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Heart Failure & Shock

Name: Heart Failure & Shock
Creator: Veli Bakalov, MD

Backward pressure, forward failure, and the four hemodynamic profiles of shock

Cardiovascular·Ischemic Heart Disease & Heart Failure·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Systolic HF (HFrEF) = EF 40% or less, impaired contractility, eccentric hypertrophy, S3; diastolic HF (HFpEF) = preserved EF, stiff ventricle from hypertensive concentric hypertrophy, S4.
Left HF floods the lungs (dyspnea, orthopnea, PND, crackles, pulmonary edema, hemosiderin-laden heart failure cells).
Right HF congests the body (JVD, pitting edema, nutmeg liver, hepatojugular reflux); left HF is its most common cause; right HF from lung disease is cor pulmonale.
Sympathetic and RAAS activation (angiotensin II, aldosterone) compensate at first but raise afterload and drive remodeling; ACE inhibitors/ARBs, β-blockers, and aldosterone antagonists improve survival.
BNP is released by ventricular myocytes on stretch and causes natriuresis and vasodilation; a low BNP has high negative predictive value and argues against heart failure.
Shock profiles: hypovolemic ↓PCWP ↓CO ↑SVR; cardiogenic ↑PCWP ↓CO ↑SVR; obstructive ↓CO ↑SVR; distributive ↓SVR with ↑CO early in sepsis.
Cold shock (high SVR) = hypovolemic, cardiogenic, obstructive; warm shock (low SVR) = distributive; PCWP separates hypovolemic (low) from cardiogenic (high).
Neurogenic shock loses sympathetic tone: hypotension with bradycardia instead of reflex tachycardia.
Obstructive shock = tamponade, tension pneumothorax, massive PE; tamponade gives equalized diastolic pressures and pulsus paradoxus.

Systolic vs diastolic heart failure

Heart failure. The heart cannot pump enough blood for the body's needs without abnormally high filling pressures, producing congestion, low output, or both.

Systolic HF (HFrEF). Ejection fraction of 40% or less (41 to 49% is termed mildly reduced) from impaired contractility. The ventricle dilates through eccentric hypertrophy (sarcomeres added in series, the pattern of volume overload), and an S3 gallop is typical. Causes include ischemic heart disease and dilated cardiomyopathy.

Diastolic HF (HFpEF). EF is preserved, but the stiff ventricle relaxes and fills poorly, so filling pressures rise. Concentric hypertrophy from hypertension (pressure overload) is the classic cause, and an S4 gallop is typical.

HFrEF vs HFpEF

Feature	Systolic (HFrEF)	Diastolic (HFpEF)
Ejection fraction	40% or less	Preserved
Core defect	Impaired contractility	Impaired relaxation and filling
Remodeling	Eccentric hypertrophy, dilated chamber	Concentric hypertrophy, small stiff chamber
Gallop	S3	S4
Classic causes	Ischemia, dilated cardiomyopathy	Hypertension

Gallops. An S3 in early diastole reflects rapid filling of a volume-overloaded, dilated ventricle (it can be normal in children, young adults, and pregnancy). An S4 in late diastole is the atrial kick striking a stiff, noncompliant ventricle, typical of diastolic HF and hypertrophy.

High-output heart failure occurs when a normal or strong heart cannot meet an abnormally high demand: anemia, thyrotoxicosis, arteriovenous fistula, wet beriberi (thiamine deficiency), and Paget disease of bone.

Left vs right heart failure

Left HF. Blood backs up into the pulmonary circulation: dyspnea, orthopnea (lying flat returns more venous blood to congested lungs), paroxysmal nocturnal dyspnea, crackles, and pulmonary edema. Chronic congestion causes microhemorrhages; alveolar macrophages that ingest the red cells become hemosiderin-laden heart failure cells.

Right HF. Systemic venous congestion: jugular venous distension, peripheral pitting edema, hepatomegaly with nutmeg liver, and hepatojugular reflux. The most common cause of right HF is left HF; isolated right HF from primary lung disease is cor pulmonale.

