Pathophysiology of Left Ventricular Failure - Essay Example

Pathophysiology Pathophysiology of Left Ventricular Failure Left Ventricular heart failure is mainly caused by ineffective left ventricular contractile function (Lippincott Williams & Wilkins, 2005, p. 182). When the ability of the left ventricle to pump is compromised, there is a decreased cardiac output. As a result, the blood that is supposed to be distributed to the body is backed up into the left atrium and then back into the lungs. Consequently, blood fills up the lungs and causes pulmonary congestion and dyspnea. If this condition persists, there will be pulmonary edema and eventually, right-sided heart failure (Lippincott Williams & Wilkins, 2005, p. 182). As was previously mentioned, patients who have left ventricular heart failure exhibit dyspnea, especially when they lie down, and at night. Since the patient’s lungs are one of the primary organs affected by this condition, the patient may exhibit bloody sputum and chest pains. He may also suffer from exhaustion, disorientation, and nocturia. The patient may also exhibit elevated respiratory and heart rates; pale, cold, and sweaty skin; pulsus alternans; rales auscultated from lungs; apical pulse displaced laterally; third and fourth heart sounds heard; on occasion, signs of right ventricular heart failure (McPhee, et.al., 2006, p. 272). The etiology of left ventricular heart failure is a conglomeration of possible causes which eventually affect the action of the left ventricles. It is related to a variety of possible diseases and affectations mostly affecting the cardio-vascular and the respiratory system. In general, heart failure may be attributed to the decreased workload for the heart – this may be caused by increased volume or increased pressure of the blood; it may also be caused by restricted filling of the heart; by myocyte loss; or by decreased contractility of the myocytes (McPhee, et.al., 2006, p. 272). Hemodynamic changes Left ventricular heart failure may initially be caused by hemodynamic changes. Hemodynamic changes may be caused by the worsening of the systolic or diastolic functions. In the worsening of systolic functions, there is a decreased systolic pressure which causes a decreased stroke volume and an eventual decrease in cardiac output. Cardiac output can be maintained through an increased or maintained preload, through the increased release of catecholamines and the hypertrophy of the cardiac muscle, which eventually increases ventricular volume. Such compensatory measures are only temporary, and the heart may fail later if the cause of the decreased cardiac output is not addressed (McPhee, et.al., 2006, p. 272-274). In diastolic dysfunction, the systolic isovolumic curve remains the same, but the diastolic pressure and volume shifts to the left. Consequently, there is an added increase in the left-ventricular end-diastolic pressure. This is seen in instances when there is decreased elasticity and increased stiffness of the ventricle. In cases of hypertension, the walls of the left ventricle are thickened and can cause diastolic dysfunction. Ischemia to the heart muscles can also cause diastolic dysfunction due to decreased relaxation (McPhee, et.al., 2006, p. 275). Neurohormonal changes Neurohormonal changes which may include the sustained and increased secretion of endogenous neurohormones and cytokines can cause the progressive deterioration of cardiac function. Increased hormones through increased sympathetic activity can also intensify cardiac contractility. Increased contractility of the heart will eventually lead to a higher preload and higher afterload. This condition can lead to heart failure if not correctly addressed (McPhee, et.al., 2006, p. 275). Pathophysiology-symptoms The shortness of breath seen in left ventricular heart failure is due to increased left ventricular pressure. The blood being backed up into the lungs by the pumping heart will increase pulmonary capillary pressure and cause the interstitial cells of the lungs to fill with fluid. “Replacement of air in the lungs by blood or interstitial fluid can cause a reduction of vital capacity, restrictive physiology and air trapping as a result of closure of small airways” (McPhee, et.al., 2006, pp. 276-277). Fatigue and confusion can arise because of the decreased oxygen being supplied to the cells of the body. Nocturia arises due to the decreased renal perfusion during the day as the patient is usually upright. When the patient is lying down, renal function becomes normal and there is increased urination at night. Chest pain may be caused by ischemia of heart muscles or by some other unexplained factors (McPhee, et.al., 2006, p. 277). Rales and pleural effusion is caused by the increased perfusion into the alveolar spaces of the lungs. There is