Cardio Nursing Course Audit 21

Cardiovascular System
By: Ms. Irene M. Magbanua
FOUR STAGES OF LIFE
CARDIOVASCULAR SYSTEM
IMPORTANT FUNCTION: - provide oxygen in every tissue in the body which is essential in performing its function CONSISTS of: HEART BLOOD VESSEL BLOOD
HEART
Hollow, muscular 4-chambered Located in middle of thoracic cavity between lungs in space called mediastinum ( The space between the lungs, which includes the heart, pericardium, aorta and vena cava) Inverted cone
The Cardiovascular System

HEART Normal Anatomy: Microscopic Consists of Three layers- epicardium, myocardium and endocardium
The epicardium covers the outer surface of the heart The myocardium is the middle muscular layer of the heart The endocardium lines the chambers and the valves
The layer that covers the heart is the PERICARDIUM There are two parts- parietal and visceral pericardium The space between the two pericardial layers is the pericardial space
PERICARDIAL EFFUSION

Normal Anatomy: Gross The heart is located in the LEFT side of the mediastinum

The heart chambers are guarded by valves The Atrio-ventricular valves
The Semilunar valves-
BLOOD VESSELS
Great
vessels: large veins and arteries leading directly to and away from heart

SUPERIOR VENA CAVA AND INFERIOR VENA CAVA PULMONARY ARTERY PULMONARY VEIN AORTA
LAUGH BREAK
BOY: Isang babaeng siopao nga! LEA: Babaeng siopao? BOY: Oo, yung may saping papel, may napkin! LEA: Ah ganun ba? Mayrun kaming siopao na bading BOY: Bading na siopao? LEA: May sapin din, pero may itlog sa loob!
LAUGH BREAK
AMO: Day, gamitin mo sa pader itong chalk pamatay ng ipis. MAID: Yis ati! NEXT DAY ... nagulat ang amo, nakasulat sa pader: EPES MAMATAY KAYUNG LAHAT! SYET! PAKYO!
LAUGH BREAK
PASYENTE: Dok bakit pag tuwing umiinm ako ng alak sumasakit ang tyan ko? Pero pag libre, di naman? DKTOR: Normal yan, manipis kasi atay mo. Tapos makapal mukha mo!
LAUGH BREAK
BUS HINOLDAP! Holdaper: Re-reypin ko lahat ng babae dito! Prosti: Ako na lang po, maawa kayo sa iba.. Lola: Sinabi na ngang LAHAT eh! Sasagot pa!
CORONARY ARTERIES
The Blood supply of the heart comes from the Coronary arteries 1. Right coronary artery 2. Left coronary artery
Cardiophysiology
Conduction system Cardiac (heart) sounds Heart rate and Blood pressure Cardiac cycle
CHARACTERISTICS OF THE CARDIAC MUSCLE

Inherent abilities of cardiac muscle cells: Automaticity Conductivity Excitability Refractoriness

The CONDUCTING SYSTEM OF THE HEART Consists of the 1. SA node- the pacemaker 2. AV node- slowest conduction 3. Bundle of His branches into the Right and the Left bundle branch 4. Purkinje fibers- fastest conduction
LAUGH BREAK
HONEYMOON: Wife: Hon wag mo ako bibiglain ha? I'm still a virgin Husband: You mean ako ang una? Wife: Yes, do it na please! Husband: I did it na, kanina pa!! Wife: Ah ganon ba? Aray pala, shit!!!

Heart rate

Normal range is 60-100 beats per minute Tachycardia is greater than 100 bpm Bradycardia is less than 60 bpm Sympathetic system INCREASES HR Parasympathetic system (Vagus) DECREASES HR
The Heart: Physiology
The amount of blood the heart pumps out in each beat is called the STROKE VOLUME When this volume is multiplied by the number of heart beat in a minute (heart rate), it becomes the CARDIAC OUTPUT When the Cardiac Output is multiplied by the Total Peripheral Resistance, it becomes the BLOOD PRESSURE
Blood pressure is:

Cardiac output X peripheral resistance
Cardiac Output Regulation
The heart pumps approximately 5 L of blood every minute The heart rate increases with exercise; therefore cardiac output increases The cardiac output will vary according to the amount of venous return.

Blood pressure
Control is neural (central and peripheral) and hormonal Baroreceptors in the carotid and aorta Hormones- ADH, Adrenergic hormones, Aldosterone and ANF

Blood pressure
Hormones- ADH, Adrenergic hormones, Aldosterone and ANF

ADH increases water retention Aldosterone increases sodium retention and water retention secondarily Epinephrine and NE increase HR and BP ANF= causes sodium excretion
LAUGH BREAK

Bakla at Macho nagkasabay sa CR... Bakla: Ang laki naman nyan sayo... Macho: Wala na tong silbi kasi iniwan na ako ng GF ko... puputulin ko na lang at ipapakain ko sa aso! Bakla: aw! aw! aw!
The Heart: Physiology
The PRELOAD is the degree of stretching of the heart muscle when it is filled-up with blood The AFTERLOAD is the resistance to which the heart must pump to eject the blood
Anatomy a& Physiology Refers to change in heart rate Chronotropic

Terminology
effect
A positive chronotropic effect refers to an increase in heart rate A negative chronotropic effect refers to a decrease in heart rate Refers to a change in the speed of conduction through the AV junction A positive dromotropic effect results in an increase in AV conduction velocity A negative dromotropic effect results in a decrease in AV conduction velocity
Dromotropic effect
Inotropic effect
Refers to a change in myocardial contractility A postive inotropic effect results in an increase in myocardial contractility A negative inotropic effect results in a decrease in myocardial contractility
LAUGH BREAK
PATIENT: Nurse bakit TAE ko may kasamang plema? NURSE: Ok lang yan! Mas delikado kung pag singa mo may kasamang TAE!
Factors regulating Stroke Volume
1. Degree of stretch of the cardiac muscle before contraction (Starlings Law); determined by the volume of blood in the ventricle at the end of diastole or diastolic filling. 2. Contactility: ability of the myocardium to contract; contractility is increased by circulating catecholamines and medications like digitalis
3. Preload : the filling of the ventricles at the end of diastole. The more the ventricles fill, the more the cardiac muscles are stretched, and the greater the force of the contraction during systole (Starlings Law). If there is a decrease in contractility and in cardiac output.
4. Afterload: the pressure in the aorta that the ventricles must overcome to pump blood into the systemic circulation. A decrease in the afterload causes a decrease in the workload of the ventricles; this in turn will assist to increase the stroke volume and the cardiac output
Factors that increase myocardial oxygen demands

Increased heart rate Increased force of contractions Increased afterload
Cardiac compensatory mechanisms
When the normal compensatory mechanisms cannot maintain cardiac output to meet body needs, the client is in a state of cardiac
decompensation.
SUKO SA MISTER:
Misis 1: Suko na ako sa mister ko, lagi na lang ako binubugbog bago niroromansa. ..
Misis 2: Mas grabe yung mister ko. Binubugbog ako tapos si Inday ang niroromansa.

