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Congestive Heart Failure

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Congestive Heart Failure (CHF) accounts for about a quarter of a million deaths a year, and currently its prevalence among the U.S. population is 4.8 million (Health Grades, Inc). CHF occurs when the heart cannot meet the demands of the body. The symptoms are breathlessness and fatigue due to a buildup of fluid in and around the lungs. The failing heart inflates like a water balloon and, over time, gets stretched out to the point where it becomes a flimsy sac saturated with blood. If this sac is agitated with vigorous exercise it can, in some cases, fail. Thus whether a CHF patient should exercise is now a controversial issue. Cardiologists are often times reluctant to prescribe exercise to CHF patients because of the possibility that their failing hearts may have a negative response to the increased workload and stress of exercise (British Journal of Sports Medicine). The negative short-term responses to exercise may include a decrease in ejection fraction (fraction of blood pumped out of the heart), arrhythmias (arrhythmic beating of the heart), and a drop in oxygen saturation of the blood. CHF patients struggle on a daily basis to perform simple tasks such as walking up stairs or even dribbling a basketball in extreme cases; this results in a drastically compromised quality of life. On the other hand, exercise may allow optimal cardiac output and other secondary therapeutic effects. The purpose of this review is to provide an overview of the positive and negative effects of cardiovascular exercise on ejection fraction, the onset of arrhythmias and dyspnea (shortness of breath), and functional capacity in congestive heart failure patients.

Ejection Fraction

Cardiac muscle works similarly to skeletal muscle in that they both follow the Frank-Starling length-tension curve. This curve indicates that the contractility (force of contraction) of the heart increases with increased venous return. Venous return is the amount of blood that returns from the body to the heart in order to be pumped back out again into the lungs for oxygenation and, eventually, to the rest of the body. As venous return increases, the heart is stretched further and produces more contractile force; this happens in a healthy heart during exercise due to the increase in demands of the active skeletal muscle. However, the Frank-Starling curve is U-shaped and there is a point beyond which increased stretching leads to decreased contractile force. This is the level that CHF patients reach while performing simple tasks such as walking up a flight of stairs. Therefore, further stressing their hearts with vigorous cardiovascular exercise can result in decreased contractility, thus a decreased ejection fraction. "It (ejection fraction) is commonly expressed as a percentage and normally ranges from 55% to 80% (mean 67%) under resting conditions; ejection fractions of less than 55% indicate depressed myocardial contractility" (Lehmann, M). With a depressed ejection fraction, the heart of a CHF patient inflates like a saggy water-balloon during exercise as fluid builds up. Syncope (fainting) and Arrhythmias are common results of poor tolerance to physical exertion in CHF patients. Therefore, the short-term effects of exercise can be detrimental to someone with Congestive Heart Failure.

However, there have been studies that show that long-term effects of exercise can significantly improve cardiac function. When sedentary men aged 60-70 with normal ejection fractions were put on a 12-month cardiovascular training program their ejection fractions improved by 7% and stroke volumes improved by 22mL. Exercise has the same effect on subjects with impaired ejection fractions such as those with CHF. "In a randomized study of patients with CHF, involving 2 weeks of in hospital ergo meter exercise for 10 minutes 4 to 6 times per day, followed by 6 months of home-based ergo meter exercise training for 20 minutes per day at 70% of peak oxygen uptake, patients in the exercise training group showed not only improvements in New York Heart Association functional class, maximal ventilation, exercise time, exercise capacity, and decreased resting heart rate, but also a 14-mL increment of stroke volume at rest, with an increase in mean resting LV" left ventricular "ejection fraction from 30% to 35%" (Zhi You Fang). Along with the increase in strength of the heart muscle, exercise causes an increase in blood plasma volume, which causes the blood to become less viscous. The increase in blood volume can assist in a larger venous return, which in turn can cause an increase in contractility of the heart (assuming it does not pass the maximum level of contractility using the principle from the Frank-Starling length-tension curve).


"The initial response to heart failure and the incomplete filling of the arterial system leads to increased discharge of the sympathetic nervous system and increased secretion of renin and aldosterone, so that Na + and water are retained. These responses are initially compensatory, but eventually the failure worsens and the ventricles dilate" (Ganong WF). When the heart of CHF patients becomes distended like a balloon, the myocardium (heart muscle) becomes irritable and can cause deadly arrhythmias such as ventricular fibrillation to occur. Ventricular fibrillation is an asynchronous contraction of the ventricles (chambers) of the heart and if a patient stays in ventricular fibrillation, death will occur due to the lack of blood flow to the brain and the rest of the body. Arrhythmias are defects in the electrical conduction pathways of the heart. If the electrical signal is disrupted or altered, the heart will not contract properly (each chamber will contract at the wrong time or the chamber itself will not contract as one unit but will essentially vibrate); the result is an inefficient pumping of blood.

Decreased vagal activity (parasympathetic stimulation via the vagus nerve), which decreases HRV (heart rate variability) in between beats, is associated with a high mortality rate due to arrhythmias. "The 'UK-Heart' study which examined 433 patients with moderate or severe heart failure, showed that those with depressed HRV had an annual mortality rate of 51.4% compared to 5.5% in those with nearly normal values" (UK-heart). One long-term effect of exercise, however, is a decrease in sympathetic nervous activation to the heart and an increase in vagal activity (Lehmann, M). The decrease in sympathetic tone will not only decrease the occurrence of arrhythmias, but will lower heart rate both at rest and during exercise. Therefore, along with an increase in ejection fraction, an endurance-trained heart operates at a lower heart rate, demanding less oxygen. The result is a heart muscle



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