Gastric intubation via the nasal passage (ie, nasogastric route) is a common procedure that provides access to the

stomach for diagnostic and therapeutic purposes. A nasogastric (NG) tube is used for the procedure. The placement of an NG tube can be uncomfortable for the patient if the patient is not adequately prepared with anesthesia to the nasal passages and specific instructions on how to cooperate with the operator during the procedure.

Indications

Diagnostic o Evaluation of upper gastrointestinal (GI) bleed (ie, presence, volume) o Aspiration of gastric fluid content o Identification of the esophagus and stomach on a chest radiograph o Administration of radiographic contrast to the GI tract Therapeutic o Gastric decompression, including maintenance of a decompressed state after endotracheal intubation, often via the oropharynx o Relief of symptoms and bowel rest in the setting of small-bowel obstruction o Aspiration of gastric content from recent ingestion of toxic material o Administration of medication o Feeding o Bowel irrigation

Contraindications

Absolute contraindications o Severe midface trauma o Recent nasal surgery Relative contraindications o Coagulation abnormality o Esophageal varices or stricture o Recent banding or cautery of esophageal varices o Alkaline ingestion

Complications
The main complications of NG tube insertion include aspiration and tissue trauma. Placement of the catheter can induce gagging or vomiting, therefore suction should always be ready to use in the case of this happening.

Universal precautions
The potential for contact with a patients blood/body fluids while starting an NG is present and increases with the inexperience of the operator. Gloves must be worn while starting an NG; and if the risk of vomiting is high, the operator should consider

face and eye protection as well as a gown. Trauma protocol calls for all team members to wear gloves, face and eye protection and gowns.

Equipment
All necessary equipment should be prepared, assembled and available at the bedside prior to starting the NG tube. Basic equipment includes:

Personal protective equipment NG/OG tube Catheter tip irrigation 60ml syringe Water-soluble lubricant, preferably 2% Xylocaine jelly Adhesive tape Low powered suction device OR Drainage bag Stethoscope Cup of water (if necessary)/ ice chips Emesis basin pH indicator strips

Procedure
1. Gather equipment. 2. Don (put on) non-sterile gloves. 3. Explain the procedure to the patient and show equipment. 4. If possible, sit patient upright for optimal neck/stomach alignment. 5. Examine nostrils for deformity/obstructions to determine best side for insertion. 6. Measure tubing from bridge of nose to earlobe, then to the point halfway between the end of the sternum and the navel. 7. Mark measured length with a marker or note the distance. 8. Lubricate 2-4 inches of tube with lubricant (preferably 2% Xylocaine). This procedure is very uncomfortable for many patients, so a squirt of Xylocaine jelly in the nostril, and a spray of Xylocaine to the back of the throat will help alleviate the discomfort. 9. Pass tube via either nare posteriorly, past the pharynx into the esophagus and then the stomach. Instruct the patient to swallow (you may offer ice chips/water) and advance the tube as the patient swallows. Swallowing of small sips of water may enhance passage of tube into esophagus.

If resistance is met, rotate tube slowly with downward advancement toward closes ear. Do not force. 10. Withdraw tube immediately if changes occur in patients respiratory status, if tube coils in mouth, if the patient begins to cough or turns pretty colors. 11. Advance tube until mark is reached. 12. Check for placement by attaching syringe to free end of the tube, aspirate sample of gastric contents. Do not inject an air bolus, as the best practice is to test the pH of the aspirated contents to ensure that the contents are acidic. The pH should be below 6. Obtain an x-ray to verify placement before instilling any feedings/medications or if you have concerns about the placement of the tube. 13. Secure tube with tape or commercially prepared tube holder. 14. If for suction, remove syringe from free end of tube; connect to suction; set machine on type of suction and pressure as prescribed. 15. Document the reason for the tube insertion, type & size of tube, the nature and amount of aspirate, the type of suction and pressure setting if for suction, the nature and amount of drainage, and the effectiveness of the intervention.

Troubleshooting
Nasal Obstruction It is important to chose the most patent side by having the patient alternatively breath through each nostril independently. The presence of polyps are generally not considered a contraindication to this procedure, but it may be made easier by the application of a topical vasoconstrictor first, allowing a minute or 2 for the medication to take effect. If the tube meets with significant obstruction, continuous, gentle pressure often allows passage. If the tube cannot be passed through either side, it may be necessary to insert the tube orally. If a tube is absolutely necessary, the oral route can be used. The technique is generally the same as for nasal insertion although greater attention to topical anesthesia is necessary as most patients find this procedure to be extremely uncomfortable. Oral tubes are generally not recommended for long term use, except in intubated patients. They may be helpful for diagnostic purposes when they can be removed in a short time. Failure of Tube to Pass Into Esophagus / Curling of the Tube Difficulty may be encountered in passing the tube from the oropharynx into the esophagus, especially if the tube tends to curl. Occasionally the NGT will curl 180 and the distal tip will protrude through the oral cavity. Several remedies are possible. Maneuvers to increase the rigidity of the tube may be employed. After several attempts at passage, NGTs tend to become more flexible, and using a new NGT may increase your chances of successful passage. Some authorities recommended cooling the NGT in an ice bath to increase rigidity. Care must be utilized when using this

technique as injuries to the soft tissues of the pharynx and esophagus are more likely with a cooled, rigid tube. Flexing the neck (in patients without cervical spine injury) brings the esophagus into a more anterior position and may facilitate passage as well. Bending the tube in the direction it will ultimately take may be helpful. The tube is inserted with the convex side up initially and then, as it reaches the lower pharynx, it is rotated 180 degrees so that the tube passes posteriorly and into the esophagus. Unconscious Patient These patients are unable to assist you by swallowing, and passage into the esophagus may be difficult. Furthermore, in the supine patient, gravity may cause the esophagus to collapse and impede passage, causing the NGT to curl. If the patient does not have intact airway reflexes, it is possible to insert a laryngoscope into the oropharynx and directly visualize the tube. This visualization alone may be enough to facilitate passage. If further manipulation is required, a Magill forceps or the operators fingers may be inserted into the posterior oral cavity to help advance the tube. Anteriorlydirected traction on the mandible (using either the jaw-thrust maneuver or gentle manual traction on the patients lower teeth and chin) will often open the esophagus and allow the tube to pass through. A variation of this technique utilizes anterior traction on the thyroid cartilage to open the esophagus. It should be noted that in the intubated patient, the Salem or Levin tube may be passed orally. Hemorrhage / Coagulopathy Bleeding disorders do not generally represent a contraindication to tube placement. However, bleeding after insertion may sometimes be significant. The likelihood of major bleeding can be diminished by application of a vasoconstrictor to the entire nasal mucosa by atomization and the waiting several minutes for the medication to take effect.

An intensive care unit, or ICU, is a specialized section of a hospital that provides comprehensive and continuous care for persons who are critically ill and who can benefit from treatment.

Purpose
The purpose of the intensive care unit (ICU) is simple even though the practice is complex. Healthcare professionals who work in the ICU or rotate through it during their training provide around-the-clock intensive monitoring and treatment of patients seven days a week. Patients are generally admitted to an ICU if they are likely to benefit from the level of care provided. Intensive care has been shown to benefit patients who are severely ill and medically unstablethat is, they have a potentially life-threatening disease or disorder.
An Intensive Care Unit (ICU) is a special facility within a hospital which is dedicated to treating patients who are critically ill. Patients in an ICU may be experiencing multiple organ failure, respiratory arrest, or other serious problems which require intensive monitoring. The ICU staff are specially trained to administer critical care, and there are sometimes several staffers to each patient to ensure that patients get the care they need. Intensive care medicine focuses on the major systems of the body, including the cardiovascular system, the gastrointestinal tract, the central nervous system, and the respiratory tract. Intensive care providers try to keep these important bodily systems running smoothly so that the patient remains stable. As the patient's underlying condition is treated, smoothly running bodily systems will greatly improve the patient's prognosis. In a very unstable patient, ICU care may require constant adjustment of medications and treatment programs, along with a very focused and dedicated staff. Patients will be moved into an ICU if it is clear that their conditions require constant and careful monitoring and adjustment. ICU staff can quickly make decisions for their patients to keep them comfortable and stable, and they have an extensive network of support staff and specialized equipment to assist them in their important work. ICU care may also be offered to some patients after surgery, especially if the surgery has been traumatic or the patient is at risk for complications.

Common equipment in an ICU includes mechanical ventilators to assist breathing through an endotracheal tube or a tracheotomy; cardiac monitors including those with telemetry; external pacemakers; defibrillators; dialysis equipment for renal problems; equipment for the constant monitoring of bodily functions; a web of intravenous lines, feeding tubes, nasogastric tubes, suction pumps, drains and catheters; and a wide

array of drugs to treat the primary condition(s) of hospitalization. Medically induced comas, analgesics, and induced sedation are common ICU tools designed to reduce pain and prevent secondary infections.

Suctioning
The upper airway warms, cleans and moistens the air we breathe. The trach tube bypasses these mechanisms, so that the air moving through the tube is cooler, dryer and not as clean. In response to these changes, the body produces more mucus. Suctioning clears mucus from the tracheostomy tube and is essential for proper breathing. Also, secretions left in the tube could become contaminated and a chest infection could develop. Avoid suctioning too frequently as this could lead to more secretion buildup.

When to suction
Suctioning is important to prevent a mucus plug from blocking the tube and stopping the patient's breathing. Suctioning should be considered

Any time the patient feels or hears mucus rattling in the tube or airway In the morning when the patient first wakes up When there is an increased respiratory rate (working hard to breathe) Before meals Before going outdoors Before going to sleep

The secretions should be white or clear. If they start to change color, (e.g. yellow, brown or green) this may be a sign of infection. If the changed color persists for more than three days or if it is difficult to keep the tracheostomy tube intact, call your surgeon's office. If there is blood in the secretions (it may look more pink than red), you should initially increase humidity and suction more gently. A Swedish or artificial nose (HME), which is a cap that can be attached to the tracheostomy tube, may help to maintain humidity. The cap contains a filter to prevent particles from entering the airway and maintains the patient's own humidity. Putting the patient in the bathroom with the door closed and shower on will increase the humidity immediately. If the patient coughs up or has bright red blood mucus suctioned, or if the patient develops a fever, call your surgeon's office immediately.

How to suction
Equipment Clean suction catheter (Make sure you have the correct size) Distilled or sterile water Normal saline Suction machine in working order Suction connection tubing Jar to soak inner cannula (if applicable) Tracheostomy brushes (to clean tracheostomy tube) Extra tracheostomy tube 1. Wash your hands. 2. Turn on the suction machine and connect the suction connection tubing to the machine. 3. Use a clean suction catheter when suctioning the patient. Whenever the suction catheter is to be reused, place the catheter in a container of distilled/sterile water and apply suction for approximately 30 seconds to clear secretions from the inside. Next, rinse the catheter with running water for a few minutes then soak in a solution of one part vinegar and one part distilled/sterile water for 15 minutes. Stir the solution frequently. Rinse the catheters in cool water and air-dry. Allow the catheters to dry in a clear container. Do not reuse catheters if they become stiff or cracked. 4. Connect the catheter to the suction connection tubing. 5. Lay the patient flat on his/her back with a small towel/blanket rolled under the shoulders. Some patients may prefer a sitting position which can also be tried. 6. Wet the catheter with sterile/distilled water for lubrication and to test the suction machine and circuit. 7. Remove the inner cannula from the tracheostomy tube (if applicable). The patient may not have an inner cannula. If that is the case, skip this step and go to number 8. a. There are different types of inner cannulas, so caregivers will need to learn the specific manner to remove their patient's. Usually rotating the inner cannula in a specific direction will remove it. b. Be careful not to accidentally remove the entire tracheostomy tube while removing the inner cannula. Often by securing one hand on the tracheostomy tube?s flange (neck plate) one can/ will prevent?accidental removal. c. Place the inner cannula in a jar for soaking (if it is disposable, then throw it out). 8. Carefully insert the catheter into the tracheostomy tube. Allow the catheter to follow the natural curvature of the tracheostomy tube. The distance to the location of catheter becomes easier to determine with experience. The least traumatic technique is to pre-measure the length of the tracheostomy tube then introduce the catheter only to that length. For example if the patient?s tracheostomy tube is 4 cm long, place the catheter 4 cm into the tracheostomy tube. Often, there will be instances when this technique of suctioning (called tip suctioning) will not clear the patient?s secretions. For those situations, the

catheter may need to be inserted several mm beyond the end of the tracheostomy tube (called deep suctioning). With experience, caregivers will be able to judge the distance to insert the tracheostomy tube without measuring. 9. Place your thumb over the suction vent (side of the catheter) intermittently while you remove the catheter. Do not leave the catheter in the tracheostomy tube for more than 5-10 seconds since the patient will not be able to breathe well with the catheter in place. 10. Allow the patient to recover from the suctioning and to catch his/her breath. Wait for at least 10 seconds. 11. Suction a small amount of distilled/sterile water with the suction catheter to clear any residual debris/secretions. 12. Insert the inner cannula from extra tracheostomy tube (if applicable). 13. Turn off suction machine and discard catheter (clean according to step 3 if to be reused). 14. Clean inner cannula (if applicable). In urinary catheterization ("cathing" for short), a latex, polyurethane or silicone tube known as a urinary catheter is inserted into a patient's bladder via his or her urethra. Catheterization allows the patient's urine to drain freely from the bladder for collection. It may be used to inject liquids used for treatment or diagnosis of bladder conditions. A clinician, often a nurse, usually performs the procedure; but selfcatheterization is also possible. The catheter may be a permanent one (indwelling catheter), or an intermittent catheter removed after each catheterization.

Catheter types
Catheters come in several basic designs:[1]

A Foley catheter (indwelling urinary catheter)is retained by means of a balloon at the tip which is inflated with sterile water. The balloons typically come in two different sizes: 5 cc and 30 cc. They are commonly made in silicone rubber or natural rubber. An intermittent catheter/Robinson catheter is a flexible catheter used for short term drainage of urine. Unlike the Foley catheter, it has no balloon on its tip and therefore cannot stay in place unaided. These can be non-coated or coated e.g. hydrophilic coated catheter that is ready to use. A Coud catheter is designed with a curved tip that makes it easier to pass through the curvature of the prostatic urethra. A hematuria (or haematuria) catheter is a type of Foley catheter used for PostTURP hemostasis. This is useful following endoscopic surgical procedures or in the case of gross hematuria. There are both 2-way and 3-way hematuria catheters (double and triple lumen).[1] An external, Texas, urisheat or condom catheter is used for incontinent males and carries a lower risk of infection than an indwelling catheter.[2]

Catheter diameters are sized by the French catheter scale (F). The most common sizes are 10 F (3.3mm) to 28 F (9.3mm). The clinician selects a size large enough to allow free flow of urine, and large enough to control leakage of urine around the catheter. A larger size can become necessary when the urine is thick, bloody or contains large amounts of sediment. Larger catheters, however, are more likely to cause damage to the urethra. Some people develop allergies or sensitivities to latex after long-term latex catheter use making it necessary to use silicone or Teflon types. Silver alloy coated urinary catheters may reduce infections.[3]

[edit] Sex differences

In males, the catheter tube is inserted into the urinary tract through the penis. A condom, urisheat or Texas catheter can also be used[clarification needed]. In females, the catheter is inserted into the urethral meatus, after a cleansing using povidone-iodine. The procedure can be complicated in females due to varying layouts of the genitalia (due to age, obesity, Female genital cutting, childbirth, or other factors), but a good clinician should rely on anatomical landmarks and patience when dealing with such a patient. In the UK it is generally accepted that cleaning the area surrounding the urethral meatus with 0.9% sodium chloride solution is sufficient for both male and female patients as there is no reliable evidence to suggest that the use of antiseptic agents reduces the risk of urinary tract infection.[4] Males may have a slightly higher incidence of Bladder Spasms. If bladder spasms occur or there is no urine in the drainage bag, the catheter may be blocked by: blood; thick sediment; a kink in the catheter or drainage tubing. Sometimes spasms are caused by the catheter irritating the bladder, prostate or penis. Such spasms can be controlled with medication such as Butylscopolamine, although most patients eventually adjust to the irritation and the spasms go away.[5] Common indications to catheterize a patient include acute or chronic urinary retention - (which can damage the kidneys), orthopedic procedures that may limit a patient's movement, the need for accurate monitoring of input and output (such as in an ICU), benign prostatic hyperplasia, incontinence, and the effects of various surgical interventions involving the bladder and prostate. For some patients the insertion and removal of a catheter causes excruciating pain, so a topical anesthetic is used. Catheterization should be performed as a sterile medical procedure and should only be done by trained, qualified personnel, using equipment designed for this purpose, except in the case of intermittent self catheterization where the patient has been trained to perform the procedure himself or herself. Intermittent self catheterization will be performed by the user 4-6 times a day using a clean technique in most cases. Nurses will use a sterile technique when performing intermittent catheterization in hospital settings. If correct technique is not used there may be trauma to the urethra or prostate (male), urinary tract infection, or a paraphimosis in the uncircumcised male. For patients with spinal cord lesions and neurogenic bladder dysfunction, intermittent catheterisation (IC) is a standard method for bladder emptying. The technique is safe and effective and results in improved kidney and upper urinary tract status, lessening of vesicoureteral reflux and amelioration of continence (Hedlund et al, 2001). In addition to the clinical benefits, patient quality of life is enhanced by the increased independence and security offered by self catheterization (Lapides et al, 1972).

