- If BP is high (i.e. hypertension induced HF), give afterload reducers (i.e. hydralazine) and diurese if they're fluid overloaded. The etiology of this is assumed to be excessive afterload.
- If BP is normal, diuresis is the cornerstone of treatment. The etiology is assumed to be fluid overload.
- If BP is low, then give dobutamine with lasix. The etiology is assumed to be insufficient contractility. If you just give lasix, it may or may not work depending on how bad the cardiac output is. If cardiac output is really low, there will be both insufficient forward flow to the kidneys (people can be up 12 liters with a BNP over 100K and edema up the wazoo and still have pre-renal azotemia) and decreased venous return, leading to back pressure in the kidneys that further worsens forward filtration rate. The addition of dobutamine gtt (start low dose 2.5mcg/kg/min, titrate up to max dose 20mc/kg/min as needed) augments contractility, allowing the lasix to actually work. If you titrate up dobutamine all the way and you're still not diuresing, add dopamine.
2. Wide complex tachycardia: SVT +aberrant conduction vs VT.
- SVT + aberrant conduction. Essentially sinus tach + bundle branch block.
- To distinguish between the two, give adenosine. Adenosine blocks conduction through the AV node and if it's SVT, the rhythm will break and it will slow down to a more normal rate so that you are able to see the P waves (although they may be oddly placed). If it's VT, adenosine won't do anything, because it's ventricularly paced. You can also distinguish with history-- a history of ischemic heart disease = its almost certainly VTach.
- Adenosine 6mg IV push, wait 2 minutes, if it doesn't change then 12mg IV push, wait another 2 minutes, then another 12mg. If after all 3 the rhythm didn't break, it's VT.
- If the rhythm does break and you get p-waves, it was SVT with aberrancy; this can be treated with a low-dose beta blocker. However, make sure its not VT before you beta-block because you can push someone into asystole doing that.
3. Management of VT
- If the patient is unstable, call a code and go down the ACLS pathway.
- If the patient is clinically stable, give Amiodarone 150mg at once, then 1mg/minute for 6 hours, and then 0.5mg/min for 18 hours. Max dose 2.2 g/day.
- DO NOT GIVE BETA BLOCKERS TO SOMEONE IN VT. Don't give any drugs that block conduction. The ventricles are the last source of pacing-- the SA/AV nodes are no longer pacing, and so if you give a drug that could potentially block the ventricular pacers you will end up with asystole.
4. Diagnosing narrow-complex tachycardia:
- Differential: sinus tach, SVTs including AVNRT, a-flutter with 2:1 block
- 100-140, think sinus tach. Upper limit of sinus tach is 220-age.
- 140-160, think aflutter with 2:1 block. Look for p-waves going at a rate of 300.
- 160 + think SVT (AVNRT, atrial tachycardia)
5. Management of regular, narrow-complex tachycardia:
- For sinus tach, fix the underlying problem-- most commonly dehydration, pain, infection, anxiety. Less common thyroid storm, etc. Don't just beta-block people, there's always a hypothetical risk of taking down all the pacers.
- For AVNRT, treat with adenosine. Warn people that they're gonna feel like crap.
- For a-flutter, see 'management of a-fib' below, its the same treatment.
- Don't give adenosine in any narrow-complex tachycardia if there is any suspicion of wolff-parkinson-white syndrome; if you take down the AV node, then all the conduction will go through the accessory pathway, which conducts fast, and you will end up with a circular conduction in the opposite direction of normal conduction that may be even faster than the original rhythm. Luckily the effects of adenosine wear off quickly so the person should hypothetically return to normal, but you don't want to go there. Definitely don't give these people any class II or IV antiarrhythmics; since they have such long half lives, they'll be in this horrible re-entrant tachycardia for a while.
6. Irregular narrow-complex tachycardia:
- A-fib with RVR (most common cause of narrow complex tachycardia that you will get paged about) a-flutter with variable conduction and MAT
- MAT is usually caused by electrolyte abnormalities (specifically K, Mg, Ca). If you think someone has MAT, send a BMP and replenish whatever is low. If nothing is low, empirically give Mg 2g over 15 minutes and 4g over the next 6 hours. At these doses, the mag will not accumulate in the blood and cause toxicity; it's a heavily intracellular ion (DNA polymerase cofactor) and it will get sucked into cells. It's only at the really high doses used by ob/gyns that you have to worry about mag toxicity
7. Management of a-fib with RVR (and also of a-flutter with variable/constant block)
- Rate control first (then anticoagulation and eventually cardioversion once they have been fully anticoagulated for 4 weeks)
- Metoprolol 5mg IV push. Can be given up to 3 times with a 5 minute wait between each one. The benefit of metop is that it's fast, but the problem is there is no drip metop so if it fails then you have to switch to dilt. If you think there's high chance of success that a few IV pushes of beta-blockade will make them better (i.e. you know the patient, metop has worked in the past, etc) then this is fine. Otherwise start with dilt. Of note, the patient will need to go home on PO metoprolol and may need to remain on it indefinitely.
