Include in your discussion an evaluation of the presence and effects of alteration in the homeostatic state secondary to gender, genetic, ethnic, and temporal variables.
Requirements:
Make sure all of the topics in the case study have been addressed.
Cite at least three sources; journal articles, textbooks or evidenced-based websites to support the content.
Two sources from the book and one other evidence-based reference no older than 3-5 years.
Do not use .com, Wikipedia, or up-to-date, etc., for your sources.
Case Study 4
APA format.
A 72-year-old man presents to the emergency department complaining of severe shortness of breath. He has long-standing poorly controlled hypertension and history of coronary artery disease and two myocardial infarctions. About 1 week before admission, he had an episode of substernal chest pain lasting approximately 30 minutes. Since then he has noted progressive shortness of breath to the point that he is now dyspneic on minimal exertion such as walking across the room. He notes a new onset of shortness of breath while lying down. He is only comfortable when propped up by three pillows. He is occasionally awakened from sleep acutely short of breath. On examination he is afebrile, with a blood pressure of 160/100 mm Hg, heart rate of 108/min, respiratory rate of 22/min, and oxygen saturation of 88% on room air. He is pale, cool, and diaphoretic. Jugular venous pressure is 10 cm H2O. Chest auscultation reveals rales in both lungs to the mid lung fields. Cardiac examination reveals tachycardia, with an audible S3 and S4. No murmurs or rubs are heard. Extremities are without edema. The ECG shows left ventricular hypertrophy and Q waves in the anterior and lateral leads, consistent with this patient’s history of hypertension and myocardial infarction. Chest x-ray film reveals bilateral fluffy infiltrates consistent with pulmonary edema. He is admitted to the ICU with a diagnosis of heart failure and possible myocardial infarction.
What are the four factors that account for almost all cases of pulmonary edema?
Which are probably responsible for this patient’s pulmonary edema?
