Материал: Internal_diseases_propedeutics._Part_II._Diagnostics_of_cardiovascular_diseases

No definition of heart failure (HF) is entirely satisfactory. Congestive heart failure (CHF) develops when plasma volume increases and fluid accumulates in the lungs, abdominal organs (especially the liver), and peripheral tissues.

Physiology At rest and during exercise, cardiac output (CO), venous return, and distribution of blood flow with O2 delivery to the tissues are balanced by neurohumoral and intrinsic cardiac factors. Preload, the contractile state, afterload, the rate of contraction, substrate availability, and the extent of myocardial damage determine left ventricular (LV) performance and myocardial O2 requirements. The Frank-Starling principle, cardiac reserve, and the oxyhemoglobin dissociation curve play a role.

Preload (the degree of end-diastolic fiber stretch) reflects the end-diastolic volume, which is influenced by diastolic pressure and the composition of the myocardial wall. For clinical purposes, the end-diastolic pressure, especially if above normal, is a reasonable measure of preload in many conditions. LV dilatation, hypertrophy, and changes in myocardial distensibility or compliance modify preload.

The contractile state in isolated cardiac muscle is characterized by the force and velocity of contraction, which are difficult to measure in the intact heart. Clinically, the contractile state is often expressed as the ejection fraction (LV stroke volume/enddiastolic volume).

Afterload (the force resisting myocardial fiber shortening after stimulation from the relaxed state) is determined by the chamber pressure, volume, and wall thickness at the time of aortic valve opening. Clinically, afterload approximates systemic BP at or shortly after aortic valve opening and represents peak systolic wall stress. The heart rate and rhythm also influence cardiac performance.

Reduced substrate availability (eg, of fatty acid or glucose), particularly if O2 availability is reduced, can impair the vigour of cardiac contraction and myocardial performance.

Tissue damage (acute with myocardial infarction or chronic with fibrosis due to various diseases) impairs local myocardial performance and imposes an additional load on viable myocardium.

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The Frank-Starling principle states that the degree of end-diastolic fiber stretch (preload) within a physiologic range is proportional to the systolic performance of the subsequent ventricular contraction

This mechanism operates in HF, but, because ventricular function is abnormal, the response is inadequate. If the Frank-Starling curve is depressed, fluid retention, vasoconstriction, and a cascade of neurohumoral responses lead to the syndrome of CHF. Over time, LV remodeling (change from the normal ovoid shape) with dilatation and hypertrophy further compromises cardiac performance, especially during physical stress. Dilatation and hypertrophy may be accompanied by increased diastolic stiffness.

Classification and Etiology

In many forms of heart disease, the clinical manifestations of HF may reflect impairment of the left or right ventricle.

Left ventricular (LV) failure characteristically develops in coronary artery disease, hypertension, and most forms of cardiomyopathy and with congenital defects (eg, ventricular septal defect, patent ductus arteriosus with large shunts).

Right ventricular (RV) failure is most commonly caused by prior LV failure (which increases pulmonary venous pressure and leads to pulmonary arterial hypertension) and tricuspid regurgitation. Causes are also mitral stenosis, primary pulmonary hypertension, multiple pulmonary emboli, pulmonary artery or valve stenosis, and RV infarction.

One distinguishes chrionic and acute heart failure. In Russian Federation clinicians use classification of chronic heart failure, stipulated by National Scientific Society of Cardiologists in 2002. It joins two classifications: one – after N.D. Strazhesko and V.H.Vasilenko (1935) and New York Heart Association functional classification (NYHA) (1964).

According to this classification stages and functional classes of chronic heart failure are distinguished (Table 1 &6).

HF is manifested by systolic or diastolic dysfunction or both. Combined systolic and diastolic abnormalities are common.

In systolic dysfunction (primarily a problem of ventricular contractile dysfunction), the heart fails to provide tissues with adequate circulatory output. A wide variety of defects in energy utilization, energy supply, electrophysiologic functions, and contractile element interaction occur, which appear to reflect abnormalities in intracellular Ca++ modulation and cyclic adenosine monophosphate (cAMP) production.

Systolic dysfunction has numerous causes; the most common are coronary artery disease, hypertension, and dilated congestive cardiomyopathy. There are many known and probably many unidentified causes for dilated myocardiopathy. More than 20 viruses have been identified as causal. Toxic substances damaging the heart include alcohol, a variety of organic solvents, certain chemotherapeutic drugs (eg, doxorubicin), β-blockers, Ca blockers, and antiarrhythmic drugs.

