Questions of the Week for 10/10/2023
Author: Christian Gerhart
A patient presents after a sotalol overdose. What is the mechanism of sotalol and what clinical manifestations does this cause?
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Sotalol has both beta blocker and potassium channel blocker properties. This can result in clinical findings consistent with a beta block overdose (bradycardia, hypotension, hypoglycemia) and potassium channel blockade (QT prolongation, Torsade de Pointes).
Describe your initial therapies for a patient who presents with a calcium channel blocker (CCB) or beta blocker (BB) overdose.
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1) Consider the need for fluids/vasopressors, stabilize vital signs: Norepinephrine or Epinephrine are probably good choices, no strong evidence for any particular pressor. IV fluids should only given if it is suspected that the patient is hypovolemic.
2) Consider decontamination: Most effective early. Discuss with toxicology whether activated charcoal or whole bowel irrigation would be recommended.
3) IV Calcium: Typically administered for either CCB or BB overdose. Usually start with 3g calcium gluconate, can redose every 10 minutes, follow ionized calcium. Can help with contractility and blood pressure.
4) Glucagon: Probably most helpful for sick BB overdose patients. Bypasses beta blocker and increases intracellular myocardial cAMP to help with contractility. Initial dosing 3-5mg IV, may require infusion. Watch out for vomiting.
5) High dose insulin therapy: Used for both CCB/BB but maybe more effective for CCB. 1 unit/kg bolus, 1 unit/kg/hr infusion (10 times DKA dosing).
You get handed the following EKG from the waiting room. The previous EKG showed normal sinus rhythm. What is the rhythm and what is on your differential?
EKG from Steve Smith’s EKG blog
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This a narrow complex, regular bradycardia with a rate of approximately 35 with no clear P waves. The rhythm is a junctional bradycardia with retrograde P waves. This should always raise concern for hyperkalemia. Peaked T waves are also present on this EKG. Remember that hyperkalemia can cause bradycardia without peaked T waves or QRS widening. Always consider hyperkalemia in your differential for bradycardia. Other considerations are drugs (beta blockers, calcium channel blockers, digoxin), hypothermia, hypothyroidism, and ischemia.
More here: https://hqmeded-ecg.blogspot.com/2014/07/bradycardia-sob-in-dialysis-patient.html
A 75 yo patient presents with dizziness and the following vitals:
HR: 32
BP: 80/30
RR: 25
SpO2: 99%
T: 37 C
EKG is shown below:
EKG from Life in the Fast Lane
Describe your initial stabilization package.
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This patient has an unstable bradycardia (hypotension, symptomatic). ACLS favors atropine as initial therapy, however this is most effective when the bradycardia is vagally mediated, such as in an acute MI. There is probably no harm in trying 1 mg of atropine, but it may not work and is a short-lived treatment. Push dose epinephrine (20-50 micrograms) can be given for blood pressure support and chronotropy while an epinephrine infusion is started. Transcutaneous pacing (start with a high amplitude and titrate down) should be started if there is not sufficient response to initial therapies. Remember that if hyperkalemia is the culprit, then the above therapies likely won’t be particularly effective. Consider calcium early in your unstable bradycardia algorithm. If these therapies don’t work and the patient continues to require transcutaneous pacing, a transvenous pacemaker is usually the next step. This particular EKG was a case of BRASH syndrome who was hyperkalemic.
A young patient presents with profound CNS depression and absent brainstem reflexes. CT/CTA head and neck is read as normal. What medication overdoses should be considered?
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Baclofen, Bupropion and Valproic acid overdose can all produce profound CNS depression and mimic brain death. Testing for Bupropion or Baclofen is not usually helpful in the acute setting due to delayed turnaround time. Valproic acid is associated with elevated ammonia (usually over 100s in severe overdose). Additionally, intoxication with barbiturates or alcohols (ethanol, ethylene glycol) can present similarly and can be tested for. Tricyclic antidepressants can also cause profound CNS depression.
Norepinephrine is an excellent vasopressor in many situations and rarely the wrong vasopressor for a hypotensive patient. What patient factors may prompt a shift to a different vasopressor in a patient with septic shock?
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Patients with tachydysrhythmias (atrial fib/flutter with RVR, ventricular tachycardia) may not tolerate the beta agonism of norepinephrine well. In these scenarios, vasopressin or phenylephrine may be a better option depending on the underlying process. Vasopressin may also be slightly preferred if right heart failure is suspected to be contributing to the patient’s shock as it has some pulmonary vasodilatory properties.
A patient with suspected sepsis requires norepinephrine, which is infusing through a good peripheral IV. The patient’s IV becomes slightly dislodged and the pump starts beeping. The patient has a small area of swelling around the IV site. What are your next steps?
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This patient’s norepinephrine likely has extravasated. First, stop the infusion or ideally switch it another IV as they probably need it. Next, do not remove the IV but rather keep it in place and us it to aspirate as much norepinephrine as possible. The antidote for norepinephrine extravasation is phentolamine, an alpha antagonist, which promotes vasodilation. This can be injected into the original IV catheter as well as subcutaneously in the surrounding skin. The dose is 0.1 to 0.2 mg/kg up to a max of 10 mg. Generally, plastic surgery should be consulted for extravasation injuries.
More here: https://emcrit.org/emcrit/peripheral-vasopressors-extravasation/