Potential negligence in the management of cardiogenic shock

Rhythm control is preferred over rate control for atrial flutter in general but especially in heart failure. More importantly, the choice of IV diltiazem was one that is contraindicated and almost certainly precipitated a decline that led to cardiac arrest.

Yes. If upon review of the records it was clear that diltiazem was initiated or continued inappropriately there is definite causation.

The care rendered raises legitimate concerns but, on the facts as presented, falls within the range of defensible clinical judgment under the circumstances. Several points support this assessment: Diltiazem administration: While IV non-dihydropyridine calcium channel blockers are relatively contraindicated in known HFrEF, the severity of this patient's systolic dysfunction (EF 12–15%) was not established at the time of administration. He presented in atrial flutter with RVR at 138–145 bpm requiring urgent rate control, and the diagnosis of severe biventricular cardiomyopathy was made on the echocardiogram performed after diltiazem was given. Although the bedside picture (peripheral edema, abdominal bloating, near-syncope, two-week dyspnea) should have raised suspicion for underlying heart failure and arguably warranted POCUS or bedside echo before IV nodal blockade, the use of diltiazem for rate control in undiagnosed flutter with RVR is a common and generally accepted ED practice. Notably, the patient achieved rate control to the 80s without immediate hemodynamic collapse, and the PEA arrest did not occur until nearly 31 hours after presentation. Neurologic deterioration at 17:00 on 11/04: This event was appropriately worked up with CT head and CTA chest, both reportedly negative, and therapeutic anticoagulation was initiated — a reasonable response given the embolic risk from flutter. Escalation and transfer timing: The patient was escalated to Impella, CRRT, and transferred to a tertiary center for ECMO within roughly 48 hours of presentation. While earlier recognition of cardiogenic shock physiology might have prompted earlier transfer, the trajectory from rate-controlled flutter to overt shock was not linear, and the response once shock was recognized appears appropriate. Rhythm vs. rate strategy: The eventual recovery of EF to ~45% following successful ablation supports a tachycardia-mediated component, which in hindsight favors earlier rhythm control. However, electrical cardioversion in unanticoagulated flutter of unknown duration carries its own embolic risk, and the initial decision to pursue rate control was reasonable given the information available at presentation. Outcome: The patient ultimately survived with significant EF recovery and was discharged with a LifeVest. While the hospital course was complicated, the ultimate outcome was favorable, which complicates any damages analysis. The strongest plaintiff theory is the diltiazem decision in the face of obvious clinical signs of decompensated heart failure on arrival, but defense experts will credibly argue that the EF was not yet known, rate control was clinically indicated, and the standard of care does not require POCUS in every flutter-with-RVR presentation. Expert review by a cardiologist and emergency medicine physician would be warranted to determine whether the constellation of presenting findings should have triggered a different initial approach, but on the current record, breach of standard of care is not clearly established and causation is further complicated by the patient's recovery.

Even assuming arguendo that a breach of the standard of care occurred (most plausibly the administration of IV diltiazem in a patient with clinical signs of decompensated heart failure without prior assessment of LV function), the causal link to a discrete, compensable injury is difficult to establish on the facts presented. Underlying disease as the dominant cause: The patient was ultimately diagnosed with dilated/noncompaction cardiomyopathy — a structural, likely genetic condition that pre-existed the ED encounter and was independently responsible for his severe biventricular dysfunction (EF 12–15%), atrial flutter, and shock physiology. His exogenous testosterone/anastrozole use also independently raises the risk of cardiomyopathy and thromboembolic events. He presented already in advanced decompensation after two weeks of progressive symptoms. The natural history of his underlying disease — not the diltiazem — is the most plausible primary driver of the subsequent PEA arrest, need for mechanical circulatory support, and prolonged hospitalization. Temporal disconnect from diltiazem: Diltiazem was given on arrival on 11/04 with successful rate control to the 80s and no immediate hemodynamic collapse. The PEA arrest did not occur until approximately 16:50 on 11/05 — nearly 31 hours later — and after diltiazem had already been discontinued at ~17:00 on 11/04 following the neurologic event. This temporal gap weakens any direct causal argument that diltiazem precipitated the arrest. Neurologic event: The acute lethargy and severe headache at 17:00 on 11/04 had a negative CT head and CTA chest. Without a documented stroke, intracranial hemorrhage, or other discrete neurologic injury, this event does not appear to have produced a permanent compensable injury. It may instead reflect low-output physiology from the underlying cardiomyopathy itself. Favorable ultimate outcome: The patient survived, underwent successful ablation, recovered EF to approximately 45%, and was discharged with a LifeVest on 11/29/24. While he endured a prolonged ICU course with ECMO, Impella, CRRT, and multiple cardioversions, much or all of this would likely have been required regardless of the initial rate-control strategy given the severity of his underlying cardiomyopathy at presentation. Damages are therefore limited to the incremental harm attributable to any alleged breach — which is difficult to isolate from the harm caused by the underlying disease. Counterfactual problem: The plaintiff would need to establish that a different initial strategy (e.g., early electrical cardioversion, amiodarone, or earlier transfer) would more likely than not have avoided the arrest and shortened the hospital course. Given the severity of the cardiomyopathy on presentation, the embolic risk of cardioversion in unanticoagulated flutter of unknown duration, and the fact that even at the tertiary center on full mechanical support the EF remained <20% until after ablation, this counterfactual is speculative. The strongest causation theory — that diltiazem worsened cardiogenic shock physiology and contributed to the cascade leading to PEA arrest — is plausible but not strongly supported by the timeline, and the contribution would be difficult to disentangle from the natural progression of severe, previously undiagnosed cardiomyopathy. Expert cardiology review would be needed, but on the current record, causation is unlikely to be established by a preponderance of the evidence.

In someone with a severe cardiac, the and a flutter with rapid ventricular raid, a beta blocker would be probably the better option. Calcium channel blockers may not be indicated, given the severe cardiomyopathy. Though it is not stated we do not know what the heart rate or vitals were prior to him coding. But so far there’s a lot of aspects of this case that make me question be attentiveness of the primary team.

It doesn’t seem like anyone is really paying attention other than to try and get the heart rate to be lower. Without regard to the biventricular dysfunction, I think that this may yield to him having some negative results.

Although it’s not unreasonable to utilize dilt as first-line therapy for unstable atrial arrhythmias if the patient is normotensive and not in obvious heart failure or show, By the time they recognize severe left ventricular dysfunction and cardiomyopathy, this should have been discontinued. dilt is known to have negative inotropic properties and, in a situation like this, can deteriorate a patient from stable heart failure and left ventricular dysfunction to unstable cardiogenic shock very easily, especially if the patient is in a state of unrecognized low cardiac output. . The patient should have been switched to either beta blocker therapy, amiodarone, or digoxin

Although it's hard to definitively know With certainty, based on the sequence of events described, I think it's very likely that the diltiazem contributed to the decline and progression to cardiogenic shock, and this may have been avoided.

The problem here is nationwide. The kneejerk reflex of starting diltiazem on any afib RVR or aflutter with RVR is a major mistake. Once the patient comes with afib or aflutter RVR, you do not know what the underlying condition is. Especially in this case, the clinical case screams CHF. Diltiazem being a negative ionotropic agent would be the worst drug of choise.

If the patient was started on amio rather then diltiazem, the outcome and the speed of recovery would be different.