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| Postoperative Complications | Respiratory Care| Cardiovascular Therapy| Fluid Management| Nutrition in Critical Patients |Traumatic Brain Injury-Stroke-Brain Death |

I. Basic considerations

The crucial goal of cardiovascular therapy in perioperative neurosurgical patients is to provide sufficient metabolic substrate to the threatened central nervous system (CNS). Because glucose is usually not a problem related to cardiovascular therapy, our attention is directed to oxygen delivery. Cardiovascular therapy can affect CNS swelling and result in irreversible injury. Therefore, while maintaining oxygen delivery is important, care must be exercised not to compromise intracerebral hemodynamics.
Autoregulation refers to the interdependence of cerebral blood flow (CBF) and mean arterial (blood) pressure (MAP). The range of MAP over which nonhypertensive patients exhibit autoregulation is 50 to 150 mm Hg. Chronically hypertensive patients have altered autoregulation and neither maintain CBF at an MAP in the low end of the normal range nor vasoconstrict when the MAP exceeds 150 mm Hg. A similar alteration of autoregulation occurs with sympathetic activation induced by shock or surgery.
When autoregulation is impaired, CBF will become more dependent on the blood pressure; minor swings in MAP might have significant impact on intracerebral hemodynamics.
Many conditions such as head injury and tumors are associated with either generalized or regional disruption of autoregulation.
Intracranial pressure (ICP). The intracranial compartment is essentially a closed space, so ICP is determined by the intracranial volume, which is comprised of cerebrospinal fluid, cerebral parenchyma, and cerebral blood volume (CBV). Increases in any of these components can contribute to intracranial hypertension and result in decreased cerebral perfusion pressure (CPP).
CPP is the difference between MAP and ICP. In most organs, venous pressure generates the back pressure that determines the pressure drop across an organ. Because venous pressure tends to be negative in the brain, parenchymal pressure (ICP) generates the back pressure for determining CPP. CPP determines CBF both globally and regionally in the CNS. Normal CBF is 50 mL/100 g brain/minute and decreases only if CPP falls from a normal value of approximately 80 mm Hg to below 50 mm Hg unless autoregulation is altered.

II. Cerebral oxygen delivery

is a function of CBF and the quantity of oxygen carried in arterial blood (Caco2. CBF is related to CPP, and, because blood pressure is a function of cardiac output (CO) and systemic vascular resistance
(SVR), CO becomes an important parameter to manipulate to preserve CBF and cerebral oxygen delivery. The normal awake brain consumes 3.3 mL O2/100 g/minute, a value reduced by approximately one-third when anesthesia is being administered.
Determinants of CO. The CO is a result of four basic factors: preload, contractility, heart rate (HR), and afterload.
1. Preload is impractical to monitor but can be best determined by measuring ventricular end-diastolic volume (EDV) by either angiography or echocardiography. Pulmonary artery occlusion pressure (PAOP) is more frequently used as a reliable estimate of left atrial preload; central venous pressure is a measure of right atrial preload. In addition to PAOP, volumetric pulmonary artery catheter (PAC) monitoring provides right ventricular EDV for preload assessment. Stroke volume variation is used to assess preload when pulse contour cardiac monitoring technology is employed.
2. Contractility. The ejection fraction measured by either angiography or echocardiography is frequently used to assess contractility, which can also be assessed by evaluating the magnitude of the CO for a given preload condition. Right ventricular ejection fraction is available when monitoring is performed with a volumetric PAC.
3. HR. CO = HR x stroke volume. When preload, contractility, or both limit stroke volume, an increase in HR often acts to maintain CO.
4. Afterload. Mean aortic pressure is the afterload against which the left ventricle ejects a stroke volume. We use MAP in neuroanesthesia as a close approximation.
Cardiac failure occurs when CO is insufficient to deliver adequate oxygen. Typical causes include cardiomyopathies from infarction, ischemia, and chronic hypertension; dysrhythmias; increased afterload from arterial hypertension; and outflow obstruction from pulmonary embolus. Neurosurgical patients who are critically ill have additional considerations.
Hypovolemia resulting in insufficient preload.
1. Blood loss. Surgical and traumatic causes including scalp lacerations should be considered.
2. Osmotic diuretic administration can result in intravascular volume contraction.
3. Fluid restriction instituted to minimize cerebral swelling can lead to hypovolemia and end-organ compromise.
4. Diabetes insipidus associated with severe traumatic brain injury (TBI) and pituitary surgery can result in hypovolemia.
CNS causes
1. Spinal cord injury and injury to the brain stem vasomotor center can result in hypotension from decreased sympathetic tone.
2. Neurogenic cardiomyopathy has been described in patients after they have suffered subarachnoid hemorrhage (SAH) and acute TBI. The etiology is thought to be the massive release of norepinephrine. The ensuing electrocardiographic changes are consistent with ischemia and myocardial dysfunction.
Drug induced. Occasionally, aggressive therapy with calcium-entry blocking drugs or beta-blocking drugs can result in suboptimal myocardial performance.
Blood pressure
Hypotension in the presence of normal intravascular volume and cardiac function occurs because of decreases in SVR.
1. Hypotension can be secondary to high cervical cord injury.
2. Brain stem damage involving the vasomotor center results in hypotension. Such an insult is usually lethal.
3. Fever and sepsis can be associated with hypotension.

