Heart failure and valvular heart disease



Heart failure and valvular heart disease



Chris L. Wells


Introduction


Despite the increase in diagnostic procedures and medical management, heart disease continues to be one of the most common causes of morbidity and mortality in the United States of America. The rise in life expectancy, increases in hypertension, obesity, diabetes mellitus and sedentary lifestyles are all contributing to the increasing cardiovascular disease. This chapter will briefly discuss heart failure and valvular disease.


Heart failure


Heart failure (HF) is defined as the inability of the heart to pump blood at a sufficient rate to meet the metabolic demands of the body. HF can be the result of many different diseases; therefore, it is important to complete a thorough history taking and evaluation of the patient with HF to identify the underlying pathology and any factors that exacerbate the HF. The heart may compensate for years before the patient reaches a level of dysfunction that leads to the clinical presentation of HF. In many cases, it is an acute event that places additional stress on the heart, beyond its ability to circulate a sufficient blood flow, leading to clinical HF. Exacerbation or progression of other chronic diseases, such as renal insufficiency, infections, cardiac arrhythmias, uncontrolled hypertension or diabetes, and poor dietary consumption, can precipitate the insidious onset of clinical signs and symptoms associated with HF (see Chapters 41 and 46).


HF can be categorized in many ways. The Heart Failure Society of America describes two types of HF. HF with reduced left ventricular function, which is commonly associated with a dilated ventricle, is referred to as systolic HF where the myocardial contraction is ineffective in circulating blood forward into the pulmonary and systemic circulations. In HF with preserved left ventricular function, also known as diastolic dysfunction, the ventricles do not relax to allow for sufficient filling. The patient with HF can be clinically present in an acute or a chronic medical state. Finally, HF can present as predominately left HF or right HF, or as biventricular failure (Lindenfeld et al., 2010).


Heart failure, a clinical syndrome, is associated with symptoms of shortness of breath with exertion and rest, fatigue and tiredness, and signs of abnormal heart rate, elevation in respiratory rate, pulmonary rales, pleural effusions, jugular vein distension, peripheral edema and hepatomegaly. The heart has structural or functional changes that lead to its inability to pump blood at a sufficient rate to meet the metabolic demands of the body (Lindenfeld et al., 2010; Shiba & Shimokawa, 2011). The body attempts to compensate by increasing sympathetic nervous system (SNS) activity which increases heart rate and contractility to improve cardiac output. This increase in the SNS also leads to increased oxygen demand and additional inflammation and stress that eventually will further impair heart function (Barnes et al., 2011).


Congestive heart failure (CHF) is a common clinical term used to describe a cluster of signs and symptoms associated with HF. When cardiac pump function is inadequate to meet the circulatory demands of the body, the body attempts to decrease the volume of blood the heart has to circulate, which leads to fluid retention. Fluid leaves the vascular system and is stored in various parts of the body, hence the term ‘congestive heart failure’. When the left ventricular pump function is impaired, excess fluid is stored in the pulmonary interstitium to decrease the workload of the left ventricle. Left ventricular dysfunction is commonly associated with an increase in stress to the right ventricle. Right ventricular myocardial dysfunction leads to an increased blood volume in the venous system and liver which is associated with jugular vein distention, peripheral edema, hepatomegaly and abdominal ascites.


Causes of ventricular failure


To understand heart failure, it is important to understand the basic cardiac cycle. Blood flows from the venous system and the pulmonary capillary beds into the right and left atria respectively. Once there is a sufficient volume and, therefore, enough pressure in the atria, the atrioventricular, tricuspid and mitral valves will open to allow filling of the ventricles. When the atria contract another 15–20% of the blood volume is delivered into the ventricles and the atrioventricular valves close. The right and left ventricles then begin to contract, generating enough force to open the semilunar, pulmonic and aortic valves and eject blood into the pulmonary circulation for gas exchange and into the systemic circulation to meet the metabolic demands of the body’s cells.


Coronary artery disease, which leads to myocardial impairment, is one of the most common causes of HF (McKenna et al., 2012); however, there are many other diseases, such as valvular lesions, viral infections, myocardial dysfunction and pulmonary disease that can also lead to the development of HF. In older adults coronary artery disease and aortic valvular disease are the most common causes of HF (McKenna et al., 2012; Vasques et al., 2012). Along with the diagnosis, it is important to identify factors that exacerbate HF or lead to an uncompensated state, such as excessive fluid consumption, arrhythmias, systematic infection and kidney failure. Understanding the pathology and contributing factors can aid in the delivery of prompt and appropriate medical intervention and patient education.


The most common cause of right ventricular failure (RVF) is left ventricular pump dysfunction. Failure to pump blood forward into the aorta leads to a backflow of blood and an increase in pressure within the left atrium and eventually within the pulmonary system. The right ventricle is not anatomically designed to pump under elevated pressure, which leads to RVF. Right HF may also result from pulmonary hypertension caused by a pulmonary disease such as emphysema and from a pulmonary embolism. Finally, RVF can also be the result of mitral or tricuspid valve disease, restrictive or hypertrophic cardiomyopathies and viral or idiopathic myocarditis.