- Diltiazem: Bolus 0.25mg/kg. Wait 15 minutes. If it didn't work, bolus 0.35 mg/kg. Wait 15 minutes. If that still doesn't work, start drip at 5-15mg/hr. Preferred drug for patients you don't know (may have atrial thrombus) and for people with tough to break a-fib who you think may need a drip.
- Amiodarone: 150mg IV push, then 1mg/min for 6 hours. The dangerous thing about amio is that it's a class III antiarrhythmic, and you can inadvertently cardiovert the patient, and if they have a mural thrombus you may have just given them an embolic stroke. So if you know the patient well and you're sure that they don't have a mural thrombus, or their a-fib is less than 48 hours old, or they are properly anticoagulated (4 weeks on warfarin), choose diltiazem instead, even in patients with heart failure.
- Digoxin: crappy drug for this purpose; 1 hour onset time. At 6 hours, a significant number of people will still be tachycardic. Only use this as an addon drug in heart failure patients who are unable to be rate controlled with amio alone.
- Esmolol: great drug, works really well for this purpose, but has to be given as a drip with constant careful titration (half life 9-12 minutes) and thus requires ICU admission.
8. Contraindications to direct thrombin inhibitors (xarelto aka rivaroxaban, pradaxa aka dabigatran)
- CYP3A4 interactions
- GFR <15. These drugs are all cleared renally. At GFR 15-30, recommend halving the dose. But really, the best thing to do is just to avoid these in people with any amount of significant renal disease.
9. Statins can help treat fatty liver disease, but it should be avoided in people who have elevated LFTs. Pravastatin is the cleanest one with the fewest LFT perturbances. Simvastatin has bad interactions and is not used much anymore.
10. The bigger the stent, the less difference there is in outcomes between bare metal and drug eluting.
- For larger vessels taking larger stents (3.5mm), there is probably no difference in restenosis rates between the bare metal and drug eluting ones. The old studies showing the superiority of drug eluting stents were done with an older technique that was less aggressive about opening the plaque with the balloon. New data with better technique shows a restenosis rate of bare metal stents that is <1%.
- For smaller stents (2.5mm) drug eluting is probably better.
2. Wide complex tachycardia: SVT +aberrant conduction vs VT.
- SVT + aberrant conduction. Essentially sinus tach + bundle branch block.
- To distinguish between the two, give adenosine. Adenosine blocks conduction through the AV node and if it's SVT, the rhythm will break and it will slow down to a more normal rate so that you are able to see the P waves (although they may be oddly placed). If it's VT, adenosine won't do anything, because it's ventricularly paced. You can also distinguish with history-- a history of ischemic heart disease = its almost certainly VTach.
- Adenosine 6mg IV push, wait 2 minutes, if it doesn't change then 12mg IV push, wait another 2 minutes, then another 12mg. If after all 3 the rhythm didn't break, it's VT.
- If the rhythm does break and you get p-waves, it was SVT with aberrancy; this can be treated with a low-dose beta blocker. However, make sure its not VT before you beta-block because you can push someone into asystole doing that.
3. Management of VT
- If the patient is unstable, call a code and go down the ACLS pathway.
- If the patient is clinically stable, give Amiodarone 150mg at once, then 1mg/minute for 6 hours, and then 0.5mg/min for 18 hours. Max dose 2.2 g/day.
- DO NOT GIVE BETA BLOCKERS TO SOMEONE IN VT. Don't give any drugs that block conduction. The ventricles are the last source of pacing-- the SA/AV nodes are no longer pacing, and so if you give a drug that could potentially block the ventricular pacers you will end up with asystole.
4. Diagnosing narrow-complex tachycardia:
- Differential: sinus tach, SVTs including AVNRT, a-flutter with 2:1 block
- 100-140, think sinus tach. Upper limit of sinus tach is 220-age.
- 140-160, think aflutter with 2:1 block. Look for p-waves going at a rate of 300.