III. Drugs used in cardiovascular therapy

Guidelines for administration of vasoactive drugs
Use a calibrated pump for all infusions.
Inject into the intravenous line as close to vein insertion site as possible.
Avoid using systolic blood pressure as the goal of therapy because this value is prone to fluctuate from a number of causes, not all of which are related to the patient's cardiovascular condition. MAP is a more reliable variable.
Potent vasoactive drugs should be administered in a graded fashion starting with a dose below one that is thought to be therapeutic.
Adrenergic agonists. See Table-1 for action of adrenergic receptors; see Tables-2 and -3 for relative adrenergic action and dosing recommendations. Sympathomimetic drugs appear to have little influence on the vascular tone of cerebral vessels. However, raising MAP above the upper threshold of autoregulation increases CBF. Some evidence suggests that beta-agonists can increase the cerebral metabolic rate for oxygen consumption and secondarily raise CBF.
Norepinephrine (Levophed) has some beta activity but is used primarily as an alpha-adrenergic agonist. Its primary use is to treat refractory hypotension.
Epinephrine (Adrenalin) possesses dose-related alpha and beta properties. Its primary uses are in cardiopulmonary resuscitation, anaphylaxis, and refractory hypotension. Toxicity from epinephrine is from arrhythmias and the sequelae of vasoconstriction.

Table-1. Action of adrenergic receptors

Receptor Site Action
a 1 Postsynaptic
a 2 Presynaptic
Peripheral and central nervous system, liver, pancreas, kidney, eye
b1 Heart Contractility, chronotropy
b2 Heart
Vascular and bronchial smooth muscle
Contractility, chronotropy
Vasodilatation Smooth muscle relaxation
Dopaminergic Presynaptic
Renal and splanchnic circulation, brain stem
Smooth muscle relaxation
Nausea and vomiting


Table-2. Adrenergic agonist and phosphodiesterase inhibitor drugs

Name Receptors Dosage
Epinephrine b2 1-2 mcg/min
  b1+ b2 2-10 mcg/min
  a >10 mcg/min
Norepinephrine a , b1 4-12 mcg/min
Dopamine Dopaminergic 0-3 mcg/kg/min
  b 3-10 mcg/kg/min
  a >10 mcg/kg/min
Dobutamine b1 2.5-10 mcg/kg/min
Phenylephrine a , b1 (slight) 0.1-0.5 mcg/kg/min
Ephedrine a , b1 5-10 mg
Isoproterenol b1+ b2 0.5-10 mcg/min
Amrinone Inhibition of phosphodiesterase 0.75 mg/kg load, then 5-10 mcg/kg/min
Milrinone Inhibition of phosphodiesterase 50-75 mg/kg load, then 0.5-0.75 mcg/kg/min


Table-3. Adrenergic antagonist drugs
Name Receptor Blocked Dosage
Phentolamine a 5-10 mg
Esmolol b2 0.15-1 mg/kg, then 50-300 mcg/kg/min
Labetalol b2 > a 5-20 mg, then 2 mg/min
Metoprolol b2 2.5-15 mg
Propranolol b2 0.25-5 mg

