Pharmacotherapy III > AHF > Flashcards

AHF Flashcards

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1
Q

Define acute heart failure (AHF).

A

Rapid onset of new or worsening HF signs/symptoms; can be life-threatening and often requires hospitalization/emergency treatment to manage fluid overload + hemodynamic compromise.

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2
Q

AHF includes what 2 main presentation types?

A

De novo (first presentation) and acute decompensated HF (ADHF)/HF exacerbation (worsening baseline HF).

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3
Q

Roughly what % of AHF presentations are ADHF vs de novo vs end-stage?

A

~80% ADHF, ~15% de novo, ~5% end-stage HF.

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4
Q

What are the 4 major mechanisms of acute HF symptoms?

A

Volume overload; pressure overload; myocardial loss; impaired ventricular filling.

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5
Q

How does RAAS contribute to congestion in AHF?

A

RAAS → ↑ sodium reabsorption → fluid retention.

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6
Q

How does SNS contribute to congestion in AHF?

A

SNS → ↑ circulating catecholamines → vasoconstriction → fluid redistribution.

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7
Q

Why can AHF symptoms occur with only modest weight gain?

A

Symptoms may be driven more by fluid redistribution (lungs/viscera) than true fluid accumulation.

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8
Q

Precipitating factors for de novo AHF (name several).

A

MI; sudden BP elevation; stress-induced cardiomyopathy; myocarditis; acute valvular insufficiency; aortic dissection; arrhythmias; hypertensive urgency/emergency.

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9
Q

Precipitating factors for ADHF (name several).

A

Dietary indiscretion; med nonadherence; inotropic use; NSAIDs; uncontrolled HTN/hypertensive crisis; substance abuse (EtOH/illicit drugs); MI; arrhythmias.

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10
Q

What % of ADHF episodes may have no identifiable cause?

A

~40–50%.

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11
Q

Common left-sided HF symptoms in AHF.

A

Dyspnea; orthopnea; bendopnea; PND; tachypnea; hypoxia; abnormal lung sounds; peripheral edema.

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12
Q

Common right-sided HF findings in AHF.

A

Pleural effusions; JVD; + hepatojugular reflux; ascites; hepatomegaly; icterus; abdominal pain/N/V; ↓ urine output; peripheral edema.

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13
Q

Key ED evaluation for suspected AHF.

A

Hx/PE; CXR; 12-lead EKG; troponin; BMP + CBC; BNP (or NT-proBNP).

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14
Q

Other diagnoses to rule out that can mimic AHF dyspnea/fatigue.

A

Pulmonary infection; severe anemia; acute renal failure (and other non-HF causes).

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15
Q

BNP/NT-proBNP role in diagnosis.

A

Supports/helps confirm clinical diagnosis; best for rule-out or rule-in at extremes; most helpful when intermediate probability.

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16
Q

BNP >100 pg/mL indicates what (test characteristic)?

A

Sensitive cutoff (around 86% sensitivity per slide set).

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17
Q

BNP <50 pg/mL suggests what?

A

High negative predictive value (around 96% NPV per slide set).

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18
Q

Common “rule-in / rule-out” BNP thresholds mentioned.

A

Rule-in often >500 pg/mL; rule-out often <100 pg/mL.

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19
Q

Why might BNP be falsely elevated on sacubitril/valsartan?

A

BNP is a neprilysin substrate; neprilysin inhibition increases BNP (but not NT-proBNP).

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20
Q

AHF bedside classification is based on what 2 axes?

A

Congestion (dry vs wet) and perfusion (warm vs cold).

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21
Q

Most common AHF hemodynamic profile.

A

Warm and wet (well-perfused but congested).

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22
Q

Warm & dry means what + associated 6-month mortality?

A

Well perfused without congestion; ~10% mortality at 6 months (per slide).

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23
Q

Cold & wet means what + associated 6-month mortality?

A

Hypoperfused and congested; ~40% mortality at 6 months (per slide).

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24
Q

Cold & dry means what?

A

Hypoperfused without congestion.

