Learning objectives

• Describe the underlying mechanisms of AR
• Recognize the symptoms of AR
• Manage patients with AR

Definition & mechanisms

• Aortic regurgitation (AR) is defined as diastolic reversal of blood flow from the aorta into the left ventricle
• Most common etiology: Atherosclerotic degeneration of the valve, especially in the presence of a bicuspid aortic valve
• Acute AR:
  • May develop from:
    • Valvular abnormalities (most commonly infective endocarditis)
    • Aortic abnormalities (mostly aortic dissection) 
    • Iatrogenic causes such as traumatic injury (i.e., motor vehicle accident) or during transcutaneous aortic valve procedures
  • Characterized by an abrupt increase in left ventricular end-diastolic volume
  • In severe cases, patients often present with pulmonary edema and even cardiogenic shock
• Chronic AR:
  • Most commonly caused by atherosclerotic degeneration of the valve and/or congenital bicuspid aortic valve
  • In the early phases, compensatory mechanisms keep the left ventricular ejection fraction in the normal range
  • Over time, the LV dilates and hypertrophies to normalize wall stress by maintaining the ratio of ventricular wall thickness to cavity radius
  • Compensatory mechanisms allow patients to remain stable and asymptomatic for many years, even in the presence of severe AR
  • If wall thickening fails to keep up with the volume overload, there is an increase in wall stress which then results in a reduction in LV systolic function and LVEF due to myocyte damage
  • As LV filling pressures rise, symptoms of fatigue and dyspnea may appear 
  • Angina can develop even in the presence of normal coronary arteries
  • Pulmonary edema and heart failure can occur due to chronically elevated left-sided filling pressures

Signs & symptoms

• Symptoms
  • Chronic AR
    • Patients with chronic AR remain asymptomatic for years. When symptoms appear, they are due to left heart failure:
      • Chest pain
      • Increasing exercise intolerance
      • Dyspnea
      • Paroxysmal nocturnal dyspnea
      • Orthopnea
  • Acute AR
    • Because of a lack of chronic compensation, patients usually present with pulmonary edema and heart failure refractory to optimal medical therapy
    • Patients are often hypotensive and clinically appear to be on the verge of cardiovascular collapse
• Diagnostic signs
  • Collapsing pulse and wide pulse pressure
  • Displaced apex inferolaterally
  • Early diastolic high-pitched murmur 
  • An Austin-Flint murmur may be heard in mid-diastole at the apex
  • De Musset’s sign – Head nodding with each pulse
  • Corrigan’s sign – Visible carotid pulsation

Severity assessment

• Echocardiography is the best diagnostic tool to evaluate the severity of AR. A rough guideline for approximating severity is the width of the AR jet compared to the width of the left ventricular outflow tract: 
  • <1/3: Mild
  • 1/3–2/3: Moderate 
  • >2/3: Severe

Management

Acute severe AR management

• Sudden aortic incompetence results in acute pulmonary congestion
• Immediate management: 
  • Afterload reduction (nitroprusside) 
  • Enhancement of contractility and heart rate (dobutamine)
  • Emergency surgical intervention is likely necessary
  • Intra-aortic balloon pump is contraindicated

Suggested reading

• Flint N, Wunderlich NC, Shmueli H, Ben-Zekry S, Siegel RJ, Beigel R. Aortic Regurgitation. Curr Cardiol Rep. 2019;21(7):65. 
• Pollard BJ, Kitchen, G. Handbook of Clinical Anaesthesia. Fourth Edition. CRC Press. 2018. 978-1-4987-6289-2.
• Hines, R. L. (2017). Stoelting’s anesthesia and co-existing disease (7th ed.). Elsevier – Health Sciences Division
• Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [published correction appears in Circulation. 2014 Jun 10;129(23):e650]. Circulation. 2014;129(23):2440-2492.