1994 In-service question

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refreshingred

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80kg, 70yo woman is scheduled for a mastectomy. Has hx of CHF tx w/ digoxin 0.25mg qd. preop exam shows NSR at 80 bpm & BP of 110/70. K is 4.2 and digoxin is 1.5ug/ml. Five minutes after induction of GA, ventricular bigeminy is noted; bp is 85/65, spo2 is 97% & etco2 is 20mmHg

What's most appropriate managment?
a) CaCl
b)ephedrine
c)lidocaine
d)KCL
e)decrease ventilation

According to the key the answer is (e). I chose (c). My reasoning was that if I control the ventricular bigeminy the bp will rise and so with it will the etco2. I couldn't find much in the textbooks regarding a scenario like this. Obviously hypocapnia is the key to the answer; can anyone explain why?

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refreshingred said:
80kg, 70yo woman is scheduled for a mastectomy. Has hx of CHF tx w/ digoxin 0.25mg qd. preop exam shows NSR at 80 bpm & BP of 110/70. K is 4.2 and digoxin is 1.5ug/ml. Five minutes after induction of GA, ventricular bigeminy is noted; bp is 85/65, spo2 is 97% & etco2 is 20mmHg

What's most appropriate managment?
a) CaCl
b)ephedrine
c)lidocaine
d)KCL
e)decrease ventilation

According to the key the answer is (e). I chose (c). My reasoning was that if I control the ventricular bigeminy the bp will rise and so with it will the etco2. I couldn't find much in the textbooks regarding a scenario like this. Obviously hypocapnia is the key to the answer; can anyone explain why?

Lidocaine, in my limited experience, has only temporarily converted bigeminy to NSR. It does not last long. I've seen it come back in 5-10 minutes. She already has low bp and lidocaine itself can cause hypotension. Also, bigeminy does not necessarily need to be treated.

Does the answer key say that hypocapnia increases bigeminy? What is the book explanation to the answer. Hyperventilation can lead to hypotension by decreasing available calcium to cells. Maybe it also causes some myocardial irritability either by the hypotension itself or due to membrane electrolyte fluctuations?
 
This question was from an ABA/ASA In-traning examanition (1994) that they released. They gave out the entire test and the answer key, but unfortunately no explanations.
 
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refreshingred said:
80kg, 70yo woman is scheduled for a mastectomy. Has hx of CHF tx w/ digoxin 0.25mg qd. preop exam shows NSR at 80 bpm & BP of 110/70. K is 4.2 and digoxin is 1.5ug/ml. Five minutes after induction of GA, ventricular bigeminy is noted; bp is 85/65, spo2 is 97% & etco2 is 20mmHg

What's most appropriate managment?
a) CaCl
b)ephedrine
c)lidocaine
d)KCL
e)decrease ventilation

According to the key the answer is (e). I chose (c). My reasoning was that if I control the ventricular bigeminy the bp will rise and so with it will the etco2. I couldn't find much in the textbooks regarding a scenario like this. Obviously hypocapnia is the key to the answer; can anyone explain why?

I am not sure.. but i think the answer lay in the fact that increasing ventilation causes a resp alkalosis. which inturn can cause hypokalemia.. which inturn can exacerbate dig toxicity............ But clearly a question of dig toxicity.. lot of thinking huh? thats how all the questions are..
 
E is the correct answer and the explanation given above is correct. Lidocaine may treat the bigeminy, but ultimately, you want to treat the underlying etiology of the bigeminy and the subsequent hypotension.
 
rainking said:
I am not sure.. but i think the answer lay in the fact that increasing ventilation causes a resp alkalosis. which inturn can cause hypokalemia.. which inturn can exacerbate dig toxicity............ But clearly a question of dig toxicity.. lot of thinking huh? thats how all the questions are..


Nice job. To take it one step further for fun:

Pco2 is 20mmhg. For every 10mm hg decrease in pCO2 ph goes up by .1. Assuming she has a ph of 7.4 that would bring her ph down to 7.2. 1.5 below normal ph.