Dobutamine is a synthetic drug that has predominantly beta-one activity. When compared with other drugs, dobutamine tends to produce less tachycardia and elevation of pulmonary vascular pressure for the same degree of inotropic enhancement. It does not have any dopaminergic agonist action.
Dopamine exhibits alpha, beta, and dopaminergic properties in a dose-related fashion. Its primary uses are to treat hypotension and provide inotropic support. Low doses inhibit renal reabsorption of sodium, resulting in a natriuresis. In high doses, dopamine's alpha properties predominate. Evidence suggests that dopamine can produce mild cerebral vasodilatation.
Phenylephrine is a synthetic drug whose chief characteristic is its relative selectivity for alpha-receptors. When used to increase MAP, a baroreceptor-mediated reflex decrease in HR often occurs. Phenylephrine can be the drug of choice when the cardiac index (CI) is sufficient but MAP is below the goal.
Isoproterenol is a synthetic drug that has remarkable beta selectivity. Administration is associated with tachycardia, decreased MAP, and bronchodilation.
Adrenergic antagonists (Table-3)
Esmolol is an ultrashort-acting (9 to 10 minutes' duration) beta-specific competitive antagonist. Its fast onset and short duration of action render it suitable for rapid intervention in the treatment of tachyarrhythmias in the perioperative period.
Metoprolol is a cardioselective beta antagonist whose duration of action is a longer than that of esmolol. Metoprolol is most commonly used to treat angina and acute myocardial infarction but can be used intravenously in the perioperative period to control tachycardia. All beta-blocking drugs are capable of inducing bronchospasm, heart failure, or both.
Labetalol blocks both alpha- and beta-receptors with more beta than alpha effects. However, a reduction in MAP usually occurs when the dose is sufficient to decrease HR. Labetalol also has a longer duration of action than either esmolol or propranolol.
Propranolol was the original clinically available beta-blocking drug. It is nonselective and has a relatively fast onset, but because the metabolism of the drug in the liver differs widely from patient to patient, dosing is variable. Curiously, propanolol shifts the hemoglobin-oxygen dissociation curve to the right.
Phentolamine specifically competes for both a1 and alpha2 receptors. Because of its duration of action, phentolamine is not frequently used as an antihypertensive in acute perioperative situations.
Phosphodiesterase inhibitors. (Information is presented in Table-2)
Milrinone is a nonadrenergic, nonglycosidic compound that enhances contractility and promotes pulmonary and arterial vasodilatation. It is thought to act by inhibiting phosphodiesterase, which increases the intracellular concentrations of cyclic AMP. Milrinone has little potential for causing cardiac arrhythmias but has a long half-life (hours) and can induce thrombocytopenia as well as hypotension.
Vasodilators (Table-4)
Nicardipine is a calcium-entry blocking drug that reliably decreases MAP when given as an intravenous infusion. It has low toxicity and a predictable response.
Sodium nitroprusside (SNP) is a potent, rapid-onset, short-acting drug that causes more arteriolar than venular vasodilatation via the release of nitric oxide. Administration of SNP is associated with the activation of the renin-angiotensin system; reflex tachycardia can interfere with blood pressure reduction. Occasionally, patients demonstrate relative resistance to SNP. They are at particular risk for developing cyanide toxicity.
Nitroglycerin (NTG) is a rapid-onset, short-acting drug that induces vasodilatation via nitric oxide. Less potent than SNP but with little toxicity, NTG causes more venular than arteriolar vasodilatation.

Table-4. Vasodilators

Name Dosage
Sodium nitroprusside 0.5-10 mcg/kg/min
Nitroglycerin 5-50 mcg/min
Trimethaphan 1-15 mg/min
Hydralazine 0.1-0.2 mg/kg
Nicardipine 5-15 mg/kg

Adenosine is an ultrafast-acting vasodilator that decreases MAP and increases CI owing to a decrease in SVR. Heart block is a potential side effect of its use.
Hydralazine is a vascular smooth muscle relaxant with no effects on contractility or chronotropy. Its use is frequently accompanied by reflex tachycardia.
Vasopressin (antidiuretic hormone) is a peptide with potent vasoconstricting properties, which can be useful in increasing arterial tone. It is administered as a constant infusion, and not titrated up to avoid severe complications of distal ischemia.