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25
Signs/symptoms of congestion (name several).
Dyspnea; fatigue; edema; abdominal bloating/nausea; S3; rales; hepatomegaly; ascites; edema; elevated JVP.
26
Signs/symptoms of hypoperfusion (name several).
Fatigue; confusion; dyspnea; sweating; hypotension; tachycardia; AMS; elevated LFTs; rising SCr; cold extremities.
27
Top goals in AHF management (high-yield).
Improve symptoms (esp congestion/low-output); restore oxygenation; optimize volume; identify etiology + precipitating factors; optimize chronic oral therapy; minimize side effects; patient education/self-management planning.
28
Initial AHF triage: what 2 emergencies to assess early?
Cardiogenic shock and respiratory failure (need circulatory/ventilatory support).
29
Key monitoring parameters in AHF inpatient care.
Volume status (daily weights, I/O); EKG; BP; labs (Na/K/Mg, SCr/BUN).
30
Who should get invasive hemodynamic monitoring?
Generally only those in cardiogenic shock.
31
General rule for chronic HF oral meds during hospitalization.
Continue unless hemodynamically unstable or contraindicated.
32
Reasons to hold/reduce chronic HF meds in AHF.
Symptomatic hypotension; hypoperfusion; bradycardia; hyperkalemia; severely impaired renal function.
33
Beta-blockers in AHF: continue or stop?
Usually continue; stop/hold mainly in cardiogenic shock or severe instability.
34
Why avoid stopping beta-blockers abruptly in hospitalized HF?
Associated with increased mortality when held (per slide summary).
35
Digoxin in AHF: what’s the caution about withdrawal?
Withdrawal can worsen HF (though digoxin is used less commonly now).
36
First-line therapy for volume overload/congestion in AHF.
IV loop diuretics (start early, even in ED).
37
Why is IV preferred over PO for loops in AHF?
More consistent bioavailability/response.
38
Typical IV furosemide start dose for diuretic-naïve patients.
20–40 mg IV (or equivalent).
39
How to dose IV loop if patient was already on PO loop at home.
At least match the outpatient PO dose (convert to IV equivalent).
40
Loop diuretics: effect on mortality in AHF?
Provide symptom relief; mortality benefit not proven.
41
Loop diuretics: time to peak effect (furosemide).
About 30–60 minutes.
42
Why can “post-diuretic sodium retention” happen with loops?
Short half-life → once drug wears off, sodium reabsorption recurs.
43
Strategies to reduce sodium reabsorption rebound with loops.
Salt restriction + more frequent dosing (or infusion strategy).
44
Major adverse effects of aggressive loop diuresis.
Electrolyte imbalances (hypoK/hypoNa), arrhythmias; hypotension/intravascular depletion; renal dysfunction; gout precipitation; possible ototoxicity.
45
If hypokalemic before giving aggressive diuresis, what should you do?
Replete potassium first (reduce arrhythmia risk).
46
Why is hypokalemia extra dangerous in patients on digoxin?
Hypokalemia potentiates digoxin toxicity.
47
Diuretic resistance: first medication steps.
Increase loop dose; add thiazide or spironolactone.
48
Which thiazide is available IV (per slides)?
Chlorthiazide.
49
How should metolazone be timed with a loop diuretic?
Give metolazone ~30 minutes before the loop.
50
Thiazide add-on risk you must watch closely.
Severe potassium wasting (and other electrolyte issues).
51
Spironolactone in diuretic resistance: what’s the main benefit?
May reduce K wasting (doesn’t massively increase diuresis).
52
Loop diuretic continuous infusion (“drip”): why use it?
Higher/more consistent tubular concentrations; avoids high peaks from bolus dosing.
53
When is dialysis/UF/hemodialysis considered in AHF congestion (per slide emphasis)?
Refractory volume overload not responsive to diuresis; reserved for severe/refractory cases.
54
Dialysis “reserve” lab triggers listed on slides (memorize).
K >6.5; pH <7.2; BUN >150; SCr >3.4 (per slide list).
55
Vasodilators in AHF: when to consider?
Adjunct to diuretics for symptom relief (esp dyspnea) in patients with adequate BP.
56
BP requirement for vasodilators (per slides).
SBP >90 mmHg and no symptomatic hypotension.
57
Hemodynamic effects of vasodilators.
↓ venous tone (↓ preload) + ↓ arterial tone (↓ afterload).
58
Nitroglycerin: low-dose predominant effect.
Venodilation → ↓ filling pressures/pulmonary congestion.
59
Nitroglycerin: high-dose effect.
Arterial dilation → ↓ afterload → ↑ stroke volume/CO.
60
Nitroglycerin limitation that develops quickly at high doses.
Tachyphylaxis within ~1–2 hours.
61
Nitroglycerin: common adverse effect and what to do.
Headache is very common—treat with analgesics rather than automatically stopping.
62
Nitroprusside: key properties.
Balanced venous + arterial vasodilator; strong afterload reduction; can markedly reduce PCWP and improve CO.
63
Nitroprusside: major risks.
Marked hypotension; rebound vasoconstriction on stopping; cyanide toxicity risk (esp renal/hepatic dysfunction); often needs arterial line monitoring.
