Heart and vascular exam medical

The cause and acuity of mitral regurgitation determines the clinical presentation; it may be asymptomatic or cause left-sided HF. • Mitral regurgitation results from Ischemia at base or rupture of papillary muscle (myocardial ischemia or infarction or infection [endocarditis]) Displacement of papillary muscles (dilated cardiomyopathy) Excessive length of chordae or myxomatous degeneration of leaflets (mitral valve prolapse) Noncontraction of annulus (annular calcification) Scarring (rheumatic fever, calcific invasion)

The blood pressure goal for most patients should be <140/<90 mm Hg; patients over age 80 years should be treated more gradually and a goal of <150/<90 mm Hg may be more reasonable. • Initiation of drug therapy is based on level of BP, cardiovascular risk factors, presence of target end-organ damage, and demographic considerations. • Medication classes include diuretics, β-adrenergic blocking agents, ACE inhibitors and angiotensin receptor blockers, calcium channel-blocking agents, α-adrenergic blockers, vasodilators, and centrally acting agents. • Choice of medication is based on presence of disease-specific indications (eg, β-blockers in CAD and heart failure, ACE inhibitors in renal disease and heart failure).

ECG shows LV hypertrophy. • Cardiac catheterization helps quantify the severity and evaluates the coronary arteries.

Diminished and delayed carotid pulses (pulsus parvus et tardus) • Soft, absent, or paradoxically split S2 • Harsh systolic murmur, classically crescendo-decrescendo, along the left sternal border, often radiating to the neck and sometimes associated with a thrill • Electrocardiography (ECG) with LVH; calcified valve on radiography; echocardiography is diagnostic

Chronic obstructive pulmonary disease (COPD) • Pneumonia • Cirrhosis • Peripheral venous insufficiency • Nephrotic syndrome

Chest radiography shows cardiomegaly with LV prominence and sometimes aortic dilatation. • Doppler echocardiography confirms the diagnosis and estimates the severity. • Annual echocardiographic assessments determine the timing of valve replacement when the aortic regurgitation is severe. • Computed tomography (CT) or magnetic resonance imaging (MRI) Can estimate aortic root size Can exclude ascending aneurysm

Left heart catheterization to detect CAD • Right heart catheterization: in patients not responding to standard therapy

Essentials of Diagnosis • Sudden development of prolonged (>30 minutes) anterior chest discomfort or pressure. • Sometimes painless, manifesting as acute HF, syncope, stroke, or shock. • ECG: ST-segment elevation or new left bundle branch block occurs with STEMI; ST depression or no ECG changes may be present in NSTEMI. • Immediate reperfusion treatment is warranted in STEMI with PCI within 90 minutes of first medical contact; fibrinolytic therapy within 30 minutes of hospital presentation and 12 hours of symptom onset if transfer to a facility with PCI will be delayed. • Early PCI and reperfusion may be indicated for NSTEMI depending on clinical factors.

High-pitched, decrescendo aortic diastolic murmur along the left sternal border without respiratory variation. • Water-hammer or Corrigan pulse: rapid rise and fall from high systolic and low diastolic pressures; Quincke pulses: pulsatile nail beds. • Duroziez sign: to-and-fro murmur over a partially compressed femoral artery. • Musset sign: head bob with each pulse. • Hill sign: leg systolic pressure higher than 40 mm Hg in the arm. • Exertional dyspnea and fatigue are the most frequent symptoms, but paroxysmal nocturnal dyspnea and pulmonary edema may also occur. • Chronic AR is usually slowly progressive; acute AR may present with acute LV failure.

Treatment must be guided by underlying etiology. Short-acting as-needed nitroglycerin, daily aspirin, β-blocker, long-acting nitrate, statin for stable angina pectoris. Empiric trial of high-dose proton pump inhibitor therapy has been reported to improve symptoms in patients with noncardiac chest pain of unknown etiology. Antidepressants may have modest benefit in reducing noncardiac chest pain. Psychological interventions (especially cognitive-behavioral) may have modest to moderate benefit. Hypnotherapy may have some benefit.

ECG. • Arterial line placement for blood pressure and arterial oxygen monitoring. • Foley catheter should be inserted to monitor urinary output. • Pulmonary artery catheter can distinguish cardiogenic from septic shock and monitor effects of volume resuscitation or pressor medications. • CVP measurement can suggest volume status. • Cardiac index is often low in cardiogenic shock and high in septic shock. • SVR is low in septic and neurogenic shock and high in hypovolemic and cardiogenic shock.

