Although the stage of CHF often determines treatment, it is essential to assess and therapeutically support the 5 primary determinants of stroke volume and cardiac output: preload, afterload, inotropic state (myocardial contractility), heart rate, and synergy (see 5 Primary Determinants of Stroke Volume & Cardiac Output). These determinants help guide the measures necessary for patients with cardiac disease, regardless of the underlying disease process.
5 Primary Determinants of Stroke Volume & Cardiac Output
Preload
Preload depends on venous return, total blood volume, and blood distribution within the vascular system. Increased diastolic stretching (ie, preload) results in more forceful cardiac contraction (ie, Frank-Starling mechanism). If diastolic myocardial function is normal, increased end-diastolic volume induces a more forceful contraction with only modest increases in end-diastolic pressure. Myocardial fibrosis and hypertrophy impede diastolic filling because they prevent optimal stretch by the myofibers even when filling pressures are increased. With many cardiac diseases, excessive preload can result in pleural effusion, ascites, pulmonary edema, or peripheral edema.
Afterload
Afterload, the intraventricular systolic tension experienced during ejection, is determined by peripheral vascular resistance, physical properties (compliance) of the arterial tree, and volume of blood in the ventricle at onset of systole. Increased afterload leads to reduced rate or amount of ejection at preload. Reducing the afterload in patients with CHF may improve forward cardiac output, reduce regurgitant jet size, and speed resolution of CHF signs.
Myocardial Contractility and/or Inotropy
Myocardial contractility, the innate property of the myocardium that defines force of contraction, is affected by sympathetic nerve activity, concentration of circulating catecholamines, and, to some extent, heart rate. Anoxia, ischemia, acidosis, and disease processes (eg, DCM, chronic mitral insufficiency with severe volume overload) can reduce contractility and inotropic state. Reduced myocardial contractility can be assessed by echocardiography and more indirectly via systemic blood pressure measurement. Drugs that can increase myocardial contractility (ie, positive inotropes) can help alleviate acute and chronic clinical signs of CHF.
Heart Rate
Heart rate is determined by automaticity of the sinoatrial (SA) node, which is subject to autonomic regulation and other environmental (eg, temperature) and metabolic (eg, thyroid levels) factors. Cardiac output increases
linearly with heart rate when stroke volume is constant; however, at extremely rapid heart rates, ventricular filling, stroke volume, and cardiac output are reduced. Patients can present with clinical signs attributed to bradyarrhythmias (eg, third-degree atrioventricular [AV] block, high-grade second degree AV block) and tachyarrhythmias (eg, ventricular or supraventricular tachycardia). Arrhythmias can contribute to clinical signs in patients with structural heart disease (eg, atrial fibrillation in patient with severe mitral insufficiency and CHF, ventricular tachycardia in patient with dilated cardiomyopathy). Addressing arrhythmias in a patient with CHF may help speed resolution of signs.
Synergy
Ventricular synergy is orderly synchronized contraction of the ventricles. Dyssynergy can lead to a reduction of stroke volume and cardiac output. Resynchronization therapy, fairly common in human cardiology, is starting to be investigated in veterinary cardiology (ie, in patients with a pacemaker-induced myocardial dysfunction).
CHF = congestive heart failure, CVD = canine valvular disease, DCM = dilated cardiomyopathy, HCM = hypertrophic cardiomyopathy, LAE = left atrial enlargement, NT proBNP = N terminal prohormone of brain natriuretic peptide, TT4 = total thyroxine