HF Flashcards
(500 cards)
1
Q
Is heart failure diagnosed primarily by echocardiography?
A
No. Heart failure is diagnosed clinically.
2
Q
What findings confirm the diagnosis of HF clinically?
A
A: A combination of congestive and low-output findings, supported by elevated BNP, echo evidence, or elevated LA pressure.
3
Q
What two symptoms are relatively specific for HF and result from increased venous return during recumbency?
A
A: Orthopnea and paroxysmal nocturnal dyspnea (PND).
4
Q
What does a nocturnal dry cough during recumbency suggest?
A
A: It may be an orthopnea equivalent, suggestive of HF.
5
Q
What causes wheezing in HF patients?
A
A: Bronchial mucosal congestion.
6
Q
What bedside test can reveal orthopnea?
A
A: Ask the patient to lie supine for 1–2 minutes.
7
Q
How does PND in COPD differ from that in HF?
A
A: COPD-related PND improves with cough and albuterol; HF-related improves with sitting upright.
8
Q
What is bendopnea and what does it indicate?
A
A: Dyspnea within 15 sec of bending forward; suggests elevated PCWP or RA pressure.
9
Q
What does quick weight gain or rapid loss in response to therapy suggest?
A
A: Volume overload or response to treatment.
10
Q
Are crackles a reliable sign of pulmonary edema in chronic HF?
A
A: No, they are absent in ~80% due to enhanced lymphatic drainage.
11
Q
What JVP level suggests congestion?
A
A: ≥8 cm H₂O.
12
Q
What is a positive hepatojugular reflux test?
A
A: Sustained JVP rise ≥3 cm H₂O with RUQ pressure >10 sec.
13
Q
What is JVD and what does it imply?
A
A: Visible external jugular distension while upright; implies elevated JVP.
14
Q
What is the specificity of S3 in patients >40 years old?
A
A: ~90% for elevated PCWP.
15
Q
What does a loud P2 suggest?
A
A: Significant pulmonary hypertension, often from left HF.
16
Q
Is peripheral edema a sensitive sign of HF?
A
A: No, it may be absent in up to 60% of patients with elevated PCWP.
17
Q
What is required to visibly see peripheral edema?
A
A: Over 4 liters of fluid overload.
18
Q
What scoring system may suggest HFpEF?
A
A: H2FPEF score.
19
Q
What is the gold standard for diagnosing HFpEF?
A
A: Elevated mean PCWP at rest (>15 mmHg) or with exercise (≥25 mmHg) via RHC.
20
Q
What four criteria are required to diagnose HFpEF per ESC?
A
Clinical HF
Normal EF and LV size
No dynamic MR or ischemic systolic dysfunction
Objective evidence of elevated LA pressure or diastolic dysfunction
21
Q
What is HFmEF?
A
A: HF with EF 40–50%, mostly diastolic dysfunction, but with some systolic involvement
22
Q
What defines HFpEF?
A
A: EF ≥50%, normal/mildly increased LV volume, clinical HF, and elevated LA pressure or diastolic dysfunction.
23
Q
What EF defines systolic HF (HFrEF)?
A
A: EF ≤ 40%.
24
Q
What is NYHA Class IV?
A
A: Symptoms at rest.
25
What is NYHA Class IIIB?
A: Symptoms with light activities (e.g., dressing).
26
What is NYHA Class IIIA?
A: Symptoms walking one block
27
What is NYHA Class II?
A: Symptoms with heavy lifting or walking two blocks/stairs.
28
What activity corresponds to NYHA Class I?
A: No limitation; can jog or carry >24 lb upstairs.
29
What respiratory pattern occurs in late-stage HF?
A: Cheyne–Stokes breathing.
30
What labs indicate advanced HF?
A: Renal failure, hyponatremia, poor diuretic response.
31
What are cold, clammy extremities a sign of?
A: Poor perfusion from low cardiac output.
32
What does pulsus alternans indicate?
A: Advanced HF with low stroke volume
33
What physical sign best predicts low cardiac output?
A: Narrow pulse pressure (<25% SBP)
34
What is the most sensitive and specific sign of elevated filling pressures?
A: Elevated JVP or positive hepatojugular reflux.
35
Name four highly reliable congestive findings in HF diagnosis.
A: Orthopnea, elevated JVP, S3, recent quick weight gain
36
How many B-lines per view suggest edema?
A: ≥3 lines bilaterally.
37
What CT finding is specific for elevated PCWP?
A: Interlobular septal thickening.
38
What EF value is typically associated with combined systolic and diastolic dysfunction?
A: EF < 40% is usually associated with variable impairment of both systolic and diastolic function.
39
What characterizes high-output heart failure?
A: Elevated left and/or right filling pressures with a cardiac index at the upper limit of normal or elevated (>3.5-4 l/min/m²), often with normal or mildly reduced EF.
40
How is isolated right heart failure clinically distinguished?
A: Peripheral edema and elevated JVP with clear lungs; invasive hemodynamics show elevated RA pressure with normal or mildly increased PCWP.
41
What is the second most common cause of systolic HF?
A: Hypertension (chronic severe hypertension causing initial diastolic dysfunction, then systolic dysfunction).
42
Which cardiomyopathies have the worst prognosis?
A: HIV cardiomyopathy, amyloidosis, and doxorubicin-associated cardiomyopathy.
43
What are catheterization criteria for HFpEF?
A: LVEDP > 16 mmHg or PCWP > 15 mmHg.
44
What BNP levels suggest HFpEF?
A: BNP > 100 pg/ml or NT-proBNP > 300-400 pg/ml (higher cutoffs if atrial fibrillation is present).
45
What echo criteria support a diagnosis of HFpEF?
A: E/E’ > 14, LA volume index > 34 ml/m², TR velocity > 2.8 m/s, septal E’ <7 cm/s or lateral E’ <10 cm/s, severe LV hypertrophy.
46
What is the H2FPEF score and what does it predict?
A: A scoring system predicting HFpEF probability based on Heavy (BMI>30), Hypertensive (≥2 drugs), Atrial Fibrillation, Pulmonary Hypertension, Elderly (>60), and Filling pressure (E/E’>9). Score ≥6 strongly predicts HFpEF.
47
Which cardiomyopathies are potentially reversible?
A: Myocarditis, alcoholic cardiomyopathy (early stage), hypertensive cardiomyopathy, peripartum cardiomyopathy, tachycardia-mediated, Takotsubo, stress-related cardiomyopathies, thyroid-related cardiomyopathy
48
What LA volume index suggests diastolic dysfunction?
A: LA volume index >34 ml/m².
49
What BNP level essentially rules out HFpEF in euvolemic dyspnea?
A: BNP <35 pg/ml or NT-proBNP <125 pg/ml.
50
What echo marker E’ values indicate diastolic dysfunction?
A: Septal E’ <7 cm/s or lateral E’ <10 cm/s.
51
How is exertional HFpEF confirmed invasively?
A: Exertional PCWP ≥25 mmHg during supine cycling.
52
What are components of the H2FPEF score?
A: Heavy (BMI>30), Hypertensive (≥2 drugs), Atrial fibrillation, Pulmonary hypertension (PA systolic >35 mmHg), Elderly (>60), Filling pressure (E/E’>9)
53
What are normal LV volumes defining normal or mildly dilated LV?
A: End-diastolic volume <75 ml/m² (normal), <96 ml/m² (mildly dilated).
54
What did the TRED-HF trial show?
A: Withdrawal of therapy in recovered HF led to 44% recurrence at 6 months.
55
What percentage of recent-onset idiopathic or myocarditis-related DCM resolves spontaneously or with treatment?
A: Approximately 35%.
56
What defines HF-recovereredEf?
A: EF improvement of ≥10% to >40%.
57
Name three advanced valvular diseases that can cause heart failure?
A: Mitral regurgitation (MR), aortic insufficiency (AI), aortic stenosis (AS).
58
What is the second most common cause of systolic heart failure?
A: Hypertension (after CAD).
59
Can hibernating myocardium recover?
A: Yes, it can recover after revascularization.
60
What conditions can cause truly isolated right heart failure?
A: Atrial septal defect (ASD), lung disease, pulmonary vascular disease.
61
What are two additional types of heart failure beyond systolic and diastolic?
A: High-output heart failure and isolated/predominant right heart failure.
62
What happens to ventricular function in severe left valvular disease?
A: Initially normal but eventually leads to LV systolic and diastolic dysfunction (except in mitral stenosis).
63
What are the two most common risk factors for HFpEF?
A1: Hypertension and obesity.
64
Can LV hypertrophy be absent in HFpEF?
A2: Yes. LV mass is normal in up to 50%, and wall thickness is normal in up to 25%.
65
What structural changes lead to stiffness in HFpEF?
A3: Increased collagen, cytoskeletal proteins, and abnormal calcium homeostasis
66
Why does SBP rise disproportionately with exercise in HFpEF?
A4: Due to arterial stiffness
67
What demographic and comorbid conditions are commonly associated with HFpEF?
A5: Age >65, diabetes, female sex, renal failure, and atrial fibrillation (AF).
68
How does AF contribute to HFpEF?
