The Cushing reflex is basically not a true reflex, but a relationship between intracranial pressure, blood pressure, and heart rate. When intracranial pressure rises, blood pressure rises to maintain O2 supply to the brain. Perfusion pressure in the brain is equal to the difference between mean arterial pressure and intracranial pressure.
What is the Cushing’s reflex?
In 1901, Harvey Cushing discovered a relationship between the increase in intracranial pressure, the decrease in heart rate, and the increase in blood pressure. In 1901, American neurologist Harvey Cushing discovered a correlation between the slope of intracranial pressure, the drop in heart rate, and the increase in blood pressure. The connection has borne his name in honor of him since it was first described and is consequently called the Cushing reflex. The formula of the reflex is CPP = MAP – ICP. In it, ICP stands for intracranial pressure (intracranial pressure), MAP stands for mean arterial pressure, and CPP stands for partial intracranial pressure. In other words, perfusion pressure in the brain is the difference between mean arterial pressure and intracranial pressure. The latter opposes the arterial pressure and is overcome by it as resistance. Sometimes, instead of the Cushing reflex, we speak of the Cushing triad, which is composed of hypertension, bradycardia, and irregular, inadequate respiration. In the true sense, the increase in blood pressure and decrease in heart rate following an increase in intracranial pressure is not a true reflex with a reflex arc.
Function and task
Increases in intracranial pressure may be due to a variety of contexts. For example, space occupying lesions of the brain parenchyma can cause the pressure to rise, including a brain tumor. The same applies to any swelling of the brain, such as is present inform cerebral edema. Brain edema is often the result of craniocerebral trauma. In addition, strokes and inflammation can increase intracranial pressure in the brain. Other causes include increases in cerebrospinal fluid volume, such as those present in cerebrospinal fluid outflow disorders. Thus, when intracranial pressure increases because of any of the phenomena just described, the perfusion pressure of the brain automatically decreases. For this reason, the brain receives less blood flow. The blood transports vital oxygen to the brain. Therefore, when the perfusion pressure drops, the nerve cells are no longer supplied with sufficient oxygen and irreversible damage to the nerve tissue is imminent. The body wants to prevent this. Therefore, the organism tries to keep the mean arterial pressure and the intracranial pressure in a certain constancy. For this purpose, the body strongly increases the blood pressure. Increases of up to 300 mmHg can be expected with respect to systolic blood pressure. The increase in blood pressure also increases the ICP. This causes the arterial pressure to rise even higher. At the same time, a decrease in heart rate occurs. This is because the organ must recover from the increased stress. Based on these relationships, the pressure pulse develops; it is caused by a sudden increase in sympathetic activity in the medulla oblongata. After a certain time, self-regulation of blood pressure is expected. Therefore, the administration of antihypertensive drugs is contraindicated in the described situation. Only in the case of active bleeding into the brain, such as a ruptured aneurysm, the physician must lower the systolic blood pressure to below 160 mmHg. In summary, then, the Cushing reflex describes the decreasing perfusion pressure, the decrease in cerebral blood flow, and the compensatory action of increasing systemic blood pressure taken by the body after an increase in intracranial pressure to keep the MAP-to-ICP ratio constant. Subsequent increases in ICP cause arterial pressure to rise again, thus creating a vicious circle.
Diseases and medical conditions
The Cushing reflex gains clinical relevance in all elevations of intracranial pressure and, accordingly, may be relevant in the context of hemorrhage, cerebrospinal fluid disorders, stroke, edema, after trauma, or in tumors. Signs of increased intracranial pressure include symptoms such as more or less severe headache, vomiting, or edema within the optic nerve papilla. The edema can be diagnosed by ophthalmoscopy. If several of the symptoms are present at the same time, a so-called intracranial pressure triad is present.Trias is often associated with accompanying symptoms such as dizziness, paralysis of the eye muscles, bradycardia or respiratory and consciousness disorders. Absence up to coma may occur in the context of increased intracranial pressure. In most cases, patients initially suffer increased restlessness and experience a general increase in blood pressure and a drop in heart rate as part of the Cushing’s reflex. Patients with high intracranial pressure are monitored intensively and positioned in bed with their upper body elevated 30 or 45 degrees. Their head must lie as straight as possible so that venous drainage can occur without obstruction. Mild hyperventilation causes the blood vessels to constrict. In this way, a slight reduction in ICP can be achieved therapeutically. Further treatment depends on the cause of the increased pressure. Edema can be resolved or reduced by the administration of diuretics. In the event that autoregulation is not effective with regard to blood pressure in the brain, patients with elevated intracranial pressure are monitored closely with regard to their blood pressure. Often invasive blood pressure measurements are used for this purpose. In this way, intervention is possible in the event of a failure of the Cushing’s reflex. Various drugs are available for intervention that can keep the blood pressure physiological and thus have an effect on the intracranial pressure on the one hand and ensure the blood supply to the brain tissue on the other. Increased intracranial pressure may be a life-threatening situation.
