Does my patient have critical aortic stenosis? How to find out and what to do?
PSLA parasternal long axis
PSSA parasternal short axis
4CPV four chamber apical view
CW continuous wave
AVA aortic valve area
MG mean gradient
AS aortic stenosis
A 76 year old male with a history of hypertension, chronic kidney disease, atrial fibrillation and hyperlipidemia presents to the emergency department with hypotension. The patient complains of chest pain and shortness of breath. BP 75/40, HR 110 ( irregular ), SpO2 82% and Afebrile. Patient given aggressive IV fluids and started on antibiotics. POCUS enthusiast on call arrives to bedside. Starting with the lung ultrasound (mage 1) and echocardiography (Image 2).
How to diagnose critical aortic stenosis ?
Any patient with a significant aortic stenosis will have some visible abnormality of the aortic valve which can be identified with a good PSLA, PSSA and a 4CA views. A thick left ventricle with concentric hypertrophy is commonly seen. After this initial screening the next step is to get a good 4 chamber view/suprasternal view/right parasternal view and place a CW doppler through the aortic valve (Image 3). The highest peak velocity is selected to trace and measure the mean gradient (MG). The machine calculates the mean gradient and the aortic valve area (AVA) can be calculated with the continuity equation (more on this in a future post).
Discordance between AVA and MG can be seen in low stroke volume and sometimes normal stroke volume states ( more on this in a future post )
What about the rhythm?
Patients need their atrial kick to maintain normal cardiac output. Cardioversion (electrical or chemical) can be helpful in some patients. In case of permanent atrial fibrillation, rate control with digoxin and/or amiodarone is the only option.
How about fluid management, vasopressors and diuresis?
A hypotensive severe AS patient is one of the most challenging and fascinating patients to manage. These patients are very preload-dependent but at the same time have a very high LVEDP with a fixed cardiac output. A low preload will lead to decrease in cardiac output and thus hypotension. A very high preload with lack of an atrial kick can lead to pulmonary edema. Our patient was labelled as septic and thus was given the magic fluid volume of 30 cc per kg saline and with the new loss of atrial kick ended up in pulmonary edema. Ideal management would be to optimize preload with gentle fluids and to use a vasopressor like phenylephrine. The high afterload in severe AS is from the valve itself and not from the blood vessels. In case of pulmonary edema preload, reduction agents need to be used with caution.
- A hypotensive patient with a thick AV with restrictive movement seen on POCUS, needs to be evaluated for severe AS.
- Patients with severe AS need the absolute correct fluid balance. Too much fluid (preload) can cause pulmonary edema and too little fluid can lead to hypotension.
- In severe AS, phenylephrine is considered by many as the least harmful vasopressor.
- Loss of atrial kick can lead to shock and pulmonary edema depending on the fluid balance