The vascular system consists of the arteries, veins and capillaries The arteries are vessels that carry blood away from the heart to the periphery The veins are the vessels that carry blood to the heart The capillaries are lined with squamous cells, they connect the veins and arteries
The lymphatic system also is part of the vascular system and the function of this system is to collect the extravasated fluid from the tissues and returns it to the blood
Differences Between Blood Vessel Types

Walls of arteries are the thickest
Lumens of veins are larger
Skeletal muscle milks blood in veins toward the heart

Walls of capillaries are only one cell layer thick to allow for exchanges between blood and tissue
Slide 11.26
Movement of Blood Through Vessels

Most arterial blood is pumped by the heart Veins use the milking action of muscles to help move blood
Figure 11.9
Slide 11.27
Tutpik!
Kustomer: Ano ba naman itong tutpik nyo, iisa na nga lang, ang dali pang mabali! Waiter (inis): Alam nyo, sir, ang dami nang gumamit nyan, pero kayo lang nakabali!
Major Arteries of Systemic Circulation
Figure 11.11
Slide 11.30
Blood Supply to:
Bone Haversian canal and Volkmanns canal Blood Vessel vasa vasorum Heart coronary arteries Brain common carotid artery external and internal carotid artery, anterior, middle and posterior cerebral artery (Circle of Willis) Upper Extremities basillic cephalic brachial radial and ulnar Lower Extremities iliac femoral popliteal saphenous tibial
Blood Supply to:

Eyes choroids (between sclera and retina) cornea gets 02 from the atmosphere Kidneys renal artery interlobar artery arcuate artery interlobular artery afferent arteriole glomerulus efferent arteriole - vasa recta back to the heart Liver celiac artery hepatic artery and hepatic portal vein (food laden) - liver sinusoids (mixed blood) hepatic cells extract 02, nutrients and detoxify toxic substances. Organs of the GIT celiac trunk Lungs bronchial arteries
Major Veins of Systemic Circulation
Figure 11.12
Slide 11.31
Arterial Supply of the Brain
Figure 11.13
Slide 11.32
Hepatic Portal Circulation
Figure 11.14
Slide 11.33
Circulation to the Fetus
Slide 11.34
LAUGH BREAK
DALAWANG MADRE NIREREYP: MADRE 1: Jusko! Patawarin nyo po sya, di po nya alam ang ginagawa nya! MADRE 2: Sister yung akin marunong!!!! Whooooo! Yeeaahhh!!!
Blood Pressure
Measure of force exerted by blood against the wall Blood moves through vessels because of blood pressure Measured by listening for Korotkoff sounds produced by turbulent flow in arteries as pressure released from blood pressure cuff
Blood Pressure: Effects of Factors

Temperature
Heat has a vasodilation effect Cold has a vasoconstricting effect
Chemicals
Various substances can cause increases or decreases
Diet
Slide 11.39b
Factors Determining Blood Pressure
Figure 11.19
Slide 11.40
Pulse
Pulse pressure wave of blood Monitored at pressure points where pulse is easily palpated
Figure 11.16
Slide 11.35
Pulse Pressure
Difference between systolic and diastolic pressures Increases when stroke volume increases or vascular compliance decreases Pulse pressure can be used to take a pulse to determine heart rate and rhythmicity
Variations in Blood Pressure

Human normal range is variable
Normal 140110 mm Hg systolic 8075 mm Hg diastolic Hypotension Low systolic (below 110 mm HG) Often associated with illness Hypertension High systolic (above 140 mm HG) Can be dangerous if it is chronic
Slide 11.41
Effects of Aging on the Heart
Gradual changes in heart function, minor under resting condition, more significant during exercise Hypertrophy of left ventricle Maximum heart rate decreases Increased tendency for valves to function abnormally and arrhythmias to occur Increased oxygen consumption required to pump same amount of blood
Cardiac Assessment

Cardiac History

Interview Focused assessment
CARDIAC ASSESSMENT
Health History Obtain description of present illness and the chief complaint Chest pain, DOB, Edema, etc. Assess risk factors
CARDIAC ASSESSMENT
Physical examination
Vital
signs- BP, PP, Inspection of the skin Inspection of the thorax Palpation of the PMI, pulses Auscultation of the heart sounds
Fig. 13.23
WHY NURSING?
Do you know why I took up nursing? It was in 4th year high school that I saw a vision of a great woman bearing a light in her right hand wearing a long gown and a headress calling me to serve her.
STATUE OF LIBERTY
CARDIAC ASSESSMENT
Laboratory and diagnostic studies

CBC Cardiac catheterization Lipid profile Arteriography Cardiac enzymes and proteins CXR CVP ECG Holter monitoring Exercise ECG

Laboratory Test Rationale 1. To assist in diagnosing MI 2. To identify abnormalities 3. To assess inflammation

Laboratory Test Rationale 4. To determine baseline value 5. To monitor serum level of medications 6. To assess the effects of medications
LABORATORY PROCEDURES
CARDIAC Proteins and enzymes
CK-
MB ( creatine kinase) Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days
CK-
MB ( creatine kinase) Normal value is 0-7 U/L
Lactic
Dehydrogenase (LDH) Elevates in MI in 24 hours, peaks in 48-72 hours
Lactic
Dehydrogenase (LDH) Normal value is 70-200 IU/L
Myoglobin Rises within 1-3 hours Peaks in 4-12 hours Returns to normal in a day
Troponin I and T
Troponin
I is usually utilized for
MI Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks! Normal value for Troponin I is less than 0.6 ng/mL
Troponin I and T
REMEMBER
to AVOID IM injections before obtaining blood sample! Early and late diagnosis can be made!
Myoglobin Not seen alone in cardiac problems Muscular and RENAL disease can have elevated myoglobin
SERUM LIPIDS Lipid profile measures the serum cholesterol, triglycerides and lipoprotein levels Cholesterol= <200 mg/dL Triglycerides- 40- 150 mg/dL
SERUM LIPIDS LDL- 130 mg/dL HDL- 30-70- mg/dL NPO post midnight (usually 12 hours)
AFTER THE WEDDING:

