Heart failure is a condition that results when the heart's cardiac output cannot meet the body's demand. It is characterised by blood being dammed in the venous system and reduced cardiac output. Left-sided heart failure is just one of the several types of heart failure, and it has a different presentation from the rest.
Several risk factors predispose to left-sided heart failure. Hypertension predisposes to heart failure. The reason is the heart is overexerted when blood pressure is high. The occurrence of a heart attack increases the risk of left-sided heart failure because it causes damage to the heart muscles which could reduce the heart's pumping ability. Coronary heart disease which causes an inadequate supply of oxygen to heart tissues, thereby weakening the muscles. Diabetes could also predispose to left-sided heart failure as it causes an increased risk of coronary artery disease and hypertension. Some medications used in the treatment of diabetes such as pioglitazone and rosiglitazone elevate the risk of left-sided heart failure. Some non-steroidal anti-inflammatory drugs (NSAIDs), certain antiarrhythmics, some anti-hypertensives, drugs used in the treatment of cancer, lung conditions, inflammatory conditions, psychiatric conditions, neurological conditions, and urological conditions also increase the risk of left-sided heart failure. Other conditions which predispose to left-sided heart failure include viruses, alcohol use, tobacco use, viruses, obesity, etc. (Eldelmann, 2015).
On most occasions, heart failure usually develops after other conditions have caused the weakening of the heart or have damaged it (Eldelmann, 2015). Heart failure can also result from the stiffness of the heart which lowers its ability to pump blood. In left-sided heart failure, the left ventricle which is the main pumping chamber could become stiff; its muscles could be damaged or weakened to the extent where the ability of the left chamber to pump blood to all body organs is compromised. Conditions which have the potential to undermine or damage heart muscles cause left-sided heart failure. Heart attack and coronary heart disease can cause left-sided heart failure. Coronary heart disease is the cause of heart failure in most instances. It is caused by deposition of fat in coronary arteries thereby impairing blood flow in the heart causing a heart attack. Systemic hypertension causes left-sided heart failure. High blood pressure causes the heart muscles to work harder than normal blood pressure. With time the muscles of the left ventricle become weak or stiff due to this extra exertion. Valvular diseases such as aortic valve disease and mitral valve disease can cause left-sided heart failure. These cause the heart to work harder, weakening over time. Cardiomyopathy, which has several causes such as toxic effects of drugs, abuse of alcohol, genetic factors and several infections and diseases can also cause left-sided heart failure. Other causes of left-sided heart failure include myocarditis, heart arrhythmias, congenital heart defects, and chronic diseases such as HIV, diabetes, hypothyroidism, hyperthyroidism, etc. acute heart failure has different causes. They include severe infections, viruses that damage muscles of the heart, allergic reactions, the presence of blood clots in the lungs, and particular medications that affect the entire body (Eldelmann, 2015).
Over time, left-sided heart failure causes changes in the heart. Apoptosis increases the amount of fibrous tissue in the heart. Neurohormonal compensatory mechanisms such as increased vasopressin release and increased sympathetic activity cause increase in the contractility of the heart and heart rate worsening the problem. The contractility of the left ventricle is reduced due to overload with blood. Stroke volume is reduced due to failing systole and diastole. Hypertrophy of the myocardium occurs following the decrease in the contractility of the heart in an attempt to increase the force of contraction of the heart. The increase in the size of the heart is disproportionate with capillary numbers. The effect of this is that the heart becomes stiffer and more strained raising the risk of cardiac arrest (Halushka, Mitchell & Padera, 2016).
The signs and symptoms of left-sided heart failure include dyspnea during exercise or when lying flat, wheezing, chronic coughing, sudden weight gain, accumulation of fluid which leads to swollen feet, legs and ankles, rapid heartbeat, lack of appetite, waking at night, and fatigue. The occurrence of these symptoms causes a strain on the heart making it pump harder which causes further damage. The damages include rapid heartbeat, decreased blood flow to legs, hypertrophy of the heart muscles, and high blood pressure (Halushka, Mitchell & Padera, 2016).
Dyspnea and coughing are caused by the accumulation of fluid in the lungs and hypoxia due to impairment in blood flow. Weight gain is due to fluid retention. Fluid retention occurs as a result of impaired venous circulation. A rapid heartbeat is a result of the heart trying to compensate for the reduced contractility.
Some laboratory blood tests are helpful in the diagnosis of left-sided heart failure. Such blood tests include urea and electrolyte levels determination and complete blood count (Tanaka, Matsumoto & Hirati, 2015). Full blood count is necessary to rule out low levels of red blood cells as a cause of hypoxia. Hypoxia characterises left-sided heart failure despite normal haemoglobin and red blood cells level. The cause of this is reduced pumping ability of the heart hence inadequate supply of oxygen-rich blood to tissues. The level of red blood cells would be significant due to the imminent hypoxia in the case where left-sided heart failure is present. White blood cells count helps to rule out low count as the cause of low immunity. Low immunity characterises left-sided heart failure despite normal levels of white blood cells (Tanaka, Matsumoto & Hirati, 2015). The reason is that left-sided heart failure causes low metabolism, hence low immunity.
