S1: the first heart sound produced by closure of the atrioventricular (mitral and tricuspid) valves S2: the

second heart sound produced by closure of the semilunar (aortic and pulmonic) valves S3: an abnormal heart sound detected early in diastole as resistance is met to blood entering either ventricle; most often due to volume overload associated with heart failure S4: an abnormal heart sound detected late in diastole as resistance is met to blood entering either ventricle during atrial contraction; most often caused by hypertrophy of the ventricle

left ventricle is situated posteriorly. As a result of this close proximity to the chest wall, the pulsation created during normal ventricular contraction, called the apical impulse (also called the point of maximal impulse [PMI]), is easily detected. In the normal heart, the PMI is located at the intersection of the midclavicular line of the left chest wall and the fifth intercostals space

Cardiac output refers to the amount of blood pumped by each ventricle during a given period. The cardiac output in a resting adult is about 5 L/min but varies greatly depending on the metabolic needs of the body. Cardiac output is computed by multiplying the stroke volume by the heart rate. Stroke volume is the amount of blood ejected per heartbeat. The average resting stroke volume is about 70 mL, and the heart rate is 60 to 80 bpm. Cardiac output can be affected by changes in either stroke volume or heart rate.

The following are the most common signs and symptoms of CVD, with related medical diagnoses in parentheses: Chest pain or discomfort (angina pectoris, ACS, dysrhythmias, valvular heart disease) Shortness of breath or dyspnea (ACS, cardiogenic shock, HF, valvular heart disease) Peripheral edema, weight gain, abdominal distention due to enlarged spleen and liver or ascites (HF) Palpitations (tachycardia from a variety of causes, including ACS, caffeine or other stimulants, electrolyte imbalances, stress, valvular heart disease, ventricular aneurysms) Vital fatigue, sometimes referred to as vital exhaustion (an early warning symptom of ACS, HF, or valvular heart disease, characterized by feeling unusually tired or fatigued, irritable, and dejected)

 Dizziness, syncope, or changes in level of consciousness (cardiogenic shock, cerebrovascular disorders, dysrhythmias, hypotension, postural hypotension, vasovagal episode)

Chest Pain
Chest pain and discomfort are common symptoms that may be caused by a number of cardiac and noncardiac problems.

During the assessment the patient is asked to identify the quantity of pain using a 0 (no pain) to 10 (worst pain) scale. Next, the nurse asks the patient to describe the character or quality of the pain or discomfort and its location. The nurse needs to determine whether there is radiation to or discomfort in other areas and must assess for associated signs and symptoms such as diaphoresis or nausea. It is important to identify the events that precipitate the onset of symptoms, the duration of the symptoms, and measures that aggravate or relieve the symptoms. The nurse should keep the following important points in mind when assessing patients reporting chest pain or discomfort:

The location of chest symptoms is not well correlated with the cause of the pain. For example, substernal chest pain can result from a number of causes as outlined in Table 26-2. The severity or duration of chest pain or discomfort does not predict the seriousness of its cause. For example, a patient experiencing esophageal spasm may rate chest pain as a 10/10 (eg, the worst pain the patient has ever felt), whereas a patient experiencing a myocardial infarction (MI) may report only mild to moderate chest pressure.

More than one clinical cardiac condition may occur simultaneously. During an MI, patients may report chest pain from myocardial ischemia, shortness of breath from HF, and palpitations from dysrhythmias. Both HF and dysrhythmias can be complications of an acute MI.
Angina pectoris Acute coronary syndrome (ACS) (unstable angina, myocardial infarction [MI])

Angina:
Uncomfortable pressure, squeezing, or fullness in substernal chest area Can radiate across chest to the medial aspect of one or both arms and hands, jaw, shoulders, upper back, or epigastrium Radiation to arms and hands, described as numbness, tingling, or aching

Duration : Angina: 515 min Precipitating Events or Aggravating Factors:

Angina: Physical exertion, emotional upset, eating large meal, or exposure to extremes in temperature

ACS: Same as angina pectoris Pain or discomfort ranges from mild to severe Associated with shortness of breath, diaphoresis, palpitations, fatigue, and nausea or vomiting Duration:
ACS: > 15 min

Precipitating Events or Aggravating Factors: ACS: Emotional upset or unusual physical exertion occurring within 24 hr of symptom onset Can occur at rest or while asleep

Alleviating factors: ACS: Morphine, reperfusion of coronary artery with thrombolytic agent or percutaneous coronary intervention

Pericarditis:
Symptoms:

Sharp, severe substernal or epigastric pain Can radiate to neck, arms, and back Associated symptoms include: Fever Malaise Dyspnea cough, nausea dizziness palpitations Duration:Intermittent

Precipitating Events or Aggravating Factors: Sudden onset Pain increases with inspiration, swallowing, coughing, and rotation of trunk

Alleviating factors:
Sitting upright, Analgesia Anti-inflammatory medications

Pulmonary disorders (pneumonia, pulmonary embolism)

Characteristics: Sharp, severe substernal or epigastric pain arising from inferior portion of pleura (referred to as pleuritic pain) Patient may be able to localize the pain Durations: > 30mins Precipitating Events or Aggravating Factors: Follows an infectious or non-infectious process (MI,cardiac surgery, cancer, immune disorders, uremia) Pleuritic pain increases with inspiration, coughing, movement, and supine positioning Occurs in conjunction with community-acquired or nosocomial lung infections (pneumonia) or deep vein thrombosis (pulmonary embolism) Early depolarizations of the atrium or ventricle cause premature contractions, placing the patient at risk for dysrhythmias. Premature ventricular contractions in certain situations, such as the presence of myocardial ischemia, are of concern because these early ventricular depolarizations can trigger lifethreatening dysrhythmias, including ventricular tachycardia or ventricularfibrillation Alleviating factors: Treat underlying cause

Esophageal disorders (hiatal hernia, reflux esophagitis or spasm) Characteristics:

Substernal pain described as sharp, burning, or heavy Often mimics angina Can radiate to neck, arm, or shoulders

Duration: 5-60 min Precipitating Events or Aggravating Factors: Recumbency, cold liquids, exercise

Alleviating factors: Food or antacid Nitroglycerin

Anxiety and panic disorders: Character: Pain described as stabbing to dull ache Associated with diaphoresis, palpitations, shortness of breath, tingling of hands or mouth, feeling of unreality, or fear of losing control Duration : Peaks IN 10 MIN Precipitating Events or Aggravating Factors: Can occur at any time including during sleep Can be associated with a specific trigger Alleviating factor: Removal of stimulus, relaxation medications to treat anxiety or underlying disorder

Musculoskeletal disorders (costochondritis) Characteristics:

Sharp or stabbing pain localized in anterior Most often unilateral Can radiate across chest to epigastrium or back

Duration: Hours to Days Percipitating Events and Aggravasting factors:

Most often follows respiratory tract infection with significant coughing, vigorous exercise, or posttrauma Some cases are idiopathic Exacerbated by deep inspiration, coughing, sneezing, and movement of upper torso or arms

Alleviating Factors:

Rest Ice Heat Anti-inflammatory medications

Symptoms of Acute Coronary Syndrome Because CAD is so prevalent, all patients reporting new or worsening cardiac symptoms, particularly those at risk for CAD or who have a history of CAD, should be evaluated initially for ACS. There are several

distinct characteristics of ACS symptoms that need to be kept in mind during assessment of the patient in which ACS is suspected: Acute coronary syndrome The majority of patients with ACS experience prodromal symptoms sometimes a month or more prior to developing this acute event.

Prodromal symptoms include fatigue, shortness of breath, sleep disturbances,anxiety, or fleeting chest discomfort (aching, pressure) that wax and wane. Approximately 50% of men and women with ACS experience chest symptoms, whereas the remainder may develop a variety of symptoms such as upper back, shoulder, arm, or neck pain; epigastric burning; or shortness of breath

diabetes may prevent these patients from experiencing pain or discomfort associated with myocardial ischemia. Instead, they may report vital fatigue or shortness of breath

When straining during defecation, the patient bears down (the Valsalva maneuver), which momentarily increases pressure on the baroreceptors. This triggers a vagal response, causing the heart rate to slow and resulting in syncope in some patients. Straining during urination can produce the same response
COMMON SKIN FINDINGS ASSOCIATED WITH CARDIOVASCULAR DISEASE

Pallor (decreased color of the skin, often noted around the fingernails, lips, and oral mucosa, or in patients with dark skin, the palms of the hands and soles of the feet) Caused by lack of oxyhemoglobin, it is a result of anemia or decreased arterial perfusion.