A8: It reduces LV filling directly and may lead to elevated LA pressure even without AF.
69
What is chronotropic incompetence and its relevance to HFpEF?
A11: Inability to increase heart rate during exercise; affects ~50% of HFpEF patients
70
What vascular issue is prominent in middle-aged women with HFpEF?
Microvascular dysfunction.
71
How does CAD contribute to HFpEF?
By impairing active relaxation and causing increased LVEDP during ischemia.
72
What ECG–echo discrepancy is common in amyloid cardiomyopathy?
Thick myocardium on echo with low voltage or pseudo-Q waves on ECG.
73
What echo features are characteristic of cardiac amyloidosis?
Small pericardial effusion, valvular thickening, and "sparkling" myocardium.
74
What are common causes of RCM?
Amyloidosis, Fabry disease, hemochromatosis, sarcoidosis, HES, radiation heart disease.
75
What does constrictive pericarditis mimic?
Restrictive cardiomyopathy and chronic right HF.
76
What mimics acute vs. chronic RHF?
Tamponade mimics acute; constrictive pericarditis/RCM mimic chronic RHF
77
Is heart rate reduction helpful in HFpEF?
Not clearly; may worsen exercise capacity in HFpEF patients.
78
What HR is acceptable in AF with HFpEF?
80–100 bpm.
79
What are the three major heart failure categories evaluated by echocardiography?
A: EF assessment, valvular function, diastolic dysfunction (E’), and LA pressure (E/E’).
80
What does a high E wave with a narrow profile in decompensated HF indicate?
A: High LA pressure with quick LA-LV pressure equalization
81
In decompensated HF, does slowing heart rate improve LV filling?
A: No, it does not; faster HR improves filling via more cardiac cycles per minute
82
What HR range may optimize cardiac output acutely in HF?
A: Up to ~110 bpm; beyond that, contractility declines due to depleted energy reserves.
83
What is the recommended HR range in compensated HFrEF?
A: 60–70 bpm.
84
What HR may be acceptable in HFpEF or AF?
A: 80–100 bpm.
85
What effect did ivabradine have in HFpEF vs. HFrEF?
A: Improved exercise capacity in HFrEF; worsened it in HFpEF.
86
What does a new tachyarrhythmia >105–110 bpm with new HF suggest?
A: Tachycardia-mediated cardiomyopathy.
87
What findings suggest HFpEF on echo?
A: Low E’, high E/E’ (>14), LA enlargement, thickened septum.
88
What is the physiological stimulus for BNP release?
A: Cardiomyocyte stretch from volume or pressure overload.
89
What is the relationship between NT-proBNP and BNP values?
A: NT-proBNP ≈ 4x BNP (may be >6x in elderly or renal failure).
90
What BNP level strongly suggests acute left HF?
A: BNP > 400–500 pg/mL or NT-proBNP > 1200 pg/mL.
91
What BNP level excludes acute HF?
A: BNP < 100 pg/mL or NT-proBNP < 300 pg/mL.
92
What is the BNP cutoff to rule out chronic HF per ESC?
A: BNP < 35 pg/mL or NT-proBNP < 125 pg/mL.
93
What factors increase BNP independent of HF?
A: Age, female sex, renal failure, atrial fibrillation, cirrhosis.
94
What condition can have normal BNP despite clinical HF signs?
A: Constrictive pericarditis.
95
What reduces BNP values?
A: Obesity (use lower cutoff: BNP < 50 pg/mL in BMI >35).
96
What BNP reduction during hospitalization predicts good outcomes?
A: A 30–50% reduction.
97
What does high QRS voltage in precordial leads combined with low voltage in limb leads suggest?
A5: Dilated LV with low ejection fraction (EF).
98
Why is nuclear perfusion scanning not very specific for ischemic cardiomyopathy?
A9: Because non-ischemic cardiomyopathy may show patchy defects, and multivessel CAD may present with balanced ischemia.
99
What does a biphasic response on stress echocardiography suggest?
A10: Viable myocardium that becomes ischemic at high stress.
100
What does a uniphasic response on stress echo indicate?
A11: Non-ischemic CM or stunned myocardium post-revascularization.
101
What are the key measurements in diastolic stress testing?
A16: E/E’ ratio >14 and TR velocity >3.4 m/s at peak exercise.
102
When is biopsy used to diagnose infiltrative cardiomyopathy?
Suspected cardiac AL amyloidosis with inconclusive abdominal fat pad biopsy
Suspected cardiac sarcoidosis without typical lung findings
103
Why is biopsy indicated in suspected drug-induced myocarditis?
A13: To confirm eosinophilic myocarditis and justify steroid therapy if HF does not improve after drug withdrawal
104
What are the biopsy indications in new or acute heart failure?
Acute HF <2 weeks with hemodynamic compromise
New HF <3 months with:
• poor response to therapy after 1–2 weeks
• intractable ventricular arrhythmias
• advanced AV block
105
What are the treatment implications for giant-cell myocarditis?
A11: Often requires cardiac transplant, immunosuppression, and possibly LVAD support
106
What is the clinical course of fulminant lymphocytic myocarditis?
Often reversible with aggressive support and may recover in a few weeks
107
When is endomyocardial biopsy indicated in myocarditis?
When severe, progressive myocarditis is suspected—especially if fulminant lymphocytic, eosinophilic, or giant-cell myocarditis is possible
108
What LGE pattern suggests Fabry disease?
Patchy inferolateral LGE.
109
What LGE pattern suggests hypertrophic cardiomyopathy (HCM)?
Patchy midwall LGE
110
What LGE pattern suggests cardiac amyloidosis?
Global subendocardial LGE.
111
What LGE pattern is typical of non-ischemic cardiomyopathy?
Subepicardial or midwall LGE in a non-coronary distribution
112
What type of LGE pattern suggests ischemic cardiomyopathy?
Subendocardial or transmural LGE.
113
What does late gadolinium enhancement (LGE) on T1-weighted MRI usually indicate?
Necrotic or fibrotic myocardial tissue.
114
How should therapy be tailored in HFpEF?
Balance afterload reduction (to improve relaxation) and preload reduction (to reduce congestion); therapeutic window is narrower than in HFrEF
115
What is the role of SGLT2 inhibitors in HFpEF?
Only drug class to show clear reduction in HF hospitalizations and quality of life improvement in trials.
116
Is there any therapy proven to improve survival in HFpEF?
No drug improves survival in HFpEF per se; management focuses on comorbidities and HFpEF features.
117
Did spironolactone improve symptoms or exercise capacity in AldoHF trial?
No, but it improved diastolic function parameters and NT-pro-BNP
118
What was the outcome of the TOPCAT trial regarding spironolactone?
Reduced CV mortality by 26% and HF hospitalizations by 20% in American patients with BNP elevation or prior HF hospitalization.
119
What is the risk of worsening renal function after ACE-I/ARB in HFpEF?
Associated with worsened cardiovascular outcomes and mortality.
120
What did ivabradine trials in HFpEF show?
Harmful effects: worsened exercise capacity and worsened E velocity and LA size.
121
Which β-blocker may benefit elderly HFpEF patients?
Nebivolol – shown to reduce cardiovascular hospitalizations in all types of HF in the elderly.
122
Do β-blockers benefit HFpEF patients?
Not routinely; may worsen symptoms in patients with chronotropic incompetence or preload-dependence.
123
Should acute heart rate reduction be aggressively pursued in decompensated HFpEf?
No, HR up to 110–120 bpm is acceptable; slowing HR may not help due to non-improvable diastolic filling.
124
What were the findings of the NEAT-HFpEF trial regarding nitrates?
Long-acting nitrates worsened activity level and did not improve exercise capacity.
125
Why should diuretic dosing be cautious in chronic HFpEF?
Due to steep pressure–volume curve; over-diuresis reduces preload and cardiac output.
126
What is the mainstay for decongestion in HFpEF?
Diuretics; nitrates are not effective and may worsen symptoms.
127
Why is BP of 110 mmHg or lower not well tolerated in HFpEF?
Because HFpEF is preload-dependent; low BP may reduce cardiac output.
128
What is the recommended BP target in HFpEF according to ACC and ESC?
<130/80 mmHg (ACC) and <140/80 mmHg (ESC).
129
Why don’t amlodipine or α-blockers improve HF outcomes despite afterload reduction?
Because they do not block the harmful RAAS or sympathetic system effects.
130
What is the special benefit of hydralazine–nitrate therapy?
It reduces mortality and symptoms particularly in black patients with HF.
131
How do ACE-I and ARBs improve outcomes in HF?
By reducing afterload and blocking harmful RAAS effects on myocardium and volume status.
132
Why is EF considered more a remodeling index than pure contractility?
Because EF is affected by preload and afterload, not just myocardial contractility.
133
What role does LV end-systolic volume (LVESV) play in HF?
A: It is the best measurement of LV remodeling.
134
What are the three harmful compensatory mechanisms inHF?
LV remodeling and dilation
Increased sympathetic activity
Activation of the renin–angiotensin–aldosterone system (RAAS)
135
When might revascularization NOT be beneficial in ischemic LV dysfunction?
