Essay: Heart failure

Heart failure occurs when the heart is unable to pump enough blood around the body and, thus, is unable to supply enough blood flow through the body, away from the heart. This results in insufficient oxygen delivery for organs and tissues. Most often in heart failure, the left ventricle fails. Right ventricle failure most often occurs secondary to left ventricle failure, but can also occur on its own (Klabunde, 2011).
Heart failure can be divided in several ways. First, there are two types of heart failure; acute heart failure and chronic heart failure. When talking about heart failure, most likely chronic heart failure is meant. Acute heart failure occurs rather spontaneously within several hours or days. In chronic heart failure the disease develops gradually (Bouman, Bernards, & Boddeke, 2008). Secondly, heart failure can be divided in mild heart failure and severe heart failure. Patients suffering from mild heart failure have a reduced exercise capacity. These patients develop a shortness of breath during physical activity, which is called exertional dyspnoea (Klabunde, 2011). Patients suffering from more severe forms of heart failure are unable to perform hardly any physical activity. These patients will most likely experience dyspnoea even when they are not doing any exercise at all. In the latter patients are unable to do their daily activities (Klabunde, 2011).
Pathophysiology
Heart failure can be caused by several factors. It can be caused by factors from the heart itself or from external factors that influence the function of the heart. The biggest cause of heart failure is coronary artery disease. This reduces the blood flow through the coronary artery and, thus, the oxygen supply to the cardiac muscle. This causes hypoxia and a disabled function of the cardiac muscle (Klabunde, 2011). Another common cause of heart failure is cardiac muscle infarction. Tissue that has been infarcted cannot contribute to the generation of heart contractions anymore. Tissue areas that are not infarcted have to take over this movement, which is very stressing on these tissues. After some time, the non-infarcted tissue cannot keep up with the demands anymore resulting in heart failure. Less common heart conditions that may lead to heart failure are valve diseases and congenital defects, diseases or inflammation of the heart muscle tissue and chronic dysrhythmia (Klabunde, 2011).
Heart failure can be the result of an impaired ability of the cardiac muscle to contract, this is called systolic heart failure. Heart failure can also be the result of impaired filling of the heart, this is called diastolic heart failure (Rutten, Walma, Kruizinga, Bakx, & Van Lieshout, 2009).
Systolic heart failure is caused by changes in the signal transduction and EC-coupling (excitation-contraction coupling), which disables the contraction of the cardiac muscle (Klabunde, 2011). A disabled contraction of the cardiac muscle results in a decrease in stroke volume and it causes an increase in preload of the heart. This increase of preload is a compensation of the body. It activated the Frank-Starling mechanism to keep the stroke volume up, since there is a loss of cardiac muscle contraction. If this preload would not undergo this increase to compensate, the stroke volume would decline even further. The longer systolic heart failure progresses, the heart will become less able to compensate this using the Frank-Starling mechanism. The sarcomeres in the heart will become exhausted, since they have to extend to their maximal length. When systolic heart failure become chronic, the ventricle anatomically remodels (Rutten et al., 2009). It dilates because of new sarcomeres added to the existing ones. This prevents the sarcomeres from overstretching in situations of raised filling pressure and volume of the ventricle. The dilated ventricle has a higher performance so that it can adapt to large end-diastolic volumes without having an outrageous raise in end-diastolic pressure (Rutten et al., 2009).
Diastolic heart failure is caused by a disabled filling of the ventricle. It can both occur by disabled ventricular performance, which happens with hypertrophy of the ventricle or by disabled relaxation. Hypertrophy of the ventricle is often a result of chronic hypertension, which thickens the wall of the ventricle by adding new sarcomeres to the existing ones (Klabunde, 2011). This hypertrophy of the ventricle allows the heart to pump with more force against aorta pressure. This results in less ventricular filling and an increase of the end-diastolic pressure. Another cause of diastolic heart failure is hypertrophic cardiomyopathy. This is a cardiac disease caused by a genetic error that changes the structure of the cardiac muscle fibres (Klabunde, 2011).
Clinically, it is pretty common that patients with chronic heart failure suffer from both systolic and diastolic heart failure. This combination of systolic and diastolic heart failure results in an increase in end-systolic volume and a decrease in end-diastolic volume (Klabunde, 2013). This results in a severe decrease of the stroke volume of the heart. Suffering from both systolic and diastolic heart failure can result in severe pulmonary congestion and, thus, shortness of breath for the patients (Klabunde, 2013).
Beneficial effects of exercise training on heart failure
Multiple studies have shown a positive relationship between physical exercise and heart failure in patients suffering from heart failure.
