Acute decompensated heart failure Flashcards
(64 cards)
A 70-year-old with known heart failure presents with increasing dyspnea, weight gain of 5 lbs in a week, and new bilateral rales. She is warm to the touch, no signs of poor perfusion. Which Forrester subset does she likely fall under?
A) Subset I (dry/warm)
B) Subset II (wet/warm)
C) Subset III (dry/cold)
D) Subset IV (wet/cold)
Answer: B
Rationale: “Wet/warm” means signs of volume overload (rales, weight gain) but normal perfusion (warm extremities, stable BP).
A 65-year-old with chronic HFrEF arrives tachypneic and hypotensive. Exam: cool extremities, JVD, pulmonary crackles. This suggests low output and volume overload. Which Forrester subset?
A) Subset I (dry/warm)
B) Subset II (wet/warm)
C) Subset III (dry/cold)
D) Subset IV (wet/cold)
Answer: D
Rationale: “Wet/cold” → signs of congestion (wet) + hypoperfusion (cold).
Which of the following most commonly triggers an acute decompensation in heart failure patients?
A) High altitude exposure
B) Medication nonadherence (excess salt/fluid)
C) Minor dehydration
D) Frequent nebulized bronchodilator use
Answer: B
Rationale: Dietary indiscretion (high salt) or med nonadherence is a very common cause of ADHF.
An NT-proBNP level is measured in a patient with acute dyspnea. A very high value (>2000 pg/mL) is typically suggestive of:
A) Asthma exacerbation
B) COPD exacerbation
C) Pulmonary embolism
D) Acute decompensated heart failure
Answer: D
Rationale: NT-proBNP is released with ventricular volume expansion; high levels → probable ADHF.
A 72-year-old with right-sided heart failure primarily presents with:
A) Pulmonary edema and orthopnea
B) Jugular venous distension, peripheral edema, hepatomegaly
C) Marked paroxysmal nocturnal dyspnea
D) Elevated troponin alone
Answer: B
Rationale: Right HF → systemic venous congestion (JVD, edema, hepatic congestion).
A 68-year-old with HFpEF is admitted with acute pulmonary edema. Which mechanism best explains why they are susceptible to fluid overload?
A) Low ejection fraction decreases forward flow
B) Impaired ventricular filling due to stiffness
C) Overly compliant ventricle
D) High stroke volume with no back pressure
Answer: B
Rationale: HFpEF = diastolic dysfunction → stiff LV impairs filling, leads to higher filling pressures & fluid backup.
7.
In acute decompensated HF with flash pulmonary edema, the priority is:
A) Increase oral beta-blocker dose
B) Diuresis + vasodilators to relieve pulmonary congestion
C) IV fluids to improve preload
D) Start a dopamine infusion at high dose
Answer: B
Rationale: Flash pulmonary edema = urgent need for diuretics, possibly vasodilators to reduce preload/afterload.
Which sign in a patient with suspected right-sided HF indicates hepatic congestion?
A) Rales at lung bases
B) Hepatojugular reflux
C) S3 gallop at apex
D) Narrow pulse pressure
Answer: B
Rationale: Hepatojugular reflux suggests fluid overload and hepatic congestion from right HF.
A patient with advanced HFrEF has acute dyspnea. Exam: JVD, S3, BP 88/50, cool extremities. The best initial management?
A) High-dose beta-blocker
B) Aggressive IV fluids
C) IV loop diuretic + consider inotropic support
D) Strict bed rest only
Answer: C
Rationale: “Wet/cold” → loop diuretic for congestion + possible inotrope for low output.
Which lab test helps distinguish acute decompensated HF from noncardiac causes of pulmonary symptoms?
A) D-dimer
B) BNP or NT-proBNP
C) Serum sodium
D) AST/ALT.
Answer: B
Rationale: BNP/NT-proBNP significantly elevated in HF vs noncardiac etiologies
A patient with chronic HF on loop diuretics presents with increased edema. No improvement with IV furosemide at their usual dose. Which approach helps overcome diuretic resistance?
A) Add a thiazide (metolazone) before loop
B) Discontinue all diuretics
C) Switch to sublingual nitrates
D) Give IV fluids to “challenge” the kidney
Answer: A
Rationale: Diuretic resistance is often addressed by combination therapy (loop + thiazide).
A 55-year-old in acute HF shows severe hypertension (BP 210/120) and pulmonary edema. Which medication combination is preferred?
A) IV vasodilator (e.g., nitroprusside) + loop diuretic
B) IV beta-blocker + fluid bolus
C) Low-dose dopamine + oral nitrates
D) High-flow oxygen only
Answer: A
Rationale: Severe HTN + ADHF → reduce afterload with a vasodilator + diuretic for volume overload.
