8/12/2019 Intracranial Pressure and Cushing Response

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EMS Recap: Intracranial Pressure and the Cushing ReflexBY ROBERT E. SIPPEL, MS, MAED, NREMT-P, LP (/CONTACT/10362618/ROBERT-

E-SIPPEL-MS-MAED-NREMT-P-LP) 

CREATED: NOVEMBER 23, 2011

Rising ICP can have serious consequences. Here’s what to know.

The Cushing response refers to the changes the body experiences to compensate for rising intracranial

pressure. Cushing’s triad of signs includes hypertension, bradycardia and apnea.

Dr. Harvey Cushing introduced bloo d pressure measurement as a method of monitoring patient status dur

neurosurgical procedures. Cushing recognized that the body’s initial response to rising intracranial pressu

a rise in systolic blood pressure. The rising systolic pressure results in widened pulse pressures, bradycard

and irregular breathing. As intracranial pressure continues to increase, the patient’s heart rate will increas

 breathing will became shallow, periods of apnea will occur, and blood pressure will begin to fall. Eventuall

agonal rhy thm will develop as herniation begins, followed soon by cessation of brain stem activity,

respirator y arrest and cardiac arrest.

Intracranial pressure is the force exerted on the inside of the skull by the brain, cerebral spinal fluid and

 blood. An increase in pressure caused by one component necessitates compensatory responses by the oth

to maintain intracranial pressure within the normal range of 0–15 mmHg. Intracranial pressure adjusts continuously with the daily activ ities of liv ing. Breath

lifting and coughing cause increases in intracranial pressure. The body is capable of autoregulating intracranial pressure increases that stay below 35 mmHg,

corresponding systolic blood pressures between 60–160 mmHg and cerebral perfusion pressures between 50–150 mmHg.

To maintain normal intracranial pressures, cerebral spinal fluid moves between the cranium and the spinal subarachnoid space, and the diameter of the arteri

can change to allow for adequate cerebral blood flow. The automatic adjustments allow cerebral perfusion pressure to remain within the normal range. When

autoregulation of cerebral perfusion pressure fails, rising carbon dioxide levels cause the arterioles to passively dilate and mirror systemic pressure changes.

Compression of the veins will occur, and venous return will be impeded. Left uncorrected, intracranial pressure will continue to rise until it equals the systolic blood pressure, and cerebral blood flow will then cease. T his is called cerebral vasoparalysis.

Early signs of rising intracranial pressure include decreased level of consciousness, restlessness, irritability and confusion. With a continued increase, speech,

 voluntary movements, sensations and extraocular movements will slow. Additionally, T -wave elevation will develop on the electrocardiogram. Your patient

only speak when stimulated, have no voluntary movements and only respond to painful stimuli. As pressure increases near the medulla, the patient may 

experience projectile vomiting with no associated nausea, and cardiac arrhythmias can range from supraventricular tachycardia to severe bradycardia. As co

develops, reaction to painful stimuli will become reflexive and may disappear completely. When herniation of the brain is imminent, loss of extraocular

movement will occur, with the pupils dilating, becoming unreactive and turning outward.

Methods to prevent or reduce the rate of a rising ICP include elevating the head 30–45 degrees, keeping the neck in a neutral position, maintaining normal

oxygen and carbon dioxide levels, avoiding overhydration, avoiding the clustering of treatments, preoxygenating prior to any suctioning, avoiding Valsalva’s

maneuvers, maintaining normal body temperature, avoiding noxious stimuli and administering appropriate medications.

To summarize, with increases in intracranial pressure, the Cushing response begins with a rise in systolic blood pressure, widening pulse pressure, bradycardi

and irregular breathing. Left uncorrected, the heart rate will increase, breathing will become shallow with periods of apnea, and the blood pressure will begin

fall. Eventually the patient will develop an agonal rhythm. Brain stem activity will cease when herniated, and the patient will experience cardiac and respirato

arrest.

Bibliography 

Molnar C, Nemes C, Szabo S, Fulesdi B. Harvey Cushing, a pioneer of neuroanesthesia. J Anesth 22(4): 483–6, 2008.

Dadlani R, Challam K, Garg A, Hegde, AS. Can bradycardia pose as a “red herring” in neurosurgery? Surgical stress ex poses an asymptomatic sick sinus

syndrome: Diagnostic and management dilemmas. Indian J Crit Care Med  14 (4): 212–216, Oct–Dec 2010.

Barker E. Avoiding increased intracranial pressure. Nursing 20(5): 64Q–64RR, May 1990.