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Table of Contents    
Year : 2019  |  Volume : 67  |  Issue : 2  |  Page : 427-432

Perioperative significance and management of electrocardiographic abnormalities in patients undergoing cerebral aneurysm surgeries

Department of Anaesthesiology and Intensive Care, GB Pant Institute of Postgraduate Medical Education and Research, New Delhi, India

Date of Web Publication13-May-2019

Correspondence Address:
Dr. Pragati Ganjoo
Department of Anaesthesiology and Intensive Care, GB Pant Institute of Postgraduate Medical Education and Research, Maulana Azad Medical College Campus, JL Nehru Marg, New Delhi - 110 002
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.258038

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 » Abstract 

Morphological electrocardiological changes and arrhythmias are commonly encountered in patients with aneurysmal subarachnoid hemorrhage. These, if undetected and unaddressed, can cause cardiovascular ailments, postsurgical poor neurological outcomes and long term medical complications.

Keywords: Anesthetic management, aneurysm, cardiac, electrocardiogram, subarachnoid hemorrhage
Key Message: The salient physiological and pathological electrocardiogram changes associated with aneurysmal subarachnoid hemorrhage and their clinical implications during anesthesia and neurosurgery are discussed.

How to cite this article:
Malik I, Ganjoo P. Perioperative significance and management of electrocardiographic abnormalities in patients undergoing cerebral aneurysm surgeries. Neurol India 2019;67:427-32

How to cite this URL:
Malik I, Ganjoo P. Perioperative significance and management of electrocardiographic abnormalities in patients undergoing cerebral aneurysm surgeries. Neurol India [serial online] 2019 [cited 2020 Sep 25];67:427-32. Available from:

Patients presenting for cerebral aneurysm surgeries are frequently detected to have abnormal preoperative electrocardiograms (ECGs) depicting morphological waveform alterations and/or cardiac rhythm irregularities; these changes are mostly presumed to be caused by subarachnoid hemorrhage (SAH).[1] However, such ECGs may not get sufficient preoperative attention, mainly due to the urgency involved with aneurysm surgeries, and also because somehow, SAH-induced cardiac abnormalities are not considered so harmful, unlike abnormalities due to a primarily cardiac origin like ischemic heart disease (IHD). However, cardiac irregularities in SAH are known to result in serious cardiovascular complications,[1],[2],[3],[4],[5],[6] and development of such complications during the already high-risk aneurysm surgeries can be disastrous.[2],[4],[7],[8] SAH-induced cardiac abnormalities have also been linked to adverse neurological outcomes,[2],[5],[6] thereby implying that patients with abnormal preoperative ECGs could possibly fare poorly after aneurysm surgeries. An association between these cardiac abnormalities and increased incidence of serious medical complications is also reported,[9] and this may potentially impact the postoperative course and recovery in neurosurgical patients. Moreover, in patients with possibly co-existent SAH and IHD, like the elderly and hypertensive patients, the preoperative ECG abnormalities may be misdiagnosed and mismanaged. It is not uncommon to blame only SAH for the ECG changes and proceed with surgery, overlooking the more ominous IHD; while conversely, attributing the ECG changes to IHD alone may result in unnecessary deferment of surgery and initiation of anticoagulant therapy. There are thus many ways in which SAH-associated cardiac irregularities can potentially impact the course and outcome of aneurysm surgeries, and hence, these abnormalities need to be understood well by the operating team. This review focuses on the implications, adverse consequences, and the best possible perioperative management of ECG abnormalities detected prior to aneurysm surgeries.

 » Background Top

ECG abnormalities manifest in over 50% of patients within the first 48 hours after SAH; the prevalence rate is 27-100%.[10] The incidence of these abnormal cardiac changes is directly proportional to the amount of bleeding, being higher in patients with Fisher grades 3 and 4 on computed tomography (CT).[11] Morphological alterations in the ECG waveform include repolarization abnormalities like ST elevation, T wave inversion, prominent U and Q waves, prolonged QTc intervals and large, flattened or notched T waves; and, atrial depolarization abnormalities like peaked P waves and short PR intervals; a prolonged QTc interval with an inverted T wave is the most commonly observed abnormality. Nearly 80% of patients undergoing surgery within 4 days of SAH have at least one morphological ECG abnormality, the commonest being non-specific ST-T changes.[12] Among the rhythm abnormalities, sinus bradycardia, sinus tachycardia and premature ventricular beats are the most common and least harmful. Serious rhythm changes, seen in approximately 1-4% of SAH patients, include ventricular tachycardia (VT), ventricular flutter and ventricular fibrillation (VF), paroxysmal supraventricular tachycardia (PSVT), atrial flutter and atrial fibrillation (AF), Torsades de pointes and atrio-ventricular (AV) blocks.

