JH IM Board Review - Heart Failure I Flashcards
1
Q
What is the prevalence of HF in the United States?
A
6million
2
Q
What is the incidence of HF in the United States?
A
Up to 550,000 each yr.
3
Q
What is the root of HF?
A
The heart can no longer meet the metabolic demands of the body.
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.
5
Q
What is the common division of HF?
A
- Systolic ==> HF w/ reduced EF = HFrEF.
2. Non systolic HF ==> HFpEF.
6
Q
What is the MC type of HF?
A
Systolic (60%).
7
Q
What is the type of HF that is increasing in prevalence?
A
Non systolic HF.
8
Q
What are the 2 MC of HF?
A
- CAD — MI.
2. HTN.
9
Q
What are the 8 major causes of acute decompensated HF?
A
- Decompensation of preexisting chronic HF from a precipitating factor.
- Hypertensive crisis (eg hypertensive emergency).
- MI.
- Acute tachyarrhythmia.
- Acute endocarditis ==> severe regurgitation.
- Acute DCM.
- Cardiac tamponade.
- High-output HF.
10
Q
What are the 7 main precipitating factors that may lead to decompensation of preexisting chronic HF?
A
- Natural progression.
- Excessive fluid/salt intake.
- Meds nonadherence.
- Infection.
- New MI.
- Metabolic stress (eg anemia, hyperthyroidism).
- Medication use (NSAIDs ==> Na retention).
11
Q
What are the 3 circumstances under which an AMI may lead to ADHF?
A
- Papillary muscle is involved ==> Mitral regurgitation.
- Massive anterior MI.
- RV infarct resulting in a low cardiac output state.
12
Q
What are the 8 main causes of high output HF?
A
- Thyrotoxicosis.
- Beri beri.
- Paget.
- Sepsis.
- Severe anemia.
- AV fistula.
- Persistent tachycardia (eg atrial arrhythmias).
- Liver disease.
13
Q
What are the 3 potential cell targets of a cardiomyopathy?
A
- Myocytes.
- Non myocytes.
- Myocardial interstitium.
14
Q
What is the MC of DCM?
A
CAD.
15
Q
What is the 2nd MCC of DCM?
A
Idiopathic.
16
Q
What is the 3rd MCC of DCM?
A
Inherited/familial.
17
Q
What is the usual presentation of DCM?
A
ADHF.
18
Q
What percentage of DCM improves spontaneously?
A
25-30%.
19
Q
What is the prognosis of a DCM with a NYHA IV?
A
1y mortality is 50%.
20
Q
What are some important predictors of poor prognosis in DCM pts?
(4)
A
- Hyponatremia.
- High cardiac filling pressures.
- Low cardiac index.
- Poor kidney function.
21
Q
What is the difference in the mechanism of systolic and nonsystolic HF?
A
Systolic ==> Impaired ejection.
Non systolic ==> Impaired filling.
22
Q
What are the main physical findings in systolic HF?
A
- S3 and/or S4.
- Weak carotid upstroke.
- Displaced apical impulse.
23
Q
What are the main physical findings in non systolic HF?
3
A
- S4 is more common.
- Normal carotid upstroke.
- Forceful apical impulse.
24
Q
What is the type of cardiomyopathy that Duchenne leads to?
A
DCM
25
What are the 3 types of HCM?
1. Hypertrophy of the LV.
2. Hypertrophy of the RV.
3. Hypertrophy of both.
26
What is the type of HF that HCM leads to?
HFpEF.
| Rarely HFrEF
27
What is the ddx of HCM?
1. Hypertrophy from HTN (Hypertensive HCM).
2. Renal failure.
3. Fabry.
28
What is the age of onset of HCM?
Hypertrophy is almost always present by age 30y and sx by age 40y.
29
What is the screening recommendation for all 1o relatives of HCM pts?
All first degree relatives should be undergo screening w/ echocardiography and electrocardiography (ECG).
30
What are the 2 functional types of HCM?
1. Obstructive.
| 2. Nonobstructive.
31
What are the 2 conditions under which obstructive HCM is worse?
1. Increased contractility.
| 2. Decreased preload.
32
What is the criterion for dx of obstructive HCM?
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
What are the physical exam points in pts w/ obstructive HCM?
| 5
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
What is the percentage of pts w/ HCM that eventually develop DCM?
5%.
35
What is the type of HF that RCM presents w/?
Typically HFpEF.
| Depending on the etiology, can lead to reduced EF and HFrEF
36
What is the ventricular morphology in RCM?