Peripheral cyanosis (a bluish tinge, most often of the nails It suggests decreased blood flow to a particular area, and skin of the nose, lips, earlobes, and extremities) which allows more time for the hemoglobin molecule to become desaturated. This may occur normally in peripheral vasoconstriction associated with a cold environment, in patients with in patients with anxiety, or in disease states such as heart failure

Xanthelasma (yellowish, slightly raised plaques in the skin observed along the nasal portion of one or both eyelids) It may indicate elevated cholesterol levels (hypercholesterolemia).

Ecchymosis (bruise, a purplish-blue color fading to green, yellow, or brown over time) Patients who are receiving platelet-inhibiting medications or anticoagulant therapy should be carefully observed for unexplained ecchymosis. In these patients, excessive bruising indicates reduced platelet function (platelet-inhibiting medications) or prolonged clotting times (prothrombin, international normalized ratio, or partial thromboplastin time) caused by an anticoagulant dosage that is too high.

Thinning of skin surrounding a pacemaker or implantable cardioverter-defibrillator (ICD) This could indicate erosion of the device through the skin.

Cool/cold and moist skin In cardiogenic shock, sympathetic nervous system stimulation causes vasoconstriction, and the skin becomes cold and clammy. During acute coronary syndrome, diaphoresis is common

Pulse Pressure The difference between the systolic and the diastolic pressures is called the pulse pressure. It is a reflection of stroke volume, ejection velocity, and systemic vascular resistance. Pulse pressure, which normally is 30 to 40 mm Hg, indicates how well the patient maintains cardiac output.

The pulse pressure increases in conditions that elevate the stroke volume (anxiety, exercise, bradycardia), reduce systemic vascular resistance (fever), or reduce distensibility of the arteries (atherosclerosis, aging, hypertension)

Decreased pulse pressure reflects reduced stroke volume and ejection velocity (shock, HF, hypovolemia, mitral regurgitation) or obstruction to blood flow during systole (mitral or aortic stenosis). A pulse pressure of less than 30 mm Hg signifies a serious reduction in cardiac output and requires further cardiovascular assessment

Although there are many causes of postural hypotension, the three most common causes in patients with cardiac problems are a reduced volume of fluid or blood in the circulatory system (intravascular volume depletion, dehydration), inadequate vasoconstrictor mechanisms, and insufficient autonomic effect on vascular constriction

Right-sided heart function can be estimated by observing the pulsations of the jugular veins of the neck and the central venous pressure (CVP), which reflects right atrial or right ventricular end-diastolic pressure (the pressure immediately preceding the contraction of the right ventricle). The veins normally are not apparent if the patients head is elevated more than 30 degrees. Obvious distention of the veins with the patients head elevated 45 to 90 degrees indicates an abnormal increase in the volume of the venous system This occurs with right ventricular failure, pulmonary hypertension, and pulmonary stenosis; less commonly with obstruction of blood flow in the superior vena cava; and rarely with acute massive pulmonary embolism. Aortic areasecond intercostal space to the right of the sternum. Pulmonic areasecond intercostal space to the left of the sternum Erbs pointthird intercostal space to the left of the sternum Tricuspid arealower half of the sternum along the left parasternal area Mitral (apical) arealeft fifth intercostal space at the midclavicular line Epigastric areabelow the xiphoid process S1First Heart Sound. Tricuspid and mitral valve closure creates the first heart sound (S1). The word lub is used to replicate its sound. S1 is usually heard the loudest at the apical area. The intensity of S1 increases during tachycardias or with mitral stenosis.

S2Second Heart Sound. Closure of the pulmonic and aortic valves produces the second heart sound (S2), commonly referred to as the dub sound. The aortic component of S2 is heard the loudest over the aortic and pulmonic areas S3Third Heart Sound. It represents a normal finding in children and adults up to 35 or 40 years of age In older adults, it is a sign of significant pathophysiology, most commonly due to volume overload of one or both ventricles If the right ventricle is involved, a right-sided S3 is heard over the tricuspid area with the patient in a supine position left-sided S3 is best heard over the apical area. Having the patient turn to the left lateral position may facilitate auscultation of an S3 generated by the left ventricle

S4Fourth Heart Sound. S4 occurs late in diastole This resistance to blood flow is due: ventricular hypertrophy caused by hypertension CAD Cardiomyopathies Aortic stenosis S4 produced in the left ventricle is auscultated over the apical area with the patient in the left lateral position.

Murmurs. Are created by turbulent flow of blood. The causes of the turbulence may be a critically narrowed valve, a malfunctioning valve that allows regurgitant blood flow, a congenital defect of the ventricular wall, a defect between the aorta and the pulmonary artery, or an increased flow of blood through a normal structure (eg, with fever, pregnancy, hyperthyroidism

Friction Rub A harsh, grating sound that can be heard in both systole and diastole is called a friction rub Caused by abrasion of the inflamed pericardial surfaces from pericarditis Can sound like a murmur. Murmur evident at both systole and diastole Heard best using the diaphragm of the stethoscope, with the patient sitting up and leaning forward. Inspection of the Extremities Decreased capillary refill time indicates a slower peripheral flow rate from sluggish reperfusion and is often observed in patients with hypotension or HF Capillary refill best to estimate rate of peripheral blood flow < 3sec

Vascular changes Decreased arterial circulation include a decrease in quality or loss of pulse, discomfort or pain, paresthesia, numbness, decrease in temperature, pallor, and loss of movement After invasive cardiac procedures (eg, cardiac catheterization), affected extremities should be assessed frequently for vascular changes Hematoma Major blood vessels of the arms and legs may be used for catheter insertion o During these procedures, systemic anticoagulation with heparin is necessary, and minor or small hematomas may occur at the catheter puncture site o However, large hematomas are a serious complication that can compromise circulating blood volume and cardiac output Peripheral edema Assessed by pressing firmly for 5 seconds with the thumb over the dorsum of eachfoot, behind each medial malleolus, and over the shin o Peripheral edema is observed in patients with HF and in those with peripheral vascular diseases such as deep vein thrombosis or chronic venous insufficiency.

Abdomen Abdominal distension: Ascites develops in patients with right ventricular or biventricular HF (both right- and left-sided HF) In the failing right heart, abnormally high chamber pressures impede the return of venous blood o the liver and spleen become engorged with excessive venous blood (hepatosplenomegaly) o Pressure in the portal system rises, fluid shifts from the vascular bed into the abdominal cavity. Hepatojugular reflux: Patient is positioned so that the jugular venous pulse is visible in the lower part of the neck firm pressure is applied over the right upper quadrant of the abdomen for 30 to 60 seconds Increase of 1 cm or more in jugular venous pressure is indicative of a positive hepatojugular reflux. This positive test aids in confirming the diagnosis of HF Bladder distention: Urine output is an important indicator of cardiac function.

Sodium (Na_) 135145 mEq/L Low or high serum sodium levels do not directly affect cardiac function. Hyponatremia: Decreased sodium levels indicate fluid excess and can be caused by heart failure or administration of thiazide diuretics. Hypernatremia: Increased sodium levels indicate fluid deficits and can result from decreased water intake or loss of water through excessive sweating or diarrhea

Blood Chemistries
Potassium (K+) Potassium. 3.55.0 mEq/L Hypokalemia: Decreased potassium levels due to administration of potassium-excreting diuretics can cause many forms of dysrhythmias, including life-threatening ventricular tachycardia or ventricular fibrillation, and predispose patients taking digitalis preparations to digitalis toxicity

Hyperkalemia: Increased potassium levels can result from an increased intake of potassium (eg, foods high in potassium or potassium supplements), decreased renal excretion of potassium, use of potassiumsparing diuretics (eg, spironolactone), or use of angiotensin-converting enzyme inhibitors (ACE inhibitors) that inhibit aldosterone function. Serious consequences of hyperkalemia include heart block, asystole, and life-threatening ventricular dysrhythmias.