Left ventricular failure (LVF) leads to lower systemic cardiac output. It can be caused by the long-term adverse effects of hypertension, aortic or mitral valve disease and coronary artery disease. Coronary artery disease can cause pump dysfunction because of the long-term subtle effects of myocardial ischemia or because of an acute ischemic event, such as an abrupt rupture of an atherosclerotic plaque, which leads to a myocardial infarction. Less frequently, LVF may also occur because of a systemic condition such as septic shock. During this critical medical state, the left ventricle attempts to increase cardiac output to meet the high oxygen demand of the body. The stress from this physiological imbalance may lead to the left ventricle being unable to meet the body’s needs, resulting in LVF.


Contributing factors


There are several factors that can lead to HF. These factors can either increase the body’s needs or further decrease cardiac output. Cardiac arrhythmias such as atrial fibrillation can decrease cardiac output in the presence of myocardial pump dysfunction. Atrial fibrillation is a common arrhythmia in older adults and is one of the most common arrhythmias associated with HF. With atrial fibrillation, the atria do not contract as a unit and therefore the ventricles do not receive the last 15–20% of blood volume, causing the loss of the ‘atrial kick’. In the presence of pump dysfunction, atrial fibrillation may lead to a loss of filling which also results in an insufficient stretch of the ventricular myocardium. This consequence is a further decrease in cardiac output. The compensatory mechanism for the loss of the atrial kick is an increase in heart rate, which further impairs filling, increases oxygen demand and decreases output (Trigo & Fischer, 2012). Others types of arrhythmias may exacerbate HF depending on the severity of the pump dysfunction and how the arrhythmia affects myocardial perfusion, ventricular filling time and cardiac output. In general, with tachycardiac rhythms there is an increase in myocardial oxygen demand and a decreased output by shortening the filling time. With bradycardiac rhythms there is sufficient filling time but the rate may not be sufficient to maintain output. Finally, arrhythmias generated from the ventricles can directly lead to insufficient filling and contraction of the ventricles.


Acute myocardial ischemia and infarction are some of the leading causes of HF in the older adult. Coronary artery disease is associated with inflammation and arterial thrombosis and plaque formation, which leads to narrowing of the lumen diameter. This decreases blood flow to the myocardium that eventually impairs the tissue. When oxygen demand exceeds supply, myocardial cells can become injured or die leading to myocardial pump dysfunction and eventually HF.


Improper utilization of medications and poor dietary choices can also precipitate HF. The discontinuation of medications such as diuretics and beta blockers, which are commonly used to manage blood pressure and volume status, can lead to the development of HF. Overuse of beta blockers can lead to an insufficient heart rate to supply sufficient output. Improper prescription/administration and monitoring of the therapeutic levels of medications like antiarrhythmics and calcium-channel blockers can also contribute to HF. In the presence of impaired myocardial function, increased consumption of sodium or large amounts of fluids can lead to fluid overload and HF.


In cases of anemia, the heart tries to compensate by increasing cardiac output to meet oxygen demands. When there is myocardial pump dysfunction, the heart may not be able to sustain this increased stress. Anemia and the increased workload may lead to further ischemia and precipitate HF. Anemia is a common comorbidity in the elderly and is a probable factor to manage during the postoperative period (van Veldhuisen et al., 2011). The therapist must consider the increase in oxygen demand during functional mobility training in an individual with both anemia and heart disease. It is therefore important to monitor laboratory results and vital signs closely.


Individuals with pulmonary disease such as interstitial pulmonary fibrosis, chronic obstructive disease and vascular disease can lead to HF. Often the progression of lung disease leads to vascular changes within the lungs which may lead to pulmonary arterial hypertension (PAH). The increase in pulmonary arterial pressure causes stress on the right ventricle which cannot sustain the increased workload and eventually fails. The failure of the right ventricle will likely lead to left ventricular dysfunction and failure.



Clinical manifestations


The most common symptoms associated with HF are dyspnea, fatigue and exercise intolerance. Dyspnea and tachypnea can be related to many factors, including pulmonary vascular congestion and an increased work of breathing. Other factors include a decrease in cardiac output to meet peripheral tissue demand, disuse atrophy, alterations in skeletal muscles and renal dysfunction. The patient will report a progressive shortness of breath with exertion, to dyspnea at rest, as pump dysfunction progresses (Shiba & Shimokawa, 2011; McKenna et al., 2012). Box 42.1 describes the signs and symptoms associated with right and left HF; however, it is important to note that it is uncommon to see isolated unilateral HF. Box 42.2 describes the signs and symptoms associated with systolic and diastolic HF.



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Jun 22, 2016 | Posted by in PHYSICAL MEDICINE & REHABILITATION | Comments Off on Heart failure and valvular heart disease

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