BACKGROUND AND PURPOSE: We know that significant cardiac involvement can occur in patients with acute intracranial hemorrhage, particularly in those with subarachnoid hemorrhage. These patients may present with electrocardiographic abnormalities that were previously thought to be benign. However, many die of cardiovascular sequelae, which suggests more serious cardiac problems. To characterize the cardiac, rhythmic, and myocardial disturbances that occur 2 to 4 hours after subarachnoid hemorrhage, we conducted an experimental study using autologous blood (7.9+/-0.3 mL) injected into the right frontal lobe and subarachnoid space in canines. METHODS: Nine adult mongrel dogs were anesthetized with isoflurane and their rectal temperatures maintained at 37 degrees C. Electrocardiogram, heart rate, mean arterial pressure, mean pulmonary artery pressure, and intracranial pressure were continuously measured. Transesophageal echocardiography was performed to assess myocardial wall motion changes and aortic and pulmonary flow velocities before, immediately after, and 2 and 4 hours after intracranial hemorrhage. Blood samples were collected and analyzed for catecholamines and cardiac enzymes, and cardiac output was measured. Animals were killed at 2 to 4 hours after subarachnoid hemorrhage, and a piece of the myocardium was freeze-clamped for analysis of tissue catecholamines. Light and electron microscopy were used for histopathologic assessment. RESULTS: Subarachnoid hemorrhage produced significant increases in intracranial pressure, cardiac output, and aortic and pulmonary flow velocities. Also, significant changes in creatine kinase and catecholamines were observed. Electrocardiographic recordings showed changes of tachycardia, ST-segment depression, inverted T wave, and premature ventricular contractions in four animals at 1 to 5 minutes after injection, and echocardiographic changes were evident in all animals at 20 to 240 minutes. Microscopic examination of the heart showed evidence of myocardial changes in one animal with the use of light microscopy and in nine with the use of electron microscopy. CONCLUSIONS: This study demonstrates the high incidence of cardiac involvement, specifically wall motion abnormalities, that occur after subarachnoid hemorrhage and suggests the importance of continuous cardiac monitoring, particularly echocardiographic measurements, in those patients.
BACKGROUND AND PURPOSE: We know that significant cardiac involvement can occur in patients with acute intracranial hemorrhage, particularly in those with subarachnoid hemorrhage. These patients may present with electrocardiographic abnormalities that were previously thought to be benign. However, many die of cardiovascular sequelae, which suggests more serious cardiac problems. To characterize the cardiac, rhythmic, and myocardial disturbances that occur 2 to 4 hours after subarachnoid hemorrhage, we conducted an experimental study using autologous blood (7.9+/-0.3 mL) injected into the right frontal lobe and subarachnoid space in canines. METHODS: Nine adult mongrel dogs were anesthetized with isoflurane and their rectal temperatures maintained at 37 degrees C. Electrocardiogram, heart rate, mean arterial pressure, mean pulmonary artery pressure, and intracranial pressure were continuously measured. Transesophageal echocardiography was performed to assess myocardial wall motion changes and aortic and pulmonary flow velocities before, immediately after, and 2 and 4 hours after intracranial hemorrhage. Blood samples were collected and analyzed for catecholamines and cardiac enzymes, and cardiac output was measured. Animals were killed at 2 to 4 hours after subarachnoid hemorrhage, and a piece of the myocardium was freeze-clamped for analysis of tissue catecholamines. Light and electron microscopy were used for histopathologic assessment. RESULTS:Subarachnoid hemorrhage produced significant increases in intracranial pressure, cardiac output, and aortic and pulmonary flow velocities. Also, significant changes in creatine kinase and catecholamines were observed. Electrocardiographic recordings showed changes of tachycardia, ST-segment depression, inverted T wave, and premature ventricular contractions in four animals at 1 to 5 minutes after injection, and echocardiographic changes were evident in all animals at 20 to 240 minutes. Microscopic examination of the heart showed evidence of myocardial changes in one animal with the use of light microscopy and in nine with the use of electron microscopy. CONCLUSIONS: This study demonstrates the high incidence of cardiac involvement, specifically wall motion abnormalities, that occur after subarachnoid hemorrhage and suggests the importance of continuous cardiac monitoring, particularly echocardiographic measurements, in those patients.
Authors: Hoang P Nguyen; Jonathan G Zaroff; Emine O Bayman; Adrian W Gelb; Michael M Todd; Bradley J Hindman Journal: Anesthesiology Date: 2010-08 Impact factor: 7.892
Authors: L B J van der Velden; L C Otterspoor; L J Schultze Kool; G J Biessels; F W A Verheugt Journal: Neth Heart J Date: 2009-08 Impact factor: 2.380
Authors: Preeti Ramappa; Deepak Thatai; William Coplin; Steven Gellman; J Ricardo Carhuapoma; Ruth Quah; Benjamin Atkinson; James D Marsh Journal: Neurocrit Care Date: 2008 Impact factor: 3.210