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American physician Austin Flint first described his namesake murmur in 1862. In his own poetic words: "The murmur is oftener rough than soft. The roughness is often peculiar. It is a blubbering sound, resembling that produced by throwing the lips or the tongue into vibration with the breath of respiration." The murmur is described in modern terms as a low-pitched mid to late diastolic rumble heard best at the apex of the heart and is associated with severe aortic regurgitation. This activity examines when this condition merits consideration in the differential diagnosis and how to evaluate it properly. This activity highlights the role of the interprofessional team in caring for patients with this condition. Objectives: Identify the pathophysiology of the Austin Flint murmur. Assess the workup of a patient with an Austin Flint murmur. Differentiate the treatment and management options available for a patient with Austin Flint murmur. Communicate interprofessional team strategies for improving care coordination to advance the treatment of aortic regurgitation and improve outcomes. Access free multiple choice questions on this topic.

American physician Austin Flint first described his namesake murmur in 1862.[1] In his own poetic words: "The murmur is oftener rough than soft. The roughness is often peculiar. It is a blubbering sound, resembling that produced by throwing the lips or the tongue into vibration with the breath of respiration." The murmur is described in modern terms as a low-pitched mid to late diastolic rumble heard best at the apex of the heart and is associated with severe aortic regurgitation.

As others had previously suggested, an echocardiogram-based study found the Austin Flint murmur was not associated with rapid mitral inflow.[2] The authors concluded that the murmur resulted from the regurgitant aortic jet alone.[2] Another study of echocardiogram findings found that the auscultated sound resulted from the abutment of the aortic regurgitant jet against the left ventricular epicardium.[3] A prior study suggested that the Austin Flint murmur arose from a regurgitant aortic jet directed at the anterior mitral leaflet, resulting in the leaflet shuddering.[4] The authors hypothesized that this shuddering resulted in vibrations and shock waves that ultimately distorted the regurgitant aortic jet and caused the familiar sound heard in the Austin Flint murmur. Ultimately, there is no consensus about the cause of the sound auscultated as the Austin Flint murmur.

One would expect the Austin Flint murmur's prevalence to correlate with severe aortic regurgitation. In the Framingham study, moderate to severe aortic regurgitation incidence was less than 1% in age groups under 70 years old.[5] In the 70 to 83-year-old age group, the incidence was 2.2% for men and 2.3% for women.[5] However, not all patients with severe aortic regurgitation have an Austin Flint murmur; therefore, the true prevalence of the murmur is currently unknown.

In developing countries, the most common cause of aortic regurgitation remains rheumatic heart disease.[6] In developed countries, aortic regurgitation occurs most often in young patients with a bicuspid aortic valve and in patients with advanced age when the burden of calcific aortic disease is highest.[5]

The Austin Flint murmur is a rumbling diastolic murmur best heard at the heart's apex associated with severe aortic regurgitation and is usually heard best in the fifth intercostal space at the midclavicular line. Younger patients are more likely to have a history of a bicuspid aortic valve or rheumatic heart disease, while older patients are more likely to suffer from calcific valvular disease. A blood pressure reading on the patient shows an increased pulse pressure due to the backflow of blood through the aortic valve during diastole. An astute clinician may be able to palpate a "water hammer" pulse, also known as "Corrigan's pulse." This finding demonstrates arterial swelling followed by a brisk diastolic fall. Patients may endorse a history of syncope or lightheadedness associated with an inability to maintain forward flow through the aortic valve and the significant difference between systolic and diastolic pressure. Decreasing exercise tolerance and the inability to perform activities of daily living should prompt screening for this condition.

The most appropriate test to order in a patient with an Austin Flint murmur is a transthoracic Doppler echocardiogram.[7] A cardiac magnetic resonance imaging scan indicates whether the echocardiogram images are suboptimal due to body habitus.[7] The American College of Cardiology and the American Heart Association recommend yearly monitoring with a transthoracic echocardiogram in severe asymptomatic aortic regurgitation.[7] Despite being asymptomatic, this monitoring interval should be shortened in patients with left ventricular dilation.

