Thousands of people have ventricular fibrillation every year, but most of them are not 29. Found gasping for air by her husband, she was shocked six times and given 3 mg of epinephrine by paramedics, with return of sinus rhythm en route to the hospital.
PE. She remained unresponsive on arrival — tachycardic to 110s, BP 110/70, and tachypneic to 29. Hypoxemic despite non-rebreather face mask, rales on the right side greater than left, and cool non-edematous extremities. We intubated her, and noted exquisite sensitivity to midazolam sedation. Her BP would drop even at 1 mg per hour, requiring us to start a norepinpehrine drip just to maintain sedation. Her cardiovascular system is strained; it cannot tolerate even a small amount of benzodiazepine.
ECG. Sinus tachycardia with lateral ST depressions and a prolonged QT interval. No STEMI. Not uncommon to have repolarization abnormalities immediately post-resuscitation, I suppose. But a congenital or acquired cause of prolonged QT should remain on the differential.
CXR. Bilateral, diffuse, alveolar infiltrates, and a normal heart size. No cardiac dilation? Likely cardiogenic pulmonary edema of an acute rather than chronic time course. She is not the dwindling cardiomyopath who battled daily compensated cardiac failure before arresting.
PE with a focus. I listen for a second time, intent on finding regurgitation of the mitral valve. Retracting breast tissue superiorly, all the way out beyond the apex to the anterior axillary line and into the axilla. New ruptured chordae? Ischemic papillary muscles that cannot maintain tension on valve leaflets? Or incompetent, infected leaflets themselves? Each could cause acute mitral insufficiency and cardiogenic pulmonary edema with a normal heart size. I hear no corroborating murmur. The valves seem OK, but what about myocytes?
ED U/S. Short axis parasternal view showed an LV chamber diameter that changed little between systole and diastole. Diffusely dysfunctional. Was this a large territory of injured myocardium? Or just stunned post-arrest tissue? Her ejection fraction at that moment was below 20% by my estimates.
Rx. Hypothermic protocol is initiated. The monitor displays short runs of ventricular tachycardia. We start a lidocaine drip to persuade her myocytes to behave more congenially. Norepinephrine is titrated up to maintain her MAP in what appeared to us as cardiogenic shock.
Norepinephrine. Non-inferior to dopamine and less arrhythmogenic, it also has vasoconstricting alpha effects that can be helpful in states of very low diastolic pressure. Clamped down peripheral and visceral arterioles may starve their respective vascular beds distally, but what they also do is increase the diastolic pressure upstream. A pressure that builds all the way back to the aortic root. Encouraging RBCs newly released by the aortic valve to take a U-turn and head down coronary arteries as the leaflets close. Myocardial perfusion is driven by diastolic pressure.
Systolic events, on the other hand, are starvation. Contracting myocytes compress intra-myocardial perforating branches of coronary arteries, and essentially cut off all flow — to themselves. The altruist in this state is not able to feed off the higher systolic pressures it produced. Instead it relies solely on diastolic backpressure for flow of nutrients at a time when its ventricular myocytes are relaxed.
Hypoxemia. The cardiology team is at the bedside arranging for admission as we attend to her secondary problem. We cannot bring her oxygen saturation above the low 80s despite standard settings on PRVC. Not good for an irritable, post-arrest myocardium with precarious diastolic coronary perfusion pressures. Tracheal suction produces minimal froth and no change in the percentages.
Fortunately, her flow loops show no prolongation of expiration. No bronchiolar obstruction and no air trapping. This means we can procure more time for inspiration. I discuss with the respiratory therapist adjusting the flow rate, increasing the inspiratory time, and nearly inverting the I:E ratio. We hope her alveoli will feel the opening pressure more homogeneously and for a longer time, in this manner recruiting more alveolar units as future contributors to gas exchange. We increase PEEP to keep the new recruits open during end-expiration. Her saturation peaks at the high 80s. The therapist and I nod in agreement, satisfied for now.
V-fib arrest followed by cardiogenic shock with runs of monomorphic v-tach and secondary, dense alveolar edema producing hypoxemia refractory to standard ED ventilation parameters. The differential started at prolonged QT, but must include stimulant abuse, arrhythmogenic right ventricular cardiomyopathy, other channelopathies like Brugada syndrome, or anatomic issues including anomalous origin or course of a coronary artery. Alternatively, she could be a precocious 29-year-old with garden-variety atherosclerotic disease or a ruptured plaque. In her favor, she did not appear to have a structural cardiomyopathy by x-ray, ECG, or U/S.
First troponin was 0.62. Urine tox negative. WBC of 9.8 with 89% lymphocytes. I am not sure how this fits in. Are we dealing with an infectious or immunologic myocarditis?
She was ill, by all accounts, and had cardiogenic shock that did not seem related to a new, intervenable ST elevation MI. And in that sense, I believed her prognosis was poor.
She found herself on phenylephrine, milrinone, and amiodarone drips in addition to our norepinephrine and lidocaine after a few hours in the CCU. Their leading diagnosis was myocarditis. Lactate peaked at 11, and her troponin peaked at 9.8.
And then … she had an ECG that caught it. A brief run of v-tach. What they noticed was that v-tach was actually “v-tach.” A wide complex tachycardia that, upon closer inspection, had p waves and an ultra short PR interval before every QRS. This was supraventricular and conducting down a bypass tract. Review of select ECGs throughout her hospital stay showed subtle delta waves preceding some but not all of her QRS complexes.
What her diagnosis became now was one I did not foresee during her ED course — a proposed atrial dysrhythmia and unregulated conduction down a bypass tract resulting in a storm of systolic events that left no time for diastole and, in doing so, cut off all coronary flow. No time to relax meant no perfusion for ventricular muscle. Soon enough she was gasping for air, and the paramedics found that her starved myocytes had decided it was every man for himself. V-fib.
She was gradually weaned off pressor and inotrope over days in the CCU as her stunned myocardium regained function and her mentation improved. She underwent ablation of a left lateral accessory pathway once stable, was extubated, and was eventually discharged home with preserved neurologic function and an ECG without delta waves.
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