Succinylcholine and Intracranial Pressure

2018 ◽  
Vol 129 (6) ◽  
pp. 1159-1162 ◽  
Author(s):  
James E. Cottrell
Keyword(s):  
Mean Arterial Pressure ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Increased Intracranial Pressure ◽  
Hemodynamic Changes ◽  
Neurosurgical Patients ◽  
Pulmonary Arterial ◽  
Increased Icp

Abstract Intracranial and Hemodynamic Changes after Succinylcholine Administration in Cats. By Cottrell JE, Hartung J, Giffin JP, and Shwiry B. Anesthesia & Analgesia 1983; 62:1006–9. Reprinted with permission. Bolus injections of succinylcholine (1.5 mg/kg) significantly increased intracranial pressure (ICP) in cats under normal conditions from control levels of 8 +/- 1 mmHg to 16 +/- 3 mmHg (+/- SEM, P less than 0.01), and in the presence of artificially increased ICP from control levels of 27 +/- 1 mmHg to 47 +/- 4 mmHg (P less than 0.01). These approximately 100% increases in ICP were accompanied by a transitory decrease in mean arterial pressure (approximately 10 s), followed by a 15 to 20% increase (P less than 0.05). Pulmonary arterial pressure increased 20 to 30% (P less than 0.05). These results, when considered in conjunction with results previously obtained in humans, suggest that succinylcholine may be contraindicated in neurosurgical patients.

A STUDY ON HAEMODYNAMIC RESPONSE ATTENUATION DURING HEAD HOLDER APPLICATION FOR CRANIOTOMY COMPARING IV DEXMEDITOMIDINE AND LOCAL LIGNOCAINE

2021 ◽  
pp. 28-30
Author(s):  
Jayadheer. D
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Demographic Data ◽  
Hemodynamic Response ◽  
P Value ◽  
Hemodynamic Parameters ◽  
Neurosurgical Patients ◽  
Head Holder

Background; One of the goals of neuro anesthesia is to ensure stable perioperative cerebral hemodynamics, thus avoiding a sudden rise in intracranial pressure and prevent acute brain swelling.1 The intense surgical stimuli associated with craniotomy frequently causes sympathetic activation, which results in changes in heart rate (HR), blood pressure (BP), and cerebral blood ow (CBF). These changes may increase intracranial pressure (ICP) and a reduction in cerebral perfusion pressure (CPP). Finally, it leads to cerebral ischemia, especially in patients with impaired autoregulation and compromised cerebral compliance2,3. Thus, it is essential to preserve cerebral homeostasis and to prevent abrupt changes in hemodynamics. Smooth and rapid recovery from anesthesia allows immediate neurological assessment. Application of skull pin head holder is a necessity for stabilizing the head during craniotomy. Mayeld device or head holder is a clamp thatconsists of a C-shaped metal piece with three sharp interchangeable metal pins arranged triangularly to one another.4 These pins forced through the layers of scalp and periosteuminto the external lamina of the skull. Skull pins support the head without allowing any direct pressure on the face, allow access to the airway, and hold head rmly in one position that can nely be adjusted for optimal neurosurgical exposure. This study was conducted in fty ASA grade 1 or 2 patients who were adm Methods: itted at Government General Hospital, Guntur afliated to Guntur Medical College, Guntur, to undergo elective craniotomies under general anesthesia. After getting Ethical committee approval, a total of fty patients were allocated into two groups of 25 each. They were connected to the non-invasive monitors, and the basal heart rate and mean arterial pressure were recorded.Patients randomized to group dexmedetomidine received 1mcg/kg of dexmedetomidine diluted to 10ml with 0.9% saline over 10 min through a syringe pump, after recording pre-induction baseline hemodynamic parameters. Before the pin application, these patients received inltration of the pin sites with 0.9% saline (3ml for each site). Patients randomized to group lidocaine received infusion of 10ml of 0.9% saline over 10min, after recording baseline hemodynamic parameters. They then received inltration of the pre-marked pin sites with 2% lidocaine (without adrenaline), 3ml for each site. Heart rate and mean arterial pressure were recorded at various time intervals.Baseline, preinltration, post inltration, pre pin, 1 minute after post pin, 2minutes after post pin, 3 minutes, 5 miutes, 10 minutes and 15 minutes after post pin application. The result was analyzed using student t-test, and a P value of less than 0.05 was taken as signicant. ResultsWith patients matched for demographic data, the results showed there was no signicant difference in baseline values between the two groups. Heart rate and mean arterial pressure were comparable between the groups at various time intervals in the study. Thus both dexmedetomidine and lidocaine are equally effective in controlling the hemodynamic response to skull pin application. Despite being comparable to lidocaine inltration, dexmedetomidine causes signicantlymore episodes of hypotension and bradycardia, which could be detrimental in neurosurgical patients. Dexmedetomidine 1mcg/kg infusion and 2% li Conclusion gnocaine inltration both are equally effective in controlling the hemodynamic response to skull pin placement. Despite being comparable to lignocaine inltration, dexmedetomidine causes signicantly more episodes of bradycardia and hypotension, so they need rescue medication, which could be detrimental in a neurosurgical patient. We conclude that 2% of local lignocaine inltration is better in controlling hemodynamic responses to skull pin head holder application and does not cause any adverse effects in any of the patients.

