Browsing by Author "Misra, Satyajeet"
Now showing 1 - 20 of 22
Results Per Page
Sort Options
Item A Novel Technique To Assess Aortic Valve Repair Before Releasing the Aortic Cross-Clamp(JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA, 2009)Item A Phantom in the Aortic Valve: Tumor, Thrombus, or Artifact?(JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA, 2011)Item A Ring Artifact in the Left Ventricle on Transesophageal Echocardiography After Mitral Valve Replacement(ANESTHESIA AND ANALGESIA, 2010)Item Accurate Localization and Echocardiographic-Pathologic Correlation of Tricuspid Valve Angiolipoma by Intraoperative Transesophageal Echocardiography(ECHOCARDIOGRAPHY-A JOURNAL OF CARDIOVASCULAR ULTRASOUND AND ALLIED TECHNIQUES, 2009)Angiolipoma (angiolipohamartoma) of the tricuspid valve (TV) is a rare tumor which may be occasionally misdiagnosed as right atrial (RA) myxoma. Transesophageal echocardiography (TEE) provides accurate information regarding the size, shape, mobility as well as site of attachment of RA tumors and is a superior modality as compared to transthoracic echocardiography (TTE). Correct diagnosis of RA tumors has therapeutic significance and guides management of patients, as myxomas are generally more aggressively managed than lipomas. We describe a rare case of a pedunculated angiolipoma of the TV which was misdiagnosed as RA myxoma on TTE and discuss the echocardiographic-pathologic correlates of the tumor as well as its accurate localization by TEE. (ECHOCARDIOGRAPHY, Volume 26, November 2009).Item Airway implications of post-ductal coarctation of the aorta and an aberrant right subclavian artery(CANADIAN JOURNAL OF ANAESTHESIA-JOURNAL CANADIEN D ANESTHESIE, 2008)Item An additional mass in the aortic root in a patient with infective endocarditis scheduled for excision of a tricuspid valve mass?(JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA, 2008)Item An Intimal Flap-like Projection in the Aortic Root(JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA, 2009)Item CASE 5-2012 Incidentally Detected Patent Foramen Ovale in A Patient Undergoing Aortic Valve Replacement: To Close or Not to Close?(JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA, 2012)Item Changes in Left Ventricular Preload, Afterload, and Cardiac Output in Response to a Single Dose of Mannitol in Neurosurgical Patients Undergoing Craniotomy: A Transesophageal Echocardiographic Study(JOURNAL OF NEUROSURGICAL ANESTHESIOLOGY, 2012)Background: Mannitol increases intravascular volume by withdrawing water from the brain and causes significant changes in stroke volume, cardiac output (CO), systemic vascular resistance, central venous pressure (CVP), and blood pressure. No previous studies have demonstrated changes in left ventricular (LV) preload, afterload, and CO using transesophageal echocardiography (TEE).Methods: Fifteen adult patients undergoing elective supratentorial craniotomy received 20% mannitol 1.0 gm/kg over 15 minutes before dural opening. The following hemodynamic and TEE-derived parameters were recorded before and after the administration of mannitol: heart rate (HR), mean arterial pressure (MAP), CVP, LV end diastolic area (EDA), end systolic area, fractional area change, stroke volume, and CO.Results: EDA and CVP significantly increased at 5 minutes (P=0.002 and < 0.001) after mannitol infusion and remained insignificantly elevated till 15 minutes, thereafter returning to baseline values. CO also increased significantly at 5 and 15 minutes (P=0.001 and 0.013) and remained insignificantly elevated till 25 minutes, and thereafter returned to baseline values. A concomitant significant decline in systemic vascular resistance was observed at 5 and 15 minutes (P=0.002 and 0.008 at 5 and 15 min, respectively). Although EDA increased significantly at 5 minutes, there were no appreciable changes in MAP and HR throughout the study period.Conclusions: In conclusion, in patients undergoing craniotomy, TEE demonstrated that a single bolus dose of 20% mannitol (1.0 gm/kg) caused significant but short-duration alterations in LV preload, afterload, and CO without concomitant changes in hemodynamic variables (MAP/HR).Item Diagnosis of Shone's Anomaly by Intraoperative Transesophageal Echocardiography in an Adult Patient Undergoing Repair of Coarctation of the Aorta(JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA, 2011)Item Embolization of Atrial Septal Occluder Device into the Pulmonary Circulation: Role of Transesophageal Echocardiography(ECHOCARDIOGRAPHY-A JOURNAL OF CARDIOVASCULAR ULTRASOUND AND ALLIED TECHNIQUES, 2009)(ECHOCARDIOGRAPHY, Volume 26, July 2009).Item False Tendons and Accessory Papillary Muscle in the Left Ventricle(ANESTHESIA AND ANALGESIA, 2011)Item Gabapentin Premedication Decreases the Hemodynamic Response to Skull Pin Insertion in Patients Undergoing Craniotomy(JOURNAL OF NEUROSURGICAL ANESTHESIOLOGY, 2011)Background: In patients undergoing craniotomy, skull pin insertion produces significant increases in heart rate (HR) and blood pressure. We investigated whether premedication with gabapentin would prevent or attenuate this increase.Methods: Forty-seven ASA I and II patients, 18 to 60 years, undergoing elective craniotomy for intracranial tumor surgery were recruited prospectively and randomly divided into 3 groups; L (oral placebo plus 2% lidocaine