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Introduction

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Objectives

  1. Describe the interactions between mechanical ventilation (increased intrathoracic pressure) and head injury.

  2. Identify neurogenic pulmonary edema.

  3. Discuss the indications, initial ventilator settings, monitoring, and ventilator weaning for the head-injured patient.

  4. Describe how an apnea test is performed.

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Head injury and its associated neurologic dysfunction are common in the United States and other developed countries. The morbidity and mortality associated with this problem are related to acute cerebral edema and other space occupying lesions that increase intracranial pressure (ICP). Head injury is often traumatic in origin. However, similar effects may be seen with surgical (eg, postcraniotomy for tumor resection) and medical (eg, cerebral vascular accident, postresuscitation hypoxia, hepatic failure) problems.

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Overview

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Physiology

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Because the skull is rigid, intracranial volume increases result in an increase in ICP. The relationship between intracranial volume and ICP is described by the cerebral compliance curve (Figure 20-1). Although small increases in intracranial volume are tolerated without an increase in ICP, larger increases in volume result in large increases in ICP. This increase in ICP decreases cerebral blood flow, resulting in cerebral hypoxia. With large increases in ICP, the swelling brain herniates through the tentorium, resulting in compression of the brain stem. Much of the management of head injury relates to efforts to control ICP.

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Figure 20-1

Cerebral compliance curve showing the relationship between intracranial pressure and intracranial volume. Normally (low intracranial volume), some cerebral swelling can occur without increasing intracranial pressure. However, a point is reached after which further increases in cerebral swelling result in a large increase in intracranial pressure.

Graphic Jump Location
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Cerebral perfusion pressure (CPP) is defined as the difference between mean arterial pressure (MAP) and ICP:

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Normally, ICP is less than 10 mm Hg and MAP is about 90 mm Hg, resulting in a normal CPP of more than 80 mm Hg. The target CPP is 50 to 70 mm Hg. CPP less than 50 mm Hg should be avoided. In patients with acute head injury, the ICP is frequently measured. CPP is decreased by either a decrease in MAP or an increase in ICP. Thus, treatments that decrease MAP (eg, positive pressure ventilation, diuresis, vasodilator therapy) decrease CPP, whereas treatments that decrease ICP (hyperventilation, mannitol) increase CPP. A normal physiologic response to an acute increase in ICP is hypertension with bradycardia, which is called the Cushing response.

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Mechanical ventilation can increase ICP and decrease CPP because the increased intrathoracic pressure associated with mechanical ventilation. Positive end-expiratory pressure (PEEP) has the potential of decreasing MAP and venous return. A decrease in venous return increases ICP and a decrease in MAP decreases CPP.

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Clinical Findings

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Increases in ICP can result in abnormal ventilatory patterns such as Cheyne-Stokes ...

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