Calcium (Ca ++) 8.610.2 mg/dL Calcium is necessary for blood coagulability, neuromuscular activity, and automaticity of the nodal cells (sinus and atrioventricular nodes). Hypocalcemia: Decreased calcium levels slow nodal function and impair myocardial contractility. The latter effect increases the risk for heart failure Hypercalcemia: Increased calcium levels can occur with the administration of thiazide diuretics because these medications reduce renal excretion of calcium. Hypercalcemia potentiates digitalis toxicity, causes

increased myocardial contractility, and increases the risk for varying degrees of heart block and sudden death from ventricular fibrillation. Glucose Glucose Fasting. 60110 mg/dL Levels are elevated in stressful situations, when mobilization of endogenous epinephrine results in conversion of liver glycogen to glucose. A1C: It reflects the blood glucose levels over 23 mo. The glycemic goal is to maintain the hemoglobin A1C below 7% reflecting consistent near-normal blood glucose levels.

Coagulation Studies
Partial Thromboplastin Time (PTT) PTT or aPTT measures the activity of the intrinsic pathway and is used to assess the effects of unfractionated heparin

Therapeutic range is 1.52.5 times baseline values

C - reactive protein Produced by the liver in response to systemic inflammation. Inflammation is thought to play a role in the development and progression of atherosclerosis Used as an adjunct to other tests to predict CVD risk (3.0 mg/dL or greater) ----- greatest risk for CVD (1.0 to 3.0 mg/dL) -----moderate (less than 1.0 mg/dL) low

Elevated hs-CRP may place patients with ACS at risk for recurrent cardiac events, including unstable angina and acute MI

Homocysteine:
Enhances the clinicians ability to assess the patients risk for CVD It can damage the endothelial lining of arteries and promote thrombus formation is thought to indicate a high risk for CAD, stroke, and peripheral vascular disease Genetic factors and a diet low in folic acid, vitamin B6, and vitamin B12 are associated with elevated homocysteine levels A 12-hour fast is necessary before drawing a blood sample for an accurate serum measurement.

Opening snaps are abnormal diastolic sounds heard during opening of an AV valve. For example, mitral stenosis can cause an opening snap, which is an unusually high-pitched sound very early in diastole

Continuous ECG monitoring is the standard of care for patients who are at high risk for dysrhythmias Hardwire cardiac monitoring and telemetry systems vary in sophistication

Cardiac Stress Testing Normally, the coronary arteries dilate to four times their usual diameter in response to increased metabolic demands for oxygen and nutrients coronary arteries affected by atherosclerosis dilate less, compromising blood flow to the myocardium and causing ischemia Noninvasive ways to evaluate the response of the cardiovascular system to stress exercise stress test pharmacologic stress test mental or emotional stress test

Helps determine the following: (1) presence of CAD, (2) cause of chest pain (3) functional capacity of the heart after an MI or heart surgery (4) effectiveness of antianginal or antiarrhythmic medications (5) dysrhythmias that occur during physical exercise

Exercise Stress Testing goal is to increase the heart rate to the target heart rate, which is 80% to 90% of the maximum predicted heart rate based on the patients age and gender Nursing Interventions Fast for 4 hours before the test avoid stimulants such as tobacco and caffeine physician may instruct the patient not to take certain cardiac medications, such as beta adrenergic blocking agents

Pharmacologic Stress Testing Vasodilating agents used dipyridamole (Persantine) effects last about 15 to 30 minutes adenosine (Adenocard) extremely short half-life (less than 10 seconds) Dobutamine, a synthetic sympathomimetic, increases heart rate, myocardial contractility, and BP Nursing Interventions Fast 4 hours before the test No caffeine Patients taking aminophylline, theophylline, or dipyridamole are instructed to stop taking these medications for 24 to 48 hours before the test (if tolerated) The patient is informed about the transient sensations that may occur during infusion of the vasodilating agent, such as flushing or nausea, which will disappear quickly

Echocardiography Noninvasive ultrasound test that is used to measure the ejection fraction and examine the size, shape, and motion of cardiac structures Useful for diagnosing - pericardial effusions , chamber size and the etiology of heart murmurs function of heart valves

Transesophageal Echocardiography: Transesophageal echocardiography (TEE), provides clearer images because ultrasound waves pass through less tissue A topical anesthetic agent and moderate sedation are used during a TEE First-line diagnostic tool for: CVD HF Valvular heart disease Dysrhythmias

Complications are caused by sedation and impaired swallowing resulting from the topical anesthesia (respiratory depression and aspiration) and by insertion and manipulation of the transducer into the esophagus and stomach (vasovagal response or esophageal perforation).

Nursing Interventions Fast for 6 hours prior to the study Recovery period, the patient must maintain bed rest with the head of the bed elevated to 45 degrees Nurse monitors patient for dyspnea assesses vital signs SpO2 level of consciousness gag reflex usually returns w/in 2hrs Myocardial Perfusion Imaging Radioisotope Tl201 crosses into the cells of healthy myocardium and is used to assess myocardial perfusion It is taken up more slowly and in smaller amounts by myocardial cells that are ischemic from decreased blood flow Thallium does not cross into areas of the myocardium that have been scarred by MI Tc99m. Technetium can be combined with various chemical compounds, giving it an affinity for different types of cells

Computed Tomography uses x-rays to provide cross-sectional images of the chest, including the heart and great vessels used to evaluate cardiac masses and diseases of the aorta and pericardium EBCT, also known as the ultrafast CT: Used to evaluate Bypass graft patency, Congenital heart lesions Left and right ventricular muscle mass Chamber volume Cardiac output, Ejection fraction A calcium score is derived that predicts the likelihood of cardiac events, such as MI Magnetic Resonance Angiography MRA uses a powerful magnetic field and computer-generated pictures to image the heart and great vessels. It is valuable in diagnosing diseases of the aorta, heart muscle, and pericardium, as well as congenital heart lesions MRA is distorted by respirations, the beating heart

Nursing Interventions Carefully screen patients for contraindications Pacemaker Metal plates Prosthetic joints, or other metallic implants Remove Transdermal patches that contain a heat-conducting aluminized layer ( NicoDerm, Androderm, Transderm Nitro, Transderm Scop, Catapres- TTS)

Cardiac Catheterization
Invasive diagnostic procedure in which radiopaque arterial and venous catheters are introduced Into selected blood vessels of the right and left sides of the heart Frequently used to diagnose CAD, assess coronary artery patency, and determine the extent of atherosclerosis and determine whether revascularization procedures, including PCI or coronary artery bypass surgery

Cardiac catheterization is also used to diagnose pulmonary arterial hypertension or to treat stenotic heart valves via percutaneous balloon valvuloplasty Radiopaque contrast agents are used to visualize the coronary arteries. Some contrast agents contain iodine, and the patient is assessed before the procedure for previous reactions to contrast agents or allergies to iodine-containing substances

Antihistamines or methylprednisolone (Solu-Medrol) may be administered before the procedure to protect patient from ARF requires 2 to 6 hours of bed rest afte

Several options to achieve arterial hemostasis after catheter removal, including manual pressure, mechanical compression devices such as the FemoStop (placed over puncture site for 30 minutes) Saline-soaked gelatin sponge (QuickSeal), collagen (VasoSeal), sutures (Perclose,Techstar)

Angiography Technique in which a contrast agent is injected into the vascular system to outline the heart and blood vessels. Common sites for selective angiography are the aorta, the coronary arteries, and the right and left sides of the heart

Aortography
An aortogram is a form of angiography that outlines the lumen of the aorta and the major arteries arising from it

Coronary Arteriography Coronary arteriography involves the introduction of a catheter into the right or left brachial or femoral artery, which is then passed into the ascending aorta and manipulated into the right and left coronary arteries Used to evaluate the degree of atherosclerosis and to determine treatment

Right Heart Catheterization Usually precedes left heart catheterization. It involves the passage of a catheter from an antecubital or femoral vein into the right atrium, right ventricle, pulmonary artery, and pulmonary arterioles Pressures and oxygen saturation levels from each of these areas are obtained and recorded Potential complications include: Cardiac dysrhythmias, Venous spasm Infection of the insertion site Cardiac perforation Rarely cardiac arrest