now increased fluid in the interstitial and the pleural space of the lungs which, when auscultated are heard as rales. The displaced and sustained apical pulse can usually be heard during left ventricular heart failure. Normally, the apical pulse is heard at the fourth or fifth intercostal space at the midclavicular line, palpable only during the first part of systole. In instances when it is heard at the latter part of systole, it is considered sustained. This usually suggests an increase in ventricular volume or mass. And when the left ventricle is compensating for increased blood volume, the pulse is displaced laterally. Experts claim that the third heart sound is caused either by the sudden deceleration of blood as the limits of the ventricle are reached or by the actual impact of the ventricles against the chest wall. The increased end-systolic volume and pressure seen in the failing heart causes the third heart sound to be heard. The fourth heart sound is heard because of increased stiffness of the ventricle. This sound is heard as low pitch and concomitantly with the atrial contraction. Experts claim that it is caused by the sudden deceleration of blood through a stiff ventricle or by the sudden impact of the stiff ventricle against the chest wall. Finally pale, cold, and sweaty skin is due to peripheral vasoconstriction. There is reduced oxygen supply and therefore more oxygen is drawn from the peripheral tissues. Sweating occurs because excess body heat cannot be released through constricted vascular beds (McPhee, et.al., 2006, p. 277). Hypoxia Hypoxia is generally about the decreased oxygen supply to the tissues and cells of the body. Hypoxia exhibits several types: hypoxemic type, anemic type, stagnant type, and histotoxic type. Hypoxemic hypoxia Hypoxemic hypoxia “is deficient tissue oxygenation due to an inadequate arterial blood oxygen tension” (Shapiro, et.al., 1977, p. 49). This condition may be due to the decrease in the amount of oxygen taken in; this is common among pilots, mountain climbers, and those living in high altitudes. Decreased oxygen breathed in through the nostrils means decreased oxygen absorbed through the lungs. Lower oxygen absorption would mean decreased oxygen perfusion into the tissues and cells of the body. The hypoxemic type of hypoxia may also be caused by cardiopulmonary failure where the lungs are unable to efficiently transfer oxygen from the alveoli to the blood (Encyclopedia Britannica, 2009). Oxygen is absorbed through the alveoli in the lungs. Such oxygen is diffused into the capillaries and is picked up by the blood for circulation into the different parts of the body (Hammer, et.al., 2003, p. 442). When the cardiopulmonary function is impaired the alveoli cannot absorb and extract oxygen to be distributed to the cells of the body. The hypoxic state ensues. Anemic Hypoxia Anemic hypoxia may be caused by a decrease in the total amount of hemoglobin which, in turn, decreases the oxygen-carrying capacity of the blood (Britannica Encyclopedia, 2009). The hemoglobin is the blood component that transports oxygen into the different parts of the body. Decreased hemoglobin in the blood will mean decreased oxygen carried by the blood. This may be seen during excessive blood loss or in instances where the hemoglobin is nonfunctional (as in carbon monoxide poisoning and methoglobinuria) (Britannica Encyclopedia, 2009). In carbon monoxide poisoning, the toxic quality of carbon monoxide alters the hemoglobin, rendering it damaged and ineffective as a vehicle for transport of oxygen. Stagnant hypoxia In stagnant hypoxia, the blood is not flowing, hence the term stagnant. Since the oxygen-rich blood is not flowing through the veins, the cells of the body are not supplied with oxygen, hence the hypoxic state. This type of hypoxia is seen in cases of shock, heart failing to pump blood effectively, a constricted artery, and during cold temperature when circulation is decreased and there is decreased blood flow to the extremities (Federal Aviation Administration, 2007, p. 15-2). The pathophysiology of this type of hypoxia basically involves decreased blood flow. Decreased blood flow will prevent or reduce the delivery of oxygen into the cells and tissues of the body resulting to a hypoxic state. Histotoxic hypoxia Finally, histotoxic hypoxia is seen when the cells are unable to effectively make use of the oxygen distributed to them (Federal Aviation Administration, 2007, p. 15-2). In instances of alcohol and narcotic drugs intake, cellular respiration becomes impaired. The cellular machinery that uses oxygen to produce energy is poisoned, hence the term toxic (Levitzky, 2007, p. 184). In this type of hypoxia, pollutants or toxic substances instead of oxygen is transported by the blood. These toxic chemicals like carbon monoxide, alcohol, cigarette