Heart Failure

In depth

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Pathophysiology: neurohormones, remodeling and phenotypes

An injury (infarction, pressure or volume overload, cardiomyopathy, toxins) lowers stroke volume or raises filling pressure. Baroreceptors and the kidney sense low effective volume and activate the sympathetic system, the renin–angiotensin–aldosterone system (RAAS) and vasopressin. Short term this holds BP and output; sustained for months, the same response becomes the disease.

Angiotensin II and aldosterone drive myocyte hypertrophy, apoptosis and fibrosis; norepinephrine is toxic to myocytes, provokes arrhythmias and downregulates β₁ receptors; vasopressin causes hyponatremia. Wall stretch releases the counterweight, ANP and BNP (natriuresis, vasodilation, RAAS inhibition), which neprilysin degrades: the reason for sacubitril. ARNi, ACE inhibitors, ARBs, β-blockers and MRAs lower mortality by blocking these pathways, and SGLT2 inhibitors by natriuretic and metabolic effects; diuretics, digoxin and inotropes relieve symptoms without lowering mortality.

In HFrEF the LV dilates and becomes spherical. By Laplace's law, wall stress = pressure × radius ÷ (2 × wall thickness), so a bigger, thinner ventricle has higher wall stress and oxygen demand; the stretched mitral annulus adds functional MR. In HFpEF, hypertension, age, obesity, diabetes and inflammation make a thick, stiff ventricle: a small volume gain or BP surge raises LVEDP sharply (flash pulmonary edema), and AF or tachycardia, which cost atrial kick and filling time, are poorly tolerated.

GDMT and CRT can reverse remodeling (HFimpEF), but recovery is remission, not cure: in TRED-HF (Lancet 2019), 44% of patients with recovered dilated cardiomyopathy relapsed within 6 months of stopping therapy, versus none who continued. In a patient labeled HFpEF, low ECG voltage despite thick walls, bilateral carpal tunnel syndrome or poor β-blocker tolerance suggests cardiac amyloidosis.

Hemodynamic profiles: Forrester, Stevenson and the bedside

Two questions frame every decompensation: congested (wet) or not, and perfused (warm) or not. Forrester, Diamond and Swan (Am J Cardiol 1977) sorted 200 AMI patients into four subsets using CI 2.2 L/min/m² and wedge 18 mm Hg; the clinical exam predicted the hemodynamic subset 83% of the time. Stevenson's bedside profiles apply the grid to HF and predict death or urgent transplant (Nohria, JACC 2003).

Crackles are often absent in chronic HF because lymphatic drainage increases: Stevenson and Perloff (JAMA 1989) found no rales, edema or raised JVP in 18 of 43 patients with a wedge ≥22 mm Hg, so a clear chest does not rule out a high wedge. In that study a proportional pulse pressure, (SBP − DBP) ÷ SBP, below 25% predicted a CI under 2.2 (sensitivity 91%, specificity 83%). Other cold signs: cool extremities, sleepiness, falling urine output, rising creatinine and lactate; a high SVR can keep BP normal.

BNP ≥100 or NT-proBNP ≥300 pg/mL supports decompensated HF (Universal Definition 2021). A PA catheter is for unclear filling pressures or perfusion, hypotension or worsening renal function despite therapy, vasoactive drugs, or advanced-therapy evaluation (ACCF/AHA 2013); in ESCAPE (JAMA 2005; 433 patients) routine use did no better than clinical assessment and caused more adverse events (21.9% vs 11.5%).

Decompensated HF in the ICU: the first hours

Find the trigger: nonadherence, ACS, arrhythmia, uncontrolled hypertension, infection, PE, thyroid disease, NSAIDs, nondihydropyridine calcium channel blockers or thiazolidinediones. For AF with rapid ventricular response in decompensated HFrEF, use amiodarone or digoxin, a cautious β-blocker if perfusion allows, or cardioversion if unstable; diltiazem and verapamil are 3: Harm in HFrEF (2022 guideline).

Positive pressure lowers preload and LV afterload (transmural pressure) while reopening flooded alveoli. In 3CPO (NEJM 2008; 1,069 patients), CPAP or BiPAP relieved dyspnea, acidosis and hypercapnia faster than oxygen without changing 7-day mortality (9.5% vs 9.8%). Expect hypotension at intubation as sympathetic tone and preload fall.