Treatment and management of a patient with an Austin Flint murmur are the same as other patients with severe aortic regurgitation, regardless of whether an Austin Flint murmur is present. Medical management consists of treating hypertension with afterload-reducing agents such as dihydropyridine calcium channel blockers or angiotensin-converting enzyme inhibitors/angiotensin receptor blockers.[7] Definitive management is with aortic valve replacement.[7] Metallic prosthetic valves are preferred in younger patients who can tolerate anticoagulation due to increased longevity compared to bioprosthetic valves.[7] Elderly patients and patients with contraindications to anticoagulation should undergo implantation of bioprosthetic valves, which do not require the same lifelong anticoagulation therapy as a metallic valve.[7] Patients who are poor surgical candidates, as determined by the Society of Thoracic Surgeons' cardiac risk score (STS score), can be evaluated for the implantation of a transcatheter aortic valve replacement.[7]

The differential diagnosis for patients with a cardiac murmur and a widened pulse pressure includes conditions associated with hyperdynamic circulation. These include: Thyrotoxicosis Severe anemia Wet beriberi or thiamine deficiency Presence of arteriovenous fistulae Pregnancy Other intracardiac causes of similar physical presentation include: Infective endocarditis Mitral stenosis Tricuspid stenosis Mitral regurgitation Pulmonic regurgitation As originally described by Flint in 1862, the murmur was "presystolic in timing and indistinguishable from that of mitral stenosis."[1] The Austin Flint murmur can be differentiated from organic mitral stenosis by an opening snap in mitral stenosis. Further differentiation is achievable with amyl nitrate inhalation, which decreases the intensity of the Austin Flint murmur due to a decrease in afterload. The murmur of mitral stenosis increases in both duration and intensity with amyl nitrate inhalation.

The prognosis of patients with severe aortic regurgitation associated with the Austin Flint murmur depends on a variety of factors. Within 10 years of diagnosis of severe aortic regurgitation, 75% of patients either pass away or require valve replacement.[8] Predictors of survival include age, functional class, comorbidities, atrial fibrillation, and left ventricular end-systolic diameter corrected for body surface area.[8] Those with severe left ventricular dysfunction have a survival rate of 62% compared to 96% in patients with preserved left ventricular function.[9]

Complications of severe chronic aortic regurgitation include progressive left ventricular dysfunction and dilation that can lead to progressive, symptomatic congestive heart failure, myocardial infarction, arrhythmias, and sudden cardiac death. Symptomatic aortic regurgitation portends a higher risk of complications, and echocardiographic findings show reduced left ventricular ejection fraction and worsening left ventricular end-systolic dimension. This highlights the importance of monitoring patients with aortic regurgitation to prevent adverse outcomes.

The first consultation for a patient with an Austin Flint murmur should be with a cardiologist. The cardiologist can medically manage the patient while they coordinate care with prompt referral to a cardiothoracic surgeon to evaluate surgical aortic valve replacement. If the patient is not a candidate for a surgical aortic valve replacement due to an elevated STS score, an interventional cardiologist trained in structural heart disease should provide a consult to evaluate the patient for a transcatheter aortic valve replacement.

Patient education is key in ensuring adequate clinical outcomes for this disease. Patient education on medical compliance, including compliance with medications and routine monitoring, can help delay left ventricular dysfunction and optimize the timing of surgery. Patients should be encouraged to follow up regularly with a cardiologist for routine echocardiography to improve long-term outcomes.

The auscultation of an Austin Flint murmur correlates with severe aortic regurgitation. Coordinated care between the cardiologist, cardiothoracic surgeon, and an interventional cardiologist is integral to managing these complex patients. Surgical aortic valve replacement is the gold standard of care for patients who are candidates for replacement. In patients with prohibitively high STS scores, the surgeon should discuss the option for a transcatheter aortic valve approach with the patient. Long-term monitoring and patient education on symptom management can help delay the need for surgery in patients who are not candidates for replacement. Specialty-trained nurses in cardiology can help educate the patient on adequate medical management of symptoms, daily weight measurements, medication compliance, and compliance with routine testing to ensure patients receive optimal care. Asymptomatic patients with this disease should be screened for changes in exercise capacity and symptoms regularly. Specialty nurses can help obtain this data from patients at regularly scheduled intervals and notify the clinicians if symptoms develop. This helps optimize the timing of surgery and prevent complications. The recovery time from an aortic valve replacement is 4 to 8 weeks.  The most important factors in recovery are nutrition and exercise. Nutritional guidance should be provided before discharge, and follow-up with a nutritionist may benefit high-risk patients. When anticoagulation is appropriate, a board-certified cardiology specialty pharmacist should also provide input. Patients who are elderly or with significant comorbidities benefit from cardiac rehabilitation, which has been shown to increase aerobic capacity and quality of life.[10]