A “cold and dry” Forrester subset III patient typically has:
A) Normal perfusion, no congestion
B) Low perfusion (cool extremities), no volume overload signs
C) Low perfusion, high volume overload
D) Normal perfusion, high volume overload
Answer: B
Rationale: “Cold” = poor perfusion, “dry” = not volume overloaded (no significant edema/rales).
A patient with severe right-sided HF might demonstrate:
A) Orthopnea as the primary complaint
B) Pulmonary edema with pink frothy sputum
C) Marked jugular venous distension and ascites
D) Widened pulse pressure
Answer: C
Rationale: Right HF → systemic venous congestion: JVD, ascites, edema.
Cardiac index <2.0 L/min/m² with elevated wedge pressure typically indicates:
A) Normal hemodynamics
B) Wet/warm profile
C) Wet/cold profile
D) Dry/warm profile
Answer: C
Rationale: Low CI = “cold,” high PCWP = “wet” → “wet/cold” Forrester IV.
A 70-year-old with EF of 25% arrives with acute HF. He’s in sinus tachycardia, BP 95/60, warm extremities, bilateral rales. The best initial therapy?
A) IV diuretic (loop)
B) IV vasopressor
C) Oral beta-blocker load
D) IV fluid challenge
Answer: A
Rationale: He’s “wet/warm” → loop diuretics for volume overload relief.
Which of the following is least likely to cause an acute decompensation of chronic HF?
A) High-salt diet noncompliance
B) New atrial fibrillation
C) Uncontrolled hypertension
D) Strict medication compliance, stable vitals
Answer: D
Rationale: Adherence typically prevents exacerbations. Nonadherence, arrhythmias, or hypertension can worsen HF.
A 75-year-old with HFpEF presents with severe hypertension and pulmonary edema. He’s Forrester subset II (wet/warm). After IV loop diuretic, BP remains 210/110. Next step?
A) IV inotrope (dobutamine)
B) IV vasodilator (e.g., nitroglycerin)
C) Increase sedation
D) IV fluid bolus
Answer: B
Rationale: HFpEF + severe HTN → vasodilator (reduce afterload/preload) to help relieve pulmonary edema.
Patients with right-sided HF due to pulmonary hypertension often benefit from:
A) High afterload to improve output
B) Diuretics + addressing underlying pulmonary vasoconstriction
C) Heavy fluid loading to increase RV stroke volume
D) Oral nitrates alone
Answer: B
Rationale: Right HF from pHTN is managed by diuretics (carefully) + pulmonary vasodilators or therapies addressing pHTN.
An ADHF patient is unresponsive to high-dose loop diuretics. They still have severe pulmonary edema. A typical next intervention?
A) Stop diuretics and give fluids
B) Add a thiazide or spironolactone to augment diuresis
C) Oral nitrates
D) Beta-blockers IV bolus
Answer: B
Rationale: If loop diuretic alone is insufficient, add a second diuretic or aldosterone antagonist (or consider IV vasodilators/inotropes if indicated).
A “wet/cold” patient (subset IV) typically requires which immediate approach?
A) IV fluids to improve perfusion
B) Vasodilators alone
C) Combine diuretics (to reduce volume) and possibly inotropes (to improve perfusion)
D) Early beta-blocker load
Answer: C
Rationale: “Wet/cold” means volume overload + low output → diuretics + possible inotropes to improve perfusion.
A 65-year-old with HFrEF is admitted with ADHF. He has an S3 gallop, crackles, mild hypotension (BP 90/60), and evidence of end-organ hypoperfusion. Which drug might improve cardiac output but risk arrhythmias?
A) Dobutamine (inotrope)
B) Furosemide only
C) Beta-blocker infusion
D) High-dose nitrates
Answer: A
Rationale: Dobutamine boosts contractility (↑CO) but can provoke tachyarrhythmias.
A 72-year-old’s EF is 25%. He’s stable, receiving guideline-directed therapy. Which best explains why he needs an ACE inhibitor?
A) ACEIs are only used in stable HFpEF
B) They reduce preload but increase mortality
C) They reduce afterload and limit maladaptive remodeling
D) They are given solely for arrhythmia prophylaxis
Answer: C
Rationale: ACE inhibitors reduce afterload & block RAAS, preventing remodeling → improved mortality in HFrEF.
A known HF patient with chronic atrial fibrillation stops taking diuretics and has rapid weight gain. He develops acute dyspnea. Why do arrhythmias often worsen HF?
A) They always reduce afterload
B) They can reduce cardiac filling time/coordinate contraction, ↓CO
C) They have no significant impact on HF
D) They permanently lower EF
Answer: B
Rationale: Arrhythmias (e.g., AF) → poor synchronization & shorter filling → decreased CO → worsen HF.