A 72-year-old man comes to the office with intermittent symptoms of dyspnea on exertion, palpitations, and cough occasionally productive of blood. On cardiac auscultation, a low-pitched diastolic rumbling murmur is faintly heard at the apex. What is the most likely cause of the murmur?
The history and physical examination findings suggest mitral stenosis. Dyspnea may be present secondary to pulmonary edema; palpitations are often related to atrial arrhythmias (PACs, SVT, atrial flutter, or fibrillation); hemoptysis may occur as a consequence of pulmonary hypertension with rupture of bronchial veins. A diastolic rumbling apical murmur is characteristic. If the patient is in sinus rhythm, a late diastolic accentuation of the murmur occurs because of increased flow across the mitral valve with atrial contraction. A loud first heart sound and early diastolic opening snap may also be present. The etiology of mitral stenosis is usually rheumatic, rarely congenital. Hypertension may cause an S4 gallop but not a diastolic murmur. Myocardial infarction may cause mitral regurgitation because of papillary muscle dysfunction and anemia may cause a pulmonic flow murmur; both of these are systolic murmurs.
You are called to see a 21-year-old man in the emergency room with new onset of slurred speech and left hemiparesis. On auscultation the patient has a systolic murmur at the pulmonic region with a diastolic rumble along the left sternal border. The second heart sound is split and fixed relative to respiration. What is the likely cause of patient’s symptom?
This patient likely has experienced a paradoxical embolus causing acute embolic stroke. In paradoxical embolism, a venous thrombus (usually from the leg or pelvic veins) passes into the systemic circulation through an intracardiac defect, typically an atrial septal defect (ASD) or less commonly through a ventricular septal defect (VSD). In ASD, a mid-systolic murmur can often be appreciated due to increased flow across the pulmonic valve. During diastole, a middiastolic rumbling murmur may be appreciated along the sternal border due to increased flow across tricuspid valve. A prominent right ventricular impulse and palpable pulmonary artery pulsation may sometime be appreciated. The second heart sound is widely split and is relatively fixed in relation to respiration. Ventricular septal defect usually presents as a holosystolic murmur at the mid-left sternal border. Both the murmur of VSD and mitral regurgitation are enhanced by exercise and diminished by amyl nitrate. Aortic insufficiency causes a diastolic decrescendo murmur at the mid left sternal border. A patent ductus arteriosus (PDA) results in a continuous “machinery” murmur heard best at the upper left sternal border. Coarctation of aorta usually presents with a midsystolic murmur over the left interscapular space which may become continuous if the lesion in the vessel is narrowed enough to cause high-velocity jet flow. Classic to this condition are arterial hypertension in the upper extremities and normal or low blood pressure, with diminished or delayed pulsations in the lower extremities. Chest x-ray findings such as sign of “3” due to indentation of the aorta at the site of coarctation with pre and post-stenotic dilatation and rib notching due to rib erosions by dilated collateral vessels are classic findings. Aortic insufficiency, PDA, and coarctation of the aorta are not associated with paradoxical embolism.
A 68-year-old man was intubated in the emergency room because of pulmonary edema. Stat echocardiogram reveals an ejection fraction of 45% and severe mitral regurgitation. In spite of aggressive diuresis with furosemide, the patient continues to require mechanical ventilation secondary to pulmonary edema. What is the best next step in treating this patient?
The patient has severe mitral regurgitation (MR) with resultant pulmonary edema. During systole, blood follows the course of least resistance. Cardiac output is determined by the amount of resistance to flow into the aorta (afterload) and the amount of resistance to flow across the malfunctioning mitral valve. As the resistance to retrograde flow across the leaky mitral valve decreases, a larger proportion of stroke volume flows into the left atrium rather than across the aortic valve. This patient’s pulmonary edema is primarily caused by retrograde flow across the MV. To increase antegrade flow (thereby increasing cardiac output and decreasing pulmonary vascular congestion) we should reduce the left ventricular afterload. Lower resistance to flow through the LV outflow tract will increase the proportion of stroke volume that enters systemic circulation. Vasodilators such as ACE inhibitors and hydralazine are frequently used. Nitroprusside is another consideration. This patient will likely benefit from MV replacement, but his perioperative risk will be reduced if he can be stabilized first. Contractility is usually preserved in mitral regurgitation, so an inotropic agent such as milrinone or the less potent digoxin will not provide as much benefit as an afterload-reducer. Beta-blockers do not have a major vasodilator effect and will not be useful in afterload reduction. A second loop diuretic is unlikely to be as beneficial as an intervention that improves the patient’s hemodynamics.
A 30-year-old woman presents with a chief complaints of palpitations. A 24-hour Holter monitor shows occasional unifocal premature ventricular contractions and premature atrial contractions. An echocardiogram reveals left ventricular ejection fraction to be greater than 60%. Which of the following is the best management for this patient?
Minimally symptomatic premature atrial and premature ventricular contractions in the absence of structural heart disease are benign and do not require treatment. Antiarrhythmic therapy in this setting has not been shown to reduce sudden cardiac death or overall mortality. A beta-blocker would be the best choice if symptoms begin to interfere with daily activities. Digoxin is not useful in this setting. Type 1 antiarrhythmics (such as quinidine) carry significant risks, including an increased incidence of ventricular tachycardia.
An active 78-year-old woman with hypertension presents with a new left hemiparesis. Cardiac monitoring reveals atrial fibrillation. She had been in sinus rhythm 3 months earlier. She takes a beta-blocker for her blood pressure. Aside from blood pressure and heart rate control, which of the following is appropriate?
Anticoagulation is important in patients with atrial fibrillation who have risk factors for stroke. Risk factors can be calculated from the CHADS2 score, an easy to remember mnemonic (C—CHF, H—hypertension, D—diabetes mellitus, A—age ≥ 75 and S—previous stroke or transient ischemic attack). Each risk factor is equivalent to 1 point except for stroke or TIA, which is 2 points. Scores of greater than 2 would benefit with anticoagulation such as warfarin with target INR of 2 to 3. Rheumatic mitral valve stenosis, marked left atrial enlargement (> 5.0 cm), and left atrial thrombus seen on echocardiography may be additional risk factors. Other scoring systems are also available. Immediate direct current cardioversion is appropriate for hemodynamically unstable patients with atrial fibrillation but would not be indicated in this patient. Antiplatelet agents might be considered in patients with a CHADS2 score less than 2 or if anticoagulation is contraindicated. An implantable defibrillator is not indicated for atrial fibrillation unless left ventricular ejection fractions is less than 35% or there is a history of sudden cardiac death. Pacemakers are usually reserved for cases refractory to standard therapy and who have received AV nodal ablation.
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