Hemodynamic changes after pneumonectomy in the exercising foxhound

1990 ◽  
Vol 69 (1) ◽  
pp. 51-57 ◽  
Author(s):  
C. C. Hsia ◽  
J. I. Carlin ◽  
S. S. Cassidy ◽  
M. Ramanathan ◽  
R. L. Johnson
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Work Load ◽  
Systemic Blood Pressure ◽  
Elastic Recoil ◽  
Hemodynamic Changes ◽  
Pressure Flow ◽  
Ventricular Afterload ◽  
Pulmonary Arterial

Pulmonary arterial pressure is higher during exercise after pneumonectomy than before. Several factors may contribute to the elevation, e.g., loss of vascular bed, overinflation of the remaining lung, and active pulmonary vasoconstriction. We measured hemodynamic changes during graded exercise in conditioned foxhounds and compared pulmonary pressure-flow relationships before and after left pneumonectomy. Pulmonary arterial pressure-flow relationship in the remaining lung is not altered by pneumonectomy, suggesting that the increase in pulmonary vascular resistance post-pneumonectomy is largely the passive consequence of increased pulmonary blood flow to the remaining lung. The potential for chronic hyperinflation of the remaining lung to increase pulmonary resistance after pneumonectomy may have been counterbalanced by a concomitant reduction in lung elastic recoil. Unexpectedly, both mean systemic blood pressure and hematocrit were higher with respect to cardiac output after pneumonectomy. Cardiac output and stroke volume at any given work load were lower after pneumonectomy than before, and heart rate response was unaltered. This pattern of responses suggests that increases in left and right ventricular afterload may have contributed to the reduction in cardiac output.

STUDIES ON THE ROLE OF THROMBOXANE IN THROMBIN-INDUCED PULMONARY INSUFFICIENCY IN THE RAT

1987 ◽  
Author(s):  
H Sandler ◽  
B Gerdin ◽  
T Saldeen
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Permeability ◽  
Lung Tissue ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Insufficiency ◽  
Albumin Concentration ◽  
Lung Weight ◽  
Pulmonary Arterial

The pathophysiology of the acute pulmonary damage that may occur in association with sepsis, hemorrhagic shock and microembolism seems to involve the activity of cyclooxygenase derived arachidonate metabolites. In the rat, pulmonary microembolism due to infusion of thrombin together with inhibition of fibrinolysis has been found to induce pulmonary insufficiency with similarities to the clinical adult respiratory distress syndrome. The infusion of thrombin results in systemic hypotension, pulmonary hypertension and platelet aggregation, and subsequently, with a certain dealy in time, to increased pulmonary vascular permeability.The main purposes of this investigation were to study the release of TxA2 and PGI2 following thrcmbin-induced pulmonary microembolizaticn in the rat and to examine the effects of a thromboxane synthetase inhibitor (DazoxibenR) on pulmonary arterial and systemic mean arterial pressure and vascular permeability.During infusion of thrcmbin in rats pulmonary arterial pressure rose from 15 ± 2 to 35 ± 3 rmHg and mean arterial pressure fell from 120 ± 6 to 49 ± 27 mmHg. Plasma thromboxane B2 (TxB2) increased from 0.3 ± 0.004 to 3.6 ± 0.5 ng/ml. Ninety minutes later the lung weight and albunin concentration in the lung were increased (2.21 ± 0.13 g and 22.7 ± 4.7 mg/g) compared with controls (1.12 ± 0.14 g and 8.5 ± 0.9 mg/g). Dazoxiben reduced the elevated pulmonary arterial pressure and the elevated plasma TxB2 concentration following infusion of thrombin. Ninety minutes after infusion of thrcmbin, the in vitro synthesis of TxB2 in lung tissue was increased. Dazoxiben and a specific rabbit anti-rat neutrophil serun reduced this synthesis of TxB in vitro. The lung weight (2.18 ± 0.20 g) and lung albumin concentration (21.4 ± 3.4 mg/g) was not affected by Dazoxiben. The results indicate that TxA2 in an important mediator of the pressure changes in the early phase after infusion of thrombin and that neutrophils are associated with thromboxane formation in the lung tissue. Rats pretreated with the antineutrophil serum had less pulmonary weight (1.69 ± 0.28 g) and the albumin concentration in the edema fluid was decreased (17.3 ± 3.6 mg/g), suggesting that polymorphonuclear leukocytes contributed to the pulmonary dysfunction. Dazoxiben when incubated with thrcmbin in a chromogenic substrate system had a linear, dose-related anti-thrombin effect. At a Dazoxiben concentration of 2.4 mM only a few percent of the thrombin activity remained.