[edit] Catheter maintenance

A catheter that is left in place for more than a short period of time is generally attached to a drainage bag to collect the urine. This also allows for measurement of urine volume. There are two types of drainage bags: The first is a leg bag, a smaller drainage device that attaches by elastic bands to the leg. A leg bag is usually worn during the day, as it fits discreetly under pants or skirts, and is easily emptied into a toilet. The second type of drainage bag is a larger device called a down drain that may be used overnight. This device is hung on a hook under the patient's bed - they are never to be placed on the floor due to the risk of bacterial infection. During long-term use, the catheter may be left in place during the entire time, or a patient may be instructed on a procedure for placing a catheter just long enough to empty the bladder and then removing it (known as intermittent self-catheterization). Patients undergoing major surgery are often catheterized and may remain so for some time. The patient may require irrigation of the bladder with sterile saline injected through the catheter to flush out clots or other matter that does not drain.[6]

[edit] Effects of long term use

The duration of cathetarization can have significance for the patient. Incontinent patients commonly are catheterized to reduce their cost of care. However, long-term catheterization carries a significant risk of urinary tract infection. Because of this risk catheterization is a last resort for the management of incontinence where other measures have proved unsuccessful. Other long term complications may include blood infections (sepsis), urethral injury, skin breakdown, bladder stones, and blood in the urine (hematuria). After many years of catheter use, bladder cancer may also develop.

[edit] Combating infection

Everyday care of catheter and drainage bag is important to reduce the risk of infection.[7] Such precautions include:

Cleansing the urethral area (area where catheter exits body) and the catheter itself. Disconnecting drainage bag from catheter only with clean hands Disconnecting drainage bag as seldom as possible. Keeping drainage bag connector as clean as possible and cleansing the drainage bag periodically. Use of a thin catheter where possible to reduce risk of harming the urethra during insertion. Drinking sufficient liquid to produce at least two liters of urine daily Sexual activity is very high risk for urinary infections, especially for catheterized women.

Recent developments in the field of the temporary prostatic stent have been viewed as a possible alternative to indwelling catheterization and the infections associated with their use.[8]

Universal precautions The potential for contact with a patient's blood/body fluids while starting a catheter is present and increases with the inexperience of the operator. Gloves must be worn while starting the Foley, not only to protect the user, but also to prevent infection in the patient. Trauma protocol calls for all team members to wear gloves, face and eye protection and gowns. Indications By inserting a Foley catheter, you are gaining access to the bladder and its contents. Thus enabling you to drain bladder contents, decompress the bladder, obtain a specimen, and introduce a passage into the GU tract. This will allow you to treat urinary retention, and bladder outlet obstruction. Urinary output is also a sensitive indicator of volume status and renal perfusion (and thus tissue perfusion also). In the emergency department, catheters can be used to aid in the diagnosis of GU bleeding. In some cases, as in urethral stricture or prostatic hypertrophy, insertion will be difficult and early consultation with urology is essential.

Contraindications Foley catheters are contraindicated in the presence of urethral trauma. Urethral injuries may occur in patients with multisystem injuries and pelvic factures, as well as straddle impacts. If this is suspected, one must perform a genital and rectal exam first. If one finds blood at the meatus of the urethra, a scrotal hematoma, a pelvic fracture, or a high riding prostate then a high suspicion of urethral tear is present. One must then perform retrograde urethrography (injecting 20 cc of contrast into the urethra).

Equipment Sterile gloves - consider Universal Precautions Sterile drapes Cleansing solution e.g. Savlon Cotton swabs Forceps Sterile water (usually 10 cc) Foley catheter (usually 16-18 French) Syringe (usually 10 cc) Lubricant (water based jelly or xylocaine jelly) Collection bag and tubing

Complications The main complications are tissue trauma and infection. After 48 hours of catheterization, most catheters are colonized with bacteria, thus leading to possible bacteruria and its complications. Catheters can also cause renal inflammation, nephro-cysto-lithiasis, and pyelonephritis if left in for prolonged periods. The most common short term complications are inability to insert catheter, and causation of tissue trauma during the insertion. The alternatives to urethral catheterization include suprapubic catheterization and external condom catheters for longer durations.

Endotracheal intubation
URL of this page: http://www.nlm.nih.gov/medlineplus/ency/article/003449.htm

Endotracheal intubation is a medical procedure in which a tube is placed into the windpipe (trachea), through the mouth or the nose. In most emergency situations it is placed through the mouth. See also: Bronchoscopy, Tracheostomy

Why the Test is Performed

Endotracheal intubation is done to open the airway to give oxygen, medication, or anesthesia, and to help with breathing. It may also be done to remove blockages (foreign bodies) from the airway or to allow the doctor to get a better view of the upper airway.

Risks
Risks for any surgery are:

Bleeding Infection

Additional risks for this procedure include trauma to the voice box (larynx), thyroid gland, vocal cords and trachea (windpipe), or esophagus. Puncture or perforation (tearing) of body parts in the chest cavity, leading to lung collapse, may also occur.

Considerations

After endotracheal intubation, you will likely be placed on a respirator, which is a machine that breathes for you while the tube is in place.

Specifically, endotracheal intubation is used for the following conditions:

respiratory arrest respiratory failure airway obstruction need for prolonged ventilatory support Class III or IV hemorrhage with poor perfusion severe flail chest or pulmonary contusion multiple trauma, head injury and abnormal mental status inhalation injury with erythema/edema of the vocal cords protection from aspiration

Read more: Endotracheal Intubation - procedure, tube, pain, complications, Definition, Purpose, Description, Preparation, Risks, Normal results, Alternatives http://www.surgeryencyclopedia.com/Ce-Fi/EndotrachealIntubation.html#ixzz1PiiI5mf0

Description
To begin the procedure, an anesthesiologist opens the patient's mouth by separating the lips and pulling on the upper jaw with the index finger. Holding a laryngoscope in the left hand, he or she inserts it into the mouth of the patient with the blade directed to the right tonsil. Once the right tonsil is reached, the laryngoscope is swept to the midline, keeping the tongue on the left to bring the epiglottis into view. The laryngoscope blade is then advanced until it reaches the angle between the base of the tongue and the epiglottis. Next, the laryngoscope is lifted upwards towards the chest and away from the nose to bring the vocal cords into view. Often an assistant has to press on the trachea to provide a direct view of the larynx. The anesthesiologist then takes the endotracheal tube, made of flexible plastic, in the right hand and starts

inserting it through the mouth opening. The tube is inserted through the cords to the point that the cuff rests just below the cords. Finally, the cuff is inflated to provide a minimal leak when the bag is squeezed. Using a stethoscope , the anesthesiologist listens for breathing sounds to ensure correct placement of the tube.

Preparation
For endotracheal intubation, the patient is placed on the operating table lying on the back with a pillow under the head. The anesthesiologist wears gloves, a gown and goggles. General anesthesia is administered to the patient before starting intubation.

Risks
The anesthesiologist should evaluate and follow the patient for potential complications that may include edema; bleeding; tracheal and esophageal perforation; pneumothorax (collapsed lung); and aspiration. The patient should be advised of the potential signs and symptoms associated with lifethreatening complications of airway problems. These signs and symptoms include but are not limited to sore throat, pain or swelling of the face and neck, chest pain, subcutaneous emphysema, and difficulty swallowing.

Normal results
The endotracheal tube inserted during the procedure maintains an open passage through the upper airway and allows air to pass freely to and from the lungs in order to ventilate them.

Alternatives
Alternatives to endotracheal intubation include:

Esophageal tracheal combitube (ETC). The ETC is a double-lumen tube, combining the function of an esophageal obturator airway and a conventional endotracheal airway. The esophageal lumen has an open upper end, perforations at the pharyngeal level, and a closed distal end. The tracheal lumen has open ends. The lumens are separated by a wall and each is linked via a short tube with a connector. An oropharyngeal balloon serves to seal the oral and nasal cavities after

Read more: Endotracheal Intubation - procedure, tube, pain, complications, Definition, Purpose, Description, Preparation, Risks, Normal results, Alternatives http://www.surgeryencyclopedia.com/Ce-Fi/EndotrachealIntubation.html#ixzz1PiiSLfDU

The doctor inserts the laryngoscope into the patient's mouth, advancing through the trachea to the vocal cords (A). An

endotracheal tube is inserted into the airway (B). The balloon cuff is inflated, and the laryngoscope is removed (C). ( Illustration by GGS Inc. ) insertion. At the lower end, a second cuff serves to seal either the trachea or esophagus. Laryngeal mask airway (LMA). The LMA consists of an inflatable silicone ring attached diagonally to a flexible tube. The ring forms an oval cushion that fills the space around and behind the larynx. It achieves a low-pressure seal between the tube and the trachea without insertion into the larynx. Tracheostomy. A tracheostomy is a surgically created opening in the neck that allows direct access to the trachea. It is kept open with a tracheostomy tube. A tracheostomy is performed when it is not possible to intubate the patient. Read more: Endotracheal Intubation - procedure, tube, pain, complications, Definition, Purpose, Description, Preparation, Risks, Normal results, Alternatives http://www.surgeryencyclopedia.com/Ce-Fi/EndotrachealIntubation.html#ixzz1PiiiHNpT

Electrocardiography
From Wikipedia, the free encyclopedia

Jump to: navigation, search "ECG" redirects here. For other uses, see ECG (disambiguation). Not to be confused with echocardiogram, electromyogram, electroencephalogram, or EEG.

Electrocardiography
Intervention

Image showing a patient connected to the 10 electrodes necessary for a 12-lead ECG ICD-9-CM MeSH 89.52 D004562

12 Lead ECG of a 26-year-old male. Electrocardiograph (ECG or EKG [from the German Elektrokardiogramm]) is a transthoracic interpretation of the electrical activity of the heart over time captured and externally recorded by skin electrodes.[1] It is a noninvasive recording produced by an electrocardiographic device. The etymology of the word is derived from the Greek electro, because it is related to electrical activity, cardio, Greek for heart, and graph, a Greek root meaning "to write". In English speaking countries, medical professionals often write EKG (the abbreviation for the German word elektrokardiogramm) in order to avoid confusion with EEG.[citation needed] The ECG works mostly by detecting and amplifying the tiny electrical changes on the skin that are caused when the heart muscle "depolarizes" during each heart beat. At rest, each heart muscle cell has a charge across its outer wall, or cell membrane. Reducing this charge towards zero is called de-polarization, which activates the

mechanisms in the cell that cause it to contract. During each heartbeat a healthy heart will have an orderly progression of a wave of depolarisation that is triggered by the cells in the sinoatrial node, spreads out through the atrium, passes through "intrinsic conduction pathways" and then spreads all over the ventricles. This is detected as tiny rises and falls in the voltage between two electrodes placed either side of the heart which is displayed as a wavy line either on a screen or on paper. This display indicates the overall rhythm of the heart and weaknesses in different parts of the heart muscle. Usually more than 2 electrodes are used and they can be combined into a number of pairs (For example: Left arm (LA), right arm (RA) and left leg (LL) electrodes form the three pairs LA+RA, LA+LL, and RA+LL). The output from each pair is known as a lead. Each lead is said to look at the heart from a different angle. Different types of ECGs can be referred to by the number of leads that are recorded, for example 3-lead, 5-lead or 12-lead ECGs (sometimes simply "a 12-lead"). A 12-lead ECG is one in which 12 different electrical signals are recorded at approximately the same time and will often be used as a one-off recording of an ECG, traditionally printed out as a paper copy. 3- and 5-lead ECGs tend to be monitored continuously and viewed only on the screen of an appropriate monitoring device, for example during an operation or whilst being transported in an ambulance. There may or may not be any permanent record of a 3- or 5-lead ECG, depending on the equipment used. It is the best way to measure and diagnose abnormal rhythms of the heart,[2] particularly abnormal rhythms caused by damage to the conductive tissue that carries electrical signals, or abnormal rhythms caused by electrolyte imbalances.[3] In a myocardial infarction (MI), the ECG can identify if the heart muscle has been damaged in specific areas, though not all areas of the heart are covered.[4] The ECG cannot reliably measure the pumping ability of the heart, for which ultrasound-based (echocardiography) or nuclear medicine tests are used. It is possible to be in cardiac arrest with a normal ECG signal (a condition known as pulseless electrical activity). 1.

Instructions
Things You'll Need

ECG machine Electrode tabs

1.
o

Place your fingers at the top of the sternum and run them down until you reach a boney lump. This is the angle of Louis. Move your fingers into the rib space on the right side of this point.

2 3 4 5 6 7 8 9 10

Move down two rib spaces to the fourth intercostal space and place the first electrode tab. This is V1.

Locate the fourth intercostal space on the left side of the sternum and place the tab for V2.

Slip your fingers down into the fifth intercostal space and line them up with the middle of the left clavicle, mid-clavicular line. Place the V4 tab here.

Place the V3 tab midway between V2 and V4.

Run your fingers along the fifth intercostal space to the beginning of the axilla. This is in line with the front of the shoulder. V5 will be placed here.

Follow further around the fifth intercostal space to the mid-axilla, or middle of the armpit. Place the V6 tab here.

Place the tab for aVR on the right wrist, tab for aVL on the left wrist and tab for aVF on the left foot.

Stick a tab for the N lead on the right foot.

Connect the corresponding wires from the ECG machine to the respective tabs.

Read more: Correct ECG Lead Placement | eHow.com http://www.ehow.com/how_6576094_correct-ecg-leadplacement.html#ixzz1PijoQZM9

Layout
By definition, a 12-lead ECG will show a short segment of the recording of each of the 12-leads. This is often arranged in a grid of 4 columns by three rows, the first columns being the limb leads (I,II and III), the second column the augmented limb leads (aVR, aVL and aVF) and the last two columns being the chest leads (V1-V6). It is usually possible to change this layout so it is vital to check the labels to see which lead is represented. Each column will usually record the same moment in time for the three leads and then the recording will switch to the next column which will record the heart beats after that point. It is possible for the heart rhythm to change between the columns of leads. Each of these segments is short, perhaps 1-3 heart beats only, depending on the heart rate and it can be difficult to analyse any heart rhythm that shows changes between heart beats. To help with the analysis it is common to print one or two "rhythm strips" as well. This will usually be lead II (which shows the electrical signal from the atrium, the P-wave, well) and shows the rhythm for the whole time the ECG was recorded (usually 56 seconds). Some ECG machines will print a second lead II along the very bottom of the paper in addition to the output described above. This printing of Lead II is continuous from start to finish of the process. The term "rhythm strip" may also refer to the whole printout from a continuous monitoring system which may show only one lead and is either initiated by a clinician or in response to an alarm or event.