The origin of cardiac abnormalities in SAH is attributed to multiple factors. Release of high levels of systemic and intra-myocardial catecholamines from hypothalamic stimulation triggered by blood in the subarachnoid space is the chief culprit;[4],[13],[14],[15] the other causes being, stimulation of the arrhythmogenic insular cortex due to raised intracranial pressure (ICP),[16],[17] and direct development of ventricular arrhythmias, acute lung injury and pulmonary edema in response to SAH-induced neuro-inflammation [Figure 1].[18],[19],[20] The catecholamine surge causes intense systemic vasoconstriction, increased myocardial wall stress and oxygen demand, myocardial cell death, development of sub-endocardial ischemia, contraction band necrosis and focal necrotic and hemorrhagic lesions in the heart, resulting in severely impaired left ventricular (LV) function. This cardiomyopathy in SAH, also known as neurogenic stunned myocardium (NSM), is characterized by global hypokinesia sparing the cardiac apex,[21] in contrast to the myocardial damage in IHD which is due to coronary occlusion and is distributed in the specific arterial territories. SAH-induced cardiomyopathy is also associated with raised cardiac biomarkers (in 20-68% of patients), though it is much less frequently observed than that seen in IHD; cardiac troponin I (cTnI) is the main biomarker in SAH while creatine kinase MB predominates in IHD.[17],[22] The biomarker rise in SAH is modest despite a markedly reduced ejection fraction (EF). The cardiac manifestations may appear even with minor increases in cTnI levels (0.5μ/l), and levels over 10μ/l are suggestive of significant cardiac injury manifesting as antero-septal regional wall-motion abnormalities (RWMAs) on echocardiography. Raised brain natriuretic peptide (BNP) levels, serum lipids concentration,[23],[24],[25] and C-reactive protein (CRP) levels in serum and CSF are the other prognostic biomarkers in SAH.[26] An increased BNP was also seen to be significantly associated with cerebral infarction in patients with absent angiographic vasospasm, suggestive of alternate mechanisms for its action like generalized microcirculatory dysfunction, release of pro-inflammatory cytokines, and reduced cerebral perfusion due to direct hypovolemia and vasodilatation.[25] The elevated serum lipid and CRP levels have also been associated with an increased incidence of vasospasm and worse clinical outcomes.[24] This unique pathophysiology of SAH-induced LV dysfunction, distinct from IHD, is an important determinant of the severity and prognosis of the disease.
Figure 1: Pathophysiology of cardiovascular complications after SAH. SAH: Subarachnoid hemorrhage, CSF: Cerebrospinal fluid, SIRS: Systemic inflammatory response syndrome, ATP: Adenosine triphosphate, ALI: Acute lung injury, LV: Left ventricle

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Complications of SAH-induced ECG changes and their impact on the neurosurgical course and outcome

SAH-induced ECG changes can lead to profound cardiac complications.[9],[27],[28],[29] Patients with SAH having raised cTnI levels, ECG abnormalities and LV systolic dysfunction were more likely to experience episodes of severe hypotension, pulmonary edema, severe disability and death at 90 days.[29] Frontera et al., reported a high risk of cardiovascular co-morbidity, prolonged hospital stay, poor functional outcome and high mortality in patients with SAH having clinically significant cardiac arrhythmias; 28% patients developed myocardial infarction (MI) with the mean troponin level raised up to 9.2ng/ml, and 11% patients had EF less than 50%.[9] Sinus tachycardia or persistently elevated heart rate (PEHR) were considered to be significantly responsible for the adverse cardiac events and poor outcome including death within 7 days post-SAH.[30],[31] van der Bilt et al., in their meta-analysis concluded that though the initial hemorrhage and neurological complications are the main culprits for death and poor outcome after SAH, development of LV dysfunction indicated by the RWMAs, raised biomarker levels, and presence of Q waves and ST-T changes also contribute significantly to the morbidity and mortality.[31]