Left Heart Catheterization

Performed to evaluate the patency of the coronary arteries and the function of the left ventricle and the mitral and aortic valves Potential complications include Dysrhythmias MI perforation of the heart or great vessels, s Systemic embolization Nursing Interventions Fast, usually for 8 to 12 hours, before the procedure (Palpitation) may be felt in the chest because of extra heartbeats that almost always occur Patient may be asked to cough and to breathe deeply, especially after the injection of contrast agent Injection of a contrast agent into either side of the heart may produce a flushed feeling throughout the body and a sensation similar to the need to void, which subsides in 1 minute or less Nursing responsibilities: Catheter access site is observed for bleeding or hematoma formation Peripheral pulses are assessed in the affected extremity (dorsalis pedis and posterior tibial pulses in the lower extremity, radial pulse in the upper extremity) every 15 minutes for 1 hour, and then every 1 to 2 hours until the pulses are stable Temperature, color, and capillary refill of the affected extremity are frequently evaluated o numbness, or tingling sensations that may indicate arterial insufficiency vasovagal reaction, consisting of: o bradycardia, hypotension, and nausea, can be precipitated by a distended bladder or by discomfort from manual pressure that is applied during removal of an arterial or venous catheter reversed by promptly elevating the lower extremities above the level of the heart, infusing a bolus of IV fluid, and administering IV atropine to treat the bradycardia

Bed rest is maintained for 2 to 6 hours after the procedure. If manual or mechanical pressure is used, the patient must remain on bed rest for up to 6 hours with the affected leg straight and the head of the bed elevated no greater than 30 degrees

Patient is instructed to report chest pain and bleeding or sudden discomfort from the catheter insertion sites promptly Patient is monitored for contrast agentinduced nephropathy by observing for elevations in serum creatinine levels Oral and IV hydration is used to increase urinary output and flush the contrast agent Monitor for bleeding at insertion site and orthostatic hypotension

Electrophysiologic Testing Invasive procedure that plays a major role in the diagnosis and management of serious dysrhythmias Indications: Syncope Palpitations or both For survivors of cardiac arrest from ventricular fibrillation

Used to distinguish atrial from ventricular tachycardias when the determination cannot be made from the 12-lead ECG Evaluate how readily a life-threatening dysrhythmia can be induced Ventricular tachycardia Ventricular fibrillation

EPS used to evaluate AV node function, evaluate the effectiveness of antiarrhythmic medications in suppressing the dysrhythmia, or determine the need for other therapeutic interventions, such as a pacemaker, implantable cardioverter-defibrillator, or radiofrequency ablation

Hemodynamic Monitoring Continuous assessment of their cardiovascular system to diagnose and manage their complex medical conditions Use of direct pressure monitoring systems. Common forms include: Central venous pressure (CVP) Pulmonary artery pressure Intra-arterial BP monitoring. Arterial catheter is introduced into the appropriate blood vessel or heart chamber. Connected to a pressure monitoring system that has several components, including: Flush system composed of IV solution (eg heparin) continuous manual flushing pressure bag placed around the flush solution that is maintained at 300 mm Hg of pressure o pressurized flush system delivers 3 to 5 mL of solution per hour transducer to convert the pressure coming from the artery or heart chamber into an electrical signal Before the system is used to obtain pressure measurements, the nurse checks that the stopcock of the transducer is positioned at the level of the atrium landmark is referred to as the phlebostatic axis nurse establishes the zero reference point in order to ensure that the system is properly functioning at atmospheric pressure Measurements of CVP, BP, and pulmonary artery pressures can be made with the head of the bed elevated up to 60 degrees, but the system must be repositioned to the phlebostatic axis to ensure an accurate reading Complications from use of hemodynamic monitoring systems are uncommon and can include: Pneumothorax Infection air embolism

nurse observes for signs of pneumothorax during the insertion of catheters using a central venous approach (CVP and pulmonary artery catheters) (after 72 to 96 hours), the greater the risk of infection. Air emboli can be introduced into the vascular system if the stopcocks attached to the pressure transducers are mishandled during blood drawing, administration of medications

Central Venous Pressure Monitoring CVP is a measurement of the pressure in the vena cava or right atrium. CVP also reflects the filling pressure of the right ventricle (preload). normal CVP is 2 to 6 mm Hg greater than 6 mm Hg indicates an elevated right ventricular preload most common cause of elevated CVP hypervolemia or right-sided HF

Low CVP can be caused by hypovolemia Dehydration excessive blood loss vomiting or diarrhea overdiuresis Diagnosis can be substantiated when a rapid IV infusion of fluid causes the CVP to increase Singlelumen or multilumen catheter through the external jugular, antecubital, or femoral vein into the vena cava just above or within the right atrium Catheter placement is confirmed by chest X-Ray

Pulmonary Artery Pressure Monitoring used in critical care for assessing: left ventricular function diagnosing the etiology of shock Evaluating the patients response to medical interventions (eg, fluid administration, vasoactive medications) Thermodilution catheter has three additional features that enable it to: measure cardiac output port for infusing IV fluids and medications

During insertion of the pulmonary artery catheter observe for: pressure and waveform dysrhythmias As the catheter progresses through the right heart to the pulmonary artery

PA-cath Measures: Right atrial Pulmonary artery systolic Pulmonary artery diastolic Wedge pressures Mean pulmonary artery Pulmonary artery

Used to evaluate left Ventricular filling pressures ( left ventricular preload).

Pulmonary artery wedge pressure is achieved by inflating the balloon tip, which causes it to float more distally into a smaller portion of the pulmonary artery until it is wedged into position.

Wedge pressure is measured immediately and the balloon is deflated promptly to restore blood flow

Serious complications include: Pulmonary artery rupture Pulmonary thromboembolism, Pulmonary infarction Catheter kinking Dysrhythmias Air embolism

Intra-Arterial Blood Pressure Monitoring Used to obtain direct and continuous BP measurements in critically ill patients have severe hypertension or hypotension. Useful when arterial blood gas measurements and blood samples need to be obtained frequently involved extremity is assessed by the Allen test or an ultrasonic Doppler study because placing an arterial catheter can further impede perfusion to an area that has poor circulation

Allen test is used to evaluate perfusion of the hand and fingers by the radial and ulnar arteries: 1. The hand is elevated and the patient is asked to make a fist for 30 seconds 2. nurse compresses the radial and ulnar arteries simultaneously, causing the hand to blanch 3. After the patient opens the fist, the nurse releases the pressure on the ulnar artery 4. If blood flow is restored (hand turns pink) within 6 seconds Circulation to the hand may be adequate enough to tolerate placement of a radial artery catheter

Doppler is the most accurate method for assessing arterial perfusion of the hand

Nursing Interventions: The nurse monitors the patient for complications which include: local obstruction with distal ischemia massive ecchymosis dissection air embolism blood loss pain arteriospasm infection After measuring the pulmonary artery wedge pressure, the nurse ensures that the balloon is deflated and that the catheter has returned to its normal position. This important intervention is verified by evaluating the pulmonary artery pressure waveform displayed on the bedside monitor

Chapter 27
Dysrhythmias
Dysrhythmias are disorders of the formation or conduction (or both) of the electrical impulse within the heart. This part of atrial contraction is frequently referred to as the atrial kick and accounts for nearly one third of the volume ejected during ventricular contraction Bundle of his R&L bundle branches Purkinje fibers located in the ventricular muscles

Electrical stimulation is called depolarization, and the mechanical contraction is called systole. Electrical relaxation is called repolarization, and mechanical relaxation is called diastole

Stimulation of the sympathetic system increases heart rate (positive chronotropy) Conduction through the AV node (positive dromotropy) Force of myocardial contraction (positive inotropy)

Sympathetic stimulation also constricts peripheral blood vessels, therefore increasing blood pressure

Parasympathetic stimulation reduces the heart rate (negative chronotropy) AV conduction (negative dromotropy) and the force of atrial myocardial contraction

The decreased sympathetic stimulation results in dilation of arteries, thereby lowering blood pressure

Chart 27-1Identifying Cardiac Rhythms

Sites of Origin Sinus (SA) node Atria Atrioventricular (AV) node or junction Ventricles Mechanisms of Formation or Conduction Normal (idio) rhythm Bradycardia Tachycardia Dysrhythmia Flutter Fibrillation Premature complexes Conduction blocks

P wave: atrial depolarization 0.11 seconds or less in duration QRS complex represents ventricular depolarization less than 0.12 seconds T wave represents ventricular repolarization