Diastolic dysfunction (resistance to ventricular filling not readily measurable at the bedside) accounts for 20 to 40% of cases of HF. It is generally associated with prolonged ventricular relaxation time, as measured during isovolumic relaxation (the time between

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aortic valve closure and mitral valve opening when ventricular pressure falls rapidly). Resistance to filling (ventricular stiffness) directly relates to ventricular diastolic pressure; this resistance increases with age, probably reflecting myocyte loss and increased interstitial collagen deposition. Diastolic dysfunction is presumed to be dominant in hypertrophic cardiomyopathy, circumstances with marked ventricular hypertrophy (eg, hypertension, advanced aortic stenosis), and amyloid infiltration of the myocardium.

Pathophysiology

In LV failure, CO declines and pulmonary venous pressure increases. Elevated pulmonary capillary pressure to the levels that exceed the oncotic pressure of the plasma proteins (about 24 mm Hg) leads to increased lung water, reduced pulmonary compliance, and a rise in the O2 cost of the work of breathing. Pulmonary venous hypertension and edema resulting from LV failure significantly alter pulmonary mechanics and, thereby, ventilation/perfusion relationships. Dyspnea correlates with elevated pulmonary venous pressure and the resultant increased work of breathing, although the precise cause is debatable. When pulmonary venous hydrostatic pressure exceeds plasma protein oncotic pressure, fluid extravasates into the capillaries, the interstitial space, and the alveoli. Pleural effusions characteristically accumulate in the right hemithorax and later bilaterally. Lymphatic drainage is greatly enhanced but cannot overcome the increase in lung water. Unoxygenated pulmonary arterial blood is shunted past nonaerated alveoli, decreasing mixed pulmonary capillary PaO2. A combination of alveolar hyperventilation due to increased lung stiffness and reduced PaO2 is characteristic of LV failure. Thus, arterial blood gas analysis reveals an increased pH and a reduced PaO2 (respiratory alkalosis) with decreased saturation reflecting increased intrapulmonary shunting. Typically, PaCO2 is reduced too. A PaCO2 above normal signifies alveolar hypoventilation possibly due to respiratory muscle failure and requires urgent ventilatory support.

In RV failure, systemic venous congestive symptoms develop. Moderate hepatic dysfunction commonly occurs in CHF secondary to RV failure, with usually moderate increases in conjugated and unconjugated bilirubin, prothrombin time, and hepatic enzymes (eg, alkaline phosphatase, AST, ALT). However, in severely compromised

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circulatory states with markedly reduced splanchnic blood flow and hypotension, increases due to central necrosis around the hepatic veins may be severe enough to suggest hepatitis with acute liver failure. Reduced aldosterone breakdown by the impaired liver further contributes to fluid retention.

In systolic dysfunction, inadequate ventricular emptying leads to increased preload, diastolic volume, and pressure. Sudden (as in MI) and progressive (as in dilated cardiomyopathy) myocyte loss induces ventricular remodeling, resulting in increased wall stress accompanied by apoptosis (accelerated myocardial cell death) and inappropriate ventricular hypertrophy. Later, the ejection fraction falls, resulting in progressive pump failure. Systolic HF may primarily affect the LV or the RV (see above), although failure of one ventricle tends to lead to failure of the other.

In diastolic dysfunction, increased resistance to LV filling as a consequence of reduced ventricular compliance (increased stiffness) results in prolonged ventricular relaxation (an active state following contraction) and alters the pattern of ventricular filling. Ejection fraction may be normal or increased. Normally, about 80% of the stroke volume enters the ventricle passively in early diastole, reflected in a large e wave and smaller a wave on pulsed-wave Doppler echocardiography. Generally, in diastolic LV dysfunction the pattern is reversed, accompanied by increased ventricular filling pressure and a-wave amplitude.

Whether the failure is primarily systolic or diastolic and regardless of which ventricle is affected, various hemodynamic, renal, and neurohumoral responses may occur.

Hemodynamic responses: With reduced CO, tissue O2 delivery is maintained by increasing A-VO2. Measurement of A-VO2 with systemic arterial and pulmonary artery blood samples is a sensitive index of cardiac performance and reflects, via the Fick equation (VO2 = CO . A-VO2), CO (inversely related) and the body's O2 consumption (VO2--directly related).

Increased heart rate and myocardial contractility, arteriolar constriction in selected vascular beds, venoconstriction, and Na and water retention compensate in the early stages for reduced ventricular performance. Adverse effects of these compensatory efforts

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