Clinical evaluation of intravenous nitroglycerin for neurosurgery

1978 ◽  
Vol 48 (5) ◽  
pp. 704-711 ◽  
Author(s):  
Julian S. Chestnut ◽  
Maurice S. Albin ◽  
Evelyn Gonzalez-Abola ◽  
Philippa Newfield ◽  
Joseph C. Maroon
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Intravenous Nitroglycerin ◽  
Control Blood Pressure ◽  
Content Type ◽  
Cerebrovascular Autoregulation ◽  
Ideal Agent ◽  
Neurosurgical Patient ◽  
Moment Control ◽  
The Ideal

✓ Moment-to-moment control of blood pressure is important in the management of the neurosurgical patient. The ideal agent to control blood pressure or induce hypotension should be non-toxic, maintain cerebrovascular autoregulation, and not alter cardiac output or change intracranial pressure. Intravenous nitroglycerin has been used to control blood pressure in 54 neurosurgical cases. This agent produces a rapid, controllable, but not precipitous fall in blood pressure without rebound, is non-toxic, may not alter cerebrovascular autoregulation, and does not raise intracranial pressure. Our clinical experience with intravenous nitroglycerin indicates that it has an important role as a hypotensive agent for the neurosurgical patient.

Effects of intravenous nitroglycerin on the intracranial pressure and volume pressure response

1983 ◽  
Vol 58 (4) ◽  
pp. 562-565 ◽  
Author(s):  
Ghaleb A. Ghani ◽  
Yung Fong Sung ◽  
Michael S. Weinstein ◽  
George T. Tindall ◽  
Alan S. Fleischer
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Fluid Pressure ◽  
Pressure Response ◽  
Mean Blood Pressure ◽  
Intravenous Nitroglycerin ◽  
Content Type ◽  
Ventricular Fluid Pressure ◽  
The Mean ◽  
Fine Print

✓ Ventricular fluid pressure (VFP) and volume-pressure response were measured during nitroglycerin (NTG) infusion in nine patients anesthetized with N2O and fentanyl. The patients' ventilation was controlled, and PaCO2 was kept at 32 ± 4 mm Hg. When an infusion of 0.01% NTG was given intravenously to decrease the mean blood pressure to 95.1%, 84.7%, and 78.2% of control, the VFP increased from control levels of 9.94 ± 2.14 mm Hg to 12.89 ± 2.25, 15.6 ± 2.85, and 14.43 ± 3.45 mm Hg, respectively. The volume-pressure response showed a significant increase when blood pressure decreased to 84.7% and 78.2% of control. These results suggest that intravenous NTG caused an increase in the intracranial pressure and a decrease in the intracranial compliance.

The relationship of blood flow velocity fluctuations to intracranial pressure B waves

1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Wave Amplitude ◽  
Transcranial Doppler Ultrasound ◽  
Normal Subjects ◽  
Content Type ◽  
Arterial Blood ◽  
Flow Fluctuations

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.

Intracranial pressure in the normal monkey while awake and asleep

1979 ◽  
Vol 51 (2) ◽  
pp. 206-210 ◽  
Author(s):  
Gündüz Gücer ◽  
Lawrence J. Viernstein
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Systemic Blood Pressure ◽  
Macaque Monkey ◽  
Short Term ◽  
Content Type ◽  
Plateau Waves ◽  
Normal Monkey ◽  
The Mean ◽  
Cervical Ganglia

✓ Intracranial pressure (ICP) was recorded continuously by telemetry in seven normal monkeys trained to eat, sleep, and live in a primate chair. Electroencephalography, electromyography, and blood pressure were also measured by conventional means. During wakefulness and all stages of sleep except desynchronized sleep, the ICP record showed small short-term variations in pressure. However, during desynchronized sleep, the mean ICP rose on the average to 170 ± 6 mm H2O above the ICP levels in the other states of sleep, and the pulsation pressure variation increased by a factor of three. The episodes occurred 10 ± 2 times during the night and lasted for 6.8 ± 1.4 minutes, during which the average systemic blood pressure decreased by 19 ± 1.6 mm Hg. These ICP waves occurring during desynchronized sleep resemble the plateau waves described by Lundberg, but are of smaller magnitude and they appear to be a normal characteristic of sleep in the macaque monkey. Bilateral sympathectomy of the superior cervical ganglia in four of the monkeys did not alter significantly the duration, amplitude, or frequency of occurrence of the ICP waves during desynchronized sleep.

