The Right Ventricle: Your First Big Fight

You had a great first date. Things are progressing nicely, but then gosh dang COVID-19 hit and made life hard for everyone. Your new girlfriend is feeling the pressure. She’s working more hours than usual at Five Guys, there is a national shortage of ground beef which further complicates her job, and she tells you she feels like a failure. You offer to leave a bottle of wine on her porch (because #socialdistancing) but you quickly realize the error of your ways. She is not like most girls. A fluid bolus is going to worsen this situation greatly.

When the RV faces resistance, it cannot create the force necessary to move blood forward against the opposing pressure. Your girlfriend is delicate, she cannot handle high-pressure situations, she tends to crumble. The LV is a muscular, pressure generating machine, it can push back against systemic resistance with decent success. The RV’s inability to push forward against increasing pulmonary artery pressure means a decreased stroke volume in the RV, and thus, a decreased stroke volume out of the LV, resulting in a reduction in perfusion. It only takes a few beats of the heart for the LV stroke volume to match up to the RV stroke volume; when the RV decreases, the LV is going to follow suit almost immediately.

If the patient has invasive hemodynamic monitoring in place, you will not initially see increases in central venous pressure (CVP) because the thin-walled RV (remember, it’s only 2-3 mm thick) easily stretches to accommodate the growing volume. This will be visible on ultrasound, and if a clinician notes RV stretch, the time for intervention was 15 minutes ago. It’s like when you ask her “What’s wrong?” And she answers, “I’m fine!” It goes without saying that things are not “fine” and the time to fix things has long passed. It is also worth noting that when the RV stretches to accommodate increased pressures, it reduces coronary perfusion to the RV free wall because there is greater tension along the wall and thus reduces the lumen of the coronary arteries.

Not many of us in EMS have ultrasound capabilities. Thankfully, we are all equipped with assessment skills and other tools that will help us put together the clinical puzzle. When there is acute RV hypertrophy from a sudden increase in RV pressure, the EKG reveals a right shift in the axis in leads I and aVF; we also might see a large R wave in leads V1 or V2. Clinically, we can expect to hear an RV gallop (S3) and will see signs of poor cardiac output, including hypotension and hypoperfusion.

Think about the reasons for RV failure: too much pressure coming INTO the RV (excessive preload), poor contractility IN the RV (right-sided MI), or too much pressure on the OUTFLOW side of the RV (pulmonary hypertension). So, you need to figure out if the problem is before, during, or after the RV to know what to look for and how to treat it. Just the same, you need to know if your girlfriend is upset about something you did, or something else that happened and she’s projecting her reaction onto you. If she’s overwhelmed by work, you’ll win major points with a pint of Haagen-Dazs, listening to her unload her complaints, and letting her take a nap. But, if it’s something you did, you’re gonna have to work a lot harder to fix it!

Let’s consider problems BEFORE the RV: Both too much and too little preload can contribute to RV strain. Many things can lend to poor preload, thus insufficient filling pressure, such as positive pressure ventilation or tension pneumothorax (it presses on the inferior vena cava, obstructing the path of blood to the right atrium), hypovolemia, and poor venous tone (sepsis, neurogenic shock, etc). In these cases, identify the cause of the insufficient RV filling pressure and treat it (ie: pressors, blood products, appropriate fluid bolus). On the flip side, too much fluid can overwhelm the RV and it is simply unable to handle the onslaught of work. Like your girlfriend, there is too much pressure placed on her at work and it’s REALLY STRESSING HER OUT, MAN! In this case, remove the volume with therapeutic bloodletting. I’M KIDDING OH MY GOSH JUST CHECKING TO SEE IF YOU’RE STILL PAYING ATTENTION. Geeze. Dialyze or give some Lasix to the patient and take yourself a chill pill.

Now let’s have a gander at problems with the RV itself: When the RV is failing in the presence of normal preload and normal pulmonary vascular resistance, it is likely the patient is experiencing a right-sided myocardial infarction (MI). This is not always the case, but you can use your handy-dandy EKG machine and assess for signs of right-sided MI (don’t forget your right-sided EKG!); just remember that an MI that only affects the RV is rare, and more commonly, there are other areas of myocardial involvement. Poor RV contractility limits its ability to apply the pressure required to eject the stroke volume; this leads to increased pressures in the RV, which causes the ventricular septal wall to bow out into the LV. The septal wall deviation creates a double whammy to the LV because the RV’s decreased stroke volume means a decreased preload pouring into the left heart, automatically reducing the stroke volume on the left. It also inhibits the contractility of the LV and then the patient can spiral into biventricular failure. Wrapping up this section, the moral of the story is to fix the RV contractility problem. Get your patient to the cath lab to remove the coronary artery occlusion and restore perfusion.

Finally, let’s talk about increased RV afterload: The most common cause of right-sided heart failure is left-sided heart failure. They say sh*t rolls downhill, but when discussing cardiology, problems flow backward. Typically, the patient with an LV pump problem worsens over longer periods of time, this isn’t an acute onset problem. What I want to focus on is acute problems that we will see crash fast in the back of our ambulances, in our ED beds, or in our helicopters. These are the folks we need to be hyperaware of and prepared to intervene. When the RV faces sudden increases in afterload, we must identify the etiology of the increased pulmonary resistance and intervene with the goal of afterload reduction specific to that cause. Increased pulmonary artery pressure is where we are going to spend the final installment of this RV series. Come back tomorrow for the wrap-up!

References:

This series was inspired by a ridiculously good podcast over at the EMCrit page and I cannot pretend to do her lecture justice with my blog. Hop on over and take a listen to Sara Crager discuss RV failure management…

https://emcrit.org/emcrit/right-heart-sara-crager/

https://litfl.com/oxygen-extraction-ratio/

Darovic, G. O. (2002). Hemodynamic monitoring: invasive and noninvasive clinical application. Philadelphia: W.B. Saunders Co.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4225807/

Clark, D. Y., Stocking, J. C., Johnson, J., Treadwell, D., & Corbett, P. (2017). Critical care transport core curriculum. Aurora, CO: ASTNA.

https://www.ncbi.nlm.nih.gov/books/NBK431048/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5537114/

https://www.emra.org/emresident/article/managing-acute-right-ventricular-failure/

https://journal.chestnet.org/article/S0012-3692(15)30257-9/fulltext

https://pubchem.ncbi.nlm.nih.gov

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