Now for every .1 change in arterial ph one would expect a decrease in K+ by .6meq which in this case would be .9 (.6x1.5). Her starting K+ was 4.2 which would make her hypokalemic at 3.3 meq. Now I don't know if this is enough to cause dig toxicity, but I suppose it is possible.

I don't know if I can explain the hypotension, unless she has developed sinus bradycardia or av block (which can be seen in dig toxicity although bigemeny is commonly seen). The question stem does not say anything about HR besides NSR. The hypotension could certainly be caused by acute hypocalcemia.

Yes, I know... a little "gobblydegook" action... Just number crunching. :D
 
never would of thought that five minute of hyperventilation and the resultant scenario just put forth could play out to dig toxicity, especially given the normal preop level. But the explanation theroretically makes sense. Perhaps the hypotension is just a result of lowered CO from the bigeminy -- not far-fetched if you consider that the she already has CHF and has just had a relative lowering in her sympethetic ouput secondary to induction . . .
 
I'll throw in my two cents as well.....studies show about 10-13% of pts show electrophysiologic symptoms of toxicity at levels above 1.5 ng/ml (not ug/ml!) altho no clinical symtoms...so she may have already been a bit high, depending upon her hydration & renal status. (As an aside...0.25mcg of digoxin seems a bit high for an 70 yo woman even at 80kg since it is dosed on lean body weight & her Crcl with age alone would be <70, but who knows......you gotta go with what you're given..)

I agree with the poster who said 5 min of hyperventilation causing the biochemical change in the K+ to increase myocardial sensitivity seems pretty fast, but all of you would know that better than I..

Another hypothesis might be the hypercapnia may cause an increase in myocardial blood flow which, I think, has been shown to cause an increase in sympathetic sensitivity of the myocardium.

At therapeutic concentrations, digoxin decreases automaticity due to an increase in vagal tone & a decrease in sympathetic activity. However, at higher concentrations (greater than 1.4ng/ml) it can increase sympathetic activity & directly affect automaticity in cardiac tissue which contribute to the arrhythmias - not only increase sensitivity, but also increase uptake. If myocardial blood flow has increased transiently....there may be more digoxin presented to an already sensitized heart - just a thought.......slow down breathing, slow down myocardial blood flow, decrease sympathetic tone, check electrolytes (K+ & Mg+ - not mentioned) & see what happens.....just another thought...
 
sdn1977 said:
I'll throw in my two cents as well.....studies show about 10-13% of pts show electrophysiologic symptoms of toxicity at levels above 1.5 ng/ml (not ug/ml!) altho no clinical symtoms...so she may have already been a bit high, depending upon her hydration & renal status. (As an aside...0.25mcg of digoxin seems a bit high for an 70 yo woman even at 80kg since it is dosed on lean body weight & her Crcl with age alone would be <70, but who knows......you gotta go with what you're given..)

I agree with the poster who said 5 min of hyperventilation causing the biochemical change in the K+ to increase myocardial sensitivity seems pretty fast, but all of you would know that better than I..

Another hypothesis might be the hypercapnia may cause an increase in myocardial blood flow which, I think, has been shown to cause an increase in sympathetic sensitivity of the myocardium.

At therapeutic concentrations, digoxin decreases automaticity due to an increase in vagal tone & a decrease in sympathetic activity. However, at higher concentrations (greater than 1.4ng/ml) it can increase sympathetic activity & directly affect automaticity in cardiac tissue which contribute to the arrhythmias - not only increase sensitivity, but also increase uptake. If myocardial blood flow has increased transiently....there may be more digoxin presented to an already sensitized heart - just a thought.......slow down breathing, slow down myocardial blood flow, decrease sympathetic tone, check electrolytes (K+ & Mg+ - not mentioned) & see what happens.....just another thought...

You always have good info to dispense here, sdn. I appreciate it.

By the way, the elbow feels a lot better after the surgery. Consider it, if you are still suffering. :thumbup:
 
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