smoke, or over-the-counter drugs attach to the hemoglobin. These toxic substances are usually absorbed faster by the hemoglobin; the hemoglobin can also become too full of these toxic chemicals and be unable to carry and transport the oxygen. These chemicals are toxic to the cells of the body. They will eventually cause the body to malfunction. If transport of these chemicals is not stopped, cell death will follow (Turner, 2000, p. 608). Dehydration Dehydration manifests mostly as excessive body fluid and electrolyte loss resulting to negative fluid balance. It is most commonly caused by diarrhea, although other conditions have been known to cause dehydration (Anderson, 2007, p. 212). Renal sources, as seen in diabetic ketoacidosis; cutaneous sources, as seen in sweating and burns; and third space losses, into the intestinal lumen in bowel obstruction also cause dehydration (Roberts, 2007). Fluid loss is normally accompanied with decreased fluid intake which exacerbates the depletion of electrolytes in the body. Dehydration may be attributed to a decreased fluid intake, an increased fluid output, or a fluid shift between the compartments. Decreased fluid intake will cause reduced fluids in both the intracellular and extracellular fluid volumes. Decreased intracellular and extracellular fluids will shrink the cell and eventually cause cell death. For organs affected, organ failure will ensue and eventually death will follow. Isonatremic dehydration Dehydration may be isonatremic, hyponatremic, and hypernatremic. In isonatremic dehydration, the fluid lost is similar in sodium concentration to the blood. In other words, the sodium and water losses are the same magnitude in the intravascular and extravascular fluid compartments. This is usually seen in children suffering from infectious diarrhea. Hyponatremic dehydration In hyponatremic dehydration, the fluid which is lost contains more sodium than the blood. As sodium in the blood becomes depleted, intravascular fluids shift to the extravascular space. The intravascular volume becomes even more depleted based on total body water loss (Huang, et.al., 2008). The intracellular fluid is preserved at the expense of the ECF. Signs and symptoms in this type of dehydration manifest with minimal fluid loss. This is seen in patients with diarrhea given only water to drink. Fluid is sufficient, but sodium is insufficient (Fine, 2008, p. 93). Hypernatremic dehydration Finally, in hypernatremic dehydration, the fluid lost contains less sodium than the blood (Huang, et.al., 2008). More water is lost as compared to sodium. Since, serum sodium is now elevated, there is a shift of extravascular water to the intravascular space. The intravascular volume becomes depleted as compared to the total water loss in the body. As sodium and chloride are confined in the ECF space, the ICF volume is preserved. This condition is seen in patients who are vomiting, who are suffering from diarrhea, and who cannot tolerate fluids. They often lose more fluids than sodium. Due to shifts of fluids from the intravascular spaces into the extravascular spaces, cells lose much needed electrolytes needed for normal cellular function. Cell death may occur because the cells literally become dehydrated. Symptoms later manifest in the decreased level of consciousness, prolonged capillary refill time, dry mucus membrane, decreased or absent tears, increased respiratory rate, decreased blood pressure, weak and thready pulse, sunken eyes, and decreased urine output (Braun & Anderson, 2007, p. 213). Works Cited Braun, C. & Anderson, C., 2007, Pathophysiology, Pennsylvania: Lippincott Williams and Wilkinson Federal Aviation Administration, 2007, Pilots Encyclopedia of Aeronautical Knowledge, New York: Skyhorse Publishing Fine, K., 2008, Pediatric Board Recertification Review, Pennsylvania: Williams & Wilkinson Huang, L., et.al., 21 July 2008, Dehydration, eMedicine Medscape, viewed 24 July 2009 from http://emedicine.medscape.com/article/906999-overview Hypoxia, 2009, Encyclopedia Britannica, viewed 24 July 2009 from http://www.britannica.com/EBchecked/topic/280144/hypoxia Levitzky, M., 2007, Pulmonary physiology, USA: McGraw-Hill Publishing Company Lippincott, Williams & Wilkins, 2005, Pathophysiology, Pennsylvania: Lippincott Williams & Wilkins. McPhee, S., et.al., 2006, Pathophysiology of disease, USA: McGraw-Hill Publishers Roberts, K., May 2007, Dehydration, Merck, viewed 24 July 2009 from http://www.merck.com/mmpe/sec19/ch276/ch276b.html Shapiro, B., et.al., 1977, Clinical application of blood gases, California: Year Book Medical Publishers Turner, T., 2000, Instrument Flying Handbook, USA: McGraw Hill Willie, H., et.al., 2003, Occupational safety management and engineering, China: Pearson Education Asia Limited Tsinghua University Press Read More