Acute RV Failure
The left ventricle (LV) gets the glory typically. Any echo request usually relates to LV ejection fraction, filing status or regional wall motion abnormality. Perhaps this is fair enough as the LV is a significant contributor to blood flow and organ perfusion, but as Pinsky said at the CICM ASM in Hobart “Right ventricle (RV) function is not considered important for cardiac function until it is … and then it’s everything”.
RV dysfunction is rife in the ICU: as a direct result of diseases such as sepsis, and indirectly by mechanical ventilation or pulmonary hypertension, and it is strongly associated with a poor prognosis. In the clinical setting, RV failure presents as a combination of hypoperfusion and congestion: cool peripheries, lactic acidosis, shock, confusion, oedema, arrhythmias, liver and renal derangement etc…. RV failure occurs when the RV can’t meet demands for blood flow without the excessive use of the Frank-Starling mechanism. RV failure is caused by any increase in pulmonary pressures, volume, decreased contractility or tachyarrhythmias. .
Echo plays a crucial role in the diagnosis and RV dilation, and dysfunction can be seen with relatively little training (e.g., RV bigger than the LV and TAPSE <16mm).
When pressures in the RV become greater than the LV, the interventricular septum becomes forced to the left (ventricular interdependence seen as a D-shaped septum). In the setting of RV failure, this is known as Cor Pulmonale. In disease states such as ARDS, its presence is not uncommon and is a bad sign.
Ventricular interdependence (D-shaped septum)
Echo is not perfect (as anyone who uses it can agree), in particular for diagnosing pulmonary embolism, where up to 30% of the pulmonary vasculature can be blocked, and echo may not determine this. CTPA will always remain the gold standard for PE diagnosis (as long as renal function is ok). Also, there may still be a role for the pulmonary artery catheter to guide therapy due to the possibility of having continuous monitoring.
Management of the patient with RV failure is tough. Understanding the cause is important and must be addressed (e.g., RV failure from PE). Further care includes optimisation of respiratory function (avoid hypoxia, hypercarbia, acidosis) and cardiovascular status (e.g., treating arrhythmias urgently), avoiding fluid overload (essential) and steer clear of increasing pulmonary pressures (e.g., with excessive PEEP). Excellent housekeeping is critical (e.g., avoid diaphragm splinting from raised intra-abdominal pressure).
An initial strategy to sustain cardiovascular homeostasis is to try and keep systemic arterial pressure higher than pulmonary pressure and vasopressors are often used: recommended first-line agents include noradrenaline, vasopressin. There is no clear evidence to make concrete recommendations of where to go after that, to be honest. Milrinone, Levosimendan and Dobutamine can all be considered, and each has their own problems. In my practice, I try to ensure proper monitoring (echo +/- PAC) and then go on first physiological/pharmacological principles and choose the catecholamine on a risk analysis. Pulmonary vasodilator drugs can be useful (inhaled nitric oxide, Sildenafil, Iloprost, Epoprostenol), mainly where there has been vascular remodelling or long-standing pulmonary hypertension. It is important to watch for decreased SBP which may reduce RV preload and can exacerbate RV flow and ischaemia. Also, watch for cases of isolated raised pulmonary venous pressure before giving pulmonary vasodilators as you could cause significant pulmonary oedema. Finally, despite optimal medical management, patients still deteriorate. In these circumstances, mechanical circulatory support can be considered (e.g.: ECMO, RVAD, Impella etc…).
In conclusion, RV failure is often seen in the critically ill, is associated with an adverse prognosis, and treatment is by-and-large based on pathophysiological and pharmacological rationale at this stage. Echo plays a crucial role in the diagnosis of RV failure as well as for monitoring of pulmonary pressures and response to therapy.
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