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What Causes Increased Heart Rate While Treating Atrial Fibrillation With Pulmonary Embolism?

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Posted on Wed, 23 Nov 2016
Question: If a patient presents with atrial fibrullation and pulmenory embolism and I administer 75 mg Metropolol without reduction of hr and hyp9tension response and then administer 25mg diltiazem also without reducion in hr, what justification is there to the further administration of verapamil?
doctor
Answered by Dr. Sukhvinder Singh (1 hour later)
Brief Answer:
please see details.

Detailed Answer:
Dear Sir
The increase in heart rate in given case is dependent upon the effect of sympathetic discharge. The higher the sympathetic discharge, the more will be ease of conduction through AV node and higher number of impulses from AF will pass to ventricles producing higher heart rates.
1. If you have given oral metoprolol, which is the most likely scenario, considering the dose of 75mg, It may take more time to show its effect and probably was not a good route considering emergency of situation.
2. IV diltiazem 25mg first dose is good choice and should be repeated in lower dose i.e. 25mg/kg if required further. Theoretically, I would not choose a third agent in such a scenario. However I have following reservations about this scenario and the management done.
A. If patient had AF and hypotension, then it speaks of a massive pulmonary embolism and all efforts should be directed towards thrombolysis or removal.
B. The increase HR in AF and its persistence despite giving rate lowering drugs again speaks about increase sympathetic discharge which in turn an indicator of stress mechanism activated by heart due to lower stroke volume. Thus Reduction in heart rate is desirable only for very high heart rates and some degree of tachycardia is physiological rather than pathological. It must be allowed. All such attempts to control tachycardia too much may in fact compromise cardiac output.
C. I would direct all my energy towards removal of thrombus burden and may use DC shock to revert AF to NSR if excessive tachycardia demands so.
Sincerely
Sukhvinder

Above answer was peer-reviewed by : Dr. Veerisetty Shyamkumar
doctor
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Follow up: Dr. Sukhvinder Singh (18 hours later)
Thank you for your assessmen. Just to make sure I understnd, would I be correct in taking the following approach when dealing wiyh cocmitant PE and AF Refeain from immediate AF countermeasures and instead administer IV heparin injection followed wi Hewparin iv infusion. Then use positive pressure O 2 until and provide sinoatrial node support rather than depressing BP as long as BP in normal range. Once the embolism is mostly clear, then address anr continuing cardiac aryyhmia.
doctor
Answered by Dr. Sukhvinder Singh (3 hours later)
Brief Answer:
kindly see details.

Detailed Answer:
Dear Sir
1. Any patient who develops AF in response to PTE will be a candidate for thrombolysis. The agent may be reteplase or alteplase, depending upon your choice. The heparin comes next to it.
2. There is no need to specifically provide sino-atrial node support.
3. After successful thrombolysis, AF should revert back to normal after some time or at least the rate will not be very high. If high rate persists despite stable BP, Oxygen saturation and respiratory rate, we may try controlling heart rate specifically.
Sincerely
Sukhvinder
Note: For further queries related to coronary artery disease and prevention, click here.

Above answer was peer-reviewed by : Dr. REMY KOSHY
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Answered by
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Dr. Sukhvinder Singh

Cardiologist

Practicing since :1998

Answered : 1306 Questions

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What Causes Increased Heart Rate While Treating Atrial Fibrillation With Pulmonary Embolism?

Brief Answer: please see details. Detailed Answer: Dear Sir The increase in heart rate in given case is dependent upon the effect of sympathetic discharge. The higher the sympathetic discharge, the more will be ease of conduction through AV node and higher number of impulses from AF will pass to ventricles producing higher heart rates. 1. If you have given oral metoprolol, which is the most likely scenario, considering the dose of 75mg, It may take more time to show its effect and probably was not a good route considering emergency of situation. 2. IV diltiazem 25mg first dose is good choice and should be repeated in lower dose i.e. 25mg/kg if required further. Theoretically, I would not choose a third agent in such a scenario. However I have following reservations about this scenario and the management done. A. If patient had AF and hypotension, then it speaks of a massive pulmonary embolism and all efforts should be directed towards thrombolysis or removal. B. The increase HR in AF and its persistence despite giving rate lowering drugs again speaks about increase sympathetic discharge which in turn an indicator of stress mechanism activated by heart due to lower stroke volume. Thus Reduction in heart rate is desirable only for very high heart rates and some degree of tachycardia is physiological rather than pathological. It must be allowed. All such attempts to control tachycardia too much may in fact compromise cardiac output. C. I would direct all my energy towards removal of thrombus burden and may use DC shock to revert AF to NSR if excessive tachycardia demands so. Sincerely Sukhvinder