Discussing morphine in Acute Heart Failure

21 Dec

Hello everybody,

Hereby as promised the post about morphine in acute heart failure.

Morphine has been considered a central drug in the treatment of pulmonary oedema for a long time. It is believed to cause venodilatation, peripheral venous pooling, reduction of pulmonary congestion and is thought to be a powerful anxiolytic. Most of these believes appears to be based on small studies, which were published during the era when there few alternatives.
In vivo experiments has shown peripheral dilatation, (1,2) probably due to histamine receptors rather that the opiate receptors (3), and a decrease in systemic vascular resistance (2). Furthermore peripheral pooling in the splanchnic region has been found. The splanchnic vascular resistance dropped by 16% after admission of morphine (4).
Next to this scientific evidence there is the strong subjective believe of a lot of doctors that it improves the short-term patient apprearance, which is another big reason we still use it, I think.

A large retrospective study from 2008 (5) looked at the outcome of patients treated with and without morphine for decompensated heart failure.The morphine group seemed to be sicker at initial presentation, but after risk adjustment for the greatest amount of in-hospital mortality risk in ADHERE and after exclusion of ventilated patients they still concluded that morphine was included with a greater frequency of mechanical ventilation, prolonged hospitalisation, more ICU admissions and higher mortality. (Even when adjusted for BUN, systolic BP, age, creatinine, dyspnoea at rest, chronic dialysis, heart rate, inotrope/vasodilator use and raised troponin the mortality odds ratio for morphine was 5.75.)

Another review article from 2008 (6) showed that there is no real evidence supporting the use of opiates in acute heart failure. They found 5 articles of which 4 which looked at the clinical results of opiates in acute heart failure. Some of the findings were:
– A trend in decreased systemic blood pressure, heart rate and pulmonary artery pressure
– A decrease in blood pressure and O2-saturation
– A reduction in circulating blood volume by about 115ml
– A decrease in dyspnoea and increase drowsiness.
But…none of these articles was able to find clinically significant improvement.

In conclusion:
Morphine has never been proven to be effective in ADH. There even seems to be a strong association between opiates and worsening of outcomes. This is in line with the article of Sacchetti (7), who found and increased need for ICU admission (odds ratio 3.08) and endotracheal intubation (odds ratio 5.04).

I have the idea that we are not treating the patient with the morphine, but the doctor. Doctors don’t like to wait and see. It is not in our nature to wait for, in this case, the NTG + NIV to do its work.
In practice that is also my experience (my subjective believe!). Without a cardiologist I never give morphine. When they come in later and NTG + NIV has done its work nobody talks about morphine. But when they are present from the beginning morphine is often given.
Although in small studies morphine has been shown to decreases dyspnea in terminal ill patients and patients with chronic heart failure, (8) its use in AHF seems to be far from proven. Theoretically it could provide benefit from its central nervous system effects, but it doesn’t seem plausible that this sedation effect is beneficial in a patient with respiratory distress.

A good randomised prospective study looking at safety or efficacy of morphine in AHF has never been done, which is strange, considering it is mentioned 3rd in the algorithm for management of AHF in the ESC guideline. This would be interesting to look at. Waiting for this research to be done, I would advise people not to use morphine as standard of care. There seems to be an association between opiates and worsening of outcome. As I will show you in the next’s posts other treatment option are superior to morphine (which you already know) and should be higher in the algorithm!

Until next time, when we will look at NTG in AHF!

Egon Zwets

list of references


4 Responses to “Discussing morphine in Acute Heart Failure”

  1. Sean Scott December 22, 2012 at 23:21 #

    Hey Egon,

    Nice summary of the evidence. I’m interested to know if morphine remains a mainstay of treatment for pulmonary edema in most hospitals in the Netherlands. It is disappointing that the ESC guidelines are still advocating morphine but how attached are your cardiologists to it? Hopefully they will take heed of the evidence you’ve just summarized

  2. sehrotterdam December 23, 2012 at 11:11 #

    Reblogged this on Maas Casualty and commented:
    Opinie stukje uit Dordrecht, van Egon over Morfine in acute astma cardiale.

  3. Iwan Dierckx December 26, 2012 at 13:38 #

    Egon: as you know I dislike morphine in CHF as much as anyone, but as you also know I can’t pass up an opportunity to wind you up either so let me play the devil’s advocate.

    Is there some association between morphine and increased mortality. Maybe, although you can never truly adjust for all variables. Is there evidence for causality ? None whatsoever.

    Morphine may well help in decreasing catecholamines, a very important component of the CHF pathophysiology. Would benzodiazepines do the same ? Maybe, but to my knowledge they are even less studied in the treatment for CHF than morphine. A Cochrane review from 2011 showed no effect of benzodiazepines for the relief of breathlessness in advanced diseases (all causes)

    Do all CHF patients benefit from decreasing catecholamines ?Probably not, and maybe this is why morphine may increase mortality in the total population. Maybe we need to be selective in whom we give morphine.

    So this is my first question to the EMdutch community: in which subset of acute CHF patients would decreasing catecholamines be beneficial and what would be clinical parameters to guide treatment ?

    Another way in which morphine may help is by decreasing rate of breathing. Yes you heard me: I said decrease ! There is a point when breathing to fast will only increase dead space ventilation and become ineffective. By slowing down breathing we might conceivably increase alveolar ventilation, make NIV (non invasive ventilation) easier and decrease work of breathing.

    And that would be my second question for you all: how do you know the optimal breathing rate for a patient and can we pharmacologically guide this ? What do you do if they over-breath and fail to trigger the NIV (Yes, yes you could always intubate. Now step away from the laryngoscope)

    Looking forward to some answers.


  1. The LITFL Review 089 - October 2, 2013

    […] Discussing morphine in Acute Heart Failure […]

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