Rapid Review·Cardiovascular
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PATHOLOGY
T1Must knowHeart Failure
FA P316, 324
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Congestion and low perfusion, the split between a weak pump and a stiff one, and the drugs that change mortality.
Key takeaways
What heart failure is
Definition
a clinical syndrome of cardiac pump dysfunction producing congestion and low perfusion. Symptoms: dyspnea, orthopnea, fatigue. Signs: S3, rales, JVD, pitting edema (normal JVP is 6 to 8 mm Hg).Systolic dysfunction (HFrEF)
raised EDV with reduced contractility, often after ischemia or MI, or from dilated cardiomyopathy.Diastolic dysfunction (HFpEF)
reduced compliance with a raised end-diastolic pressure, usually from myocardial hypertrophy. Both loops are contrasted on the heart failure PV loops and neurohormonal cascade.Right from left
right heart failure most often results from left heart failure. Cor pulmonale is isolated right heart failure from a pulmonary cause.| Feature | Systolic (HFrEF) | Diastolic (HFpEF) |
|---|---|---|
| EF | Reduced | Preserved |
| Primary defect | Reduced contractility | Reduced compliance, raised EDP |
| EDV | Raised | Normal or reduced |
| Usual cause | Ischemia or MI, dilated cardiomyopathy | Myocardial hypertrophy |
| Heart sound | S3 | S4 |
| Mortality benefit from drugs | Yes: ACEi/ARB/ARNI, beta-blockers, spironolactone, SGLT2i | Less established |
| Disease | Diastolic function | Cavity size | Wall thickness | Contractility |
|---|---|---|---|---|
| Ischemic heart disease, dilated cardiomyopathy | Normal or impaired | Large | Normal or thin | Reduced |
| Hypertensive heart disease | Impaired | Small | Thick | Normal |
| Hypertrophic cardiomyopathy | Impaired | Small | Thick (septal) | Normal or raised |
| Restrictive cardiomyopathy | Impaired | Normal or small | Normal or thick | Normal |
The drugs that change mortality
Drugs that lower mortality in HFrEF
ACE inhibitors, ARBs, angiotensin receptor-neprilysin inhibitors, beta-blockers (not in acute decompensation), aldosterone antagonists (spironolactone, eplerenone; ENaC blockers have no role), plus hydralazine with nitrates (symptoms and mortality) and SGLT2 inhibitors.Diuretics
loop and thiazide diuretics relieve symptoms only, with no mortality benefit. That distinction is heavily tested.Sacubitril
a neprilysin inhibitor. Neprilysin normally degrades bradykinin, natriuretic peptides, angiotensin II, and substance P, so inhibiting it produces vasodilation and lowers extracellular fluid volume. The circuit is drawn on the sacubitril/valsartan mechanism.- Given combined with valsartan, an ARB, for HFrEF, because blocking neprilysin also raises angiotensin II, which the ARB then blocks.
- Adverse: hypotension, hyperkalemia from the ARB component, cough, dizziness.
- Contraindicated with ACE inhibitors, because both raise bradykinin and the combination causes angioedema.
| Feature | Sacubitril | ACE inhibitors |
|---|---|---|
| Mechanism | Inhibits neprilysin, reducing bradykinin degradation | Inhibits ACE, reducing bradykinin degradation |
| Effect on bradykinin | Raised | Raised |
| Together | Angioedema, so the combination is contraindicated | Paired with an ARB instead |
Left versus right
Left heart failure manifestations
- Orthopnea: lying flat redistributes venous return, worsening pulmonary congestion.
- Paroxysmal nocturnal dyspnea: raised venous return plus reabsorption of peripheral edema overnight.
- Pulmonary edema: raised pulmonary venous pressure causes transudation. Hemosiderin-laden macrophages are the "heart failure cells" seen in the lungs.
Right heart failure manifestations
- Congestive hepatomegaly: raised central venous pressure resists portal flow, giving a nutmeg liver and rarely cardiac cirrhosis.
- JVD and peripheral edema. In chronic failure, increased lymphatic drainage offsets the edema for a while, which is why it appears late.
| Feature | Left heart failure | Right heart failure |
|---|---|---|
| Findings | Pulmonary: dyspnea, orthopnea, PND, pulmonary edema | Systemic: JVD, peripheral edema, hepatomegaly |
| Mechanism | Raised pulmonary capillary hydrostatic pressure | Raised central venous pressure |
| Pathology | "Heart failure cells", hemosiderin-laden macrophages | Nutmeg liver, rarely cardiac cirrhosis |
| PCWP | Raised | Normal if isolated, i.e. cor pulmonale |
| Most common cause | Ischemia, hypertension | Left heart failure |
Cor pulmonale
| Feature | Cor pulmonale | Congestive heart failure |
|---|---|---|
| Definition | Right heart failure from a pulmonary cause | Left plus right heart failure |
| Left heart | Completely normal | Diseased |
| PCWP | NORMAL | Elevated |
| Findings | JVD and edema plus overt lung disease | Dyspnea, JVD, edema |
| Shared | Pulmonary hypertension, raised endothelin 1, loud P2, tricuspid regurgitation | Same |
High-output heart failure
What it is
uncommon; the output is raised to meet peripheral oxygen demand, driven by low systemic vascular resistance from vasodilation or arteriovenous shunting, so heart rate and stroke volume climb. It still presents as pulmonary and/or systemic venous congestion.Causes
severe obesity, advanced cirrhosis, severe anemia, hyperthyroidism, wet beriberi, Paget disease of bone, and an AV fistula, which bypasses the high-resistance arterioles.| Cause | Mechanism |
|---|---|
| Severe anemia | Lower viscosity and oxygen delivery |
| Hyperthyroidism | Raised metabolic demand |
| Wet beriberi (thiamine deficiency) | Vasodilation |
| Paget disease of bone | Arteriovenous shunting |
| AV fistula | Bypasses the high-resistance arterioles |
| Advanced cirrhosis | Vasodilation and shunting |
| Severe obesity | Raised demand |
Cardiorenal syndrome
What it is
kidney function declines progressively because of severe cardiac dysfunction; it occurs in about 30% of acute decompensated heart failure.Three routes
systolic dysfunction lowers output and hypoperfuses the kidney (prerenal failure); diastolic dysfunction congests the systemic veins, including the renal veins, which flattens the transglomerular pressure gradient and lowers GFR; and RAAS activation retains salt and water, raising blood pressure toward hypertensive nephropathy.JVD, ankle edema, a 100-pack-year history, and a normal wedge pressure. Biventricular failure?
No, cor pulmonale. A normal PCWP exonerates the left heart; the right heart failed because of the lungs.
How it's tested
The distinction Mehlman drives hardest is that cor pulmonale has a NORMAL wedge pressure because the left heart is untouched, whereas congestive heart failure has an elevated one. So a patient with JVD, edema, and a hundred-pack-year smoking history has cor pulmonale, not biventricular failure. The other reliably tested point is that loop and thiazide diuretics relieve symptoms but confer no mortality benefit, while the cascade blockers do. On the drug side, sacubitril and an ACE inhibitor are contraindicated together because both raise bradykinin, and stacking them produces angioedema, which is exactly why sacubitril is paired with an ARB instead.
Go deeper
First Aid 2026 — CV/Pathology (p.316, 324) · B&B — Heart failure; heart failure drugs · Mehlman — HY Cardio (HFrEF vs HFpEF, cor pulmonale, JVP measurement, neprilysin)
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