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► Med - Internal Medicine > JH IM Board Review - Heart Failure I > Flashcards

JH IM Board Review - Heart Failure I Flashcards

1
Q

What is the prevalence of HF in the United States?

A

6million

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2
Q

What is the incidence of HF in the United States?

A

Up to 550,000 each yr.

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3
Q

What is the root of HF?

A

The heart can no longer meet the metabolic demands of the body.

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4
Q

What is the definition of HF?

A

A complex clinical syndrome that occurs when the heart or circulation is unable to meet the metabolic demands of peripheral tissue at normal cardiac filling pressures.

==> It can occur in pts w/ nl or depressed systolic function.

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5
Q

What is the common division of HF?

A
  1. Systolic ==> HF w/ reduced EF = HFrEF.

2. Non systolic HF ==> HFpEF.

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6
Q

What is the MC type of HF?

A

Systolic (60%).

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7
Q

What is the type of HF that is increasing in prevalence?

A

Non systolic HF.

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8
Q

What are the 2 MC of HF?

A
  1. CAD — MI.

2. HTN.

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9
Q

What are the 8 major causes of acute decompensated HF?

A
  1. Decompensation of preexisting chronic HF from a precipitating factor.
  2. Hypertensive crisis (eg hypertensive emergency).
  3. MI.
  4. Acute tachyarrhythmia.
  5. Acute endocarditis ==> severe regurgitation.
  6. Acute DCM.
  7. Cardiac tamponade.
  8. High-output HF.
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10
Q

What are the 7 main precipitating factors that may lead to decompensation of preexisting chronic HF?

A
  1. Natural progression.
  2. Excessive fluid/salt intake.
  3. Meds nonadherence.
  4. Infection.
  5. New MI.
  6. Metabolic stress (eg anemia, hyperthyroidism).
  7. Medication use (NSAIDs ==> Na retention).
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11
Q

What are the 3 circumstances under which an AMI may lead to ADHF?

A
  1. Papillary muscle is involved ==> Mitral regurgitation.
  2. Massive anterior MI.
  3. RV infarct resulting in a low cardiac output state.
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12
Q

What are the 8 main causes of high output HF?

A
  1. Thyrotoxicosis.
  2. Beri beri.
  3. Paget.
  4. Sepsis.
  5. Severe anemia.
  6. AV fistula.
  7. Persistent tachycardia (eg atrial arrhythmias).
  8. Liver disease.
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13
Q

What are the 3 potential cell targets of a cardiomyopathy?

A
  1. Myocytes.
  2. Non myocytes.
  3. Myocardial interstitium.
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14
Q

What is the MC of DCM?

A

CAD.

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15
Q

What is the 2nd MCC of DCM?

A

Idiopathic.

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16
Q

What is the 3rd MCC of DCM?

A

Inherited/familial.

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17
Q

What is the usual presentation of DCM?

A

ADHF.

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18
Q

What percentage of DCM improves spontaneously?

A

25-30%.

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19
Q

What is the prognosis of a DCM with a NYHA IV?

A

1y mortality is 50%.

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20
Q

What are some important predictors of poor prognosis in DCM pts?

(4)

A
  1. Hyponatremia.
  2. High cardiac filling pressures.
  3. Low cardiac index.
  4. Poor kidney function.
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21
Q

What is the difference in the mechanism of systolic and nonsystolic HF?

A

Systolic ==> Impaired ejection.

Non systolic ==> Impaired filling.

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22
Q

What are the main physical findings in systolic HF?

A
  1. S3 and/or S4.
  2. Weak carotid upstroke.
  3. Displaced apical impulse.
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23
Q

What are the main physical findings in non systolic HF?

3

A
  1. S4 is more common.
  2. Normal carotid upstroke.
  3. Forceful apical impulse.
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24
Q

What is the type of cardiomyopathy that Duchenne leads to?

A

DCM

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25
Q

What are the 3 types of HCM?

A
  1. Hypertrophy of the LV.
  2. Hypertrophy of the RV.
  3. Hypertrophy of both.
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26
Q

What is the type of HF that HCM leads to?

A

HFpEF.

Rarely HFrEF

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27
Q

What is the ddx of HCM?

