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Emergency And Acute Medicine – Heart Murmur
Basics And Description
Heart murmurs are sounds produced by normal physiologic flow or by functional and structural abnormalities of the heart. Stenotic lesions result in pressure overload of the chamber proximal to the valve, leading to compensatory hypertrophy. Regurgitant lesions cause volume overload of the preceding chamber, resulting in chamber dilatation. Genetic abnormalities and congenital defects may also produce abnormal cardiac blood flow and murmurs.
Etiology
Aortic stenosis may result from rheumatic heart disease, congenital bicuspid valve, calcification, or prosthetic valves. Aortic regurgitation is associated with rheumatic disease, endocarditis, aortic dissection, and prosthetic valves. Mitral stenosis is commonly caused by rheumatic heart disease, rheumatologic disorders such as systemic lupus erythematosus, calcification, atrial myxoma, congenital abnormalities, or prosthetic valves.
Acute mitral regurgitation may occur due to endocarditis, papillary muscle rupture or dysfunction, rupture of chordae tendineae, or prosthetic valve failure, while chronic mitral regurgitation is associated with rheumatic disease, mitral valve prolapse, and connective tissue disorders such as Marfan syndrome. Mitral valve prolapse itself may be congenital or related to connective tissue disease.
Tricuspid stenosis is usually rheumatic in origin, whereas tricuspid regurgitation may result from rheumatic disease, endocarditis, or pulmonary hypertension. Pericardial friction rubs arise from pericarditis or pericardial effusion. Ventricular septal defects may be congenital, traumatic, or postinfarction. Ventricular assist devices produce mechanical flow sounds due to implantable pumps supporting ventricular function.
Pediatric And Congenital Causes
Pulmonic stenosis is often congenital and may be associated with maternal–fetal rubella exposure or rheumatic disease. Pulmonic regurgitation may be congenital or related to pulmonary hypertension. Atrial septal defects and patent ductus arteriosus are congenital, with PDA also associated with prematurity and maternal rubella exposure. Coarctation of the aorta is congenital and linked to Turner syndrome. Hypertrophic cardiomyopathy, also known as idiopathic hypertrophic subaortic stenosis, is a congenital condition with a genetic predisposition.
Clinical Features And Murmur Characteristics
Aortic stenosis presents with a systolic crescendo–decrescendo murmur radiating to the carotids, diminished and delayed carotid upstroke (parvus et tardus), angina, exertional dyspnea, and syncope. Aortic regurgitation produces a diastolic blowing murmur along the left sternal border with findings such as widened pulse pressure, pulmonary edema, tachycardia, chest pain, Austin Flint murmur, Corrigan pulse, Quincke pulse, and de Musset sign.
Mitral stenosis causes a diastolic rumbling murmur at the apex with a loud S1 and opening snap, accompanied by dyspnea, orthopnea, hemoptysis, pulmonary edema, atrial fibrillation, and systemic emboli. Acute mitral regurgitation presents with a harsh systolic murmur at the apex and pulmonary edema, while chronic mitral regurgitation produces a holosystolic murmur radiating to the axilla with dyspnea, fatigue, and atrial fibrillation.
Mitral valve prolapse is characterized by an early- to mid-systolic click followed by a systolic murmur and may cause palpitations and chest pain. Tricuspid stenosis causes a diastolic murmur with peripheral edema, hepatosplenomegaly, ascites, atrial fibrillation, and prominent jugular venous A waves. Tricuspid regurgitation presents with a holosystolic murmur along the left sternal border and large V waves in the jugular venous pulse.
Patent ductus arteriosus produces a continuous machinery murmur and may lead to heart failure. Pericardial friction rubs are intermittent with systolic and/or diastolic components. Ventricular septal defects cause a harsh holosystolic murmur at the lower left sternal border. Ventricular assist devices generate a continuous or pulsatile mechanical hum, often with adequate perfusion despite absent palpable pulses.
Pediatric Murmur Features
Pulmonic stenosis presents with a systolic ejection murmur at the left upper sternal border, possible thrill, widely split S2, exertional dyspnea, and signs of right heart failure in severe cases. Pulmonic regurgitation causes a high-pitched early diastolic murmur with a widely split S2 and may be associated with pulmonary hypertension. Atrial septal defects often present with a systolic ejection murmur and wide fixed S2, while patent foramen ovale produces no murmur. Coarctation of the aorta may cause a continuous or late systolic murmur with differential upper and lower extremity pulses. Hypertrophic cardiomyopathy presents with a harsh systolic murmur that increases with Valsalva and may cause dyspnea, chest pain, syncope, or sudden death.
