A 79 year old female presented to the emergency room with worsening dyspnea on exertion. She reported orthopnea, leg swelling, and only being able to walk a few steps without getting short of breath. She denied chest pain, fever, or productive cough, and she had been compliant with her medications. Of note, the patient was seen 3 weeks ago for chest pain, at which point she had a dobutamine stress echo that demonstrated non-reversible ischemic changes. During examination, the providers noted JVD, crackles at bilateral bases, and bilateral lower extremity pitting edema.
Vitals: T 97.3 BP 152/81 HR 83 RR 18 SPO2 97% on RA
Your initial impression is a slamdunk heart failure exacerbation. However, a bedside ECHO is performed normal ejection fraction. This doesn’t appear to be the classic HFrEF exacerbation you’ve seen countless times before. What do we see in the echo below? What does it tell us about this patient's diastolic function?
Answer and Learning Points
Answer:
The two images above are an apical four chamber view with the doppler gait measuring mitral inflow velocity and tissue doppler, respectively. They show Grade 1 diastolic dysfunction.
Assessing for diastolic dysfunction is best achieved with an apical four chamber view and involves two measurements: mitral inflow and tissue doppler. Mitral inflow velocity is measured by placing pulsed-wave doppler at the mitral valve leaflet tips. During diastole, there are two surges of blood flow through the mitral valve. The first is Early filling immediately after the valve opens (E wave), representing ventricular relaxation. The second wave comes from the Atrial kick (A wave). In normal diastolic function, the E wave should be larger than the A wave because most of the blood enters the ventricle during relaxation, with the atrial kick subsidizing this.
Look at the diagram below to see how the E/A wave changes with the different grades of diastolic dysfunction. In our patient, the A wave was larger than the E wave so we knew this patient had grade 1 diastolic dysfunction, i.e. impaired relaxation. This happens when the stiff ventricle no longer pulls most of the blood in with relaxation (as relaxation is impaired), so the atrial kick does most of the diastolic filling. Our patient was admitted to cardiology for IV diuresis and medical optimization.
For patients whose E wave is larger than their A wave, it can be unclear whether this is a normal, pseudonormal or restrictive pattern. Tissue doppler can help further assess whether this. Place the doppler gate at the mitral valve annulus to assess left ventricular muscle relaxation. As diastolic dysfunction worsens, the ability of the left ventricle to relax will progressively worsen. Looking at the diagram below again, we see that in normal diastolic function the e' wave will be larger than the a', but as the ventricle loses its ability to relax the e' wave will get smaller. If the e' is the same size or smaller than the a' this represents diastolic dysfunction.
Learning Points:
- Heart failure with preserved ejection fraction makes up half of the patients with heart failure.
- HFpEF can be assessed in the apical four chamber view by evaluating the mitral valve inflow at the leaflet tips and tissue doppler at the annulus.
- The E wave is blood flow through the mitral valve during early diastole and the A wave is during the atrial kick.
- In one study, sensitivity and specificity of diagnosing clinically significant diastolic dysfunction was 92% and 69% respectively for emergency physician conducted echocardiography (1).
References
- Dinh, Vi. How to Measure and Grade Diastolic Dysfunction Using Echocardiography. POCUS 101. https://www.pocus101.com/how-to-measure-and-grade-diastolic-dysfunction-using-echocardiography/ Accessed August 2nd, 2020.
- Ehrman, Robert, et al. Can emergency physicians diagnose and correctly classify diastolic dysfunction using bedside echocardiography? American Journal of Emergency Medicine. 2015; 33:1178-1183.
This post was written by Megan Jackson, PGY1 at UCSD Emergency Medicine Residency Program, Charles Murchison, MD and Amir Aminlari MD