U wave hypokalemia, hypertension, or heart disease

PR interval ranges from 0.12 to 0.20 seconds is measured from the beginning of the P wave to the beginning of the QRS complex and represents the time needed for sinus node stimulation, atrial depolarization, and conduction through the AV node before ventricular depolarization ST segment must be isometric (flat against line) if not may indicate cardiac ischemia Which represents early ventricular repolarization, lasts from the end of the QRS complex to the beginning of the T wave QT interval usually 0.32 to 0.40 seconds which represents the total time for ventricular depolarization and repolarization, is measured from the beginning of the QRS complex to the end of the T wave If QT interval becomes prolonged, the patient may be at risk for a lethal ventricular dysrhythmia called torsades de pointes

PP interval is measured from the beginning of one P wave to the beginning of the next. The PP interval is used to determine atrial rhythm and atrial rate RR interval is measured from one QRS complex to the next QRS complex. The RR interval is used to determine ventricular rate and rhythm

count the number of RR intervals in 6 seconds and multiply that number by 10 = HR

Analyzing the Electrocardiogram Rhythm Strip Normal sinus rhythm occurs when the electrical impulse starts at a regular rate and rhythm in the sinus node and travels through the normal conduction pathway Normal sinusrhythm has the following characteristics (Fig. 27-5): Ventricular and atrial rate: 60 to 100 in the adult Ventricular and atrial rhythm: Regular QRS shape and duration: Usually normal, but may be regularly abnormal P wave: Normal and consistent shape; always in front of the QRS PR interval: Consistent interval between 0.12 and 0.20 seconds P:QRS ratio: 1:1

Chart 27-2Interpreting Dysrhythmias: Systematic Analysis of the Electrocardiogram

When examining an ECG rhythm strip to learn more about a patient's dysrhythmia: 1. Determine the ventricular rate. 2. Determine the ventricular rhythm. 3. Determine QRS duration. 4. Determine whether the QRS duration is consistent throughout the strip. If not, identify other duration. 5. Identify QRS shape; if not consistent, then identify other shapes. 6. Identify P waves; is there a P in front of every QRS? 7. Identify P-wave shape; identify whether it is consistent or not. 8. Determine the atrial rate. 9. Determine the atrial rhythm. 10. Determine each PR interval. 11. Determine if the PR intervals are consistent, irregular but with a pattern to the irregularity, or just irregular. 12. Determine how many P waves for each QRS (P:QRS ratio). In many cases, the nurse may use a checklist and document the findings next to the appropriate ECG criterion.

Sinus Node Dysrhythmias Sinus Bradycardia. Sinus bradycardia occurs when the sinus node creates an impulse at a slower-thannormal rate. Causes include: Lower metabolic needs (eg, sleep, athletic training, hypothyroidism) Vagal stimulation (eg, from vomiting, suctioning, severe pain, extreme emotions) Medications (eg, calcium channel blockers, amiodarone, beta-blockers) Idiopathic sinus node dysfunction Increased intracranial pressure (ICP) myocardial infarction (MI), especially of the inferior wall Other causes H&Ts Hypovolemia, Hypoxia Hydrogen ion (acidosis) Hypokalemia Hyperkalemia Hypoglycemia Hypothermia Toxins Tamponade (cardiac) Tension pneumothorax Thrombosis (coronary or pulmonary) Trauma

Bradycardia has the following characteristics (Fig. 27-6): Ventricular and atrial rate: Less than 60 in the adult Ventricular and atrial rhythm: Regular QRS shape and duration: Usually normal, but may be regularly abnormal P wave: Normal and consistent shape; always in front of the QRS PR interval: Consistent interval between 0.12 and 0.20 seconds P:QRS ratio: 1:1 If patient symptomatic: eg SOB, Decreased LOC, angina hypotension, ST-segment changes, or premature ventricular complexes: TX: Atropine, 0.5 mg given rapidly as an intravenous (IV) bolus every 3 to 5 minutes to a maximum total dose of 3 mg, is the medication of choice in treating symptomatic sinus bradycardia

Sinus Tachycardia. Sinus tachycardia occurs when the sinus node creates an impulse at a faster-thannormal rate

Causes may include the following: Physiologic or psychological stress: Blood loss Anemia Shock Hypervolemia Hypovolemia, Heart failure Pain Hypermetabolic states Fever Exercise, Anxiety

Medications that stimulate the sympathetic response Catecholamines, aminophylline, atropine Stimulants caffeine, alcohol, nicotine, Illicit drugs amphetamines, cocaine, Ecstasy)

Enhanced automaticity of the SA node and/or excessive sympathetic tone with reduced parasympathetic tone, a condition called inappropriate sinus tachycardia Autonomic dysfunction, which results in a type of sinus tachycardia called postural orthostatic tachycardia syndrome (POTS).

Sinus tachycardia has the following characteristics (Fig. 27-7): Ventricular and atrial rate: Greater than 100 in the adult, but usually less than 120 Ventricular and atrial rhythm: Regular QRS shape and duration: Usually normal, but may be regularly abnormal P wave: Normal and consistent shape; always in front of the QRS, but may be buried in the preceding T wave PR interval: Consistent interval between 0.12 and 0.20 seconds P:QRS ratio: 1:1 The diastolic filling time decreases, possibly resulting in reduced cardiac output and subsequent symptoms of syncope and low blood pressure If the rapid rate persists and the heart cannot compensate for the decreased ventricular filling the patient may develop acute pulmonary edema Treatment of sinus tachycardia is usually determined by the severity of symptoms and directed at identifying and abolishing its cause Beta-blockers and calcium channel blockers

Sinus Arrhythmia: Sinus arrhythmia occurs when the sinus node creates an impulse at an irregular rhythm; The rate usually increases with inspiration and decreases with expiration

Sinus arrhythmia has the following characteristics (Fig. 27-8): Ventricular and atrial rate: 60 to 100 in the adult Ventricular and atrial rhythm: Irregular QRS shape and duration: Usually normal, but may be regularly abnormal P wave: Normal and consistent shape; always in front of the QRS PR interval: Consistent interval between 0.12 and 0.20 seconds P:QRS ratio: 1:1 Sinus arrhythmia does not cause any significant hemodynamic effect and usually is not treated. Atrial Dysrhythmias Premature Atrial Complex: A premature atrial complex (PAC) is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus node PAC may be caused by: Caffeine Alcohol Nicotine Stretched atrial myocardium (as in hypervolemia) Anxiety Hypokalemia Atrial ischemia, Injury Infarction PACs are often seen with sinus tachycardia

PACs have the following characteristics (Fig. 27-9): Ventricular and atrial rate: Depends on the underlying rhythm (eg, sinus tachycardia) Ventricular and atrial rhythm: Irregular due to early P waves, creating a PP interval that is shorter than the others. This is sometimes followed by a longer-than normal PP interval, but one that is less than twice the normal PP interval This type of interval is called a noncompensatory pause.

QRS shape and duration: The QRS that follows the early P wave is usually normal, but it may be abnormal (aberrantly conducted PAC). It may even be absent (blocked PAC).

