Arterial blood gases during raised intracranial pressure in anesthetized cats under controlled ventilation

1978 ◽  
Vol 48 (3) ◽  
pp. 390-401 ◽  
Author(s):  
Sheila Jennett ◽  
Julian T. Hoff
Keyword(s):  
Intracranial Pressure ◽  
Respiratory Activity ◽  
Pulmonary Hemorrhage ◽  
Blood Gases ◽  
Minute Volume ◽  
Raised Intracranial Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Minor Degree ◽  
A Minor

✓ In anesthetized paralyzed cats ventilated with air, blood gases were analyzed repeatedly before and during episodes of raised intracranial pressure (ICP). The ICP was raised by infusion via the lumbar subarachnoid or intraventricular route, and increases were maintained for at least 30 minutes. A minor degree of hypoxemia commonly developed, but was always associated with hypercapnia; normoxia was restored by increasing the ventilation sufficiently to restore normocapnia. Relative under-ventilation is thus liable to develop if the minute volume is maintained constant when ICP is raised, probably because of increased metabolic rate which may be associated with a rise in temperature; there is no evidence to implicate more obscure causes of hypoxemia in this circumstance. Pulmonary hemorrhage and edema were found post mortem in nine of 20 animals, but only two of these had developed greater hypoxemia than could be accounted for by under-ventilation. Phrenic electroneurograms were recorded, and respiratory activity was shown to persist during prolonged periods of cerebral ischemia.

Effect of positive end expiratory pressure ventilation on intracranial pressure in man

1977 ◽  
Vol 46 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Michael L. J. Apuzzo ◽  
Martin H. Weiss ◽  
Viesturs Petersons ◽  
R. Baldwin Small ◽  
Theodore Kurze ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Venous Pressure ◽  
Blood Gases ◽  
Pulmonary Injury ◽  
Positive End Expiratory Pressure ◽  
Central Venous ◽  
Content Type ◽  
Arterial Blood ◽  
Peep Ventilation

✓ This study was designed to define the effect of positive end expiratory pressure (PEEP) ventilation on intracranial pressure (ICP). In 25 patients with severe head trauma with and without associated pulmonary injury the following parameters were simultaneously monitored under mechanical ventilation with and without PEEP: ICP, arterial blood pressure, central venous pressure, arterial blood gases, and cardiac rate. In addition, the volume-pressure response (VPR) was evaluated in each patient to assess cerebral elastance. The results indicate a significant increase in ICP with the application of PEEP only in the 12 patients who manifested increased cerebral elastance by VPR. Half of this latter group manifested impairment of cerebral perfusion pressure to levels less than 60 mm Hg. Return to baseline ICP levels was observed with termination of PEEP. No significantly consistent changes in other parameters were noted.

Release of antidiuretic hormone during mass-induced elevation of intracranial pressure

1977 ◽  
Vol 46 (5) ◽  
pp. 627-637 ◽  
Author(s):  
Lynn Gaufin ◽  
W. Ronald Skowsky ◽  
Stanley J. Goodman
Keyword(s):  
Intracranial Pressure ◽  
Antidiuretic Hormone ◽  
Rhesus Monkeys ◽  
Infusion Pump ◽  
Blood Gases ◽  
Content Type ◽  
Temporal Lobes ◽  
Balloon Catheters ◽  
Arterial Blood ◽  
Mass Expansion

✓ There are complex osmotic and non-osmotic factors regulating release of antidiuretic hormone (ADH). A wide variety of intracranial pathological processes may trigger ADH release sufficient to produce clinically recognizable hyponatremia, or the “inappropriate ADH syndrome.” We systematically studied one non-osmotic trigger, namely mass-induced elevated intracranial pressure (ICP). Initial experiments established baseline data in normal rhesus monkeys: anesthetized animals displayed appropriate rises and falls in immunoreactive urinary ADH in response to intravenously administered hypertonic and hypotonic infusions. Next, balloon catheters were implanted subdurally over temporal lobes and the animals were allowed to recover. The final experiment consisted of anesthetizing the animals, monitoring arterial blood pressure and blood gases, and retrieving timed urinary specimens while continuously recording ICP during infusion-pump expansion of the subdural balloon. A nonlethal and a lethal series of balloon-expansion experiments were done. Control values of urinary ADH were 783 ± 125 µU/15 min, and ICP was less than 10 mm Hg. During nonlethal mass expansion ADH output rose to 3433 ± 269 µU/15 min while ICP averaged 65 mm Hg (measured at completion of mass expansion). While the mass was maintained, hypotonic infusion produced unchanged urinary ADH output of 3452 ± 277 µU/15 min. During lethal experiments, urinary ADH rose still higher to 4339 ± 1887 µU/15 min associated with ICP averaging 100 mm Hg. We concluded that there is a direct relationship between the magnitude of ICP and the amount of ADH release, and that during elevated ICP the ADH release is not suppressed by hypotonic infusion.

