Browse Tag: hypotension

Emergency Department


Rapid sequence induction (RSI) for intubation is an effective method for securing the airway in combative or agitated patients.


If hypotension is detected at any time in the course of the emergent management of a head-injured patient, a cause should be sought other than the head injury. Hypotension is rarely caused by head injury except as a terminal event, but important exceptions include profound blood loss from scalp lacerations and pediatric patients with relatively small circulating blood volumes. In small children, hemorrhage into an epidural or subgaleal hematoma can produce profound hypovolemic shock. In the presence of concomitant spinal cord injury, spinal cord hypotension may occur. This is rare and can be differentiated from hypovolemic hypotension by its nonresponsiveness to fluid administration.

Recently, it has been suggested that hypotensive patients with penetrating abdominal trauma may have better outcomes if fluids are restricted before operation. These studies did not include head-injured patients. In the case of the head-injured patient, systematic hypotension cannot be tolerated without profound worsening of neurologic outcome; fluids should therefore be delivered to maintain a systolic blood pressure of at least 90 mm Hg. Several laboratory and clinical studies have investigated the effects of the delivery of large amounts of fluid to severely head-injured patients who are hypotensive from other injuries and have not demonstrated clinically significant increases in ICP. Fluids should not be withheld in the hypovolemic hypotensive head trauma patient for fear of increasing cerebral edema and ICP. Hypotension from any cause increases mortality from the head injury by 30%. Hypotension may interfere with the accurate neurologic assessment of the brain-injured patient. Often, when blood pressure is restored, an improved neurologic status is observed.

As many as 60% of patients with severe head injury are victims of multiple trauma. The dramatic presentation of the head injury should not distract the clinician from a thorough search for other life threats.

The ED neurologic assessment should be compared with the initial prehospital examination, focusing on evidence of neurologic deterioration or signs of increasing ICP. If the patient is deteriorating or has signs of increased ICP, active intervention must be initiated in the ED.


Hyperventilation to produce an arterial P CO2 of 25 to 30 mm Hg will temporarily reduce ICP by promoting cerebral vasoconstriction and subsequent reduction of CBF. The onset of action is within 30 seconds and probably peaks within 8 minutes after the P CO2 drops to the desired range. In most patients hyperventilation lowers the ICP by 25%; if the patient does not rapidly respond, the prognosis for survival is generally poor. Prolonged hyperventilation probably loses its effectiveness and therefore is of limited value beyond the acute phase. The partial pressure of carbon dioxide should not fall below 25 mm Hg because this may cause profound vasoconstriction and ischemia in normal and injured areas of the brain. Prophylactic hyperventilation has been associated with worsened neurologic outcome when measured at 3 and 6 months after severe trauma and is therefore not recommended in head-injured patients who are not exhibiting signs of increased ICP.

Cerebral edema

Cerebral edema is an increase in brain volume caused by an absolute increase in cerebral tissue water content.Diffuse cerebral edema may develop soon after head injury. Vasogenic edema arises from transvascular leakage caused by mechanical failure of the tight endothelial junctions of the BBB. Vasogenic edema is frequently associated with focal contusions or hematomas. It eventually resolves as edema fluid is reabsorbed into the vascular space or the ventricular system.

Cytotoxic edema is an intracellular process that results from membrane pump failure. It is very common after head injury and is frequently associated with posttraumatic ischemia and tissue hypoxia. Normal membrane pump activity depends on adequate CBF to ensure adequate substrate and oxygen delivery to brain tissue. If the CBF is reduced to 40% or less of baseline, cytotoxic edema begins to develop. If CBF drops to 25% of baseline, membrane pumps fail and cells begin to die. Congestive brain swelling can contribute to cytotoxic edema if it becomes severe enough to increase ICP and reduce CPP so that cerebral circulation cannot be maintained.

Alteration in Consciousness

Consciousness is a state of awareness of the self and of the environment and requires intact functioning of the cerebral cortices and the reticular activating system (RAS) of the brain stem. An altered level of consciousness is the hallmark of brain insult from any cause and results from an interruption of the RAS or a global event that affects both cortices.

A patient who has sustained TBI commonly has an altered level of consciousness. Head-injured patients may be hypoxic from injury to respiratory centers or from concomitant pulmonary injury. Hypotension from other associated injuries can compromise CBF and affect consciousness. Global suppression may be present as a result of an intoxicating substance consumed before the injury. With increasing ICP from brain swelling or an expanding mass lesion, brain stem compression and subsequent RAS compression can occur.

Patients with altered levels of consciousness require careful monitoring and observation. Reversible conditions that can alter mental status, such as hypoxia, hypotension, hypoglycemia, should be corrected as they are identified.