SomewhatLoved
I now know the depths I reach are limitless
- Apr 12, 2023
- 441
Hi all. Was recently reading up on a pharmacology textbook and came across the following excerpt in a chapter about cardiovascular medications:
"The concomitant blocking of slow calcium channels by verapamil, and the B-receptor antagonism caused by propranolol, may result in asystole"
Verapamil is a calcium channel blocker. As the excerpt says, it more specifically blocks slow calcium channels, which help maintain a positive charge in cardiac myocytes (heart muscle cells) and preventing the cell from repolarizing ("recharging" essentially) so that it can then depolarize/"beat" again.
Propranolol is a beta-receptor antagonizing/blocking medication. It is most selective to the Beta-1 receptor, which increases chronotropy (rate of heart contraction/beating), inotropy (strength of heart contraction), and dromotropy (speed at which electrical impulses conduct through the heart, more specifically the atrioventricular node). When you block the effects of this receptor, the heart does not beat as fast or as strongly.
Together, at least according to this textbook, these medications have an effect which may result in asystole ("flatline"). Asystole is the heart rhythm, which has the worst outcomes in cardiac arrests. Where I work, in certain cases, resuscitation may even be discontinued 15 minutes early if a patient is in an asystole rhythm on the initial rhythm analysis at the beginning of a resuscitation attempt as the outcomes in these patients is so poor. Asystole essentially signifies that any electrical impulse in the heart at all has stopped. The electrical system which controls the heart is essentially turned off, and at that stage it can be extremely difficult to restart the heart and chances of survival (especially in outside-of-hospital cardiac arrests, OHCAs) is extremely low. Even when people do survive, it is often with neurological injury/brain damage, so the argument is often made that quality of life, even following revival, is extremely low and so in some instances should not be attempted.
I personally don't see this method as the "most appealing", but I think it is interesting and worth discussion. When discussing pharmacological methods of CTB, I see the sedative route (barbiturates) as the most appealing. If mixed with an excess dose of sedatives though, I could see verapamil and propranolol potentially "strengthening" another method as a failsafe and as a way to persuade the heart to stop beating.
Please note this was written without double-checking any sources. Do your own research, don't take medications of untested methods. This post is for discussion and educational purposes.
"The concomitant blocking of slow calcium channels by verapamil, and the B-receptor antagonism caused by propranolol, may result in asystole"
Verapamil is a calcium channel blocker. As the excerpt says, it more specifically blocks slow calcium channels, which help maintain a positive charge in cardiac myocytes (heart muscle cells) and preventing the cell from repolarizing ("recharging" essentially) so that it can then depolarize/"beat" again.
Propranolol is a beta-receptor antagonizing/blocking medication. It is most selective to the Beta-1 receptor, which increases chronotropy (rate of heart contraction/beating), inotropy (strength of heart contraction), and dromotropy (speed at which electrical impulses conduct through the heart, more specifically the atrioventricular node). When you block the effects of this receptor, the heart does not beat as fast or as strongly.
Together, at least according to this textbook, these medications have an effect which may result in asystole ("flatline"). Asystole is the heart rhythm, which has the worst outcomes in cardiac arrests. Where I work, in certain cases, resuscitation may even be discontinued 15 minutes early if a patient is in an asystole rhythm on the initial rhythm analysis at the beginning of a resuscitation attempt as the outcomes in these patients is so poor. Asystole essentially signifies that any electrical impulse in the heart at all has stopped. The electrical system which controls the heart is essentially turned off, and at that stage it can be extremely difficult to restart the heart and chances of survival (especially in outside-of-hospital cardiac arrests, OHCAs) is extremely low. Even when people do survive, it is often with neurological injury/brain damage, so the argument is often made that quality of life, even following revival, is extremely low and so in some instances should not be attempted.
I personally don't see this method as the "most appealing", but I think it is interesting and worth discussion. When discussing pharmacological methods of CTB, I see the sedative route (barbiturates) as the most appealing. If mixed with an excess dose of sedatives though, I could see verapamil and propranolol potentially "strengthening" another method as a failsafe and as a way to persuade the heart to stop beating.
Please note this was written without double-checking any sources. Do your own research, don't take medications of untested methods. This post is for discussion and educational purposes.