In recent STEMI or Q-wave infarcts 1–28 days old without angina or symptoms (OAT trial findings).
136
What did the STICH ischemia sub-study conclude about ischemia testing?
A: Ischemia did not predict prognosis or response to CABG in LV dysfunction.
137
How does ischemia impact prognosis and treatment in LV dysfunction?
Ischemia is a stronger predictor of prognosis and myocardial recovery than viability alone.
138
What is the difference between ischemia and viability?
Viability is metabolic activity of dysfunctional myocardium at rest; ischemia is worsened perfusion or function under stress.
139
Does revascularization improve outcomes even without viability or EF improvement?
A: Yes, it improves symptoms, HF progression, and mortality by preventing further remodeling and arrhythmias.
140
What are some limitations of viability testing?
A: Moderate sensitivity and specificity (~75-80%), non-uniform definitions, and inability to perfectly predict mortality benefit.
141
How is global viability defined in the STICH trial?
Viability in ≥65% of myocardial segments (11 out of 17 segments)
142
Can Q waves on ECG rule out myocardial viability?
A: No, Q waves may be present even in viable, hibernating myocardium.
143
How does cardiac MRI indicate non-viability?
Late gadolinium enhancement involving >50% transmural thickness indicates scar and non-viability.
144
What does a biphasic response in low-dose dobutamine echo indicate?
It indicates ischemia and myocardial contractile reserve, predictive of viability.
145
What imaging modalities assess myocardial viability?
A:
Thallium/technetium nuclear imaging
Low-dose dobutamine echocardiography
PET scan
Cardiac MRI with late gadolinium enhancement
-Thallium/technetium nuclear imaging
-Low-dose dobutamine echocardiography
-PET scan
-Cardiac MRI with late gadolinium enhancement
146
What is "global viability"?
A significant improvement (>5%) in overall EF after revascularization.
147
Does viability testing affect the decision to perform CABG in ischemic cardiomyopathy?
A: No, CABG showed benefit regardless of viability testing results in the STICH trial.
148
How urgent is CABG for ischemic cardiomyopathy based on the STICH trial?
A: Not urgent; the benefit appears after 2 years and is given a class IIb indication for HF.
149
What did the STICH trial show about CABG in ischemic cardiomyopathy?
CABG was associated with a mortality reduction trend at 5 years and significant benefit at 10 years, mainly in patients with EF ≤35%, especially with 3-vessel CAD.
150
Should HF drugs be withheld due to low blood pressure in systolic HF?
No, HF drugs should be given regardless of blood pressure, as long as SBP is ≥90–100 mmHg and clinically tolerated.
151
What is the blood pressure (BP) goal for hypertension treatment in systolic heart failure (HF)?
A: BP should be treated to a goal of <130/80 mmHg.
152
What is the goal regarding β-blocker dosing in HF?
A: Reach high target doses proven beneficial (e.g., carvedilol 25 mg BID).
153
How do hydralazine–nitrate and other HF drugs affect BP in hypotensive HF patients vs. hypertensive patients?
A: They reduce BP in hypertensive patients, but may increase BP in hypotensive HF patients after a few days.
154
What did the COPERNICUS trial find about β-blocker use in patients with SBP <95 mmHg?
These patients had similar or greater benefit without significant SBP drop; SBP often increased over time.
155
Does a low SBP (<100 mmHg) reduce the benefit of β-blockers or vasodilators in HF?
No, even patients with low SBP derive similar or greater benefit.
156
Can patients with SBP of 85–90 mmHg tolerate hydralazine–nitrate?
Yes, unless symptomatic with low perfusion.
157
What common side effect does hydralazine cause in 5–10% of patients?
A: Drug-induced lupus (rash and arthralgia).
158
What is BiDil and how is it dosed?
BiDil combines 37.5 mg hydralazine and 20 mg ISDN; start at ½ pill TID, titrate to 2 pills TID.
159
What are the starting and target doses for isosorbide dinitrate in HF?
Start at 20 mg TID, titrate up to 40 mg TID
160
What are the starting and target doses for hydralazine in HF?
Start at 12.5 mg TID, increase to 25 mg TID in 2–4 days, then titrate weekly to 50–75 mg TID.
161
Why might black patients benefit more from hydralazine–nitrate?
Many have a genetic variant of NO synthase that reduces NO availability
162
What is the mechanism behind the benefit of hydralazine–nitrate therapy?
Nitrates provide nitric oxide (NO), and hydralazine prevents its oxidation, preserving vasodilation and myocardial remodeling.
163
When can hydralazine–nitrate be used instead of ACE-I/ARB?
In cases of intolerance due to renal failure or hyperkalemia (Class IIa recommendation regardless of race).
164
When is hydralazine–nitrate considered for non-black patients?
In cases of persistent symptoms or uncontrolled HTN (>140/90 mmHg).
165
What is the guideline recommendation for using hydralazine–nitrate in black patients with HF?
A: Class I recommendation for class III–IV black patients already on ACE-I/ARB and β-blocker.
166
What were the outcomes of the A-HeFT trial in class III–IV black HF patients already on ACE-I and β-blockers?
Hydralazine–nitrate further reduced mortality by 43% and HF hospitalizations by 40%
167
How did white patients respond to hydralazine–nitrate in V-HeFT-II?
It improved exercise tolerance and EF more than enalapril, but enalapril had lower mortality.
168
How did hydralazine–nitrate compare to ACE inhibitors in the V-HeFT-II trial among black patients?
It reduced mortality as much as ACE-I and was superior in improving exercise tolerance and EF.
169
In which patient group did the V-HeFT-I trial show the most benefit from hydralazine–nitrate?
Black patients
170
What should you do if β-blockers worsen HF symptoms during titration?
A: Increase diuretic dose; if not effective, reduce β-blocker and titrate more slowly.
171
What's the preferred therapy initiation order?
Start ACE-I → Start β-blocker → Add spironolactone → Add SGLT2 inhibitor.
172
Is it necessary to reach full ACE-I dose before starting β-blockers?
No. Start both at low doses and uptitrate in alternating fashion.
173
What to do if gynecomastia develops with spironolactone?
Switch to eplerenone.
174
How do you manage hyperkalemia from aldosterone antagonists?
K 5.5–5.9: Hold, then resume at half dose
K ≥6.0: Discontinue
K <5.5: Continue current dose
175
What are key monitoring parameters for aldosterone antagonists?
Check K and creatinine at day 3, 1 week, then Q2–4 weeks for 3 months
176
What's the initial dose of spironolactone in HFrEF?
A: 12.5–25 mg QD; may titrate cautiously up to 50 mg.
177
What are contraindications to aldosterone antagonists?
A: Creatinine >2.0 mg/dL, GFR <30 mL/min, or K >5.0 mEq/L
178
Which patients benefit from aldosterone antagonists?
NYHA class II–IV with EF ≤35%
Post-MI with EF <40% + HF or diabetes
Class II with high BNP or recent HF hospitalization
179
Can β-blockers benefit patients with EF 40–50% or AF?
A: Yes, evidence supports benefit even in EF 40–50% and in patients with AF
180
Can β-blockers benefit patients with EF 40–50% or AF?
A: Yes, evidence supports benefit even in EF 40–50% and in patients with AF
181
What is the initial dose and goal for carvedilol?
Start 3.125 mg BID → Goal 25 mg BID (<85 kg) or 50 mg BID (>85 kg)
182
What are the contraindications to β-blocker initiation?
SBP <90 mmHg, symptomatic hypotension, bradycardia <55 bpm, heart block, bronchospasm
183
Should β-blockers be stopped during HF hospitalization?
No, unless the patient is in shock or requires inotropes. Otherwise, reduce dose or continue.
184
What is the preferred initiation strategy for β-blockers in HFrEF?
Start low and slow in stable, euvolemic patients. Titrate every 2 weeks.
185
Give examples of ACE-I and ARB dosing in HFrEF?
Lisinopril: Start 5 mg QD → Goal 20–40 mg QD
Enalapril: Start 2.5 mg BID → Goal 10 mg BID
Candesartan: Start 4 mg QD → Goal 32 mg QD
Valsartan: Start 40 mg BID → Goal 160 mg BID
186
What's the usual titration schedule for ACE-Is?
Titrate every 5 days to ~½ maximal trial doses.
187
Can ACE-I/ARB be used in patients with renal failure?
Yes, with caution. Patients with moderate renal impairment can still benefit, but avoid if GFR < 30 mL/min.
188
What potassium level is a contraindication to starting ACE-I/ARB?
A: K > 5.0 mEq/L at baseline or >5.5 mEq/L during therapy.
189
How should you manage ACE-I/ARB in patients with elevated creatinine after initiation?
If creatinine rises <50%, continue therapy; if ≥50% or ≥0.5 mg/dL, hold ACE-I, correct contributing factors, and restart at a lower dose.
190
What is the alternative to ACE-Is if a patient develops cough or angioedema?
A: Use an ARB, but with caution due to a small cross-risk (<5%) of angioedema.
191
What is a renal contraindication for SGLT-2 inhibitors?
A: GFR < 30 ml/min.
