Note: This info is only relevant to intravenously administered morphine.
When we give morphine intravenously, they may have orthostatic hypotension, a form of hypotension in which a person’s blood pressure suddenly falls when standing up or stretching. (Postural hypotension, Head rush, dizzy spell)
They may also have a decreased cardiac workload during myocardial infarction. This is a great thing. If a person is having a heart attack, oxygen demand exceeds delivery and cardiac tissue dies. Most of our muscles can survive anaerobically with a lack of oxygen but cardiac muscle cannot. It has a very limited duration where it cannot survive without oxygen. If you have an area that has died due to a MI, that person has already lost muscle that will never regenerate. The next several hours is a very critical time because if the surrounding tissue dies and can’t get to balance with the oxygen delivery (versus demand), heart failure will occur.
If we give someone IV morphine, it will increase venous pooling of blood due to the dilation of the vessels. As blood pulls on the venous side, what happens to the return of blood from the vena cava to the right atrium? It will decrease the return of blood to the heart and decrease the volume of the blood to pump. That will cause the work load to decrease, in turn decreasing oxygen demand, giving us a better chance of salvaging the surrounding tissue.
So what you’ll find in your coronary unit protocol, is that if a person is complaining of chest pain, they will be administered IV morphine. In this very one situation with narcotics, not only are we blocking the perception of pain, but we are actually treating the cause of the pain.