Husband: Sinungaling ka, sabi mo virgin ka! Bakit kagabi maluwag na!
Wife: Ulol ka! Dahil lasing ka, katabi mo kagabi si mama!
ELECTROCARDIOGRAM (ECG) A non-invasive procedure that evaluates the electrical activity of the heart Electrodes and wires are attached to the patient
ELECTROCARDIOGRAM (ECG) Tell the patient that there is no risk of electrocution Avoid muscular contraction/movement
Holter Monitoring A non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded continuously over a period of 24 hours
The Cardiovascular System LABORATORY PROCEDURES
Holter Monitoring
Instruct
the client to resume normal activities and maintain a diary of activities and any symptoms that may develop
ECHOCARDIOGRAM Non-invasive test that studies the structural and functional changes of the heart with the use of ultrasound No special preparation is needed
Stress Test A non-invasive test that studies the heart during activity and detects and evaluates CAD Exercise test, pharmacologic test and emotional test
Stress Test Treadmill testing is the most commonly used stress test Used to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise
Stress Test
Pre-test:
consent may be required, adequate rest, eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine

Post-test:
instruct client to notify the physician if any chest pain, dizziness or shortness of breath Instruct client to avoid taking a hot shower for 10-12 hours after the test
Pharmacological stress test Use of dipyridamole Maximally dilates coronary artery Side-effect: flushing of face
Pharmacological stress test

Pre-test:
4 hours fasting, avoid alcohol, caffeine Post test: report symptoms of chest pain
CARDIAC catheterization Insertion of a catheter into the heart and surrounding vessels Determines the structure and performance of the heart valves and surrounding vessels
CARDIAC catheterization Used to diagnose CAD, assess coronary artery patency and determine extent of atherosclerosis
Pretest:
Ensure Consent, assess for allergy to seafood and iodine, NPO, document weight and height, baseline VS, blood tests and document the peripheral pulses
Pretest:
Fast for 8-12 hours, teachings, medications to allay anxiety
Intra-test:
inform patient of a fluttery feeling as the catheter passes through the heart; - inform the patient that a feeling of warmth and metallic taste may occur when dye is administered
Post-test:
Monitor VS and cardiac rhythm Monitor peripheral pulses, color and warmth and sensation of the extremity distal to insertion site Maintain sandbag to the insertion site if required to maintain pressure Monitor for bleeding and hematoma formation
Maintain strict bed rest for 6-12 hours Client may turn from side to side but bed should not be elevated more than 30 degrees and legs always straight Encourage fluid intake to flush out the dye Immobilize the arm if the antecubital vein is used Monitor for dye allergy
CVP The CVP is the pressure within the SVC Reflects the pressure under which blood is returned to the SVC and right atrium
CVP
Normal
CVP is 0 to 8 mmHg/ 4-10 cm H2O
CVP
Elevated
CVP indicates increase in blood volume, excessive IVF or heart/renal failure
CVP
Low
CVP may indicate hypovolemia, hemorrhage and severe vasodilatation
Measuring CVP
1. Position the client supine with bed elevated at 45 degrees (CBQ) 2. Position the zero point of the CVP line at the level of the right atrium. Usually this is at the MAL, 4th ICS 3. Instruct the client to be relaxed and avoid coughing and straining.
CARDIAC IMPLEMENTATION
1. Assess the cardio-pulmonary status
VS, BP, Cardiac assessment
2. Enhance cardiac output Establish IV line to administer fluids
3. Promote gas exchange Administer O2 Position client in SEMI-Fowlers Encourage coughing and deep breathing exercises
4. Increase client activity tolerance Balance rest and activity periods Assist in daily activities Provide strict bed rest if indicated Soft foods Assistance in self-care
5. Promote client comfort Assess the clients description of pain and chest discomfort Administer medication as prescribed
Morphine
for MI Nitroglycerine for Angina Diuretics to relieve congestion (CHF)
6. Promote adequate sleep 7. Prevent infection Monitor skin integrity of lower extremities Assess skin site for edema, redness and warmth Monitor for fever Change position frequently
8. Minimize patient anxiety Encourage verbalization of feelings, fears and concerns Answer client questions. Provide information about procedures and medications
Activity Intolerance
Monitor TPR and BP Space activities in the day Permit rest periods before activity Limit activity 1 hour before meals Teach energy conservation measures like bed rest
Edema
Instruct patient to avoid constricting garments Instruct to elevate edematous areas Instruct patient to avoid dependent positions Teach patient to prepare low sodium meals Apply anti-embolic stockings
Pain
Instruct patient to stop activity when pain occurs Administer nitroglycerine for angina Pace activities within patients limits Instruct patient to avoid cold temperatures and smoking Instruct to report unrelieved pain immediately
CARDIAC DISEASES
Coronary
Artery Disease Myocardial Infarction Congestive Heart Failure Infective Endocarditis Cardiac Tamponade Cardiogenic Shock
VASCULAR DISEASES
Hypertension Buergers Aneurysm Varicose
disease
veins Deep vein thrombosis
CAD
CORONARY
results
ARTERY DSE
from the focal narrowing of the large and medium-sized coronary arteries due to deposition of atheromatous plaque in the vessel wall
CAD
RISK FACTORS 1. Age above 45/55 and Sex- Males and post-menopausal females 2. Family History 3. Hypertension 4. DM 5. Smoking 6. Obesity 7. Sedentary lifestyle 8. Hyperlipedimia
CAD
RISK FACTORS Most important MODIFIABLE factors: Smoking Hypertension Diabetes Cholesterol abnormalities
CAD: Pathophysiology
Fatty streak formation in the vascular intima
T-cells and monocytes ingest lipids in the area of deposition

Atheroma narrowing of the arterial lumen
reduced coronary blood flow

myocardial ischemia
CAD
Pathophysiology There is decreased perfusion of myocardial tissue and inadequate myocardial oxygen supply If 50% of the left coronary arterial lumen is reduced or 75% of the other coronary artery, this becomes significant
CAD
Pathophysiology Potential for Thrombosis and embolism
Angina Pectoris
Chest pain resulting from coronary atherosclerosis or myocardial ischemia
Angina Pectoris: Clinical Syndromes