Effect of intermittently raised intracranial pressure on breathing pattern, ventilatory response to CO2, and blood gases in anesthetized cats

1976 ◽  
Vol 44 (2) ◽  
pp. 156-167 ◽  
Author(s):  
Sheila Jennett ◽  
J. Brian North
Keyword(s):  
Intracranial Pressure ◽  
Gas Exchange ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Blood Gases ◽  
Raised Intracranial Pressure ◽  
Content Type ◽  
Central Depression ◽  
Ventilatory Response To Co2 ◽  
Fine Print

✓ In anesthetised cats, breathing pattern, blood gases, and ventilatory response to CO2 were recorded before and during intermittent 10-minute episodes of hydrostatically raised intracranial pressure. The first effect on breathing was a stimulation which was followed at higher pressures by irregularity, depression, and periods of apnea; hyperventilation at high intracranial pressure (ICP) was rare. Raised ICP did not consistently depress the ventilatory response to CO2 until ventilation during airbreathing was already depressed; therefore, we cannot experimentally justify applying this test clinically to detect incipient ventilatory depression. When hypoxemia developed during raised ICP, it was compatible with the degree of hypoventilation due to central depression of breathing; thus, there was no evidence of a neurally mediated effect on the lungs, causing defective gas exchange.

The effects of mass-induced intracranial pressures on arterial hypertension and survival in awake cats

1972 ◽  
Vol 37 (5) ◽  
pp. 514-527 ◽  
Author(s):  
Stanley J. Goodman ◽  
Donald P. Becker ◽  
John Seelig
Keyword(s):  
Intracranial Pressure ◽  
Systemic Hypertension ◽  
Content Type ◽  
Arterial Blood ◽  
Mass Size ◽  
Intracranial Pressures ◽  
Relationship Of ◽  
The Relationship ◽  
Awake Cats ◽  
Supratentorial Mass

✓ Intracranial pressures above and below the tentorium, arterial blood pressure, heart rate, and respiratory rate were recorded continuously before, during, and after expansion of a supratentorial mass in awake unsedated cats. In general, as the mass enlarged, the intracranial pressure rose; however, considerable variation was observed among animals with respect to specific mass size and associated intracranial pressures. There was considerable variation in the relationship of supratentorial pressure to infratentorial pressure. No animal survived that had sustained a mass-induced pressure exceeding 1100 mm H2O, and survival was shorter with greater pressures. Systemic hypertension occurred always and only when the infratentorial pressure exceeded 600 mm H2O, regardless of the magnitude of the associated supratentorial intracranial pressure. The methodological limitations of previous studies of mass-induced intracranial hypertension appear to have been substantially reduced by the technique described.

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.

Dural posterior fossa AVM producing raised sagittal sinus pressure

1977 ◽  
Vol 46 (6) ◽  
pp. 804-810 ◽  
Author(s):  
Eduardo Lamas ◽  
Ramiro D. Lobato ◽  
Javier Esparza ◽  
Luis Escudero
Keyword(s):  
Intracranial Pressure ◽  
Posterior Fossa ◽  
Considerable Increase ◽  
Selective Embolization ◽  
Content Type ◽  
Sagittal Sinus ◽  
Arterial Blood ◽  
Sagittal Sinus Pressure ◽  
Dural Avm ◽  
Sinus Pressure

✓ A patient with raised intracranial pressure secondary to a dural arteriovenous malformation (AVM) of the posterior fossa is presented. Direct shunting of arterial blood into the transverse sigmoid sinus caused a considerable increase of the sagittal sinus pressure (SSP) and elevation of intracranial pressure (ICP). Both ICP and SSP returned to normal values following obliteration of the dural AVM by selective embolization.