- 160 + think SVT (AVNRT, atrial tachycardia)
5. Management of regular, narrow-complex tachycardia:
- For sinus tach, fix the underlying problem-- most commonly dehydration, pain, infection, anxiety. Less common thyroid storm, etc. Don't just beta-block people, there's always a hypothetical risk of taking down all the pacers.
- For AVNRT, treat with adenosine. Warn people that they're gonna feel like crap.
- For a-flutter, see 'management of a-fib' below, its the same treatment.
- Don't give adenosine in any narrow-complex tachycardia if there is any suspicion of wolff-parkinson-white syndrome; if you take down the AV node, then all the conduction will go through the accessory pathway, which conducts fast, and you will end up with a circular conduction in the opposite direction of normal conduction that may be even faster than the original rhythm. Luckily the effects of adenosine wear off quickly so the person should hypothetically return to normal, but you don't want to go there. Definitely don't give these people any class II or IV antiarrhythmics; since they have such long half lives, they'll be in this horrible re-entrant tachycardia for a while.
6. Irregular narrow-complex tachycardia:
- A-fib with RVR (most common cause of narrow complex tachycardia that you will get paged about) a-flutter with variable conduction and MAT
- MAT is usually caused by electrolyte abnormalities (specifically K, Mg, Ca). If you think someone has MAT, send a BMP and replenish whatever is low. If nothing is low, empirically give Mg 2g over 15 minutes and 4g over the next 6 hours. At these doses, the mag will not accumulate in the blood and cause toxicity; it's a heavily intracellular ion (DNA polymerase cofactor) and it will get sucked into cells. It's only at the really high doses used by ob/gyns that you have to worry about mag toxicity
7. Management of a-fib with RVR (and also of a-flutter with variable/constant block)
- Rate control first (then anticoagulation and eventually cardioversion once they have been fully anticoagulated for 4 weeks)
- Metoprolol 5mg IV push. Can be given up to 3 times with a 5 minute wait between each one. The benefit of metop is that it's fast, but the problem is there is no drip metop so if it fails then you have to switch to dilt. If you think there's high chance of success that a few IV pushes of beta-blockade will make them better (i.e. you know the patient, metop has worked in the past, etc) then this is fine. Otherwise start with dilt. Of note, the patient will need to go home on PO metoprolol and may need to remain on it indefinitely.
- Diltiazem: Bolus 0.25mg/kg. Wait 15 minutes. If it didn't work, bolus 0.35 mg/kg. Wait 15 minutes. If that still doesn't work, start drip at 5-15mg/hr. Preferred drug for patients you don't know (may have atrial thrombus) and for people with tough to break a-fib who you think may need a drip.
- Amiodarone: 150mg IV push, then 1mg/min for 6 hours. The dangerous thing about amio is that it's a class III antiarrhythmic, and you can inadvertently cardiovert the patient, and if they have a mural thrombus you may have just given them an embolic stroke. So if you know the patient well and you're sure that they don't have a mural thrombus, or their a-fib is less than 48 hours old, or they are properly anticoagulated (4 weeks on warfarin), choose diltiazem instead, even in patients with heart failure.
- Digoxin: crappy drug for this purpose; 1 hour onset time. At 6 hours, a significant number of people will still be tachycardic. Only use this as an addon drug in heart failure patients who are unable to be rate controlled with amio alone.
- Esmolol: great drug, works really well for this purpose, but has to be given as a drip with constant careful titration (half life 9-12 minutes) and thus requires ICU admission.
8. Contraindications to direct thrombin inhibitors (xarelto aka rivaroxaban, pradaxa aka dabigatran)
- CYP3A4 interactions
- GFR <15. These drugs are all cleared renally. At GFR 15-30, recommend halving the dose. But really, the best thing to do is just to avoid these in people with any amount of significant renal disease.
9. Statins can help treat fatty liver disease, but it should be avoided in people who have elevated LFTs. Pravastatin is the cleanest one with the fewest LFT perturbances. Simvastatin has bad interactions and is not used much anymore.
10. The bigger the stent, the less difference there is in outcomes between bare metal and drug eluting.
- For larger vessels taking larger stents (3.5mm), there is probably no difference in restenosis rates between the bare metal and drug eluting ones. The old studies showing the superiority of drug eluting stents were done with an older technique that was less aggressive about opening the plaque with the balloon. New data with better technique shows a restenosis rate of bare metal stents that is <1%.
- For smaller stents (2.5mm) drug eluting is probably better.
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