Amidarone ?

Diltiazem is perfectly fine to treat any tachycardia as long as there is no re-entry. It tends to last longer than metoprolol, too.

Not that ACLS is the be-all, end-all anyway, but it says so in the very next bullet point.
 
Remi said:
Diltiazem is perfectly fine to treat any tachycardia as long as there is no re-entry. It tends to last longer than metoprolol, too.

Not that ACLS is the be-all, end-all anyway, but it says so in the very next bullet point.
Click to expand...
What about the negative inotropic effects of Non-DI CCBs?
 
I'm certainly no cardiac guru, but I do use cardizem, metoprolol and esmolol quite liberally in the OR and the perioperative period. Uncontrolled or poorly controlled hypertension and AF are things I see quite a bit. I try to remain abreast of ACLS recommendations, but they are just that - recommendations.
 
Im used to trying a few metop pushes before dilt load /drip if metop is not showing good signs. and esmolol drip if metop works but only shortly.

Amio is a weird one because it is not really effective until the pt is loaded with a whole lot over time (multiple grams like 8 or 10) and iv amio is pricy. Some discussion with a cardiologist i recall that iv amio load has effects via pharm mechanism not directly associated with the drug but I'll have to check on that
 
As I understand it Metoprolol takes a while to work while Esmolol has a very fast onset. I am not sure about the two Non-DI CCBs (Diltiazem and Verapamil). Our system has us use Metoprolol because it slows the rate and also enables better coronary perfusion which may have suffered during the tachycardia of AFib. I had to look it up just now but it seems that the coronary arteries are perfused during diastole only (the heart literally blocks their inlets during systole) and a lot of the chest pain associated with a rapid AFib is due to mycardial-oxygen mismatch. I imagine the same is true for the non-DI CCBs but they also reduce inotropy (contraction force) but I don't think that has any effect on coronary artery flow.

I can't wait until we start doing mitral valve replacements in the field. I heard you can do it by taking a 5 hour CE online course and then a quiz at the end.


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Alan L Serve said:
As I understand it Metoprolol takes a while to work while Esmolol has a very fast onset. I am not sure about the two Non-DI CCBs (Diltiazem and Verapamil). Our system has us use Metoprolol because it slows the rate and also enables better coronary perfusion which may have suffered during the tachycardia of AFib. I had to look it up just now but it seems that the coronary arteries are perfused during diastole only (the heart literally blocks their inlets during systole) and a lot of the chest pain associated with a rapid AFib is due to mycardial-oxygen mismatch. I imagine the same is true for the non-DI CCBs but they also reduce inotropy (contraction force) but I don't think that has any effect on coronary artery flow.

I can't wait until we start doing mitral valve replacements in the field. I heard you can do it by taking a 5 hour CE online course and then a quiz at the end.


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Click to expand...

Any drug that slows the heart rate and reduces wall tension will improve coronary perfusion and the Mv02 supply:demand ratio. It seems to me that diltiazem would actually do a better job of improving coronary perfusion than metoprolol, because of its smooth muscle relaxant effects. I don't know if that is actually the case, but if I had to guess which one did a better job of that, I'd pick the vasodilator.
 
[QUOTE="Alan L Serve, post: 614104, member: 29025" I had to look it up just now but it seems that the coronary arteries are perfused during diastole only (the heart literally blocks their inlets during systole) and a lot of the chest pain associated with a rapid AFib is due to mycardial-oxygen mismatch. I imagine the same is true for the non-DI CCBs but they also reduce inotropy (contraction force) but I don't think that has any effect on coronary artery flow.[/QUOTE]

This is demand ischemia.

Myocardial O2 demand (or MvO2) is proportional to heart rate and wall tension (i.e. preload, afterload and contractility).

Myocardial Oxygen supply (DO2) is proportional to coronary perfusion pressure (i.e. MAP - right atrial or central venous pressure), arterial oxygen content, and is inversely proportional to heart rate and coronary vascular resistance.

Chest pain can be present for a number of reasons. This may be demand ischemia simply from the rapid heart rate in an otherwise "normal" heart. The demand ischemia may also occur from increases in afterload (e.g. pulmonary embolus), or preload (heart failure). Chest pain may also result from inadequate supply, e.g. acute MI, or may be a combination of increase demand with limited supply, e.g. exertional angina.

In MI we typically manipulate oxygen demand by reducing preload (e.g. nitrates). In tachycardic (typically anterior) MIs, it used to be common to slow the rate with beta-blockers to reduce demand. The heart may become bradycardic (especially inferior wall MI), which reduces demand (Bezold-Jarisch relflex). Sometimes we may have to balance the beneficial effects of bradycardia and decreased preload against the need to have enough cardiac output to generate adequate myocardial oxygen supply, e.g. pressors and atropine +/- fluid in the hypotensive patient.
 
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