Cardiac Flashcards

1
Q

Which artery on the heart is often called the “widowmaker”?

A

left anterior descending coronary artery

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2
Q

Where is the point of maximal impulse (PMI)? Why is it significant?

A

– PMI = 5th intercostal space, midclavicular line, left of the sternum

– where the apical pulse can be located = loudest heart sounds

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3
Q

Which valves make up S1 sounds? Which valves make up S2 sounds?

A

– atrioventricular valves (mitral/tricuspid) = S1

– semilunar valves (aortic/pulmonic) = S2

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4
Q

Describe the pathway of electrical conduction in the heart.

A
  • sinoatrial (SA) node = natural pacemaker of the heart; where conduction starts
  • atrioventricular node
  • bundle branches (left and right)
  • perkinje fibers
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5
Q

What are the 2 types of cells located in the heart, and what kinds of electrolytes do they require?

A

– electrical cells

  • require
    • sodium
    • potassium
    • calcium
  • in order to initiate impulses

– mechanical cells

  • require calcium in order to initiate contraction
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6
Q

What is normal mean arterial pressure (MAP) that is required to maintain adequate blood flow?

A

must be at least 60 mm Hg, but normal is 70 - 110

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7
Q

What is the difference between cardiac output (CO), stroke volume (SV), preload, and afterload?

A

cardiac output: amount of blood pumped from the left ventricle each minute

stroke volume: amount of blood ejected from the left ventricle with each contraction

preload: volume of blood in the ventricles at the end of diastole

afterload: resistance the left ventricle must overcome to circulate blood (semilunar valve pressure and peripheral blood vessel pressure)

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8
Q

What kinds of factors could impact preload? Afterload?

A

– preload:

  • hypervolemia
  • regurgitation of cardiac valves
  • heart failure

– afterload:

  • hypertension
  • vasoconstriction

– an increase in afterload results in an increase in cardiac workload (the heart has to work that much harder to overcome greater amounts of pressure)

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9
Q

What are 2 types of receptors that are a part of the autonomic nervous system that help to regulate blood pressure?

A

baroreceptors: detect pressure in the blood vessels (vena cava, right atrium, and aorta) and regulate BP

chemoreceptors: detect concentrations of electrolytes in the blood and controls amount of fluid that permeates through blood vessel walls to control BP

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10
Q

What are the different pulse grades?

A
  • 0 = absent pulse
  • 1+ = weak and thready
    • possibly due to hypovolemia
  • 2+ = normal
  • 3+ = full
    • possibly due to elevated temperature or exercise
  • 4+ = full and bounding
    • abnormal
    • can indicate hypervolemia or elevated BP
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11
Q

What are the different edema grades? What are possible causes of edema?

A
  • 0 = 0 mm = none
  • +1 = 2 mm = trace
  • +2 = 4 mm = moderate
  • +3 = 6 mm = deep/severe
  • +4 = 8 mm = very deep/severe

– edema could be the result of cardiac, hepatic, or renal problems

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12
Q

What is the best indicator of fluid balance?

A

daily weights

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13
Q

What are some common signs and symptoms of cardiovascular problems?

A
  • pain, discomfort
  • dyspnea, DOE (dyspnea on exertion), orthopnea, PND (proximal noctural dyspnea)
  • fatigue
  • palpitations
  • edema
  • syncope
  • N/V
  • SOB
  • diaphoresis
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14
Q

What are S3 and S4 sounds? What are murmurs, rubs, and clicks?

A

– S3 sounds are an extra sound after S2 sounds due to rapid filling of left ventricle

  • could be caused by CHF, left ventricular failure, or mitral valve regurgitation

– S4 sounds are an extra sound before S1 sounds due to atrial contraction if ventricles are noncompliant

  • could indicate left ventricle hypertrophy, hypertension or aortic stenosis

murmurs: whoosing sounds

rubs: scratching sounds

clicks: metallic sounds

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15
Q

What are the lab tests that can indicate cardiac problems?

