Pathophysiology and Pharmacology of Cardiac Diseases - Essay Example

Pathophysiology & Pharmacology of Cardiac Diseases Pathophysiology of Heart Failure Heart failure refers to the condition characterized by a malfunction of the heart muscles to pump and distribute a sufficient supply of blood to cater for the body’s requirements. In this condition, the heart muscles become damaged and are therefore less efficient. This results in an overload of the heart while performing its functions. There are several conditions that can induce heart failure in humans. One such condition occurs when damage to the heart muscles is induced by a myocardial infarction or a heart attack. Under this condition, the amount of blood transmitted to the tissues in the heart muscle is inadequate (Department of Health, 2008). As a consequence, muscle tissue dies due to starvation from oxygen and the necessary nutrients. Muscles in the heart, therefore, fail to operate as they are designed to. This significantly increases the chance of heart failure. Another condition that may lead to heart failure is anemia. In this case, air circulation to and from the vital body organs is insufficient. As a result, cardiac muscles are subjected to a significant amount of strain as they are required to work harder to ensure that enough oxygen is distributed throughout the body. Other cardiac diseases that may cause damage to the muscle tissue include amyloidosis and cardiomyopathy (McMurray et al., 2009). In heart failure, contractions by the cardiac muscles may weaken as a result of excessive supply of blood to the ventricles during diastole. In healthy people, this surplus amount of blood in the ventricles may trigger an increased rate of muscle contraction. This condition if referred to as the Frank-Starling law of the heart and its intention is to increase the cardiac output. The chances of this mechanism working under heart failure are, however, minimal. This is because cardiac muscles are weakened and as such, the heart fails to pump a sufficient amount of blood in the body. To make up for the low cardiac output, a rise in the heart rate is observed. The condition is as a result worsened as the cardiac muscles require significantly more nutrients to work. The rate of pumping by myocardial muscles is also increased. As the systole and diastole contractions begin to fail, stroke volume is observed to reduce. In the instance where the blood volume in the ventricle rises at the end of systole, it means that less blood has been ejected. Little blood is considered to have entered the heart if the blood volume at the end of diastole is decreased. The heart’s reserve may reduce (NHFA & CSNZ, 2011). As such, the heart is required to possess the necessary capacity that will enable it to cope with the regular metabolic demands during normal and elevated levels. In heart failure, however, this reserve capacity is compromised. As time passes, the heart begins to enlarge, a condition referred to as hypertrophy. Initially, muscle fibers in the heart increase in size to enhance contractions. With time, they stiffen and become too unyielding to be of use. Blood pressure in the arteries falls and blood flow to vital organs such as the kidneys is reduced (McMurray et al., 2009). Pharmacological Treatment Aims of Acute Myocardial Infarction Acute myocardial infarction (AMI) is a condition that arises due to necrosis of myocardial tissue. This occurs usually as a result of an occlusion by a thrombus in a coronary artery. Whereas the primary objective of physicians is to avert death, those tending to victims suffering from myocardial infarction strive to minimize patient’s distress and discomfort. This is done to limit the extent to which damage is caused from the disease. Treatment of AMI can be conducted over four phases. The first involves care when the intent is to undertake early risk assessment and rapid diagnosis (Bolooki, 2010). This is done majorly to avert or treat cardiac arrest. The second phase revolves around early care in which the main concern is to begin reperfusion therapy as soon as necessary. This therapy is aimed at preventing the extension of infarcts and to effectively address complications like pump failure and shock. In the third phase, subsequent care is provided. Here, complications ensuing in later stages are dealt with. During the final phase, measures are undertaken to prevent the spread of coronary artery diseases and new infarctions (Alowayesh, 2009). In the treatment of AMI, aspirin helps to prevent the formation of blood clots. It does so by reducing the ability of platelets to stick to each other. Failure to do so would mean that clots forming in the heart would block the flow of blood. The long-term use of low dose aspirin helps to reduce overall mortality, nonfatal strokes and nonfatal re-infarction. Clopidogrel in particular is is recommended for the treatment of AMI together with ST-segment elevation. Beta-blockers ease cardiac workload by preventing the stimulation of beta receptors in heart muscle. As such, the heart rate and blood pressure remain minimal. Beta-blockers also reduce nonfatal re-infarctions and mortality when taken within a few hours of infarction. In addition, they are also used in the treatment of angina and high-blood pressure (ESC, 2008). Angiotensin-Converting Enzyme (ACE) Inhibitors give protection to the heart. The do so by interfering with angiotensin, a chemical enzyme in the bloodstream. This action results in the dilation of blood vessels and subsequently a reduction in blood pressure. As such, the work of the heart is reduced. Angiotensin-II receptor antagonists bear the same effect as ACE inhibitors and they are sometimes supplemented for the same. ACE inhibitors reduce mortality and the likelihood of nonfatal heart failure. Statins reduce cholesterol levels in the liver. In so doing, the formation of atheroma is inhibited (ESC, 2008). Atheroma builds up on the interior lining of blood vessels and may cause stroke, cardiac diseases and blood flow problems. Heparin infusion may be used as an adjunctive agent among patients undergoing alteplase without streptokinase. Insulin-glucose infusion is usually followed by rigorous glucose control with subcutaneous insulin for type 1 and 2 diabetes victims. Analgesics such as morphine are useful in reducing pain evident in victims of AMI. All these drugs are aimed at countering early manifestations of AMI and preventing their progression. In addition, they are aimed at improving patient’s comfort and preventing mortality (ESC, 2008). References McMurray John, Mark Petrie, Karl Swedberg, Micheal Komajda, Stefan Anker & Roy Gardner (2009) The ESC Textbook of Cardiovascular Medicine, Oxford University Press, 2nd Ed. New York, USA. pp. 835-845 National Heart Foundation of Australia (NHFA) & the Cardiac Society of Australia and New Zealand (CSNZ) (2011) Guidelines for the prevention, detection and management of chronic heart failure in Australia, p. 80. Retrieved from http://www.heartfoundation.org.au/SiteCollectionDocuments/Chronic_Heart_Failure_Guidelines_2011.pdf Department of Health, Western Australia (2008) Cardiovascular Health Network: Heart Failure Model of Care. Perth: Health Networks Branch, Department of Health, Western Australia, pp. 10-11. Retrieved from http://www.healthnetworks.health.wa.gov.au/modelsofcare/docs/Heart_Failure_Model_of_Care.pdf European Society of Cardiology (2008) Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation, European Heart Journal 29, pp. 2927-2928. Retrieved from http://www.escardio.org/guidelines-surveys/esc-guidelines/Documents/AMI/guidelines-AMI-FT-2008.pdf Bolooki H. Michael &Arman Askari (2010) Acute Myocardial Infarction, Cleveland Clinic. Web. Available at http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/acute-myocardial-infarction/ (Accesses May 18 2014) Alowayesh Maryam S. (2009) Acute Pharmacological Treatment Given to Older Adults with Acute Myocardial Infarction: A Nationwide Emergency Department Study, 1992–2010. University of London, London, UK. pp. 12-18 Read More