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Heart failure

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Abstract

Heart failure arises when structural or functional abnormalities prevent the heart from properly filling with or ejecting blood, so that the heart cannot meet the metabolic needs of the peripheral tissue or can do so only in the face of elevated filling pressures. Additional terminology describing failure of the cardiovascular system is based upon the specific organs or tissues involved. The haemodynamic and circulatory consequences of heart failure involve decreased cardiac output, vasoconstriction, retention of sodium and water, and activation of neurohormonal pathways, including the sympathetic nervous system and the renin-angiotensin-aldosterone axis. The chapter looks at Mechanisms of heart failure; Global cardiac function; and Clinical presentation of heart failure.

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Figures

Image of 15.1
15.1 Calcium cycling in the myocardial cell. The majority of intracellular calcium is stored in the sarcoplasmic reticulum. During cardiac depolarization, calcium is released through the ryanodine receptor2 channel into the cytosol, where it is free to bind to troponin-C. The troponin complex normally inhibits interaction between the myosin head and actin filaments, preventing crossbridging and contraction. Binding of calcium to troponin-C relieves this inhibition and initiates systolic contraction. Once contraction is complete, calcium is released from troponin-C and taken back up into the sarcoplasmic reticulum by the SERCA2a transporter, regulated by phospholamban. The uptake of calcium by SERCA2a as well as crossbridging of myosin and actin utilize a large amount of energy, hence both systole and diastole are energy-dependent events. ADP = Adenosine diphosphate; ATP = Adenosine triphosphate.
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15.2 Frank–Starling curves demonstrating the relationship between preload (ventricular volume or pressure and end-diastole) and cardiac performance (cardiac output). In healthy patients, the Frank–Starling relationship is curvilinear and steep, such that small increases in preload effect significant improvements in cardiac output. In diseased patients, the Frank–Starling relationship is depressed and flattened such that cardiac output is decreased for any given level of preload, and the incremental gains in cardiac output for any increase in preload are less than in a healthy patient. Development of CHF occurs as the kidneys retain sodium and fluid, and preload increases above approximately 25 mmHg in the pulmonary veins and capillaries. Low output heart failure (blue circle) and combined low output and CHF (green circle) in instances of severely depressed myocardial function. Treatment of heart failure with preload reducers (i.e. diuretics or venous vasodilators) shifts a patient leftward along the Frank–Starling curve, helping to reduce signs of congestion. Treatment of heart failure with afterload reducers (i.e. arterial vasodilators) or positive inotropes (i.e. dobutamine, pimobendan) shifts the Frank–Starling curve upwards with a steeper slope, helping to restore the normal relationship between preload and cardiac performance.
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15.3 Relationship between pressure and volume within the ventricle during the three phases of diastole. In the healthy patient, increases in ventricular volume are achieved with little change in ventricular pressure because of normal early ventricular relaxation and high ventricular compliance during mid- and late-diastole. In patients with impaired ventricular relaxation, early filling is only achieved at the expense of higher ventricular pressures. In patients with poor ventricular compliance, mid- and late-diastolic filling is hindered and only achieved at the expense of higher ventricular pressures. In patients with pericardial restraint (i.e. pericardial tamponade), the entirety of diastole is affected by external compression of the ventricle, and filling throughout all phases of diastole is accomplished only at higher ventricular pressures.
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15.4 Evolution of pulmonary oedema. In the healthy individual, transudation of small amounts of fluid from the capillary across the capillary–alveolar membrane and into the interstitial space is balanced by removal of the fluid by the lymphatic system. In Stage 1 of pulmonary oedema formation, elevated hydrostatic pressure within the capillary system increases the transudation of fluid into the interstitial space; however, no oedema forms due to increased lymphatic removal of fluid from the tissue. In Stage 2, the degree of transudation overwhelms the capacity of the lymphatic system to clear fluid, and interstitial oedema results. This occurs when capillary hydrostatic pressures achieve 20–25 mmHg. In Stage 3, the degree of transudation is sufficient to accumulate in both the interstitial space as well as in the pulmonary alveoli, and overt clinical signs would be anticipated in these patients.

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