Sometimes, the worst thing you can do is hold your breath and hope for the best.
- Young woman
- Hx of PE on warfarin
- Brief unconscious episode in the surf in Autumn, brief CPR prior to rousing.
- Now extubated in ICU, BP 95/50
Echo requested to assess for a cause of syncope.
This is the first loop, a parasternal long axis window. What are the major findings?
RV appears dilated (the RV , LVOT and LA should all be roughly the same diameter in the PLAX window), with RV hypertrophy (the normal RV wall is <0.5cm) and the moderator band looks thick too. The LV systolic function appears normal. The walls come in ~ 1/3 of the LV internal diameter, and uniformly thicken by 50%. Slow the loop down if you aren’t convinced. There is no pericardial effusion seen here. We can also see B lines shooting down from the pleura.
The parasternal short axis window (PSAX). What do you think of the interventricular septum and what is the significance?
The interventricular septum is bowed to the right through both systole and diastole. This denotes right ventricular volume overload (diastolic D shape) and pressure overload (systolic D shape).
OK, so she has had another PE and we should tell the team to thrombolyse?
Well, no. Sure, the picture is pretty bad, even without an estimation of pulmonary pressures from TR. The RV appears dilated (the RV should be narrow and wrapping around the LV) but it is very thick, and there is a small pericardial effusion seen here with a tiny rim anteriorly and slightly thicker posteriorly. This all suggests a more chronic course.
PSAX, mid pap level. How severe is the RV volume and pressure overload?
Are you serious? This is very severe. Lets have a look at what the pulmonary pressures are:
CWD through tricuspid valve, A4C. Note isosystemic pulmonary pressures.
Subcostal 4 chamber
Subcostal IVC view. Note the IVC is dilated but there is some respiratory variation in the size.
Before wrapping up, here is one last look at the PSAX, repeated at the end of the study as the patient was becoming more sweaty . What do you think and what should you do?
Looks like that LV isn’t being delivered much blood by the failing RV. It is imperative to optimise:
- RV preload (not too much filling, definitely not dry though)
- RV contractility (Don’t let the RV become ischaemic while it is working so hard, keep the systemic blood pressure up with pressors if needed) and use inotropes. Milrinone might be of benefit for the RV but beware with hypotension it might not be your best option.
- RV afterload (pulmonary vasodilators? iNO can be used but with difficulty in the non-intubated patient. Certainly keep the CO2 low normal and provide supplemental O2 to prevent all hypoxic pulmonary vasoconstriction.)
Think about an exit strategy: ECMO? Lung transplant? pulmonary artery endarterectomy?
That’s all for now…
Cover image: Smurf, by Vik NandaTags: acute vs chronic pulmonary hypertension RV syncope