A
  • sodium
  • magnesium
  • potassium
  • lipid panel
    • total cholesterol
      • < 170 mg/dL for pts 20 and younger
      • 100 - 199 mg/dL for pts 21+
    • HDL
      • > 45 - 55 mg/dL
    • LDL
      • < 70 mg/dL for very high risk pts
      • < 130 mg/dL for low risk pts
    • triglycerides
      • < 150 mg/dL
  • enzymes & protein panel
    • highly sensitive CRP (hsCRP)
      • indicates inflammation of cardiac tissue
    • creatinine kinase (CK)
      • 30 - 220 U/L
      • enzyme in heart and muscle tissue that increases with damage
      • will see this with rhabdo, MI, and laying down for a while
    • myoglobin (Mb)
      • 30 - 90 ng/mL
      • produced during injury to muscle cells
    • troponin T (cTNT)
      • 0.0 - 0.10 ng/mL
      • this is the gold standard lab for cardiac problems
      • protein directly related to cardiac damage
  • B-type natriuretic peptide (BNP)
    • increased production when there is an increase in blood volume in the heart chambers – indicates HF
    • < 100 pg/mL = no HF
    • 100 - 300 pg/mL = HF present
    • 300+ pg/mL = mild HF
    • 600+ pg/mL = moderate HF
    • 900+ pg/mL = severe HF
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16
Q

What are some diagnostic tests that can identify cardiac problems?

A
  • CXR
  • EKG
  • Holter monitor
    • records EKG continously over long periods
  • echocardiography
    • measures
      • amount of blood flow through chambers (ejection fraction)
        • normal = 60 - 70%
      • contraction under stress
      • tumors and clots
      • congenital abnormalities
  • thallium stress test
    • thallium injected
    • thallium doesn’t enter damaged tissue
    • dark spots with no thallium can be visualized
  • cardiac catheterization
  • coronary angiography
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17
Q

What is the difference between ischemia and infarction?

A

ischemia: insufficient oxygen supply to sustain myocardial contraction

  • does not always result in permanent damage

infarction: necrosis due to prolonged severe ischemia

  • causes irreversible damage to tissue
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18
Q

What conditions make up coronary artery disease?

A
  • stable angina
  • acute coronary syndrome
    • unstable angina
    • acute myocardial infarction
    • new onset angina
    • variant (Prinzmetal’s) angina
    • pre-infarction angina
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19
Q

What is chronic stable angina pectoris?

A
  • “strangling of the chest”
  • temporary imbalance between
    • coronary arteries’ ability to supply oxygen
    • the cardiac muscles’ demand for oxygen
  • limited in duration
  • does not cause permanent damage
  • usually relieved by
    • nitroglycerin
    • rest
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20
Q

What is acute coronary syndrome (ACS)?

A
  • pts with either
    • unstable angina
    • acute myocardial infarction
    • new onset angina
    • variant (Prinzmetal’s) angina
    • pre-infarction angina
  • atherosclerotic plaque in coronary arteries ruptures, causing platelet clumping and clot foramtion
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21
Q

Differentiate between the diseases under ACS.

A

unstable angina: chest pain during rest; exertion causes severe limitations; chest pains last 15+ minutes

  • poorly relieved by nitroglycerin or rest
  • exertion can increase the number and severity of attacks

acute myocardial infarction: heart attack due to blockage of blood flow to heart via coronary arteries

new onset angina: first few incidences of chest pain; usually occurs with exertion

variant (Prinzmetal’s) angina: usually result of coronary artery spasms; usually occurs after rest

pre-infarction angina: days or weeks leading up to MI

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22
Q

What are STEMIs and NSTEMIs?