THREE COMMON TYPES OF ANGINA
1. STABLE ANGINA The typical angina that occurs during exertion, relieved by rest and drugs and the severity does not change

Three Common Types of ANGINA
2. Unstable angina Occurs unpredictably during exertion and emotion, severity increases with time and pain may not be relieved by rest and drug

Three Common Types of ANGINA
3. Variant angina Prinzmetal angina, results from coronary artery VASOSPASMS, may occur at rest
Angina Pectoris
ASSESSMENT FINDINGS 1. Chest pain- ANGINA The most characteristic symptom PAIN is described as mild to severe retrosternal pain, squeezing, tightness or burning sensation Radiates to the jaw and left arm
Angina Pectoris
ASSESSMENT FINDINGS 1. Chest pain- ANGINA Precipitated by Exercise, Eating heavy meals, Emotions like excitement and anxiety and Extremes of temperature Relieved by REST and Nitroglycerin
Angina Pectoris
ASSESSMENT FINDINGS 2. Diaphoresis 3. Nausea and vomiting 4. Cold clammy skin 5. Sense of apprehension and doom 6. Dizziness and syncope
Angina Pectoris
LABORATORY FINDINGS 1. ECG may show normal tracing if patient is pain-free. - Ischemic changes may show ST depression and T wave inversion
Angina Pectoris
LABORATORY FINDINGS
2. Cardiac catheterization Provides the MOST DEFINITIVE source of diagnosis by showing the presence of the atherosclerotic lesions
Angina Pectoris
NURSING DIAGNOSES: Decreased cardiac output Impaired gas exchange Activity intolerance Anxiety
Angina Pectoris
NURSING MANAGEMENT 1. Administer prescribed medications
Nitrates- to dilate the venous vessels decreasing venous return and to some extent dilate the coronary arteries Aspirin- to prevent thrombus formation Beta-blockers- to reduce BP and HR Calcium-channel blockers- to dilate coronary artery and reduce vasospasm
Angina Pectoris
2. Teach the patient management of
anginal attacks

Advise patient to stop all activities Put one nitroglycerin tablet under the tongue Wait for 5 minutes If not relieved, take another tablet and wait for 5 minutes Another tablet can be taken (third tablet) If unrelieved after THREE tablets seek medical attention
Angina Pectoris
3. Obtain
a 12lead ECG
Angina Pectoris
4. Promote myocardial perfusion Instruct patient to maintain bed rest Administer O2 @ 3 lpm Advise to avoid valsalva maneuvers Provide laxatives or high fiber diet to lessen constipation Encourage to avoid increased physical activities
Angina Pectoris
5. Assist in possible treatment modalities PTCA- percutaneous transluminal coronary angioplasty To compress the plaque against the vessel wall, increasing the arterial lumen CABG- coronary artery bypass graft To improve the blood flow to the myocardial tissue
Angina Pectoris
6. Provide information to family members to minimize anxiety and promote family cooperation 7. Assist client to identify risk factors that can be modified 8. Refer patient to proper agencies
Myocardial infarction
Death of myocardial tissue in regions of the heart with abrupt interruption of coronary blood supply
ETIOLOGY and Risk factors 1. CAD 2. Coronary vasospasm 3. Coronary artery occlusion by embolus and thrombus 4. Conditions that decrease perfusion- hemorrhage, shock
Risk factors 1. Hypercholesterolemia 2. Smoking 3. Hypertension 4. Obesity 5. Stress 6. Sedentary lifestyle
PATHOPHYSIOLOGY Interrupted coronary blood flow myocardial ischemia anaerobic myocardial metabolism for several hours myocardial death depressed cardiac function triggers autonomic nervous system response further imbalance of myocardial O2 demand and supply
ASSESSMENT findings 1. CHEST PAIN Chest pain is described as severe, persistent, crushing substernal discomfort Radiates to the neck, arm, jaw and back
ASSESSMENT findings 1. CHEST PAIN Occurs without cause, primarily early morning NOT relieved by rest or nitroglycerin Lasts 30 minutes or longer
Assessment findings 2. Dyspnea 3. Diaphoresis 4. Cold clammy skin 5. N/V 6. restlessness, sense of doom 7. tachycardia or bradycardia 8. hypotension 9. S3 and dysrhythmias
Laboratory findings 1. ECG- the ST segment is ELEVATED, T wave inversion, presence of Q wave
2.
Myocardial enzymeselevated CK-MB, LDH and Troponin levels
Laboratory findings 3. CBC- may show elevated WBC count 4. Test after the acute stageExercise tolerance test, thallium scans, cardiac catheterization
Pain Decreased cardiac output Impaired gas exchange Activity intolerance Altered tissue perfusion Constipation
Nursing Interventions 1. Provide Oxygen at 2 lpm, Semifowlers 2. Administer medications Morphine to relieve pain Nitrates, thrombolytics, aspirin and anticoagulants Stool softener and hypolipidemics
Nursing Interventions 3. Minimize patient anxiety Provide information as to procedures and drug therapy Allow verbalization of feelings Morphine can be administered
4. Provide adequate rest periods Bed rest during acute stage 5. Minimize metabolic demands Provide soft diet Provide a low-sodium, low cholesterol and low fat diet
6. Assist in treatment modalities such as PTCA and CABG 7. Monitor for complications of MIespecially dysrhythmias, since ventricular tachycardia can happen in the first few hours after MI 8. Provide client teaching
MI
Medical Management 1. ANALGESIC
The
choice is MORPHINE It reduces pain and anxiety Relaxes bronchioles to enhance oxygenation
MI
Medical Management 2. ACE inhibitors
Prevents
formation of angiotensin II Limits the area of infarction
MI
Medical Management 3. Thrombolytic therapy
Streptokinase,
Alteplase Dissolve clots in the coronary artery allowing blood to flow
NURSING INTERVENTIONS AFTER ACUTE EPISODE
1. Maintain bed rest for the first 3 days 2. Provide passive ROM exercises 3. Progress with dangling of the feet at side of bed
4.
Proceed with sitting out of bed, on the chair for 30 minutes TID 5. Proceed with ambulation in the room toilet hallway TID
Cardiac rehabilitation