Intraoperative development of these cardiac complications resulting in hemodynamic instability and consequent decrease in cerebral perfusion adds to the inherent risk of aneurysm surgery. A study of cardiac arrhythmias in 70 patients with SAH using Holter monitoring demonstrated that 7 out of 10 patients undergoing surgery within 48 hours developed serious intraoperative arrhythmias.[5] Malik et al., have reported recurrent episodes of intraoperative and postoperative AF and subsequent death of the patient following aneurysm clipping.[2] A patient with SAH and QT prolongation in ECG was reported to suffer from episodes of bradycardia and premature ventricular contractions (PVCs) intraoperatively, followed by polymorphic ventricular tachycardia (VT) and ventricular fibrillation (VF) and hemodynamic collapse, necessitating cardioversion; the abnormal rhythm was eventually controlled with postoperative antiarrhythmic drugs.[7] Intraoperative bigeminal pulse and Torsades de pointes treated by lignocaine infusion have also been reported.[7],[8]

Patients with abnormal rhythm are also reported to develop medical complications like frequent blood stream infections, fever, anemia, repeated pulmonary edema, myocardial ischemia and cardiac arrest. At least one life-threatening medical complication was reported in up to 40% of patients with arrhythmias with a 23% mortality; the complications included, pulmonary edema (23%), pneumonia (22%), hepatic dysfunction (24%), electrolyte abnormalities (33%), renal dysfunction (7%) and thrombocytopenia (4%).[32] The length of intensive care unit (ICU) and hospital stay after SAH increased significantly due to the medical complications.[7] Development of such complications postoperatively in patients undergoing aneurysm surgeries can potentially worsen their overall recovery and outcome.

A significant correlation between SAH-induced cardiac changes and life-threatening neurological complications like symptomatic vasospasm (28%), herniation (32%), cerebral infarction (44%), seizures (8%) and aneurysmal re-bleed (8%) has recently come to the fore.[9],[32] Brouwers et al., reported death in 87% of patients with fast rhythm disturbances and ECG alterations, mostly due to neurological causes like re-bleeding, cerebral ischemia, hydrocephalus, and postoperative subdural hematoma.[5] Delayed cerebral ischemia (DCI), one of the commonest causes of poor outcome after SAH, was found to be closely associated with cardiac abnormalities by different authors. A statistically significant correlation between ST segment depression and DCI,[33] between BNP levels and vasospasm severity,[34] and association of elevated cTnI levels with severe disability and death at 90 days[9] are some observations endorsing this close relationship. Hyponatremia secondary to release of BNP and persistent hyperglycemia, frequently encountered in aneurysmal SAH, have also been linked with the development of DCI.[35],[36] RWMA due to left ventricular (LV) dysfunction in SAH is an independent risk factor for the occurrence of DCI and contributes substantially to the poor outcome; apical RWMAs are linked more with ischemia while mid-ventricular RWMAs are associated with death. Late onset (day 3-10) prolonged elevated heart rate (PEHR) is also significantly associated with the development of DCI following vasospasm.[29] A recent study from the CONSCIOUS I trial has also shown that prolonged QTc interval was associated with an increased incidence of vasospasm, since QT prolongation remained the most prevalent finding (25% cases) in patients having angiographic vasospasm; sinus tachycardia was also associated with vasospasm and a poor outcome.[37] It has also been observed that among the patients with ECG abnormalities undergoing early surgery, causes of death occurring from neurological causes included primary neurological injury in the form of cerebral infarction, edema, intracranial hypertension and hydrocephalus.[38] Thus, these neurological complications associated with SAH-induced cardiac changes may perhaps be contributing in some way to the poor outcomes seen after aneurysm surgery; anticipation and early institution of neuroprotective measures in patients with preoperative ECG changes may help to improve the prognosis.