192
What is the mechanism of benefit in HF for SGLT-2 inhibitors?
Osmotic diuresis, natriuresis, improved cardiac metabolism (↑ ketones), and renal protection.
193
What is a key contraindication to ivabradine?
A: Atrial fibrillation—ineffective in absence of sinus rhythm.
194
In which patients is ivabradine indicated?
A: Class II–IV HFrEF (EF ≤ 35%) with sinus rhythm and resting HR ≥70 bpm despite max β-blocker.
195
What is ivabradine's mechanism of action?
A: Pure sinus node inhibitor—reduces HR without affecting contractility or blood pressure.
196
What are classic signs of digoxin toxicity?
A: Brady- or tachyarrhythmias (e.g., bidirectional VT), nausea, visual halos, neurologic symptoms.
197
What is the goal serum level for digoxin in HF?
A: Trough level ≤ 0.8 ng/ml; ideally 0.5–0.8 ng/ml. Levels >1.1 ng/ml are associated with increased mortality.
198
What is the recommended maintenance dose of digoxin?
Usually 0.125 mg/day; 0.25 mg/day may be used in young, large males with normal kidneys.
199
What supplements should be considered with loop diuretics?
Oral potassium (20–40 mEq/day) and possibly magnesium if K remains low.
200
What should a patient do if weight increases >3 lb in <5 days?
Take extra diuretic doses until weight returns to baseline; if ineffective in 1–2 days, seek medical evaluation and consider adding metolazone.
201
What is the best strategy if 40 mg furosemide QD is effective but not enough?
A: Switch to 40 mg BID rather than increasing to 80 mg QD.
202
Why split the total daily dose of furosemide in severe HF?
To avoid sodium retention between doses and provide sustained natriuresis.
203
Why is torsemide potentially superior to furosemide?.
A: Longer duration (~12 hrs), better absorption, hepatic metabolism, and evidence of reduced HF hospitalizations.
204
What is the equivalent dosing: bumetanide vs. furosemide?
A: 1 mg bumetanide = 40 mg furosemide (20 mg in renal failure).
A: 1 mg bumetanide = 40 mg furosemide (20 mg in renal failure).
205
How does oral bioavailability compare among furosemide, bumetanide, and torsemide?
Furosemide has variable absorption (~50%); bumetanide and torsemide are more consistently absorbed (80–100%).
206
Which thiazide-like diuretic remains effective in advanced CKD?
Metolazone – acts on both proximal and distal tubules and accumulates with a prolonged effect
207
Why are thiazides less effective in GFR < 30 ml/min?
Less sodium is filtered and remaining nephrons are already maximizing sodium excretion, but combining with loop diuretics can restore efficacy.
208
What limits the effectiveness of diuretics in hypoalbuminemia or nephrotic syndrome?
Low albumin reduces drug delivery to the nephron and binds diuretics in the urine, limiting their action.
209
Why might higher doses of diuretics be needed in renal failure?
Reduced renal perfusion decreases diuretic delivery and sodium filtration, necessitating higher doses for the same effect.
210
Why are loop diuretics preferred over thiazides in heart failure (HF)?
Loop diuretics are more potent and act on a part of the nephron responsible for a larger portion of sodium reabsorption (~25%) vs. thiazides (~3–5%), making them more effective in volume overload.
211
What is the primary site of action of loop diuretics, and how much sodium reabsorption do they block?
Loop diuretics act on the ascending loop of Henle and block the Na-K-2Cl transporter, preventing ~25% of sodium reabsorption.
212
When is echo dyssynchrony evaluation useful for CRT selection?
For QRS 130–150 ms or RBBB; not useful for QRS <130 ms
213
Class IIa CRT indications?
LBBB with QRS 130–150 ms, or RBBB with QRS >150 ms.
214
CRT indications?
: EF ≤35% + QRS ≥150 ms (LBBB or RV-paced) + class II–ambulatory IV, on optimal meds
215
How is DigiFab dose calculated in chronic digoxin toxicity?
Vials = (digoxin level × weight) / 100.
216
What lab abnormality should be monitored post-DigiFab?
Hypokalemia.
217
When should you wait before ICD post-MI or revascularization?
>40 days post-MI; >3 months post-revascularization.
218
Define iron deficiency in HF.
Ferritin <100 ng/mL, or 100–300 with TSAT <20%.
219
How is central sleep apnea in HF treated?
Nocturnal O₂; avoid non-invasive ventilation (↑ mortality in SERVE-HF trial).
220
What dose of omega-3 reduces mortality in HF?
1 g/day (850 mg omega-3 acids); 9% RR reduction (GISSI-HF).
221
What are the recommended salt and fluid restrictions in advanced/decompensated HF?
Salt <2–3 g/day; fluid 1.5–2 L/day.
222
What lab abnormalities are associated with poor prognosis in HF?
A: Hyponatremia <133 mmol/L, anemia (Hb <12 g/dL), low BP <100 mmHg.
223
What lab abnormalities are associated with poor prognosis in HF?
A: Hyponatremia <133 mmol/L, anemia (Hb <12 g/dL), low BP <100 mmHg.
224
Why is the right ventricle (RV) more sensitive to afterload increases than the left ventricle (LV)?
A: The RV has a thinner wall than the LV, so according to Laplace's law (wall stress = pressure × radius / [2 × wall thickness]), it poorly tolerates increases in pulmonary artery (PA) pressure and quickly fails in acute pressure overload.
225
How does chronic pulmonary hypertension affect the RV wall?
A: It stimulates thickening of the RV wall, which helps reduce wall tension, unlike the acute setting where the RV is intolerant to afterload increases.
226
What happens to RV wall stress and tricuspid regurgitation (TR) as the RV dilates severely?
A: Progressive RV dilatation increases wall stress on the thin walls, leading to a vicious cycle of further dilatation and worsening TR.
227
How does the pericardium affect RV dilatation?
A: The pericardium helps contain the RV; removing it (e.g., pericardiotomy or cardiac surgery) may lead to massive RV dilatation.
228
How does LV failure contribute to RV failure?
A: LV failure leads to RV failure via pulmonary hypertension and loss of septal contribution to RV function; 20–40% of RV systolic pressure and output comes from LV contraction.
229
How can acute RV failure lead to LV failure?
A: RV dilatation causes pericardial stretching and functional constriction, compressing the LV in diastole, reducing LV distensibility, preload, and contractility via paradoxical septal motion.
230
What is the consequence of high right atrial (RA) pressure in severe RV failure patients with patent foramen ovale (PFO)?
A: It may cause large right-to-left shunting, leading to refractory hypoxemia.
231
What does a high systolic PA pressure indicate in severe pulmonary hypertension with RV failure?
A: It predicts better RV function recovery and outcomes than patients with lower systolic PA pressure.
232
: How is RV-PA coupling assessed on echocardiography?
A: By the ratio of RV TAPSE to systolic PA pressure; normal is >0.31 mm/mmHg.
233
What is the recommended preload management in acute RV failure?
A: Aggressive diuresis (2-3 L negative balance/day) in acute-on-chronic cases; gentler diuresis (0.5-1 L/day) in chronic cases.
234
When is volume loading recommended in acute RV failure?
A: If RV is non-dilated and central venous pressure (CVP) is <10-14 mmHg, a 500–1000 ml saline load can be given; avoid volume if RV is dilated or CVP >14 mmHg.
235
What treatments help reduce RV afterload (pulmonary vascular resistance, PVR)?
A: Treatment of hypoxemia, inhaled nitric oxide (NO), inhaled milrinone, or inhaled epoprostenol reduce PVR and RV distension.
236
Why is norepinephrine often preferred in RV failure?
A: It increases RV contractility and systemic vascular resistance (SVR) without significantly increasing PVR at low/medium doses, improving the SVR/PVR ratio.
237
Why systemic vasodilators poorly tolerated in RV failure?
A: They reduce SVR but the underfilled LV cannot increase output to match the vasodilated circulation, worsening hemodynamics.
238
How should sinus rhythm and AV synchrony be managed in RV failure?
A: Maintain sinus rhythm and AV synchrony; prompt DC cardioversion is advised in AF with acute RV shock due to the dependence on atrial contraction for RV and LV filling.
239
What is the effect of mechanical ventilation on RV failure?
A: It reduces hypoxemia (improving PVR and RV output) but positive pressure ventilation increases RV afterload (PA pressure), so low tidal volumes and limited plateau pressure are recommended.
240
How does right-to-left shunting through a PFO affect patients with severe RV failure?
A: It unloads the RV, reduces RA pressure, and increases LV filling and cardiac output, despite causing some hypoxemia; some shunting improves overall oxygen delivery and symptoms.
241
When can right-to-left shunting become harmful in RV failure?
A: Excessive shunting with very high RA pressure (>20 mmHg) and poor RV function can drastically reduce pulmonary blood flow and cause profound hypoxemia
242
How does the RV coronary flow differ from LV coronary flow and why is this important?
A: RV coronary flow is at least 50% systolic and depends on the gradient between systemic systolic blood pressure (SBP) and systolic RV pressure; low SBP reduces this gradient, causing RV ischemia and failure
243
What is the clinical significance of the SBP/systolic PA pressure or SVR/PVR ratio in RV failure?