Physical Examination Focus
Evaluation includes careful auscultation of the heart and lungs, assessment of peripheral pulses, perfusion, edema, and jugular venous findings.
Essential Evaluation
Further assessment is guided by suspected pathology, with reference to specific valvular or congenital heart disease entities when appropriate.
Diagnostic Testing And Interpretation
Electrocardiography and chest radiography are commonly obtained. Echocardiography is essential for evaluating valves, chamber size, and flow patterns. CT imaging may be required to exclude aortic dissection. Acute regurgitant lesions may require cardiac catheterization.
Differential Diagnosis
Differential considerations mirror the underlying etiologies of murmurs and associated cardiac conditions.
Initial And Emergency Management
Prehospital care includes cautious IV fluid administration, especially in critical aortic stenosis, and oxygen as needed. In the emergency department, management focuses on oxygen, IV access, cardiac monitoring, and treatment of associated conditions such as heart failure or arrhythmias. Fluids and medications must be used cautiously in patients with aortic stenosis.
Medications
Therapy may include digoxin for rate control, calcium channel blockers or beta blockers for arrhythmias, diuretics for volume overload, anticoagulation when indicated, and vasodilators such as nitroglycerin or nitroprusside with careful monitoring. Medication choice depends on the underlying lesion and hemodynamic status.
Disposition And Follow-Up
Admission is required for patients with ischemia, syncope, pulmonary edema, hemodynamic instability, endocarditis, or significant arrhythmias. Asymptomatic and hemodynamically stable patients may be discharged with follow-up. New murmurs warrant referral to a primary provider or cardiologist.
Follow-Up Advice
Patients should inform all medical and dental providers of their heart murmur. Antibiotic prophylaxis may be necessary before certain procedures to prevent endocarditis.
Clinical Insights And Pitfalls
New heart murmurs accompanied by fever must prompt evaluation for infective endocarditis.
Basics And Description
Heart murmurs are sounds produced by normal physiologic flow or by functional and structural abnormalities of the heart. Stenotic lesions result in pressure overload of the chamber proximal to the valve, leading to compensatory hypertrophy. Regurgitant lesions cause volume overload of the preceding chamber, resulting in chamber dilatation. Genetic abnormalities and congenital defects may also produce abnormal cardiac blood flow and murmurs.
Etiology
Aortic stenosis may result from rheumatic heart disease, congenital bicuspid valve, calcification, or prosthetic valves. Aortic regurgitation is associated with rheumatic disease, endocarditis, aortic dissection, and prosthetic valves. Mitral stenosis is commonly caused by rheumatic heart disease, rheumatologic disorders such as systemic lupus erythematosus, calcification, atrial myxoma, congenital abnormalities, or prosthetic valves.
Acute mitral regurgitation may occur due to endocarditis, papillary muscle rupture or dysfunction, rupture of chordae tendineae, or prosthetic valve failure, while chronic mitral regurgitation is associated with rheumatic disease, mitral valve prolapse, and connective tissue disorders such as Marfan syndrome. Mitral valve prolapse itself may be congenital or related to connective tissue disease.
Tricuspid stenosis is usually rheumatic in origin, whereas tricuspid regurgitation may result from rheumatic disease, endocarditis, or pulmonary hypertension. Pericardial friction rubs arise from pericarditis or pericardial effusion. Ventricular septal defects may be congenital, traumatic, or postinfarction. Ventricular assist devices produce mechanical flow sounds due to implantable pumps supporting ventricular function.
Pediatric And Congenital Causes
Pulmonic stenosis is often congenital and may be associated with maternal–fetal rubella exposure or rheumatic disease. Pulmonic regurgitation may be congenital or related to pulmonary hypertension. Atrial septal defects and patent ductus arteriosus are congenital, with PDA also associated with prematurity and maternal rubella exposure. Coarctation of the aorta is congenital and linked to Turner syndrome. Hypertrophic cardiomyopathy, also known as idiopathic hypertrophic subaortic stenosis, is a congenital condition with a genetic predisposition.
