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.
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!