A: It reflects how well systemic pressure supports RV coronary perfusion and function; a low ratio indicates poor RV perfusion and higher risk of failure.
244
What is Type 1 acute cardiorenal syndrome?
it refers to worsening renal function and volume overload in a patient with acute heart failure (HF).
245
What causes reduced diuretic response in acute cardiorenal syndrome?
Reduced renal perfusion, even with preserved cardiac output at the central level.
246
What is the main driver of renal blood flow in HF patients?
✅ The gradient between mean arterial pressure and renal venous pressure.
247
What is the most important hemodynamic factor predicting renal deterioration in acute HF?
✅ Right atrial (RA) pressure (admission and post-therapy values).
248
How does systemic blood pressure reduction during therapy affect renal function?
✅ A drop >15% or >10–15 mmHg from baseline SBP (~115 mmHg) strongly correlates with renal deterioration.
249
Why is renal autoregulation impaired in HF and CKD?
✅ Due to pre-existing maximal afferent arteriolar dilation and vasoconstrictor activation (e.g., angiotensin II, sympathetic activity).
250
What is plasma refill time?
✅ The time required for interstitial fluid to refill the intravascular space during diuresis
251
What can happen if diuresis exceeds the plasma refill rate?
✅ Transient effective hypovolemia, neurohormonal activation, reduced GFR.
252
How does intra-abdominal pressure affect the kidneys?
✅ Increased intra-abdominal pressure (e.g., from ascites) raises renal venous pressure, reducing perfusion.
253
Which condition impairs renal hemodynamic tolerance the most during diuresis?
✅ Baseline chronic kidney disease (CKD).
254
In patients with predominant ascites, what limits volume removal?
✅ Peritoneal volume clearance is limited to 500 mL/day.
255
What preserves GFR in early HF when renal perfusion drops?
✅ Afferent vasodilation and efferent vasoconstriction increase filtration fraction (FF).
256
When is GFR fully dependent on pressure gradient (ΔP)?
✅ In severe HF when afferent vasodilation and FF compensation are exhausted.
257
How do loop diuretics and vasodilators improve renal function?
✅ By reducing renal venous pressure (“afterload”) and intra-abdominal pressure.
258
What clinical sign may suggest acute tubular necrosis instead of cardiorenal syndrome?
.
✅ Oliguria and resistance to diuretics
259
What should be evaluated to rule out intrinsic kidney disease in acute HF?
✅ Urinalysis and urine microscopy.
260
Which type of HF most commonly leads to renal failure?
✅ Combined RV and LV failure.
261
What two features predict poor renal tolerance of diuresis?
✅ (1) Minimal peripheral edema, (2) Non-dilated LV/RV with steep pressure-volume relationship.
262
What is the recommended fluid balance target for patients with poor renal tolerance of diuresis?
✅ Mild diuresis with a target negative fluid balance of 1–1.5 liters/day.
263
What are the 5 types of cardiorenal syndrome?
Type 1 – Acute HF causes acute kidney injury
Type 2 – Chronic HF leads to chronic kidney dysfunction
Type 3 – Acute kidney injury leads to acute HF
Type 4 – CKD leads to chronic cardiac dysfunction
Type 5 – Systemic diseases (e.g., diabetes, HTN, vasculitis) cause both HF and CKD
264
Why does aggressive decongestion improve renal and cardiac function?
✅ It reduces congestion, improves organ perfusion, lowers diuretic requirements, and allows better tolerance of low systemic BP
265
What is the prognostic significance of aggressive decongestion in acute HF, even if creatinine rises?
A: Aggressive decongestion is associated with a 70% reduction in 6-month mortality, despite a rise in creatinine. It’s the relief of congestion, not preservation of creatinine, that improves outcomes.
266
Does a rising creatinine during diuresis always mean worsening renal function?
A: No. It may reflect hemoconcentration, not injury. Studies show no increase in tubular injury markers with rising creatinine during effective diuresis.
267
What did the DOSE trial reveal about diuretic dosing and outcomes?
A: High-dose diuretics caused more transient creatinine rise but better decongestion and clinical outcomes. Creatinine eventually improved by 60 days.
268
What does a high BUN or BUN/Cr ratio ≥20 typically indicate in acute HF?
A: Congestion rather than hypovolemia. These patients are sicker but more likely to recover renal function with decongestion.
269
When does a rising BUN actually suggest hypovolemia?
A: When it rises after several liters of fluid removal and the patient is fully decongested (no edema, normal JVP).
270
What are the theoretical downsides of bolus loop diuretics?
A: They may exceed the plasma refill rate, cause transient hypovolemia, activate RAAS/sympathetic systems, and result in post-diuretic Na+ rebound.
271
What are the benefits of continuous loop diuretic infusion?
A: Allows fluid removal at the plasma refill rate, potentially reducing neurohormonal activation, though DOSE trial showed no clinical advantage over bolus dosing.
272
How does ultrafiltration differ from diuresis in fluid removal?
A: It removes isotonic fluid at a steady rate, potentially matching the plasma refill rate more closely and reducing neurohormonal activation.
273
What did the CARRESS-HF trial show about ultrafiltration?
A: It did not outperform high-dose diuretics in weight loss or symptom relief and caused more creatinine rise at 60 days due to technical interruptions and complications.
274
What is diuretic resistance?
A: Reduced natriuresis and diuresis despite high loop diuretic doses, preventing resolution of congestion.
275
How is diuretic resistance diagnosed?
A: One or more of:
<1 L urine within 6 hours of a loop diuretic dose
<2 L negative balance/day despite >160–240 mg IV furosemide
Post-diuretic urine Na+ <50–70 mEq/L
276
How is diuretic resistance managed?
Increase loop diuretic dose and frequency
Add thiazide or tolvaptan
Consider inotropes or ultrafiltration if output remains low
Address metabolic alkalosis or RAAS activation
277
When should vasodilators be avoided?
A: When SBP < 110 mmHg, or if the patient is dependent on catecholamines for BP.
278
How should vasodilators be initiated?
A: Only after confirming stable BP. Start low and slow, particularly in “warm-wet” patients or those with fluid redistribution-type HF.
279
Which patients are more sensitive to vasodilators?
A: Patients with diastolic HF, even if hypertensive—may experience precipitous BP drops.
280
What did the GALACTIC trial show about vasodilators in ADHF?
A: No benefit in terms of mortality or symptom relief → ESC gives class IIb recommendation.
281
What are common vasodilators used acutely?
*IV Nitroglycerin (NTG): Venodilator; arterial effects at medium doses. Titrate from 10 mcg/min upward if SBP ≥ 110 mmHg
*IV Nitroprusside: Balanced vasodilator; effective in “cold” HF but requires close BP monitoring.
*Oral vasodilators (ACE-I, hydralazine + nitrates): Start after 12–24h when BP is stable.
282
Should IV inotropic agents be routinely used in acute HF?
A: No. They may worsen long-term survival and should be avoided unless essential.
283
What were the key findings of the OPTIME-HF trial?
A: Milrinone increased in-hospital death, 60-day death or rehospitalization in ischemic HF, and arrhythmias in all HF types.
284
Why can inotropes worsen outcomes despite short-term hemodynamic improvement?
A: They cause exogenous cardiac stimulation in an energy-depleted myocardium, leading to ischemic and apoptotic damage.
285
When are IV inotropes indicated in acute HF?
Wet and cold HF with SBP < 90 mmHg
Wet and cold HF not responding to diuretics
286
What is the next step if low-dose inotropes fail to improve hemodynamics?
A: Consider a percutaneous ventricular assist device (IABP or Impella) as a bridge to recovery or surgical VAD.
287
What is the mechanism of action of milrinone?
A: Phosphodiesterase-3 inhibitor → ↑ intracellular cAMP → inotropy + vasodilation.
288
When should milrinone be avoided or adjusted?
Avoid if SBP < 80 mmHg
Reduce dose by 50% in renal failure
Avoid bolus dose (very hypotensive)
289
How should milrinone be started?
A: Begin with 0.2 mcg/kg/min drip, titrate slowly to allow cardiac output to improve before vasodilation causes hypotension.
290
What arrhythmia is most common with milrinone?
A: Atrial fibrillation (AF)
291
How do β-blockers affect milrinone?
A:
Enhance its effects (milrinone acts downstream of β-receptors, unaffected by β-blockade).
292
What is the mechanism of action of dobutamine?
A: β1-agonist (strong) + β2-agonist and α1-agonist (weaker, opposing vascular effects).
293
What are the typical doses of dobutamine?
A: Start at 2–5 mcg/kg/min; may increase to 10 mcg/kg/min if patient is on chronic β-blockers.
294
What are the vascular effects of dobutamine?
.
A: Usually minimal hypotension; may even increase BP via improved cardiac output
295
In what situation might dobutamine cause vasodilation?
A: In critically ill patients with α-receptor saturation, β2 effects may predominate.
296
What arrhythmia is most common with dobutamine?
A: Sinus tachycardia; PVCs and NSVT are also common, but VT is rare.