Chest radiograph: signs of heart failure, often lagging behind the clinical findings • Echocardiography: assesses global and regional LV function, wall motion

Drug therapy should be based on overall risk of cardiovascular events and LDL cholesterol level. • Indications for high intensity and moderate intensity statins have been formulated by the American Heart Association and American College of Cardiology. • Treatment guidelines no longer recommend treating to a goal LDL level, but rather selecting a statin intensity for each given risk level. • Most aggressive therapy is required for patients with CHD, diabetes mellitus, cerebrovascular disease, peripheral vascular disease, 10-year risk of CHD more than 20%. • HMG-CoA reductase inhibitors (statins) such as atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, and simvastatin reduce LDL, coronary events, and mortality. • Niacin can reduce LDL, increase HDL, and reduce triglycerides but commonly causes flushing. • Bile acid-binding resins (eg, cholestyramine, colestipol, and colesevelam) mainly reduce LDL; they have many gastrointestinal side effects. • Fibric acid derivatives (eg, gemfibrozil, fenofibrate) reduce LDL and triglycerides and raise HDL; side effects are greater when they are taken with statins. • There is no evidence that statins combined with other agents lead to better outcomes and such combination may increase side effects, even if cholesterol levels are reduced.

Chest radiography: cardiomegaly, pulmonary edema, and pleural effusions • Echocardiography: ventricular size and function, valvular abnormalities, pericardial effusions, intracardiac shunts, and segmental wall motion abnormalities • Radionuclide angiography and cardiac MRI: measure LV ejection fraction and assess regional wall motion • Stress imaging: indicated if ECG abnormalities or suspected myocardial ischemia

LV failure: exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, chronic nonproductive cough (often worse in recumbency), nocturia, fatigue, and exercise intolerance • Physical examination in LV failure: crackles and dullness to percussion at bases, parasternal lift, an enlarged and sustained LV impulse, S3 gallop, S4 gallop in diastolic dysfunction • RV failure: anorexia, nausea, right upper quadrant pain caused by chronic passive congestion of the liver and gut • Physical examination in RV failure: elevated and abnormal jugular venous pulsations, hepatic enlargement, hepatojugular reflux, ascites, and peripheral pitting edema • Tachycardia, hypotension, reduced pulse pressure, cold extremities, and diaphoresis • Long-standing severe HF: cachexia or cyanosis

Complete blood count, serum electrolytes, glucose and lactate, coagulation parameters, type and cross-match • Arterial blood gas determinations • Blood cultures

ACE inhibitors started at low dosages decrease mortality; angiotensin II receptor blockers are given for ACE-intolerant patients. • β-Blockers in stable patients (not acute exacerbation) have mortality benefit. • Aldosterone blockers such as spironolactone or eplerenone decrease mortality. • Diuretics such as loop or thiazides reduce symptoms of fluid overload. • Digoxin can reduce symptoms but does not have a mortality benefit. • Inotropic agents (eg, dobutamine or milrinone) may be given in cardiogenic shock or while awaiting transplantation. • Angiotensin receptor–neprilysin inhibitors (eg, sacubitril) are in the process of FDA approval and reduce the risk of death and hospitalization in patients with heart failure and reduced ejection fraction. • In heart failure with preserved ejection fraction, diuretics and rigorous blood pressure control are the only medications that are beneficial.

Low-fat diets may produce a moderate (5%–10%) decrease in LDL cholesterol. • Substituting monounsaturated fats for saturated fats can lower LDL without affecting HDL. • Exercise and moderate alcohol consumption can increase HDL levels. • Reducing alcohol, fatty food, and excessive dietary carbohydrate intake and controlling hyperglycemia in diabetics are effective for hypertriglyceridemia.

Mitral valve prolapse • Atrial myxoma • Cor triatriatum (congenital atrial anomaly)

Usually, asymptomatic • Headaches are the most frequent symptom but are nonspecific • Elevated BP • Loud A2 on cardiac examination • Retinal arteriolar narrowing with “silver-wiring,” arteriovenous nicking • Flame-shaped retinal hemorrhages

Congenital bicuspid valve is the most common etiology in middle-aged patients. • The cause in elderly patients is usually valvular degeneration from progressive calcification. • It is more frequent in men, smokers, and patients with hypercholesterolemia and hypertension. • Coronary artery disease is often coincident because risk factors are the same.

Pansystolic murmur at the apex, radiating into the axilla; associated with S3 when regurgitant volume is great. • ECG with LA abnormality, left ventricular hypertrophy (LVH), and often atrial fibrillation; LA and LV enlargement on chest radiograph. • Echocardiographic findings are diagnostic and can help decide when to operate.

