Left-handed intensivist defending the right side of the heart. Often found ordering diuretics in the Cardiothoracic Surgery ICU or posting cat photos on twitter.
Pre-Brief:
ARDS isn’t going anywhere, and is more prevalent now thanks to COVID-19.
RV failure due to ARDS is often underrecognized – nearly ¼ of your patients with ARDS may have it.
What are you going to do when faced with acute cor pulmonale (ACP) in ARDS? Will you even know it’s there?
Follow this top 10 list for a quick review! For more detail, see the in-depth video discussion (parts 1 & 2) here and here.
Top 10 List
1. In ARDS, pulmonary vascular resistance (PVR) – and therefore RV afterload – is often elevated, which can lead to RV failure.
The RV is accustomed to low pressures, and low afterload, which makes this rise in PVR intolerable.
Lung volumes contribute significantly to PVR. The closer to functional residual capacity (FRC), the better. In ARDS, both overdistention and poorly recruited alveoli can move the patient farther from FRC.
(Abbreviations: WU = Wood units, RV = residual volume, TLC = total lung capacity)
2. Acute cor pulmonale is right heart failure due to an abrupt increase in PVR. ARDS and pulmonary embolism are common causes. It is most commonly diagnosed with transthoracic or transesophageal echo, though invasive hemodynamics (e.g. pulmonary artery catheterization) may be used.
By echocardiography, ACP in the literature is often defined as RV end-diastolic area to LV end-diastolic area ratio (RVEDA:LVEDA) > 0.6 with septal dyskinesia. It is often difficult to obtain adequate views with TTE, and TEE may be necessary. Additionally, measures of RV systolic function such as TAPSE or S’ are easier to obtain via TTE, and may help identify RV dysfunction.
There are no specific pulmonary artery catheterization criteria for ACP due to ARDS. One would expect to find signs of pre-capillary pulmonary hypertension (elevated PA pressures, elevated CVP, and low/normal PCWP), potentially with reduced measured or calculated cardiac output.
3. A multitude of pathophysiologic forces contribute to ACP in ARDS.
4…. and many iatrogenic actions can worsen ACP
5. Gas exchange and acidemia independently affect PVR.
This example from an animal study shows how quickly PVR can rise in the face of acidemia, hypoxemia, hypercapnia, or a combination thereof.
6. Know the risk factors for ACP in ARDS!
The four risk factors above have been identified in observational studies. Notably, even with zero risk factors present, there is 20% prevalence of ACP!
It may be possible to mitigate ACP progression if these factors can be modified, but this has not been demonstrated in a prospective intervention trial.
If hypercapnia is a problem, it is tempting to increase minute ventilation by raising tidal volume, which is not generally advised in ARDS. Instead, try to optimize the respiratory rate, I:E ratio, and remove sources of dead space ventilation.
7. Lung-protective ventilation is RV-protective ventilation: negative fluid balance, prone position ventilation, & safe driving pressures are physiologically-sound ways to treat or prevent ACP.
See this companion post for tips on driving pressure and PEEP titration!
Alveolar overdistention not only worsens PVR, but may also insidiously impair gas exchange by increasing dead space!
8. Rescue therapies to consider in ACP: Know your exit strategy!
Inhaled pulmonary vasodilators have not shown benefit beyond improved oxygenation in ARDS, but are a physiologically plausible treatment for ACP to decrease PVR.
Inotropes (namely, dobutamine and milrinone) can be considered for ACP-related RV failure, but evidence is sparse.
Finally, extracorporeal life support (ECLS) can be considered in very severe cases. Venovenous ECLS would be the first consideration, though mechanical support of the RV may be necessary as well.
If your patient is sick enough from ARDS and ACP to consider these options, please involve your ECLS and advance lung failure teams early!
9. New hypotension in your patient with ARDS? Think about ACP!
The majority of ARDS cases result from pneumonia and/or sepsis, so it is natural to assume that the development of shock is directly related to the underlying disease process (i.e. septic shock).
However, RV failure should be considered as an etiology of shock, as treatment may differ. Serial hemodynamic assessment is key!
10. Bringing it home: the debrief!
- RV function is directly influenced by lung function
- Hypoxemia, hypercarbia, and acidemia increase PVR
- In ACP, RV dysfunction is due to acute increase in PVR
- ACP is probably still underrecognized
- ARDS patient turning “septic?”- think about ACP
- Diagnose it! TTE/TEE, invasive monitoring.
- Prevent strategies include RV-protective ventilation, decongestion, and consideration rescue therapies early.
References
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Rosenberg AL, Dechert RE, Park PK, Bartlett RH; NIH NHLBI ARDS Network. Review of a large clinical series: association of cumulative fluid balance on outcome in acute lung injury: a retrospective review of the ARDSnet tidal volume study cohort. J Intensive Care Med. 2009 Jan-Feb;24(1):35-46. doi: 10.1177/0885066608329850. Epub 2008 Dec 22. PMID: 19103612.
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de Asua, Ignacio, and Alex Rosenberg. “On the right side of the heart: Medical and mechanical support of the failing right ventricle.” Journal of the Intensive Care Society vol. 18,2 (2017): 113-120. doi:10.1177/1751143716684357
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