cardiovascular disorders
Heart Failure (HF)
Physiology of Heart Failure
Cardiac contractility (force and velocity of contraction), ventricular performance, and myocardial oxygen requirements are determined by Preload Afterload Substrate availability (eg, oxygen, fatty acids, glucose) Heart rate and rhythm Amount of viable myocardium Cardiac output(CO) is the product of stroke volume and heart rate; it is also affected by venous return, peripheral vascular tone, and neurohumoral factors. Preloadis the loading condition of the heart at the end of its relaxation and filling phase (diastole) just before contraction (systole). Preload represents the degree of end-diastolic fiber stretch and end-diastolic volume, which is influenced by ventricular diastolic pressure and the composition of the myocardial wall. Typically, left ventricular (LV) end-diastolic pressure, especially if higher than normal, is a reasonable measure of preload. LV dilation, hypertrophy, and changes in myocardial distensibility (compliance) modify preload. Afterloadis the force resisting myocardial fiber contraction at the start of systole. It is determined by LV chamber pressure, radius, and wall thickness at the time the aortic valve opens. Clinically, systemic systolic blood pressure at or shortly after the aortic valve opens correlates with peak systolic wall stress and approximates afterload. TheFrank-Starling principledescribes the relationship between preload and cardiac performance. It states that, normally, systolic contractile performance (represented by stroke volume or CO) is proportional to preload within the normal physiologic range (see figure). Contractility is difficult to measure clinically (because it requires cardiac catheterization with pressure-volume analysis) but is reasonably reflected by the ejection fraction (EF), which is the percentage of end-diastolic volume ejected with each contraction (stroke volume/end-diastolic volume). EF can generally be adequately assessed noninvasively with echocardiography, nuclear imaging, or MRI. Theforce-frequency relationshiprefers to the phenomenon in which repetitive stimulation of a muscle within a certain frequency range results in increased force of contraction. Normal cardiac muscle at typical heart rates exhibits a positive force-frequency relationship, so a faster rate causes stronger contraction (and corresponding greater substrate requirements). During some types of heart failure, the force-frequency relationship may become negative, so that myocardial contractility decreases as heart rate increases above a certain rate. Cardiac reserveis the ability of the heart to increase its performance above resting levels in response to emotional or physical stress; body oxygen consumption may increase from 250 to≥1500 mL/minute during maximal exertion. Mechanisms include Increasing heart rate Increasing systolic and diastolic volumes Increasing stroke volume Increasing tissue extraction of oxygen (the difference between oxygen content in arterial blood and in mixed venous or pulmonary artery blood) In well-trained young adults during maximal exercise, heart rate may increase from 55 to 70 beats/minute at rest to 180 beats/minute, and CO may increase from 6 to≥25 L/minute. At rest, arterial blood contains about 18 mL oxygen/dL of blood, and mixed venous or pulmonary artery blood contains about 14 mL/dL. Oxygen extraction is thus about 4 mL/dL. When demand is increased, oxygen extraction may increase to 12 to 14 mL/dL. This mechanism also helps compensate for reduced tissue blood flow in heart failure. Normally (top curve), as preload increases, cardiac performance also increases. However at a certain point, performance plateaus, then declines. In heart failure (HF) due to systolic dysfunction (bottom curve), the overall curve shifts downward, reflecting reduced cardiac performance at a given preload, and as preload increases, cardiac performance increases less. With treatment (middle curve), performance is improved, although not normalized. 