Regularly performing physical activity stimulates vasodilation in skeletal muscles, which improves the blood flow to the muscles. The cardiac output also increases. Both these mechanisms result in an improvement of exercise capacity. Exercise training also leads to remodelling of the cardiac muscle, especially the left ventricle, which results in an improved contractility of the heart muscle (Hambrecht, Gielen, Linke, & et al., 2000). This improved contractility results in an increase in ejection fraction and a decrease in end-systolic volume and end-diastolic. These changes lead to an increase of the stroke volume. Since a decreased stroke volume is the greatest limiting factor for physical exercise in patients suffering from heart failure, the increase of stroke volume is a beneficial effect of physical exercise training. So when the stroke volume increases, patients will be able to perform higher (Hambrecht et al., 2000).
A study conducted by Hambrecht et al. (2000) was performed to determine the effects of exercise training on heart failure. The results of this study show the changes in the main hemodynamic values in rest and during peak exercise. In the exercise group, the stroke volume and cardiac output increased, both in rest and during peak exercise from baseline to 6 month follow up (Hambrecht et al., 2000). This means that the heart is more capable of pumping blood around the body and supplying the tissues with sufficient oxygen. In the control group, the stroke volume and cardiac output remained almost the same from baseline to 6 month follow up (Hambrecht et al., 2000). This means that the exercise program conducted in this study has a positive effect on the stroke volume and cardiac output of the heart and, thus, on the pump capacity of the heart. When the pump function of the heart increases, patients suffering from heart failure will experience less symptoms and discomforts.
Exercise program
Before starting an exercise program the patients have to be checked to determine whether they are stable enough to participate in an exercise program. The maximum heart rate has to be estimated. This maximal heart rate is estimated with the equation 220-age (Beale et al., 2010). In patients using beta blockers, an extra 30 beats/minute have to be extracted from the 220 beats/minute. Both these factors determine the intensity of the exercise program the patient has to follow (Beale et al., 2010).
The exercise program consists of endurance training which is executed at a submaximal level. The endurance training consists of three different exercises; walking a treadmill, cycling and aerobics. Each these exercises are performed once a week, so the patients exercise three times a week. The exercises are executed in a group of patients. The exercises are executed in a gym. This gym is equipped for heart failure patients, and equipped with all necessary medical equipment possibly needed. During every training session, the patients wear a portable heart rate monitor to make sure they do not exceed their estimated maximum heart rate. Patients are asked to give a sign when they experience symptoms like dyspnea, angina pectoris of other discomforts.
Each training session consists of a warming up, main exercise, cool down and an evaluation.
The warming up always consists of 15 minutes of walking on low intensity. Low intensity walking is defined as 3-5 km/h (Funk et al., 2012). During this warming up, patients should not experience any discomfort. If they do, they are not stable enough to perform the main exercise.
After the warming up the main exercise training starts. Depending on the exercise program that day, the patients walk on the treadmill, cycle or participate in aerobics. All these trainings are executed at 50-70% of their maximal heart rate for 20 to 40 minutes, depending on the patients physical condition and discomforts (Beale et al., 2010).
After the main training, patients walk the treadmill again for 15 minutes at 3-5 km/h (Funk et al., 2012).
Every time the patients have completed a training, patients are asked to fill in a short questionnaire about their experiences during the training. They are asked about the intensity of the training, the duration of the training and the possible discomforts or symptoms they experienced during exercising.
References
Beale, L., Carter, H., Doust, J., Brickley, G., Silberbauer, J., & Lloyd, G. (2010). Exercise heart rate guidelines overestimate recommended intensity for chronic heart failure patients. from http://bjcardio.co.uk/2010/05/exercise-heart-rate-guidelines-overestimate-recommended-intensity-for-chronic-heart-failure-patients/
Bouman, L. N., Bernards, J. A., & Boddeke, H. W. G. M. (2008). Medische fysiologie: Bohn Stafleu van Loghum.
Funk, R. E., Taylor, M. L., Creekmur, C. C., Ohlinger, C. M., Cox, R. H., & Berg, W. P. (2012). EFFECT OF WALKING SPEED ON TYPING PERFORMANCE USING AN ACTIVE WORKSTATION. Perceptual and Motor Skills, 115(1), 309-318. doi: 10.2466/06.23.26.PMS.115.4.309-318
Hambrecht, R., Gielen, S., Linke, A., & et al. (2000). Effects of exercise training on left ventricular function and peripheral resistance in patients with chronic heart failure: A randomized trial. JAMA, 283(23), 3095-3101. doi: 10.1001/jama.283.23.3095
Klabunde, R. (2011). Cardiovascular physiology concepts: Lippincott Williams & Wilkins.
Klabunde, R. (2013). Regulation of Stroke Volume. from http://www.cvphysiology.com/Cardiac%20Function/CF002.htm
Rutten, F., Walma, E., Kruizinga, G., Bakx, H., & Van Lieshout, J. (2009). NHG-standaard hartfalen NHG-Standaarden 2009 (pp. 193-212): Springer.