P wave: An early and different P wave may be seen or may be hidden in the T wave; other P waves in the strip are consistent. PR interval: The early P wave has a shorter-than-normal PR interval, but still between 0.12 and 0.20 seconds P:QRS ratio: usually 1:1 PACs are common in normal hearts. The patient may say, My heart skipped a beat. A pulse deficit (a difference between the apical and radial pulse rate) may exist

Treats and prevents atrial and ventricular dysrhythmias: quinidine (Quinaglute, Quinidex, Cardioquin) procainamide (Pronestyl, Procan SR) disopyramide (Norpace) Decreased cardiac contractility Prolonged QRS, QT Proarrhythmic Hypotension with IV administration Diarrhea with quinidine, constipation with disopyramide Cinchonism with quinidine Lupus-like syndrome with procainamide Anticholinergic effects: dry mouth, urinary hesitancy with disopyramid

Minimal depression of depolarization; shortened repolarization Treats ventriculardysrhythmias: lidocaine (Xylocaine) mexiletine (Mexitil) tocainide (Tonocard)

CNS changes (eg, confusion, lethargy) Bradycardia GI distress Tremors Treats atrial and ventricular dysrhythmias flecainide (Tambocor)

propafenone (Rythmol)

S/E Dizziness, visual disturbances, dyspnea

Decreases automaticity and conduction Treats atrial and ventricular dysrhythmias: acebutolol (Sectrol) atenolol (Tenormin) bisoprolol/HCTZ (Ziac, Zebeta) esmolol (Brevibloc) labetalol (Trandate) metoprolol (Lopressor, Toprol-XL) nadolol (Corgard) nebivolol (Bystolic) propranolol (Inderal) sotalol (Betapace; Sorine; also has class III actions) amiodarone (Cordarone) dofetilide (Tikosyn) ibutilide (Corvert S/E: Bradycardia, AV block Decreased contractility Bronchospasm Nausea Asymptomatic and symptomatic hypotension Masks hypoglycemia and thyrotoxicosis CNS disturbances (eg, confusion, dizziness, fatigue, depression)

Blocks calcium channel Treats and prevents paroxysmal atrial dysrhythmias:

verapamil (Calan, Isoptin) diltiazem (Cardizem,Dilacor, Tiazac, Diltia, Cartia)

Bradycardia AV blocks Hypotension with IV administration HF, peripheral edema Constipation, dizziness, Headache Nausea

Monitor heart rate, PR interval Monitor blood pressure closely with IV administration Monitor for signs and symptoms of HF Do not crush sustained-release medications

Atrial Flutter. Atrial flutter occurs because of a conduction defect in the atrium and causes a rapid, regular atrial rate, usually between 250 and 400 times per minute Atrial flutter often occurs in patients with: Chronic obstructive pulmonary disease Valvular disease, Thyrotoxicosis, Following open heart surgery Repair of congenital cardiac defects

Atrial flutter has the following characteristics (Fig. 27-10): Ventricular and atrial rate: Atrial rate ranges between 250 and 400 Ventricular rate usually ranges between 75 and 150

Ventricular and atrial rhythm: The atrial rhythm is regular; the ventricular rhythm is usually regular but may be irregular because of a change in the AV conduction

QRS shape and duration: Usually normal, but may be abnormal or may be absent P wave: Saw-toothed shape; these waves are referred to as F waves PR interval: Multiple F waves may make it difficult to determine the PR interval P:QRS ratio: 2:1, 3:1, or 4:1 TX: Vagal maneuvers or administration of adenosine (Adenocard, Adenoscan), which causes sympathetic block and slowing of conduction in the AV node signs and symptoms: chest pain shortness of breath Low blood pressure

Atrial Fibrillation: Atrial fibrillation is an uncoordinated atrial electrical activation that causes a rapid, disorganized, and uncoordinated twitching of atrial musculature

Regular RR intervals in atrial fibrillation may indicate the presence of complete AV block, junctional tachycardia, or ventricular tachycardia Atrial fibrillation may be transient, starting and stopping suddenly and occurring for a very short time (paroxysmal dysrhythmia)

Atrial fibrillation has the following characteristics (Fig. 27-11): Ventricular and atrial rate: Atrial rate is 300 to 600 ventricular rate is usually 120 to 200 in untreated atrial fibrillation Ventricular and atrial rhythm: Highly irregular QRS shape and duration: Usually normal, but may be abnormal P wave: No discernible P waves; irregular undulating waves that vary in amplitude and shape are seen and are referred to as fibrillatory or f waves PR interval: Cannot be measured P:QRS ratio: Many Atrial fibrillation causes a loss in AV synchrony (the atria and ventricles contract at different times) May lead to irregular palpitations and symptoms of heart failure such as shortness of breath, fatigue, exercise intolerance, and malaise. Patients may be asymptomatic or experience significant hemodynamic collapse (hypotension, chest pain, pulmonary edema, and altered level of consciousness)

In many patients, atrial fibrillation converts to sinus rhythm within 24 hours and without treatment If A-FIB has lasted longer than 48hrs do not cardiovert unless PT has received warfrin (coumain) for at least 3-4 wks before. May release blood clot into blood stream

Medications that may be administered to achieve cardioversion: Flecainide propafenone, sotalol Other choices include dofetilide (Tikosyn) amiodarone or Norpace ibutilide may cause torsades de points monitor for at least 4hrs after Electrical cardioversion is the treatment of choice for atrial fibrillation in the presence of WPW syndrome

To control the heart rate in persistent atrial fibrillation, an IV beta-blocker or a nondihydropyridine calcium channel blocker: (diltiazem and verapamil)

Premature Ventricular Complex: A premature ventricular complex (PVC) is an impulse that starts in a ventricle and is conducted through the ventricles before the next normal sinus impulse. PVCs can occur in healthy people, especially with intake of Caffeine Nicotine Alcohol PVCs may be caused by: Cardiac ischemia Infarction, Increased workload on the heart (eg, heart failure, and tachycardia) Digitalis toxicity Hypoxia Acidosis Electrolyte imbalances, especially hypokalemia.

PVCs have the following characteristics (Fig. 27-15): Ventricular and atrial rate: Depends on the underlying rhythm (eg, sinus rhythm) Ventricular and atrial rhythm: Irregular due to early QRS, creating one RR interval that is shorter than the others. PP interval may be regular, indicating that the PVC did not depolarize the sinus node. QRS shape and duration: Duration is 0.12 seconds or longer; shape is bizarre and abnormal P wave: Visibility of P wave depends on the timing of the PVC; may be absent (hidden in the QRS or T wave) or in front of the QRS. If the P wave follows the QRS, the shape of the P wave may be different.PR interval: If the P wave is in front of the QRS PR interval is less than 0.12 seconds P:QRS ratio: 0:1; 1:1

PVCs that are frequent and persistent may be treated with amiodarone or sotalol Not dangerous if not pathological

Ventricular Tachycardia: VT is defined as three or more PVCs in a row, occurring at a rate exceeding 100 bpm. Patients with larger MIs and lower ejection fractions are at higher risk of lethal ventricular tachycardia VT is an emergency because the patient is usually (although not always) unresponsive and pulseless

VT has the following characteristics (Fig. 27-16): Ventricular and atrial rate: Ventricular rate is 100 to 200 bpm atrial rate depends on the underlying rhythm (eg, sinus rhythm) Ventricular and atrial rhythm: Usually regular Atrial rhythm may also be regular QRS shape and duration: Duration is 0.12 seconds ormore bizarre, abnormal shape P wave: Very difficult to detect, so atrial rate and rhythm may be indeterminable PR interval: Very irregular, if P waves are seen P:QRS ratio: Difficult to determine, but if P waves are apparent, there are usually more QRS complexes than P waves

IV procainamide is the antiarrhythmic medication of choice a patient with stable acute MI with VT IV amiodarone is the medication of choice for a patient with unstable VT or impaired cardiac function Cardioversion is the treatment of choice for monophasic VT in a symptomatic patient Defibrillation is the treatment of choice for pulseless VT Defibrillation is the treatment of choice for pulseless VT.

Ventricular Fibrillation. The most common dysrhythmia in patients with cardiac arrest is ventricular fibrillation, which is a rapid, disorganized ventricular rhythm that causes ineffective quivering of the ventricles

Ventricular fibrillation has the following characteristics (Fig. 27-17): Ventricular rate: Greater than 300 per minute Ventricular rhythm: Extremely irregular, without a specific pattern QRS shape and duration: Irregular, undulating waves without recognizable QRS complexes Early defibrillation is critical to survival, with administration of immediate bystander cardiopulmonary resuscitation (CPR) until defibrillation is available

Epinephrine should be administered as soon as possible after the second rhythm check (immediately before or after the second defibrillation) and then every 3 to 5 minutes One dose of vasopressin (Pitressin) may be administered instead of epinephrine if the cardiac arrest persists amiodarone, lidocaine, or possibly magnesium should be administered as soon as possible after the third rhythm check (immediately before or after the third defibrillation

For refractory ventricular fibrillation, amiodarone may be the medication of choice Ventricular Asystole: Commonly called flatline, ventricular asystole (Fig. 27-19) is characterized by absent QRS Complexes Ventricular asystole is treated the same as PEA, focusing on high-quality CPR with minimal interruptions and identifying underlying and contributing factors

IV epinephrine is administered and repeated at 3- to 5-minute intervals One dose of vasopressin may be administered for the first or second dose of epinephrine A bolus of IV atropine may also be administered as soon as possible after the rhythm check

Conduction Abnormalities AV blocks occur when the conduction of the impulse through the AV nodal or His bundle area is decreased or stopped These blocks can be caused by medications (eg, digitalis, calcium channel blockers, beta-blockers), Lyme disease, myocardial ischemia and infarction, valvular disorders, cardiomyopathy, endocarditis, or myocarditis First-Degree Atrioventricular Block; First-degree AV block occurs when all the atrial impulses are conducted through the AV node into the ventricles at a rate slower than normal.

