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Cardiology Exam > CHF 1 > Flashcards

CHF 1 Flashcards

1
Q

congestive heart failure (CHF) - physiologic definition

A

*the inability of the heart to maintain the circulatory demands of an organism without a rise in left ventricular filling pressure
*simply put, if you have a high filling pressure, you have heart failure

*translation: ELEVATED CARDIAC FILLING PRESSURES with normal/abnormal cardiac output and normal/abnormal LV ejection fraction

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2
Q

heart failure - first aid

A

*clinical syndrome of cardiac pump dysfunction → congestion and low perfusion

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3
Q

heart failure - clinical definition

A

*clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to either fill with or eject blood

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4
Q

high-output vs. low-output CHF

A

*causes of low-output CHF: aortic stenosis, hypertension, myocardial infarction

*causes of high-output CHF: anemia, thyrotoxicosis (thyroid storm), AVM, pregnancy

note: the vast majority of CHF is LOW output

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5
Q

cardiogenic shock vs. acute heart failure

A

*cardiogenic shock and acute heart failure are not different entities, but rather, CARDIOGENIC SHOCK IS ACUTE HEART FAILURE WITH HYPOTENSION

*acute heart failure: increased PCWP, high SVR
*cardiogenic shock: decreased CO, increased PCWP, high SVR, HYPOTENSION

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6
Q

common signs of CHF

A

*jugular venous distention
*S3 gallop [most specific sign on physical exam]
*pulmonary edema (crackles/rales)
*leg edema
*ascites
*hepatomegaly

recall: signs are objective features of an illness, detected by a practitioner

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7
Q

common symptoms of CHF

A

*dyspnea
*dyspnea on exertion
*orthopnea
*paroxysmal nocturnal dyspnea [most specific symptom]
*fatigue
*weakness

recall: symptoms are subjective features of an illness as related by a patient

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8
Q

signs/symptoms of left-sided heart failure

A

*signs: S3 gallop, pulmonary edema
*symptoms: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, weakness

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9
Q

signs/symptoms of right-sided heart failure

A

*jugular venous distention
*leg edema
*ascites
*hepatomegaly

note: usually these are in addition to the s/s of left CHF (pulmonary edema, S3 gallop, dyspnea/orthopnea) b/c left CHF usually precedes right CHF

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10
Q

number 1 leading cause of right-sided CHF is?

A

LEFT-sided CHF

*meaning: right HF most often results from left HF

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11
Q

left-sided CHF pathogenesis: increased LV filling pressure

A

*increased LV end-diastolic pressure → increased left atrial pressure → increased pulmonary venous pressure → increased pulmonary capillary pressure → pulmonary edema

*increased left atrial pressure is translated back to the lungs where it produces shortness of breath (dyspnea)
*initially, it primarily affects the base of the lungs (due to gravity), but as the pressure increases, it can affect all the way to the lung apices

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12
Q

orthopnea in CHF

A

*shortness of breath when supine (when a patient lies down, venous return increases from the legs)
*increased venous return form redistribution of blood (immediate gravity effect) exacerbates pulmonary vascular congestion
*commonly associated with left-sided CHF

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13
Q

paroxysmal nocturnal dyspnea in CHF

A

*breathless awakening from sleep (sensation of shortness of breath that awakens the patient; usually relieved in an upright position)
*increased venous return from redistribution of blood, reabsorption of peripheral edema, etc
*commonly associated with left-sided CHF

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14
Q

pulmonary edema in CHF

A

*increased pulmonary venous pressure → pulmonary venous distention and transudation of fluid
*presence of hemosiderin-laden macrophages (“HF cells”) in lungs
*commonly associated with left-sided CHF

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15
Q

congestive hepatomegaly in CHF

A

*increased central venous pressure → increased resistance to portal flow
*rarely, leads to “cardiac cirrhosis”
*associated with NUTMEG LIVER (mottled appearance) on gross exam
*commonly associated with right-sided CHF

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16
Q

jugular venous distention in CHF

A

*increased venous pressure → distention of jugular veins in the neck
*commonly associated with right-sided CHF

17
Q

peripheral edema in CHF

A

*increased venous pressure → fluid transudation
*commonly associated with right-sided CHF

18
Q

S3 heart sound in CHF

A

*occurs in EARLY DIASTOLE (heard shortly after S2)
*“caused” by oscillation of blood back and forth between the walls of the ventricles initiated by blood rushing in from atria
*in CHF, it is because of increased left atrial pressure filling against a stiff left ventricle

19
Q

right-sided CHF pathogenesis: increased RV filling pressure

A

*increased RV end-diastolic pressure → increased right atrial pressure → increased systemic venous pressure → increased systemic capillary pressure → jugular venous distention, ascites, and lower extremity edema

20
Q

CHF signs & symptoms related to decreased cardiac output vs. increased ventricular filling pressures

A

*s/s due to decreased cardiac output: fatigue, weakness
*s/s due to increased ventricular filling pressures:
-JVD, S3, pulmonary edema, leg edema, ascites, hepatomegaly
-dyspnea, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea

21
Q

clinical profiles in acute heart failure (cold vs. warm; wet vs. dry)

A

*congestion at rest = WET (s/s: orthopnea/PND, S3/rales, JV distention, hepatomegaly, edema)
*low perfusion at rest = COLD (s/s: narrow pulse pressure, cool extremities, sleepy/obtunded, low serum sodium, renal dysfunction, hypotension with ACE inhibitor)