A

– STEMI = ST elevation MI

  • traditional manifestation of MI where the ST segment is elevated on the EKG

– NSTEMI (non-STEMI) = non-ST elevation MI

  • uncommon manifestation of MI where the ST segment appears abnormal but it is not necessarily elevated or the ST segment appears normal but the pt is clearly having cardiac issues
  • common presentation in women
  • diagnose NSTEMIs with trope labs
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23
Q

What is a myocardial infarction? What are some ways it can result?

A

myocardial infarction: most serious acute coronary syndrome; myocardial tissue is abruptly and severly deprived of oxygen

– possible causes:

  • occlusion of blood flow
  • necrosis – can extend an MI if left untreated
  • hypoxia – can extend an MI if left untreated
  • ventricular remodeling (scarring of heart tissue; long-term damage to cardiac function)
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24
Q

What can exacerbate damage to the heart during an MI?

A

catecholamines

released during stress –> causes release of epi and norepi –> increases damage to the heart

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25
Q

Which demographics have a higher risk of MIs?

A
  • Hispanic and African American women have a higher risk of MIs, especially in older age
  • men tend to experience MIs in younger age
  • women tend to experience MIs in older age
  • men experience STEMIs more often
  • women experience NSTEMIs more often
    • higher risk of death due to MIs because of non-traditional symptoms
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26
Q

What are the 5 descriptors of chest pain? (PQRST)

A
  • Precipitating factors
  • Quality
  • Region and raditation
  • Severity and associated symptoms
  • Timing
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27
Q

What are some immediate interventions for pts with MI?

A
  • place on non-rebreather – 10 - 15 L/min
  • place on IV immediately
  • administer medications
  • place on EKG
  • diet:
    • restrict sodium
    • restrict cholesterol
    • restrict caffeine
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28
Q

What are serum lab tests that can indicate cardiac problems? Which tests are gold standard?

A
  • creatine kinase of muscle band (CK-MB)
    • used when trope tests aren’t available
    • aren’t as useful anymore
  • cardiac troponin (cTn)
    • determine cardiac injury
    • any positive amount suggest cardiac injury
  • myoglobin (Mb)
    • high sensitivity but low specificity for skeletal and muscle issues
    • can be used to rule out MI
  • lactate dehydrogenase (LDH)
    • not specific for cardiac tissue
  • hsCRP
  • BNP

– gold standard = tropes + EKG

29
Q

Other than women, what other demographic presents MIs differently?

A

DM pts – have silent MIs

30
Q

What are some interventions for acute cardiac pain?

A
  • pain relief
  • decrease myocardial oxygen demand
  • increase myocardial oxygen supply
    • oxygen
      • 100% non-rebreather @ 10 - 15 L/min
      • ensure pt sats 95+%
    • deep breathing exercises
  • drugs
    • nitroglycerine
      • vasodilator –> increases oxygen available to tissues
      • contraindicated in pts with erectile dysfunction
    • morphine sulfate
      • vasodilator
    • beta-blockers (lopressor)
      • blocks catecholamines
      • decreases heart’s oxygen demand
      • just keep an eye on BP
    • ACE inhibitors (-pril meds)
      • given within 48H of MI to prevent scarring
    • MONA
      • morphine
      • oxygen
      • nitrogen
      • aspirin
  • reposition
    • comfort
    • semi-Fowler’s
  • provide quiet and calm environment
31
Q

What are some interventions for ineffective tissue perfusion?

A
  • drugs
    • aspirin
    • thrombolytic agents
  • restore perfusion to injured area
32
Q

What are some drug interventions for acute coronary syndrome?