infiltration at pin sites; n = 12), G (oral gabapentin 900 mg plus normal saline infiltration; n = 21) and GL (oral gabapentin 900mg plus 2% lidocaine infiltration; n = 14). The oral medications were administered 2 hours before induction of anesthesia. Measurements were made at preinduction baseline, before skull pin insertion and at every 1 minute from pin insertion till end of 10 minutes.Results: Forty-three patients completed the study (L, n = 11; G, n = 20; GL, n = 12). Premedication with gabapentin significantly attenuated the rise in systolic (SBP) and mean arterial pressure (MAP) after pin insertion when compared with placebo (for SBP, P < 0.001 at 1 and 2 min and < 0.05 at 3 to 5 min between L and G; P < 0.001 at 1 to 4 min and < 0.05 at 5 min between L and GL; for MAP, P < 0.05 at 1 min, < 0.001 at 2 min and < 0.05 at 3 to 4 min between L and G; P < 0.001 at 1 to 2 min and < 0.05 at 3 to 5 min between L and GL). HR responses were also attenuated in patients premedicated with gabapentin; however, the responses were more variable in group G (P = 0.03 between L and G at 4 min after pin insertion) as compared with group GL (P < 0.05 at 1 min, < 0.001 at 2 min and < 0.05 at 3 to 10 min between L and GL).Conclusion: In conclusion, 900mg of gabapentin, administered orally 2 hours before induction of anesthesia along with lidocaine scalp infiltration abolished the hemodynamic response after skull pin insertion. Premedication with gabapentin alone significantly attenuated the SBP and MAP; however, HR responses were more variable. A larger trial is required to corroborate the findings of the study before clinical recommendations would be warranted.Item Horseshoe lung secondary to hypoplastic left lung for pneumonectomy(JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA, 2007)Item Is Collapse of the Lung With Increased Lucency on a Chest X-Ray Always a Pneumothorax?(JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA, 2009)Item Large pseudoaneurysm of aortic root after aortic valve replacement for rheumatic heart disease: a rare complication.(Annals of cardiac anaesthesia, 2009)Item Oral Clonidine Attenuates the Fall in Mean Arterial Pressure Due to Scalp Infiltration With Epinephrine-lidocaine Solution in Patients Undergoing Craniotomy A Prospective, Randomized, Double-blind, and Placebo Controlled Trial(JOURNAL OF NEUROSURGICAL ANESTHESIOLOGY, 2009)Background: Scalp infiltration with epinephrine-lidocaine solution in patients undergoing neurosurgery may result in transient but significant hypotension. We investigated whether premedication with alpha(2)-adrenoreceptor agonist clonidine, which also exhibits alpha(1)-adrenoreceptor mediated vasoconstriction, would prevent or attenuate this fall in mean arterial pressure (M A P).Methods: Sixty-six American Society of Anesthesiologists 1 and 11 adult patients, 18 to 50 years, undergoing elective tumor decompression were recruited into this prospective, randomized, double-blind, placebo controlled study, and scheduled to receive either oral pantoprazole 40 mg (placebo group) or oral clonidine 3 mu g/kg (clonidine group), 90 minutes before induction of anesthesia. Primary end points studied were heart rate (HR) and MAP in both groups measured just before scalp infiltration (preinfiltration baseline) and then every 30 seconds for 5 minutes after initiation of scalp infiltration with 2.5 mu g/mL epinephrine contained in 15 in L of 1%, lidocaine solution.Results: There was no significant change in HR in the 2 groups during the study period compared with baseline values; however, patients in clonidine group had significantly lower HR compared with placebo (*P < 0.05). In both groups, MAP fell significantly below baseline I minute after start of infiltration. It recovered in the clonidine group after 2.5 minutes but not in the placebo group where it continued to remain low even at 5 minutes. MAP in the placebo group was also significantly lower compared with the clonidine group from 2.5 minutes to 5 minutes.Conclusion: In conclusion, oral clonidine 3 mu g/kg administered 90 minutes before induction of anesthesia attenuates the fall in MAP due to scalp infiltration with a dilute concentration of epinephrine-lidocaine solution in patients undergoing craniotomy under isoflurane anesthesia.Item Pericardial cyst.(Annals of cardiac anaesthesia, 2008)Item Resolution of Airway Compression Induced by Transesophageal Echocardiography Probe Insertion in a Pediatric Patient After Repair of an Atrial Septal Defect and Partial Anomalous Pulmonary Venous Connection(JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA, 2008)Item Sudden decrease in end-tidal carbon-dioxide in a neonate undergoing surgery for type B interrupted aortic arch.(Annals of cardiac anaesthesia, 2011)Interruption of the aortic arch is a rare anomaly affecting 1% of children with congenital heart disease. The systemic circulation is ductal dependent and is determined principally by the ratio of the resistances in the systemic and the pulmonary vascular bed. Any increase in the pulmonary vascular resistance may increase the dead space ventilation due to acute pulmonary hypoperfusion. We report a case where sudden decreases in the end-tidal carbon-dioxide due to pulmonary hypoperfusion mimicked accidental endotracheal tube extubation in an infant undergoing repair of interrupted aortic arch.