[edit] Leads
The term "lead" in electrocardiography causes much confusion because it is used to refer to two different things. In accordance with common parlance the word lead may be used to refer to the electrical cable attaching the electrodes to the ECG recorder. As such it may be acceptable to refer to the "left arm lead" as the electrode (and its cable) that should be attached at or near the left arm. There are usually ten of these electrodes in a standard "12-lead" ECG. Alternatively (and some would say properly, in the context of electrocardiography) the word lead may refer to the tracing of the voltage difference between two of the electrodes and is what is actually produced by the ECG recorder. Each will have a specific name. For example "Lead I" (lead one) is the voltage between the right arm electrode and the left arm electrode, whereas "Lead II" (lead two) is the voltage between the right limb and the feet. (This rapidly becomes more complex as one of the "electrodes" may in fact be a composite of the electrical signal from a combination of the other electrodes (see later). Twelve of this type of lead form a "12-lead" ECG

To cause additional confusion the term "limb leads" usually refers to the tracings from leads I, II and III rather than the electrodes attached to the limbs.

[edit] Placement of electrodes

Ten electrodes are used for a 12-lead ECG. The electrodes usually consist of a conducting gel, embedded in the middle of a self-adhesive pad onto which cables clip. Sometimes the gel also forms the adhesive.[12] They are labeled and placed on the patient's body as follows:[13][14]

Proper placement of the limb electrodes, color coded as recommended by the American Heart Association (a different colour scheme is used in Europe). Note that the limb electrodes can be far down on the limbs or close to the hips/shoulders, but they must be even (left vs right).[15] . * Note that when exercise stress tests are performed, limb leads may be placed on the trunk to avoid aftifact while ambulatory (arm leads moved sub-clavicularly and leg leads medial to and above the iliac crest).

12 leads Electrode label (in the USA) RA LA RL LL V1 V2 V3 V4

Electrode placement On the right arm, avoiding thick muscle. In the same location that RA was placed, but on the left arm. On the right leg, lateral calf muscle In the same location that RL was placed, but on the left leg. In the fourth intercostal space (between ribs 4 & 5) just to the right of the sternum (breastbone). In the fourth intercostal space (between ribs 4 & 5) just to the left of the sternum. Between leads V2 and V4. In the fifth intercostal space (between ribs 5 & 6) in the mid-clavicular line (the imaginary line that extends down from the midpoint of the

V5

V6

clavicle (collarbone)). Horizontally even with V4, but in the anterior axillary line. (The anterior axillary line is the imaginary line that runs down from the point midway between the middle of the clavicle and the lateral end of the clavicle; the lateral end of the collarbone is the end closer to the arm.) Horizontally even with V4 and V5 in the midaxillary line. (The midaxillary line is the imaginary line that extends down from the middle of the patient's armpit.)

[edit] Additional electrodes

The classical 12-lead ECG can be extended in a number of ways in an attempt to improve its sensitivity in detecting myocardial infarction involving territories not normally "seen" well. This includes an rV4 lead which uses the equivalent landmarks to the V4 but on the right side of the chest wall and extending the chest leads onto the back with a V7, V8 and V9.

[edit] Limb leads

In both the 5- and 12-lead configuration, leads I, II and III are called limb leads. The electrodes that form these signals are located on the limbsone on each arm and one on the left leg.[16][17][18] The limb leads form the points of what is known as Einthoven's triangle.[19]

Lead I is the voltage between the (positive) left arm (LA) electrode and right arm (RA) electrode:

I = LA RA.

Lead II is the voltage between the (positive) left leg (LL) electrode and the right arm (RA) electrode:

II = LL RA.

Lead III is the voltage between the (positive) left leg (LL) electrode and the left arm (LA) electrode:

III = LL LA.
Simplified electrocardiograph sensors designed for teaching purposes at e.g. high school level are generally limited to three arm electrodes serving similar purposes.[20]

[edit] Unipolar vs. bipolar leads

There are two types of leads: unipolar and bipolar. Bipolar leads have one positive and one negative pole.[21] In a 12-lead ECG, the limb leads (I, II and III) are bipolar leads. Unipolar leads also have two poles, as a voltage is measured; however, the negative pole is a composite pole (Wilson's central terminal, or WCT) made up of

signals from lots of other electrodes.[22] In a 12-lead ECG, all leads besides the limb leads are unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6). Wilson's central terminal VW is produced by connecting the electrodes, RA; LA; and LL, together, via a simple resistive network, to give an average potential across the body, which approximates the potential at infinity (i.e. zero):

[edit] Augmented limb leads

Leads aVR, aVL, and aVF are augmented limb leads (after their inventor Dr. Emanuel Goldberger known collectively as the Goldberger's leads). They are derived from the same three electrodes as leads I, II, and III. However, they view the heart from different angles (or vectors) because the negative electrode for these leads is a modification of Wilson's central terminal. This zeroes out the negative electrode and allows the positive electrode to become the "exploring electrode". This is possible because Einthoven's Law states that I + (II) + III = 0. The equation can also be written I + III = II. It is written this way (instead of I II + III = 0) because Einthoven reversed the polarity of lead II in Einthoven's triangle, possibly because he liked to view upright QRS complexes. Wilson's central terminal paved the way for the development of the augmented limb leads aVR, aVL, aVF and the precordial leads V1, V2, V3, V4, V5 and V6.

Lead augmented vector right (aVR) has the positive electrode (white) on the right arm. The negative electrode is a combination of the left arm (black) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the right arm:

Lead augmented vector left (aVL) has the positive (black) electrode on the left arm. The negative electrode is a combination of the right arm (white) electrode and the left leg (red) electrode, which "augments" the signal strength of the positive electrode on the left arm:

Lead augmented vector foot (aVF) has the positive (red) electrode on the left leg. The negative electrode is a combination of the right arm (white) electrode and the left arm (black) electrode, which "augments" the signal of the positive electrode on the left leg:

The augmented limb leads aVR, aVL, and aVF are amplified in this way because the signal is too small to be useful when the negative electrode is Wilson's central terminal. Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of the hexaxial reference system, which is used to calculate the heart's electrical axis in the frontal plane. The aVR, aVL, and aVF leads can also be represented using the I and II limb leads:

[edit] Precordial leads

The electrodes for the precordial leads (V1, V2, V3, V4, V5 and V6) are placed directly on the chest. Because of their close proximity to the heart, they do not require augmentation. Wilson's central terminal is used for the negative electrode, and these leads are considered to be unipolar (recall that Wilson's central terminal is the average of the three limb leads. This approximates common, or average, potential over the body). The precordial leads view the heart's electrical activity in the so-called horizontal plane. The heart's electrical axis in the horizontal plane is referred to as the Z axis.

[edit] Waves and intervals

Schematic representation of normal ECG

Animation of a normal ECG wave.

Detail of the QRS complex, showing ventricular activation time (VAT) and amplitude. A typical ECG tracing of the cardiac cycle (heartbeat) consists of a P wave, a QRS complex, a T wave, and a U wave which is normally visible in 50 to 75% of ECGs.[23] The baseline voltage of the electrocardiogram is known as the isoelectric line. Typically the isoelectric line is measured as the portion of the tracing following the T wave and preceding the next P wave. Feature Description RR The interval between an R wave and the next R wave . interval Normal resting heart rate is between 60 and 100 bpm Duration 0.6 to 1.2s

P wave

PR interval

PR segment

QRS complex J-point ST segment

T wave

ST interval QT interval

U wave

J wave

During normal atrial depolarization, the main electrical vector is directed from the SA node towards the AV node, 80ms and spreads from the right atrium to the left atrium. This turns into the P wave on the ECG. The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. The PR interval reflects the time the electrical impulse takes to travel from the 120 to 200ms sinus node through the AV node and entering the ventricles. The PR interval is therefore a good estimate of AV node function. The PR segment connects the P wave and the QRS complex. This coincides with the electrical conduction from the AV node to the bundle of His to the bundle branches and then to the Purkinje Fibers. This electrical activity does not produce 50 to 120ms a contraction directly and is merely traveling down towards the ventricles and this shows up flat on the ECG. The PR interval is more clinically relevant. The QRS complex reflects the rapid depolarization of the right and left ventricles. They have a large muscle mass 80 to 120ms compared to the atria and so the QRS complex usually has a much larger amplitude than the P-wave. The point at which the QRS complex finishes and the ST segment begins. Used to measure the degree of ST elevation N/A or depression present. The ST segment connects the QRS complex and the T wave. The ST segment represents the period when the ventricles are 80 to 120ms depolarized. It is isoelectric. The T wave represents the repolarization (or recovery) of the ventricles. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the 160ms absolute refractory period. The last half of the T wave is referred to as the relative refractory period (or vulnerable period). The ST interval is measured from the J point to the end of the 320ms T wave. The QT interval is measured from the beginning of the QRS complex to the end of the T wave. A prolonged QT interval is 300 to a risk factor for ventricular tachyarrhythmias and sudden 430ms[citation needed] death. It varies with heart rate and for clinical relevance requires a correction for this, giving the QTc. The U wave is hypothesized to be caused by the repolarization of the interventricular septum. They normally have a low amplitude, and even more often completely absent. They always follow the T wave and also follow the same direction in amplitude. If they are too prominent we suspect hypokalemia, hypercalcemia or hyperthyroidism usually. [24] The J wave, elevated J-Point or Osborn Wave appears as a late delta wave following the QRS or as a small secondary R

wave . It is considered pathognomonic of hypothermia or hypocalcemia.[25] There were originally four deflections, but after the mathematical correction for artifacts introduced by early amplifiers, five deflections were discovered. Einthoven chose the letters P, Q, R, S, and T to identify the tracing which was superimposed over the uncorrected labeled A, B, C, and D.[26] In intracardiac electrocardiograms, such as can be acquired from pacemaker sensors, an additional wave that can be seen is the H deflection, which reflects the depolarization of the bundle of His.[27] The H-V interval, in turn, is the duration from the beginning of the H deflection to the earliest onset of ventricular depolarization recorded in any lead.[28]

[edit] Vectors and views

Graphic showing the relationship between positive electrodes, depolarization wavefronts (or mean electrical vectors), and complexes displayed on the ECG. Interpretation of the ECG relies on the idea that different leads (by which we mean the ECG leads I,II,III, aVR, aVL, aVF and the chest leads) "view" the heart from different angles. This has two benefits. Firstly, leads which are showing problems (for example ST segment elevation) can be used to infer which region of the heart is affected. Secondly, the overall direction of travel of the wave of depolarisation can also be inferred which can reveal other problems. This is termed the cardiac axis . Determination of the cardiac axis relies on the concept of a vector which describes the motion of the depolarisation wave. This vector can then be described in terms of its components in relation to the direction of the lead considered. One component will be in the direction of the lead and this will be revealed in the behaviour of the QRS complex and one component will be at 90 degrees to this (which will not). Any net positive deflection of the QRS complex (i.e. height of the R-wave minus depth of the S-wave) suggests that the wave of depolarisation is spreading through the heart in a direction that has some component (of the vector) in the same direction as the lead in question.

[edit] Axis

Diagram showing how the polarity of the QRS complex in leads I, II, and III can be used to estimate the heart's electrical axis in the frontal plane. The heart's electrical axis refers to the general direction of the heart's depolarization wavefront (or mean electrical vector) in the frontal plane. With a healthy conducting system the cardiac axis is related to where the major muscle bulk of the heart lies. Normally this is the left ventricle with some contribution from the right ventricle. It is usually oriented in a right shoulder to left leg direction, which corresponds to the left inferior quadrant of the hexaxial reference system, although 30 to +90 is considered to be normal. If the left ventricle increases its activity or bulk then there is said to be "left axis deviation" as the axis swings round to the left beyond -30, alternatively in conditions where the right ventricle is strained or hypertrophied then the axis swings round beyond +90 and "right axis deviation" is said to exist. Disorders of the conduction system of the heart can disturb the electrical axis without necessarily reflecting changes in muscle bulk. Normal 30 to Normal 90 May indicate left anterior 30 to fascicular block or Q waves 90 from inferior MI. Normal

Left axis deviation is Left axis considered normal in pregnant deviation women and those with emphysema. May indicate left posterior Right deviation is considered Right axis +90 to fascicular block, Q waves from normal in children and is a deviation +180 high lateral MI, or a right standard effect of ventricular strain pattern. dextrocardia. Extreme right +180 Is rare, and considered an axis deviation to 90 'electrical no-man's land'.

The hexaxial reference system showing the orientation of each lead. For example, if the bulk of heart muscle is oriented at +60 degrees with respect to the SA node, lead II will show the greatest deflection and aVL the least. In the setting of right bundle branch block, right or left axis deviation may indicate bifascicular block.

[edit] Clinical lead groups

There are twelve leads in total, each recording the electrical activity of the heart from a different perspective, which also correlate to different anatomical areas of the heart for the purpose of identifying acute coronary ischemia or injury. Two leads that look at neighbouring anatomical areas of the heart are said to be contiguous (see color coded chart). The relevance of this is in determining whether an abnormality on the ECG is likely to represent true disease or a spurious finding.

Diagram showing the contiguous leads in the same color Color on Category Leads Activity chart Leads II, Inferior Look at electrical activity from the vantage point of Yellow III and leads the inferior surface (diaphragmatic surface of heart). aVF Look at the electrical activity from the vantage point of the lateral wall of left ventricle.

Lateral leads

Green

I, aVL, V5 and V6

The positive electrode for leads I and aVL should be located distally on the left arm and because of which, leads I and aVL are sometimes referred to as the high lateral leads.

Septal leads Anterior leads

Orange Blue

Because the positive electrodes for leads V5 and V6 are on the patient's chest, they are sometimes referred to as the low lateral leads. Look at electrical activity from the vantage point of V1 and V2 the septal wall of the ventricles (interventricular septum). Look at electrical activity from the vantage point of V3 and V4 the anterior surface of the heart (sternocostal surface of heart).

In addition, any two precordial leads that are next to one another are considered to be contiguous. For example, even though V4 is an anterior lead and V5 is a lateral lead, they are contiguous because they are next to one another.

Wiggers diagram, showing a normal ECG curve synchronized with other major events during the cardiac cycle. Lead aVR offers no specific view of the left ventricle. Rather, it views the inside of the endocardial wall to the surface of the right atrium, from its perspective on the right shoulder.

[edit] Filter selection

Modern ECG monitors offer multiple filters for signal processing. The most common settings are monitor mode and diagnostic mode. In monitor mode, the low frequency filter (also called the high-pass filter because signals above the threshold are allowed to pass) is set at either 0.5 Hz or 1 Hz and the high frequency filter (also called the low-pass filter because signals below the threshold are allowed to pass) is set at 40 Hz. This limits artifact for routine cardiac rhythm monitoring. The high-pass filter helps reduce wandering baseline and the low-pass filter helps reduce 50 or 60 Hz power line noise (the power line network frequency differs between 50 and 60 Hz in different countries). In diagnostic mode, the high-pass filter is set at 0.05 Hz, which allows accurate ST segments to be recorded. The low-pass filter is set to 40, 100, or 150 Hz. Consequently, the monitor mode ECG display is more filtered than diagnostic mode, because its passband is narrower.[29]

[edit] Indications
Symptoms generally indicating use of electrocardiography include:

Cardiac murmurs [30] Syncope or collapse[30] Seizures[30] Perceived cardiac dysrhythmias[30] Symptoms of myocardial infarction. See Electrocardiography in myocardial infarction

It is also used to assess patients with systemic disease as well as monitoring during anesthesia and critically ill patients
A defibrillator is a machine used to shock the victim's heart and restore the heart's normal rythmic patterns. When a defibrillator is used, it in effect kicks the heart into action again, causing it to resume sending blood throughout the body.