To extend and improve quality of life Physical conditioning Patients who are able to walk 3-4 mph are usually ready to resume sexual activities
CARDIOMYOPATHIES
Heart
muscle disease associated with cardiac dysfunction
CARDIOMYOPATHIES
1.
Dilated Cardiomyopathy 2. Hypertrophic Cardiomyopathy 3. Restrictive cardiomyopathy
DILATED CARDIOMYOPATHY
ASSOCIATED FACTORS 1. Heavy alcohol intake 2. Pregnancy 3. Viral infection 4. Idiopathic
DILATED CARDIOMYOPATHY PATHOPHYSIOLOGY Diminished contractile proteins poor contraction decreased blood ejection increased blood remaining in the ventricle ventricular stretching and dilatation. SYSTOLIC DYSFUNCTION
HYPERTROPHIC CARDIOMYOPATHY
Associated factors: 1. Genetic 2. Idiopathic
HYPERTROPHIC CARDIOMYOPATHY
Pathophysiology Increased size of myocardium reduced ventricular volume increased resistance to ventricular filling diastolic dysfunction
RESTRICTIVE CARDIOMYOPATHY
Pathophysiology Rigid ventricular wall impaired stretch and diastolic filling decreased output Diastolic dysfunction
CARDIOMYOPATHIES
Assessment findings 1. PND 2. Orthopnea 3. Edema 4. Chest pain 5. Palpitations 6. dizziness 7. Syncope with exertion
CARDIOMYOPATHIES
Laboratory Findings 1. CXR- may reveal cardiomegaly 2. ECHOCARDIOGRAM 3. ECG 4. Myocardial Biopsy
CARDIOMYOPATHIES
Medical Management 1. Surgery= heart transplant 2. pacemaker insertion 3. Pharmacological drugs for symptom relief
CARDIOMYOPATHIES
Nursing Management 1. Improve cardiac output Adequate rest Oxygen therapy Low sodium diet
CARDIOMYOPATHIES
Nursing Management 2. Increase patient tolerance Schedule activities with rest periods in between
CARDIOMYOPATHIES
Nursing Management 3. Reduce patient anxiety Support patient Offer information about transplantations Support family in anticipatory grieving
Infective endocarditis
Infection
of the heart valves and the endothelial surface of the heart
Can
be acute, sub-acute or chronic
Etiologic factors 1. Bacteria- Organism depends on several factors 2. Fungi
Infective Endocarditis
Risk factors 1. Prosthetic valves 2. Congenital malformation 3. Cardiomyopathy 4. IV drug users 5. Valvular dysfunctions
Pathophysiology Direct invasion of microbes microbes adhere to damaged valve surface and proliferate damage attracts platelets causing clot formation
erosion of valvular leaflets and the clot and vegetation can embolize
Assessment findings 1. Intermittent high grade fever 2. anorexia, weight loss 3. cough, back pain and joint pain 4. splinter hemorrhages under nails
Assessment findings 5. Oslers nodes- painful nodules on fingerpads 6. Roths spots- pale hemorrhages in the retina
Assessment findings 7. Heart murmurs 8. Heart failure= usually acute heart failure
Prevention Antibiotic prophylaxis if patient is undergoing procedures like dental extractions, bronchoscopy, surgery, etc.
Prevention Any invasive procedure that is associated with transient bacteremia may cause the microrganism to lodge in the damaged, irregular valves
LABORATORY EXAM Blood Cultures to determine the exact organism

Usually,
3 culture specimens are obtained and antibiotic sensitivity done
Nursing management 1. Regular monitoring of temperature, heart sounds 2. Manage infection 3. Long-term antibiotic therapy is given to ensure eradication of bacteria
Medical management 1. Pharmacotherapy IV antibiotic for 2-6 weeks Antifungal agents are given amphotericin B
Medical management 2. Surgery Valvular replacement
CHF
A
syndrome of congestion of both pulmonary and systemic circulation caused by inadequate cardiac function and inadequate cardiac output to meet the metabolic demands of tissues
CHF
Inability
of the heart to pump sufficiently The heart is unable to maintain adequate circulation to meet the metabolic needs of the body
CHF This can happen acutely or chronically

Acute in Myocardial infarction Chronic cardiomyopathies
CHF Classified according to the major ventricular dysfunction: 1. Left Ventricular failure 2. Right ventricular failure
CHF
Etiology of CHF
1. CAD 2. Valvular heart diseases 3. Hypertension 4. MI 5. Cardiomyopathy 6. Lung diseases 7. Post-partum 8. Pericarditis and cardiac tamponade
New York Heart Association

Class 1 Ordinary physical activity does NOT cause chest pain and fatigue No pulmonary congestion Asymptomatic NO limitation of ADLs
New York Heart Association

Class 2 SLIGHT limitation of ADLs NO symptom at rest Symptoms with INCREASED activity Basilar crackles and S3
New York Heart Association Class 3 Markedly limitation on ADLs Comfortable at rest BUT symptoms present in LESS than ordinary activity
New York Heart Association Class 4 SYMPTOMS are present at rest
CHF
PATHOPHYSIOLOGY LEFT Ventricular pump failure back up of blood into the pulmonary veins increased pulmonary capillary pressure pulmonary congestion (edema)
CHF
PATHOPHYSIOLOGY LEFT ventricular failure Decreased cardiac output Decreased perfusion to the brain, kidney and other tissues Cerebral anoxia, fatigue, oliguria, dizziness
CHF
PATHOPHYSIOLOGY RIGHT ventricular failure
blood pooling in the venous circulation increased hydrostatic pressure

peripheral edema
CHF
PATHOPHYSIOLOGY RIGHT ventricular failure
Venous blood pooling venous congestion in the kidney, liver and GIT
LEFT SIDED CHF ASSESSMENT FINDINGS 1. Dyspnea on exertion, activity intolerance 2. PND 3. Orthopnea 4. Pulmonary crackles/rales 5. Cough with Pinkish, frothy sputum 6. Tachycardia
LEFT SIDED CHF ASSESSMENT FINDINGS

7.
Cool extremities 8. Cyanosis 9. decreased peripheral pulses 10. Fatigue 11. Oliguria 12. signs of cerebral anoxia
RIGHT SIDED CHF ASSESSMENT FINDINGS

