DrankTheKoolaid
Forum Deputy Chief
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Had a call the other day that i haven't quite figured out.
Called to local clinic for a 76 YO/Female with chest pain. Get to clinic to find female patient lying low fowler's on exam table pink warm dry, RR16 non labored Lungs CTA without complaint. While partner was getting her hooked up get report from FNP who states patient at home had 4/10 chest pain not relieved by single 0.4ntg. FNP upon patient arrival assessed and put her on "7" literes O2 via NC and administered a second NTG at which point patient states pain down to a zero which patient relates was from the O2 and not the NTG. FNP doesnt keep CM in the clinic as she cant read em. FNP states patient prior MI 1 year ago with no meds or allergies. While im receiving report I hear the familiar alarm on the monitor as my partner hooked her up look over and she's in a rapid atrial tach 170's 180's with a bp of 128/70. Initially appeared to be SVT but after getting her to vagal down pretty clear was a A-fib W/RVR.
Anyways i get the order for Verapamil and CA++ as it's one of the few we have to mother may I for. So i get everything drawn up and after giving the CA++ over 5 minutes patient HR increased to 220 with a complaint of 4/10 CP. Since i already had it drawn up and the patient remained PWD with no shortness of breath with no drop in BP i gave the Verapamil 2.5mg. First dose no change other then complete relief of the CP and bringing her rate back to a uncontrolled Afib w/RVR at 160's 180's.. Second 2.5mg dose coverted her to a ST at 120 without ectopy.
Now my question is was the CA++ the cause of the increasing atrial rate? I fully understand the slow and fast CA channels and expected the rate to increase. But after the call i dbl checked in the field guide and it shows a SE of the CA++ as a decrease in heartrate which doesnt make sense to me. Any of you guru's that can step up and set me straight it would be much appreceited.
Corky
Called to local clinic for a 76 YO/Female with chest pain. Get to clinic to find female patient lying low fowler's on exam table pink warm dry, RR16 non labored Lungs CTA without complaint. While partner was getting her hooked up get report from FNP who states patient at home had 4/10 chest pain not relieved by single 0.4ntg. FNP upon patient arrival assessed and put her on "7" literes O2 via NC and administered a second NTG at which point patient states pain down to a zero which patient relates was from the O2 and not the NTG. FNP doesnt keep CM in the clinic as she cant read em. FNP states patient prior MI 1 year ago with no meds or allergies. While im receiving report I hear the familiar alarm on the monitor as my partner hooked her up look over and she's in a rapid atrial tach 170's 180's with a bp of 128/70. Initially appeared to be SVT but after getting her to vagal down pretty clear was a A-fib W/RVR.
Anyways i get the order for Verapamil and CA++ as it's one of the few we have to mother may I for. So i get everything drawn up and after giving the CA++ over 5 minutes patient HR increased to 220 with a complaint of 4/10 CP. Since i already had it drawn up and the patient remained PWD with no shortness of breath with no drop in BP i gave the Verapamil 2.5mg. First dose no change other then complete relief of the CP and bringing her rate back to a uncontrolled Afib w/RVR at 160's 180's.. Second 2.5mg dose coverted her to a ST at 120 without ectopy.
Now my question is was the CA++ the cause of the increasing atrial rate? I fully understand the slow and fast CA channels and expected the rate to increase. But after the call i dbl checked in the field guide and it shows a SE of the CA++ as a decrease in heartrate which doesnt make sense to me. Any of you guru's that can step up and set me straight it would be much appreceited.
Corky