Defibrillation is a common treatment for life-threatening cardiac arrhythmias, ventricular fibrillation and pulseless ventricular tachycardia. Defibrillation consists of delivering a therapeutic dose of electrical energy to the affected heart with a device called a defibrillator. This depolarizes a critical mass of the heart muscle, terminates the arrhythmia, and allows normal sinus rhythm to be reestablished by the body's natural pacemaker, in the sinoatrial node of the heart. Defibrillators can be external, transvenous, or implanted, depending on the type of device used or needed. Some external units, known as automated external defibrillators (AEDs), automate the diagnosis of treatable rhythms, meaning that lay responders or bystanders are able to use them successfully with little, or in some cases no training at all.

Placement

Anterio-apical placement of external defibrillator electrodes (When defibrillation is unsuccessful, anterior-posterior placement is also sometimes attempted) Resuscitation electrodes are placed according to one of two schemes. The anteriorposterior scheme (conf. image) is the preferred scheme for long-term electrode placement. One electrode is placed over the left precordium (the lower part of the chest, in front of the heart). The other electrode is placed on the back, behind the heart in the region between the scapula. This placement is preferred because it is best for non-invasive pacing. The anterior-apex scheme can be used when the anterior-posterior scheme is inconvenient or unnecessary. In this scheme, the anterior electrode is placed on the right, below the clavicle. The apex electrode is applied to the left side of the patient, just below and to the left of the pectoral muscle. This scheme works well for defibrillation and cardioversion, as well as for monitoring an ECG The cardiac monitor is a device that shows the electrical and pressure waveforms of the cardiovascular system for measurement and treatment. Parameters specific to respiratory function can also be measured. Because electrical connections are made between the cardiac monitor and the patient, it is kept at the patient's bedside.

Purpose
The cardiac monitor continuously displays the cardiac electrocardiogram (EKG) tracing. Additional monitoring components allow cardiovascular

pressures and cardiac output to be monitored and displayed as required for patient diagnosis and treatment. Oxygen saturation of the arterial blood can also be monitored continuously. Most commonly used in emergency rooms and critical care areas, bedside monitors can be interconnected to allow for continual observation of several patients from a central display. Continuous cardiovascular and pulmonary monitoring allows for prompt identification and initiation of treatment.

Description
The monitor provides a visual display of many patient parameters. It can be set to sound an alarm if any parameter changes outside of an expected range determined by the physician. Parameters to be monitored may include, but are not limited to, electrocardiogram, noninvasive blood pressure, intravascular pressures, cardiac output, arterial blood oxygen saturation, and blood temperature. Equipment required for continuous cardiac monitoring includes the cardiac monitor, cables, and disposable supplies such as electrode patches, pressure transducers, a pulmonary artery catheter (Swan-Ganz catheter), and an arterial blood saturation probe.

Preparation
As the cardiac monitor is most commonly used to monitor electrical activity of the heart, the patient can expect the following preparations. The sites selected for electrode placement on the skin will be shaved and cleaned causing surface abrasion for better contact between the skin and electrode. The electrode will have a layer of gel protected by a film, which is removed prior to placing the electrode to the skin. Electrode patches will be placed near or on the right arm, right leg, left arm, left leg, and the center left side of the chest. The cable will be connected to the electrode patches for the measurement of a five-lead electrocardiogram. Additional configurations are referred to as three-lead and

12-lead electrocardiograms. If noninvasive blood pressure is being measured, a blood pressure cuff will be placed around the patient's arm or leg. The blood pressure cuff will be set to inflate manually or automatically. If manual inflation is chosen, the cuff will only inflate at the prompting of the health care provider, after which a blood pressure will be displayed. During automatic operation, the blood pressure cuff will inflate at timed intervals and the display will update at the end of each measurement. Disposable pressure transducers require a reference to atmosphere, called zeroing, which is completed before monitoring patient pressures. This measurement will

Cardiac monitors display such vital signs as heart rate, pulse, and blood pressure for patients in the intensive care unit. ( Photograph by Hank Morgan. Science Source/Photo Researchers. Reproduced by permission. ) occur once the patient is comfortably positioned since the transducer must be level with the measurement point. The pressure transducer will then be connected to the indwelling catheter. It may be necessary for as many as four or five pressure transducers to be connected to the patient. The arterial blood saturation probe will be placed on the finger, toe, ear, or nasal septum of the patient, providing as little discomfort as possible, while achieving a satisfactory measurement.

Aftercare

After connecting all equipment, the health care provider will observe the monitor and evaluate the quality of the tracings, while making size and position adjustments as needed. The provider will confirm that the monitor is detecting each heartbeat by taking an apical pulse and comparing the pulse to the digital display. The upper and lower alarm limits should be set according to physician orders, and the alarm activated. A printout may be recorded for the medical record, and labeled with patient name, room number, date, time, and interpretation of the strip. Maintenance and replacement of the disposable components may be necessary as frequently as every eight hours, or as required to maintain proper operation. The arterial saturation probe can be repositioned to suit patient comfort and to obtain a tracing. All connections will be treated in a gentle manner to avoid disruption of the signal and to avoid injury to the patient.

Normal results
The monitor will provide waveforms and/or numeric values associated with the patient status. These may include, but are not limited to, heart rate, arterial blood pressure, central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, left atrial pressure, cardiac output, arterial blood saturation, and blood temperature. Furthermore, these values can be used to calculate other values, or parameters, or used to diagnose and treat the patient's condition. Patient movement may cause measurement errors; the patient will be requested to remain motionless. Depending on the mobility of the patient, assistance should be provided by the health care provider prior to changing from a laying down position to sitting or standing. As the patient's condition improves, the amount of monitoring equipment may be decreased. However, the electrocardiogram and arterial blood saturation probe should be expect to remain attached until discharge is imminent.

Read more: Cardiac Monitor - blood, time, operation, heart, rate, Definition, Purpose, Description, Preparation, Aftercare, Normal results http://www.surgeryencyclopedia.com/A-Ce/CardiacMonitor.html#ixzz1Piruu49k An infusion pump infuses fluids, medication or nutrients into a patient's circulatory system. It is generally used intravenously, although subcutaneous, arterial and epidural infusions are occasionally used. Infusion pumps can administer fluids in ways that would be impractically expensive or unreliable if performed manually by nursing staff. For example, they can administer as little as 0.1 mL per hour injections (too small for a drip), injections every minute, injections with repeated boluses requested by the patient, up to maximum number per hour (e.g. in patient-controlled analgesia), or fluids whose volumes vary by the time of day. Because they can also produce quite high but controlled pressures, they can inject controlled amounts of fluids subcutaneously (beneath the skin), or epidurally (just within the surface of the central nervous system- a very popular local spinal anesthesia for childbirth). A syringe driver or syringe pump is a small infusion pump (some include infuse and withdraw capability), used to gradually administer small amounts of fluid (with or without medication) to a patient or for use in chemical and biomedical research. The most popular use of syringe drivers is in palliative care, to continuously administer analgesics (painkillers), antiemetics (medication to suppress nausea and vomiting) and other drugs. This prevents periods during which medication levels in the blood are too high or too low, and avoids the use of multiple tablets (especially in people who have difficulty swallowing). As the medication is administered subcutaneously, the area for administration is practically limitless, although edema may interfere with the action of some drugs. Syringe drivers are also useful for delivering IV medications over several minutes. In the case of a medication which should be slowly pushed in over the course of several minutes, this device saves staff time and reduces errors. Syringe pumps are also useful in microfluidic applications, such as microreactor design and testing, and also in chemistry for slow incorporation of a fixed volume of fluid into a solution. In enzyme kinetics syringe drivers can be used to observe rapid kinetics as part of a stopped-flow apparatus.[1] Cardiopulmonary resuscitation (CPR) is an emergency procedure which is performed in an effort to manually preserve intact brain function until further

measures are taken to restore spontaneous blood circulation and breathing in a person in cardiac arrest. It is indicated in those who are unresponsive with no breathing or abnormal breathing, for example agonal respirations. It may be performed both in and outside of a hospital. CPR involves chest compressions at least 5 cm deep and at a rate of at least 100 per minute in an effort to create artificial circulation by manually pumping blood through the heart. In addition, the rescuer may provide breaths by either exhaling into the subject's mouth or utilizing a device that pushes air into the subject's lungs. This process of externally providing ventilation is termed artificial respiration. Current recommendations place emphasis on high-quality chest compressions over artificial respiration; a simplified CPR method involving chest compressions only is recommended for untrained rescuers. CPR alone is unlikely to restart the heart; its main purpose is to restore partial flow of oxygenated blood to the brain and heart. The objective is to delay tissue death and to extend the brief window of opportunity for a successful resuscitation without permanent brain damage. Administration of an electric shock to the subject's heart, termed defibrillation, is usually needed in order to restore a viable or "perfusing" heart rhythm. Defibrillation is only effective for certain heart rhythms, namely ventricular fibrillation or pulseless ventricular tachycardia, rather than asystole or pulseless electrical activity. CPR may succeed in inducing a heart rhythm which maybe shockable. CPR is generally continued until the subject regains return of spontaneous circulation (ROSC) or is declared dead. CPR is indicated for any person who is unresponsive with no breathing, or who is only breathing in occasional agonal gasps, as it is most likely that they are in cardiac arrest.[1]:S643 If a person still has a pulse, but is not breathing (respiratory arrest), artificial respirations may be more appropriate, but due to the difficulty people have in accurately assessing the presence or absence of a pulse, CPR guidelines recommend that lay persons should not be instructed to check the pulse, while giving health care professionals the option to check a pulse.[2] In those with cardiac arrest due to trauma CPR is considered futile but still recommended.[3]

Standard
A universal compression to ventilation ratio of 30:2 is recommended for adult and in children and infant if only a single rescuer is present.[5]:8 If at least 2 rescuers are present a ratio of 15:2 is preferred in children and infants.[5]:8 In newborns a rate of 3:1 is recommended unless a cardiac cause is known in which case a 15:2 ratio is reasonable.[1]:S647 If an advanced airway such as an endotracheal tube or laryngeal mask airway is in place delivery of respirations should occur without pauses in compressions at a rate of 8-10 per minute.[6] The recommended order of interventions is chest compressions, airway, breathing or CAB in most situations.[1]:S642 With a compression rate of at least 100 per minute in all groups.[5]:8 Recommended compression depth in adults and children is about 5 cm (2 inches) and in infants it is 4 cm (1.5 inches.[5]:8 As of 2010 the Resuscitation Council (UK) still recommends ABC for children.[7] As it can be difficult to determine the presence or absence of a pulse the pulse check has been removed for lay providers and should not be performed for more than 10 seconds by health care providers.[5]:8 In adults rescuers

should use two hands for the chest compressions, while in children they should use one, and with infants two fingers (index and middle fingers).[8]

[edit] Compression only

Compression only (hands-only or cardiocerebral resuscitation) CPR is a technique that involves chest compressions without artificial respiration.[1]:S643 It is recommended as the method of choice for the untrained rescuer or those who are not proficient as it is easier to perform and instructions are easier to give over the phone.[1]:S643[5]:8[9] In adults with out-of-hospital cardiac arrest, compression-only CPR by the lay public has a higher success rate than standard CPR.[9] The exceptions are cases of drownings, drug overdose, and arrest in children. Children who receive compression only CPR have the same outcomes as those who received no CPR.[1]:S646 The method of delivering chest compressions remains the same, as does the rate (at least 100 per minute). It is hoped that the use of compression only delivery will increase the chances of the lay public delivering CPR.[10] For those with non cardiac arrest and people less than 20 years of age standard CPR is superior to compression only CPR. CPR is used on people in cardiac arrest in order to oxygenate the blood and maintain a cardiac output to keep vital organs alive. Blood circulation and oxygenation are required to transport oxygen to the tissues. The brain may sustain damage after blood flow has been stopped for about four minutes and irreversible damage after about seven minutes.[21][22][23][24][25] Typically if blood flow ceases for one to two hours, the cells of the body die. Because of that CPR is generally only effective if performed within seven minutes of the stoppage of blood flow.[26] The heart also rapidly loses the ability to maintain a normal rhythm. Low body temperatures as sometimes seen in near-drownings prolong the time the brain survives. Following cardiac arrest, effective CPR enables enough oxygen to reach the brain to delay brain death, and allows the heart to remain responsive to defibrillation attempts. A bag valve mask (also known as a BVM or Ambu bag) is a hand-held device used to provide positive pressure ventilation to a patient who is not breathing or who is breathing inadequately. The device is a normal part of a resuscitation kit for trained professionals, such as ambulance crew. The BVM is frequently used in hospitals, and is an essential part of a crash cart. The device is used extensively in the operating room to ventilate an anaesthetised patient in the minutes before a mechanical ventilator is attached. The device is self-filling with air, although additional oxygen (O2) can be added. Use of the BVM to ventilate a patient is frequently called "bagging" the patient.[1] Bagging is regularly necessary in medical emergencies when the patient's breathing is insufficient (respiratory failure) or has ceased completely (respiratory arrest). The BVM resuscitator is used in order to manually provide mechanical ventilation in preference to mouth-to-mouth resuscitation (either direct or through an adjunct such as a pocket mask).

Myocardial infarction
From Wikipedia, the free encyclopedia

Jump to: navigation, search "Heart attack" redirects here. For other uses, see Heart attack (disambiguation).

Myocardial infarction
Classification and external resources

Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the (left coronary artery = LCA, right coronary artery = RCA). ICD-10 ICD-9 DiseasesDB MedlinePlus eMedicine MeSH I21.-I22. 410 8664 000195 med/1567 emerg/327 ped/2520 D009203

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, is the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is

an unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium). Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety (often described as a sense of impending doom).[1] Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue.[2] Approximately one quarter of all myocardial infarctions are "silent", without chest pain or other symptoms. Among the diagnostic tests available to detect heart muscle damage are an electrocardiogram (ECG), echocardiography, and various blood tests. The most often used markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels. Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual nitroglycerin.[3] Most cases of STEMI (ST elevation MI) are treated with thrombolysis or percutaneous coronary intervention (PCI). NSTEMI (non-ST elevation MI) should be managed with medication, although PCI is often performed during hospital admission. In people who have multiple blockages and who are relatively stable, or in a few emergency cases, bypass surgery may be an option. Heart attacks are the leading cause of death for both men and women worldwide.[4] Important risk factors are previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (triglycerides, low-density lipoprotein) and low levels of high density lipoprotein (HDL), diabetes, high blood pressure, obesity, chronic kidney disease, heart failure, excessive alcohol consumption, the abuse of certain drugs (such as cocaine and methamphetamine), and chronic high stress levels.[5][6]

Contents
[hide]

1 Classification 2 Signs and symptoms 3 Causes o 3.1 Risk factors 4 Pathophysiology 5 Diagnosis 6 Prevention 7 Management 8 Complications 9 Prognosis 10 Epidemiology 11 Legal implications

12 Research 13 References 14 External links

[edit] Classification
There are two basic types of acute myocardial infarction:

Transmural: associated with atherosclerosis involving major coronary artery. It can be subclassified into anterior, posterior, or inferior. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply.[7] Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. Subendocardial infarcts are thought to be a result of locally decreased blood supply, possibly from a narrowing of the coronary arteries. The subendocardial area is farthest from the heart's blood supply and is more susceptible to this type of pathology.[7]

Clinically, a myocardial infarction can be further subclassified into a ST elevation MI (STEMI) versus a non-ST elevation MI (non-STEMI) based on ECG changes.[8] The phrase "heart attack" is sometimes used incorrectly to describe sudden cardiac death, which may or may not be the result of acute myocardial infarction. A heart attack is different from, but can be the cause of cardiac arrest, which is the stopping of the heartbeat, and cardiac arrhythmia, an abnormal heartbeat. It is also distinct from heart failure, in which the pumping action of the heart is impaired; severe myocardial infarction may lead to heart failure, but not necessarily.[citation needed] A 2007 consensus document classifies myocardial infarction into five main types:[9]

Type 1 Spontaneous myocardial infarction related to ischaemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection Type 2 Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension Type 3 Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by presumably new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood Type 4 Associated with coronary angioplasty or stents: o Type 4a Myocardial infarction associated with PCI o Type 4b Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy Type 5 Myocardial infarction associated with CABG

[edit] Signs and symptoms

Rough diagram of pain zones in myocardial infarction (dark red = most typical area, light red = other possible areas, view of the chest).