1.
Peripheral dependent, pitting edema 2. Weight gain 3. Distended neck vein 4. hepatomegaly 5. Ascites
RIGHT SIDED CHF ASSESSMENT FINDINGS 6. Body weakness 7. Anorexia, nausea 8. Pulsus alternans 9. Nocturia= urination at night at frequent intervals as the blood moves from interstitial space to the intravascular space and is excreted
CHF
LABORATORY FINDINGS 1. CXR may reveal cardiomegaly 2. ECG may identify Cardiac hypertrophy 3. Echocardiogram may show hypokinetic heart
CHF
LABORATORY FINDINGS
4.
ABG and Pulse oximetry may show decreased O2 saturation 5. PCWP is increased in LEFT sided CHF and CVP is increased in RIGHT sided CHF
CHF
NURSING INTERVENTIONS 1. Assess patient's cardiopulmonary status 2. Assess VS, CVP and PCWP. Weigh patient daily to monitor fluid retention
CHF
NURSING INTERVENTIONS
3. Administer medicationsusually cardiac glycosides are given- DIGOXIN or DIGITOXIN, Diuretics, vasodilators and hypolipidemics are prescribed
CHF
Cardiotonics
Positive inotropic agents

Diuretics
To increase cardiac contractility To decrease the intravascular volume in the circulation
Low Sodium Diet

Hypolipidemics
To minimize water retention

To decrease the lipid levels of high risk patients
CHF
NURSING INTERVENTIONS Digoxin Health teaching
Oral
tablet usually once a day Increases force of contraction DECREASES heart rate Assess: Apical pulse, ECG, hypokalemia
CHF
NURSING INTERVENTIONS Digoxin Health teaching
Withhold
the drug if apical pulse is less than 60 Note for early signs of toxicity: NAVDA Provide potassium supplements
CHF
4.
Provide a LOW sodium diet. Limit fluid intake as necessary 5. Provide adequate rest periods to prevent fatigue
CHF
6.
Position on semi-fowlers to fowlers for adequate chest expansion 7. Prevent complications of immobility
CHF
NURSING INTERVENTION AFTER THE ACUTE STAGE 1. Provide opportunities for verbalization of feelings 2. Instruct the patient about the medication regimen- digitalis, vasodilators and diuretics 3. Instruct to avoid OTC drugs, Stimulants, smoking and alcohol
CHF
NURSING INTERVENTION AFTER THE ACUTE STAGE
4.
Provide a LOW fat and LOW sodium diet 5. Provide potassium supplements 6. Instruct about fluid restriction
CHF
NURSING INTERVENTION AFTER THE ACUTE STAGE
7.
Provide adequate rest periods and schedule activities 8. Monitor daily weight and report signs of fluid retention
CARDIOGENIC SHOCK
Heart
fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion
CARDIOGENIC SHOCK
ETIOLOGY
1. Massive MI 2. Severe CHF 3. Cardiomyopathy 4. Cardiac trauma 5. Cardiac tamponade
CARDIOGENIC SHOCK
ASSESSMENT FINDINGS 1. HYPOTENSION 2. Oliguria (less than 30 ml/hour) 3. Tachycardia 4. Narrow pulse pressure 5. weak peripheral pulses 6. cold clammy skin 7. changes in sensorium/LOC 8. pulmonary congestion
CARDIOGENIC SHOCK
LABORATORY FINDINGS Increased CVP due to pooling of blood in the venous system
Normal
is 4-10 cmH2O
Metabolic
acidosis
CARDIOGENIC SHOCK
1. Place patient in a modified Trendelenburg (shock ) position

2. Administer IVF, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE
CARDIOGENIC SHOCK
3.
Administer O2
4.
Morphine is administered to decreased pulmonary congestion and to relieve pain, relieve anxiety
CARDIOGENIC SHOCK
5.
Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz cath and IABP 6. Monitor urinary output, BP and pulses 7. cautiously administer diuretics and nitrates
CARDIAC TAMPONADE
A
condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial effusion)
CARDIAC TAMPONADE
Causative factors 1. Cardiac trauma 2. Complication of Myocardial infarction 3. Pericarditis 4. Cancer metastasis
CARDIAC TAMPONADE
This
condition restricts ventricular filling resulting to decreased cardiac output Acute tamponade may happen when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac
CARDIAC TAMPONADE
ASSESSMENT FINDINGS 1. BECKs Triad- Jugular vein distention, hypotension and distant/muffled heart sound 2. Pulsus paradoxus 3. Increased CVP 4. Decreased cardiac output
CARDIAC TAMPONADE
ASSESSMENT FINDINGS 5. Syncope 6. Anxiety 7. Dyspnea 8. Percussion- Flatness across the anterior chest
CARDIAC TAMPONADE
Laboratory FINDINGS 1. Echocardiogram= shows accumulated fluid in the pericardial sac 2. Chest X-ray
CARDIAC TAMPONADE
NURSING INTERVENTIONS 1. Assist in PERICARDIOCENTESIS 2. Administer IVF 3. Monitor ECG, urine output and BP 4. Monitor for recurrence of tamponade
Pericardiocentesis
Patient
is monitored by ECG Maintain emergency equipments Elevate head of bed 45-60 degrees Monitor for complicationscoronary artery rupture, dysrhythmias, pleural laceration and myocardial trauma
General Measures to Improve Peripheral Circulation

