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. Continue reading →