Vasodilators (2022 guideline 2b, with diuretics when BP allows) suit the warm-wet hypertensive patient. Nitroglycerin is mostly venous at low doses; nitroprusside (0.3–10 mcg/kg/min) is balanced, needs an arterial line, and risks cyanide and thiocyanate toxicity with high doses, long infusions or renal failure. In sympathetic crashing acute pulmonary edema, NIV plus nitroglycerin above 100 mcg/min resolved symptoms by 6 h in 65% vs 12% with low doses (Siddiqua, Emerg Med J 2024; 54 patients). Nesiritide failed to change death or readmission (ASCEND-HF, NEJM 2011).

Inotropes are for hypoperfusion, not congestion. In OPTIME-CHF (JAMA 2002; 951 patients without shock), milrinone caused more sustained hypotension (10.7% vs 3.2%) and atrial arrhythmias with no benefit, and low-dose dopamine did not protect the kidney in ROSE-AHF (JAMA 2013). The 2022 guideline supports continuous inotropes only as a bridge to MCS or transplant (2a) or as palliation (2b) and calls other long-term use potentially harmful (3: Harm).

Decongestion, diuretic resistance and cardiorenal syndrome

Loop diuretics must be secreted into the tubule to block Na-K-2Cl transport in the thick ascending limb, so low renal flow, uremia and hypoalbuminemia blunt them. The dose–response curve has a threshold: a poor response needs a higher dose, not a repeat. Oral furosemide absorption averages about 50% (10–100%); roughly 40 mg oral furosemide = 20 mg IV = 1 mg bumetanide = 20 mg torsemide. Sodium retention between doses and distal tubular hypertrophy explain why repeated dosing and blocking other segments work.

DOSE (NEJM 2011; 308 patients) found boluses every 12 h and a continuous infusion equivalent; 2.5 times the oral dose given IV produced more diuresis and only a transient creatinine rise. A spot urine sodium below 50–70 mEq/L at 2 h, or urine output below 100–150 mL/h over the first 6 h, signals an inadequate response: double the dose (HFA position statement, Mullens 2019), then add a second diuretic (2022 guideline 2a).

Metolazone acts within an hour for 24 h or more (label), so timing it 30 min before the loop matters less than daily K, Na and creatinine.

Type 1 cardiorenal syndrome (Ronco 2008) is AKI from acute cardiac dysfunction. Congestion drives it more than low output: among 145 patients managed with PA catheters (Mullens, JACC 2009), worsening renal function followed a higher admission CVP (18 vs 12 mm Hg), not a lower cardiac index. A creatinine rise of 0.3 mg/dL or more predicts harm when congestion persists, but not with hemoconcentration and effective decongestion (Testani 2010, Metra 2012); reassess when BP or perfusion falls or the patient is dry.

Ultrafiltration removed more fluid in UNLOAD (JACC 2007), but in CARRESS-HF (NEJM 2012; patients with worsening renal function) it raised creatinine (+0.23 vs −0.04 mg/dL) for the same weight loss, with more serious adverse events (72% vs 57%); it is kept for congestion that drugs cannot clear.

HFrEF therapy: GDMT, in-hospital starts, ICD and CRT

The pillars are additive: versus an ACE inhibitor or ARB plus β-blocker, all four carry an estimated HR of 0.38 for CV death or HF admission and add 6.3 years of life at age 55 (Vaduganathan, Lancet 2020).

The 2022 guideline (Class 1) says continue GDMT in hospital unless the patient is unstable, start it once stable (PIONEER-HF and EMPULSE found in-hospital starts safe), restart anything stopped early, and do not stop it for a mild creatinine rise or asymptomatic low BP. In practice the β-blocker is held or halved in shock or marked low output, RAAS inhibitors and MRAs are held for hypoperfusion, AKI or K above 5.5, and the SGLT2 inhibitor is held while NPO. STRONG-HF (Mebazaa, Lancet 2022) titrated to half the target dose before discharge and full dose within 2 weeks, with four visits over 2 months: 180-day death or HF readmission 15.2% vs 23.3% (RR 0.66).

