3.2 Heart Failure & Mechanical Circulatory Support

Key Takeaways

  • Left-sided heart failure causes pulmonary congestion (crackles, dyspnea, PAWP over 18 mmHg); right-sided failure causes systemic congestion (jugular venous distension, hepatomegaly, elevated CVP, peripheral edema).
  • HFrEF (systolic) has an ejection fraction of 40% or less; HFpEF (diastolic) has an EF of 50% or more with impaired relaxation.
  • The intra-aortic balloon pump inflates in diastole at the dicrotic notch to augment coronary perfusion and deflates just before systole to reduce afterload and myocardial oxygen demand.
  • IABP is contraindicated in aortic regurgitation and aortic dissection; the Impella pulls blood from the LV into the aorta and provides up to 2.5-5.5 L/min of forward flow.
  • Continuous-flow LVAD patients often have no palpable pulse; assess perfusion by Doppler-measured mean arterial pressure and monitor for pump thrombosis, GI bleeding, and driveline infection.
Last updated: July 2026

Acute Decompensated Heart Failure

Acute decompensated heart failure (ADHF) is a sudden worsening of the heart's ability to maintain adequate cardiac output and/or normal filling pressures. The CCRN expects you to classify failure two ways: by side and by ejection fraction.

Left versus Right

  • Left-sided failure backs blood up into the lungs, producing pulmonary congestion: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, bilateral crackles, S3 gallop, frothy pink sputum, and an elevated pulmonary artery wedge pressure (PAWP) above 18 mmHg.
  • Right-sided failure backs blood up into the systemic veins, producing systemic congestion: jugular venous distension (JVD), hepatomegaly, hepatojugular reflux, ascites, dependent peripheral edema, and an elevated central venous pressure (CVP). The most common cause of right failure is left failure.

Systolic versus Diastolic

  • Systolic failure (HFrEF) — impaired contraction with a reduced ejection fraction of 40% or less; a dilated, weak ventricle that cannot eject.
  • Diastolic failure (HFpEF) — impaired relaxation/filling with a preserved ejection fraction of 50% or more; a stiff, hypertrophied ventricle. Congestion occurs despite a normal EF.

B-type natriuretic peptide (BNP or NT-proBNP) rises with ventricular wall stretch and helps confirm that dyspnea is cardiac. The wet/dry (congestion) and warm/cold (perfusion) grid guides therapy: most decompensations are warm-and-wet (congested, perfusing) and respond to diuresis and vasodilation, while cold-and-wet signals low output needing inotropes or mechanical support.

Precipitants and Hemodynamic Profiles

Common triggers of acute decompensation include dietary sodium or fluid excess, medication nonadherence, uncontrolled hypertension, a new dysrhythmia (especially atrial fibrillation), myocardial ischemia, infection, and worsening renal function. Invasive or noninvasive hemodynamics define the profile: an elevated PAWP combined with a low cardiac index below 2.2 L/min/m2 identifies the cold-and-wet patient at highest risk of death. The four-quadrant framework — warm-and-dry (compensated), warm-and-wet (congested, the most common ADHF picture), cold-and-dry (hypoperfused and underfilled), and cold-and-wet (congested and hypoperfused, the worst prognosis) — tells you whether the immediate priority is diuresis, vasodilation, cautious volume, inotropy, or escalation to mechanical support.

Cardiogenic Pulmonary Edema

When left-heart filling pressures rise abruptly, fluid floods the alveoli, causing cardiogenic pulmonary edema — severe dyspnea, hypoxemia, and diffuse crackles. Management targets preload and afterload, captured by the mnemonic LMNOP:

  • Loop diuretic (furosemide) to remove volume in fluid-overloaded patients.
  • Morphine — historically used but now de-emphasized because of respiratory depression.
  • Nitrates (nitroglycerin, or nitroprusside for severe hypertension) to venodilate (reduce preload) and dilate arteries (reduce afterload).
  • Oxygen and non-invasive positive-pressure ventilation (CPAP/BiPAP) to recruit alveoli, improve oxygenation, and reduce work of breathing and preload.
  • Position upright to reduce venous return.

When output is inadequate (cold-and-wet), add an inotropedobutamine (beta-1 agonist) or milrinone (phosphodiesterase-3 inhibitor that is also a vasodilator, useful when systemic vascular resistance is high). Watch for hypotension and tachydysrhythmias with both.

Mechanical Circulatory Support

When pharmacology fails, mechanical circulatory support (MCS) temporarily unloads the ventricle and augments perfusion.

Intra-Aortic Balloon Pump (IABP)

The IABP sits in the descending aorta below the left subclavian and cycles with the cardiac rhythm through counterpulsation:

  • Inflates during diastole, timed to the dicrotic notch of the arterial waveform (aortic valve closure). This raises diastolic pressure and augments coronary artery perfusion.
  • Deflates just before systole (before the QRS/aortic valve opening), which lowers afterload, reduces myocardial oxygen demand, and improves forward stroke volume.

Timing errors (early or late inflation, early or late deflation) reduce benefit or increase workload and must be recognized on the waveform. Contraindications include aortic regurgitation (augmentation worsens regurgitation) and aortic dissection; severe peripheral arterial disease limits insertion. Monitor the affected limb for ischemia and never let the balloon sit idle (thrombus risk).

Impella

The Impella is a percutaneous axial-flow pump placed across the aortic valve. It continuously pulls blood from the left ventricle and expels it into the ascending aorta, directly unloading the LV and providing up to 2.5-5.5 L/min depending on the model. Monitor for hemolysis, suction alarms (from hypovolemia or malposition), and migration.

Ventricular Assist Device (VAD)

A left ventricular assist device (LVAD) is a durable continuous-flow pump for advanced heart failure, used as a bridge to transplant or destination therapy. Because flow is continuous, patients frequently have no palpable pulse and a narrow pulse pressure — assess perfusion using a Doppler-measured mean arterial pressure, not a standard cuff. Lifelong anticoagulation is required; complications include pump thrombosis, gastrointestinal bleeding (acquired von Willebrand deficiency), driveline infection, and right-heart failure.

Escalation and VA-ECMO

When one device cannot maintain perfusion, or when cardiac and respiratory failure coexist, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) provides full cardiopulmonary support by draining venous blood, oxygenating and warming it through a membrane, and returning it to the arterial circulation. Every escalation weighs the added support against complications — limb ischemia, bleeding, hemolysis, stroke, and infection — and requires a defined exit strategy (myocardial recovery, durable VAD, or transplant). The critical care nurse tracks device flows and alarms, anticoagulation targets, distal limb perfusion, and emerging right-heart failure, which frequently unmasks once the left ventricle is mechanically unloaded and preload to the right heart rises.

DeviceMechanismSupportKey Caution
IABPDiastolic counterpulsation in aorta~0.5-1 L/min effectAortic regurgitation/dissection; timing errors
ImpellaAxial pump across aortic valveUp to 2.5-5.5 L/minHemolysis, suction events, migration
LVADContinuous-flow LV-to-aorta pumpFull LV supportNo pulse; Doppler MAP, anticoagulation, driveline infection
Test Your Knowledge

For correct timing, the intra-aortic balloon pump inflates during:

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D
Test Your Knowledge

A patient with acute decompensated systolic heart failure has a PAWP of 28 mmHg, bilateral crackles, and dyspnea but an adequate blood pressure. Appropriate initial therapy includes:

A
B
C
D
Test Your Knowledge

A patient with a continuous-flow LVAD is being assessed. Blood pressure and perfusion are best evaluated by:

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B
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D