As morphological changes in ECG wave forms may resolve spontaneously within 2-3 weeks, these are often considered innocuous compared to the rhythm abnormalities. However, these simple-looking ECG changes were seen to have an independent value in predicting mortality and disability after SAH.[5],[6],[7],[10] A high mortality rate was observed in SAH patients with S-T segment changes, T wave abnormalities, pathological Q waves and QTc prolongation.[3],[6],[7],[33] Sakr et al., using the Glasgow Outcome Score (GOS), reported poor outcomes in 36% of patients having ST segment abnormalities (15%) and arrhythmias (12%).[12] A postmortem study on patients with numerous ECG abnormalities confirmed the development of extensive sub-endocardial hemorrhage and fibrosis as the cause of death.[5] Tall T waves, T wave inversion in anterolateral leads and sinus bradycardia co-existing with the World Federation of Neurosurgical Societies (WFNS) grade > 1, indicate a 100% risk of poor outcome.[6] Excessive QTc prolongation may also lead to dismal outcomes and sudden cardiac death.[16] In another study involving 301 patients, 48% were found to have QTc prolongation, of which, 51% developed DCI and had a poor outcome including death.[31] It is thus important to know that even morphological waveform changes in ECG can be dangerous and require a thorough evaluation and management prior to aneurysm surgery.

Perioperative approach to patients with ECG abnormalities undergoing aneurysm surgeries

Any ECG abnormality detected preoperatively should ideally be thoroughly investigated and treated before undertaking surgery, which however, may not be possible in case of aneurysm surgery due to paucity of time. The preoperative work up should hence be directed towards correctly interpreting the abnormalities, especially differentiating SAH-induced abnormalities from those that are IHD-induced, and their maximum possible management within the limited time constraints should be instituted; besides IHD, the other causes of cardiac irregularities like electrolyte imbalance, hypoxia, hypercarbia, and hypothyroidism also need to be ruled out.[2],[3],[10],[20] Diagnosing SAH-induced cardiomyopathy based on clinical symptoms and signs may not be easy due to the patient's altered sensorium and presence of confounding factors like intracranial hemorrhage or ischemia and raised ICP, conditions that also have cardiovascular manifestations. Among the investigations, a 12-lead ECG, chest radiography, serum electrolytes and thyroid function tests are important, but the latter may not be possible before surgery. Cardiac enzymes should be evaluated if time permits.[2] A screening echocardiogram is recommended, particularly if there is acute cTnI elevation (more than 2 μg/l) following SAH.[15] A preoperative diagnosis of SAH-induced ECG abnormalities can thus be confirmed by the absence of a previous cardiac history, a temporal association between the SAH and cardiovascular changes, presence of isolated ECG changes, a modest elevation in cTnI, a new onset LV dysfunction, and a normal echocardiogram, or presence of RWMAs not corresponding with any coronary territory. Presence of IHD is suspected if there are well-established cardiac symptoms and signs, features of an old MI in ECG, higher values of cTnI, presence of RWMAs identifiable with specific coronary territories on echocardiogram, and possibly, severe myocardial dysfunction.[15] Coronary angiography is the best preoperative diagnostic tool for establishing a clear diagnosis but may not be plausible in such situations. Management of any preoperatively detected ECG change, irrespective of the cause, includes close hemodynamic monitoring, correction of the precipitating cause wherever possible, and initiation of specific treatment for the cardiac irregularities in consultation with the cardiologist. Preoperative reversion of arrhythmias using pharmacological or electrical methods should be attempted to avoid an intraoperative circulatory compromise. Patients with AF and hemodynamic instability require cardioversion by direct current (DC) shock of 200J, while stable patients can be managed by intravenous (IV) beta blockers like esmolol or calcium channel blockers (CCBs) to control the ventricular rate. Congestive heart failure accompanying the arrhythmias can be managed with digitalis, diltiazem or amiodarone. Ventricular arrhythmias usually do not require therapy unless associated with hemodynamic compromise or LV dysfunction. Wide QRS tachycardia or polymorphic VT with hemodynamic instability should be electrically cardioverted, while calcium channel blockers (CCBs) and trans-venous catheter pacing can be attempted in patients who are refractory to cardioversion, amiodarone, procainamide and lignocaine.[39],[40] Torsades de pointes is best managed by intravenous (IV) magnesium sulphate; temporary atrial or ventricular pacing and IV lignocaine and isoproteronol can also be used in the acute period.[41],[42] Despite a satisfactory preoperative correction, the cardiac abnormalities can re-develop in the intraoperative period causing sudden hemodynamic instability. Intraoperative management includes aggressive cardiac monitoring, continuation of preoperative anti-arrhythmic drugs, and correction of electrolyte abnormalities and hyperglycemia. Fluid therapy should be central venous pressure (CVP)-guided and vasopressors kept ready for sudden emergencies; a tight perioperative heart rate control and maintenance of normotension are recommended.[29],[43],[44] Vasopressors should be started early if the patient is hypotensive, and new episodes of arrhythmias should be immediately tackled by pharmacological or electrical cardioversion. Hypothermia is detrimental in the presence of arrhythmias, and hence avoided. A close hemodynamic monitoring and anti-arrhythmic therapy should continue postoperatively, and hypotension due to the cardiac irregularities strictly avoided; vasopressors may have to be started to maintain an adequate cerebral perfusion. Over-hydration and electrolyte imbalance need to be avoided, and measures to prevent DCI including nimodipine, magnesium sulphate and statins should be continued. Since these patients may be more vulnerable to DCI, a strict neurological monitoring is necessary for the early detection and management of postoperative deterioration. An algorithm on the perioperative approach to patients with cardiac abnormalities undergoing aneurysm surgeries is depicted in [Figure 2].
Figure 2: Perioperative management of a patient with SAH and ECG changes. ECG: Electrocardiogram, SAH: Subarachnoid hemorrhage, cTnI: Cardiac troponin I, RWMA: Regional wall motion abnormality, IHD: Ischemic heart disease, NSM: Neurogenic stunned myocardium, CVP: Central venous pressure, HTN: Hypertension, DAPT: Dual anti-platelet therapy, Preop: Preoperative