Clinical Features And Murmur Characteristics
Aortic stenosis presents with a systolic crescendo–decrescendo murmur radiating to the carotids, diminished and delayed carotid upstroke (parvus et tardus), angina, exertional dyspnea, and syncope. Aortic regurgitation produces a diastolic blowing murmur along the left sternal border with findings such as widened pulse pressure, pulmonary edema, tachycardia, chest pain, Austin Flint murmur, Corrigan pulse, Quincke pulse, and de Musset sign.
Mitral stenosis causes a diastolic rumbling murmur at the apex with a loud S1 and opening snap, accompanied by dyspnea, orthopnea, hemoptysis, pulmonary edema, atrial fibrillation, and systemic emboli. Acute mitral regurgitation presents with a harsh systolic murmur at the apex and pulmonary edema, while chronic mitral regurgitation produces a holosystolic murmur radiating to the axilla with dyspnea, fatigue, and atrial fibrillation.
Mitral valve prolapse is characterized by an early- to mid-systolic click followed by a systolic murmur and may cause palpitations and chest pain. Tricuspid stenosis causes a diastolic murmur with peripheral edema, hepatosplenomegaly, ascites, atrial fibrillation, and prominent jugular venous A waves. Tricuspid regurgitation presents with a holosystolic murmur along the left sternal border and large V waves in the jugular venous pulse.
Patent ductus arteriosus produces a continuous machinery murmur and may lead to heart failure. Pericardial friction rubs are intermittent with systolic and/or diastolic components. Ventricular septal defects cause a harsh holosystolic murmur at the lower left sternal border. Ventricular assist devices generate a continuous or pulsatile mechanical hum, often with adequate perfusion despite absent palpable pulses.
Pediatric Murmur Features
Pulmonic stenosis presents with a systolic ejection murmur at the left upper sternal border, possible thrill, widely split S2, exertional dyspnea, and signs of right heart failure in severe cases. Pulmonic regurgitation causes a high-pitched early diastolic murmur with a widely split S2 and may be associated with pulmonary hypertension. Atrial septal defects often present with a systolic ejection murmur and wide fixed S2, while patent foramen ovale produces no murmur. Coarctation of the aorta may cause a continuous or late systolic murmur with differential upper and lower extremity pulses. Hypertrophic cardiomyopathy presents with a harsh systolic murmur that increases with Valsalva and may cause dyspnea, chest pain, syncope, or sudden death.
Physical Examination Focus
Evaluation includes careful auscultation of the heart and lungs, assessment of peripheral pulses, perfusion, edema, and jugular venous findings.
Essential Evaluation
Further assessment is guided by suspected pathology, with reference to specific valvular or congenital heart disease entities when appropriate.
Diagnostic Testing And Interpretation
Electrocardiography and chest radiography are commonly obtained. Echocardiography is essential for evaluating valves, chamber size, and flow patterns. CT imaging may be required to exclude aortic dissection. Acute regurgitant lesions may require cardiac catheterization.
Differential Diagnosis
Differential considerations mirror the underlying etiologies of murmurs and associated cardiac conditions.
Initial And Emergency Management
Prehospital care includes cautious IV fluid administration, especially in critical aortic stenosis, and oxygen as needed. In the emergency department, management focuses on oxygen, IV access, cardiac monitoring, and treatment of associated conditions such as heart failure or arrhythmias. Fluids and medications must be used cautiously in patients with aortic stenosis.
Medications
Therapy may include digoxin for rate control, calcium channel blockers or beta blockers for arrhythmias, diuretics for volume overload, anticoagulation when indicated, and vasodilators such as nitroglycerin or nitroprusside with careful monitoring. Medication choice depends on the underlying lesion and hemodynamic status.
Disposition And Follow-Up
Admission is required for patients with ischemia, syncope, pulmonary edema, hemodynamic instability, endocarditis, or significant arrhythmias. Asymptomatic and hemodynamically stable patients may be discharged with follow-up. New murmurs warrant referral to a primary provider or cardiologist.
Follow-Up Advice
Patients should inform all medical and dental providers of their heart murmur. Antibiotic prophylaxis may be necessary before certain procedures to prevent endocarditis.
Clinical Insights And Pitfalls
New heart murmurs accompanied by fever must prompt evaluation for infective endocarditis.
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