Ventricular thickness is norma or increased, BUT the ventricular cavity is not enlarged.
37
What is the usual clinical presentation of RCM?
Right HF.
38
What is the characteristic echo appearance of RCM due to amyloidosis?
Starry-night appearance ==> Refractile ground-glass myocardial appearance.
39
What is the ECG in RCM?
Low-voltage ==> a/w arrhythmias.
40
What is the typical presentation of RCM due to sarcoidosis?
Typically subclinical — often w/ conduction abnormalities.
41
What is the percentage of pts w/ hemochromatosis have cardiac involvement?
15%.
42
What is the prognosis of idiopathic RCM?
Slow, progressive decline.
43
What is the prognosis of RCM due to amyloidosis?
High mortality in sx HF pts ==> 90% mortality in 6mo.
44
What is the NYHA classification?
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
What are the 4 stages of HF?
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
What is the method by which the dx of HF is made?
Clinical ==> Hx and PEx.
47
What is the most effective method to evaluate HFrEF vs HFpEF?
Echo.
48
What is the lab finding that is especially useful in distinguishing between cardiac and pulmonary causes of dyspnea?
BNP
49
What is the lab value of BNP in most pts w/ ADHF?
What is the exception to this?
>400pg/mL.
The MORBIDLY OBESE HF pts (normal BNP).
50
What is an important lab test to order in a pt w/ a-fib older than 60y?
Thyroid function tests.
51
What is the ADHF tx?
| 4
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
What is the goal in chronic HFrEF tx?
1. If asx ==> Delay onset of sx.
2. If sx ==> Ameliorate sx.
3. Prevent SCD.
53
What is the first line tx in chronic HFrEF?
ACEIs + beta blockers.
54
What is necessary to monitor in each dose change of ACEIs?
K + Cr.
55
What is the limit of ACEI’s dose increase?
Do not stop increasing the dose unless creatinine increases by more than 30% or hyperkalemia is present.
56
What is the group of pts which is more prone to complications w/ ACEIs?
Pts w/
1. Hyponatremia.
2. Hypotension.
3. DM.
57
What are the 2 beta blockers that have shown benefits in pts w/ HFrEF?
Carvedilol or bisoprolol.
58
What is an important condition in which beta blockers should NOT be started?
ADHF.
59
What is the group of pts in which aldosterone inhibitors have a mortality benefit?
Pts w/ NYHA II-IV, normal renal function, and normal K.
60
What is the group of pts in which hydralazine and isosorbide dinitrate is recommended?
For African American pts who continue to be symptomatic on ACEI and beta-blocker therapy.
61
What is the effect of digoxin on morbidity?
Decrease.
62
What is the effect of digoxin on mortality?
None.
63
What is the electrolyte disturbance that exacerbates digoxin toxicity?
Hypokalemia.
64
What is the tx for digoxin toxicity?
1. Digoxin immune abs.
2. Atropine.
3. K.
4. Temporary pacing.
65
What is to be avoided in HF pts?
| 4
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
What is the target group of CRT or biventricular pacing?
| 3
1. LVEF is <35%.
2. ECG shows sinus rhythm w/ an LBBB w/ QRS >150ms.
3. NYHA III or IV despite maximal therapy.
67
What is the benefit of CRT or biventricular pacing?
Decreases morbidity—and, possibly, mortality.
68
What is the benefit of ICD in HF pts?
Prevents SCD in pts w/ LVEF <35% + NYHA II/III despite maximal therapy.
69
What are the survival rates a/w heart transplantation?
90% 1y survival and 70% 5y survival.
70
What are the major EARLY problems w/ heart transplanation?
Infection and rejection.
71
What are the major LATE problems w/ heart transplantation?
Transplant-associated coronary artery vasculopathy.
72
What is the medication class which has been shown to decrease morbidity or mortality in chronic HFpEF?
There is none.
73
What are the 5 main recommendation in HFpEF tx?
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
What is the indication for invasive septal reduction (surgical myomectomy rather than catheter-based alcohol ablation) in HCM?
Drug-refractory sx and a gradient >50mmHg at rest or w/ provocation.
75
What are the indications for ICD in HCM pts?
| 4
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
What is the tx option that should be monitored cautiously in RCM pts?
Judicious diuretic use.
==> The noncompliant ventricle is PRELOAD-DEPENDENT and will need higher filling pressures.
77
What is that should be avoided in RCM tx?
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
What is an important dx that should be r/o in RCM pts?
Make sure the pt does not have constrictive pericarditis, which is different and surgically correctable.
