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[Subarachnoid hemorrhage and the heart]
P P Martorano1, G Bini, L Tanara
1Istituto delle Emergenze Medico-Chirurgiche, Università degli Studi, Ancona.
Insights
Electrocardiographic abnormalities are common in patients with subarachnoid hemorrhage (SAH), often appearing within 48 hours. While usually transient, cardiac monitoring is vital for managing potential severe complications.
Area of Science:
- Cardiology
- Neurology
- Critical Care Medicine
Context:
- Subarachnoid hemorrhage (SAH) is frequently associated with cardiac complications.
- Electrocardiographic (ECG) abnormalities are reported in 2-91% of SAH patients.
- These changes can manifest within 48 hours of symptom onset.
Purpose:
- To review the spectrum and significance of ECG abnormalities in subarachnoid hemorrhage.
- To discuss potential mechanisms underlying these cardiac changes.
- To emphasize the importance of cardiac monitoring in SAH patients.
Summary:
- Common ECG findings include T wave inversion, ST elevation/depression, and various arrhythmias.
- While often benign and transient, severe SAH can lead to ventricular asynergy, vasospasm, or necrosis.
- Arrhythmias may result from autonomic dysregulation or direct cerebral damage.
Impact:
- Highlights the need for vigilant ECG monitoring in SAH patients.
- Suggests ECG changes may serve as indirect indicators of neurological severity.
- Underscores the potential link between SAH and cardiac morbidity/mortality, though further research is needed.
Abstract:
Electrocardiographic abnormalities had been reported, in patients with subarachnoid hemorrhage, with variable percentage from 2% to 91%, according to several studies. The most common changes are T wave inversion, ST segment elevation or depression, QT prolongation, U waves, atrial flutter and fibrillation, ventricular fibrillation, supraventricular tachycardia, premature atrial and ventricular contractions. These findings occur within the first forty-eight hours after the onset of the symptoms; they usually are benign and transient. In a small percentage of cases generally in severe ESA, the ECG changes are associated with ventricular asynergy, coronary vasospasm or subendocardic necrosis. The arrhythmias could be produced either by autonomic discharges to the heart, during increased sympathetic activity due to ESA, or by a damage of cerebral areas with arrhythmogenic capacity. The importance of ECG abnormalities towards mortality and morbidity in patients with ESA has not yet been cleared; however, a careful monitoring is recommended to prevent severe cardiac complications and to obtain an indirect, further evaluation of the neurologic pathology.