Back view. The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.[10] Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm,[not in citation given] back, and epigastrium, where it may mimic heartburn. Levine's sign, in which the patient localizes the chest pain by clenching their fist over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value.[11] Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating),[1] weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system[12] which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral

perfusion and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.[citation needed] Women and older patients report atypical symptoms more frequently than their male and younger counterparts.[13] Women also report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men).[13] The most common symptoms of MI in women include dyspnea (shortness of breath), weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms which may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men.[14] Approximately one fourth of all myocardial infarctions are silent, without chest pain or other symptoms.[15] These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. A silent course is more common in the elderly, in patients with diabetes mellitus[16] and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient.[17] In diabetics, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.[16] Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.[18] The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, and esophageal rupture. Other non-catastrophic differentials include gastroesophageal reflux and Tietze's syndrome.[19]

[edit] Causes
Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if the exertion is more intense than the individual usually performs.[20] Quantitatively, the period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are physically very fit.[20] For those in poor physical condition, the rate differential is over 35-fold higher.[20] One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat which, as has been observed with intravascular ultrasound, increases mechanical "shear stress" on atheromas and the likelihood of plaque rupture.[20] Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.[21] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.[21] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.[22]

There is an association of an increased incidence of a heart attack in the morning hours, more specifically around 9 a.m.[23][24][25] Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation.[26]

[edit] Risk factors

Risk factors for atherosclerosis are generally risk factors for myocardial infarction:
[citation needed]

Diabetes (with or without insulin resistance) the single most important risk factor for ischaemic heart disease (IHD) Tobacco smoking Hypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density lipoprotein and low high density lipoprotein) Low HDL High Triglycerides High blood pressure Family history of ischaemic heart disease (IHD) Obesity[27] (defined by a body mass index of more than 30 kg/m, or alternatively by waist circumference or waist-hip ratio). Age: Men acquire an independent risk factor at age 45, Women acquire an independent risk factor at age 55; in addition individuals acquire another independent risk factor if they have a first-degree male relative (brother, father) who suffered a coronary vascular event at or before age 55. Another independent risk factor is acquired if one has a first-degree female relative (mother, sister) who suffered a coronary vascular event at age 65 or younger. Hyperhomocysteinemia (high homocysteine, a toxic blood amino acid that is elevated when intakes of vitamins B2, B6, B12 and folic acid are insufficient) Stress (occupations with high stress index are known to have susceptibility for atherosclerosis) Alcohol Studies show that prolonged exposure to high quantities of alcohol can increase the risk of heart attack Males are more at risk than females.[20]

Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile.[28] Non-modifiable risk factors include age, sex, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition.[20] Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation may also contribute to the risk of MI.[29] To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.[29] Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.[30]

Inflammation is known to be an important step in the process of atherosclerotic plaque formation.[31] C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation. Elevated CRP blood levels, especially measured with high sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes.[31] Moreover, some drugs for MI might also reduce CRP levels.[31] The use of high sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion, in patients who already present with other risk factors or known coronary artery disease.[32] Whether CRP plays a direct role in atherosclerosis remains uncertain.[31] Inflammation in periodontal disease may be linked to coronary heart disease, and since periodontitis is very common, this could have great consequences for public health.[33] Serological studies measuring antibody levels against typical periodontitiscausing bacteria found that such antibodies were more present in subjects with coronary heart disease.[34] Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines;[35] thus, periodontitis may mediate its effect on MI risk via other risk factors.[36] Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells.[37][38] A role for specific periodontal bacteria has been suggested but remains to be established.[39] There is some evidence that influenza may trigger an acute myocardial infarction.[40] Baldness, hair greying, a diagonal earlobe crease (Frank's sign[41]) and possibly other skin features have been suggested as independent risk factors for MI.[42] Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.[43] Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with CT scans. Several studies have shown that coronary calcium can provide predictive information beyond that of classical risk factors.[44][45][46] The European Society of Cardiology and the European Association for Cardiovascular Prevention and Rehabilitation have developed an interactive tool for prediction and managing the risk of heart attack and stroke in Europe. HeartScore is aimed at supporting clinicians in optimising individual cardiovascular risk reduction. The Heartscore Programme is available in 12 languages and offers web based or PC version.[47]

[edit] Pathophysiology
See also: Acute coronary syndrome

A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, causing catastrophic thrombus formation, totally occluding the artery and preventing blood flow downstream.

Drawing of the heart showing anterior left ventricle wall infarction. Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated myocardial infarction and ST-elevated myocardial infarction, which are most frequently (but not always) a manifestation of coronary artery disease.[8] The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery.[48][49] Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades.[50] Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis.[51] Plaques can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).[48][49] If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the occluded coronary artery die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.[52] As a result, the patient's heart will be permanently damaged. This Myocardial scarring also puts the patient at risk for potentially life threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences. Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life threatening arrhythmia is ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood

effectively. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct. The cardiac defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.

[edit] Diagnosis
Main article: Myocardial infarction diagnosis The diagnosis of myocardial infarction can be made after assessing patient's complaints and physical status. ECG changes, coronary angiogram and levels of cardiac markers help to confirm the diagnosis. ECG gives valuable clues to identify the site of myocardial damage while coronary angiogram allows visualization of narrowing or obstructions in the heart vessels.[53] At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings. A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist.[54] In stable patients whose symptoms have resolved by the time of evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmocologic stress.[54][55] Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned.[56] WHO criteria[57] formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied: 1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes 2. Changes in serial ECG tracings 3. Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.[58] According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.

[edit] Prevention
The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a

sensible diet for those with heart disease, and limitation of alcohol intake. People are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:[59][60]

Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased.[61] Beta blocker therapy such as metoprolol or carvedilol should be commenced. [62] These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia.[63] Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI. ACE inhibitor therapy should be commenced 2448 hours post-MI in hemodynamically-stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI.[64] Statin therapy has been shown to reduce mortality and morbidity post-MI.[65][66] The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.[67] The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above.[68] Spironolactone is another option that is sometimes preferable to eplerenone due to cost. Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease.[69] Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality post-MI.[70] While the mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that the survival benefit is due to electrical stabilization and the prevention of ventricular fibrillation.[71] However, further studies in a high-risk subset have not shown a clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids.[72][73]

Blood donation may reduce the risk of heart disease for men,[74] but the link has not been firmly established. A Cochrane review found that giving heparin to people who have heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of suffering from minor bleeding.[75]

[edit] Management
Main article: Myocardial infarction management An MI is a medical emergency which requires immediate medical attention. Treatment attempts to salvage as much myocardium as possible and to prevent further complications, thus the phrase "time is muscle".[76] Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI.[77] A 2009 and 2010 review of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use.[78][79] Percutaneous coronary intervention (PCI) or fibrinolysis are recommended in those with an STEMI.

[edit] Complications
Main article: Myocardial infarction complications Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). Acute complications may include heart failure if the damaged heart is no longer able to adequately pump blood around the body; aneurysm or rupture of the myocardium; mitral regurgitation, particularly if the infarction causes dysfunction of the papillary muscle; and arrhythmias, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation and heart block. Longer-term complications include heart failure, atrial fibrillation, and the increased risk of a second myocardial infarction.

[edit] Prognosis
The prognosis post myocardial infarction varies greatly, depending on a person's health, the extent of the heart damage and the treatment given. For the period 2005 2008 in the United States the median mortality at 30 days was 16.6% with a range from 10.9% to 24.9% depending on the hospital.[80] Using variables available in the emergency room, people with a higher risk of adverse outcome can be identified. One study found that 0.4% of patients with a low risk profile died after 90 days, whereas in high risk people it was 21.1%.[81] Some of the more reproduced risk stratifying factors include: age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular disease and elevation of cardiac markers.[81][82][83] Assessment of left ventricular ejection fraction may increase the predictive power.[84] The prognostic importance of Q-waves is debated.[85] Prognosis is significantly worsened if a mechanical complication such as papillary muscle or myocardial free wall rupture occur.[86] Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.[87]

[edit] Epidemiology

Myocardial infarction is a common presentation of ischemic heart disease. The WHO estimated in 2002, that 12.6 percent of worldwide deaths were from ischemic heart disease[4] with it the leading cause of death in developed countries, and third to AIDS and lower respiratory infections in developing countries.[88] Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.[89] Coronary heart disease is responsible for 1 in 5 deaths in the United States. It is becoming more common in the developing world such that in India, cardiovascular disease (CVD) is the leading cause of death.[90] The deaths due to CVD in India were 32% of all deaths in 2007 and are expected to rise from 1.17 million in 1990 and 1.59 million in 2000 to 2.03 million in 2010.[91] Although a relatively new epidemic in India, it has quickly become a major health issue with deaths due to CVD expected to double during 19852015.[92][93] Mortality estimates due to CVD vary widely by state, ranging from 10% in Meghalaya to 49% in Punjab (percentage of all deaths). Punjab (49%), Goa (42%), Tamil Nadu (36%) and Andhra Pradesh (31%) have the highest CVD related mortality estimates.[94] State-wise differences are correlated with prevalence of specific dietary risk factors in the states. Moderate physical exercise is associated with reduced incidence of CVD in India (those who exercise have less than half the risk of those who don't).[92]

[edit] Legal implications

At common law, a myocardial infarction is generally a disease, but may sometimes be an injury. This has implications for no-fault insurance schemes such as workers' compensation. A heart attack is generally not covered;[95] however, it may be a workrelated injury if it results, for example, from unusual emotional stress or unusual exertion.[96] Additionally, in some jurisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person who has suffered from a myocardial infarction may be prevented from participating in activity that puts other people's lives at risk, for example driving a car or flying an airplane.[97]

[edit] Research
Patients who receive stem cell treatment by coronary artery injections of stem cells derived from their own bone marrow after a myocardial infarction (MI) show improvements in left ventricular ejection fraction and end-diastolic volume not seen with placebo. The larger the initial infarct size, the greater the effect of the infusion. Clinical trials of progenitor cell infusion as a treatment approach to ST elevation MI are proceeding.[98] There are currently 3 biomaterial and tissue engineering approaches for the treatment of MI, but these are in an even earlier stage of medical research, so many questions and issues need to be addressed before they can be applied to patients. The first involves polymeric left ventricular restraints in the prevention of heart failure. The second utilizes in vitro engineered cardiac tissue, which is subsequently implanted in vivo. The final approach entails injecting cells and/or a scaffold into the myocardium to create in situ engineered cardiac tissue.[99]

Cardiovascular disease
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Cardiovascular disease
Classification and external resources ICD-10 ICD-9 DiseasesDB MeSH I51.6 429.2 28808 D002318

Heart disease or cardiovascular disease are the class of diseases that involve the heart or blood vessels (arteries and veins).[1] While the term technically refers to any disease that affects the cardiovascular system (as used in MeSH C14), it is usually used to refer to those related to atherosclerosis (arterial disease). These conditions usually have similar causes, mechanisms, and treatments. Most countries face high and increasing rates of cardiovascular disease. Each year, heart disease kills more Americans than cancer. In recent years, cardiovascular risk in women has been increasing and has killed more women than breast cancer.[2] A large histological study (PDAY) showed vascular injury accumulates from adolescence, making primary prevention efforts necessary from childhood.[3][4] By the time that heart problems are detected, the underlying cause (atherosclerosis) is usually quite advanced, having progressed for decades. There is therefore increased emphasis on preventing atherosclerosis by modifying risk factors, such as healthy eating, exercise and avoidance of smoking.

Contents
[hide]

1 Pathophysiology 2 Diagnosis o 2.1 Associated diagnostic markers 3 Screening 4 Prevention 5 Management 6 Epidemiology 7 See also

8 References 9 External links

[edit] Pathophysiology
Population based studies show that the precursors of heart disease start in adolescence. The process of atherosclerosis evolves over decades, and begins as early as childhood. The Pathobiological Determinants of Atherosclerosis in Youth Study demonstrated that intimal lesions appear in all the aortas and more than half of the right coronary arteries of youths aged 79 years. However, most adolescents are more concerned about other risks such as HIV, accidents, and cancer than cardiovascular disease.[5] This is extremely important considering that 1 in 3 people will die from complications attributable to atherosclerosis. In order to stem the tide education and awareness that cardiovascular disease poses the greatest threat and measures to prevent or reverse this disease must be taken. Obesity and diabetes mellitus are often linked to cardiovascular disease [6] In fact, cardiovascular disease is the most life threatening of the diabetic complications and diabetics are two- to four-fold more likely to die of cardiovascular-related causes than nondiabetics.[7][8][9]

[edit] Diagnosis
[edit] Associated diagnostic markers

Low-density lipoprotein Lipoprotein(a) Apolipoprotein A1 Apolipoprotein Bho This section requires expansion.

[edit] Screening
Some biomarkers are thought to offer a more detailed risk of cardiovascular disease. However, the clinical value of these biomarkers is questionable.[10] Currently, biomarkers which may reflect a higher risk of cardiovascular disease include:

Higher fibrinogen and PAI-1 blood concentrations Elevated homocysteine, or even upper half of normal Elevated blood levels of asymmetric dimethylarginine Inflammation as measured by C-reactive protein Elevated blood levels of brain natriuretic peptide (also known as B-type) (BNP) [11]

[edit] Prevention
Evidence shows that the Mediterranean diet improves cardiovascular outcomes.[12] As of 2010 however vitamins have not been found to be effective at preventing cardiovascular disease.[13] Modifiable risk factors to improve or prevent atherosclerosis include:

diet high in fibers from vegetables and nuts while low in saturated fat and cholesterol; tobacco cessation and avoidance of second-hand smoke[citation needed]; decreased alcohol consumption; lower blood pressures if elevated through the use of antihypertensive medications; strict diabetes management; decrease BMI if overweight or obese; increase daily activity to 30 minutes of moderate to vigorous exercise; and decrease emotional stress in day to day life[citation needed]. (Sources: www.americanheart.org, www.world-heart-federation.org/cardiovascularhealth/cardiovascular-disease-risk-factors/)[unreliable medical source?]

[edit] Management
Cardiovascular disease is treatable with initial treatment primarily focused on diet and lifestyle interventions. [14] [15] [16] Medication may also be useful for prevention.

[edit] Epidemiology

Disability-adjusted life year for cardiovascular diseases per 100,000 inhabitants in 2004.[17] no data less than 900 900-1650 1650-2300 2300-3000 3000-3700 3700-4400 4400-5100 5100-5800 5800-6500 6500-7200 7200-7900 Over 7900

The first studies on cardiovascular health were performed in 1949 by Jerry Morris using occupational health data and were published in 1958.[18] The causes, prevention, and/or treatment of all forms of cardiovascular disease remain active fields of biomedical research, with hundreds of scientific studies being published on a weekly basis. A trend has emerged, particularly in the early 2000s, in which numerous studies have revealed a link between fast food and an increase in heart disease. These studies include those conducted by the Ryan Mackey Memorial Research Institute, Harvard University and the Sydney Center for Cardiovascular Health. Many major fast food chains, particularly McDonald's, have protested the methods used in these studies and have responded with healthier menu options. A fairly recent emphasis is on the link between low-grade inflammation that hallmarks atherosclerosis and its possible interventions. C-reactive protein (CRP) is an common inflammatory marker that has been found to be present in increased levels in patients at risk for cardiovascular disease.[19] Also osteoprotegerin which involved with regulation of a key inflammatory transcription factor called NF-B has been found to be a risk factor of cardiovascular disease and mortality.[20][21] Some areas currently being researched include possible links between infection with Chlamydophila pneumoniae and coronary artery disease. The Chlamydia link has become less plausible with the absence of improvement after antibiotic use.[22]

Symptoms
Symptoms of Heart Disease Here's a fast, easy-to-understand guide to the symptoms of each type of heart disease.