IV. Goal-directed pharmacologic intervention for cardiovascular dysfunction

The two goals of cardiovascular therapy in neurosurgical patients "adequate CPP and sufficient CO to maintain oxygen delivery" can require different drug regimens. Optimal fluid therapy should be instituted either prior to or in conjunction with drug therapy.
Increasing MAP is indicated in a number of clinical settings.
Decreased SVR from impaired sympathetic tone, sepsis, fever, or anesthetic drugs can be associated with inadequate MAP. CO can be normal or even high while CPP is too low to optimize cerebral perfusion. Norepinephrine, phenylephrine, and vasopressin are vasoconstrictor drugs that are appropriate in this setting.
Increasing CPP by raising MAP could be needed to protect cerebral perfusion after carotid endarterectomy and cerebral vasospasm. With intracerebral hemorrhage after head injury, it can be desirable to increase MAP to maintain CPP and prevent cerebral hypoperfusion if ICP cannot be controlled.
Anaphylactic reactions. Hypotension accompanying an allergic reaction is treated with epinephrine.
Cardiopulmonary resuscitation. Drugs are administered according to advanced cardiac life-support guidelines.
Therapy. MAP can be increased by administering a drug possessing vasoconstrictive properties that works by direct and/or indirect adrenergic stimulation (Table-2) with varying effects on HR. Pulmonary artery pressure and PAOP also tend to rise, even if no change in intravascular volume has occurred.
1. Myocardial risks. Increasing MAP (after-load) in a patient who has coronary artery disease could increase myocardial oxygen demand sufficiently to outstrip delivery, causing myocardial ischemia and failure.
2. Left ventricular (LV) dysfunction. Increasing MAP could decrease CO if LV dysfunction exists. Therefore, CO monitoring could be indicated during the induction of hypertension in patients suspected of having LV dysfunction.
3. Hypovolemia is treated by augmentating intravascular volume rather than further masking it by the use of adrenergic drugs that only increase the risk of end-organ ischemia.
4. Impaired renal function. Pharmacologically increasing MAP could cause vasoconstriction of renal vessels and could result in deterioration of renal function if perfusion is marginal.
Increasing CO is indicated in a number of clinical settings.
Low CO owing to cardiomyopathy can be caused by ischemia, viral disease, chemotherapy, or drug overdose. Goals recommended for inotropic therapy include the following:
1. MAP of 80 mm Hg.
2. Mixed venous saturation (Sco2) of 65%.
3. CI (CO/body surface area) of 3.5 L/m2/minute.
4. Evidence of adequate end-organ perfusion. Monitoring urine output can be unreliable after diuretics have been administered.
Cerebral vasospasm. Supernormal CO can reduce the risk of permanent neurologic deficit.
Therapy. If CO is insufficient after intravascular volume has been optimized, inotropic drugs should be administered.
1. Beta-agonists are the first-line drugs because their onset and duration allow rapid titration to effect. Empiric therapy is replaced by goal-directed dosing as soon as appropriate monitoring is available.
2. Phosphodiesterase inhibitors. Milrinone can be used as an adjunct to enhance the increase of CO.
3. Digoxin possesses mild to moderate inotropic activity. It can be given orally or intravenously and can increase CO by 10% to 20% in otherwise stable patients who have chronic heart failure.
1. In doses that are high enough, all adrenergic drugs cause tachycardia; patients who have coronary artery disease are at risk for ischemia in this setting. HRs above 120 beats per minute (bpm) should be avoided.
2. When the dose of an adrenergic drug reaches the range in which alpha activity predominates, renal perfusion can be compromised, risking renal failure.
3. While digoxin is useful in the management of chronic cardiac failure, its onset is not immediate, nor is it easily titratable. Undocumented previous administration of digoxin, hypokalemia from diuretics, and the onset of renal failure increase the risk of digoxin toxicity.
Lowering MAP can be indicated in a number of clinical settings.
1. Unclipped aneurysm. Hypertension in the presence of an unclipped cerebral aneurysm is believed to be a significant risk factor for rebleeding.
2. Disrupted cerebral microvascular membrane. In the presence of the disruption of the blood-brain barrier, hypertension can exacerbate the formation of vasogenic edema so that blood pressure control should be considered.
Surgical exposure. Surgeons can request iatrogenic hypotension to enhance exposure, reduce risk of aneurysmal rupture, or assist with the control of bleeding.
1. Analgesics. Clearly, the control of pain can be sufficient to return the MAP to a more acceptable level.
2. Vasodilators. Although many vasodilator drugs are available, the patient's comorbidities and the urgency of the situation often guide the choice. Regardless, a target MAP should be chosen concomitantly with the start of therapy. In the absence of preexisting hypertension, MAP, measured at the level of the external auditory meatus, can be decreased 20% from the baseline without undue risk.
(a) Rapid control can require the use of vasodilators such as SNP or NTG.
(b) Drugs that have slower onset but fewer drawbacks, such as the beta-blocking drugs, nicardipine, and hydralazine, can adequately treat less urgent situations.
1. Hypovolemia. Even small doses of vasodilators can cause dramatic hypotension in the presence of hypovolemia.
2. Decreased intracranial compliance. Vasodilators have the potential for cerebral vascular relaxation with a resultant increase in CBV. If intracranial compliance is decreased, increases in CBV might raise ICP.
Lowering HR can be indicated in a number of clinical settings.
Reduced myocardial oxygen consumption. Tachycardia can increase myocardial oxygen demand and induce ischemia in susceptible patients.
Atrial fibrillation with a rapid ventricular response can compromise the heart's ability to deliver an adequate CO.
Hypertension. Although slowing the HR is not usually sufficient to decrease MAP by a significant degree, a smaller dose of an antihypertensive drug is subsequently required owing to the abatement of the reflex tachycardia.
Therapy. Adenosine and beta-blocking drugs, such as esmolol, metoprolol, propranolol, and labetalol, are often used as first-line drugs owing to their rapid onset and relative safety. Calcium-entry blocking drugs such as verapamil and diltiazem are also used to control ventricular rate, particularly supraventricular tachycardias.
1. The drugs to decrease HR have negative inotropic and vasodilatory properties that can result in both low CO and hypotension. Particular caution is necessary when beta-blocking and calcium-entry blocking drugs are combined.
2. Some patients who have bronchospastic disease experience exacerbation of their symptoms when they receive beta-blocking drugs.