The effect of nimodipine on intracranial pressure

1987 ◽  
Vol 67 (3) ◽  
pp. 387-393 ◽  
Author(s):  
Mark N. Hadley ◽  
Robert F. Spetzler ◽  
Mary S. Fifield ◽  
William D. Bichard ◽  
John A. Hodak
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Systemic Blood Pressure ◽  
Artery Occlusion ◽  
Content Type ◽  
Arterial Blood ◽  
Increased Risk ◽  
Before And After ◽  
The Right ◽  
Cerebral Artery Occlusion

✓ Nimodipine was administered by intravenous infusion to six male baboons before, during, and after 6 hours of middle cerebral artery occlusion. Intracranial pressure (ICP) and systemic blood pressure were monitored continuously. An epidural balloon was inflated at regular intervals at three levels of arterial CO2 tension (25, 35, and 50 mm Hg) before and after the administration of nimodipine, and volume-pressure curves were generated. In every case, curves generated after intravenous nimodipine infusion were lower and shifted more to the right than the same set of curves generated before nimodipine administration, regardless of the baseline ICP. The reduction in ICP following nimodipine infusion was not due to a reduction in mean arterial blood pressure and was statistically significant at all three levels of pCO2 (p < 0.01). These results suggest that, in the presence of elevated ICP due to cerebral infarction, there is no increased risk of exacerbating intracranial hypertension with the addition of nimodipine.

Enflurane anesthesia and changes of intracranial pressure

1978 ◽  
Vol 48 (2) ◽  
pp. 228-231 ◽  
Author(s):  
Warren C. Boop ◽  
Richard Knight
Keyword(s):  
Intracranial Pressure ◽  
Significant Alteration ◽  
Clinical Impression ◽  
Elevated Intracranial Pressure ◽  
Content Type ◽  
Ideal Agent ◽  
Enflurane Anesthesia ◽  
Fine Print

✓ Enflurane has been recommended by some as an ideal agent for use in neuroanesthesia. There is no statistically significant alteration of normal intracranial pressure with enflurane anesthesia. However, supporting a clinical impression, this study demonstrates in dogs that enflurane will significantly increase an already elevated intracranial pressure.

Hydrostatically raised intracranial pressure

1972 ◽  
Vol 37 (6) ◽  
pp. 695-699 ◽  
Author(s):  
Timo Kuurne ◽  
Henry Troupp
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Respiratory Arrest ◽  
Carbon Dioxide Tension ◽  
Experimental Models ◽  
Raised Intracranial Pressure ◽  
Acid Base Balance ◽  
Content Type ◽  
Base Balance ◽  
The Brain

✓ Hydrostatic pressure with artificial cerebrospinal fluid (CSF) was applied through a needle inserted into the cisterna magna of rabbits breathing spontaneously. Blood pressure, confluens sinuum pressure and oxygen tension, respiratory rate and volume, and acid-base balance were recorded until respiratory arrest. Blood pressure and confluens sinuum pressure and respiratory volume rose; confluens sinuum oxygen and arterial carbon dioxide tension dropped. The significant similarities and differences in changes in the same parameters following local cold injury to the brain are discussed. Comparisons between different experimental models for raised intracranial pressure must take into consideration the differing reactions of the brain.

Efficacy of hyperventilation, blood pressure elevation, and metabolic suppression therapy in controlling intracranial pressure after head injury

2002 ◽  
Vol 97 (5) ◽  
pp. 1045-1053 ◽  
Author(s):  
Matthias Oertel ◽  
Daniel F. Kelly ◽  
Jae Hong Lee ◽  
David L. McArthur ◽  
Thomas C. Glenn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Induced Hypertension ◽  
Metabolic Suppression ◽  
Gcs Score ◽  
Injured Patients ◽  
Fine Print

Object. Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP. Methods. Thirty-three patients with a mean age of 33 ± 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 ± 5 to 27 ± 5 mm Hg and in ICP from 20 ± 11 to 13 ± 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 ± 5 mm Hg and ICP increased from 16 ± 9 to 19 ± 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 ± 10 to 16 ± 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression. Conclusions Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.

Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury

1978 ◽  
Vol 48 (5) ◽  
pp. 689-703 ◽  
Author(s):  
Erna M. Enevoldsen ◽  
Finn T. Jensen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Damage ◽  
Severely Injured ◽  
Content Type ◽  
Cerebrovascular Autoregulation ◽  
Decerebrate Rigidity ◽  
Arterial Blood ◽  
Fine Print

✓ Regional cerebral blood flow (rCBF), cerebral intraventricular pressure (IVP), systemic arterial blood pressure, and cerebral ventricular fluid (CSF) lactate and pH were studied repeatedly in 23 patients during the acute phase of severe brain injury lasting from 3 to 21 days after the trauma. Cerebrovascular autoregulation was tested repeatedly by means of angiotensin infusion in 21 of the patients, and CO2 response in 14 by means of passive hyperventilation. The pressure in the brain ventricles was measured continuously in all patients and kept below 45 mm Hg during the study. If the IVP increased more than 10 mm Hg during the angiotensin infusion (as in one case), the autoregulation test was considered contraindicated and the angiotensin infusion was discontinued. Dissociation between cerebrovascular autoregulation and CO2 response was a common phenomenon. Typically, autoregulation appeared preserved in the most severely injured areas of the cerebral cortex when the patient was deeply comatose, but deteriorated concomitantly with recovery; by the time the patient became alert, the autoregulation was always impaired. The CO2 response was impaired only in patients who were deeply comatose and had attacks of decerebrate rigidity; during recovery the CO2 response became normal. Thus, preserved autoregulation associated with impaired CO2 response indicated very severe brain damage, whereas impaired autoregulation associated with preserved CO2 response suggested moderate or severe brain damage in recovery. These paradoxical observations raise the question whether the preserved autoregulation seen in severely injured brain tissue is a true autoregulation caused by an active vasoconstrictor response to an increase in blood pressure.

Experimental intracranial hypertension due to vascular blockade

1970 ◽  
Vol 33 (2) ◽  
pp. 156-166 ◽  
Author(s):  
J. Donald McQueen ◽  
Lawrence F. Jelsma ◽  
Fernando Bacci ◽  
Isauro Pereira
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Edema ◽  
Content Type ◽  
Vascular Bed ◽  
Pressor Responses ◽  
Pressure Transmission ◽  
Fine Print

✓ High intracranial hypertension was induced in dogs by intracarotid injections of oil. Cerebrospinal fluid pressures continued to rise as Cushing pressor responses were evoked, but were not exceeded by the blood pressure. Transmission of blood pressure through a dilated vascular bed has been suggested as the mechanism. There was no correlation between levels of cerebral edema and the rise in intracranial pressure. This increase in pressure due to vascular blockade has been differentiated from that caused by subarachnoid blockade.

Intracranial pressure changes induced during papaverine infusion for treatment of vasospasm

1995 ◽  
Vol 83 (3) ◽  
pp. 430-434 ◽  
Author(s):  
William McAuliffe ◽  
Murphy Townsend ◽  
Joseph M. Eskridge ◽  
David W. Newell ◽  
M. Sean Grady ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Carotid Artery ◽  
Pulse Rate ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Clinical Signs ◽  
Average Dose ◽  
Content Type ◽  
Arterial Blood ◽  
Fine Print

✓ The authors reviewed the cases of 21 patients who received intraarterial infusions of papaverine to determine the drug's effects on intracranial pressure (ICP), mean arterial blood pressure, pulse rate, and cerebral perfusion pressure (CPP). The study focused on patients with aneurysmal subarachnoid hemorrhage who developed clinical signs and symptoms of vasospasm, which was documented by cerebral angiography. In 18 patients, an average dose of 300 mg papaverine was administered over 20 to 35 minutes using a No. 5 French catheter inserted into the high cervical internal carotid artery or vertebral artery. Two other patients received superselective infusions via a microcatheter placed in the anterior cerebral artery. Sixteen patients (76%) experienced good angiographic results, and 11 (52%) obtained objective clinical improvement within 48 hours. Significant elevations in ICP, blood pressure, and pulse rate were noted during papaverine infusion. In contrast, no statistically significant sustained change in CPP was observed, although it tended to decrease during papaverine infusion. In one elderly patient, infusion of the common carotid artery resulted in profound bradycardia and hypotension with a subsequent significant increase in ICP and a marked decrease in CPP. The increase in ICP in these patients correlates well with changes seen in animal models and is probably related to increased cerebral blood flow. A careful, titrated infusion of papaverine, with constant reference to the patient's ICP, blood pressure, and pulse rate, minimizes the transient increase in ICP while maintaining adequate blood pressure and CPP. Failure to monitor these parameters during the infusion, with appropriate modification of the rate of titration, could potentially produce an uncontrolled change in ICP or CPP.

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