A
  • glycoprotein (IIb and IIIa) inhibitors (RePro, Integrilin, Aggrastat)
    • antiplatelet
    • prevents fibrinogen from attaching to activated platelets
  • heparin
    • anticoagulant
    • can be used in conjunction with glycoprotein inhibitors
    • draw baseline aPTT prior to heparin administration (bolus or infusion)
    • after 6H, baseline should be higher than the control
      • 1.5 - 2x higher
    • indicates therapeutic effect
  • fibrinolytics (Reteplase, Tenecteplase)
    • clot buster to help reperfuse the tissues
    • IV or intracoronary administration
    • ensure pt has no hx of injury 90 prior
      • could result in bleeding out
  • beta-adrenergic blocking agents (carvedilol)
    • long-acting vasodilators
  • ACE inhibitors
    • relaxes BVs
  • calcium channel blockers
    • increase cardiac perfusion and vasodilation
33
Q

What are some surgical interventions for acute coronary syndrome?

A
  • percutaneous transluminal coronary angioplasty (PTCA)
    • angioplasty = reshape blood vessels by inflating a balloon
    • may involve stent placement
    • prior to procedure, administer Plavix to prevent platelet/clot formation
    • IV heparin after procedure
    • other IV meds to use for procedure
      • nitroglycerine
      • diltiazem – BV relaxer
      • glycoprotein inhibitors
    • long-term medications
      • antiplatelets
      • beta blockers
      • ACE inhibitors
34
Q

What are the 3 phases of cardiac rehabilitation?

A
  1. phase 1: D/C from hospital
    • pt has limited mobility
    • must be careful with activity
  2. phase 2: clinic
    • routine exercise
    • DM checks
  3. phase 3: long-term adherance to exercise
35
Q

What are dysrhythmias? What are some interventions?

A

dysrhythmias: irregular beating of heart

– interventions:

  • identify dysrhythmias
  • assess hemodynamic status
  • evaluate discomfort
  • keep heart monitors and 12-leads on pt
36
Q

What is cardiogenic shock? What are some signs and symptoms?

A

cardiogenic shock (AKA class 4 HF): necrosis of more than 40% of left ventricle

– s/s

  • tachycardia
  • hypotension
    • can lead to renal insufficiency and eventually renal failure
  • BP < 90 mm Hg or 30 mm Hg less than pt’s baseline
  • urine output < 30 mL/hr
  • cold, clammy skin
  • poor peripheral pulses
  • agitation, restlessness
  • confusion
  • pulmonary congestion
  • tachypnea
  • chest discomfort/pain
  • pts are typically unresponsive
37
Q

What are some interventions for cardiogenic shock?

A
  • pain relief
    • reduce preload and afterload
  • drugs
    • vasopressors
    • reperfusion therapies
  • intra-aortic balloon pump
    • last resort
  • arthrectomy
    • retrieval of clots/plaques
  • stent placement
  • rheolytic thrombectomy
    • saline jets break up clots/plaque
    • aspirate out broken clots/plaque
  • coronary artery bypass graft (CABG)
    • grafts are taken from mammary and saphenous veins
    • only use for
      • > 70% stenosis
      • unstable angina
      • CAD in DM pts
38
Q

What is heart failure? What are some causes? What are some risk factors?

A

heart failure (pump failure): inability of the heart to work effectively as a pump, causing the blood to back up, liver congestion, and peripheral edema

– causes:

  • coronary artery disease
  • HTN
  • valvular heart disease

– risk factors:

  • aging
  • DM
  • obesity
  • hyperlipidemia
  • chemical dependencies
    • drugs
    • alcohol
    • smoking
39
Q

What are the 2 types of heart failure?

A
  1. left-sided (CHF)
  2. right-sided
40
Q

Describe left-sided heart failure. What are some signs and symptoms? What are the 2 subtypes of left-sided heart failure?

A

– stroke volume is reduced

  • blood backs up into left side of heart and pulmonary circulation
  • pulmonary pressure increases

– s/s:

  • fluid overload in pulmonary circulation results in
    • dyspnea
    • paroxysmal noctural dyspnea
  • weakness
  • fatigue
  • dizziness
  • acute confusion
  • pulmonary congestion (pink-tinged sputum)
  • oliguria

– 2 subtypes:

  • systolic dysfunction (AKA foreward failure): ventricular dilation (dilated myopathy) – left ventricle stretches and dilates
    • reduced ejection fraction (<40%) because the heart cannot contract forcefully enough to pump blood into circulation
    • preload increases, stroke volume decreases
  • diastolic dysfunction: left ventricular stiffness
    • left venticle inadequately relaxes due to hypertrophic/restrictive cardiomyopathy
    • ventricular filling during diastole are impaired
    • common in women with chronic HTN
41
Q

Discuss the etiology of left-sided heart failure.