64
Nesiritide: what is it?
Recombinant peptide identical to human BNP.
65
Nesiritide: overall role today (per slides).
Use has diminished; sometimes used when nitro/nitroprusside not options.
66
Nesiritide: main adverse effects.
Hypotension; headache; worsening renal function; longer half-life so AEs can last longer.
67
Inotropes: which patient profile (“warm/cold”)?
Cold patients (hypoperfusion/low output).
68
Inotropes: general rule in reversible hypotension causes.
Avoid if underlying cause is reversible (e.g., hypovolemia).
69
When are inotropes generally reserved?
Severe reduced CO compromising perfusion—often hypotensive patients; sometimes as bridge to transplant/decision.
70
Inotropes: outcomes concern.
Associated with increased mortality and arrhythmias.
71
Milrinone MOA.
PDE-3 inhibitor → ↑ cAMP → ↑ Ca influx → ↑ contractility; not dependent on β-receptors.
72
Why can milrinone work even if patient is on beta-blocker?
MOA not reliant on β receptors.
73
Milrinone hemodynamic effect besides inotropy.
Significant vasodilation (pulmonary + peripheral) → ↓ LV filling pressure.
74
Milrinone bolus concern.
Risk of symptomatic hypotension (noted up to ~10% in one trial per slides).
75
Dobutamine MOA (high-yield).
Catecholamine with β1 and β2 agonist activity → ↑ contractility/CO.
76
Dobutamine vs milrinone: pulmonary vasodilation difference.
Dobutamine has little effect on PVR compared with milrinone.
77
How do beta-blockers affect dobutamine response?
They can mask the inotropic effect (carvedilol more than metoprolol).
78
Vasopressors in AHF: when to initiate?
Only with marked hypotension to raise BP/maintain organ perfusion.
79
Major tradeoff of vasopressors in HF.
↑ LV afterload.
80
Preferred vasopressor option vs dopamine (per slides).
Norepinephrine may have fewer side effects/mortality than dopamine.
81
Epinephrine in AHF shock: place in therapy.
Usually last-line; consider persistent hypotension despite adequate filling pressures.
82
Vasopressin antagonists: what problem do they treat?
Hypervolemic hyponatremia.
83
Tolvaptan: what improves and what does NOT improve?
Modest hemodynamics/dyspnea/weight/hyponatremia improvements; no mortality/readmission benefit if continued post-discharge.
84
Conivaptan: what’s the key limitation in ADHF?
No evidence for improved signs/symptoms in ADHF (per slides).
85
Entresto (sacubitril/valsartan) in hospitalized stabilized ADHF with reduced EF: key takeaway.
Supported for in-hospital initiation after stabilization; associated with greater NT-proBNP reduction and reduced HF rehospitalization vs enalapril in study summary.
86
Sacubitril/valsartan vs enalapril: tolerability outcomes listed.
Comparable rates of worsening renal function, hyperkalemia, symptomatic hypotension, angioedema (per slide summary).
87
VTE prophylaxis in hospitalized HF: why?
HF increases VTE risk → prophylaxis recommended.
88
VTE prophylaxis options/doses listed.
Enoxaparin 40 mg SC daily (adjust for renal fxn); or heparin 5000 units SC BID/TID.
89
Discharge planning: IV→PO loop diuretic transition.
Transition loops back to PO before discharge; ensure patient stable on oral regimen.
90
Why are “target doses” of chronic HF meds emphasized at discharge?
Up-titration toward target doses is key for chronic outcomes (guideline-directed care).
91
Lifestyle discharge counseling targets listed.
Na <2 g/day; fluids <2 L/day; moderate exercise; tobacco cessation; limit alcohol; flu + pneumococcal vaccines; daily weights.
92
Beta-blockers in HFrEF: early timeline for mortality benefit.
By ~8 weeks (per slides).
93
Beta-blocker initiation in hospital: when?
Low-dose pre-discharge in hemodynamically stable patients; generally well tolerated.
94
Beta-blockers in hospitalized HF: observed benefits.
Lower risk of rehospitalization and post-discharge mortality when continued.
95
What to monitor with beta-blockers in hospitalized HF.
Bradycardia/heart block risk; also watch tachycardia (may be compensatory for low stroke volume).
96
ACE-I/ARB in AHF hospitalization: what do observational studies suggest?
In-hospital initiation/continuation associated with ↓ 30-day readmissions + mortality; trend can persist to 12 months.
97
Common reasons to discontinue ACE-I/ARB in AHF.
Hyperkalemia and renal dysfunction.
98
ACE-I/ARB caution situation mentioned.
Hypovolemia (higher hypotension risk).
99
Transitions of care: what % had death or unplanned readmission within 30 days in one study?
~19%.
100
Transitions of care: besides drugs, what patient factors impact rehospitalization?
Physiological, functional, social, cultural, psychological—treat the whole person.
101
Medication safety at transitions: key action on admission.
Proper medication reconciliation.
Pharmacotherapy III
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