Warning Signs
When to Call the Doctor If you or a loved one has heart disease, when must you call the doctor? When should you head for the emergency room? Click here for clear, fast information. Related Web Site: Heart Attack Warning Signs Don't wait, click here for heart attack warning signs. For easy reference, you'll also find stroke and cardiac arrest warning signs -- and no-nonsense advice on what to do now. This link will take you to the American Heart Association. Related Web Site: Women and Heart Disease Symptoms Women are more likely than men to have a heart attack without chest pain. Read more data on gender-specific heart disease. This link takes you to another web site. Angina Doctors call it angina pectoris. You call it chest pain. It may feel like indigestion -- or like an elephant just stepped on your chest. Here's what it means.

Types
Coronary Artery Disease Coronary artery disease is America's No.1 killer, affecting more than 13 million Americans. Tool: CAD View this illustrative guide to coronary artery disease. Heart Attack

You know there's nothing funny about a heart attack. There's a lot more to learn. Here's what you need to know: no more, no less. Irregular Heart Rhythm Irregular heart rhythm -- arrhythmia -- is when your heart doesn't keep up a good beat. Learn what it means here. Atrial Fibrillation It's the most common kind of irregular heart beat. Here's where to find out what it is, and what to do about it. Tool: Heart Rhythm Disorders Irregular heart rhythms can cause the pumping function of the heart to fail. See how. Heart Valve Disease You may not know what a heart valve is -- until it stops working right. It's a common form of heart disease. Here's an illustrated guide. Sudden Cardiac Death This is the cause of half of all heart disease deaths. Find out why here. Congenital Heart Disease Not everyone gets heart disease. Some are born with it. Here are the facts on congenital heart disease. Heart Muscle Disease Heart muscle disease -- what doctors call cardiomyopathy -- is as serious as it sounds. Here's a brief overview. Dilated Cardiomyopathy Symptoms of DC --dilated cardiomyopathy -- can appear at any age. Learn to recognize them here. Hypertrophic Cardiomyopathy HCM -- hypertrophic cardiomyopathy -- is a thickening of the walls of the heart. Here's a brief overview. Restrictive Cardiomyopathy Restrictive cardiomyopathy is the rarest form of heart-muscle disease. Here's an overview. Pericarditis Did you know that your heart is held by a little sac? That sac -- the pericardium -- can get infected. It's called pericarditis or pericardial disease. Here's more. Pericardial Effusion Fluid around the heart can be caused by various types of infection/inflammation or cancer, kidney disease or heart surgery. This fluid can impair heart function. Read more in this technical article written for doctors. Marfan Syndrome This inherited genetic defect weakens connective tissues -- including those in the heart. Click here to learn more.

What is heart disease?

Heart disease, or cardiovascular disease, is a general name for a wide variety of diseases, disorders and conditions that affect the heart and blood vessels. Heart disease is the number one cause of death in the United States, according to the Centers for Disease Control and Prevention. http://www.cdc.gov/features/heartmonth/ Heart attack risks and blood types The heart is composed of muscle tissue that requires a steady supply of oxygen in order to pump blood effectively through the body. Heart diseases can damage the coronary arteries, which provide oxygen-rich blood to the heart muscle. Heart diseases can also impair the functioning or structure of the heart and blood vessels. Coronary artery disease causes most heart attacks and is the most common form of heart disease. Do you know your triglyceride score? The types of heart disease include:

Atherosclerosis is a buildup of cholesterol, calcium and blood clotting material on the walls of the arteries. The material that builds up is called plaque. Cardiac arrhythmia is an abnormal heart rhythm. Cardiomyopathy is a weakened and enlarged heart muscle. Congenital heart defect is a problem with the structure of the heart. Coronary artery disease is a narrowing of the coronary arteries that supply the heart. Heart attack (myocardial infarction) is a lack of oxygenated blood to the heart muscle. Heart failure is a condition in which the heart has been damaged from a heart attack or other type of heart disease. Heart valve disorder is a malfunctioning heart valve that causes abnormal stress on the heart. Myocarditis is an infection of the middle layer of the heart wall. Pericarditis is an infection of the lining that surrounds the heart.

Left untreated, heart disease can result in serious complications, such as lethal cardiac arrhythmias, severe heart failure, cardiac arrest, and death. Some complications can occur suddenly and require immediate treatment. Immediate emergency treatment best minimizes the risk of complications. Seek immediate medical care (call 911) if you, or someone you are with, have chest pain, difficulty breathing, or palpitations, which may be combined with dizziness, sweating, fainting, and anxiety.

What are the symptoms of heart disease?

In addition, not all people who have heart disease experience chest pain. Some people even have a heart attack without having chest pain. By the time a person experiences

chest pain, he or she may have had a form of heart disease, such as atherosclerosis, for many years.... Read more about heart disease symptoms

What causes heart disease?

The heart is a muscle that requires a steady supply of oxygen in order to pump blood effectively through the body. Oxygen is supplied to the heart by blood that flows through the coronary arteries. Some types of heart disease damage or block the coronary arteries and the flow of oxygen to the heart. Other forms of heart disease damage or impair the functioning of the heart and blood vessels. These disorders include:... Read more about heart disease causes

How is heart disease treated?

Intensive monitoring and stabilization of heart rhythm and vital signs. This may require cardiopulmonary resuscitation (CPR) and advanced life support measures, such as intubation and mechanical ventilation to support breathing.... Read more about heart disease treatments

What are the symptoms of heart disease?

Symptoms of heart disease can differ depending on the type and severity of heart disease and individual factors. One well-known symptom of heart disease is chest pain, but not all chest pain is caused by heart disease. In addition, not all people who have heart disease experience chest pain. Some people even have a heart attack without having chest pain. By the time a person experiences chest pain, he or she may have had a form of heart disease, such as atherosclerosis, for many years. It is common for a person with certain types of heart disease, such as atherosclerosis, not to have noticeable symptoms until complications occur. The only definite way to detect heart disease in its earliest, most treatable stage is through regular medical care that includes comprehensive evaluations from a licensed physician or health care professional.

Symptoms of heart disease

Heart disease symptoms can be vague, mild and subtle. Symptoms include:

A feeling of indigestion Anxiety and restlessness Backache Difficulty feeding and poor weight gain in infants Erectile dysfunction Fatigue Mild, transient shortness of breath with exertion Mild weakness and feeling lightheaded

Nausea and vomiting Pain, numbness, and mild swelling in the feet and ankles Pale skin with or without sweating Wet cough

Serious symptoms that might indicate a life-threatening condition

Some symptoms of heart disease and its complications are severe and may indicate a serious or life-threatening condition that needs immediate treatment. Seek immediate medical care (call 911) if you, or someone you are with, have any of these symptoms:

Bluish discoloration of the lips and fingernails (cyanosis) Change in level of consciousness or alertness, such as passing out or unresponsiveness Chest pain, tightness, pressure, squeezing, or fullness (angina) Extreme sweating and clammy, pale skin Loss of pulse Nausea and vomiting Pain in the shoulders, back, neck, jaw, or arms that radiates from the chest. Chest pain can also occur by itself. Respiratory or breathing problems, such as shortness of breath, difficulty breathing, labored breathing, wheezing, not breathing, or choking Severe dizziness Severe swelling that can affect the arms, legs, and abdomen

What is heart disease?

Heart disease, or cardiovascular disease, is a general name for a wide variety of diseases, disorders and conditions that affect the heart and blood vessels. Heart disease is the number one cause of death in the United States, according to the Centers for Disease Control and Prevention. http://www.cdc.gov/features/heartmonth/... Read more about heart disease introduction

What causes heart disease?

The heart is a muscle that requires a steady supply of oxygen in order to pump blood effectively through the body. Oxygen is supplied to the heart by blood that flows through the coronary arteries. Some types of heart disease damage or block the coronary arteries and the flow of oxygen to the heart. Other forms of heart disease damage or impair the functioning of the heart and blood vessels. These disorders include:... Read more about heart disease causes

How is heart disease treated?

Advanced or critical stages of heart disease generally require hospitalization and some combination of:... Read more about heart disease treatments

What causes heart disease?

The heart is a muscle that requires a steady supply of oxygen in order to pump blood effectively through the body. Oxygen is supplied to the heart by blood that flows through the coronary arteries. Some types of heart disease damage or block the coronary arteries and the flow of oxygen to the heart. Other forms of heart disease damage or impair the functioning of the heart and blood vessels. These disorders include:

Abnormal electrical conduction in the heart causing cardiac arrhythmias or abnormal heart rhythms. These include ventricular tachycardia, heart blocks, ventricular fibrillation, asystole, supraventricular tachycardia, and bradycardia. Atherosclerosis, a buildup of plaque on the walls of the coronary arteries. Atherosclerosis narrows the coronary arteries and results in angina. It can also lead to the formation of a blood clot that blocks blood flow to the heart (heart attack). Birth defects, also called congenital heart or blood vessel defects. These include atrial septal defect, coarctation of the aorta, and atrioventricular septal defect. Heart damage, such as heart failure or cardiomyopathy, that weakens the pumping action of the heart Heart valve abnormalities, which are also called heart valve disorders. Heart valve disorders include mitral valve insufficiency, mitral valve prolapse, mitral valve stenosis, tricuspid valve insufficiency, and tricuspid valve stenosis. Infection and inflammation caused by myocarditis or pericarditis

What are the risk factors for heart disease?

A number of factors are thought to increase your chances of having heart disease. These risk factors include:

African American, Hispanic American, or Native American ancestry Excessive alcohol consumption Exposure of a baby to certain maternal diseases during pregnancy Exposure of a baby to certain toxins during pregnancy Family history of heart disease High blood pressure (hypertension) History of atherosclerosis History of diabetes Long-term stress Male gender and postmenopausal females aged 45 years and older Obesity and sedentary lifestyle Smoking Having high levels of certain substances in the body, which can be seen on blood tests, can also increase the risk for heart disease. These include: High cholesterol, which can lead to atherosclerosis High C-reactive protein (CRP) level, which increases atherosclerosis

High homocysteine level, which is associated with heart disease; however, no causal link has been established

Reducing your risk of heart disease

Not all people who are at risk for heart disease will develop heart disease, and not all people who develop heart disease have risk factors. You can reduce your risk of some forms of heart disease by:

Eating a diet that is low in saturated fat and high in fiber, whole grains, fruits, and vegetables Maintaining a healthy weight Not drinking alcohol or limiting alcohol consumption to one drink per day for women and two drinks per day for men Not smoking or quitting smoking Participating in a regular exercise program Reducing excessive stress Seeking regular medical care and following your treatment plan for such conditions as high cholesterol, hypertension and diabetes

What is heart disease?

Heart disease, or cardiovascular disease, is a general name for a wide variety of diseases, disorders and conditions that affect the heart and blood vessels. Heart disease is the number one cause of death in the United States, according to the Centers for Disease Control and Prevention. http://www.cdc.gov/features/heartmonth/... Read more about heart disease introduction

What are the symptoms of heart disease?

In addition, not all people who have heart disease experience chest pain. Some people even have a heart attack without having chest pain. By the time a person experiences chest pain, he or she may have had a form of heart disease, such as atherosclerosis, for many years.... Read more about heart disease symptoms

How is heart disease treated?

Intensive monitoring and stabilization of heart rhythm and vital signs. This may require cardiopulmonary resuscitation (CPR) and advanced life support measures, such as intubation and mechanical ventilation to support breathing.... Read more about heart disease treatments

How is heart disease treated?

Some heart diseases that are diagnosed early can be successfully treated before the development of permanent heart damage and complications, such as heart failure and cardiac arrest. Heart disease treatment plans use a multifaceted approach and are

individualized to the type and severity of your heart disease, risk factors, lifestyle, medical history, and other diseases and conditions you have.

Treatment for advanced or critical stages of heart disease

Advanced or critical stages of heart disease generally require hospitalization and some combination of:

Intensive monitoring and stabilization of heart rhythm and vital signs. This may require cardiopulmonary resuscitation (CPR) and advanced life support measures, such as intubation and mechanical ventilation to support breathing. Monitoring your heart rate and rhythm with an electrocardiogram (EKG) and lab tests, such as cardiac enzymes, to determine the extent of heart damage Supplemental oxygen to increase the amount of oxygen that is delivered to the heart tissue and the rest of the body Treatment of abnormal heart rhythms (cardiac arrhythmias) with medications and possibly cardioversion or electrical defibrillation

Medications used to treat heart disease

The following medications may be prescribed for a variety of types of heart disease during and after hospitalization:

ACE inhibitors (ramipril, lisinopril, enalapril, or captopril), which lower high blood pressure and help prevent heart failure Aspirin, which helps prevent new blood clots Beta blockers (metoprolol, atenolol, and propranolol), which lower high blood pressure and reduce strain on the heart Heparin, which helps prevent new blood clots Medications to lower high cholesterol, including statins, niacin, and selective cholesterol absorption inhibitors Medications to raise low blood pressure, which may be used in certain situations, such as in cardiogenic shock Medications to treat cardiac arrhythmias, which include digitalis, beta blockers, verapamil, adenosine, lidocaine, or calcium channel blockers Morphine, which reduces pain and anxiety and lowers the amount of oxygen the heart needs Nitroglycerine, which helps widen narrowed coronary arteries and improves blood flow to the heart Thrombolytic (clot-dissolving) drugs, which break up and dissolve the clot that is causing a heart attack. Thrombolytic drugs are most effective if given within three hours of the onset of chest pain.

Surgical treatments for heart disease

Surgical treatments vary depending on the specific type of heart disease and other factors. Surgical treatments may include:

Angioplasty and stent placement to widen the artery using a balloon device. In most cases, a stent (hollow tube) is placed in the artery to keep it open.

Coronary artery bypass to graft new arteries to bypass the blocked coronary artery or arteries. Blood flow is then redirected through healthy new grafted arteries to the affected heart tissues. Surgery to correct congenital heart defects Surgery to replace or repair abnormal heart valves Surgical implantation of a cardioverter-defibrillator or pacemaker to deliver electrical stimulation to the heart using a small device and electrical wires placed in the body. The electrical stimulation corrects abnormal heart rhythms (cardiac arrhythmias).

Other treatments for heart disease

Other treatments and therapies that may be recommended as part of a complete treatment program for heart disease include:

Cardiac rehabilitation and physical therapy to help strengthen your body, reduce complications, increase alertness, reduce fatigue, and improve overall health and functional ability Complementary or alternative treatments, such as acupuncture, massage therapy, and yoga to reduce stress, increase flexibility, and improve wellbeing. Complementary treatments are not a substitute for full medical care. Palliative care to improve the overall quality of life for families and patients with serious diseases. Regular follow-up care is very important to help monitor your treatment and progress and to address any problems or complications promptly.

What are the possible complications of heart disease?