PR interval: Greater than 0.20 seconds; PR interval measurement is constant

Second-Degree Atrioventricular Block, Type I (Wenckebach) Each atrial impulse takes a longer time for conduction than the one before, until one impulse is fully blocked.

Second-Degree Atrioventricular Block, Type II: Only some of the atrial impulses are conducted through the AV node into the ventricles P wave: In front of the QRS complex; shape depends on underlying rhythm PR interval: PR interval is constant for those P waves just before QRS complexes

Third-Degree Atrioventricular Block:

Third-degree AV block occurs when no atrial impulse is conducted through the AV node into the ventricles In third-degree AV block, two impulses stimulate the heart: one stimulates the ventricles (eg, junctional or ventricular escape rhythm), represented by the QRS complex, and one stimulates the atria (eg, sinus rhythm or atrial fibrillation), represented by the P wave. P:QRS ratio: More P waves than QRS complexes Medical Management of Conduction Abnormalities; If the patient is stable and has no symptoms, no treatment may be indicated other than decreasing or eliminating the cause (eg, withholding the medication or treatment) The initial treatment of choice is an IV bolus of atropine, although it is not effective in second-degree AV block, type II, or third-degree AV block If the patient does not respond to atropine, has advanced AV block, or has had an acute MI, temporary transcutaneous pacing may be started If the patient has no pulse, treatment is the same as for ventricular asystole

THE PATIENT WITH A DYSRHYTHMIA Assessment: Identify Possible cause O2 sat Syncope Dizziness Fatigue Chest discomfort Decreased cardiac output leads to: Decreased LOC Fluid retention o Neck vein distention o Crackles Decreased pulse pressure o Indicates decreased cardiac output

Diagnosis
Nursing Diagnoses Based on assessment data, major nursing diagnoses of the patient may include: Decreased cardiac output Anxiety related to fear of the unknown Deficient knowledge about the dysrhythmia and its treatment

Collaborative Problems/Potential Complications Potential complications that may develop include the following: Cardiac arrest (see Chapter 30) Heart failure (see Chapter 30) Thromboembolic event, especially with atrial fibrillation (see Chapter 30)

Planning and Goals

The major goals for the patient may include eliminating or decreasing the occurrence of the dysrhythmia (by decreasing contributory factors) to maintain cardiac output, minimizing anxiety, and acquiring knowledge about the dysrhythmia, tests used to diagnose the problem, and its treatment

Nursing Interventions
Monitoring and Managing the Dysrhythmia Evaluates the patient: blood pressure, pulse rate and rhythm rate and depth of respirations breath sounds To determine the dysrhythmias hemodynamic effect

Minimizing Anxiety The nurse stays with the patient and provides assurance of safety and security while maintaining a calm and reassuring attitude

Promoting Home and Community-Based Care

TEACHING PATIENTS SELF-CARE:

The nurse first assesses the patients understanding, clarifies misinformation, and then shares needed information in terms that are understandable and in a manner that is not frightening or threatening The nurse explains the importance of maintaining therapeutic serum levels of antiarrhythmic medications so that the patient understands why medications should be taken regularly each day and the importance of regular blood testing The patient should be taught how to take his or her pulse before each dose and to notify the health care provider if the pulse is abnormal Explain S&S of decreased cardiac output If life threatening dysrhythmia have plan of action for family

Home care may be warranted if the patient has significant comorbidities, socioeconomic issues, or limited self-management skills that could increase the risk of nonadherence to the therapeutic regimen

Evaluation
Expected Patient Outcomes

Expected patient outcomes may include: 1. Maintains cardiac output a. Demonstrates heart rate, blood pressure, respiratory rate, and level of consciousness within normal ranges b. Demonstrates no or decreased episodes of dysrhythmia 2. Experiences reduced anxiety a. Expresses a positive attitude about living with the dysrhythmia b. Expresses confidence in ability to take appropriate actions in an emergency 3. Expresses understanding of the dysrhythmia and its treatment a. Explains the dysrhythmia and its effects b. Describes the medication regimen and its rationale c. Explains the need to maintain a therapeutic serum level of the medication d. Describes a plan to eliminate or limit factors that contribute to the dysrhythmia e. States actions to take in the event of an emergency

Cardioversion and Defibrillation One major difference between cardioversion and defibrillation is the timing of the delivery of electrical current. In cardioversion, the delivery of the electrical current is synchronized with the patients electrical events; in defibrillation, the delivery of the current is immediate and unsynchronized

May be external w/paddles or conductor pads

When using paddles, the appropriate conductant is applied between the paddles and the patients skin. Any other type of conductant, such as ultrasound gel, should not be substituted Whether using pads or paddles, the nurse must observe two safety measures. 1. Good contact to patients skin w/conductive medium between them] 2. No one should be in contact with patient

During cardioversion, ensure that the monitor leads are attached to the patient and that the defibrillator is in the synchronized mode If using paddles, exert 20 to 25 pounds of pressure to ensure good skin contact Before pressing the discharge button, call Clear! three times Record the delivered energy. After the defibrillation, immediately resume CPR, starting with chest compressions After five cycles (about 2 minutes) of CPR, check the cardiac rhythm and deliver another shock if indicated After the event is complete, inspect the skin under the pads or paddles for burns

Electrical Cardioversion:

Involves the delivery of a timed electrical current to terminate a tachydysrhythmia In cardioversion, the defibrillator is set to synchronize with the ECG on a cardiac monitor so that the electrical impulse discharges during ventricular depolarization (QRS complex If the cardioversion is elective and the dysrhythmia has lasted longer than 48 hours, anticoagulation for a few weeks before cardioversion may be indicated Digoxin usually withheld for 48hrs before Instruct patient not to eat for at least 4hrs before Patient receives moderate sedation Because of the sedation, airway patency must be maintained and the patients state of consciousness assessed

Defibrillation Defibrillation is used in emergency situations as the treatment of choice for ventricular fibrillation and pulseless VT, Defibrillation is not used for patients who are conscious or have a pulse If it is used within 1 minute of the onset of VT or fibrillation, the survival rate is 90%; if it is delayed for 12 minutes, the survival is only 2% to 5% If immediate CPR is provided and defibrillation is performed within 5 minutes, more adults in ventricular fibrillation may survive with intact neurologic function Epinephrine or vasopressin is administered after defibrillation to make it easier to convert the dysrhythmia to a normal rhythm with the next defibrillation o May also increase cerebral and coronary artery blood flow. o amiodarone, lidocaine, or magnesium are administered if ventricular dysrhythmia persists

Pacemaker Therapy
o o o Pacemakers are usually used when a patient has a permanent or temporary slower-than-normal impulse formation, or a symptomatic AV or ventricular conduction disturbance. may also be used to control some tachydysrhythmias that do not respond to medication biventricular (resynchronization) pacing may be used to TX HF thats does not respond to Meds

If a patient suddenly develops a bradycardia, is symptomatic but has a pulse, and is unresponsive to atropine, emergency pacing may be started with transcutaneous pacing Can cause significant discomfort (only for temporary)

loss of AV synchrony and atrial kick, which may cause a decrease in cardiac output and an increase in atrial distention and venous congestion.