Chest X-ray can be done to determine to check for any abnormalities of the heart. Heart enlargement characterises left-sided heart failure. In the presence of left-sided heart failure, chest X-ray also reveals Kerley B and C lines which are caused by pulmonary changes, perivascular and interstitial oedema specifically in the interlobular septa (Tanaka, Matsumoto & Hirati, 2016). ECG can be done to reveal abnormal ventricular contraction as depicted by different ECG graphs.
Treatment of left-sided heart failure
Medical treatment of left-sided heart failure entails the use of several classes of drugs. Digitalis such as digoxin can be used in the management of left-sided heart failure. It improves the heart rhythm and its contraction efforts. The therapeutic effects of digoxin are achieved through the slowing of the heart rate, therefore stabilising heart rhythms. However, digoxin has a very narrow therapeutic window requiring keen monitoring of doses as an overdose may result in heart arrest and bradycardia. Angiotensin Converting Enzyme Inhibitors (ACEs) are used to manage left-sided heart failure (Eldelmann, 2015). They prevent the conversion of angiotensin I to angiotensin II thereby regulating angiotensin II levels. The effect of this is reduced aldosterone, lowering the risk of systemic oedema as there is limited reabsorption of salt and water. Care should be taken by the nurse to prevent an imbalance of serum electrolytes. ACEs can cause severe electrolyte depletion and dehydration. Diuretics such as furosemide are used to manage left-sided heart failure (Eldelmann, 2015). These drugs enhance excess fluid elimination via urination. However, at therapeutic doses of diuretics, there is a loss of essential electrolytes mainly potassium and sodium. The loss of potassium could be a cause of arrhythmia in an already failing heart. For this reason, these drugs are used primarily to provide quick relief to congestion symptoms. Beta blockers such as metoprolol succinate, bisoprolol, and carvedilol can also be used in the management of symptomatic hypotension characteristic of left-sided heart failure (Eldelman, 2015).
Left-sided heart failure can also be treated via surgical interventions such as mitral valve repair, coronary revascularisation, and ventricular reconstruction. All these surgical procedures are, however, not recommended due to their unclear long-term benefits and high mortality rates.
Prevention of left-sided heart failure entails avoiding the factors that predispose individuals and education on its causes. Lifestyle changes are fundamental in the prevention of this type of heart failure. They include regulating diabetes and hypertension, exercising regularly, eating healthy, avoidance of smoking, managing and reducing stress, and maintenance of healthy weight (Halushka, Mitchell & Padera, 2016).
For the treatment of acute left-sided heart failure, oxygen should be administered where saturation is lower than 90 percent. ACEs, diuretics, and vasodilators are administered in acute condition to relieve symptoms. For chronic left-sided heart failure, management entails pharmacotherapy and lifestyle adjustments such as exercising regularly, avoidance of smoking and alcohol use, low sodium and fat diet, etc.
The most important patient problems in the acute phase of left-sided heart failure include increasing shortness of breath during rest (cardiopulmonary instability), oedema, and hemodynamically significant arrhythmia (Carolina, Pacheco & Hernandez, 2016).
Cardiopulmonary instability is managed by administration of diuretics such as bumetanide, torsemide, and furosemide. The diuretics help to relieve dyspnea. The reason is an accumulation of fluid in the lungs is the cause of shortness of breath, and therefore by removing excess fluid from the lungs, normal breathing can be restored. Where the patient's saturation is below 90 percent, oxygen should be administered. The dose of diuretics administered is dependent on the response produced after two to four on first administration. If adequate response is not elicited, increasing the frequency and dose of application could help in relieving the symptoms. Vasodilators such as nitroprusside and nitroglycerin can also be administered to relieve dyspnea (Eldelmann, 2015). The two are very potent vasodilators and therefore lower the filling pressure of the left ventricle and relieve shortness of breath. Nitroprusside also helps in myocardial ischemia as it causes vasodilation of epicardial coronary artery. Besides medications, oxygen administration ensures sufficient oxygen concentration. Care should be taken to ensure there is no overflow of oxygen which could lead to hyperinflation of lungs risking emphysema. Nasal cannulas are preferable for oxygen therapy as the use of an oxygen mask gives the sensation of suffocation.
Edema is managed by administration of drugs that promote excess fluid elimination and prevent fluid retention. Diuretics can be used to relieve congestion. Loop diuretics are preferred because of their high potency. Where left-sided heart failure is accompanied by high blood pressure, thiazide diuretics are used. The reason is that they have a persistent effect on blood pressure. Ensuring that the dosage of diuretics is effective and safe is essential. The dosage should be just enough to resolve congestion and not cause volume shrinking leading to hypotension. Low doses would be ineffective thereby fluid retention will not be resolved. The levels of electrolytes specifically potassium and magnesium should be monitored with the use of diuretics. The reason for this is that diuretics cause the loss of these electrolytes lowering their levels which could re...
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