Complications of heart disease are serious and can be life threatening. You can best help minimize the risk of serious complications of heart disease by following the treatment plan you and your health care professional design specifically for you. Serious complications of heart disease include:

Aneurysm, a life-threatening bulging and weakening of the wall of an artery that can burst and cause severe hemorrhage Blood clots that cause heart attack, stroke and pulmonary embolism (blood clots in the lungs) Cardiac arrest Cardiogenic shock Disability Heart failure Heart valve damage Lethal cardiac arrhythmias

Meningitis
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Meningitis
Classification and external resources

Meninges of the central nervous system: dura mater, arachnoid, and pia mater. ICD-10 ICD-9 DiseasesDB MedlinePlus eMedicine MeSH G00.G03. 320322 22543 000680 med/2613 emerg/309 emerg/390 D008581

Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges.[1] The inflammation may be caused by infection with viruses, bacteria, or other microorganisms, and less commonly by certain drugs.[2] Meningitis can be life-threatening because of the inflammation's proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency.[1][3] The most common symptoms of meningitis are headache and neck stiffness associated with fever, confusion or altered consciousness, vomiting, and an inability to tolerate light (photophobia) or loud noises (phonophobia). Sometimes, especially in small children, only nonspecific symptoms may be present, such as irritability and drowsiness. If a rash is present, it may indicate a particular cause of meningitis; for instance, meningitis caused by meningococcal bacteria may be accompanied by a characteristic rash.[1][4] A lumbar puncture may be used to diagnose or exclude meningitis. This involves inserting a needle into the spinal canal to extract a sample of cerebrospinal fluid

(CSF), the fluid that envelops the brain and spinal cord. The CSF is then examined in a medical laboratory.[3] The usual treatment for meningitis is the prompt application of antibiotics and sometimes antiviral drugs. In some situations, corticosteroid drugs can also be used to prevent complications from overactive inflammation.[3][4] Meningitis can lead to serious long-term consequences such as deafness, epilepsy, hydrocephalus and cognitive deficits, especially if not treated quickly.[1][4] Some forms of meningitis (such as those associated with meningococci, Haemophilus influenzae type B, pneumococci or mumps virus infections) may be prevented by immunization.[1]

Signs and symptoms

[edit] Clinical features
In adults, a severe headache is the most common symptom of meningitis occurring in almost 90% of cases of bacterial meningitis, followed by nuchal rigidity (inability to flex the neck forward passively due to increased neck muscle tone and stiffness).[5] The classic triad of diagnostic signs consists of nuchal rigidity, sudden high fever, and altered mental status; however, all three features are present in only 4446% of all cases of bacterial meningitis.[5][6] If none of the three signs is present, meningitis is extremely unlikely.[6] Other signs commonly associated with meningitis include photophobia (intolerance to bright light) and phonophobia (intolerance to loud noises). Small children often do not exhibit the aforementioned symptoms, and may only be irritable and look unwell.[1] In infants up to 6 months of age, bulging of the fontanelle (the soft spot on top of a baby's head) may be present. Other features that might distinguish meningitis from less severe illnesses in young children are leg pain, cold extremities, and an abnormal skin color.[7] Nuchal rigidity occurs in 70% of adult cases of bacterial meningitis.[6] Other signs of meningism include the presence of positive Kernig's sign or Brudzinski's sign. Kernig's sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. In a patient with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip. Although Kernig's and Brudzinski's signs are both commonly used to screen for meningitis, the sensitivity of these tests is limited.[6] [8] They do, however, have very good specificity for meningitis: the signs rarely occur in other diseases.[6] Another test, known as the "jolt accentuation maneuver" helps determine whether meningitis is present in patients reporting fever and headache. The patient is told to rapidly rotate his or her head horizontally; if this does not make the headache worse, meningitis is unlikely.[6] Meningitis caused by the bacterium Neisseria meningitidis (known as "meningococcal meningitis") can be differentiated from meningitis with other causes by a rapidly spreading petechial rash which may precede other symptoms.[7] The rash consists of numerous small, irregular purple or red spots ("petechiae") on the trunk, lower extremities, mucous membranes, conjuctiva, and (occasionally) the palms of the hands or soles of the feet. The rash is typically non-blanching: the redness does not disappear when pressed with a finger or a glass tumbler. Although this rash is not necessarily present in meningococcal meningitis, it is relatively specific for the disease; it does, however, occasionally occur in meningitis due to other bacteria.[1]

Other clues as to the nature of the cause of meningitis may be the skin signs of hand, foot and mouth disease and genital herpes, both of which are associated with various forms of viral meningitis.[9]

[edit] Early complications

A severe case of meningococcal meningitis in which the petechial rash progressed to gangrene and required amputation of all limbs. The patient, Charlotte CleverleyBisman, survived the disease and became a poster child for a meningitis vaccination campaign in New Zealand. People with meningitis may develop additional problems in the early stages of their illness. These may require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure, fast heart rate, high or abnormally low temperature and rapid breathing. Very low blood pressure may occur early, especially but not exclusively in meningococcal illness; this may lead to insufficient blood supply to other organs.[1] Disseminated intravascular coagulation, the excessive activation of blood clotting, may cause both the obstruction of blood flow to organs and a paradoxical increase of bleeding risk. In meningococcal disease, gangrene of limbs can occur.[1] Severe meningococcal and pneumococcal infections may result in hemorrhaging of the adrenal glands, leading to Waterhouse-Friderichsen syndrome, which is often lethal.[10] The brain tissue may swell, with increasing pressure inside the skull and a risk of swollen brain tissue causing herniation. This may be noticed by a decreasing level of consciousness, loss of the pupillary light reflex, and abnormal posturing.[4] Inflammation of the brain tissue may also obstruct the normal flow of CSF around the brain (hydrocephalus).[4] Seizures may occur for various reasons; in children, seizures are common in the early stages of meningitis (30% of cases) and do not necessarily indicate an underlying cause.[3] Seizures may result from increased pressure and from areas of inflammation in the brain tissue.[4] Focal seizures (seizures that involve one limb or part of the body), persistent seizures, late-onset seizures and those that are difficult to control with medication are indicators of a poorer long-term outcome.[1] The inflammation of the meninges may lead to abnormalities of the cranial nerves, a group of nerves arising from the brain stem that supply the head and neck area and control eye movement, facial muscles and hearing, among other functions.[1][6] Visual symptoms and hearing loss may persist after an episode of meningitis (see below).[1] Inflammation of the brain (encephalitis) or its blood vessels (cerebral vasculitis), as well as the formation of blood clots in the veins (cerebral venous thrombosis), may all lead to weakness, loss of sensation, or abnormal movement or function of the part of the body supplied by the affected area in the brain.[1][4]

[edit] Causes
Meningitis is usually caused by infection from viruses or micro-organisms. Most cases are due to infection with viruses,[6] with bacteria, fungi, and parasites being the next most common causes.[2] It may also result from various non-infectious causes.[2]

[edit] Bacterial
The types of bacteria that cause bacterial meningitis vary by age group. In premature babies and newborns up to three months old, common causes are group B streptococci (subtypes III which normally inhabit the vagina and are mainly a cause during the first week of life) and those that normally inhabit the digestive tract such as Escherichia coli (carrying K1 antigen). Listeria monocytogenes (serotype IVb) may affect the newborn and occurs in epidemics. Older children are more commonly affected by Neisseria meningitidis (meningococcus), Streptococcus pneumoniae (serotypes 6, 9, 14, 18 and 23) and those under five by Haemophilus influenzae type B (in countries that do not offer vaccination, see below).[1][3] In adults, N. meningitidis and S. pneumoniae together cause 80% of all cases of bacterial meningitis, with increased risk of L. monocytogenes in those over 50 years old.[3][4] Since the pneumococcal vaccine was introduced, however, rates of pneumococcal meningitis have declined in children and adults.[11] Recent trauma to the skull gives bacteria in the nasal cavity the potential to enter the meningeal space. Similarly, individuals with a cerebral shunt or related device (such as an extraventricular drain or Ommaya reservoir) are at increased risk of infection through those devices. In these cases, infections with staphylococci are more likely, as well as infections by pseudomonas and other Gram-negative bacilli.[3] The same pathogens are also more common in those with an impaired immune system.[1] In a small proportion of people, an infection in the head and neck area, such as otitis media or mastoiditis, can lead to meningitis.[3] Recipients of cochlear implants for hearing loss are at an increased risk of pneumococcal meningitis.[12] Tuberculous meningitis, meningitis due to infection with Mycobacterium tuberculosis, is more common in those from countries where tuberculosis is common, but is also encountered in those with immune problems, such as AIDS.[13] Recurrent bacterial meningitis may be caused by persisting anatomical defects, either congenital or acquired, or by disorders of the immune system.[14] Anatomical defects allow continuity between the external environment and the nervous system. The most common cause of recurrent meningitis is skull fracture,[14] particularly fractures that affect the base of the skull or extend towards the sinuses and petrous pyramids.[14] A literature review of 363 reported cases of recurrent meningitis showed that 59% of cases are due to such anatomical abnormalities, 36% due to immune deficiencies (such as complement deficiency, which predisposes especially to recurrent meningococcal meningitis), and 5% due to ongoing infections in areas adjacent to the meninges.[14]

[edit] Aseptic
The term aseptic meningitis refers loosely to all cases of meningitis in which no bacterial infection can be demonstrated. This is usually due to viruses, but it may be due to bacterial infection that has already been partially treated, with disappearance of the bacteria from the meninges, or by infection in a space adjacent to the meninges (e.g. sinusitis). Endocarditis (infection of the heart valves with spread of small clusters of bacteria through the bloodstream) may cause aseptic meningitis. Aseptic meningitis may also result from infection with spirochetes, a type of bacteria that includes Treponema pallidum (the cause of syphilis) and Borrelia burgdorferi (known for causing Lyme disease). Meningitis may be encountered in cerebral malaria (malaria infecting the brain). Fungal meningitis, e.g. due to Cryptococcus neoformans, is typically seen in people with immune deficiency such as AIDS. Amoebic meningitis, meningitis due to infection with amoebae such as Naegleria fowleri, is contracted from freshwater sources.[2]

[edit] Viral
Viruses that can cause meningitis include enteroviruses, herpes simplex virus type 2 (and less commonly type 1), varicella zoster virus (known for causing chickenpox and shingles), mumps virus, HIV, and LCMV.[9]

[edit] Parasitic
A parasitic cause is often assumed when there is a predominance of eosinophils (a type of white blood cell) in the CSF. The most common parasites implicated are Angiostrongylus cantonensis, Gnathostoma spinigerum, Schistosoma, as well as the conditions cysticercosis, toxocariasis, baylisascariasis, paragonimiasis, and a number of rarer infections and noninfective conditions.[15]

[edit] Non-infectious
Meningitis may occur as the result of several non-infectious causes: spread of cancer to the meninges (malignant meningitis)[16] and certain drugs (mainly non-steroidal anti-inflammatory drugs, antibiotics and intravenous immunoglobulins).[17] It may also be caused by several inflammatory conditions such as sarcoidosis (which is then called neurosarcoidosis), connective tissue disorders such as systemic lupus erythematosus, and certain forms of vasculitis (inflammatory conditions of the blood vessel wall) such as Behet's disease.[2] Epidermoid cysts and dermoid cysts may cause meningitis by releasing irritant matter into the subarachnoid space.[2][14] Mollaret's meningitis is a syndrome of recurring episodes of aseptic meningitis; it is thought to be caused by herpes simplex virus type 2. Rarely, migraine may cause meningitis, but this diagnosis is usually only made when other causes have been eliminated.[2]

[edit] Mechanism
The meninges comprise three membranes that, together with the cerebrospinal fluid, enclose and protect the brain and spinal cord (the central nervous system). The pia

mater is a very delicate impermeable membrane that firmly adheres to the surface of the brain, following all the minor contours. The arachnoid mater (so named because of its spider-web-like appearance) is a loosely fitting sac on top of the pia mater. The subarachnoid space separates the arachnoid and pia mater membranes, and is filled with cerebrospinal fluid. The outermost membrane, the dura mater, is a thick durable membrane, which is attached to both the arachnoid membrane and the skull. In bacterial meningitis, bacteria reach the meninges by one of two main routes: through the bloodstream or through direct contact between the meninges and either the nasal cavity or the skin. In most cases, meningitis follows invasion of the bloodstream by organisms that live upon mucous surfaces such as the nasal cavity. This is often in turn preceded by viral infections, which break down the normal barrier provided by the mucous surfaces. Once bacteria have entered the bloodstream, they enter the subarachnoid space in places where the blood-brain barrier is vulnerablesuch as the choroid plexus. Meningitis occurs in 25% of newborns with bloodstream infections due to group B streptococci; this phenomenon is less common in adults.[1] Direct contamination of the cerebrospinal fluid may arise from indwelling devices, skull fractures, or infections of the nasopharynx or the nasal sinuses that have formed a tract with the subarachnoid space (see above); occasionally, congenital defects of the dura mater can be identified.[1] The large-scale inflammation that occurs in the subarachnoid space during meningitis is not a direct result of bacterial infection but can rather largely be attributed to the response of the immune system to the entrance of bacteria into the central nervous system. When components of the bacterial cell membrane are identified by the immune cells of the brain (astrocytes and microglia), they respond by releasing large amounts of cytokines, hormone-like mediators that recruit other immune cells and stimulate other tissues to participate in an immune response. The blood-brain barrier becomes more permeable, leading to "vasogenic" cerebral edema (swelling of the brain due to fluid leakage from blood vessels). Large numbers of white blood cells enter the CSF, causing inflammation of the meninges, and leading to "interstitial" edema (swelling due to fluid between the cells). In addition, the walls of the blood vessels themselves become inflamed (cerebral vasculitis), which leads to a decreased blood flow and a third type of edema, "cytotoxic" edema. The three forms of cerebral edema all lead to an increased intracranial pressure; together with the lowered blood pressure often encountered in acute infection, this means that it is harder for blood to enter the brain, and brain cells are deprived of oxygen and undergo apoptosis (automated cell death).[1] It is recognized that administration of antibiotics may initially worsen the process outlined above, by increasing the amount of bacterial cell membrane products released through the destruction of bacteria. Particular treatments, such as the use of corticosteroids, are aimed at dampening the immune system's response to this phenomenon.[1][4]

[edit] Diagnosis
CSF findings in different forms of meningitis[18] Type of meningitis Glucose Protein Cells Acute bacterial low high PMNs,

Acute viral Tuberculous Fungal Malignant

normal low low low

often > 300/mm mononuclear, normal or high < 300/mm mononuclear and high PMNs, < 300/mm high < 300/mm usually high mononuclear

[edit] Blood tests and imaging

In someone suspected of having meningitis, blood tests are performed for markers of inflammation (e.g. C-reactive protein, complete blood count), as well as blood cultures.[3][19] The most important test in identifying or ruling out meningitis is analysis of the cerebrospinal fluid through lumbar puncture (LP, spinal tap).[20] However, lumbar puncture is contraindicated if there is a mass in the brain (tumor or abscess) or the intracranial pressure (ICP) is elevated, as it may lead to brain herniation. If someone is at risk for either a mass or raised ICP (recent head injury, a known immune system problem, localizing neurological signs, or evidence on examination of a raised ICP), a CT or MRI scan is recommended prior to the lumbar puncture.[3][19][21] This applies in 45% of all adult cases.[4] If a CT or MRI is required before LP, or if LP proves difficult, professional guidelines suggest that antibiotics should be administered first to prevent delay in treatment,[3] especially if this may be longer than 30 minutes.[19][21] Often, CT or MRI scans are performed at a later stage to assess for complications of meningitis.[1] In severe forms of meningitis, monitoring of blood electrolytes may be important; for example, hyponatremia is common in bacterial meningitis, due to a combination of factors including dehydration, the inappropriate excretion of the antidiuretic hormone (SIADH), or overly aggressive intravenous fluid administration.[4][22]

[edit] Lumbar puncture

A lumbar puncture is done by positioning the patient, usually lying on the side, applying local anesthetic, and inserting a needle into the dural sac (a sac around the spinal cord) to collect cerebrospinal fluid (CSF). When this has been achieved, the "opening pressure" of the CSF is measured using a manometer. The pressure is normally between 6 and 18 cm water (cmH2O);[20] in bacterial meningitis the pressure is typically elevated.[3][19] The initial appearance of the fluid may prove an indication of the nature of the infection: cloudy CSF indicates higher levels of protein, white and red blood cells and/or bacteria, and therefore may suggest bacterial meningitis.[3]

