Mohamed, a listener from Sudan, emailed asking about the treatment of acute pulmonary edema in patients with low blood pressure. This is in distinction to SCAPE patients (see podcast 1).
If the patients have pulmonary edema and low BP from a cardiac cause, then they are in
Cardiogenic shock.
First, consider the etiology:
- Rate-related
- Valve Disorder
- Ischemic (Right sided infarct, STEMI, NSTEMI)
- Cardiomyopathy
- Toxicologic
At the same time, you are treating the patient with:
- Inotropes (dobutamine, milrinone, calcium)
- Pressors to achieve a MAP > 65 (allows coronary perfusion) (Meta-Analysis demonstrates norepi superior to dopamine Medicine. 96(43):e8402, OCT 2017)
- Oxygenation support, most likely with intubation
- Optimize O2 carrying capacity (Hb>10)
Here is a fantastic set of guidelines to manage these patients
Update:
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An ED Intensivist from NY. No conflicts of interest (coi).
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Hey Scott,
Great lecture. I had a question on how to manage severe AS patients with heart failure in your ED. Conventional wisdom has taught that we should not vasodilate this patient because it can produce a precipitous drop in BP, since the heart can’t increase cardiac output against the fixed stenosis. But I am aware of one study in NEJM where they gave nitroprusside and it improved cardiac output. What do you recommend? Also what are your thoughts on nicardipine for SCAPE?
Raghu
Hey Scott, and to the other readers out there! I am in my first year of practice, and since my 2nd year residency I’ve been listening to these podcasts, I think they are awesome, and love every bit of it. I just wanted to share my first case of cardiogenic shock that I managed just 2 days ago according to your teachings. Wonderful. It was the end of my shift 5 minutes before midnight, and this 65 yo male is wheeled in by EMS, had been complaining of Chest pain for 1 hour, was pale, diaphoretic, had a pulse of 35 and a BP that had dropped in the ambulance to 85/55 from a previous 130 systolic. He was alert and oriented and initially had warm feet and clear lungs. He had a history of heart disease but was a poor historian. EKG showed new flipped T waves in the anterolateral leads and a new 3rd degree AV Block with afib. Bedside EDE showed a grossly preserved EF. I started him on ASA, Plavix and Heparin from the get go and tried 2 atropine and a 500 cc Bolus. No improvement. Since he was on Beta-blokers I tried to reverse… Read more »
Hi Dr Weingart,
great articles with great references. I was wondering if you also had a reference nearby for the use and efficacy of CaCl as an inotrope?
Thank you!
Eric Sauvageau
The Annals of Thoracic SurgeryVolume 37, Issue 2, February 1984, Pages 133-140
Hi Scott! I’d like to thank you again for all your educational material. O a recent shift, I used information I’ve learned from at least three of your podcasts on different critically ill patients. I was hoping for some advice. I had a patient in cardiogenic shock from an inferior wall STEMI with a heart rate in the 30-40s, a MAP around 50, massive JVD and pulmonary edema though not in respiratory distress. EMS had given him a dose of atropine which temporarily raised his HR to the 50-60s with improvement in his chest pain but not BP. I’m in a very small community hospital with the nearest cath lab about an hour away, and this guy wasn’t stable enough for transport anyway. He had a history of multiple craniotomies for head injuries (in Vietnam), history of 6 cm AAA, surgery within the last 3 months with subsequent GI bleed, and a wide mediastinum on CXR … I had the nurses put the TNK back in the box! I gave him 1L of NS, amp of Calcium chloride, and tried transcutaneous pacing but couldn’t get consistent capture with levels he could tolerate even with some fentanyl and versed. I used… Read more »
Wow, sounds like you did amazing work! My threshold to intubate would have been nil; then you can up your trans-cut pacing to where you want at that point and you’ve markedly lowered the metabolic requirements. Also positive pressure vent has the potential to bolster squeeze (referred to confusingly as decreased afterload). The whole stressing the heart becomes academic in these circumstances. You need to perfuse heart and brain. Pressors for MAP of 65, then inotropy until hands feel warm is usually how I play. Love that you thought of calcium, it is critical.
Sounds like end-of-life issues were primary just as you mentioned.
Strong work!
Thanks for the quick response! Would you have gone with propofol for sedation and compensate with NE for anticipated drop in MAP, then dobutamine for perfusion?
Thanks again.
I’d prob use fentanyl/midaz myself.