V. Management of cardiovascular complications of neurologic disorders

Cerebral vasospasm
Pathophysiology. Vasospasm is a potentially devastating complication that occurs after SAH and acute TBI. If extensive, vasospasm can decrease CBF to ischemic levels, causing permanent neurologic deficits or death. Although transcranial Doppler (TCD) is proving to be a useful diagnostic modality, vasospasm is traditionally diagnosed by angiography in which beaded narrowing of the cerebral arteries confirms the diagnosis.
Monitoring. Angiography is the gold standard for the diagnosis of vasospasm but is impractical for monitoring. TCD has the advantage of being portable, noninvasive, and amenable to regular or even continuous monitoring. TCD detects vasospasm by measuring the velocity of blood flow in a cerebral artery. Because vasospasm narrows a vessel, the velocity of blood traveling through the constriction increases.
Prevention. A statistical decrease in permanent neurologic deficits in patients at risk has been demonstrated when a cerebral-selective calcium-entry blocking drug is used. This improvement is not associated with an increase in the diameter of the affected vessels.
Triple-H therapy: hypervolemia, hypertension, hemodilution
a. Rationale. Triple-H therapy seeks to increase blood flow through the narrowed arteries by decreasing the viscosity (hemodilution), increasing the driving pressure (hypertension), and expanding the blood volume (hypervolemia).
b. Invasive monitoring, usually including pulmonary artery catheterization, is needed because the knowledge of intravascular volume and the CI are of central importance. Monitoring CO with pulse contour technology can prove sufficient.
(1) Fluids. Hypervolemia is accomplished by infusion of isotonic fluids or colloids.
(2) Vasoactive drugs. The two hemodynamic goals are to increase MAP and CO. Vasoactive drugs are chosen to increase SVR or contractility, as desired. A selective approach is achieved through the use of norepinephrine for the former and dobutamine for the latter.
c. Precautions. Pulmonary edema is the primary concern with triple-H therapy, even with its conscientious management. Treatment goals must be adjusted after pulmonary edema has been detected.
Cerebral salt wasting frequently accompanies SAH and other intracranial pathology. Urinary sodium is elevated in the presence of hyponatremia, an electrolyte presentation seen also with the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. With cerebral salt wasting, unlike SIADH, depletion of intravascular volume develops, which is undesirable when cerebral vasospasm is a risk.
Autonomic hypotension (neurogenic shock)
Pathophysiology. Hypotension can occur after spinal cord injury at a cervical or high thoracic level. Interruption of the sympathetic nervous system causes vasodilatation from the loss of sympathetic vascular tone and bradycardia because of the involvement of the cardioaccelerator nerves. Young individuals who have a high resting vagal tone, normally balanced by sympathetic activity, could experience bradycardia to the point of asystole.
Treatment. Care should be taken in managing low blood pressure in patients after they suffer a spinal cord injury because they do not have intact compensatory mechanisms. They tend to tolerate lower blood pressures without adverse sequelae as compared to neurologically intact patients.
1. Hypotension without bradycardia can be treated with careful administration of fluids if adequacy of end-organ perfusion is a concern. Urine output in the acute phase of spinal cord injury is typically low regardless of the CI or intravascular volume status.
2. If a vasoactive drug is administered, the clinician should remember that denervation hypersensitivity could result in a much larger response than expected.
3. Bradycardia can require atropine for the first 72 hours after spinal cord injury. Bradycardic episodes rarely persist to the point at which a pacemaker is needed.
Carotid endarterectomy: postoperative hypotension