Gram stain of meningococci from a culture showing Gram negative (pink) bacteria, often in pairs The CSF sample is examined for presence and types of white blood cells, red blood cells, protein content and glucose level.[3] Gram staining of the sample may demonstrate bacteria in bacterial meningitis, but absence of bacteria does not exclude bacterial meningitis as they are only seen in 60% of cases; this figure is reduced by a further 20% if antibiotics were administered before the sample was taken, and Gram staining is also less reliable in particular infections such as listeriosis. Microbiological culture of the sample is more sensitive (it identifies the organism in 7085% of cases) but results can take up to 48 hours to become available.[3] The type of white blood cell predominantly present (see table) indicates whether meningitis is bacterial (usually neutrophil-predominant) or viral (usually lymphocyte-predominant),[3] although in the beginning of the disease this is not always a reliable indicator. Less commonly, eosinophils predominate, suggesting parasitic or fungal etiology, among others.[15] The concentration of glucose in CSF is normally above 40% that in blood. In bacterial meningitis it is typically lower; the CSF glucose level is therefore divided by the blood glucose (CSF glucose to serum glucose ratio). A ratio 0.4 is indicative of bacterial meningitis;[20] in the newborn, glucose levels in CSF are normally higher, and a ratio below 0.6 (60%) is therefore considered abnormal.[3] High levels of lactate in CSF indicate a higher likelihood of bacterial meningitis, as does a higher white blood cell count.[20] Various more specialized tests may be used to distinguish between various types of meningitis. A latex agglutination test may be positive in meningitis caused by Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Escherichia coli and group B streptococci; its routine use is not encouraged as it rarely leads to changes in treatment, but it may be used if other tests are not diagnostic. Similarly, the limulus lysate test may be positive in meningitis caused by Gram-negative bacteria, but it is of limited use unless other tests have been unhelpful. [3] Polymerase chain reaction (PCR) is a technique used to amplify small traces of bacterial DNA in order to detect the presence of bacterial or viral DNA in cerebrospinal fluid; it is a highly sensitive and specific test since only trace amounts of the infecting agent's DNA is required. It may identify bacteria in bacterial meningitis and may assist in distinguishing the various causes of viral meningitis (enterovirus, herpes simplex virus 2 and mumps in those not vaccinated for this).[9] Serology (identification of antibodies to viruses) may be useful in viral meningitis.[9] If tuberculous meningitis is suspected, the sample is processed for Ziehl-Neelsen stain, which has a low sensitivity, and tuberculosis culture, which takes a long time to process; PCR is being used increasingly.[13] Diagnosis of cryptococcal meningitis can be made at low cost using an India ink stain of the CSF; however, testing for

cryptococcal antigen in blood or CSF is more sensitive, particularly in persons with AIDS.[23][24][25] A diagnostic and therapeutic conundrum is the "partially treated meningitis", where there are meningitis symptoms after receiving antibiotics (such as for presumptive sinusitis). When this happens, CSF findings may resemble those of viral meningitis, but antibiotic treatment may need to be continued until there is definitive positive evidence of a viral cause (e.g. a positive enterovirus PCR).[9]

[edit] Postmortem

Histopathology of bacterial meningitis: autopsy case of a patient with pneumococcal meningitis showing inflammatory infiltrates of the pia mater consisting of neutrophil granulocytes (inset, higher magnification). Meningitis can be diagnosed after death has occurred. The findings from a post mortem are usually a widespread inflammation of the pia mater and arachnoid layers of the meninges covering the brain and spinal cord. Neutrophil granulocytes tend to have migrated to the cerebrospinal fluid and the base of the brain, along with cranial nerves and the spinal cord, may be surrounded with pusas may the meningeal vessels.[26]

[edit] Prevention
[edit] Behavioral
Bacterial and viral meningitis are contagious. Neither are as contagious as the common cold or flu [27] Both can be transmitted through droplets of respiratory secretions during close contact such as kissing, sneezing or coughing on someone, but cannot be spread by only breathing the air where a person with meningitis has been.[27] Viral meningitis is typically caused by Enteroviruses, and is most commonly spread through fecal contamination.[27] By changing behavior to prevent the causes of transmission, infection by viruses and bacteria can be prevented.

[edit] Pharmaceutical
For some causes of meningitis, prophylaxis can be provided in the long term with vaccine, or in the short term with antibiotics.

Since the 1980s, many countries have included immunization against Haemophilus influenzae type B in their routine childhood vaccination schemes. This has practically eliminated this pathogen as a cause of meningitis in young children in those countries. In the countries where the disease burden is highest, however, the vaccine is still too expensive.[28][29] Similarly, immunization against mumps has led to a sharp fall in the number of cases of mumps meningitis, which prior to vaccination occurred in 15% of all cases of mumps.[9] Meningococcus vaccines exist against groups A, C, W135 and Y.[30] In countries where the vaccine for meningococcus group C was introduced, cases caused by this pathogen have decreased substantially.[28] A quadrivalent vaccine now exists, which combines all four vaccines. Immunization with the ACW135Y vaccine against four strains is now a visa requirement for taking part in the Hajj.[31] Development of a vaccine against group B meningococci has proved much more difficult, as its surface proteins (which would normally be used to make a vaccine) only elicit a weak response from the immune system, or cross-react with normal human proteins.[28][30] Still, some countries (New Zealand, Cuba, Norway and Chile) have developed vaccines against local strains of group B meningococci; some have shown good results and are used in local immunization schedules.[30] In Africa, the current approach for prevention and control of meningococcal epidemics is based on early detection of the disease and emergency reactive mass vaccination of the at-risk population with bivalent A/C or trivalent A/C/W135 polysaccharide vaccines.[32] Routine vaccination against Streptococcus pneumoniae with the pneumococcal conjugate vaccine (PCV), which is active against seven common serotypes of this pathogen, significantly reduces the incidence of pneumococcal meningitis.[28][33] The pneumococcal polysaccharide vaccine, which covers 23 strains, is only administered in certain groups (e.g. those who have had a splenectomy, the surgical removal of the spleen); it does not elicit a significant immune response in all recipients, e.g. small children.[33] Childhood vaccination with Bacillus Calmette-Gurin has been reported to significantly reduce the rate of tuberculous meningitis, but its waning effectiveness in adulthood has prompted a search for a better vaccine.[28] Short-term antibiotic prophylaxis is also a method of prevention, particularly of meningococcal meningitis. In cases of meningococcal meningitis, prophylactic treatment of close contacts with antibiotics (e.g. rifampicin, ciprofloxacin or ceftriaxone) can reduce their risk of contracting the condition, but does not protect against future infections.[19][34]

[edit] Treatment
[edit] Initial treatment
Meningitis is potentially life-threatening and has a high mortality rate if untreated;[3] delay in treatment has been associated with a poorer outcome.[4] Thus treatment with wide-spectrum antibiotics should not be delayed while confirmatory tests are being conducted.[21] If meningococcal disease is suspected in primary care, guidelines

recommend that benzylpenicillin be administered before transfer to hospital.[7] Intravenous fluids should be administered if hypotension (low blood pressure) or shock are present.[21] Given that meningitis can cause a number of early severe complications, regular medical review is recommended to identify these complications early,[21] as well as admission to an intensive care unit if deemed necessary.[4] Mechanical ventilation may be needed if the level of consciousness is very low, or if there is evidence of respiratory failure. If there are signs of raised intracranial pressure, measures to monitor the pressure may be taken; this would allow the optimization of the cerebral perfusion pressure and various treatments to decrease the intracranial pressure with medication (e.g. mannitol).[4] Seizures are treated with anticonvulsants.[4] Hydrocephalus (obstructed flow of CSF) may require insertion of a temporary or long-term drainage device, such as a cerebral shunt.[4]

[edit] Bacterial meningitis

[edit] Antibiotics

Structural formula of ceftriaxone, one of the third-generation cefalosporin antibiotics recommended for the initial treatment of bacterial meningitis. Empiric antibiotics (treatment without exact diagnosis) must be started immediately, even before the results of the lumbar puncture and CSF analysis are known. The choice of initial treatment depends largely on the kind of bacteria that cause meningitis in a particular place. For instance, in the United Kingdom empirical treatment consists of a third-generation cefalosporin such as cefotaxime or ceftriaxone.[19][21] In the USA, where resistance to cefalosporins is increasingly found in streptococci, addition of vancomycin to the initial treatment is recommended.[3][4][19] Empirical therapy may be chosen on the basis of the age of the patient, whether the infection was preceded by head injury, whether the patient has undergone neurosurgery and whether or not a cerebral shunt is present.[3] For instance, in young children and those over 50 years of age, as well as those who are immunocompromised, addition of ampicillin is recommended to cover Listeria monocytogenes.[3][19] Once the Gram stain results become available, and the broad type of bacterial cause is known, it may be possible to change the antibiotics to those likely to deal with the presumed group of pathogens.[3] The results of the CSF culture generally take longer to become available (2448 hours). Once they do, empiric therapy may be switched to specific antibiotic therapy targeted to the specific causative organism and its sensitivities to antibiotics.[3] For an antibiotic to be effective in meningitis, it must not only be active against the pathogenic bacterium, but also reach the meninges in adequate quantities; some antibiotics have inadequate penetrance and therefore have little use in meningitis.

Most of the antibiotics used in meningitis have not been tested directly on meningitis patients in clinical trials. Rather, the relevant knowledge has mostly derived from laboratory studies in rabbits.[3] Tuberculous meningitis requires prolonged treatment with antibiotics. While tuberculosis of the lungs is typically treated for six months, those with tuberculous meningitis are typically treated for a year or longer.[13] In tuberculous meningitis there is a strong evidence base for treatment with corticosteroids, although this evidence is restricted to those without AIDS.[35]

[edit] Steroids
Adjuvant treatment with corticosteroids (usually dexamethasone) has been shown in some studies to reduce rates of mortality, severe hearing loss and neurological damage in adolescents and adults from high income countries which have low rates of HIV.[36] The likely mechanism is suppression of overactive inflammation.[37] Professional guidelines therefore recommend the commencement of dexamethasone or a similar corticosteroid just before the first dose of antibiotics is given, and continued for four days.[19][21] Given that most of the benefit of the treatment is confined to those with pneumococcal meningitis, some guidelines suggest that dexamethasone be discontinued if another cause for meningitis is identified.[3][19] Adjuvant corticosteroids have a different role in children than in adults. Though the benefit of corticosteroids has been demonstrated in adults as well as in children from high-income countries, their use in children from low-income countries is not supported by evidence; the reason for this discrepancy is not clear.[38] Even in highincome countries, the benefit of corticosteroids is only seen when they are given prior to the first dose of antibiotics, and is greatest in cases of H. influenzae meningitis,[3][39] the incidence of which has decreased dramatically since the introduction of the Hib vaccine. Thus, corticosteroids are recommended in the treatment of pediatric meningitis if the cause is H. influenzae and only if given prior to the first dose of antibiotics, whereas other uses are controversial.[3] A 2010 analysis of previous studies has shown that the benefit from steroids may not be as significant as previously found. The one possible significant benefit is reduction of hearing loss in survivors,[40] and adverse neurological outcomes.[41]

[edit] Viral meningitis

Viral meningitis typically requires supportive therapy only; most viruses responsible for causing meningitis are not amenable to specific treatment. Viral meningitis tends to run a more benign course than bacterial meningitis. Herpes simplex virus and varicella zoster virus may respond to treatment with antiviral drugs such as aciclovir, but there are no clinical trials that have specifically addressed whether this treatment is effective.[9] Mild cases of viral meningitis can be treated at home with conservative measures such as fluid, bedrest, and analgesics.[42]

[edit] Fungal meningitis

Fungal meningitis, such as cryptococcal meningitis, is treated with long courses of highly dosed antifungals, such as amphotericin B and flucytosine.[23][43] Raised intracranial pressure is common in fungal meningitis, and frequent (ideally daily) lumbar punctures to relieve the pressure are recommended,[23] or alternatively a lumbar drain.[24]

[edit] Prognosis
Untreated, bacterial meningitis is almost always fatal. Viral meningitis, in contrast, tends to resolve spontaneously and is rarely fatal. With treatment, mortality (risk of death) from bacterial meningitis depends on the age of the patient and the underlying cause. Of the newborn patients, 2030% may die from an episode of bacterial meningitis. This risk is much lower in older children, whose mortality is about 2%, but rises again to about 1937% in adults.[1][4] Risk of death is predicted by various factors apart from age, such as the pathogen and the time it takes for the pathogen to be cleared from the cerebrospinal fluid,[1] the severity of the generalized illness, decreased level of consciousness or abnormally low count of white blood cells in the CSF.[4] Meningitis caused by H. influenzae and meningococci has a better prognosis compared to cases caused by group B streptococci, coliforms and S. pneumonia.[1] In adults, too, meningococcal meningitis has a lower mortality (37%) than pneumococcal disease.[4] In children there are several potential disabilities which result from damage to the nervous system. Sensorineural hearing loss, epilepsy, learning and behavioral difficulties, as well as decreased intelligence, occur in about 15% of survivors.[1] Some of the hearing loss may be reversible.[44] In adults, 66% of all cases emerge without disability. The main problems are deafness (in 14%) and cognitive impairment (in 10%).[4]

[edit] Epidemiology

Demography of meningococcal meningitis. meningitis belt epidemic zones sporadic cases only

Disability-adjusted life year for meningitis per 100,000 inhabitants in 2002.[45] no data 10 10-25 25-50 50-75 75-100 100-200 200-300 300-400 400-500 500-1000 1000-1500 1500 Although meningitis is a notifiable disease in many countries, the exact incidence rate is unknown.[9] Bacterial meningitis occurs in about 3 people per 100,000 annually in Western countries. Population-wide studies have shown that viral meningitis is more common, at 10.9 per 100,000, and occurs more often in the summer. In Brazil, the rate of bacterial meningitis is higher, at 45.8 per 100,000 annually.[6] Sub-Saharan Africa has been plagued by large epidemics of meningococcal meningitis for over a century,[46] leading to it being labeled the "meningitis belt". Epidemics typically occur in the dry season (December to June), and an epidemic wave can last two to three years, dying out during the intervening rainy seasons.[47] Attack rates of 100-800 cases per 100,000 are encountered in this area,[48] which is poorly served by medical care. These cases are predominantly caused by meningococci.[6] The largest epidemic ever recorded in history swept across the entire region in 19961997, causing over 250,000 cases and 25,000 deaths.[49] Meningococcal disease occurs in epidemics in areas where many people live together for the first time, such as army barracks during mobilization, college campuses[1] and the annual Hajj pilgrimage.[31] Although the pattern of epidemic cycles in Africa is not well understood, several factors have been associated with the development of epidemics in the meningitis belt. They include: medical conditions (immunological susceptibility of the population), demographic conditions (travel and large population displacements), socioeconomic conditions (overcrowding and poor living conditions), climatic conditions (drought and dust storms), and concurrent infections (acute respiratory infections).[48] There are significant differences in the local distribution of causes for bacterial meningitis. For instance, while N. meningitides groups B and C cause most disease episodes in Europe, group A is found in Asia and continues to predominate in Africa, where it causes most of the major epidemics in the meningitis belt, accounting for about 80% to 85% of documented meningococcal meningitis cases.[48]

[edit] History
Some suggest that Hippocrates may have realized the existence of meningitis,[6] and it seems that meningism was known to pre-Renaissance physicians such as Avicenna.[50]

The description of tuberculous meningitis, then called "dropsy in the brain", is often attributed to Edinburgh physician Sir Robert Whytt in a posthumous report that appeared in 1768, although the link with tuberculosis and its pathogen was not made until the next century.[50][51] It appears that epidemic meningitis is a relatively recent phenomenon.[52] The first recorded major outbreak occurred in Geneva in 1805.[52][53] Several other epidemics in Europe and the United States were described shortly afterward, and the first report of an epidemic in Africa appeared in 1840. African epidemics became much more common in the 20th century, starting with a major epidemic sweeping Nigeria and Ghana in 19051908.[52] The first report of bacterial infection underlying meningitis was by the Austrian bacteriologist Anton Weichselbaum, who in 1887 described the meningococcus.[54] Mortality from meningitis was very high (over 90%) in early reports. In 1906, antiserum was produced in horses; this was developed further by the American scientist Simon Flexner and markedly decreased mortality from meningococcal disease.[55][56] In 1944, penicillin was first reported to be effective in meningitis.[57] The introduction in the late 20th century of Haemophilus vaccines led to a marked fall in cases of meningitis associated with this pathogen,[29] and in 2002 evidence emerged that treatment with steroids could improve the prognosis of bacterial meningitis.[37][38]
[56]