297
How do β-blockers affect dobutamine?
A: Blunt its effect, especially carvedilol > metoprolol → higher doses may be needed.
298
When are norepinephrine and dopamine used in HF?
A: In severe hypotension (SBP < 70–80 mmHg).
299
Which agent causes more arrhythmias: dopamine or norepinephrine?
A:
Dopamine causes more tachycardia and arrhythmias for a similar cardiac output increase.
300
What is the mechanism of action of levosimendan?
A: Calcium sensitizer that increases myofilament sensitivity to calcium without increasing intracellular Ca²⁺.
301
What are the additional actions of levosimendan?
A: Direct vasodilation by opening ATP-dependent K⁺ channels in vascular smooth muscle.
302
What are its key benefits over traditional inotropes?
Does not increase myocardial oxygen demand or ischemia
May reduce mortality (vs dobutamine/placebo)
Works even with β-blockers
303
How long are inotropes typically used in acute HF?
A: Usually weaned within a few days (levosimendan effects persist ≥1 day due to long half-life).
304
When should ACE-I and β-blockers be continued in acute HF?
A: In most cases, except in severe renal dysfunction (stop ACE-I) or low-output HF with hypotension/inotrope need (stop both).
305
What is the effect of chronic β-blockers on dobutamine?
A: Decreases its hemodynamic response—higher dobutamine doses may be needed
306
What is the effect of chronic β-blockers on milrinone?
A: Enhances its effect, since milrinone acts downstream of β-receptors via cAMP.
307
Should ACE-I/ARB be continued in acute HF if renal function worsens?
A: Yes, holding them impairs outcomes and worsens diuretic response.
308
When can ACE-I/ARB be started in a patient not previously on them?
A: 12–24 hours after ensuring hemodynamic stability.
309
How does ACE-I/ARB improve renal perfusion in acute HF?
A: By reducing excessive angiotensin II–mediated afferent vasoconstriction.
310
What drug has superior outcomes when started in-hospital versus ACE-I?
A: Angiotensin-neprilysin inhibitor (e.g., sacubitril/valsartan).
311
When should β-blockers be started if they were previously stopped or never started?
A: ≥24 hours before discharge, after cold state and azotemia resolve.
312
When can β-blockers be started after stopping inotropes?
A: ≥1 day after discontinuation, with continued monitoring.
313
When is CPAP/BiPAP indicated in acute HF?
A: In severe respiratory distress as a bridge until diuretics relieve pulmonary edema.
314
When should CPAP/BiPAP be stopped?
A: Within 30 minutes if ineffective—otherwise risk increased respiratory work and aspiration.
315
How does positive pressure ventilation improve LV function?
A: Reduces LV preload and afterload by decreasing transmural pressure.
316
How does positive pressure ventilation affect RV function?
A: Increases RV afterload—may worsen output in RV failure.
317
What guides initial therapy in acute HF?
A: Clinical assessment of “wet” (volume overload) and “cold” (low perfusion) status.
318
When is a PA catheter (Swan–Ganz) indicated?
A: In unclear volume status, shock, or need for escalation (e.g., IABP, Impella).
319
What trial showed routine PA catheter use is not helpful in acute HF?
A: ESCAPE trial.
320
How does reduced LVEDP affect perfusion?
A: Improves LV perfusion by increasing the aortic DBP–LVEDP gradient.
321
What are the pre-discharge clinical targets in acute HF?
A: Normal JVP, no orthopnea/edema/bendopnea, BNP drop >30%, stable on oral diuretics.
322
What is the usual oral furosemide dose at discharge if IV 80 mg Q12h was used?
A: 40 mg orally BID (0.5–0.75x the total IV dose used).
323
When should outpatient follow-up occur post-discharge?
A: Within 1 week, to check symptoms, labs (Cr/K/BNP), and adjust diuretics.
324
: What are the four major mortality predictors in acute HF (ADHERE)?
↑ BUN/Cr, SBP <115 mmHg, “cold” HF, positive troponin >1 ng/ml.
325
What medication can be used to maintain blood pressure during dialysis-induced hypotension in severe HF patients?
Norepinephrine, which constricts the empty circulation and raises SBP to 90–100 mmHg without significantly increasing afterload.
326
What is the easiest method for outpatient monitoring of fluid status in HF patients?
A: Daily monitoring of body weight.
327
What weight gain suggests the need for extra diuretics in HF patients?
A: Gain of over 3 pounds in less than a week.
328
What parameter rises about 20 days before HF hospitalization and predicts decompensation better than weight?
A: Pulmonary artery (PA) diastolic pressure.
329
What does a PA pressure > 50 mmHg or increased pulmonary vascular resistance (PVR) indicate in RV failure?
A: Pulmonary hypertension, possibly secondary to left HF.
330
What does normal PA pressure (<50 mmHg) and normal PVR suggest in RV failure?
A: Isolated right HF due to volume overload (ASD, TR) or intrinsic RV disease (cardiomyopathy, RV MI).
331
What RV echo sign indicates volume overload?
A: RV expands and pushes the septum toward LV in diastole; septum moves paradoxically toward RV in systole.
332
Name two echocardiographic indices used to assess RV systolic function.
A: TAPSE (>16 mm normal) and tissue Doppler S’ velocity (>10 cm/s normal)
333
Which imaging modalities better assess RV volume and EF?
A: Cardiac MRI and first-pass nuclear scans.
334
What RA pressure indicates severe RV failure?
A: RA pressure >15 mmHg or RA pressure/PCWP ratio >0.63-1.
335
What diagnostic study is warranted for unexplained right ventricular (RV) dilatation or unexplained pulmonary hypertension?
Transesophageal echocardiography (TEE) with a bubble study.
336
What condition should be suspected in cases of unexplained RV dilatation or pulmonary hypertension?
An overlooked atrial septal defect (ASD), especially a sinus venosus ASD
337
What is the significance of contraction metabolic alkalosis during diuresis?
A: It signals chloride depletion; slow diuresis and replace potassium.
338
Should diuresis continue despite rising creatinine if the patient is still congested?
A: Yes, because rising creatinine may reflect cardiorenal syndrome, not overdiuresis.
339
What percent of ADHF patients have worsening renal function?
A: ~30%
340
What should be added if urine output is only moderate after max dose (e.g., 500 ml after 160–200 mg)?
A: A thiazide or ADH antagonist for sequential nephron blockade.
341
What should you consider if there is no response to max furosemide dose?
Poor renal perfusion (low cardiac output or BP ~90–100 mmHg)
Acute intrinsic kidney injury (e.g., ATN)
342
Example: What IV dose should a patient on 60 mg PO BID receive?
A: ~120 mg IV Q12h, or ~100 mg IV Q8h.
343
How do you calculate initial IV furosemide dosing from oral use?
A: Use 2.5x the total daily oral dose (or ~5x in dose equivalence).
344
What is a safe maximum single IV furosemide dose to avoid ototoxicity?
A: ≤120 mg IV, given slowly over 30 minutes
345
What dose is effective in renal failure?
Up to 200 mg IV over 30 minutes.
346
What dose of IV furosemide is typically effective in HF without renal failure?
A: 40–80 mg IV.
347
How do you determine diuretic resistance?
A: Urine output <500 ml in 1–2 hours after a dose means the dose is below threshold; double the dose.
348
What is used to counteract metabolic alkalosis during aggressive diuresis?
A: Acetazolamide – a proximal tubule carbonic anhydrase inhibitor.
349
How do thiazides affect sodium and potassium?
A: They cause more marked hyponatremia and hypokalemia than loop diuretics alone.
350
What drug blocks ADH and creates aquaresis in hyponatremia?
A: Tolvaptan (15–30 mg/day PO).
351
What are thiazide options to boost diuresis?
Metolazone: 2.5–20 mg PO Qday
Hydrochlorothiazide: 25–50 mg PO Qday
Chlorothiazide: 500–1000 mg IV Qday
352
What is the goal of fluid loss per day with diuresis?
A: 2–3 liters of net negative balance (~3.5–5 L of urine output/day).
353
What is the recommended dosing frequency for IV furosemide in acute HF?
A: Every 6–12 hours (e.g., 40 mg Q6h), or continuous drip.
354
When is a continuous IV furosemide drip considered?
A: When >250 mg/day is required. Start only after an effective bolus.
355
When should IV doses >80 mg of furosemide be considered?
A: In cases of renal failure or diuretic resistance (up to 200 mg IV).
356
In ADHF, what symptom may mimic angina but is not specific for CAD?
A21: Chest tightness – often just a manifestation of dyspnea, not angina.
357
Why can volume overload alone reduce cardiac output in HF?
A20: It raises LVEDP, reducing coronary perfusion pressure, leading to myocardial ischemia and worsening output
358
What is the target HR for AF in decompensated HF?
100–110 bpm = ideal (supports CO and LA emptying)
>110–120 bpm = harmful; slows contractility
>130 bpm with hemodynamic compromise = often requires urgent DCCV
359
What is the “dry and cold” profile in acute HF?
A7: Low output without edema, either due to hypovolemia or severe euvolemic HF (~5% of cases)
This has the worst prognosis among ADHF profiles
360
What lab findings support the “cold” profile?