A
  • systemic HTN is the most common cause of heart failure
  • structural heart changes (like valvular dysfunction) can cause pressure or volume overload on the heart
  • 1/3 of MI pts develop heart failure
42
Q

Describe right-sided heart failure. What are some signs and symptoms?

A

– right ventricle cannot empty completely

  • usually caused by left ventricular failure
  • can also be caused by pulmonary diseases

– s/s:

  • peripheral edema
    • due to increased volume and pressure in venous system
  • jugular vein distention
  • increased abdominal girth
  • swollen hands/feet
  • dependent edema
  • hepatomegaly
  • ascites
  • weight changes
    • indicative of fluid gain
43
Q

What are some lab tests to assess for heart failure? What are some diagnostic tests?

A

– lab tests:

  • electrolytes
  • H&H
    • determine if the pt is anemic from heart failure
  • B-type natriuretic peptide (BNP)
    • enzyme in chambers of the heart to detect pressure
    • levels increase with HF
    • levels decrease when the heart is stable
  • urinalysis
    • proteinuria
    • high specific gravity
  • ABGs

– diagnostic tests:

  • CXR
    • shows enlarged heart
    • visualizes PE
  • echocardiography = best diagnostic tool
  • EKG
  • hemodynamic monitoring
    • pulmonary artery catheter assesses for cardiac function and fluid volume
    • pressures are increased with heart failure
44
Q

What are the 4 classes of heart failure?

A
  1. class 1: no limitation of physical activity
  2. class 2: slight limitation of physical activity
  3. class 3: marked limitation of physical activity
  4. class 4: inability to carry out any physical activity without discomfort
45
Q

What is the difference between acute and chronic heart failure?

A

acute HF: rapid onset; body doesn’t have time to activate compensatory mechanisms to improve cardiac performance

  • compensatory mechanisms:
    • activation of SNS
    • activation of RAS system
      • angiotensin causes ventricular remodeling
    • ventricular remodeling
      • scarring that can occur due to prolonged activation of SNS and RAS

chronic HF: heart failure that develops more slowly

46
Q

What are some drugs that can be used to reduce afterload?

A
  • ACE inhibitors: angiotensin-converting-enzyme inhibitors that cause vasodilation (decreased resistance to ventricular contraction)
    • can cause respiratory side effects – dry, nagging cough
    • suppress RAS system
    • prevent ventricular remodeling
    • -pril medications
      • enalapril
      • fosinopril
  • angiotensin retension blockers (ARB): reduce ventricular ejection
    • suppress RAS system
    • prevent ventricular remodeling
    • -sartan medications
      • valsartan
      • losartan
  • human B-type natriuretic peptides (hBNP): lower pulmonary wedge pressure (vasodilates) and improves GFR
    • nesiritide
47
Q

What are some interventions to reduce preload?

A
  • diet
    • restrict sodium
    • restrict fluid
  • drugs
    • morphine
      • for acute HF
      • helps with anxiety
      • promotes vasodilation
    • diuretics
      • first choice for older pts with HF
      • monitor BP
      • examples:
        • furosemide (Lasix)
        • bumetanide (Bumex)
        • thiazide (HCTZ)
    • venous vasodilators
      • monitor BP
      • example:
        • isosorbide mononitrate
48
Q

What are some drugs that enhance contractility?