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 » Conclusion Top

Morphological ECG changes and arrhythmias, which are commonly encountered in patients with aneurysmal SAH, can thus have potentially serious implications in the form of perioperative cardiovascular complications, post-surgical poor neurological outcomes and various long-term medical complications. Despite the urgency required in undertaking aneurysm surgeries, it would be prudent to preoperatively diagnose and manage these cardiac abnormalities as best as possible, to enable a safe surgical and anesthetic outcome.

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 » References Top

Sommargren CE. Electrocardiographic abnormalities in patients with subarachnoid hemorrhage. Am J Crit Care 2002;11:48-56.  Back to cited text no. 1
Malik I, Ganjoo P, Roy R, Haloi P, Tandon MS, Sinha S. Recurrent perioperative atrial fibrillation in a patient with aneurysmal subarachnoid haemorrhage: A case report and review of literature. J Neuroanaesthesiol Crit Care 2014;1:140-3.  Back to cited text no. 2
Eisalo A, Perasalo J, Halonen PI. Electrocardiographic abnormalities and some laboratory findings in patients with subarachnoid haemorrhage. Br Heart J 1972;34:217-26.  Back to cited text no. 3
Andreoli A, Di Pasquale G, Pinelli G, Grazi P, Tognetti F, Testa C. Subarachnoid hemorrhage: Frequency and severity of cardiac arrhythmias. A survey of 70 cases studied in the acute phase. Stroke 1987;18:558-64.  Back to cited text no. 4
Brouwers PJ, Wijdicks EF, Hasan D, Vermeulen M, Wever EF, Frericks H, et al. Serial echocardiographic recording in aneurysmal subarachnoid hemorrhage. Stroke 1989;20:1162-7.  Back to cited text no. 5
Kumar SM, Choudhary D, Arulkumar A, Anees T, Nair S, Tharakan JA. Prevalence of electrocardiographic changes in patients with acute aneurysmal subarachnoid hemorrhage and their relationship with outcome. Indian J Neurosurg 2013;1:52-7.  Back to cited text no. 6
Takenaka I, Aoyama K, Iwagaki T, Ishimura H, Kadoya T. Development of torsades de pointes caused by exacerbation of QT prolongation during clipping of cerebral artery aneurysm in a patient with subarachnoid hemorrhage. Br J Anaesth 2006;97:533-5.  Back to cited text no. 7
Tajiri O, Ito H, Yago Y, Masumori Y. Torsades de pointes observed during general anesthesia for cerebral aneurysm clipping in a patient with QT prolongation. Masui 2011;60:1090-3.  Back to cited text no. 8
Frontera JA, Parra A, Shimbo D, Fernandez A, Schmidt JA, Peter P, et al. Cardiac arrhythmias after subarachnoid hemorrhage: Risk factors and impact on outcome. Cerebrovasc Dis 2008;26:71-8.  Back to cited text no. 9
Coghlan LA, Hindman BJ, Bayman EO, Banki NM, Gelb AW, Todd MM, et al. Independent associations between electrocardiographic abnormalities and outcomes in patients with aneurysmal subarachnoid hemorrhage. Stroke 2009;40:412-8.  Back to cited text no. 10
Pong RP, Lam AM. Anesthetic management of cerebral aneurysm surgery. In: Cottrell JE, Young WL, editors. Cottrell and Young's Neuroanesthesia. 5th ed.. Philadelphia: Mosby Elsevier; 2010. p. 218-46.  Back to cited text no. 11