Left vs right heart failure

Feature	Left HF	Right HF
Congestion	Pulmonary	Systemic venous
Symptoms and signs	Dyspnea, orthopnea, PND, crackles, pulmonary edema	JVD, pitting edema, hepatomegaly, hepatojugular reflux
Pathology	Heart failure cells in alveoli	Nutmeg liver (centrilobular congestion)
Common cause	Ischemia, hypertension, cardiomyopathy, valve disease	Left HF; cor pulmonale if from lung disease

Neurohormonal compensation and BNP

Low cardiac outputReduced perfusion is sensed by baroreceptors and the kidney.
Sympathetic and RAAS activationMore heart rate, contractility, and vasoconstriction; angiotensin II and aldosterone.
Vasoconstriction and volume retentionAldosterone-driven Na+ and water retention raise preload; vasoconstriction raises afterload.
RemodelingChronic neurohormonal exposure causes hypertrophy and fibrosis, and failure progresses.

Compensation becomes the disease. These responses initially support blood pressure and output, but the extra afterload and chronic remodeling worsen the failing heart.

Blocking the loop prolongs survival in HFrEF: ACE inhibitors or ARBs (or sacubitril-valsartan), β-blockers, and aldosterone antagonists, joined by SGLT2 inhibitors and, in Black patients, hydralazine with a nitrate. Loop diuretics relieve congestion and digoxin eases symptoms without a survival benefit.

BNP. Ventricular myocytes release BNP (and NT-proBNP) in response to wall stretch and volume overload; BNP causes vasodilation and natriuresis, counterbalancing RAAS, as ANP does from the atria. Its greatest clinical value is a high negative predictive value: a low BNP in a dyspneic patient argues strongly against heart failure. Neprilysin degrades BNP, so sacubitril raises BNP levels.

Shock: classification by hemodynamics

Shock. Inadequate tissue perfusion, usually with hypotension, leading to anaerobic metabolism and lactic acidosis. Classify it by three levers — preload (PCWP), cardiac output, and systemic vascular resistance (SVR). One lever fails first and the others move in compensation.

Hemodynamic profiles of shock

Type	Examples	PCWP	CO	SVR	Skin
Hypovolemic	Hemorrhage, dehydration, burns	↓	↓	↑	Cold, clammy
Cardiogenic	Large MI, arrhythmia, decompensated HF	↑	↓	↑	Cold
Obstructive	Tamponade, tension pneumothorax, massive PE	↑ in tamponade; ↓ or normal in PE	↓	↑	Cold
Distributive	Septic, anaphylactic, neurogenic	↓	↑ early in sepsis; ↓ in neurogenic	↓	Warm, flushed

Cold shock (high SVR): hypovolemic, cardiogenic, obstructive. Warm shock (low SVR): distributive.

Reading the table. SVR first separates warm from cold shock. Within cold shock, PCWP separates the empty tank (low in hypovolemic) from the failing pump (high in cardiogenic).

Mixed venous O2 saturation is low when output is low (hypovolemic, cardiogenic, obstructive) because tissues extract more, but is often high in septic shock, where tissues fail to extract O2.

The four shocks in practice

Hypovolemic. Low preload drops output; compensatory vasoconstriction raises SVR, giving cold, clammy skin and reflex tachycardia. Treat with volume or blood.

Cardiogenic. The failing pump drops output while blood backs up, so PCWP is high (pulmonary edema, often an S3); SVR is high and skin cold. The high wedge distinguishes it from hypovolemic shock.

Obstructive. A mechanical block to filling or ejection: output falls, SVR rises, skin is cold, and neck veins distend. Tamponade shows equalized diastolic pressures and pulsus paradoxus.

Distributive. Profound vasodilation drops SVR, giving warm, flushed skin. Early septic shock has high output (warm shock) and low PCWP; anaphylaxis adds histamine-driven capillary leak and is treated with epinephrine. Neurogenic shock loses sympathetic tone, so it uniquely pairs hypotension with bradycardia instead of the reflex tachycardia of other shocks.