A
  • digoxin:
    • increases contractility
    • reduces HR
    • slows conduction through AV node
  • inotropic drugs
    • improves cardiac output and perfusion
    • increases contractility
    • used short-term for acute HF
    • example:
      • dobutamine
  • beta-adrenergic blockers
    • reverses sympathetic stimulation
    • reduces catecholamine levels
    • examples:
      • carvedilol
      • metoprolol
  • hyperpolarization-activated cyclic nucleotide-gated blocker
    • ivabradine
49
Q

What are some other interventions (other than drugs and preload interventions) for heart failure?

A
  • continuous positive airway pressure (CPAP)
    • decreases preload and afterload
      • improves cardiac output
      • improves ejection fraction
  • cardiac resynchronization therapy (CRT)
    • AKA bi-ventricular pacing
    • stabilizes ventricular contraction
    • examples:
      • pacemakers
      • defibrilators
  • gene therapy
    • injection of growth factors into cardiac cells to help with scarred cardiac cells
  • surgery
    • heart transplant
      • last choice for end stage HF
    • ventricular assist device (VADs)
      • mechanical pump that works with pt’s own heart
    • heart reduction
50
Q

What is one type of heart reduction surgery? How does it work? What disease does it treat?

A

– Batista left ventricular reduction

  • removes a piece of myocardium
  • sutures together the 2 sides
  • decreases ventricular size, causing more effective and more vigorous pumping

– treats Chagas’ disease

51
Q

What part of the heart is replaced in a heart transplant? What is important to note about pts after heart transplants? What are some medications for heart transplant pts? What are some potential complications for heart transplants?

A

– all parts of the heart are replaced except for the back wall of the atria

– new hearts:

  • beat faster (100 - 110 beats/min)
  • slow to respond to increases in activity
  • ^these are due to nerves of the heart being cut during transplant

– heart transplant pts have to be on the following meds for life:

  • immunosuppressants
  • antihypertensives
  • diuretics

– complications:

  • rejection
  • infection
  • renal failure
  • HTN
  • osteoporosis
  • lymphoma
  • CAD
52
Q

What are some indications that heart failure is worsening or recurring?

A
  • rapid weight gain
  • decrease in exercise tolerance
  • cold symptoms
  • excessive nocturia
  • development of dyspnea/angina at rest
  • increased edema in feet, ankles, or hands
53
Q

What is heart valve disease? What are some risk factors? What are some causes?

A

heart valve disease: either stenosis of valves (narrowed valves) or valve insufficiency/regurgitation (widened or scarred valves that cause backflow of blood)

– risk factors:

  • aging – 60+
    • usually the cause of aortic and mitral valve disease
    • big risk factor
  • hx of heart valve disease
  • pregnancy
  • fatigue/overwork of heart
  • congenital abnormalities
  • drug use
  • HTN

– causes:

  • rheumatic fever
  • strep throat
  • atherosclerosis
  • high BP
  • congenital heart defects
  • endocarditis
  • IV drug abuse
  • increased pressure on left side of heart
  • lung disease
    • increased pressure in lungs
    • can cause right-sided valve disease
54
Q

What are the 5 types of valvular heart disease?

A
  1. mitral stenosis
    • results from rheumatic carditis due to hx of rheumatic fever or strep
  2. mitral regurgitation
    • mitral valve doesn’t close all the way
    • causes backflow of blood in the left atrium
  3. mitral valve prolapse
    • mitral valve becomes enlarged and prolaspes into the left atrium during systole
    • often asymptomatic
  4. aortic stenosis
    • wear and tear disease – happens a lot with aging
  5. aortic regurgitation
    • aortic valve doesn’t close completely
55
Q

What are some diagnostic tests for heart valve disease?

A
  • CXR
  • EKG
  • stress test
  • echocardiogram
    • helps evaluate structure and ejection fraction
56
Q

What are some interventions for heart valve disease?