Elevated lactic acid
Low SvO₂ < 60
361
What is the “wet and cold” profile in acute HF?
A5: Pulmonary/peripheral edema with signs of low output (~30% of ADHF cases)
362
What is the most common hemodynamic profile in acute HF?
A4: Wet and warm – pulmonary/peripheral edema without signs of low output (~⅔ of ADHF cases)
363
What percentage of acute HF episodes have no known precipitating cause?
A19: 40–50%
364
What are the six common triggers for acute decompensated heart failure?
Non-compliance (medications, salt/fluid restrictions, NSAIDs)
Acute hypertension
Acute ischemia (including ACS)
Arrhythmias (especially AF with RVR)
Systemic infections or anemia
Acute valvular insufficiency
365
How long before clinical symptoms do hemodynamic changes usually begin in HF?
A5: Several days to weeks before symptoms appear.
366
What is the difference between clinical and hemodynamic congestion?
Clinical congestion = overt signs of volume overload
Hemodynamic congestion = elevated LV filling pressure without significant volume overload
367
What are the three main clinical presentations of acute heart failure?
Acutely decompensated heart failure (ADHF) – most common (~70%)
De novo acute HF – ~25%
Chronic severe systolic HF with progressive low-output deterioration – ~5%
368
How long does it typically take for arrhythmia-induced cardiomyopathy to reverse after rhythm control?
A: 2–12 weeks.
369
Is arrhythmia-induced cardiomyopathy typically associated with significant LV scar?
No
370
What can arrhythmia do to an existing cardiomyopathy?
A: Aggravate it and further reduce EF.
371
What is the minimum duration of tachyarrhythmia that may cause biventricular failure?
A: As short as 3 days, usually over 2 weeks.
372
What HR is typically tolerated but can still cause cardiomyopathy over time?
.
A: 105–110 bpm
373
Which arrhythmias are commonly associated with tachycardia-induced cardiomyopathy?
A: Uncontrolled AF, atrial flutter, atrial tachycardia, PJRT.
374
What HR goal should be targeted after decongestion in HF due to tachycardia-induced cardiomyopathy?
A: <100 bpm (similar to <80 bpm per RACE-II HF substudy).
375
What PVC burden on Holter is associated with cardiomyopathy risk?
A: >10%, especially >24%.
376
What mechanism underlies PVC-induced cardiomyopathy?
A: Calcium mishandling and LV dyssynchrony.
377
Which PVCs are more likely to cause cardiomyopathy?
A: QRS >150 ms or epicardial origin.
378
What phenomenon strongly predicts LV recovery after ablation?
A: Post-PVC potentiation (↑SBP by ≥10 mmHg).
379
What is the first-line treatment for symptomatic PVCs before cardiomyopathy develops?
A: Beta-blockers or verapamil (efficacy 10–24%).
380
What are the treatment options once PVC cardiomyopathy develops?
A: Ablation or amiodarone.
381
Should asymptomatic patients with frequent PVCs and normal LV get therapy?
A: No; monitor LV function every 6–12 months.
382
Can AF cause cardiomyopathy even if rate controlled?
A: Yes, due to loss of atrial kick and rhythm irregularity.
383
What is the expected EF improvement after AF ablation in HF patients?
A: 10–18% (e.g., CAMERA-MRI trial).
384
What findings raise suspicion for AF-induced cardiomyopathy?
A: No LV scar on MRI and low EF despite rate control.
385
What type of cardiomyopathy can isolated LBBB lead to in the absence of other heart disease?
A: Dilated cardiomyopathy due to LV dyssynchrony.
386
What percentage of patients with LBBB may develop cardiomyopathy over time?
A: <5–10%.
387
What LBBB duration is associated with increased risk of cardiomyopathy?
A: LBBB ≥150 ms.
388
What is the mean time to cardiomyopathy development in LBBB patients?
.
A: 11.6 years
389
What evidence supports LBBB-induced cardiomyopathy?
A: 2–3× increased HF risk in isolated LBBB (Swedish and Framingham data); 20–25% are CRT super-responders.
390
Which group is more likely to be a super-responder to CRT?
A: Women with non-ischemic cardiomyopathy and LBBB ≥150 ms.
391
Does standard HF therapy improve EF in cardiomyopathy with LBBB?
.
A: No
392
What is subclinical myocarditis?
A: Asymptomatic myocarditis, often self-limited but may lead to chronic HF.
393
How does mild acute myocarditis usually present and resolve?
A: LVEF 40–50% with possible mild HF and pericarditis; >90% recover in weeks to months.
394
What are the outcomes of severe acute myocarditis?
A: 35% recover, 40% improve, 25% worsen; 5-year mortality ~50% if persistent HF.
395
Describe fulminant lymphocytic myocarditis.
A: Rapid onset HF with shock/arrhythmia; high early instability but potential full recovery with support.
396
What is the gold standard for diagnosing myocarditis?
A: Endomyocardial biopsy.
397
What treatments improve outcomes in giant-cell myocarditis?
A: Immunosuppressive therapy (e.g., prednisone, mycophenolate, azathioprine).
398
What imaging modality helps diagnose myocarditis and how?
A: Cardiac MRI; T2 for edema, LGE for necrosis/scarring
399
How does MRI enhancement differ between myocarditis and MI?
A: Myocarditis: subepicardial/mid-wall; MI: subendocardial/transmural.
400
What is spared in myocarditis but involved in MI on MRI?
Subendocardium
401
What are causes of acute eosinophilic myocarditis?
A: Drug reactions, Churg-Strauss, hypereosinophilic syndrome, idiopathic.
402
What are the primary causes of HIV cardiomyopathy?
A: Direct myocardial HIV infection, autoimmune processes, coinfections (CMV, Toxoplasma, EBV), and selenium deficiency.
403
What CD4 count is typically associated with HIV cardiomyopathy?.
A: CD4 <400
404
What is the 2-year mortality rate for HIV-associated dilated cardiomyopathy?
A: >50%.
405
What organism causes Chagas disease?
.
A: Trypanosoma cruzi
406
What is the classic chronic cardiac manifestation of Chagas disease?
A: Progressive biventricular failure and large apical aneurysm.
407
What antiparasitic drug is used in Chagas disease?.
A: Benznidazole
408
What cardiac structures are most commonly involved in sarcoidosis?
A: Basal septum and lateral LV wall.
409
What conduction abnormalities are common in cardiac sarcoidosis?
A: ≥2nd-degree AV block, RBBB, LBBB, and pseudo-Q waves.
410
What percentage of sarcoidosis patients have myocardial involvement?
A: 20–30%; only 5% are clinically evident.
411
What is the most common cause of death in cardiac sarcoidosis?
A: Sudden death from ventricular arrhythmias or conduction blocks (30–65%).
412
What imaging modality detects early granulomas and fibrosis in cardiac sarcoidosis?
A: Cardiac MRI (for scar) and FDG-PET (for inflammation).
413
What does MRI typically show in sarcoid cardiomyopathy?
A: Late gadolinium enhancement in basal septum and basal inferolateral wall.
414
What justifies ICD placement in sarcoidosis according to 2017 ACC guidelines?
A: AV block, unexplained syncope, low RVEF, LVEF<35%, or LVEF>35% with LGE on MRI.
415
What determines prognosis in LV non-compaction?
A: Underlying EF and heart failure status.
416
Can LV non-compaction be seen in healthy individuals?
A: Yes, up to 8% (especially in Black individuals, pregnant women, and athletes).
417
What is the diagnostic echo ratio for LV non-compaction?
A: End-systolic ratio of non-compacted to compacted myocardium ≥ 2.
418
What are typical ECG findings in Takotsubo Cariomyoparhy?
A: Anterior ST elevation evolving to deep anterior T-wave inversion, prolonged QT.
419
What is the prognosis of Takotsubo C?
A: Good; ~1% in-hospital mortality, complete recovery in ≤2 months.
420
What percent of TC cases involve the RV?
.
A: ~1/3
421
How long does septic cardiomyopathy usually take to resolve?.
A: 7–10 days
422
What heart segments are affected in neurogenic stress cardiomyopathy?
A: Basal and mid-ventricular segments; apex is spared.
423
Which group of HF patients is least tolerant of vasodilators?
A: Those with restrictive cardiomyopathy (e.g., amyloidosis) or no baseline hypertension.
424
Why do vasodilators increase stroke volume more in systolic HF than in diastolic HF?
A: Diastolic HF is more preload-sensitive and has a stiffer arterial system.
425
What treatment is typically avoided in HOHF due to worsening vasodilation?
A: Calcium channel blockers (CCBs).
426
Is LVEF typically low in high-output HF?
A: No, it is normal or high; may decline over time due to wall stress.
427
What is the most critical pathophysiologic mechanism in high-output HF?
A: Systemic vasodilation or AV fistula → high CO demand → volume overload.
428
What are the top 3 causes of high-output HF?
A: Morbid obesity, severe anemia, lung disease.
429
What defines high-output heart failure?
A: Elevated filling pressures with CI ≥4 L/min/m² or CO ≥8 L/min and wide pulse pressure.