scholarly journals EFFECT OF 30° HEAD-UP POSITION ON INTRACRANIAL PRESSURE CHANGE IN PATIENTS WITH HEAD INJURY IN SURGICAL WARD OF GENERAL HOSPITAL OF Dr. R. SOEDARSONO PASURUAN

2017 ◽  
Vol 3 (3) ◽  
pp. 89-95 ◽  
Author(s):  
Sumirah Budi Pertami ◽  
Sulastyawati Sulastyawati ◽  
Puthut Anami
Keyword(s):  
Mean Arterial Pressure ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Control Group ◽  
P Value ◽  
Increased Intracranial Pressure ◽  
Head Injured ◽  
Injured Patients ◽  
The Impact

Background: Head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the 15 degrees head-up position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of 30 and 15 degrees on intracranial pressure change.Methods: This was a quasi-experimental study with posttest only control time series time design.  There were 30 head-injured patients was selected using consecutive sampling, with 15 assigned in the treatment (30° head-up position) and control group (15° head-up position). Intracranial pressure variable was identified using the level of consciousness and mean arterial pressure parameters. Wilcoxon signed rank test was used for data analysisResults: Findings showed p-value 0.010 (0.05) on awareness level and p-value 0.031 (0.05) on mean arterial pressure, which indicated that there was a statistically significant effect of the 30° head-up position on level of awareness and mean arterial pressure.Conclusion: There was a significant effect of the 30° head-up position on intracranial pressure changes, particularly in the level of awareness and mean arterial pressure in patients with head injury. It is recommended that for health workers to provide knowledge regarding this intervention to prevent increased intracranial pressure.

scholarly journals Hemodynamic trajectories and outcomes in patients with pulmonary arterial hypertension

2020 ◽  
Vol 10 (4) ◽  
pp. 204589402094134
Author(s):  
Myriam Amsallem ◽  
Shadi P. Bagherzadeh ◽  
David Boulate ◽  
Andrew J. Sweatt ◽  
Kristina T. Kudelko ◽  
...  
Keyword(s):  
New York ◽  
Mean Arterial Pressure ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Pressure ◽  
Arterial Hypertension ◽  
Pulmonary Arterial Pressure ◽  
Heart Association ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

The relative pulmonary to systemic pressure ratio (mean pulmonary arterial pressure/mean arterial pressure) has been proven to be valuable in cardiac surgery. Little is known on the prognostic value of baseline and trajectory of mean pulmonary arterial pressure/mean arterial pressure in pulmonary arterial hypertension. Patients with confirmed idiopathic, familial, drug and toxins, or connective tissue disease-related pulmonary arterial hypertension and at least one complete right heart catheterization were included and prospectively followed-up for 5.9 ± 4.03 years. Correlates of the primary end point (i.e. death or lung transplant need) during follow-up were determined using Cox regression modeling. Results showed that among the 308 patients included, 187 had at least one follow-up catheterization (median time between catheterizations: 2.16 (1.16–3.19) years). In the total cohort (mean age 47.3 ± 14.9 years, 82.8% of female and 58.1% in New York Heart Association class 3 or 4), mean pulmonary arterial pressure/mean arterial pressure (1.38 (1.07–1.77)) was associated with outcome ( p = 0.01). Mean pulmonary arterial pressure/mean arterial pressure was incremental to a basic model (including right atrial pressure, systolic blood pressure, New York Heart Association class 3 or 4, and connective tissue disease) for outcome prediction, while mean pulmonary arterial pressure was not. In the 187 patients with a follow-up catheterization, both delta mean pulmonary arterial pressure and delta mean pulmonary arterial pressure/mean arterial pressure were associated with outcome (1.32 (1.11–1.58) and 1.31 (1.1–1.57) respectively, p < 0.01). Mean pulmonary arterial pressure and mean pulmonary arterial pressure/mean arterial pressure were both incremental to the basic model, while worsening in mean pulmonary arterial pressure or mean pulmonary arterial pressure/mean arterial pressure did not reach significance. In conclusion, mean pulmonary arterial pressure/mean arterial pressure at baseline prognosticates long-term outcome with a significant, albeit modest, incremental value to basic variables.

