Cardiovascular System And Nursing Implications

Front 1

What is the pericardium?

Back 1

-is a double layer of fibroserous membrane that covers the heart
-anchors heart to surrounding structures forming the pericardial sac

Front 2

What is the parietal pericardium?

Back 2

-is the outermost layer of the heart

Front 3

What is the epicardium?

Back 3

-adheres to the heart surface

Front 4

What 3 layers make up the heart wall?

Back 4

3 layers of the heart wall are the epicardium, the myocardium and the endocardium

Front 5

What do the each segment on EKG represent?

Back 5

:-P wave is the atrial depolarization (contraction)
-QRS wave is the ventricular depolarization (contraction) and atrial repolarization (relaxation)
-T wave is the ventricular repolarization (relaxation) and also known as the refractory period

Front 6

What is the natural pacemaker of the heart? And where is it located?

Back 6

The SA node is the natural pacemaker of the heart (60-100 impulses per minute) and located at the junction of the superior vena cava and right atrium

Front 7

Where is the AV node located and what is its purpose?

Back 7

AV node is located in the floor of the interatrial septum; the small junctional fibers of the AV node slows the impulse, slightly delaying its transmission to the ventricles

Front 8

When during the cardiac cycle does the myocardium perfuse with blood?

Back 8

Myocardium perfuses during diastole, in which ventricles refill, atria contracts

Front 9

What is the stroke volume?

Back 9

Stroke volume is the amount of blood pumped into the aorta with each contraction of the left ventricle (60-100mL/beat)

Front 10

What is Cardiac Output and how can it be calculated?

Back 10

Cardiac Output is the amount of blood pumped by the ventricles into the pulmonary and systemic circulations in 1 minute and can be calculated by:
CO=Stroke Volume x Heart Rate
(usually 4-8mL)

Front 11

What is the ejection fraction?

Back 11

Ejection Fraction is the stroke volume divided by the end diastolic volume and represents a fraction of the volume ejected from the heart during systole (contraction); normal range is from 50%-70%

Front 12

What affects cardiac output?

Back 12

Cardiac output is affected by activity level, metabolic rate, psychologic/physiologic stress responses, age, and body size

Front 13

How is cardiac output determined?

Back 13

Cardiac Output is determined by four factors: heart rate, preload, afterload and contractility

Front 14

What is contractility?

Back 14

Contractility is the heart muscle fibers’ capability to shorten. Poor contractility reduces forward flow of blood and increases ventricular pressure and increase

Front 15

What is preload?

Back 15

Preload is the amount of cardiac muscle fiber tension, or stretch, that exists after diastole just before the ventricular contraction; influenced by venous return and ventricular compliance

Front 16

What is Starling's Law of the heart? And what is it based on?

Back 16

Starling's Law states that the greater the volume of blood, the greater the stretch of cardiac muscle fibers, and the greater the force of contraction to accomplish the emptying

Front 17

What is afterload?

Back 17

Afterload is the force the ventricles must overcome(resistance) to eject their blood volume

Front 18

What four factors determine the oxygen consumption?

Back 18

1. heart rate-the more heart pumps, the more oxygen is needed
2. preload-amount of blood brought to heart increases blood return, increases oxygen consumption to pump out blood
3. afterload-increase in resistance increases work of heart to pump out blood which increases oxygen consumption
4. the stretch of ventricles-if ventricles stretch before it is stimulated to contract, has to contract harder to empty which increases oxygen consumption

Front 19

What causes the S1 and S2 heart sounds(a.k.a. "lub", "dub")

Back 19

S1-atrioventricular valves close
S2-semilunar valves close

Front 20

What type of history should be taken when interviewing patient with presenting cardiac problems?

Back 20

-childhood diseases(i.e. rheumatic fever)
-history of chest pain
-gout or diabetes
-sudden weight gain
-emotional problems
-personal habits

Front 21

What are some of the clinical symptoms of Heart Disease?

Back 21

-chest pain
-dypsnea
-fatigue
-palpitations
-syncope or near syncope
-edema
-jugular vein distention

Front 22

Where are the four sites for auscultating heart sounds?