A
  1. Hypertrophy from HTN (Hypertensive HCM).
  2. Renal failure.
  3. Fabry.
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28
Q

What is the age of onset of HCM?

A

Hypertrophy is almost always present by age 30y and sx by age 40y.

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29
Q

What is the screening recommendation for all 1o relatives of HCM pts?

A

All first degree relatives should be undergo screening w/ echocardiography and electrocardiography (ECG).

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30
Q

What are the 2 functional types of HCM?

A
  1. Obstructive.

2. Nonobstructive.

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31
Q

What are the 2 conditions under which obstructive HCM is worse?

A
  1. Increased contractility.

2. Decreased preload.

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32
Q

What is the criterion for dx of obstructive HCM?

A

Pressure difference more than 30mm Hg in the areas before and after the obstruction.

Can occur at rest or w/ inotropic stimulation (exercise, postventricular premature beat)

33
Q

What are the physical exam points in pts w/ obstructive HCM?

5

A
  1. Outflow murmur may be present b/c of turbulent blood flow in the obstructed LV outflow tract region.
  2. Augmented w/ maneuvers that DECREASE PRELOAD (Valsalva, squat-to-stand).
  3. Meds that DECREASE AFTERLOAD (amyl nitrite, vasodilators).
  4. Carotid upstroke is rapid (delayed in AS).
  5. Parasternal heave may be present.
34
Q

What is the percentage of pts w/ HCM that eventually develop DCM?

A

5%.

35
Q

What is the type of HF that RCM presents w/?

A

Typically HFpEF.

Depending on the etiology, can lead to reduced EF and HFrEF

36
Q

What is the ventricular morphology in RCM?

A

Ventricular thickness is norma or increased, BUT the ventricular cavity is not enlarged.

37
Q

What is the usual clinical presentation of RCM?

A

Right HF.

38
Q

What is the characteristic echo appearance of RCM due to amyloidosis?

A

Starry-night appearance ==> Refractile ground-glass myocardial appearance.

39
Q

What is the ECG in RCM?

A

Low-voltage ==> a/w arrhythmias.

40
Q

What is the typical presentation of RCM due to sarcoidosis?

A

Typically subclinical — often w/ conduction abnormalities.

41
Q

What is the percentage of pts w/ hemochromatosis have cardiac involvement?

A

15%.

42
Q

What is the prognosis of idiopathic RCM?

A

Slow, progressive decline.

43
Q

What is the prognosis of RCM due to amyloidosis?

A

High mortality in sx HF pts ==> 90% mortality in 6mo.

44
Q

What is the NYHA classification?

A

I ==> sx none to mild.

II ==> sx mild to moderate w/ moderate exertion.

III ==> sx moderate to severe w/ minimal exertion.

IV ==> sx severe at rest.

45
Q

What are the 4 stages of HF?

A

A ==> Risk factors only — no structural disease — no sx.

B ==> Structural heart disease — no sx.

C ==> Structural heart disease — sx (previous or present).

D ==> Structural heart disease — sx refractory, end-stage.

46
Q

What is the method by which the dx of HF is made?

A

Clinical ==> Hx and PEx.

47
Q

What is the most effective method to evaluate HFrEF vs HFpEF?

A

Echo.

48
Q

What is the lab finding that is especially useful in distinguishing between cardiac and pulmonary causes of dyspnea?

A

BNP

49
Q

What is the lab value of BNP in most pts w/ ADHF?

What is the exception to this?

A

> 400pg/mL.

The MORBIDLY OBESE HF pts (normal BNP).

50
Q

What is an important lab test to order in a pt w/ a-fib older than 60y?

A

Thyroid function tests.

51
Q

What is the ADHF tx?

4

A
  1. Reduce preload — preferably w/ loops.
  2. O2 — if hypoxemia is present.
  3. Reduce afterload — if SBP >100mmHg.
  4. Increase inotropy if signs of hypoperfusion (dobutamine, milrinone), but beware of increase in ventricular arrhythmias.
52
Q

What is the goal in chronic HFrEF tx?

A
  1. If asx ==> Delay onset of sx.
  2. If sx ==> Ameliorate sx.
  3. Prevent SCD.
53
Q

What is the first line tx in chronic HFrEF?