1. Implement Regular Physical Activity to facilitate movement of venous blood 2. Eliminate cigarette smoking- to prevent vasoconstriction 3. Control hyperlipidemia and cholesterol levels- to prevent the progression of atherosclerosis
HYPERTENSION
A
systolic BP greater than 140 mmHg and a diastolic pressure greater than 90 mmHg over a sustained period, based on two or more BP measurements.
HYPERTENSION
Types of Hypertension 1. Primary or ESSENTIAL Most common type 2. Secondary Due to other conditions like Pheochromocytoma, renovascular hypertension, Cushings, Conns , SIADH
HYPERTENSION
PATHOPHYSIOLOGY Multi-factorial etiology BP= CO (SV X HR) x TPR Any increase in the above parameters will increase BP
HYPERTENSION
Risk factors for Cardiovascular Problems in Hypertensive patients Major Risk factors 1. Smoking 2. Hyperlipidemia 3. DM 4. Age older than 60 5. Gender- Male and post menopausal women 6. Family History
HYPERTENSION
PATHOPHYSIOLOGY Any increase in the above parameters will increase BP 1. Increased sympathetic activity 2. Increased absorption of Sodium, and water in the kidney
HYPERTENSION
PATHOPHYSIOLOGY
Any increase in the above parameters will increase BP 3. Increased activity of the RAAS 4. Increased vasoconstriction of the peripheral vessels 5. Insulin resistance
HYPERTENSION
ASSESSMENT FINDINGS 1. Headache 2. Visual changes 3. chest pain 4. dizziness 5. N/V
HYPERTENSION
DIAGNOSTIC STUDIES 1. Health history and PE 2. Routine laboratory- urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS 3. Other lab- CXR, creatinine clearance, 24-huour urine protein
HYPERTENSION
MEDICAL MANAGEMENT 1. Lifestyle modification 2. Diet therapy 3. Drug therapy
HYPERTENSION
MEDICAL MANAGEMENT Drug therapy Diuretics Beta blockers Calcium channel blockers ACE inhibitors A2 Receptor blockers Vasodilators
HYPERTENSION
NURSING INTERVENTIONS 1. Provide health teaching to patient Teach about the disease process Elaborate on lifestyle changes Assist in meal planning to lose weight
HYPERTENSION
NURSING INTERVENTIONS 1. Provide health teaching to the patient Provide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/day Limit alcohol intake to 30 ml/day Regular aerobic exercise Advise to completely stop smoking
HYPERTENSION
Nursing Interventions 2. Provide information about antihypertensive drugs Instruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition Instruct to avoid over-the-counter drugs that may interfere with the current medication
HYPERTENSION
Nursing Intervention 3. Promote Home care management Instruct regular monitoring of BP Involve family members in care Instruct regular follow-up
HYPERTENSION
Nursing Intervention 4. Manage hypertensive emergency and urgency properly
ANEURYSM
Dilation
involving an artery formed at a weak point in the vessel wall
ANEURYSM
Saccular= when one side of the vessel

is affected
Fusiform= when the entire segment

becomes dilated
ANEURYSM
RISK FACTORS 1. Atherosclerosis 2. Infection= syphilis 3. Connective tissue disorder 4. Genetic disorder= Marfans Syndrome
ANEURYSM
PATHOPHYSIOLOGY Damage to the intima and media weakness outpouching of vessel wall Dissecting aneurysm tear in the intima and media with dissection of blood through the layers
ANEURYSM
ASSESSMENT 1. Asymptomatic 2. Pulsatile sensation on the abdomen 3. Palpable bruit
ANEURYSM
LABORATORY: CT scan Ultrasound X-ray Aortography
ANEURYSM
Medical Management: Anti-hypertensives Synthetic graft
ANEURYSM
Nursing Management: Administer medications Emphasize the need to avoid increased abdominal pressure No deep abdominal palpation Remind patient the need for serial ultrasound to detect diameter changes
PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Refers
to arterial insufficiency of the extremities usually secondary to peripheral atherosclerosis. Usually found in males age 50 and above The legs are most often affected
ARTERIOSCLEROSIS OF THE EXTREMITIES
Arteriosclerosis of the extremities is a disease of the peripheral blood vessels that is characterized by narrowing and hardening of the arteries that supply the legs and feet. The narrowing of the arteries causes a decrease in blood flow. Symptoms include leg pain, numbness, cold legs or feet and muscle pain in the thighs, calves or feet.

Risk factors for Peripheral Arterial occlusive disease Non-Modifiable 1. Age 2. gender 3. family predisposition

Risk factors for Peripheral Arterial occlusive disease Modifiable 1. Smoking 2. HPN 3. Obesity 4. Sedentary lifestyle 5. DM 6. Stress
WALANG ORIGINALITY! HHMMPP!
PERIPHERAL ARTERIAL OCCLUSIVE DISEASE ASSESSMENT FINDINGS 1. INTERMITTENT CLAUDICATION- the hallmark of PAOD This is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with the same degree of exercise or activity
PERIPHERAL ARTERIAL OCCLUSIVE DISEASE ASSESSMENT FINDINGS 1. INTERMITTENT CLAUDICATION- the hallmark of PAOD This pain is RELIEVED by REST This commonly affects the muscle group below the arterial occlusion
PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Assessment Findings 2. Progressive pain on the extremity as the disease advances
3.
Sensation of cold and numbness of the extremities
ARTERIOSCLEROSIS OF THE EXTREMITIES
PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Assessment Findings 4. Skin is pale when elevated and cyanotic and ruddy when placed on a dependent position
5.
Muscle atrophy, leg ulceration and gangrene

Diagnostic Findings 1. Unequal pulses between the extremities 2. Duplex ultrasonography 3. Doppler flow studies
PAOD
Medical Management 1. Drug therapy Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation 2. Surgery- Bypass graft and anastomoses

Nursing Interventions 1. Maintain Circulation to the extremity Evaluate regularly peripheral pulses, temperature, sensation, motor function and capillary refill time Administer post-operative care to patient who underwent surgery Administer heat modalities to the leg cautiously to promote vasodilatation