430
Which HFpEF phenotype is especially sensitive to preload reduction?
A: Restrictive cardiomyopathy (e.g., cardiac amyloidosis).
431
Why are vasodilators poorly tolerated in some HFpEF patients?
A: Due to preload dependence, arterial stiffness, and risk of hypotension.
432
Is pulmonary hypertension in HFpEF only postcapillary?
A: No; often includes precapillary component (disproportionate PA pressure to PCWP).
433
What is a common finding in LA function in HFpEF?
A: LA is stiff and poorly contractile, often worsened by atrial fibrillation.
434
What is a common cause of exercise intolerance in HFpEF related to HR?
A: Chronotropic incompetence (inability to raise HR adequately with exertion).
435
Can β-blockers worsen symptoms in HFpEF?
A: Yes, especially if chronotropic incompetence is due to autonomic dysfunction.
436
What is the gold standard for measuring intrinsic contractility?
A: End-systolic elastance (Ees = SBP / end-systolic volume).
437
Why is EF a poor measure of contractility in HF?
A: EF is load-dependent and reflects remodeling more than intrinsic contractility.
438
What echo finding helps detect subtle systolic dysfunction in HFpEF?
A: Reduced LV longitudinal strain.
439
What is the typical LV end-diastolic volume in HFpEF during decompensation?
A: <75–96 mL/m² (non-dilated or mildly dilated).
440
Is HFpEF purely diastolic dysfunction?
A: No; it includes impaired contractility, arterial stiffness, and exercise-induced afterload mismatch.
441
What determines the end-systolic pressure–volume relationship (ESPVR)?
A: Myocardial contractility (Ees = SBP / end-systolic volume).
442
What does the area within the PV loop represent?
A: Stroke work (stroke volume × pressure gradient).
443
Why do HF patients have early fatigue with exertion despite normal cardiac output at rest?
A: Because they have blunted stroke volume index increase during exercise.
444
What is the main limitation to stroke volume increase in HFpEF during exercise?
A: Lack of preload reserve due to stiff, small LV.
445
What HR is considered counterproductive in HF patients?
A: Tachycardia >110 bpm.
446
Why is HR control with ivabradine beneficial in HFrEF but not HFpEF or HFrEF with AF?
A: Because it improves metabolic efficiency and LA emptying only in sinus rhythm HFrEF.
447
In decompensated heart failure with a high E/A ratio, what is the role of heart rate control?
A: Little benefit from HR reduction; tachycardia up to 110 bpm may help by increasing contractility and LA emptying.
448
What is the optimal chronic heart rate target in compensated systolic heart failure (HFrEF)?
A: Less than 70 bpm.
449
What is the typical behavior of LV diastolic pressure in early diastole under normal conditions?
A1: It dips initially in early diastole, "sucking" blood from the LA, especially in young patients with a compliant LV.
450
What is the significance of elevated LVEDP (>16 mmHg)?
A2: It indicates LV dysfunction (systolic or diastolic) and is a key surrogate marker for LV failure.
451
diastolic HF with preserved EF and normal LV volume, what confirms the diagnosis?
A3: Elevated LVEDP.
452
What are the two main features of diastolic dysfunction?
A4: Poor LV relaxation and reduced LV compliance.
453
What echocardiographic findings support diastolic dysfunction?
A5: Reversed E/A ratio, reduced E’, elevated E/E’
454
What is the role of tissue Doppler in assessing LV relaxation?
A6: It measures E’, which reflects myocardial recoil/relaxation.
455
In compensated HF, what causes elevated LVEDP?
A7: Increased LV pressure after atrial contraction despite normal or mildly elevated mean diastolic pressure.
456
What physical exam finding suggests elevated LVEDP with normal pre-A pressure?
A8: Isolated S4.
457
What does an S3 indicate in decompensated HF?
Early diastolic volume overload and rapid LV filling due to LA “push.”
458
What does a high E but short deceleration time on Doppler suggest?
High LA pressure with poor LV compliance – typical of decompensated HF.
459
What does a large E/A ratio (>1.5–2) indicate in HF?
High LA pressure pushing blood rapidly into a non-compliant LV.
460
Define afterload in cardiac physiology.
Wall stress the myocardium contracts against; determined by systolic pressure, ventricular size, wall thickness, and pericardial pressure.
461
Why is the RV more afterload-dependent than the LV?.
Because it has a thinner wall
462
How does wall thickness affect afterload?
Thicker walls decrease stress per sarcomere, reducing afterload.
463
What four main factors determine cardiac output?.
Inotropism, chronotropism, preload, afterload
464
Why does tachycardia increase CO in decompensated states?
Because stroke volume cannot increase with longer filling; HR must compensate.
465
What is the effect of increasing preload beyond optimal in HF?
It worsens cardiac output due to increased afterload and LV dilatation.
466
What is the position of decompensated systolic HF patients on the Frank-Starling curve?
On the flat or descending limb – not preload-dependent.
467
Why is diuresis beneficial in systolic HF?
It reduces LV volume, wall stress (afterload), MR severity, and RV compression on LV.
468
What distinguishes systolic from diastolic LV failure on the pressure–volume curve?
Systolic failure shows dilated LV with high volume; diastolic failure shows steep pressure rise with normal volume.
469
What does a steep pressure–volume curve with normal LV size suggest?
.
Diastolic dysfunction
470
Why do patients with diastolic HF tolerate diuresis poorly?
Because their stroke volume depends heavily on maintaining normal LVEDV.
471
What is the goal PCWP in chronic systolic HF management?
10–12 mmHg – corresponds to optimal stroke volume and minimal congestion.
472
How does afterload reduction exert a lusitropic effect?
By improving LV relaxation and shifting the pressure–volume curve leftward.
473
In what HF scenario must preload not be reduced too aggressively?
Acute systolic HF or severe diastolic HF (e.g., restrictive cardiomyopathy) – they are preload-dependent.
474
What defines Stage A HF?
Risk factors for HF (e.g., HTN, CAD, diabetes) without structural heart disease or HF symptoms
475
What defines Stage B HF?
Structural heart disease (e.g., prior MI, LVH, valvular disease) but no HF symptoms.
476
What defines Stage C HF?
Structural heart disease with prior or current HF symptoms (functional class II-IV).
477
What defines Stage D HF?
Refractory HF (Class IV or advanced III), unresponsive to medical therapy, often with recurrent hospitalizations.
478
Which medications are trialed in Stage D HF if SBP ≥85 mmHg and no hypoperfusion?
ACE inhibitors, β-blockers, and spironolactone at very low doses.
479
What device is superior to inotropes for improving SvO₂ and cardiac power in Stage D HF?
(IABP).
480
What is the 5-year survival rate post-cardiac transplantation?
A: 70–75%.
481
What peak O₂ consumption suggests indication for transplant?
A: ≤14 ml/kg/min (≤12 ml/kg/min if on β-blockers).
482
What metabolic equivalent (MET) corresponds to 14 ml/kg/min?
A: 4 METs
483
What are absolute contraindications to heart transplantation?
Severe PHTN (PVR >3 Wood units), uncontrolled diabetes, GFR <40, cirrhosis, active/recent cancer, active tobacco/alcohol/drug use.
484
What are relative contraindications to transplant?
A: Age >70, BMI >30.
485
What defines vasculopathy on IVUS?
A: Intimal thickening >0.5 mm over >180° arc.
486
What are indications for LVAD placement?
Refractory class IIIB/IV HF, EF ≤25%, peak O₂ ≤14 ml/kg/min, inotrope or IABP dependence.
487
Can LVAD be used in fixed pulmonary hypertension?
Yes, it often reverses the pulmonary hypertension.
488
What is the main cause of RV failure post-LVAD?
A: Septal shift, increased RV preload, or baseline RV dysfunction.
489
What is the PA pulsatility index threshold suggesting RV failure risk?
A: <2.
490
How is LV suction treated in LVAD patients?
A: Decrease pump speed, give fluids
491
What is the only adjustable parameter in LVADs?
Pump speed (rpm).
492
What does a low pulsatility index indicate?
High LVAD support and severe LV dysfunction.
493
What are causes of decreased LVAD power?
RV failure, low preload, HTN, or inflow/outflow obstruction.
494
What are causes of increased LVAD power consumption?
High pump flow (e.g., sepsis, high demand) or pump thrombosis.
495
What are the three forms of cardiac amyloidosis?
AL amyloidosis, mutant transthyretin (TTR) amyloidosis, and wild-type (senile) TTR amyloidosis.
496
What causes AL amyloidosis?
Deposition of light chains, often related to multiple myeloma.
497
What are key systemic features of AL amyloidosis?.
Renal failure, nephrotic syndrome, macroglossia, jaw claudication, periorbital bruising
498
What is the most common form of cardiac amyloidosis?
Wild-type (senile) transthyretin amyloidosis.
499
How does progression differ between AL and TTR amyloidosis?
AL is more aggressive (survival ~15 months), TTR is slower (~5 years).
500
What musculoskeletal condition is often an early sign of amyloidosis?
Bilateral carpal tunnel syndrome.
