The ICU Gotchas: Pulmonary hypertension and right heart failure (part II)

After part I, you should understand what pulmonary hypertension is, the dangers of right heart failure, and the reasons why your ICU patient with PH might suddenly crump. But you’re probably wondering…

What the heck should you do about it?

Hopefully we’ve inspired a little bit of fear in your heart. The path away from fear, of course, lies in having a plan.

Risk factors

Start by stratifying which PH patients are most at-risk for decompensated right heart failure. A few elements to consider:

  • Cause of PH: PAH (Group 1) patients should be handled with particularly gentle hands. Other groups may be slightly less concerning.
  • Severity of PH: An RVSP in the 40s is fairly common and usually not clinically significant. As a rough rule, however, once the RVSP starts to reach 2/3 of the systemic SBP, you should become concerned about the chances of decompensation.
  • Acuity of PH: Longstanding PH caused by many years of COPD is likely to be better-tolerated than new PH caused by something like a large PE.


The best way to dodge trouble with known PH is to avoid provoking it. These are the ultimate Goldilocks patients, and they need to steer a tight homeostatic ship. Minor derangements that other patients would shrug off may send them into a spiral.

Start by avoiding hypoxia, hypercarbia, and acidosis. Although no ICU patient needs to be hyperoxic, keep their sat comfortably in the high 90s. Avoid periods of apnea, such as during intubation attempts, and be extremely cautious with any sedation that could hypoventilation. Even if you’re normally a bicarb-skeptic, consider liberalizing your use of bicarbonate to help normalize pH.

Keep their blood pressure and cardiac output supported, but don’t let them get overloaded on volume; comfortable euvolemia is the goal. Be cautious when introducing any additional intrathoracic pressure, whether by intubation, NIPPV, or increased levels of PEEP.

Be wary of anesthesia or procedures of any kind, due to their tendency to introduce all of the above insults. (Even the CO2 absorbed during laparoscopy can cause problems on its own.) Mere vagal episodes, such as those caused by bowel movements or vomiting, can induce bradycardia and stimulate decompensation. To avoid this, proactively treat and prevent pain, nausea, constipation, and stress.


Once the RV does start to go, you’re in the thick of it. Once shock begins to develop, stay ahead of the curve by remembering the right heart; confirm the diagnosis with bedside echocardiography showing a weak, dilated RV and a poorly-mobile TAPSE.

A full look at the management of decompensated right heart failure is too much for this post, but the basics are simple enough.

  1. Support cardiac output: Use inotropes to augment RV function. Epinephrine or dobutamine are reasonable options, but milrinone may be especially helpful, since it’s also a pulmonary vasodilator. A PA catheter, that oft-forgotten tool, can be a real help here; in its absence, consider trending the CVP as a surrogate for the PA pressure.
  2. Support blood pressure: Maintain adequate coronary perfusion by avoiding hypotension. Any pressor can be used, but it might be particularly clever to use one which doesn’t cause pulmonary vasoconstriction: this makes vasopressin a nice choice and perhaps first line. (Being poorly titratable, you’ll probably need something else on top, such as norepinephrine.)
  3. Restore euvolemia: Most of these patients will be relatively volume overloaded, with a dilated right venticle that would actually function better with less preload. Resist the urge to bolus fluids, and instead consider diuresis—or even hemodialysis—to start unloading that right heart.
  4. Reduce PVR: Use all of the supportive techniques above, such as maintaining normoxia and a normal pH. Avoid high airway pressures or PEEP to the extent possible. (APRV can be especially fraught.) Then think about adding a pulmonary vasodilator, which in this setting usually means inhaled agents: epoprostenol (Flolan) or nitric oxide, with the choice mostly depending on institutional preference. These drugs will enter ventilated alveoli and help dilate the pulmonary vessels, without significantly affecting the systemic circulation.
  5. Address the underlying cause: If a persistent insult provoked this decompensation, such as the PE in our case study, it will need to be removed by appropriate interventions such as thrombolysis or embolectomy.
  6. Get help: Depending on patient appropriateness and local availability, mechanical support devices such as VA ECMO or a VAD may be indicated. Remember, though, that it’s the right heart in trouble, not the left, so techniques like intra-aortic balloon pumps won’t be much help.


The takeaway points on pulmonary hypertension in the ICU:

  • More often than not, it will be a bystander to the patient’s chief complaint. However, it portends a high risk for decompensation that must be appreciate in order to prevent sudden disasters and “mysterious” cardiac arrests.
  • The right heart likes low PA pressures. Maintaining that milieu requires good oxygenation, a normal CO2 and pH, a low intrathoracic pressure, and normal catecholamine tone.
  • When things start to fall apart, respect the immediacy of the problem and get ahead of it: support the RV with inotropes, unload it with volume removal, and reduce the PVR as best you can.

These are tricky patients, and the best medicine for them is prevention. Keep your eyes open, go forth, and respect the people’s ventricle.

[Read the next Gotcha here: OverPEEPing]