A
  • rest
  • drugs
    • diuretics
    • beta blockers
    • digoxin
    • oxygen
    • nitrates
    • vasodilators
    • anticoagulants
      • prevents thrombus formation due to valve replacement
        • a. fib and a. flutter (and general conduction abnormalities) are common complications of valve replacements
  • surgery
    • reparative procedures
      • valve replacement
      • remodeling – removal of scarred tissue
    • balloon valvuloplasty
      • used for pts at high risk for surgical complications
      • benefits are short-term (~6 months)
    • transcatheter aortic valve replacement (TAVR)
      • for pts who are not surgical candidates and high risk pts
    • direct or open commissurotomy
      • removing thromboli or damaged leaflets
      • debridement of vegetation on valves
        • valves do not have their own circulation so WBCs can’t reach them
    • mitral valve annuloplasty
      • reconstruction of leaflets
    • replacement procedures
      • prostetic valves
        • can be mechanical, cadaver, or bovine tissue
        • need to be replaced Q7 - 10 years
        • xenographs: tissue that comes from biological origin but not human
      • still need to be on anticoagulants
57
Q

What is infective endocarditis? What are some risk factors?

A

infective endocarditis: microbial infection of the endocardium

  • infection by vegetation that grows on the endocardium
  • vegetation: clusters of growing bacteria that commonly develop on heart valves and linings of large arteries
    • these can sometimes be seen on echocardiograms

– risk factos:

  • IV drug abusers
  • valve replacement recipients
  • pts with systemic infections
  • pts with structural cardiac defects
58
Q

What are some portals of entry for infective endocarditis? What are common pathogens?

A

– portals of entry:

  • oral cavity
  • skin rash
  • lesion/abscess
  • infection
  • surgery/invasive procedure

– pathogens:

  • strep
  • staph
59
Q

What are some signs and symptoms of endocarditis?

A
  • murmurs
  • heart failure
  • arterial embolization
    • can be blood emboli or vegetative emboli
      • vegetative emboli will not respond to anticoagulants
  • splenic infarction
    • blood flow to spleen is compromised
    • can result in ischemia or necrosis
  • neurologic changes
  • petechiae
  • splinter hemorrhages
60
Q

How is infective endocarditis diagnosed? What are some interventions?

A

– diagnosis:

  • blood cultures
  • new regurgitant murmur
  • echocardiography
    • demonstrates endocardial involvement

– interventions:

  • antimicrobials
    • IV administration 4 - 6 weeks
  • balance activities with rest
  • surgery
    • repair/removal of infected valve
    • repair/removal of congenital shunts
    • draining of abscesses in heart or elsewhere
61
Q

What is pericarditis? What is chronic constrictive pericarditis? What are some causes of pericarditis?

A

pericarditis: inflammation of pericardium

  • can be bacterial, viral, or fungal

chronic constrictive pericarditis: thickening of pericardium due to chronic inflammation

  • can be caused by infection, cancer, or radiation therapy

– causes:

  • post-MI
    • Dressler’s syndrome
  • post-heart surgery
    • post-pericardiotomy syndrome
    • can occur 1 - 6 weeks after procedure
62
Q

What are some signs and symptoms of pericarditis?

A
  • substernal precordial pain
    • radiates to left side
  • grating, oppressive pain
    • aggravated by breathing, coughing, swallowing
  • pain when lying supine
    • alleviated by sitting up and leaning forward
  • percardial friction rub upon auscultation
63
Q

What are some interventions for percarditis?

A
  • NSAIDs
  • antibiotics
  • cortiosteroids
  • immunosuppressants
  • pericardial drainage
64
Q

What is pericardial effusion (cardiac tamponade)? What are some signs and symptoms? What are some risk factors? What are some interventions?