Effects of ANP-(95-126) in dogs before and after induction of heart failure

1990 ◽  
Vol 259 (6) ◽  
pp. H1643-H1648
Author(s):  
G. A. Riegger ◽  
D. Elsner ◽  
W. G. Forssmann ◽  
E. P. Kromer
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Right Atrial ◽  
Peripheral Vascular ◽  
Before And After ◽  
Pulmonary Arterial

In conscious dogs with and without congestive heart failure, we investigated hemodynamic, hormonal, and renal effects of a new natriuretic peptide [ANP-(95-126)]. Unlike ANP-(99-126), which is secreted in the heart and rapidly inactivated in the kidney, ANP-(95-126) most likely originates from the kidney and is not destroyed by proteolysis in membrane preparations of kidney cortex. In healthy animals intravenous ANP-(95-126) significantly decreased mean arterial pressure, cardiac output, stroke volume, and right atrial pressure and increased heart rate without changing mean pulmonary arterial pressure and total peripheral vascular resistance. In dogs with congestive heart failure, ANP-(95-126) showed no effects on mean arterial pressure, cardiac output, stroke volume, and peripheral vascular resistance but reduced right atrial pressure and pulmonary arterial pressure. Both, in dogs before and after the induction of heart failure, the new peptide led to a significant increase of urine flow and sodium and chloride excretion. In healthy dogs there were indirect indications for a small inhibitory effect on renin and aldosterone secretion. Thus, in contrast to the considerable attenuation of renal effects of ANP-(99-126) in heart failure, the efficacy of ANP-(95-126) on renal excretory function is well preserved, which may be because of the lack of proteolytic degradation in the kidney. These results suggest that ANP-(95-126) may have clinical implications for the treatment of patients with congestive heart failure.

PAF increases vascular permeability without increasing pulmonary arterial pressure in the rat

2001 ◽  
Vol 90 (1) ◽  
pp. 261-268 ◽  
Author(s):  
Leonardo C. Clavijo ◽  
Mary B. Carter ◽  
Paul J. Matheson ◽  
Mark A. Wilson ◽  
William B. Wead ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Ex Vivo ◽  
Platelet Activating Factor ◽  
Microvascular Permeability ◽  
Blue Dye ◽  
E Coli ◽  
Pulmonary Arterial

In vivo pulmonary arterial catheterization was used to determine the mechanism by which platelet-activating factor (PAF) produces pulmonary edema in rats. PAF induces pulmonary edema by increasing pulmonary microvascular permeability (PMP) without changing the pulmonary pressure gradient. Rats were cannulated for measurement of pulmonary arterial pressure (Ppa) and mean arterial pressure. PMP was determined by using either in vivo fluorescent videomicroscopy or the ex vivo Evans blue dye technique. WEB 2086 was administered intravenously (IV) to antagonize specific PAF effects. Three experiments were performed: 1) IV PAF, 2) topical PAF, and 3) Escherichia coli bacteremia. IV PAF induced systemic hypotension with a decrease in Ppa. PMP increased after IV PAF in a dose-related manner. Topical PAF increased PMP but decreased Ppa only at high doses. Both PMP (88 ± 5%) and Ppa (50 ± 3%) increased during E. coli bacteremia. PAF-receptor blockade prevents changes in Ppa and PMP after both topical PAF and E. coli bacteremia. PAF, which has been shown to mediate pulmonary edema in prior studies, appears to act in the lung by primarily increasing microvascular permeability. The presence of PAF might be prerequisite for pulmonary vascular constriction during gram-negative bacteremia.

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