A

ACEIs + beta blockers.

54
Q

What is necessary to monitor in each dose change of ACEIs?

A

K + Cr.

55
Q

What is the limit of ACEI’s dose increase?

A

Do not stop increasing the dose unless creatinine increases by more than 30% or hyperkalemia is present.

56
Q

What is the group of pts which is more prone to complications w/ ACEIs?

A

Pts w/

  1. Hyponatremia.
  2. Hypotension.
  3. DM.
57
Q

What are the 2 beta blockers that have shown benefits in pts w/ HFrEF?

A

Carvedilol or bisoprolol.

58
Q

What is an important condition in which beta blockers should NOT be started?

A

ADHF.

59
Q

What is the group of pts in which aldosterone inhibitors have a mortality benefit?

A

Pts w/ NYHA II-IV, normal renal function, and normal K.

60
Q

What is the group of pts in which hydralazine and isosorbide dinitrate is recommended?

A

For African American pts who continue to be symptomatic on ACEI and beta-blocker therapy.

61
Q

What is the effect of digoxin on morbidity?

A

Decrease.

62
Q

What is the effect of digoxin on mortality?

A

None.

63
Q

What is the electrolyte disturbance that exacerbates digoxin toxicity?

A

Hypokalemia.

64
Q

What is the tx for digoxin toxicity?

A
  1. Digoxin immune abs.
  2. Atropine.
  3. K.
  4. Temporary pacing.
65
Q

What is to be avoided in HF pts?

4

A
  1. NSAIDs.
  2. CCBs (only vasoelective agents—eg amlodipine—are safe).
  3. Antiarrhythmics (only amiodarone and dofetilide do not affect mortality).
  4. Alcohol/smoking.
66
Q

What is the target group of CRT or biventricular pacing?

3

A
  1. LVEF is <35%.
  2. ECG shows sinus rhythm w/ an LBBB w/ QRS >150ms.
  3. NYHA III or IV despite maximal therapy.
67
Q

What is the benefit of CRT or biventricular pacing?

A

Decreases morbidity—and, possibly, mortality.

68
Q

What is the benefit of ICD in HF pts?

A

Prevents SCD in pts w/ LVEF <35% + NYHA II/III despite maximal therapy.

69
Q

What are the survival rates a/w heart transplantation?

A

90% 1y survival and 70% 5y survival.

70
Q

What are the major EARLY problems w/ heart transplanation?

A

Infection and rejection.

71
Q

What are the major LATE problems w/ heart transplantation?

A

Transplant-associated coronary artery vasculopathy.

72
Q

What is the medication class which has been shown to decrease morbidity or mortality in chronic HFpEF?

A

There is none.

73
Q

What are the 5 main recommendation in HFpEF tx?

A
  1. Tx HTN aggressively.
  2. Avoid a-fib b/c shortens diastolic filling time, loses atrial kick.
  3. Treat myocardial ischemia.
  4. Use diuretics cautiously.
  5. Avoid digoxin and other inotropes.
74
Q

What is the indication for invasive septal reduction (surgical myomectomy rather than catheter-based alcohol ablation) in HCM?

A

Drug-refractory sx and a gradient >50mmHg at rest or w/ provocation.

75
Q

What are the indications for ICD in HCM pts?

4

A
  1. FHx of SCD or unexplained syncope.
  2. Sustained or nonsustained V-tach (on telemetry monitoring).
  3. Extreme hypertrophy (>30mm).
  4. Abnormal systolic BP response to exercise, or a high-risk genotype.
76
Q

What is the tx option that should be monitored cautiously in RCM pts?

A

Judicious diuretic use.

==> The noncompliant ventricle is PRELOAD-DEPENDENT and will need higher filling pressures.

77
Q

What is that should be avoided in RCM tx?

A

Avoid DIGOXIN and VERAPAMIL — especially in pts w/ amyloid.

**High local cardiac digoxin levels lead to increased arrhythmias, and verapamil leads to an exaggerated decline in inotropy.

78
Q

What is an important dx that should be r/o in RCM pts?

A

Make sure the pt does not have constrictive pericarditis, which is different and surgically correctable.

► Med - Internal Medicine (101 decks)

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