Back 22

1. aortic-right of sternum, 2nd intercostal space
2. pulmonic-left of sternum, 2nd intercostal space
3. tricuspid-left of sternum, 4th intercostal space
4. mitral-midclavicular, 5th intercostal space

Front 23

What are the causes of heart murmurs?

Back 23

-stenosis of the valves
-partial obstruction
-aneurysms
-mitral regurgitation
-septal defect

Front 24

What are two types of murmurs?

Back 24

1. systolic-occurs during systole
2. diastolic-occurs during diastole

Front 25

What range for total cholesterol is acceptable?

Back 25

Total cholesterol level should be between 140-200mg/dL

Front 26

What is the acceptable level of LDL?
What is the acceptable level of HDL?

Back 26

-LDL(less desirable lipoprotein) should be less than 130mg/dL
-HDL(highly desirable lipoprotein) should be 30-70mg/dL but it is desirable to have higher levels

Front 27

What is an acceptable level of triglycerides?

Back 27

Triglyceride levels should be 40-190mg/dL
(fasting for 12hrs, no alcohol for 24hrs)

Front 28

What are some of the risk factors for cardiovascular disease? Which ones are modifiable risk factors?

Back 28

Risk factors are age, gender, race, heredity, smoking, obesity, sedentary lifestyle, and diet
-modifiable risk factors are smoking, obesity, sedentary lifestyle, and diet

Front 29

What pharmacological treatment for hyperlipidemia?

Back 29

1. bile acid sequestriants-bind with bile acids and excrete through feces, decreasing plasma lipid levels; works in gallbladder(ex. cholestyramine, colesevelam, colestipol)
2. HMG-CoA Reduction Inhibitors-block formation of cellular lipids; works in liver(ex. atorvastatin, fluvastatin)
3. Cholesterol absorption inhibitors-decrease small intestine absorption of dietary cholesterol(ex. ezetimibe)
4. other:
fibrates-stimulates breakdown of lipoproteins; works in liver(ex. fenofibrate, gemfibrozil)
niacin(vit. B3)-inhibits release of fatty acids, decreasing LDL and increasing HDL; works in liver

Front 30

What is the pathophysiology of CAD?

Back 30

formation of plaque--> blood cells adhere to plaque--> ability of artery to dilate affected--> plaque extends--> cells occlude artery--> ischemia and/or infarction occurs
(asymptomatic until 75% occluded)

Front 31

What is Angina Pectoris?

Back 31

Angina is chest pain related to decrease coronary blood flow that causes an imbalance in between O2 supply and demand

Front 32

What are some of the symptoms of angina?

Back 32

-chest pain that can radiate to jaw, back, shoulders, arm(relieved by rest)
-dypsnea
-pallor
-anxiety and fear

Front 33

What are some of the causes of angina?

Back 33

causes:
exercise, cocaine, hyperthyroidism, emotional stress, anemia, heart failure, ventricular hypertrophy, or pulmonary disease

Front 34

Name 3 types of angina

Back 34

1. stable angina-most common, predictable; usually caused when work of heart increases through exertion, exposure to cold, or stress; relieved by rest and nitrates
2. Prinzmetal's angina-atypical angina that is unpredictable because it is unrelated to activity; often occurs at night; caused by coronary artery spasms
3. unstable angina-occurs with increased frequency, severity, and duration; pain is unpredictable, may occur w/decreasing activity or stress, or at rest; increased risk for MI

Front 35

Pharmacological treatment of angina

Back 35

1. nitrates-relaxes smooth muscle relaxation, increasing blood flow(ex. nitro)
2. beta blockers-decreases HR, contractility, BP(cannot be given to pts with asthma or COPD, risk for bronchospasm); ex. metoprolol
3. calcium channel blockers-blocks calcium uptake, relaxes smooth muscles,increases blood flow, decreases workload/preload/afterload(ex. nifedipine, verapamil, diltiazem)
4. antiplatelets-reduces platelet aggregation/thrombus formation(low dose aspirin)

Front 36

Coronary Artery Bypass Grafting (CABG)

Back 36

Revascularization of myocardium with graft to bypass obstructed area
-grafts from saphenous vein
-temporary pacer placed
-heart is stopped during surgery
-done laparoscopic or incision
-if vein used, must be reversed so valves don't obstruct blood flow

Front 37

What are the benefits of not using a cardiopulmonary bypass machine during CABG?