Low doses of all four come before a target dose of any one (2021 ACC HFrEF decision pathway). Recheck K and creatinine 1–2 weeks after RAAS changes; for MRAs at about 1 week, 4 weeks, then every 6 months (2022 guideline 7.3.3). IV iron is 2a in HFrEF with iron deficiency (ferritin <100 ng/mL, or 100–299 with transferrin saturation <20%).

A primary-prevention ICD (2022, Class 1) needs LVEF ≤35%, NYHA II–III on GDMT, expected survival over 1 year and at least 40 days after MI (and 90 days after revascularization, 2017 AHA/ACC/HRS). SCD-HeFT (NEJM 2005) cut mortality 23%; DANISH (NEJM 2016) halved sudden death in nonischemic cardiomyopathy (4.3% vs 8.2%) but not all-cause death (21.6% vs 23.4%), so that indication is debated.

LBBB makes the septum contract before the lateral wall, wasting work and worsening MR; CRT adds a coronary sinus LV lead to pace both ventricles together. Class 1: LVEF ≤35%, sinus rhythm, LBBB with QRS ≥150 ms and NYHA II to ambulatory IV on GDMT; 2a: LBBB 120–149 ms or non-LBBB ≥150 ms; no benefit with QRS <120 ms (2022). CARE-HF (NEJM 2005) cut mortality from 30% to 20%. Survival is best above 98% biventricular pacing (Hayes, Heart Rhythm 2011), so report AF with fast rates, frequent PVCs or lost LV capture; new hiccups suggest phrenic nerve pacing.

Right heart failure and pulmonary hypertension in the ICU

The RV is a thin-walled volume pump coupled to a low-resistance circuit, and its stroke volume falls steeply as PVR rises. A pressure-loaded RV dilates, its oxygen demand rises and its coronary perfusion falls as RV pressure nears aortic pressure. The dilated RV pushes the septum left (D-shaped LV on echo) and underfills the LV, so LV output falls even with normal LV muscle.

Pulmonary hypertension is a mean PA pressure above 20 mm Hg (2022 ESC/ERS): precapillary with wedge ≤15 mm Hg and PVR >2 Wood units, postcapillary with wedge >15. Left heart disease (group 2) is the commonest cause, and PAH drugs are not recommended there. RV failure shows as high CVP with clear lungs, a CVP/wedge ratio above 0.63 (predicted RV failure after LVAD, Kormos 2010), TAPSE 17 mm or less (ASE 2025), and congested liver and kidneys.

• Volume: fluid only for an underfilled RV; most are overloaded, and diuresis or CRRT often raises output by letting the septum move back.
• Pressure: norepinephrine keeps aortic pressure above PA pressure so the RV stays perfused; vasopressin raises SVR with little effect on PVR.
• Contractility: dobutamine or milrinone, which lowers PVR more but also SVR.
• PVR: correct hypoxemia, hypercapnia and acidosis; lowest PEEP that keeps the lungs open; inhaled nitric oxide (often 20 ppm; check methemoglobin, wean slowly) or inhaled epoprostenol.
• Rhythm: keep sinus rhythm and AV synchrony; cardiovert unstable AF, pace heart block.
• Support: Impella RP, ProtekDuo or VA-ECMO when drugs fail.

Advanced HF: shock bridge, MCS, transplant and palliative care

Stage D shows in the trajectory: repeated admissions, GDMT cut back for hypotension or renal function, furosemide-equivalent needs above 160 mg/day or added metolazone, persistent NYHA III–IV symptoms, persistent hyponatremia, frequent ICD shocks or inotrope dependence (2022 guideline indicators). Refer early to an advanced HF center.

HF-related cardiogenic shock now outnumbers AMI shock in US cardiac ICUs (Critical Care Cardiology Trials Network), yet the AMI device trials do not answer its questions. Temporary MCS needs a stated goal: bridge to decision, recovery, durable LVAD or transplant. An axillary IABP or Impella 5.5 lets the patient walk while waiting; since the 2018 US heart allocation policy (VA-ECMO status 1, IABP or percutaneous pump status 2), temporary MCS is a common direct bridge to transplant.

