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 ◽  
...  

✓ 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.

1977 ◽  
Vol 47 (2) ◽  
pp. 195-200 ◽  
Author(s):  
Elizabeth A. M. Frost

✓ Hypoxic pulmonary disorders and head injuries associated with increased intracranial pressure (ICP) frequently co-exist. Positive end-expiratory pressure (PEEP) improves hypoxemia but has been reported to impede cerebral venous return, potentially causing a further increase in ICP. This study examined the effects of PEEP on ICP at different levels of brain compliance. Continuous ICP recordings were obtained after insertion of Scott cannulas to the lateral ventricles of seven comatose patients. Brain compliance was assessed by calculation of the pressure volume index. Patients were maintained in a 30° head-up position. Maintenance of PEEP to levels of 40 cm H2O pressure for as long as 18 hours did not increase ICP in patients with either normal or low intracranial compliance, and did not increase ICP in the absence of pulmonary disease. Central venous pressure and pulmonary artery wedge pressure increased proportionately as PEEP was increased. No consistent changes were found in blood pressure recordings, nor were there any reductions in cardiac output found during the studies. Abrupt discontinuation of PEEP did not result in increased ICP except for a transient rise on two occasions when respiratory secretions became copious and the patients were inadequately ventilated. Improved oxygenation in two patients as a result of PEEP was concomitant with improved intracranial compliance and neurological status. In patients with brain injuries, PEEP improves arterial oxygenation without increasing ICP as previously supposed. Consequently, PEEP is a valuable form of therapy for the comatose patient with pulmonary disorders such as pneumonia or pulmonary edema.


1992 ◽  
Vol 77 (6) ◽  
pp. 908-910 ◽  
Author(s):  
Dale M. Swift ◽  
Robert A. Solomon

✓ After a ruptured aneurysm has been clipped in patients with multiple aneurysms, the question often arises whether to use volume expansion and/or hypertensive treatment to prevent delayed cerebral ischemia (vasospasm). There is understandable concern regarding the possible rupture of unprotected aneurysms under additional hemodynamic stress. In a series of 199 patients with aneurysmal subarachnoid hemorrhage who underwent early surgery, 31 were left with one or more unprotected aneurysms postoperatively. All patients were treated with prophylactic volume expansion based on a previously reported protocol. Mean central venous pressure during treatment was 10.3 cm H2O and mean arterial blood pressure 141/76 mm Hg; volume expansion was continued for 7 to 10 days. Eight patients developed symptoms of delayed cerebral ischemia and required additional volume expansion and induced hypertension. After institution of hypertension, four of these patients experienced a reversal of their symptoms, while four others developed cerebral infarcts. One patient died from massive cerebral infarction following vasospasm refractory to all measures. No patient suffered rupture of an unprotected aneurysm during hypervolemic treatment. It is concluded that the benefit of prophylactic hypervolemic hypertension in postoperative aneurysm patients warrants its use even in patients with unprotected aneurysms.


1986 ◽  
Vol 65 (5) ◽  
pp. 636-641 ◽  
Author(s):  
Michael J. Rosner ◽  
Irene B. Coley

✓ Previous investigations have suggested that intracranial pressure waves may be induced by reduction of cerebral perfusion pressure (CPP). Since pressure waves were noted to be more common in patients with their head elevated at a standard 20° to 30°, CPP was studied as a function of head position and its effect upon intracranial pressure (ICP). In 18 patients with varying degrees of intracranial hypertension, systemic arterial blood pressure (SABP) was monitored at the level of both the head and the heart. Intracranial pressure and central venous pressure were assessed at every 10° of head elevation from 0° to 50°. For every 10° of head elevation, the average ICP decreased by 1 mm Hg associated with a reduction of 2 to 3 mm Hg CPP. The CPP was not beneficially affected by any degree of head elevation. Maximal CPP (73 ± 3.4 mm Hg (mean ± standard error of the mean)) always occurred with the head in a horizontal position. Cerebrospinal fluid pressure waves occurred in four of the 18 patients studied as a function of reduced CPP caused by head elevation alone. Thus, elevation of the head of the bed was associated with the development of CPP decrements in all cases, and it precipitated pressure waves in some. In 15 of the 18 patients, CPP was maintained by spontaneous 10- to 20-mm Hg increases in SABP, and pressure waves did not occur if CPP was maintained at 70 to 75 mm Hg or above. It is concluded that 0° head elevation maximizes CPP and reduces the severity and frequency of pressure-wave occurrence. If the head of the bed is to be elevated, then adequate hydration and avoidance of pharmacological agents that reduce SABP or prevent its rise are required to maximize CPP.


Author(s):  
Anthea Hatfield

Routine monitoring is an essential part of recovery room procedure. Respiration, a vital concern while awakening after anaesthesia, is given specific attention with reference to modern capnography. This chapter also describes additional monitoring in detail: pulse oximetry, blood pressure, central venous pressure, and arterial blood gases are clearly described. A comprehensive description of electrocardiography guides the student through this complicated subject. The monitoring of temperature and warming blankets, with suggestions for purchasing equipment, are included.