Sakr YL, Lim N, Amaral AC, Ghosn I, Carvalho FB, Renard M, et al. Relation of ECG changes to neurological outcome in patients with aneurysmal subarachnoid hemorrhage. Internet J Cardiol 2004;96:369-73.  Back to cited text no. 12
Cruickshank JM, Neil-Dwyer G, Stott AW. Possible role of catecholamines, corticosteroids and potassium in production of electrocardiographic abnormalities associated with subarachnoid haemorrhage. Br Heart J 1974;36:697-706.  Back to cited text no. 13
Kawahara E, Ikeda S, Miyahara Y, Kohno S. Role of autonomic nervous dysfunction in electrocardiographic abnormalities and cardiac injury in patients with acute subarachnoid hemorrhage. Circulation J 2003;67:753-6.  Back to cited text no. 14
Weintraub BM, McHenry L Jr. Cardiac abnormalities in subarachnoid hemorrhage: A resume. Stroke 1974;5:384-92.  Back to cited text no. 15
Gregory T, Smith M. Cardiovascular complications of brain injury. Contin Educ Anaesth Crit Care Pain 2012;12:67-71.  Back to cited text no. 16
Lim HB, Smith M. Systemic complications after head injury: A clinical review. Anesthesia 2007;62:474-82.  Back to cited text no. 17
Nguyen H, Zaroff JG. Neurogenic stunned myocardium. Curr Neurol Neurosci Rep 2009;9:486-91.  Back to cited text no. 18
Frangiskakis JM, Hravnak M, Crago EA, Tanabe M, Kip KE, Gorscan J, et al. Ventricular arrhythmia risk after subarachnoid hemorrhage. Neurocrit Care 2009;10:287-94.  Back to cited text no. 19
Bagga S, Sharma YP, Jain M. Cardiac dysfunction after subarachnoid hemorrhage: Neurogenic stress cardiomyopathy or Takotsubo cardiomyopathy. Neurol India 2011;59:304-6.  Back to cited text no. 20
[PUBMED]  [Full text]  
Bruder N, Rabinstein A. Cardiovascular and pulmonary complications of aneurysmal subarachnoid hemorrhage. Neurocrit Care 2011;15:257-69.  Back to cited text no. 21
Tung PP, Olmstead E, Kopelnik A, Banki NM, Drew BJ, Ko N, et al. Plasma B-type natriuretic peptides are associated with early cardiac dysfunction after subarachnoid hemorrhage. Stroke 2005;36:1567-69.  Back to cited text no. 22
Taub PR, Fields JD, Wu AH, Miss JC, Lawton MT, Smith WS, et al. Elevated BNP is associated with vasospasm-independent cerebral infarction following aneurysmal subarachnoid hemorrhage. Neurocrit Care 2011;15:13-8.  Back to cited text no. 23
Vesley DL, deBold AJ. Cardiac natriuretic peptides gene expression and secretion in inflammation. J Investig Med 2009;57:29-32.  Back to cited text no. 24
Tykochi T, Kostyra K, Bojanowski K, Kostkiewicz B. Analysis of serum components in acute period after subarachnoid hemorrhage. Turk Neurosurg 2014;24:672-8.  Back to cited text no. 25
Fountas KN, Tasiou A, Kapsalaki EZ, Paterakis KN, Gregorian AA, Lee GP, et al. Serum and cerebrospinal fluid C-reactive protein levels as predictors of vasospasm in aneurysmal subarachnoid hemorrhage. Clinical article. Neurosurg Focus 2009;26:E22.  Back to cited text no. 26
Chatterjee S. ECG changes in subarachnoid haemorrhage: A synopsis. Neth Heart J 2011;19:31-4.  Back to cited text no. 27
Beard EF, Robertson JW, Robertson RCL. Spontaneous subarachnoid hemorrhage simulating acute myocardial infarction. Am Heart J 1959;58:755-9.  Back to cited text no. 28