A

pericardial effusion: accumulation of fluid in the space between pericardium and the heart

  • results in compressing of the heart
  • causes ineffective pumping, HR issues, BP issues, and decreased ejection fraction

– s/s:

  • jugular vein distention
  • paradoxical pulse
    • abnormally large decrease in systolic pressure and pulse during inspiration
  • decreased cardiac output
  • muffled heart sounds
  • circulatory collapse

– risk factors:

  • cancer pts
  • chemotherapy pts
  • hemodialysis pts
  • hx of pericarditis

– interventions:

  • pericardiocentesis
  • pericardial window
    • a portion of the pericardium is removed, allowing fluid to drain
  • diuretics
  • anti-inflammatories
65
Q

What is rheumatic carditis? Which population experiences it more frequently? What are some signs and symptoms?

A

rheumatic carditis: inflammation of all layers of the heart

  • sensitivity response from upper respiratory tract infection by group A beta-hemolytic streptococci
  • characterized by:
    • Aschoff bodies
      • nodules in the myocardium which form scar tissue
    • impaired contractile function of myocardium
    • thickening of pericardium
    • valvular damage

– population = pts with rheumatic fever

  • 50% of pts develop
66
Q

What is cardiomyopathy? What are the 2 types?

A

cardiomyopathy: when the heart loses the ability to pump effectively; arrhythmias

  • leading reason for heart transplant

– 2 types:

  • ischemic: heart muscle damage from coronary artery disease or MI
  • non-ischemic: 3 types
    • dilated
    • hypertrophic
    • restrictive
67
Q

What is dilated cardiomyopathy? What are some causes? What are some signs and symptoms? How is it diagnosed? What are some interventions?

A

dilated cardiomyopathy: when the heart muscles get stretched out, resulting in an inability for the heart to pump effectively

  • can affect 1 or all of the heart’s chambers

– causes:

  • ETOH
  • pregnancy
  • viral infection
  • toxins
  • genetics

– s/s:

  • same as HF
    • activity intolerance
    • fatigue
    • SOB
    • edema
    • arrhythmias

– diagnosis:

  • CXR
  • EKG
  • cath
  • echo

– interventions:

  • drugs:
    • digoxin
    • calcium channel blockers
    • beta blockers
    • diuretics
    • vasodilators
  • rhythm control
  • VAD
  • transplant
68
Q

What is hypertrophic cardiomyopathy? What are some causes? What are some signs and symptoms? How is it diagnosed? What are some interventions?

A

hypertrophic cardiomyopathy: thicker arrangement of heart muscle fibers, usually in the left ventricle or septum

  • thicker muscles are non-functional
  • high risk of sudden death

– causes:

  • genetics

– s/s:

  • abnormal S3 and S4 sounds
  • murmurs
  • mitral regurgitation
  • activity intolerance

– diagnosis:

  • H&P
  • EKG
  • echo

– interventions:

  • decrease activities
  • drugs:
    • beta blockers
    • calcium channel blockers
    • antiarrhythmias
    • diuretics
  • surgery:
    • pacemakers
    • valve replacement
    • thinning of septum
69
Q

What is restrictive cardiomyopathy? How is it different from other cardiomyopathies? What are some causes? What are some signs and symptoms? How is it diagnosed? What are some interventions?

A

restrictive cardiomyopathy: a rare, not very obvious disease in which the walls of the ventricles are very stiff but not necessarily thickened

  • different than other cardiomyopathies because the heart doesn’t necessarily present as enlarged – stiff walls make the ventricles non-functional

– causes:

  • secondary disease – usually results from another disease
  • commonly related to amyloidosis
    • amyloids (abnormal protein fibers) accumulate in the heart muscle cells
    • cause inflammation
    • results in formation of lumps on organs and iron overload
    • stiffens the ventricular tissue

– s/s:

  • same as CHF
  • nausea
  • bloating
  • fluid retention around liver, stomach, and intestines

– diagnosis:

  • H&P
  • echo
    • heart size is small
    • reduced ejection fraction
  • MRI
  • CT
  • cath
  • biopsy

– interventions:

  • no specific treatments
  • palliative care – symptom management
  • diuretics may help with fluid accumulation