1988 ◽  
Vol 69 (2) ◽  
pp. 213-215 ◽  
Author(s):  
Akio Tateishi ◽  
Takanobu Sano ◽  
Hiroshi Takeshita ◽  
Toshihisa Suzuki ◽  
Hisao Tokuno

✓ The effects of nifedipine, 20 mg administered via a nasogastric tube, on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were examined. Nifedipine was administered to treat arterial hypertension (> 180 mm Hg, systolic). Ten measurements were made in eight patients with cerebrovascular disease or head trauma. The mean arterial blood pressure (MABP) and ICP were measured before and for 30 minutes after the administration of nifedipine. The MABP gradually decreased and reached its lowest value at approximately 10 minutes after initiation of nifedipine administration, and thereafter remained unchanged. The MABP decreased significantly from 128 ± 8 (mean ± standard deviation) to 109 ± 7 mm Hg, and the CPP decreased from 105 ± 11 to 84 ± 10 mm Hg. The ICP increased by 1 to 10 mm Hg in eight of 10 measurements, and the mean change of ICP from 19 ± 7 to 22 ± 6 mm Hg was statistically significant. These changes were not accompanied by alterations in neurological signs. The results suggest that enteral nifedipine produces a small but statistically significant increase in ICP. Accordingly, neurological signs must be closely observed to detect deterioration, which can be caused by an increase in ICP and/or a decrease in CPP.


Author(s):  
Anne Craig ◽  
Anthea Hatfield

Routine monitoring is an essential part of recovery room procedure. Respiration, a vital concern while awakening after anaesthesia, is given specific attention with reference to modern capnography. This chapter also describes additional monitoring in detail: pulse oximetry, blood pressure, central venous pressure, and arterial blood gases are clearly described. A comprehensive description of electrocardiography guides the student through this complicated subject. The monitoring of temperature and warming blankets, with suggestions for purchasing equipment, are included.


1977 ◽  
Vol 46 (5) ◽  
pp. 627-637 ◽  
Author(s):  
Lynn Gaufin ◽  
W. Ronald Skowsky ◽  
Stanley J. Goodman

✓ 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.


2021 ◽  
pp. 1-14
Author(s):  
Gabriela Maissen ◽  
Gagan Narula ◽  
Christian Strässle ◽  
Jan Willms ◽  
Carl Muroi ◽  
...  

BACKGROUND: Intracranial pressure (ICP) and arterial blood pressure (ABP) are related to each other through cerebral autoregulation. Central venous pressure (CVP) is often measured to estimate cardiac filling pressures as an approximate measure for the volume status of a patient. Prior modelling efforts have formalized the functional relationship between CVP, ICP and ABP. However, these models were used to explain short segments of data during controlled experiments and have not yet been used to explain the slowly evolving ICP increase that occurs typically in patients after aneurysmal subarachnoid hemorrhage (SAH). OBJECTIVE: To analyze the functional relationship between ICP, ABP and CVP recorded from SAH patients in the first five days after aneurysm. METHODS: Two methods were used to elucidate this relationship on the running average of the signals: First, using Spearman correlation coefficients calculated over 30 min segments Second, for each patient, linear state space models of ICP as the output and ABP and CVP as inputs were estimated. RESULTS: The mean and variance of the data and the correlation coefficients between ICP-ABP and ICP-CVP vary over time as the patient progresses through their stay in the ICU. On average, after an SAH event, the models show that a) ABP is the bigger driver of changes in ICP than CVP and that increasing ABP leads to reduction in ICP and (b) increasing CVP leads to an increase in ICP. CONCLUSIONS: Finding a) agrees with the hypothesis that patients with subarachnoid hemorrhage have defective autoregulation, and b) agrees with the positive correlation observed between central venous pressure and intracranial pressure in the literature.


1981 ◽  
Vol 55 (5) ◽  
pp. 704-707 ◽  
Author(s):  
Jon S. Huseby ◽  
John M. Luce ◽  
Jeffrey M. Cary ◽  
Edward G. Pavlin ◽  
John Butler

✓ Positive end-expiratory pressure (PEEP) is used to improve oxygenation in patients with the adult respiratory distress syndrome. Nevertheless, this treatment may increase intracranial pressure (ICP) and be detrimental to certain neurosurgical patients. This clinical situation was simulated by administering PEEP to dogs with normal and elevated ICP. Increases in PEEP increased ICP in all animals. However, the presence of intracranial hypertension diminished the increase in ICP seen at a given level of PEEP. Cerebral perfusion pressure also fell less in the presence of intracranial hypertension than it did in its absence, although in the former situation cerebral perfusion pressure was at the lower limits of the range of cerebral autoregulation. These findings suggest that PEEP is no more detrimental to patients with elevated ICP than it is to patients whose ICP is normal, assuming that their cerebral autoregulation is not impaired.


1978 ◽  
Vol 48 (3) ◽  
pp. 390-401 ◽  
Author(s):  
Sheila Jennett ◽  
Julian T. Hoff

✓ 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.


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