Schimdt JM, Crimmins M, Lantigua H, Fernandez A, Zammit C, Falo C, et al. Prolonged elevated heart rate is a risk factor for adverse cardiac events and poor outcome after subarachnoid hemorrhage. Neurocrit Care 2014;20:390-8.  Back to cited text no. 29
Melin J, Fogelholm R. Electrocardiographic findings in subarachnoid hemorrhage. Acta Med Scand 1983;213:5-8.  Back to cited text no. 30
van der Bilt IA, Hasan D, Vandertop WP, Wilde AA, Algra A, Visser FC, et al. Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: A meta analysis. Neurology 2009;72:635-42.  Back to cited text no. 31
Solenski NJ, Haley EC Jr Kassel NF, Kongable G, Germanson T, Truskowski L et al. Medical complications of aneurysmal subarachnoid hemorrhage: A report of the multicenter, cooperative aneurysm study. Crit Care Med 1995;23:1007-17.  Back to cited text no. 32
Shuiling WJ, Algra A, de Weerd AW, Leemans P, Rinkel GJ. ECG abnormalities in predicting secondary cerebral ischemia after subarachnoid haemorrhage. Acta Neurochir (Wien) 2006;148:853-8.  Back to cited text no. 33
Sviri GE, Shik V, Raz B, Soustiel JF. Role of brain natriuretic peptide in cerebral vasospasm. Acta Neurochir (Wien) 2003;145:851-60.  Back to cited text no. 34
Chandy D, Sy R, Aronow WS, Lee WN, Maguire G, Murali R. Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage. Neurol India 2008;54:273-5.  Back to cited text no. 35
Ghosh S, Dey S, Maltenfort M, Vibbert M, Urtecho J, Rincon F, et al. Impact of Hunt-Hess grade on the glycemic status of aneurysmal subarachnoid hemorrhage patients. Neurol India 2012;60:283-7.  Back to cited text no. 36
  [Full text]  
Ibrahim GM, Macdonald RL. Electrocardiographic changes predict angiographic vasospasm after aneurysmal subarachnoid hemorrhage. Stroke 2012;43:2102-07.  Back to cited text no. 37
Gupta SK, Ghanta RK, Chhabra R, Mohindra S, Mathuriya SN, Mukherji KK, et al. Poor-grade subarachnoid hemorrhage: Is surgical clipping worthwhile? Neurol India 2011;59:212-7.  Back to cited text no. 38
[PUBMED]  [Full text]  
Fuster V, Ryden LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, et al. ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: A report of the ACCF/AHA task force on practice guidelines. Circulation 2011;123:e269-367.  Back to cited text no. 39
Amar D. Perioperative atrial tachyarrhythmias. Anesthesiology 2002;97:1618-23.  Back to cited text no. 40
Thomson A, Balser JR. Perioperative cardiac arrhythmias. Br J Anaesth 2004;93:86-94.  Back to cited text no. 41
Zipes DP. Specific arrhythmias: Diagnosis and treatment. In: Braunwald E editor. Heart disease: A text book of cardiovascular medicine. 4th ed. Philadelphia: WB Saunders; 1992. p. 667-725.  Back to cited text no. 42
Dernbac PD, Little JR, Jones SC, Ebrahim ZY. Altered cerebral autoregulation and CO2 reactivity after aneurysmal subarachnoid hemorrhage. Neurosurgery 1988;23:705-9.  Back to cited text no. 43
Chang HS, Hongo K, Nakagawa H. Adverse effects of limited hypotensive anesthesia on the outcome of patients with subarachnoid hemorrhage. J Neurosurg 2000;92:971-5.  Back to cited text no. 44


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