Nursing Interventions 2. Monitor and manage complications

Note for bleeding, hematoma, and decreased urine output Elevate the legs to diminish edema Encourage exercise of the extremity while on bed Teach patient to avoid leg-crossing
Nursing Interventions 3. Promote Home management Encourage lifestyle changes Instruct to AVOID smoking Instruct to avoid leg crossing
BUERGERS DISEASE
Thromboangiitis obliterans A disease characterized by recurring inflammation of the medium and small arteries and veins of the lower extremities
BUERGERS DISEASE
Thromboangiitis obliterans Occurs in MEN ages 20-35 RISK FACTOR: SMOKING!
BUERGERS DISEASE
PATHOPHYSIOLOGY Cause is UNKNOWN Probably an Autoimmune disease Inflammation of the arteries and veins thrombus formation occlusion of the vessels
BUERGERS DISEASE
ASSESSMENT FINDINGS
1. Leg PAIN Foot cramps in the arch (INSTEP CLAUDICATION) after exercise Relieved by rest Aggravated by smoking, emotional disturbance and cold chilling
BUERGERS DISEASE
ASSESSMENT FINDINGS
2. Digital rest pain not changed by activity or rest
BUERGERS DISEASE
ASSESSMENT FINDINGS 3. Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as disease advances
4.
Paresthesias
BUERGERS DISEASE
Diagnostic Studies 1. Duplex ultrasonography 2. Contrast angiography
BUERGERS DISEASE
Nursing Interventions 1. Assist in the medical and surgical management
Bypass
graft amputation
2. Strongly advise to AVOID smoking 3. Manage complications appropriately
BUERGERS DISEASE
Nursing Interventions
Post-operative care: after amputation Elevate stump for the FIRST 24 HOURS to minimize edema and promote venous return Place patient on PRONE position after 24 hours several times a day Assess skin for bleeding and hematoma Wrap the extremity with elastic bandage
RAYNAUDS DISEASE
A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain and pallor of the fingertips or toes
RAYNAUDS DISEASE
Cause : UNKNOWN Most commonly affects WOMEN, 16- 40 years old
RAYNAUDS DISEASE
ASSESSMENT FINDINGS 1. Raynauds phenomenon A localized episode of vasoconstriction of the small arteries of the hands and feet that causes color and temperature changes
RAYNAUDS DISEASE
W-B-R is the acronym for the color change Pallor- due to vasoconstriction, then Blue- due to pooling of Deoxygenated blood Red- due to exaggerated reflow or hyperemia
RAYNAUDS DISEASE
ASSESSMENT FINDINGS 2. Tingling sensation 3. Burning pain on the hands and feet
RAYNAUDS DISEASE
Medical management Drug therapy with the use of CALCIUM channel blockers
To
prevent vasospasms
RAYNAUDS DISEASE
Nursing Interventions
1. instruct patient to avoid situations that may be stressful 2. instruct to avoid exposure to cold and remain indoors when the climate is cold 3. instruct to avoid all kinds of nicotine 4. instruct about safety. Careful handling of sharp objects
LAUGH BREAK
Bisaya 1: " Gara ng kutsi, siguro kay Miyur iyan."! Bisaya 2: " Dili bay!" Bisaya 1: " Kay Hipi?" Bisaya 2: " Tuntu ka man. Kay FATHER iyan. Gisulat niya sa likud o,"'SAFARI'."
VARICOSE VEINS
THESE
are dilated veins usually in the lower extremities
VARICOSE VEINS
Predisposing
Pregnancy Prolonged
Factors
standing or
sitting Incompetent venous valves
VARICOSE VEINS
Pathophysiology
Factors
venous stasis increased hydrostatic pressure edema
VARICOSE VEINS
Assessment
Tortuous
findings
superficial veins on the legs Leg pain and Heaviness Dependent edema
VARICOSE VEINS
Laboratory
findings
Venography
Duplex
scan pletysmography
VARICOSE VEINS
Medical
management
Pharmacological
therapy Leg vein stripping and ligation Anti-embolic stockings
VARICOSE VEINS
Nursing management 1. Advise patient to elevate the legs with pillow to increase venous return 2. Caution patient to avoid prolonged standing or sitting
VARICOSE VEINS
Nursing management 3. Provide high-fiber foods to prevent constipation 4. Teach simple exercise to promote venous return
VARICOSE VEINS
Nursing management 5. Caution patient to avoid constrictive clothing
VARICOSE VEINS
Nursing management 6. Apply anti-embolic stockings as directed 7. Avoid massage on the affected area
DVT- Deep Vein Thrombosis

Inflammation
of the deep veins of the lower extremities and the pelvic veins The inflammation results to formation of blood clots in the area

Predisposing
Prolonged
factors
immobility Varicosities Traumatic procedures Increased age Malignancy Estrogen therapy Smoking

Complication
PULMONARY
thromboembolism
Assessment findings Leg tenderness Leg pain and edema Positive HOMANs SIGN
HOMANs SIGN
The foot is FLEXED upward (dorsiflexed) , there is a sharp pain felt in the calf of the leg indicative of venous inflammation
Laboratory findings Venography Duplex scan

Medical
management
Antiplatelets-
aspirin Anticoagulants Vein stripping and grafting Anti-embolic stockings
Nursing management 1. Provide measures to avoid prolonged immobility Repositioning Q2 Provide passive ROM Early ambulation
Nursing management 2. Provide skin care to prevent the complication of leg ulcers 3. Provide anti-embolic stockings

Nursing management 4. Administer anticoagulants as prescribed 5. Monitor for signs of pulmonary embolism sudden respiratory distress
The End Thank You!

Cardio Nursing Course Audit 21

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Cardiovascular System

By: Ms. Irene M. Magbanua

FOUR STAGES OF LIFE

The Cardiovascular System

The Cardiovascular System

The Cardiovascular System

The Cardiovascular System

The Cardiovascular System

The Semilunar valves-

CHARACTERISTICS OF THE CARDIAC MUSCLE

The Cardiovascular System

The Cardiovascular System

The Heart: Physiology

The Cardiovascular System

Blood pressure is:

Cardiac Output Regulation

The Cardiovascular System

The Cardiovascular System

Hormones- ADH, Adrenergic hormones, Aldosterone and ANF

The Heart: Physiology

Anatomy a& Physiology Refers to change in heart rate Chronotropic

Factors regulating Stroke Volume

Factors regulating Stroke Volume

Factors regulating Stroke Volume

Factors that increase myocardial oxygen demands

Cardiac compensatory mechanisms

The Cardiovascular System

The Cardiovascular System

Differences Between Blood Vessel Types

Skeletal muscle milks blood in veins toward the heart

Movement of Blood Through Vessels

Major Arteries of Systemic Circulation

Blood Supply to:

Blood Supply to:

Major Veins of Systemic Circulation

Arterial Supply of the Brain

Hepatic Portal Circulation

Circulation to the Fetus

Blood Pressure: Effects of Factors

Factors Determining Blood Pressure

Variations in Blood Pressure

Effects of Aging on the Heart

The Cardiovascular System

The Cardiovascular System

Interview Focused assessment

The Cardiovascular System

The Cardiovascular System

MB ( creatine kinase) Normal value is 0-7 U/L

Dehydrogenase (LDH) Elevates in MI in 24 hours, peaks in 48-72 hours

Dehydrogenase (LDH) Normal value is 70-200 IU/L

I is usually utilized for

AFTER THE WEDDING:

The Cardiovascular System LABORATORY PROCEDURES

The Cardiovascular System LABORATORY PROCEDURES

The Cardiovascular System LABORATORY PROCEDURES

The Cardiovascular System LABORATORY PROCEDURES

The Cardiovascular System LABORATORY PROCEDURES

Pharmacological stress test

Fast for 8-12 hours, teachings, medications to allay anxiety

CVP is 0 to 8 mmHg/ 4-10 cm H2O

CVP indicates increase in blood volume, excessive IVF or heart/renal failure

CVP may indicate hypovolemia, hemorrhage and severe vasodilatation