Male, 78-year-old patient, hypertensive (he couldn’t tell about his medication), dyspnea, productive cough and fever not measured for 15 days, with worsening the day he was admitted. He had been taking Ceftriaxone (a cephalosporin antibiotic) with no improvement.
Clinical history: social drinker; former smoker (he quitted 20 years before).
Admission: General regular state, agitated, tachypneic, cooperative, oriented. BP = 150 x 70 mmHg
Cardiac examination: regular cardiac rhythm, normal heart sounds and no murmurs, HR: 76 bpm.
Pulmonary examination: globally decreased gross vesicular murmurs with crepitations at the bases. Respiratory rate: 32.
He evolved into respiratory failure.
Associated to symptoms of kidney insufficiency
New regimen is started: antibiotics + mechanical ventilation + hemodialysis
Chest X-ray: compatible with pneumonia.
5 days after the admission he developed mixed shock with renal function worsening associated with metabolic acidosis and hyperkalemia, all refractory in spite of therapeutic measures (K=10.2mEq/L). High doses of noradrenaline were applied.
ECG was performed, revealing ST segment elevation, so he was referred to the hemodynamic lab.
Coronary angiography revealed significant obstructive lesions; however it showed diffuse coronary artery spasm (RCA + left main coronary artery) that was reverted with intracoronary isosorbide mononitrate.
After the result of left heart catheterization, a therapeutic dilemma arose: reducing the dose of noradrenaline (because of the spasm) or keep the high dose to increase BP and allow the hemodialysis.
Hemodialysis was contraindicated by the nephrologist due to refractory hypotension.
After the catheterization, he died in asystole/pulseless electrical activity.
Which are the diagnosis of the ECGs?
Which is/are the responsible mechanism(s) for the ECG-2 and ECG-3 pattern?