Case Based Learning for August 2025

46-year-old male arrived to the ED in January via EMS who reported the patient had abdominal pain and shortness of breath and was initially anxious but then fell asleep en route.  On arrival, the patient was calm and kept his eyes closed without speaking much.  He mumbled that he was having trouble breathing recently and gave vague history of recent chest pain, abdominal pain, and coughing.  The patient fell asleep during history taking but was arousable to voice.  He had been seen the day before in our ED complaining of shortness of breath.   That chart revealed he had a history of methamphetamine abuse, cardiomyopathy, LV mural thrombus on Eliquis, and PTSD.  The day before, a full cardiac workup was unremarkable and he was discharged.

The patient appeared withdrawn and somnolent, not speaking much.  I considered whether he was coming off of a meth binge, and experiencing the hypersomnia and encephalopathy sometimes seen with a meth crash.  It was noted that his hands and feet were cold and cyanotic, but the medics stated that the house was very cold and perhaps cold exposure was causing vasoconstriction.  Initial blood pressure was 100/70, heart rate of 76, SaO2 97%.  Initial EKG is shown below.

The workup was ordered and the patient was rechecked and condition was not improving.  Pulse ox was not showing good waveform.  The medical student called me when the patient became agitated and profusely diaphoretic.  Subsequently, the patient said “I’m going to die!”, laid back, and lost consciousness.  He continued breathing and had a very weak femoral pulse.  While trying to decide whether to begin CPR, I noted a flurry of dysrhythmias on the monitor.  There were several beats of bradycardia followed by a few multifocal PVCs followed by a very wide-complex tachycardia with giant T waves with a rate of 103.  Repeat EKG was done.

Hyperacute T waves can be an early manifestation of acute MI but this EKG showed global abnormalities with giant T waves arising from the very widened QRS complexes.  This should always raise suspicion of hyperkalemia, one of the H’s and T’s conditions that can cause cardiac arrest.  He was given an amp of calcium chloride, an amp of sodium bicarb, D50 and insulin.  The QRS immediately narrowed and the P waves were again visible.

Despite the improvement in the EKG, the patient remained hypotensive and unconscious so he was intubated and placed on a Levophed infusion.  He was given a bolus of IV NS and Lasix 40 mg IV.  Subsequently his lactic acid level came back at 7 and potassium of 7, GFR 34.  After calling multiple hospitals, he was transferred to Deaconess.  Prior to transfer, he was given another dose of calcium chloride and sodium bicarb.  Diagnoses included severe hyperkalemia causing LBBB and dysrhythmia, cardiogenic shock with lactic acidosis and acute kidney injury, and methamphetamine induced cardiomyopathy.

The patient’s potassium had been normal the day before, and his GFR was the same.  I considered the possibility of hyperkalemia caused by taking his potassium tabs and spironolactone, rhabdomyolysis (CPK came back nml), or that the patient may have taken a potassium overdose, but the most likely explanation appeared to be that he developed cardiogenic shock from meth-induced cardiomyopathy, resulting in lactic acidosis.  This caused sudden potassium shift in the face of inability to excrete potassium due to his hypoperfused damaged kidneys.  As he became more acidotic and hyperkalemic, his cardiac contractility was further impaired, leading to worsening shock and acidosis in a death spiral.

This case reminded me of the danger in attributing objective physical findings to benign causes.  In retrospect, his initial lethargy and cold extremities were a manifestation of shock, not cold exposure or a meth crash.  When he developed cardiovascular collapse, an immediate EKG provided the diagnosis of hyperkalemia, a reminder to consider the H’s and T’s of correctable causes of cardiac arrest/near-arrest.   Waiting for the potassium result from lab likely would have resulted in his death.

The patient spent 2 weeks at Deaconess where cardiogenic shock was confirmed, he developed shock liver, and required CRRT.  He was supposed to continue dialysis upon discharge but did not show up.  He came back to our ER in critical condition with heart failure a few weeks later and was again intubated and transferred.  He is currently still alive and going to wound care for an arm wound that allegedly occurred where an IV infiltrated; he asked his PCP if he could sue the hospital for this.  He recently told cardiology that he feels great and rides his bike 2 miles into town a few times per week.

Written by Mark Scott, D.O. 

ERx Clinical Partners Medical Director, North Valley Hospital, Tonasket, WA

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This is for informational purposes only. For medical advice or diagnosis, consult a physician.

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