Congestive Heart Failure - Diastolic Topic Review
Congestive heart failure occurs when the cardiac output is not adequate enough to meet the demands of the body. This can occur for several reasons, as congestive heart failure is the predominant clinical presentation in multiple disease states.
Heart failure can be due to the following:
- Systolic dysfunction (reduced ejection fraction)
- Diastolic dysfunction (relaxation or filling abnormality)
- Valvular heart disease
- Right heart failure
- High output congestive heart failure (i.e. severe anemia, arteriovenous malformations)
A review of diastolic congestive heart failure is presented here. Reviews of systolic congestive HF, valvular heart disease, right HF and high output HF are presented elsewhere.
Pathophysiology – Congestive Heart Failure - Diastolic
Diastolic dysfunction occurs when the left ventricular myocardium is noncompliant and not able to accept blood return in a normal fashion from the left atrium. This can be a normal physiologic change with aging of the heart or result in elevated left atrial pressures, leading to the clinical manifestations of diastolic congestive heart failure.
Although there is some degree of activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system in states of diastolic HF, it is not as dramatic as seen with systolic HF. Also, these neurohormonal systems do not exert the same negative remodeling effect on the heart during diastolic heart failure as occurs during systolic congestive HF.
Below is a schematic of the neurohormal mechanisms present in congestive heart failure:
Etiology – Congestive Heart Failure - Diastolic
The various causes for diastolic congestive heart failure are listed below:
- Hypertensive heart disease
- Aging of the heart
- Restrictive cardiomyopathy
- Valvular heart disease
- Constrictive pericarditis
Hypertension causes left ventricular hypertrophy, or LVH, and impaired relaxation. Over time, this progresses, resulting in higher degrees of diastolic dysfunction, low cardiac output and symptoms of congestive HF.
The aging process of the heart is not well understood, but fibrotic changes are seen within the myocardium. This results in a relaxation abnormality that is almost universally present by the age of 60. In the elderly, this can progress, causing significant diastolic impairment and congestive heart failure.
Restrictive cardiomyopathies frequently cause deposition of substances (i.e. amyloid protein) within the myocardium, causing diastolic relaxation abnormalities and, when severe, diastolic congestive HF.
Valvular heart disease such as mitral stenosis technically causes heart failure due to diastolic dysfunction of the left ventricle. Severe aortic stenosis causes LVH, and when left ventricular pressures increase a significant amount, diastolic HF can occur.
When a tachyarrhythmia such as atrial fibrillation occurs with an uncontrolled ventricular response, congestive HF can occur in the setting of normal systolic function from a shortened diastolic filling time. This is technically a form of diastolic HF; however, once ventricular rates are controlled, the cardiac hemodynamics should dramatically improve.
Symptoms – Congestive Heart Failure - Diastolic
The general symptoms of congestive heart failure are the same regardless of the etiology (systolic or diastolic) and attributed to either fluid retention (related to the activated RAAS) or low cardiac output. They can also be categorized as from left HF versus right HF.
Left HF will result in low cardiac output symptoms and transmission of the increased left-sided cardiac pressures into the lungs, causing pulmonary edema and a sense of dyspnea. With physical exertion, the heart demands increased cardiac output that is not able to be satisfied in states of HF, and thus left heart pressures increase significantly, causing this transient pulmonary edema.
As those increased pressures from the left heart affect the right ventricle, right heart failure can ensue. The most common cause of right HF is left HF.
Right heart failure symptoms include lower extremity-dependent edema. When the legs are elevated at night, the fluid redistributes centrally, causing pulmonary edema that results in orthopnea (dyspnea while laying flat) or paroxysmal nocturnal dyspnea, or PND. Hepatic congestion can occur, causing right upper quadrant abdominal pain.
Symptoms related to low cardiac output include fatigue and weakness. In extreme cases, cardiac cachexia can occur.
The New York Heart Association functional classification system helps to categorize patients based on their symptoms of heart failure.
Class I: No symptoms of heart failure
Class II: Symptoms of heart failure with moderate exertion such as ambulating two blocks or two flights of stairs
Class III: Symptoms of heart failure with minimal exertion such as ambulating one block or one flight of stairs, but no symptoms at rest
Class IV: Symptoms of heart failure at rest
Recall that the NYHA functional classification differs from the American College of Cardiology/American Heart Association heart failure classification, in that the former allows movement from one class to the other while the latter classification does not.
Diagnosis – Congestive Heart Failure - Diastolic
Echocardiography is the gold standard to diagnose diastolic dysfunction. There are four grades of diastolic dysfunction, as described below. Clinical manifestations of congestive heart failure may start to occur once grade II diastolic dysfunction is present, but not in the presence of grade I diastolic dysfunction (impaired relaxation).
Grade I (impaired relaxation): This is a normal finding. The E wave velocity is reduced, resulting in E/A reversal (ratio < 1). The left atrial pressures are normal. The deceleration time of the E wave is prolonged, measuring greater than 200 milliseconds. The e/e’ ratio measured by tissue Doppler is normal.
Grade II (pseudonormal): This is pathological and results in elevated left atrial pressures. The E/A ratio is normal (0.8 +- 1.5), and the deceleration time is normal (160-200 ms), but the e/e’ ratio is elevated. The E/A ratio will be less than 1 with Valsalva. A major clue to the presence of grade II diastolic dysfunction vs. normal diastolic function is the presence of structural heart disease such as left atrial enlargement, left ventricular hypertrophy or systolic dysfunction. If significant structural heart disease is present, and the E/A ratio as well as the deceleration time appear normal, suspect a pseudonormal pattern. Valsalva distinguishes pseudonormal from normal as well as the e/e’ ratio. Diuresis can frequently reduce the left atrial pressure, relieving symptoms of HF and returning the hemodynamics to those of grade I diastolic dysfunction.
Grade III (reversible restrictive): This results in significantly elevated left atrial pressures. Also known as a “restrictive filling pattern,” the E/A ratio is greater than 2, the deceleration time is less than 160 ms and the e/e’ ratio is elevated. The E/A ratio changes to less than 1 with Valsalva. Diuresis can frequently reduce the left atrial pressure, relieving symptoms of HF and returning the hemodynamics to those of grade I diastolic dysfunction.
Grade IV (fixed restrictive): This indicates a poor prognosis and very elevated left atrial pressures. The E/A ratio is greater than 2, the deceleration time is low, and the e/e’ ratio is elevated. The major difference distinguishing grade III from grade IV diastolic dysfunction is the lack of E/A reversal with the Valsalva maneuver (no effect will be seen with Valsalva). Diuresis will not have a major effect on the left atrial pressures, and clinical HF is likely permanent. Grade IV diastolic dysfunction is present only in very advanced HF and frequently seen in end-stage restrictive cardiomyopathies such as amyloid cardiomyopathy.
Treatment – Congestive Heart Failure - Diastolic
There is a relative lack of data to guide medical therapy in patients with diastolic congestive heart failure, especially when compared with systolic congestive heart failure.
The ACC/AHA guidelines give three class I recommendations to medically treat chronic diastolic congestive HF.
The first is to control the heart rate in patients with atrial fibrillation in order to improve diastolic filling. Tachycardia shortens diastolic filling time, and thus keeping heart rates below 100 beats per minute (and preferably 60-80 bpm) will improve cardiac output when significant diastolic HF is present. Rate control can be achieved using beta-blockers, nondihydropyridine calcium channel blockers or digoxin.
The second is to control systolic and diastolic blood pressure using the standard treatment for hypertension.
The third is to use diuretics to control pulmonary congestion and peripheral edema.