Left Heart Failure
| Overview |
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- Heart Failure is a clinical syndrome which occurs when the left heart is unable to produce sufficient cardiac output to meet physiological demands. A wide variety of etiological processes can result in heart failure; however, common pathophysiological and clinical sequelae result as discussed below.
| Basic Subtypes |
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- Overview
- The heart's cardiac output is ultimately a product of the heart's stroke volume and heart rate. In general, etiologies of heart failure result in deficiencies of total stroke volume. Such etiologies can be subdivided by assessing the clinical status of the patient's ejection fraction. Epidemiologically, each subtype accounts for nearly half of all heart failure patients.
- Systolic Failure
- Systolic Failure, sometimes termed "Forward Failure", is defined by a failing heart with a depressed left ventricular ejection fraction (<40%). Systolic Failure occurs when the left ventricle cannot eject sufficient blood during systole, thus resulting in reduced stroke volume. Defects in myocardial contractility or a pathologically increased afterload are often the cause of systolic dysfunction.
- Diastolic Failure
- Diastolic Failure, sometimes termed "Backward Failure", is defined by a failing heart with a largely intact left ventricular ejection fraction (>40%). Diastolic Failure occurs when the left ventricle does not fill sufficiently with blood during diastole, thus resulting in reduced stroke volume. Defects in relaxation or physical stiffness of the left ventricle are often the cause of Backward Failure.
| Etiologies |
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- Overview
- As mentioned, a wide variety of etiologies can result in heart failure although each tends to produce either Systolic or Diastolic Failure. In developed countries, Ischemic Heart Disease and hypertension likely contribute to the most cases
- Below we have listed possible etiologies and categorized them according to the basic subtypes discussed above.
- Systolic Dysfunction
- Ischemic Heart Disease, myocarditis, dilated cardiomyopathy: Cardiomyocyte dysfunction either due to direct damage or a disease process manifests as globally reduced contractility:
- Aortic Valve Regurgitation, Mitral Valve Regurgitation, dilated cardiomyopathy: Pathologically high preload pushes Frank-Starling Relationship into pathological zone, thus reducing ventricular ejection. These etiologies are sometimes referred to "Volume Overload".
- Hypertension, Aortic Valve Stenosis: Pathologically high afterload prevents sufficient left ventricular emptying
- Diastolic Dysfunction
- Hypertrophic Cardiomyopathy, that is, hypertrophy secondary to chronic hypertension: Results in a hypertrophied left ventricle that cannot relax sufficiently during diastole
- Restrictive Cardiomyopathy, amyloidosis, hemochromatosis: Abnormally stiff left ventricular wall cannot accept sufficient blood during diastole
- Cardiac Tamponade: Fluid-filled pericardial sac places external pressure on the heart and prevents proper diastolic filling of the ventricle.
| Compensation |
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- Overview
- The etiologies described above ultimately reduce cardiac output either by directly insulting left ventricular contractility, placing an excessive afterload on the heart, or preventing sufficient filling during diastole. Whatever the etiology, a wide variety of compensatory mechanisms are engaged to maintain sufficient systemic arterial pressure in the face of declining cardiac output. Although these compensatory mechanisms are able to help maintain arterial pressure, they often do so by placing additional functional burdens on the heart, thus compounding the initial insult.
- Frank-Starling Relationship
- Etiologies which reduce the ejection fraction will result in elevated Ventricular End Systolic Volumes (VESVs). Given normal ventricular entry of blood during diastole, a higher VEDV will result. Because of the Frank-Starling Relationship, this higher preload will improve ventricular ejection and this can help compensate for the reduced contractility. However, this only occurs if the Frank-Starling Relationship is operating in its "Physiological Range". If the VEDV exceeds beyond a certain threshold, into the "Pathological Range", further ventricular filling can reduce ventricular ejection and compound heart failure.
- SNS Activation
- Reduced cardiac output in the presence of normal systemic vascular resistance will cause a reduction in the systemic arterial pressure (See: Systemic Arterial Pressure Regulation). As discussed in Short-term regulation of arterial pressure, such a reduction will be sensed by baroreceptors which will activate the vasomotor center to increased cardiovascular SNS tone. The following effects of cardiovascular SNS tone are discussed more fully in Systemic Arterial Pressure - Autonomic Control; however we mention them briefly below. Increased SNS tone to the heart boosts cardiac contractility and heart rate, thus increasing cardiac output. Increased SNS tone to arterioles causes vasoconstriction and boosts systemic vascular resistance, helping maintain arterial pressure. Increased SNS tone to veins causes venoconstriction and boosts venous return, which increases preload on the heart and helps increase cardiac output courtesy of the Frank-Starling Relationship.