Pathophysiology. Patients who have atherosclerosis sufficient to require carotid endarterectomy often have cardiovascular disease as well and are prone to instability of blood pressure, HR, and rhythm in the perioperative period. Bradycardia and dysrhythmias occur because of abnormal carotid sinus baroreceptor responses.
Treatment includes the administration of fluids to correct preexisting intravascular volume deficits: atropine if carotid sinus stimulation causes bradycardia, and either phenylephrine or dopamine to prevent end-organ compromise if hypotension persists.
Carotid endarterectomy: postoperative hypertension
Pathophysiology. Manipulation of the carotid sinus can contribute to postoperative hypertension, which is associated with a higher risk of postoperative bleeding, stroke, and death.
Treatment. Hypertension can be effectively managed by the intravenous administration of labetalol, nicardipine, hydralazine, or, if severe, SNP.
Acute TBI with hypotension
Pathophysiology. Hypotension in the patient who survives transport to the hospital after suffering a TBI is most likely the result of blood loss. TBI sufficient to damage the brain stem vasomotor center is almost always fatal.
Treatment needs to be prompt because the injured brain is particularly vulnerable to low perfusion pressure, which can already be compromised by elevated ICP.
1. As with any trauma victim suspected of having hypovolemia, intravascular volume needs to be expanded.
2. Positive inotropic drugs or vasoconstrictors can be used for rapid restoration of the MAP to an acceptable level until intravascular volume is expanded.
Acute TBI with hypertension
1. Patients are commonly hypertensive after TBI because they secrete excessive catecholamines. This secretion begins within the first ten days of the traumatic event and can continue for as long as 3 months. Hypertension can be accompanied by tachycardia, tachypnea, restlessness, and diaphoresis limited to the upper body, probably from disinhibition of central sympathetic reflexes.
2. Cushing reflex. MAP could also be elevated if ICP is approaching systemic values as a protective mechanism to maintain CPP. Original descriptions of the Cushing reflex in animals involved bradycardia, whereas tachycardia occurs more commonly in humans.
Treatment. Hypertension after TBI is typically associated with elevated ICP, and there are two possible etiologies. First, with impaired autoregulation, arterial hypertension increases CBF and therefore ICP. Second, elevated ICP induces arterial hypertension via the Cushing reflex. Treatment must be cautious with concurrent monitoring of the effect on ICP.
1. Sympathetic overactivity. Hypertension from the post-TBI syndrome is responsive to beta-blocking drugs, but large doses can be necessary to compete with the high levels of endogenous catecholamines. Beta-blocking drugs also have the benefit of improving intracranial compliance and do not cause cerebral vascular relaxation. If beta blockade does not decrease the MAP adequately, then SNP, NTG, or nicardipine can be considered. SNP and NTG can cause cerebral vascular relaxation, increasing CBV and ICP, an effect that can be ameliorated by slowly infusing the drug.
2. Cushing reflex. If hypertension is thought to occur as a result of the Cushing reflex, attention should be directed to decreasing ICP because decreasing MAP alone can result in a critical reduction in CPP.
Postoperative hypertension
Pathophysiology. Patients who have no prior history of hypertension can become hypertensive after a craniotomy. In the absence of intracranial hypertension, postcraniotomy hypertension should be treated to reduce the risk of cerebral swelling and bleeding in the operative site. However, if ICP is elevated, the treatment of hypertension can decrease CPP to ischemic levels.
Treatment. Hypertension after craniotomy can be treated with analgesics and either labetalol or nicardipine with predictable results. If intracranial hypertension is suspected, management should follow that outlined in the preceding text for TBI.


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