Evaluation of a method for noninvasive intracranial pressure assessment during infusion studies in patients with hydrocephalus

2000 ◽  
Vol 92 (5) ◽  
pp. 793-800 ◽  
Author(s):  
Bernhard Schmidt ◽  
Marek Czosnyka ◽  
Jens Jürgen Schwarze ◽  
Dirk Sander ◽  
Werner Gerstner ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Intracranial Pressure ◽  
Time Course ◽  
Cerebral Blood Flow Velocity ◽  
Absolute Error ◽  
Content Type ◽  
Arterial Blood ◽  
Potential Clinical Benefit ◽  
The Mean ◽  
Fine Print

Object. A mathematical model previously introduced by the authors allowed noninvasive intracranial pressure (nICP) assessment. In the present study the authors investigated this model as an aid in predicting the time course of raised ICP during infusion tests in patients with hydrocephalus and its suitability for estimating the resistance to outflow of cerebrospinal fluid (Rcsf).Methods. Twenty-one patients with hydrocephalus were studied. The nICP was calculated from the arterial blood pressure (ABP) waveform by using a linear signal transformation, which was dynamically modified by the relationship between ABP and cerebral blood flow velocity. This model was verified by comparison of nICP with “real” ICP measured during lumbar infusion tests. In all simulations, parallel increases in real ICP and nICP were evident. The simulated Rcsf was computed using nICP and then compared with Rcsf computed from real ICP. The mean absolute error between real and simulated Rcsf was 4.1 ± 2.2 mm Hg minute/ml. By the construction of simulations specific to different subtypes of hydrocephalus arising from various causes, the mean error decreased to 2.7 ± 1.7 mm Hg minute/ml, whereas the correlation between real and simulated Rcsf increased from R = 0.73 to R = 0.89 (p < 0.001).Conclusions. The validity of the mathematical model was confirmed in this study. The creation of type-specific simulations resulted in substantial improvements in the accuracy of ICP assessment. Improvement strategies could be important because of a potential clinical benefit from this method.

Furosemide in the Intraoperative Reduction of Intracranial Pressure in the Patient with Subarachnoid Hemorrhage

Neurosurgery ◽  
1982 ◽  
Vol 10 (2) ◽  
pp. 167-169 ◽  
Author(s):  
Duke Samson ◽  
Chester W. Beyer
Keyword(s):  
Mean Arterial Pressure ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Blood Gases ◽  
Base Line ◽  
Arterial Pco2 ◽  
Arterial Blood ◽  
Ruptured Intracranial Aneurysm ◽  
Intracranial Lesions ◽  
Sequential Measurements

Abstract The effect of furosemide in the intraoperative reduction of intracranial pressure was measured in 25 patients undergoing the operative repair of a ruptured intracranial aneurysm. Seven patients with similar intracranial lesions served as controls. A single bolus of 80 mg of furosemide was administered intravenously after the induction of anesthesia, and sequential measurements were made of intracranial pressure, mean arterial pressure, and arterial blood gases. A mean decrease of intracranial pressure of 56% was measured in the furosemide-treated patients, whereas the control patients demonstrated a mean decline of subarachnoid pressures of 18%. These changes are significant at the P &lt; 0.005 confidence level, whereas changes in mean arterial pressure, mean arterial pCO2, and base line arterial pCO2 were statistically insignificant. This study suggests that intravenous furosemide is a quick, dependable, and effective mechanism for the intraoperative reduction of intracranial pressure in the postsubarachnoid hemorrhage aneurysm patient.

Effect of parenteral nutrition on cold-induced vasogenic edema in cats

1986 ◽  
Vol 64 (3) ◽  
pp. 460-465 ◽  
Author(s):  
David C. Waters ◽  
Julian T. Hoff ◽  
Keith L. Black
Keyword(s):  
White Matter ◽  
Vasogenic Edema ◽  
Blood Gases ◽  
Serum Osmolality ◽  
Edema Formation ◽  
Content Type ◽  
Arterial Blood ◽  
Gravity Measurements ◽  
Hyperosmolar Solutions

✓ The effect of standard parenteral nutritional formulas on cold-induced vasogenic edema formation in cats was examined and compared to the effects of 5% dextrose, 0.9% saline, and 40.5% mannitol. The amount of vasogenic edema formed during a 3-hour period of fluid infusion following cold injury was quantified by a computerized graphics tablet determination of the volume of Evans blue-dyed white matter. Specific gravity measurements were taken as a measure of white matter water content. Serum osmolality, urine output, arterial blood gases, hematocrit, body temperature, and systolic blood pressure were measured periodically throughout the infusion period. Parenteral nutritional formulas and a 40.5% mannitol solution produced greater changes in serum osmolality than did 5% dextrose or 0.9% saline. Greater changes in serum osmolality were associated with larger calculated volumes of edema in the injured hemisphere and lower water contents in the uninjured hemisphere. The data indicate that hyperosmolar solutions may potentiate vasogenic edema formation when the blood-brain barrier is open.

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.

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