This can lead to pacemaker syndrome, causing symptoms such as chest discomfort, shortness of breath, fatigue, activity intolerance, and postural hypotension Because AOO pacing stimulates only the atrium, it may be used in a patient who has undergone open heart surgery and develops sinus bradycardia

Complications of Pacemaker Use

Local infection at the entry site of the leads for temporary pacing, or at the subcutaneous site for permanent generator placement Pneumothorax Bleeding and hematoma, manage w/cold compress and D/C antiplatelets Hemothorax from puncture of the subclavian vein or internal mammary artery Ventricular ectopy and tachycardia from irritation of the ventricular wall by the endocardial electrode Movement or dislocation of the lead placed transvenously (perforation of the myocardium) Phrenic nerve, diaphragmatic (hiccuping may be a sign), or skeletal muscle stimulation if the lead is dislocated or if the delivered energy (mA) is set high Cardiac perforation resulting in pericardial effusion and rarely, cardiac tamponade, which may occur at the time of implantation or months later. Twiddler syndrome may occur when the patient manipulates the generator, causing lead dislodgement or fracture of the lead Pacemaker syndrome (hemodynamic instability caused by ventricular pacing and the loss of AV synchrony o Causes mild symptoms in 20% ventricular PTs

Loss of capturecomplex does not follow pacing spike: Inadequate stimulus Lead dislodgement Lead wire fracture Catheter malposition Battery depletion Electronic insulation break Medication change Myocardial ischemia o increase milliamperage. o Reposition extremity; turn patient to left side. o Change battery. o Change generator

Rhythmic diaphragmatic or chest wall twitching or hiccupping Output too high Myocardial wall perforation o Decrease milliamperage. o Turn pacer off. Contact physician at once. o Monitor closely for decreased cardiac output.

Undersensing-pacing spike occurs at preset interval despite patient's intrinsic rhythm Sensitivity too high Electrical interference (eg, by a magnet) Faulty generator o Remove interference o Decrease sensitivity o Change battery o Replace generator

Change in pacing QRS shape Septal perforation o 12 lead EKG o Assess for murmur o Contact MD

Loss of pacing-total absence of pacing spikes Oversensing Battery depletion Loose or disconnected wires Perforation o Change battery o Check leads o Apply magnet over permanent generator

Implantable cardioverter defibrillator (ICD) is an electronic device that detects and terminates life-threatening episodes of tachycardia or fibrillation, especially those that are ventricular in origin

Nursing Management of the Patient With an Implantable Cardiac Device

cardiac output and hemodynamic stability are assessed to identify the patients response to pacing and the adequacy of pacing. If VT develops record time between onset and time charge is delivered Observe for infection, hematoma at insertion site X-ray to document placement and to confirm there is no pneumothorax Assess PT for anxiety, depression, and anger Teach importance of medication regimen compliance

Home care; Observe for signs of infection No tight clothing Initially avoid soaking in tub or lotions Do not raise arm above head for 2wks No heavy lifting for a few wks Discuss safety w/MD (driving) Avoid large magnets Keep D/C log Teach what to do if symptoms occur Discuss psychological effects Check pulse daily To promote effective coping strategies, the nurse must recognize the patients as well as the familys perceptions of the situation and their resulting emotional state and assist them to explore their reactions and feelings. Patient most vulnerable to feelings of helplessness, leading to depression. The patient and family should be encouraged to talk about their experiences and emotions with each other and the health care team

Electrophysiologic Studies Indicated for a dysrhythmia that has gone undetected and undiagnosed by other methods Elicits a dysrhythmia View electrical and propagation through cardiac electrical conduction system Assess function of SA and AV nodes Identify location (mapping) of and mechanism of dysrhythmias Assess the effectiveness of antiarrhythmic medications and devices for the patient with a dysrhythmia Treat certain dysrhythmias through the destruction of the causative cells (ablation)

Catheter w/multiple electrodes is inserted through femoral vein Paces heart faster than SA node and then stops and records time necessary for SA node to take over again. If prolonged amy indicate SA node dysfunction If dysrhythmia is induced it is called inducible.. after regimen it is tried again if not induced it means TX is successful Before the procedure, the patient should receive instructions about the procedure and its usual duration, the environment where the procedure is performed, and what to expect
Catheter Ablation Therapy Catheter ablation destroys specific cells that are the cause or central conduction route of a tachydysrhythmias Usual indications for ablation are AVNRT, a recurrent atrial dysrhythmia (especially atrial fibrillation), or VT unresponsive to previous therapy (or for which the therapy produced significant side effects)

Also indicated in Preexcitation syndromes may cause VF During the ablation procedure, defibrillation pads, an automatic blood pressure cuff, and a pulse oximeter are used and an indwelling urinary catheter is inserted. Monitor patient for another 30 to 60 minutes and then retested to ensure that the dysrhythmia does not recur

Chapter 28
Myocardial Infarction (ACS)
In unstable angina, there is reduced blood flow in a coronary artery, often due to rupture of an atherosclerotic plaque, but the artery is not completely occluded. This is an acute situation that is sometimes referred to as preinfarction angina because the patient will likely have an MI if prompt interventions do not occur

Clinical Manifestations

Acute Coronary Syndrome and (ACS) Persistent chest pain despite rest and medication May present with: SOB Indigestion Nausea Anxiety Cool pale and moist skin
Pharmacologic Therapy Aspirin NTG Morphine decrease preload, after load enhances oxygenation Beta blocker long term

ACE inhibitors; Decrease B/P Kidneys excrete Na+ Causes dieresis (excretes fluids)

Thrombolytics:
Thrombolytics should not be used if the patient is bleeding or has a bleeding disorder
Indications Chest pain for longer than 20 minutes, unrelieved by nitroglycerin ST-segment elevation in at least two leads that face the same area of the heart Less than 6 hours from onset of pain (usually 3-6hrs) Agents most commonly used: alteplase (Activase) and reteplase)

Aspirin and unfractionated heparin or LMWH may be used with t-PA to prevent another clot from forming at the site of the lesion

Cardiac Rehabilitation Goal: Prolong life and quality Immediate goals Limit progression of atherosclerosis Return patient to former job and lifestyle Prevent another cardiac event ACTIVITY TOLERANCE GOASL ACHEVED GRADUALLY Cardiac efficiency is achieved when work and activities of daily living can be performed at a lower heart rate and lower blood pressure, thereby reducing the hearts oxygen requirements and reducing cardiac workload. MONITORED PROGRAM: HR no more than 120bpm B/P no more than 20mm Hg Decrease in systolic O2 > 93% Phase III is a long-term outpatient program that focuses on maintaining cardiovascular stability and longterm conditioning Phase I Teach plan of action: S&S that indicate when to call 911 Medication regimen Rest activity balance F/U appts Phase II PT attends sessions 4-6 wk ECG monitoring Exercise training (individualized) Patient assessed at each session for adherence to regimen Dietary education

Phase III Long Term Focuses on maintaining cardiovascular stability and long-term conditioning

NURSING PROCESS THE PATIENT WITH ACUTE CORONARY SYNDROME

Assessment Establishes baseline Identifies patient needs Helps priotitrze needs Evaluate symptoms: Time Duration Factors that precipitate and alleviate Assess IV sites Diagnosis
Nursing Diagnoses: Ineffective cardiac tissue perfusion related to reduced coronary blood flow Risk for imbalanced fluid volume Risk for ineffective peripheral tissue perfusion related to decreased cardiac output from left ventricular dysfunction Death anxiety related to cardiac event Deficient knowledge about post-ACS self-care

Based on the assessment data, potential complications that may develop include the following: Acute pulmonary edema (see Chapter 30) Heart failure (see Chapter 30) Cardiogenic shock (see Chapter 15) Dysrhythmias and cardiac arrest (see Chapters 27 and 30) Pericardial effusion and cardiac tamponade (see Chapter 30)

Planning and Goals: Relief of pain or ischemic signs Symptoms prevention of myocardial damage Absence Respiratory dysfunction Adequate tissue perfusion Reduced anxiety Adherence to the self-care program Absence or early recognition of complications

Nursing Interventions
Relieving Pain and Other Signs and Symptoms of Ischemia Balancing myocardial oxygen supply with demand (eg, as evidenced by the relief of chest pain) Oxygen should be administered along with medication therapy to assist with relief of symptoms rest in bed with the backrest elevated or in a supportive chair helps decrease chest discomfort and dyspnea o Tidal volume improves because of reduced pressure from abdominal contents on the diaphragm and better lung expansion. o Drainage of the upper lung lobes improves. o Venous return to the heart (preload) decreases, reducing the work of the heart Improving Respiratory Function: Deep breathing Change position frequently O2 sat Promoting Adequate Tissue Perfusion Bed or chair rest during the initial phase of treatment helps reduce myocardial oxygen consumption Limitation on mobility until stable Monitor extremities for adequate perfusion