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P Ganjoo

Publications and source records attributed to P Ganjoo.

10 recordsLinked to original sources
PubMed2000

Effects of intrathecal ketamine added to bupivacaine for spinal anaesthesia.

We prospectively studied 30 healthy female patients undergoing intracavitory brachytherapy applicator insertion for carcinoma of the cervix under spinal anaesthesia. Patients were randomly allocated to receive either intrathecal bupivacaine 10 mg alone or bupivacaine 7.5 mg combined with preservative-free ketamine 25 mg. Spinal block onset, maximum sensory level, duration of blockade, haemodynamic variables, postoperative analgesic requirements and adverse events were recorded. Onset of sensory and motor block and duration of spinal analgesia were comparable between groups. Duration of motor blockade was shorter (p = 0.0416) and requirement for intravenous fluids in the peri-operative period was less (p = 0.0159) in the ketamine group. Significantly more patients in the ketamine group had adverse events, such as sedation, dizziness, nystagmus, 'strange feelings' and postoperative nausea and vomiting. Although the addition of ketamine to spinal bupivacaine had local anaesthetic sparing effects, it did not provide extended postoperative analgesia or decrease the postoperative analgesic requirements. Moreover, the central adverse effects of ketamine limit its spinal application.

Adult↗
PubMed1999

Pretreatment with dexmedetomidine: altered indices of anesthetic depth for halothane in the neuraxis of cats.

UNLABELLED: The sedative and anesthetic-sparing ability of the alpha2-adrenergic agonist dexmedetomidine is well documented. In this study, we identified the effects of halothane, with and without dexmedetomidine, on hemodynamic and electroencephalographic (EEG) variables and quantified the concentration of halothane resulting in various anesthetic depth indices mediated through the central nervous system (CNS) in chronically instrumented cats. Halothane was given alone or after dexmedetomidine (15 microg/kg p.o.). In both groups, four indices of anesthetic depth--minimum alveolar anesthetic concentration (MAC; no movement to noxious stimuli), MAC(BAR) (no autonomic response to noxious stimuli), MAC(BS) (EEG burst suppression), and MAC(ISOELECTRIC) (EEG isoelectricity)--were determined. Halothane decreased arterial blood pressure, heart rate, and higher frequency components of the EEG before the onset of burst suppression and isoelectricity. Dexmedetomidine pretreatment augmented the actions of halothane on arterial pressure, heart rate, and the EEG. Dexmedetomidine reduced the halothane concentrations resulting in MAC (from 1.22% +/- 0.06% to 0.89% +/- 0.08%) and MAC(BAR) (from 1.81% +/- 0.05% to 1.1% +/- 0.10%), but not those resulting in MAC(BS) (3.01% +/- 0.17% vs 3.14% +/- 0.10%) or MAC(ISOELECTRIC) (4.39% +/- 0.26% vs 4.65% +/- 0.12%). These results suggest that dexmedetomidine does not alter various CNS-mediated indices of anesthetic action to equivalent degrees and that there are dissimilar degrees of an anesthetic-sparing action at different levels of the neuraxis. IMPLICATIONS: The anesthetic adjuvant dexmedetomidine seems to differentially alter central nervous system-mediated indices of anesthetic action. Lower brainstem or spinal determinants of anesthetic depth (movement and hemodynamic responses) are more attenuated than those of higher brain functions, such as the electroencephalogram.

Adrenergic alpha-Agonists↗
PubMed1998

In vivo effects of dexmedetomidine on laser-Doppler flow and pial arteriolar diameter.

BACKGROUND: The alpha2-adrenergic agonist dexmedetomidine alters global cerebral blood flow (CBF). However, few studies have investigated the action of dexmedetomidine on the cerebral microcirculation. This investigation examined the effects of dexmedetomidine on (1) regional CBF in the rat cerebral cortex using laser-Doppler flowmetry and (2) on pial arteriolar diameter. METHODS: Halothane-anesthetized rats were fitted with instruments to measure CBF as determined by laser-Doppler flow (CBFldf) or to measure pial arteriolar diameter by preparing a cranial hollow deepened until a translucent plate of skull remained, thereby maintaining the integrity of the cranial vault. In both groups, 20 microg/kg dexmedetomidine was infused intravenously. Thirty minutes later, the mean arterial pressure was restored to control values with an infusion of phenylephrine (0.5 to 5 microg/kg/min). RESULTS: Administration of dexmedetomidine was associated with decreases in end-tidal and arterial carbon dioxide. The CBFldf and pial arteriolar diameter were measured during normocapnia (controlled carbon dioxide) and during dexmedetomidine-induced hypocapnia. Intravenous administration of dexmedetomidine significantly decreased systemic arterial pressure concurrent with a decrease in CBFldf (22% in normocapnic animals, 36% in hypocapnic animals). Restoration of mean arterial pressure increased CBFldf in normocapnic but not in hypocapnic animals. Similarly, dexmedetomidine significantly reduced pial vessel diameter in both normocapnic (9%) and hypocapnic animals (17%). However, vessel diameters remained decreased in the normocapnic and hypocapnic animals after the mean arterial pressure was restored. CONCLUSIONS: These results suggest a modulation of cerebral vascular autoregulation by dexmedetomidine which may be mediated, in part, by alterations in carbon dioxide. Dexmedetomidine may have a direct action on the cerebral vessels to reduce the CBF during normo- or hypocapnia. The differences between CBFldf and pial arteriole responses to restoration of mean arterial pressure may reflect the difference in measurement techniques because laser-Doppler measurements reflect the net effect of several arterial segments on microvascular perfusion, whereas diameter measurements specifically examined individual pial arterioles, suggesting that dexmedetomidine vasoconstriction in the cerebral vasculature may be differentially and regionally mediated.