- However, increased systemic vascular resistance also increases the afterload on the heart, which significantly increases cardiac oxygen demand and can compound heart failure. Increased venous return can also push the Frank-Starling Relationship into its pathological range and thus further reduce ventricular ejection, especially due to etiologies associated with "Volume Overload".
- RAAS System Activation
- The RAAS System is activated in scenarios of reduced systemic arterial pressure (See: RAAS System). Released Angiotensin II increases systemic vascular resistance and thus helps maintain arterial pressure; however, as discussed above this adds a significant functional burden on the failing heart. Released Angiotensin II and aldosterone also enhances salt and water resorption by the kidneys which increases the total blood volume and thus venous return to the heart. Normally, increased venous return boosts cardiac preload, courtesy of the Frank-Starling Relationship, and thus increases ventricular ejection. However, as described above, further venous return to a volume overloaded heart can compound heart failure by pushing the Frank-Starling relationship into the pathological range.
- Ventricular Remodeling
- Over time, the failing heart undergoes physical remodeling in an attempt to counteract hemodynamic stress. This process of ventricular hypertrophy initially helps relieve some of this stress encountered by the failing. However, as remodeling progresses the physical changes become maladaptive and contribute to further heart failure.
| Clinical Consequences |
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- Overview
- The failing left heart results in a characteristic clinical syndrome described below. In certain cases, heart failure manifests rapidly following a clear insult to the myocardium, such as a myocardial infarction. However, in many cases the pathogenic processes responsible for heart failure can occur subclinically for months to years and suddenly come to clinical attention. In such cases, the insidious decline of cardiac function may not be apparent due to the heart's significant functional reserve; however, symptomology may manifest rapidly following a transient increase in physiological demand on the heart.
- Pulmonary Symptoms
- Pulmonary symptomology is perhaps the most dominant clinical feature of left heart failure. This occurs in the context of forward or backward failure and results from an inability of the left heart to eject blood into the systemic circulation, yielding backup of blood into the pulmonary circulation and ultimately pulmonary edema. The consequent presence of fluid within the pulmonary interstitium and alveoli ultimately reduces lung compliance, yielding a restrictive lung disease which increases the work required to breathe.
- Additionally, irritation of pulmonary J Receptors changes the patient's breathing pattern to one characterized by rapid, shallow breaths. In early stages, patient's often complain of dyspnea on exertion which progresses to dyspnea even at rest as cardiac function continues to decline. Because edema fluid redistributes to cover more of the lung upon laying down, patients will complain of orthopnea or a nocturnal cough and frequently sleep with several pillows under their backs to elevate their position during rest. Certain patients will display "Paroxysmal Nocturnal Dyspnea" (PND) characterized by severe fits of dyspnea and coughing that wake the patient several hours after sleeping. The pathophysiology of this condition is still somewhat unclear.
- Right Heart Failure
- Backup of blood into the pulmonary circulation will eventually result in pulmonary hypertension which over time will yield Right Heart Failure. Consequently, the symptomology of right heart failure will ultimately manifest if left cardiac function does not improve.
- Other Symptoms
- Fatigue and muscle weakness: Likely due to skeletal muscle abnormalities
- Altered Mental Status: Manifests as a dullness of mental status possibly due to reduced cerebral perfusion
- Nocturnal polyuria: Reduced renal perfusion during the day results in excessive diurnal fluid retention. When the patient lies down to sleep, renal perfusion improves and the kidney begins excreting the retained fluid, manifesting as nocturnal polyuria
- Physical Signs
- Rales: Due to pulmonary edema
- Tachycardia and diaphoresis: Due to chronic SNS tone
- Reduced pulse pressure: Due to reduced stroke volume
- Cachexia: A late-stage manifestation with cryptic pathogenesis
| High-output Heart Failure |
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- The discussion above refers to conditions in which the heart cannot meet a normal physiological demand for its cardiac output. However, in certain cases, a primary pathophysiologic process can substantially increase the demand for cardiac output beyond that normally required of the heart. Even so, a fully healthy heart should be able to meet this extra functional demand; however, given some underlying cardiac pathology, this extra demand can lead to the clinical syndrome of left heart failure. Although encountered with much less frequency, such "High-output Heart Failure" scenarios may be encoutered in the following contexts: Hyperthyroidism, Wet Beri-Beri (Vitamin B1 deficiency), Chronic Anemia, or a Large arteriovenous fistula.