Heart failure is a pathophysiologic condition characterized by the heart’s inability to generate sufficient cardiac output, resulting in either inefficient tissue perfusion or increase in the diastolic filling pressure of the left ventricle, or both, which lead to increased pulmonary capillary pressure (McCance, Huether, Brashers, & Rote, 2014). Heart failure is a leading cause of death in the US (McCance et al., 2014; Mozaffarian et al., 2015). American Heart Association has estimated that in 2013, cardiovascular diseases were responsible for 30.8% of all deaths in the US, or 222.9 per 100,000 deaths (Mozaffarian et al., 2015). The 2013 overall rate of death suggested that about one American die every 40 seconds as a result of a cardiovascular disease (Mozaffarian et al., 2015).
Left heart failure, also known congestive heart failure, is characterized by reduced ejection fraction or preserved ejection fraction, which might occur together or singly. Reduced ejection fraction is a consequence of systolic heart failure while preserved ejection fraction occurs following a diastolic heart failure (McCance et al., 2014). Systolic heart failure occurs when the ejection fraction goes below 40%, which impairs the ability of the heart to generate sufficient cardiac output to supply critical tissues. An injury to the myocardium is responsible for heart failure (McCance et al., 2014).
An injury to the myocardium impairs the contractility, which in turn leads to decreased stroke volume. Stroke volume, together with the heart rate, influences cardiac output. In addition to contractility, other factors that affect stroke volume are preload and afterload. As the stroke volume falls, the left ventricular end-diastolic volume (LVEDV) increases. The result of this is heart dilation and an increase in preload. An increase in preload (LVEDV) is associated with a decrease in contractility or an excess of plasma volume. Although elevated levels of LVEDV might enhance cardiac output, the improvement is short-lived and goes only to a certain point. At such a point, continuously rising preload results in the stretching of the myocardium, whose eventual result might be the dysfunction of the sarcomeres and decreased contractility.
Increased peripheral vascular resistance (PVR) results in increased afterload, which is an increased resistance to ventricular ejection. The increase in PVR leads to an increase in the left ventricle workload due to resistance to the ventricular empting. The result of the sustained afterload is the hypertrophy of the myocardium, which is mediated by angiotensin II and catecholamines. The result of this pathologic increase in muscle mass is an increased demand for oxygen and energy. When myocardium’s demand for metabolic energy exceeds the ability of myocytes to produce adequate ATP, the contractility of the myocardium is grossly impaired.
Lack of energy also affects the myocytes themselves and ventricular remodeling, that severely degrades contractility and consequently the ventricular function (Opie, Commerford, Gersh, & Pfeffer, 2006). Remodeling may also depose the collagen between the myocytes, which may interfere with the integrity cardiac muscle, decrease contractility, and increase the vulnerability of the ventricle to dilation and failure (Opie et al., 2006). The falling cardiac output is associated with diminished renal perfusion as RAAS is activated, which result in increased PVR and plasma volume. This results in further increases in afterload and preload. Additionally, underperfusion triggers central circulation baroreceptors which stimulate the SNS, leading to additional vasoconstriction and trigger production of antidiuretic hormone from by the hypothalamus. The decreasing contractility-increasing preload-increasing afterload vicious progressively worsens the left ventricle heart failure (McCance et al., 2014). The symptoms of systolic heart failure are a consequence of pulmonary vascular congestion and inadequate perfusion of the systemic circulation (McCance et al., 2014). The major symptoms are dyspnea, orthopnea, fatigue, edema, cough of frothy sputum, pulmonary edema, and decreased urine output (McCance et al., 2014).
Heart failure with preserved ejection, or diastolic heart failure, might occur singly or together with systolic heart failure. Accounting for about half of all left heart failure cases, isolated diastolic heart failure is described as pulmonary congestion despite normal stroke volume and cardiac output (McCance et al., 2014). The most important causes of diastolic heart failure are myocardial hypertrophy due to hypertension and myocardial ischemia resulting in ventricular remodeling. Hypertrophy and ischemia impair the ability of the myocytes to engage in active pumping of calcium from the cytosol, which results in deficient relaxation. As it is the case with systolic heart failure, the major feature of diastolic heart failure is the sustained activation of the RAAS and SNS (McCance et al., 2014).
Therefore, decreased compliance of the left ventricle and abnormal diastolic relaxation are the major pathophysiologic changes. Reduced ventricular compliance is associated with alterations in myocardial structure, such as the changes in the molecular structure of collagen. Abnormal diastolic relaxation (lusitrophy) occur following alterations in calcium transport from myocytes, and may be linked to the ATPase. The result of the two is a noncompliant and poorly lusitropic ventricle, which is unable to allow filling with blood without a meaningful resistance and increased wall tension. Therefore, diastolic heart failure occurs because a normal LVEDV is linked to an increased LVEDP. This results in an increase in left atrial pressure, which is reflected back into the pulmonary circulation, resulting in pulmonary edema. The increase in left atrial pressure is worsened by increased speed in the ventricular filling. Thus symptoms are made worse with tachycardia such as exercise. People with diastolic heart failure might have dyspnea on exertion, fatigue, pulmonary edema, pulmonary hypertension, and right ventricular failure (McCance et al., 2014).
In conclusion, heart failure is a major cause of death in the US. Left heart failure may be categorized into systolic heart failure (characterized by reduced ejection fraction) or diastolic heart failure (characterized by preserved ejection fraction), which might occur together or singly. Both systolic and diastolic left heart failure types occur as a result of the inability of the ventricles to fill with and eject blood, which might be due to functional or structural damage to the myocardium (McCance et al., 2014).
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2014). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). ST. Louis, MI: Elsevier/Mosby.
Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M., & Howard, V. J. (2015). Heart disease and stroke statistics—2016 update: A report from the American Heart Association. Circulation, 132(000-000), e1-e323.
Opie, L. H., Commerford, P. J., Gersh, B. J., & Pfeffer, M. A. (2006). Controversies in ventricular remodelling. The Lancet, 367(9507), 356-367.