Jul 21, 2026 · 1 hr 39 min · 17 segments
In this month’s EM Quick Hits Podcast, Amna Karabegovic joins us for an EMC² case of pediatric altered LOA and neurocritical care, Anand Swaminathan simplifies the high-risk management of pulmonary…
Brit LongPanelistAnton HellmanHostAnand SwaminathanPanelist
Jesse McLarenPanelistWhat we're gonna focus on is treatment, because treatment is wrought with challenges as well.
The most common places that we see this in the emergency department is patients with acute pulmonary embolism resulting in right heart strain and pulmonary hypertension, and of course, we also see patients with primary pulmonary hypertension who are presenting with acute worsening.
The first thing that we want to address is hypercarbia and hypoxemia, because both of these are gonna worsen pulmonary hypertension.
Of course, we know one of the easy ways to fix both of those parameters is by intubating the patient, but we wanna avoid intubation at all costs.
Switching these patients from negative to positive pressure ventilation can drop pulmonary venous return, it can increase RV afterload, which is gonna worsen RV stress and failure, and the patient's gonna decompensate pretty rapidly.
Even though BiLevel does produce positive pressure, the patient still has to initiate breaths.
There's still gonna be that negative pressure ventilation going on, so it's not gonna result in the same acute worsening that we see with intubation and mechanical ventilation.
Of course, that being said, it's all a trade-off, just like everything in medicine.
That's gonna improve pulmonary hypertension and lead to improved RV performance.
But you are providing positive pressure, and that can worsen the patient, although I think that the benefits of BiLevel far outweigh the risks.
High-flow nasal cannula is reasonable, though it's not really gonna help with that hypercarbia.
Under some circumstances, fixing hypercarbia, fixing hypoxemia can be enough to stabilize the patient, but typically, we're gonna need to think about direct pulmonary vasodilators.
The classic gold standard agent in acute presentations is inhaled nitric oxide.
That can drop pulmonary pressure rapidly, but it's expensive, it's not always available, and depending on where you work, it could take hours to get it going.
I've worked in a number of quaternary care centers where nitric oxide is technically available, but I've never been able to get it to the bedside of a patient who needed it in the emergency department.
Inhaled epoprostenol is another great option, but again, it's not always available in the emergency department, and delays can occur in getting this to the bedside from pharmacy, delays in getting it administered, and time is really critical in these patients.
Because of all of these issues with nitric oxide and with epoprostenol, inhaled nitroglycerin is a great option.
Inhaled nitroglycerin is rapidly converted to nitric oxide in the lungs.
There's almost no systemic absorption, so you're not gonna see a drop in blood pressure, which can be really harmful depending on the pathology the patient has going on.
The best part about nitroglycerin is that it is rapidly available in just about every emergency department.
What we're gonna focus on is treatment, because treatment is wrought with challenges as well.
The most common places that we see this in the emergency department is patients with acute pulmonary embolism resulting in right heart strain and pulmonary hypertension, and of course, we also see patients with primary pulmonary hypertension who are presenting with acute worsening.
The first thing that we want to address is hypercarbia and hypoxemia, because both of these are gonna worsen pulmonary hypertension.
Of course, we know one of the easy ways to fix both of those parameters is by intubating the patient, but we wanna avoid intubation at all costs.
Switching these patients from negative to positive pressure ventilation can drop pulmonary venous return, it can increase RV afterload, which is gonna worsen RV stress and failure, and the patient's gonna decompensate pretty rapidly.
Even though BiLevel does produce positive pressure, the patient still has to initiate breaths.
There's still gonna be that negative pressure ventilation going on, so it's not gonna result in the same acute worsening that we see with intubation and mechanical ventilation.
Of course, that being said, it's all a trade-off, just like everything in medicine.
That's gonna improve pulmonary hypertension and lead to improved RV performance.
But you are providing positive pressure, and that can worsen the patient, although I think that the benefits of BiLevel far outweigh the risks.
High-flow nasal cannula is reasonable, though it's not really gonna help with that hypercarbia.
Under some circumstances, fixing hypercarbia, fixing hypoxemia can be enough to stabilize the patient, but typically, we're gonna need to think about direct pulmonary vasodilators.
The classic gold standard agent in acute presentations is inhaled nitric oxide.
That can drop pulmonary pressure rapidly, but it's expensive, it's not always available, and depending on where you work, it could take hours to get it going.
I've worked in a number of quaternary care centers where nitric oxide is technically available, but I've never been able to get it to the bedside of a patient who needed it in the emergency department.
Inhaled epoprostenol is another great option, but again, it's not always available in the emergency department, and delays can occur in getting this to the bedside from pharmacy, delays in getting it administered, and time is really critical in these patients.
Because of all of these issues with nitric oxide and with epoprostenol, inhaled nitroglycerin is a great option.
Inhaled nitroglycerin is rapidly converted to nitric oxide in the lungs.
There's almost no systemic absorption, so you're not gonna see a drop in blood pressure, which can be really harmful depending on the pathology the patient has going on.
The best part about nitroglycerin is that it is rapidly available in just about every emergency department.
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