Description of the Physiology in the Development of Disease
Pulmonary embolism is the third highest cause of mortality from cardiovascular diseases behind myocardial infarction and cerebrovascular stroke. According to the Center for Disease Prevention and Control (2012), pulmonary embolism occurs when a clot breaks free and finds its way into the arteries of the lungs impairing with supply of oxygenated blood to lung tissues. Usually, the thrombus originates from the dep venous systems of lower extremities; and rarely from the pelvic, renal, upper extremity veins or right heart chambers. As a component of venous thromboembolism, pulmonary has become a major health concern in the US, with PE being diagnosed in 277,459 hospitalized cases annually between 2007 and 2009. The pathophysiological factors in the development of PE include inflammation, hypercoagulability, and endothelial injury. These characteristics are critical in the formation of an embolus that can break off and find enter pulmonary arteries. Therefore, the development of PE can be attributed to: the pre-existing cardiopulmonary condition of the patient; extent to which the vascular tree is occulated and the size of the emboli; chemical vasoconstriction from the release of serotonin and thromboxane which adhere to the embolus, and also fibropeptide B; and reflex vasoconstriction, and outcome of pulmonary artery dilatation. Pulmonary embolism can be followed by a sequel of manifestations including chronic thromboembolic pulmonary hypertension and post thrombotic syndrome.
Myocardial failure is a common phenomenon on patients with cardiovascular conditions. Cor pulmonale refers to a condition where the right side of the heart fails, and is usually a consequence of sustained high blood pressure in pulmonary arteries and the right ventricle of the heart as a compensatory mechanism for forcing blood through the lungs. Pulmonary hypertension is responsible for small changes in small blood vessels of the lungs, consequently raising pressure on the right side of the heart, and sustained pressure causes train on the right side of the heart leading to failure – Cor pulmonale. Sustained hypoxia in the blood due to lung conditions can also cause Cor pulmonale.
Delegate your assignment to our experts and they will do the rest.
Considerations for Treatment
Clinicians treating PE must understand that the condition is a dramatic and life-threatening complication, hence diagnosis is important. Of special consideration is the fact that PE is symptomatic in 30% of the affected cases and that 50-60% of patients with deep vein thromboembolism develop PE (Kostadima & Zakynthinos, 2007). Understanding of the classic presentation of PE in the form of abrupt onset of pleuritic chest pain, shortness of breath, and hypoxia is necessary in the diagnosis process. It is most important to note that regardless of the expected outcome of diagnosis, it should not delay administration of anticoagulant for all cases suspected to be DVT. Mechanisms through which medicaments interact with the body should also be understood. For instance, patients with acute pulmonary embolism with hypertension and low bleeding risk, and those whose initial diagnosis suggest high risk of developing hypertension, should be administered with thrombolytic therapy.
The treatment of Cor pulmonale is dependent on the treatment of the underlying cause of pulmonary hypertension. Prescription medicines can be used to lower blood pressures and encourage oxygen flow to the lungs, and diuretics can be employed where fluid retention must be addressed to keep blood sodium levels normal. Blood thinners may also be taken, but emphasis should be placed on contraindications. Oxygen therapy may also be used where severe cases are involved, or a heart or lung transplant for more aggressive cases.
According to Repessé, Charron, and Vieillard-Baron (2013), ventilator strategy for improving pulmonary efficiency has taken into consideration the impacts of pulmonary injury on the right ventricle of the heart and hemodynamics. This implies that there is causation and effect between PE and Cor pulmonale. Cor pulmonale is caused by pulmonary hypertension, which may be an outcome of pulmonary embolism, hence PE can contribute to formation of the former. Pulmonary emboli that cause PE rarely originate from the right heart ventricles, but in case they do, they can also cause Cor pulmonale in a counter-mechanism. However, Cor pulmonale can easily result to formation of such emboli leading to PE, thus exacerbating the existing condition of Cor pulmonale.
References
Centers for Disease Control and Prevention (CDC. (2012). Venous thromboembolism in adult hospitalizations-United States, 2007-2009. MMWR. Morbidity and mortality weekly report , 61 (22), 401.
Kostadima, E., & Zakynthinos, E. (2007). Pulmonary embolism: pathophysiology, diagnosis, treatment. Hellenic Journal of Cardiology , 48 (2), 94-107.
Repessé, X., Charron, C., & Vieillard-Baron, A. (2015). Acute cor pulmonale in ARDS: rationale for protecting the right ventricle. Chest , 147 (1), 259-265.
