Introduction: Left ventricle hypertrophy can cause congestive heart failure to the patient. Common cause of the disease is due to the hypertension. If left ventricle hypertrophy is untreated, it will easily causes congestive heart failure. Abstract: The reasons that why I setup this hypothesis is because the patient have chest pain, this pain may come from congestive heart failure. Besides, the patient has medical history, such as hypertension and diabetes which increase the chance of chronic heart failure.
This type of shock occurs when the heart is unable to pump blood effectively. This is evident to patients who have had myocardial infarction, such as John’s case. In this illness, the heart has decreased contractility resulting to decreased cardiac output. Such decrease will stimulate the sympathetic nervous system to activate the compensatory mechanism by increasing the heart rate as evident in John’s vital sign to increase the peripheral pressure and ventricular
The priorities are to detect intraoperative MI early, give effective treatment, and transfer the patient to ICU urgently for further cardiac care.  When myocardial ischemia is because of hypovolemia, hypotension should be primarily managed with IV fluids in the form of crystalloids or colloids and blood products. Inotropic support is required when there is no response to fluid administration.In this case myocardial ischemic changes were because of hypovolemic shock. Hence by correcting hypotension secondary to hypovolemia the myocardial ischemic changes were reversed.
A similar patient who declines any treatment and decides to let nature take its course comes back one month later to the emergency room with headache, blurred vision, confusion and mucosal bleeding. What is the likely cause of this patient’s condition? A. Disseminated intravascular coagulation B. Hyperviscosity syndrome C. Hypercalcemia D. Acute renal failure Ans: B Exp: The sudden onset and mucosal bleeding rule out acute renal failure and hypercalcemia respectively. Hyperviscosity syndrome results from increased serum viscosity due to high protein content in multiple myeloma. Clinical pearls: • Multiple Myeloma is a plasma cell malignancy that causes end organ damage- CRAB Calcium elevated Renal failure Anemia Bone lesions • Median age of diagnosis is 70 years • Male > Female.
Remington Stotler Advanced Adult Care Pre-clinical assignment Common Conditions: 1. Acute myocardial infarction/coronary artery disease is when the arteries that supply the myocardium are clogged up; the heart cannot pump blood effectively to adequately perfuse vital organs and peripheral tissues. It affects the arteries that provide blood oxygen, and nutrients to the myocardium. When blood flow through the coronary arteries is partially or completely blocked, ischemia and infarction of the myocardium could occur. Nitroglycerin (NTG) increases collateral blood flow, redistributes blood flow toward the sub endocardium, and dilates the coronary arteries.
INTRODUCTION:  Valsartan is an Angiotensin II Receptor Antagonist (commonly called an ARB, or angiotensin receptor blocker), that is selective for the type I (AT1) angiotensin receptor. It is used to treat high blood pressure, congestive heart failure, and to reduce death for people with left ventricular dysfunction after having had a heart attack. Figure 1: Valsartan Nifedipine is a dihydropyridine calcium channel blocker that primarily blocks L-type calcium channels. Its main uses are as an antianginal and antihypertensive, although a large number of other indications have recently been found for this agent, such as Raynaud's phenomenon, premature labour, and painful spasms of the esophagus such as in cancer and tetanus patients.
Silent myocardial infarctions have a prevalence of 10% to 20% in diabetic patients. Autonomic neuropathy is a very common, yet serious condition that many diabetic patients suffer from which upset the balance between cardiac supply and demand. It’s defined as a disorder that affects nerves that are part of the autonomic system which control things such as the heart and blood vessels. This disorder can cause the heart to have to overcome more resistance from the blood vessels, afterload, which can lead to chronic high blood pressure causing left ventricular hypertrophy as well as a dysfunctional heart rate. The cardiac denervation is responsible for the patient’s having no chest pain which we normally associate with myocardial infarctions which, unfortunately, lead to many such patient’s to go undiagnosed and in some cases can cause death of it is severe
This can lead to heart and damage the heart muscle permanently crisis; • high blood pressure, which is also called hypertension; • disease of the heart valves - there may be a leak in the valves or those may stiffen, especially the sigmoid valves and mitral; • a disorder of cardiac muscle, which is also called cardiomyopathy. That may be caused by a virus, bacterium or other infections; • damage to the heart caused by the abuse of alcohol or drugs; • congenital heart disease and heart defects that exist at birth; • an irregular heartbeat, especially if there is rapid or chaotic. The heart does not pump enough blood when his rhythm is abnormal; • certain lung disorders, such as pulmonary hypertension, which occurs when the right ventricle dilates, causing heart failure on the right. Normal Heart congestive heart é START T How is the diagnosis? During physical examination: lungs - produce a sizzling; heart - heart murmur, gallop rhythm, noise third; neck - distended veins; enlarged liver; expansion of the abdomen due to the accumulation of fluid; leg swelling (edema).
A thorough search for a predisposing factor should be made. A cardiac cause is frequently overlooked (occult endocarditis and septal defects). In a recent case report, the authors described the rare case of a patient with an echocardiographically proven patent foramen ovale who developed a brain abscess (8) and brain abscess in an adult with atrial septal defect (ASD) (28). Perhaps such intracardiac lesions (with occult bacteremia from an abdominal source) account for some of the cryptic cases identified in previous reports, although larger studies would be needed to identify the frequency and clinical relevance of such
2010; Franchini et al. 2008). Surprisingly, 15-20% of patients with myocardial infarction (MI) have none of the traditional risk factors for CAD (Thanassoulis G. & O’Donnell C.J 2009). Such patients often have a family history of MI, which has long been associated with CAD and confers a nearly twofold increase in risk (Lloyd-Jones et al, 2004). Following this discovery, it has stimulated an intense search for the genetic determinants of