*warm & wet: congestion at rest, but normal perfusion
*cold & wet: congestion AND low perfusion at rest
*cold & dry: low perfusion at rest, but no congestion
*warm & dry (normal)

22
Q

types of heart failure (based on ejection fraction)

A
  1. HFpEF: normal (preserved) LV ejection fraction (LVEF 50%+)
  2. HFmrEF: mildly reduced LV ejection fraction (LVEF 41-49%)
  3. HFrEF: reduced LV ejection fraction (LVEF 40% or less)
23
Q

heart failure with preserved ejection fraction (HFpEF) - overview

A

*defined by LV ejection fraction of 50% or more
*DIASTOLIC dysfunction [associated with inability of LV to adequately relax & fill with blood due to decresaed compliance]
*normal EDV, decreased compliance (increased EDP)
*CONCENTRIC hypertrophy with preserved systolic function
*often secondary to myocardial hypertrophy

24
Q

heart failure with reduced ejection fraction (HFrEF) - overview

A

*defined by LV ejection fraction of 40% or less
*SYSTOLIC dysfunction [ventricles unable to adequately pump blood out]
*increased EDV, decreased contractility
*ECCENTRIC hypertrophy with reduced systolic and diastolic function
*often secondary to ischemia/MI or dilated cardiomyopathy

25
Q

heart failure with preserved ejection fraction (HFpEF) - CAUSES

A

*PRESSURE OVERLOAD:
-hypertension
-diabetes mellitus
-aortic stenosis

26
Q

heart failure with reduced ejection fraction (HFrEF) - CAUSES

A

*VOLUME OVERLOAD:
-myocardial infarction
-alcohol
-idiopathic

27
Q

clinical observations in HFpEF vs. HFrEF

A

*s/s are nearly the same
*PULSUS ALTERNANS indicates HF with REDUCED EF (pulsus alternans means pulse strength in which every other beat feels stronger)

28
Q

demographic features that differ between HFpEF vs. HFrEF

A

*HFpEF: older, female

*HFrEF: younger, male

29
Q

left ventricular remodeling: response to injury

A

*remodeling response to maintain cardiac output/stroke volume:
-LEFT VENTRICLE DILATES in an effort to increase the stroke volume

*pathogenesis: myocardial insult (ex. MI) → myocardial dysfunction → reduced system perfusion → inflammation & hemodynamic defense systems (sympathetic nervous system, RAS) → altered gene expression & apoptosis → REMODELING

30
Q

normal major hemodynamic defense systems

A
  1. sympathetic nervous system [NE at beta and alpha adrenergic receptors increase automaticity, contractility, afterload, preload]
  2. renin angiotensin system [angiotensin 2 binds to AT1 and AT2 receptors in kidney, lungs, and blood vessels → increased afterload and preload]
  3. aldosterone [aldosterone binds to mineralocorticoid receptors in kidney and heart → increased afterload and preload]

note: under NORMAL CIRCUMSTANCES, these systems are only TRANSIENTLY upregulated

31
Q

disturbances to the hemodynamic defense systems in heart failure

A
  1. sympathetic nervous system: chronic upregulation → myocyte death & arrhythmia
  2. renin-angiotensin system: chronic upregulation → myocyte hypertrophy & ischemia
  3. aldosterone: chronic upregulation → cardiac fibrosis
32
Q

beta-1 receptor in heart failure

A

*beta-1 receptors are DOWNREGULATED (fewer receptors) and DESENSITIZED (less likely to stimulate cAMP production)

33
Q

BNP and ANP in CHF

A

*BNP and ANP are both increased in congestive heart failure, as a result of ventricular stretch (increased BNP) and atrial stretch (increased ANP)
*ELEVATED BNP CAN HELP DIAGNOSE CHF (optimal cutpoint = 100 pg/mL, based on the receiver operating curve)

34
Q

ACC/AHA heart failure staging

A

*stage A: at risk for HF
*stage B: pre-HF (patients without current or previous s/s of HF but evidence of structural changes)
*stage C: symptomatic HF (patients with current or previous s/s of HF)
*stage D: advanced HF (marked HF s/s that interfere with daily life & with recurrent hospitalizations)

35
Q

new york heart association heart failure classification

A

*class 1 symptoms: structural myocardial changes (e.g. left ventricular hypertrophy)
*class 2 symptoms: small decrease in exercise tolerance
*class 3 symptoms: significant decrease in exercise tolerance
*class 4 symptoms: symptoms of heart failure in rest or during small exercise

note: we use these classes for people in stage C and stage D HF (based on ACC/AHA staging)

36
Q

ACC/AHA staging with NYHA classification for heart failure

A
37
Q

components of diastolic function

A

*active relaxation:
1. ATP is needed for the actin & myosin to separate
2. ATP is needed for calcium to be removed by SERCA-2 pump into sarcoplasmic reticulum
3. Na+ gradient is used to remove calcium from the intracellular environment through the Na/Ca exchanger

*passive relaxation:
-when actin and myosin dissociate, the energy stored in titin causes it to unspring and results in the elastic recoil of the LV (LV recoil leads to LV suction of blood from the left aftrium)

38
Q

abnormal LV relaxation (diastolic dysfunction) in CHF

A

*when the LV relaxes slowly, it can’t generate the lower pressures to “suck” the blood from the left atrium
*with impaired ability to generate LV suction, the left atrial pressure INCREASES, which leads to dyspnea with exertion (INCREASED PRELOAD to try to meet the metabolic demands)
*as heart failure worsens and LV suction diminishes, the LV filling becomes more dependent on the atrial kick

Cardiology Exam (52 decks)

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