Adrenergic alpha-Agonists↗
PubMed1996

Desflurane attenuates the somatosympathetic reflex in rats.

Arterial blood pressure and heart rate changes after afferent somatic sensory nerve stimulation are termed the "somatosympathetic reflex" (SSR). Inhibition of the SSR may partially represent an antinociceptive action. This investigation examined the actions of the volatile anesthetic, desflurane, on the SSR evoked by peripheral nerve stimulation. Rats anesthetized with alpha-chloralose (50 mg/kg) and urethane (500 mg/kg) were mechanically ventilated and cannulated with arterial and venous catheters for monitoring arterial pressure and for fluid administration, respectively. The sciatic (n = 7) or tibial (n = 6) nerves were isolated and stimulated at one, two, and four times the voltage threshold required to elicit a change in systemic hemodynamics. These cardiovascular responses were recorded before, during, and after varying concentrations of desflurane, 1.8% (0.25 minimum alveolar anesthetic concentration [MAC]), 3.6% (0.5 MAC), 7.2% (1.0 MAC), and 10.8% (1.5 MAC). Desflurane decreased arterial pressure at 1.0 and 1.5 MAC and heart rate (at more than 0.5 MAC) compared to baseline levels. Tibial nerve stimulation decreased mean arterial pressure (MAP) with no consistent changes in heart rate. Desflurane significantly attenuated this depressor response to tibial nerve stimulation (MAP decrease: control; -20 +/- 2 mm Hg versus 1.0 MAC desflurane; -6 +/- 4 mm Hg). The increases in MAP after sciatic nerve stimulation were also significantly inhibited by increasing concentrations of desflurane. At more than 0.5 MAC desflurane, the pressor response to sciatic nerve stimulation was significantly converted to a depressor response in four of seven rats (MAP: control; increase 24 +/- 2 mm Hg versus 1.0 MAC desflurane; decrease -2 +/- 4 mm Hg). Sciatic nerve stimulation also elicited increases in heart rate which were significantly attenuated by desflurane (control; 37 +/- 6 bpm versus 1.5 MAC desflurane; 0 +/- 2 bpm). These findings demonstrate that desflurane produces dose-dependent cardiovascular depression in rats and, despite previous reports of sympathoexcitation, desflurane significantly attenuated both excitatory and inhibitory types of SSR. The results of this study also support a potential antinociceptive action for this anesthetic.

Anesthetics, Inhalation↗
PubMed1994

Posterior fossa surgery in postshunt endocarditis patients: some anesthetic issues.

A patient with an intracranial fourth ventricular cyst developed right heart endocarditis from an infected ventriculoatrial shunt inserted previously. Investigation revealed pneumonic involvement of the right lung, moderate tricuspid regurgitation, mild pulmonary artery hypertension, and a large right atrial vegetation. The shunt was removed and treatment of endocarditis started, before undertaking excision of the cyst under general anesthesia. During the operation there was a sudden deterioration in the patient's condition rapidly leading to death. Clinical features suggested intraoperative pulmonary embolism; both venous air embolism and a dislodged atrial vegetation were considered. However, in the absence of specific monitoring equipment and autopsy, the actual cause could not be ascertained. This clinical report highlights the anesthetic problems related to posterior fossa surgery in patients with right-sided endocarditis and suggests some possible management strategies.

Adult↗
PubMedDate not supplied

Postblock epidural hematoma causing paraplegia. Case report.

BACKGROUND AND OBJECTIVES: An elderly man with no obvious preexisting coagulation disorder had paraplegia following epidural block for transurethral prostatectomy that was later found to be due to a large epidural hematoma requiring surgical decompression of the spinal cord. METHODS: There was a delay in starting treatment since the cause was not initially suspected. RESULTS: The patient did not improve much after the operation. CONCLUSIONS: The anesthesiologist should be alert to the possibility of epidural hematoma forming in otherwise normal patients to avoid such unfavorable outcomes.

Aged↗