Norepinephrine is generally used for vasodilatory shock, but may be used in all causes. • Dopamine has dopaminergic and β-agonist effect at low doses and α-adrenergic effects at high doses; it should only be used as an alternative to norepinephrine in select patients with septic shock, including those with significant bradycardia or low potential for tachyarrhythmias. • Phenylephrine can sometimes be used as a first-line agent for hyperdynamic septic shock. • Dobutamine is the first-line drug for cardiogenic shock without hypotension. Amrinone or milrinone can be substituted for dobutamine. • Epinephrine is the treatment of choice in anaphylactic shock and may be used in severe shock and during acute resuscitation. • Vasopressin is indicated for distributive or vasodilatory shock; it is also used in sepsis if requiring two drugs. • Broad-spectrum antibiotics are administered in septic shock. • Activated protein C (drotrecogin α) was proven ineffective for decreasing mortality in sepsis and withdrawn from the market.

ECG typically shows LA abnormality and often atrial fibrillation. • Cardiac catheterization can detect valve, coronary, or myocardial disease; it is usually done only after a decision to intervene has been made.

Hypovolemic shock: loss of blood from the gastrointestinal tract, uterus, or urinary tract or loss of fluids and electrolytes as from vomiting or diarrhea • Cardiogenic shock: myocardial infarction, cardiomyopathy, myocardial contusion, valvular regurgitation or stenosis, arrhythmias • Obstructive shock: cardiac tamponade, tension pneumothorax, massive pulmonary embolism • Distributive shock: sepsis, systemic inflammatory response syndrome from burns or severe pancreatitis, anaphylaxis, traumatic spinal cord injury, acute adrenal insufficiency Septic shock: gram-negative bacteremia, gram-positive cocci, gram-negative anaerobes; polymicrobial infections are almost as likely; incidence of sepsis caused by fungal organisms is increasing, but remains less than that for bacterial infections Anaphylactic shock: allergen exposure via injection, ingestion, contact, or inhalation Neurogenic shock: spinal cord injury, epidural of spinal anesthesia, vagal parasympathetic stimulation leading to hypotension, bradycardia, and syncope (eg, fright, pain, and gastric dilatation) Acute adrenal insufficiency: adrenal crisis in Addison disease or other hypocortisolism

An opening snap following A2 caused by a stiff mitral valve. • Low-pitched diastolic murmur (rumble) at the apex with the patient in the left decubitus position; increased by brief exercise. • Mild-to-moderate stenosis (valve area 1.5–1.0 cm2): LA pressure and cardiac output may be essentially normal; the patient may be asymptomatic or have dyspnea and fatigue with exertion, especially with tachycardia. • Severe stenosis (valve area <1.0 cm2): pulmonary hypertension, dyspnea, fatigue, right-sided HF, orthopnea, paroxysmal nocturnal dyspnea, and occasional hemoptysis. • Sudden increase in heart rate may precipitate pulmonary edema. • Atrial fibrillation is common and may precipitate dyspnea or pulmonary edema.

Urinalysis. • Serum creatinine, blood urea nitrogen, potassium, fasting glucose, cholesterol, uric acid. • Hemoglobin. • ECG. • When a secondary cause is suspected, consider chest radiography, plasma metanephrine levels, plasma aldosterone concentration, plasma renin activity, or urine electrolytes, as indicated.

Dyslipidemia is usually asymptomatic. • Extremely high levels of chylomicrons or very-low-density lipoprotein (VLDL) particles are associated with eruptive xanthomas. • Very high serum LDL levels are associated with tendinous xanthomas. • Very high serum triglycerides (>2000 mg/dL) are associated with lipemia retinalis (cream-colored vessels in the fundus) or pancreatitis. • The metabolic syndrome consists of a large waist circumference, elevated blood pressure, elevated serum triglycerides, low serum HDL cholesterol, and elevated serum glucose level (insulin resistance).

Can be classified as hypovolemic, cardiogenic, obstructive, and distributive (including septic, anaphylactic, and neurogenic). Hypovolemic results from decreased intravascular volume. Cardiogenic results from cardiac failure with inability of heart to maintain tissue perfusion. Obstructive results from acute decrease in cardiac output. Distributive causes include septic (most common), anaphylactic, and neurogenic; a reduction in systemic vascular resistance (SVR) results in inadequate cardiac output and tissue hypoperfusion despite normal circulatory volume. Septic shock may be caused by gram-negative or gram-positive bacteria. Anaphylactic shock is caused by an IgE-mediated allergic response. Neurogenic shock is caused by spinal cord injury or epidural anesthetic agents.

B-type natriuretic peptide (BNP) may be useful in diagnosis and prognostication of heart failure resulting from AS.