Back 37

OR time and recovery time are less

Front 38

What is Myocardial Infarction?

Back 38

Death of myocardial cells to to hypoxemia

Front 39

What are the symptoms of an MI?

Back 39

Chest pain(women pay present with jaw pain), tachychardia, decreased pulses, dysrhythmias, diaphoresis, mottled skin, dyspnea, decreased LOC, anxiety, N/V, EKG changes, heart failure; older adults present with confusion and abdominal pain

Front 40

What is the purpose of angioplasty for MI patient?

Back 40

to increase coronary circulation; goal is to relieve chest pain and limit damage done

Front 41

Medical management of MI

Back 41

-oxygen
-aspirin
-morphine
-nitro
-thrombolytics
-ACE
-anticoagulants
-IV nitro
-antidysrhythmics

Front 42

Patient teaching for MI

Back 42

-avoid extreme heat/cold
-alternate rest/activity
-avoid heavy lifting/bearing down (valsalva)
-eat small frequent meals
-low fat/low salt diet
-take meds as prescribed
-look for signs of activity intolerance(SOB, fatigue, increased HR, chest pain)

Front 43

Define Congestive Heart Failure (CHF)

Back 43

CHF: failure of the heart as a pump
-the cardiac muscle is unable to pump sufficient blood to meet body's needs

Front 44

Causative Factors of CHF

Back 44

-decreased flow to heart
-increased flow to heart
-outflow from heart is obstructed
-heart muscle damage
-increased metabolic needs of body

Front 45

Compensatory responses of CHF

Back 45

-increased workload causes ventricular dilation--> increases force of contraction--> increases cardiac output
-ventricular hypertrophy decreases contractility(heart so large, not enough oxygen, causes ischemia)
-tachychardia tries to increase cardiac output-->decreases time for ventricular fill

Front 46

Markers for MI

Back 46

Troponin-proteins released during MI; 2-4 hr after, peaks at 4-24hrs, remains elevated for 1-3 wks
Myoglobin-detected within 1hr after muscle damage, not specific to cardiac
CK-MB-subset of CK enzymes found only in cardiac muscle and is elevated after MI; 48hrs after MI
*higher the levels, the more damage

Front 47

Signs and Symptoms of Right (Ventricular) Heart Failure
-weakened right heart fails to pump to pulmonary arteries causing venous congestion

Back 47

-elevated central venous pressure(CVP)
-jugular vein distention
-hepatomegaly(enlarged liver)
-ascites(excess excess fluid in the space between the tissues lining the abdomen and abdominal organs (the peritoneal cavity)
-abdominal distention
-nausea
-fatigue
-weight gain(+2lbs overnite)
-bounding pulses
-olyguria

Front 48

Signs and Symptoms of Left (Ventricular) Failure
-weakened left heart, causes blood backup in the left atria; causing pulmonary congestion

Back 48

-dyspnea, SOB
-Crackles
-Orthopnea
-Cough, frothy sputum
-decreased urine output
-fatigue
-pallor
-syncope
-decreased CO
-activity intolerance
-S3 heart sounds

Front 49

What is one of the important interventions for a patient with Left-sided heart failure?

Back 49

Only one pillow at night for sleeping

Front 50

What is paroxysmal nocturnal dyspnea?

Back 50

edema during the day is reabsorbed into the system at night causing fluid overload and breathing difficulties

Front 51

What are some causes of edema?

Back 51

accumulation of extracellular fluid caused by:
1. right-sided failure(abdominal & peripheral congestion)
2. left-sided failure(pulmonary congestion)
3. fluid overload
4. abnormal renal retention
5. increased capillary permeability