Heart Failure And INFLammation Quiz: Trivia!

The patient's symptoms of shortness of breath, cough, and palpitations, along with his history of hypertension and the fact that his symptoms occur at night, suggest that he may be experiencing left ventricular failure. Left ventricular failure can cause fluid to accumulate in the lungs, leading to symptoms such as shortness of breath and cough. An ECG, chest X-ray, and ECHO can help assess the function of the heart and identify any abnormalities that may be causing the symptoms. Therefore, consulting his doctor for these tests is necessary to evaluate his condition and determine the appropriate treatment.

The most likely diagnosis in this case is hypertrophic cardiomyopathy. This condition is characterized by the thickening of the interventricular septum, which can lead to decreased end-diastolic volume. It is commonly seen in young athletes and can cause symptoms such as chest pain during physical activity. Endomyocardial fibrosis, heart amyloidosis, and physiologic heart hypertrophy are not consistent with the findings described in the question.

The patient's symptoms and physical examination findings suggest a diagnosis of congestive heart failure (CHF). The presence of dyspnea, fatigue, lower leg edema, dry cough with rusty sputum, and abdominal distension are all consistent with CHF. The physical examination findings of cyanosis, pedal edema, ascites, and rales in both lower lung fields further support this diagnosis. The chest X-ray revealing left atrial enlargement and pulmonary edema indicate chronic left-sided heart failure (LSHF). However, the combination of symptoms and findings, including the presence of rales in both lower lung fields, suggests the involvement of both sides of the heart, indicating chronic combined LSHF and RSHF.

Hypertrophic cardiomyopathy is the most likely cause of the 21-year-old NCAA basketball player's death during a game. This condition is characterized by the thickening of the heart muscle, which can disrupt the normal flow of blood and cause various complications, including sudden cardiac arrest. It is often hereditary and can go undiagnosed until a tragic event occurs, as in this case. Given the player's young age, lack of known medical problems or previous history of illness, and the sudden nature of his death, hypertrophic cardiomyopathy is a plausible explanation.

ARTERIOLOSCLEROSIS A. Narrowing of small arterioles; divided into hyaline and hyperplastic types B. Hyaline arteriolosclerosis is caused by proteins leaking into the vessel wall, producing vascular thickening; proteins are seen as pink hyaline on microscopy (Fig. 7.7). 1. Consequence of long-standing benign hypertension or diabetes 2. Results in reduced vessel caliber with end-organ ischemia; classically produces glomerular scarring (arteriolonephrosclerosis) that slowly progresses to chronic renal failure C. Hyperplastic arteriolosclerosis involves thickening of the vessel wall by hyperplasia of smooth muscle ('onion-skin' appearance, Fig. 7.9). l. Consequence of malignant hypertension 2. Results in reduced vessel caliber with end-organ ischemia 3. May lead to fibrinoid necrosis of the vessel wall with hemorrhage; classically causes acute renal failure with a characteristic 'flea-bitten' appearance

The correct answer is viral myocarditis. This diagnosis is supported by the patient's symptoms of cough, high fever, and severe muscle aches, as well as the development of signs of heart failure within a day. The myocardial biopsy reveals characteristic features of viral myocarditis, confirming the diagnosis. Rheumatic heart disease, hypertrophic cardiomyopathy, dilated cardiomyopathy, and cardiac angiosarcoma are less likely based on the clinical presentation and biopsy findings.

The most likely mechanism for heart failure in this case is reduced preload. Preload refers to the amount of blood that fills the ventricles of the heart during diastole, and reduced preload means that there is a decreased amount of blood filling the ventricles. In this case, the widely distended pericardial sac filled with serous fluid suggests the presence of pericardial effusion, which can compress the heart and reduce the amount of blood that can fill the ventricles. This can lead to decreased cardiac output and heart failure.

Diagnostic significance The main clinical utility of either BNP or NT-BNP is that a normal level rules out heart failure.[2] Either marker can also be used for screening and prognosis of heart failure.[3] Both are also typically increased in patients with left ventricular dysfunction, with or without symptoms (BNP accurately reflects current ventricular status, as its half-life is 20 minutes, as opposed to 1–2 hours for NT-ProBNP).[4] BNP less than 100 pg per milliliter sensitivity = 90% specificity = 76% BNP less than 50 pg per milliliter sensitivity = 97% specificity = 62% some laboratories report in units ng per Litre (ng/L) which is equivalent to pg/ml For patients with congestive heart failure, BNP values will generally be above 100 pg/ml. FUN FACT: BNP is also one of the reasons why people will feel the need to urinate after getting into the bathtub or pool. The increased pressure on the body drives more fluid back into systemic circulation which in turn leads to a slight increase in preload. The left ventricle, and to a small degree the left atrium, secrete BNP in response. The natriuretic effect of BNP leads to an increase in urine production

CAUSES OF HIGH-OUTPUT FAILURE — The disorders contributing to high-output heart failure include: ■Systemic arteriovenous fistulas ■Hyperthyroidism ■Anemia, including the anemia of chronic kidney disease ■Beriberi (vitamin B1 or thiamine deficiency) ■Dermatologic disorders (eg, psoriasis) ■Renal disease ■Hepatic disease ■Skeletal disorders (eg, Paget disease, multiple myeloma) Other potential causes of high-output HF include obesity and carcinoid syndrome

THORACIC ANEURYSM A. Balloon-like dilation of the thoracic aorta B. Due to weakness in the aortic wall. Classically seen in tertiary syphilis; endarteritis of the vasa vasorum results in luminal narrowing decreased flow and atrophy of the vessel wall. Results in a 'tree-bark' appearance of the aorta (Fig. 7.12) C. Major complication is dilation of the aortic valve root, resulting in aortic valve insufficiency. 1. Other complications include compression of mediastinal structures (e.g., airway or esophagus) and thrombosis/embolism.

The x-ray shows a pattern consistent with pulmonary edema, which is a condition characterized by the accumulation of fluid in the lungs. This is supported by the patient's symptoms of shortness of breath and non-productive cough, which are commonly seen in pulmonary edema. Congestive heart failure and right-sided heart failure can both lead to pulmonary edema, but the x-ray alone does not provide enough information to differentiate between the two. Hypertension alone would not typically cause the findings seen on the x-ray. Therefore, pulmonary edema is the most likely diagnosis based on the information provided.

The most likely mechanism of heart failure in this patient is increased pressure overload. This is indicated by the presence of left atrial enlargement and pulmonary edema on the chest X-ray, as well as the physical examination findings of cyanosis, pedal edema, ascites, and rales in both lower lung fields. Increased pressure overload occurs when there is an increased resistance to blood flow out of the left ventricle, leading to increased pressure within the ventricle and ultimately causing heart failure.

The given information states that the examination of the endomyocardial biopsy obtained from a 14-year-old African girl reveals certain changes. Based on this information, the most likely diagnosis is rheumatic myocarditis. This is because rheumatic fever, which is caused by a streptococcal infection, can lead to inflammation of the heart muscle (myocarditis) in some cases. The patient's age and the presence of changes in the biopsy support this diagnosis.