Man Mike, nice job given the resources you had! Only two things this patient made me think of is maybe initially using dopamine over NE for the chronotropy + an inotrope? Also, thought you were gonna say his K came back at 9… HyperK always being a thought with Symptomatic bradycardia refractory to pacing… Regardless, awesome job.
John,
great thought on the hyperK. Norepi is actually the pressor of choice for cards shock based on SOAP trial http://www.nejm.org/doi/full/10.1056/NEJMoa0907118
Agreed. The De Backer study was a game changer for NE ,but in their study the patients were mostly tachycardic to start. Would you apply the findings in the SOAP Study to all-comers in cardiogenic shock?
Dopa is definitely down, but I’m not sure the final nail is in the coffin…. I believe that in the upcoming Surviving Sepsis Recommendations there will still be a rec for Dopa as an alternative for a select group of patients (those with bradycardia).
The funny thing is, this patient unfortunately progressed to vtach/vfib and if dopa would have been used it would have gotten blamed. Ah well. Maybe could have gone with a good old precordial thump.
I just think dopamine is a dirty drug that brings nothing to the table. Rather titrate norepi and dobut independently. If you really want a drug for brady hypotension, epi prob. makes more sense than dopa.
Scott,
What if you can’t get MAP above 60-65 quickly with norepi? Any thoughts on a threshold for starting dobu or epi? You suggest 20 mcg/min in septic patients, but this is a different population. You don’t want to stress the heart muscle further, but more often than not you must…
Thanks for great effort
Now many icu/anesthesiologist still believe in dopamine as first choice for cardiogenic shock due to its beta agonist features ..they claim that norepi is worsening the heart because you are constricting the basculature and making high resistance for a sick heart to pump! any way the SOAP trial showed the actual answer. ..
Now what about dobutamine infusion and at what systolic BP we can start?And how often we see the vasodilatory effects of it?
I had a patient with new onset flash pulmonary edema with BP 220 systolic and saturation of 60% who was treated initially with lasix abd morphine and metoprolol then transferred to me.. on arrival he was obtunded with bp 97/50. Pulse 80 co2 70 ph 7.24… I intubated him with fent and atracurium (due to suspicion of hyperK) 1mg of midaz…. he developed marked hypotension with levophed 20 and dopamine 25 mic going on bp 120 systolic. . When I started dobutamine’ the bp start to drop and didn’t responde to increasing the other inotropes…
Second question.. is it possible that he migh develop transient worsening of LV sys function after intubation?
Thank you again and thanks to the readers
The rule of thumb with dobutamine is that 1/3 will increase BP, 1/3 will stay the same, and 1/3 will drop. No literature to support that. So I like to see a MAP of >60 before I’ll add it in. Though the beauty is you can just turn it off if BP drops.
As to your APE pt, I wonder if the problem wasn’t volume depletion. It is why I avoid lasix early on. Little downside to trying these patients on some fluid in these cases. Other possibility is hypocalcemia. Volume and calcium are the main failures of inotropes.
I think if high dose NTG was started instead of lasix might have better outcome.. but when i received this patient, IVC was > 1.5cm with no respiratory variation in diameter, that’s why i tried only 500cc NS without response.. any comment regarding Atracurium-related ?hypotension??
possible given the histamine release; but i have no experience with the drug
Hey Dr Weingart. Thought I’d drop a line and thank you for your great podcasts. I’m a fourth year med student and just happened to find your podcasts during my ED rotation. Your podcasts are a fantastic resource. Thank you for taking the time and effort to put them together.
Correct me if I am wrong: strictly speaking diastolic BP correlates better with coronary perfusion. Vasopressors elevate SVR and increase diastolic pressure. This increases coronary perfusion of the LV, which occurs usually in diastole.
That being said, MAP target of 65mmHg is reasonable given that it is the most accurate value from oscillimetry. In addition, DBP is a calculated value when using NON-invasive/DINAMAP.
But if an arterial line is in place, I would prefer to look at the diastolic value.
DBP is reasonable surrogate for cor. perfusion; MAP is the best surrogate of the 3 BP measurements for distal organ perfusion.
I had 45 y male with cardiogenic shock due to extensive anterior wall mi. . Bp unrecordable.. cold extremity.. diaphoretic & irritable. . Fluids.. norepi. Started.. with minimal response but bp still 60 systolic..
Anesthesia didn’t intubate him and agree to transfer to pci facility but arrested in the ambulance. .
I know intubation woul kill this patient, but are u going to transfer like this? What about Ketamine in such case?
Thanks
ketamine or etomidate seem to be the way to go