0071643192.pdf

■ Acute heart failure vs chronic heart failure
■ Cor pulmonale: enlargement of the right ventricle from underlying lung
disease

PATHOPHYSIOLOGY

What determines ideal myocyte contraction?

■ Preload—the force (volume) stretching the myocytes beforecontraction
■ Afterload—the force needed to overcome both the volume of blood in the
ventricle and the peripheral vascular resistance duringcontraction
■ Contractilityof myocytes

Underlying disease process →myocyte cell death and/or hypertrophy.

■ Predominance of cell death →↓contractility and low EF →neurohor-
monal response with aldosterone, renin, and circulating catecholamines
→fluid retention (above ideal preload) and afterload.
■ Predominance of cell hypertrophy →stiff, less compliant heart →poor
ventricular filling with a preserved EF.
■ Often both are present simultaneously.

Decompensated Heart Failure and Pulmonary Edema

CAUSES

Triggers of acute decompensation include:

■ ACS
■ Dysrhythmia
■ Acute HTN
■ Acute valvular dysfunction
■ Severe high output state: Anemia, thyrotoxicosis, acute AV shunt
■ Myocarditis
■ PE
■ Increased metabolic demand: Infection, exertion

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CARDIOVASCULAR EMERGENCIES

TABLE 2.10. Common Causes of Heart Failure

Ischemic heart disease—most common

Cardiomyopathy

Congenital heart disease

Valvular disease

Hypertension

Myocarditis

Constrictive pericarditis

Tamponade

Pulmonary disease (from pulmonary HTN)

High-output states

(thyrotoxicosis, anemia, beriberi, Paget disease, arteriovenous fistula)

Ideal myocyte contraction is

determined by preload,

afterload, and contractility.