A peak VO₂ ≤12 mL/kg/min on a β-blocker supports transplant listing (ISHLT 2016), and median survival after transplant is about 12.5 years (ISHLT registry, 2002–2009 era). The denervated heart rests at 90–110 bpm, does not respond to atropine (use isoproterenol, epinephrine or pacing), needs a reduced adenosine dose, and develops allograft vasculopathy without angina.

The 2022 guideline makes prognosis, goals of care and symptom management Class 1 for all patients with HF and specialist palliative care 2a in stage D; PAL-HF (JACC 2017; 150 patients) improved quality of life (KCCQ +9.5 points) and mood without changing survival. Discuss turning off ICD shocks early (ethically and legally accepted, HRS 2010). Diuretics and low-dose opioids ease symptoms; home inotropes (2b) can be palliative.

Nursing care, monitoring and discharge teaching

• Perfusion: mentation, skin temperature, capillary refill, hourly urine output during titration.
• Cardiac: rhythm; HR and BP before each GDMT dose (hold limits per order); JVP, S3, edema.
• Respiratory: work of breathing, pillows needed, crackles, SpO₂, skin under the NIV mask.
• Fluid: strict I&O; daily weight on the same scale, at the same time, after voiding (1 kg ≈ 1 L).
• Labs: daily BMP and Mg while titrating; most units keep K ≥4.0 mEq/L and Mg ≥2.0 mg/dL during diuresis.
• Skin and mobility: edematous skin breaks down; offload heels, mobilize early, give VTE prophylaxis (2022, Class 1).

Record urine output for 2–6 h after each diuretic dose and report a poor response early, not at the next dose. Over-diuresis shows as falling BP, dizziness, a BUN rising faster than creatinine and contraction alkalosis.

Diuretics waste K and Mg, which provokes arrhythmias and digoxin toxicity; RAAS inhibitors, MRAs and AKI raise K. For digoxin in HF, DIG trial analyses favor levels of 0.5–0.9 ng/mL, while the Lanoxin label ties levels above 1.2 ng/mL to more adverse reactions; watch for nausea, visual changes, bradycardia, atrial tachycardia with block and bidirectional VT. Tolvaptan corrected hyponatremia but did not lower mortality (EVEREST, JAMA 2007).

Teach back: the weight log and call limits, why GDMT continues when well, sick-day rules (hold the SGLT2 inhibitor, and often the diuretic and RAAS inhibitor, when unable to eat or drink, as the team directs), sodium and alcohol limits, no NSAIDs or decongestants, vaccines, cardiac rehabilitation, and the ICD shock plan (one shock and well: call the clinic; repeated shocks or symptoms: 911). Book a visit within 7 days (2022 guideline 2a). Document weights, net balance, diuretic response, replacements, GDMT held and why, and teaching.

The 2022 guideline, later updates and open questions

Unsettled: whether natriuresis-guided or combination diuretic strategies improve outcomes rather than speed; the ICD in nonischemic cardiomyopathy on modern GDMT; device choice in HF-related shock; and sodium targets (SODIUM-HF found no benefit from <1,500 mg/day).

Exam pearls

• Mortality falls with ARNi or ACEi/ARB, β-blockers, MRAs and SGLT2 inhibitors; diuretics, digoxin and inotropes treat symptoms.
• Forrester: CI 2.2 L/min/m² and wedge 18 mm Hg; cold-wet (subset IV) has the highest mortality.
• Proportional pulse pressure below 25% suggests CI below 2.2; cold patients can be normotensive.
• Poor diuretic response: double the IV loop dose, then add acetazolamide or a thiazide; bolus equals infusion (DOSE).
• A creatinine rise during effective decongestion is acceptable; high CVP, not low output, drives cardiorenal worsening.
• Milrinone works during β-blockade and lowers PVR but needs renal dosing; dobutamine's 2-minute half-life suits borderline BP.
• CRT Class 1: LVEF ≤35%, LBBB, QRS ≥150 ms, NYHA II to ambulatory IV; aim for >98% biventricular pacing.
• Primary-prevention ICD: LVEF ≤35%, NYHA II–III on GDMT, ≥40 days after MI, expected survival over 1 year.
• Transplanted heart: resting HR 90–110, no response to atropine, vasculopathy without angina.
• RV failure: keep aortic pressure above PA pressure, avoid hypoxemia and hypercapnia, never interrupt IV epoprostenol.