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Updated: Apr 7, 2026

Murine Isolated Heart Model of Myocardial Stunning Associated with Cardioplegic Arrest
Published on: August 6, 2015
Management of catecholamine-induced stunned myocardium--a case report
Mohit Mittal1, M Radhakrishnan1, G S UmamaheswaraRao1
1Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, Bangalore, India.
Insights
Triple-H therapy for cerebral vasospasm can cause cardiac failure, which may be missed by monitoring blood pressure alone. Noninvasive cardiac output monitoring aided diagnosis and treatment, preventing neurological deficits.
Area of Science:
- Neurology
- Cardiology
- Critical Care Medicine
Background:
- Cerebral vasospasm is a common complication after subarachnoid hemorrhage.
- Hypertensive, hypervolumic, and hemodilution (Triple-H) therapy is a standard treatment for symptomatic cerebral vasospasm.
- Triple-H therapy can induce a hyperadrenergic state, potentially leading to cardiac dysfunction.
Observation:
- A patient undergoing Triple-H therapy developed cardiac failure.
- Cardiac dysfunction was not apparent when monitoring blood pressure alone.
- Bioreactance noninvasive cardiac output monitoring was utilized for diagnosis.
Findings:
- Continuous cardiac output monitoring identified cardiac failure during Triple-H therapy.
- The patient's cardiac failure was successfully treated with milrinone and dobutamine.
- The patient recovered without neurological deficits.
Implications:
- Relying solely on blood pressure may lead to missed diagnoses of cardiac complications during Triple-H therapy.
- Noninvasive cardiac output monitoring is a valuable tool for guiding therapy in patients receiving Triple-H therapy.
- Early detection and management of cardiac dysfunction can prevent adverse neurological outcomes.
Abstract:
Hypertensive, hypervolumic, and hemodilution therapy (triple-H therapy) is administered to patients with symptomatic cerebral vasospasm after intracranial aneurysm clipping. This therapy can sometimes result in cardiac dysfunction because of pharmacologically induced hyperadrenergic state. The diagnosis may be missed if blood pressure alone is monitored to guide triple-H therapy. In this report, we describe one such patient who developed cardiac failure after triple-H therapy. This was diagnosed by using a bioreactance noninvasive cardiac output monitoring. Continuous cardiac output monitoring by this technique facilitated treatment of cardiac failure with milrinone and dobutamine. At discharge, the patient had no neurologic deficits.
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