Fluid Management| Nutrition in Critical Patients
|Traumatic Brain Injury-Stroke-Brain Death
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
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
Many conditions such as head injury and tumors are
associated with either generalized or regional
disruption of autoregulation.
(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
II. Cerebral oxygen
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
(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
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
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.
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.
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
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.
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.
Occasionally, aggressive therapy with calcium-entry
blocking drugs or beta-blocking drugs can result in
suboptimal myocardial performance.
MAP = CO x SVR.
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
2. Brain stem damage involving the vasomotor center
results in hypotension. Such an insult is usually
3. Fever and sepsis can be associated with
III. Drugs used in
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.
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.
(Levophed) has some beta activity but is used
primarily as an alpha-adrenergic agonist. Its
primary use is to treat refractory hypotension.
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
Peripheral and central nervous system,
liver, pancreas, kidney, eye
Vascular and bronchial smooth muscle
Vasodilatation Smooth muscle relaxation
Renal and splanchnic circulation, brain stem
Nausea and vomiting
agonist and phosphodiesterase inhibitor
||0.75 mg/kg load,
then 5-10 mcg/kg/min
||50-75 mg/kg load,
then 0.5-0.75 mcg/kg/min
Table-3. Adrenergic antagonist drugs
||0.15-1 mg/kg, then
||5-20 mg, then 2
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.
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.
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.
specifically competes for both
and alpha2 receptors. Because of its duration of
action, phentolamine is not frequently used as an
antihypertensive in acute perioperative situations.
inhibitors. (Information is presented in
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.
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.
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.
(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.
pharmacologic intervention for cardiovascular
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.
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.
Hypotension accompanying an allergic reaction is
treated with epinephrine.
Drugs are administered according to advanced cardiac
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
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
4. Impaired renal function.
Pharmacologically increasing MAP could cause
vasoconstriction of renal vessels and could result
in deterioration of renal function if perfusion is
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
3. CI (CO/body surface area) of
4. Evidence of adequate end-organ perfusion.
Monitoring urine output can be unreliable after
diuretics have been administered.
Supernormal CO can reduce the risk of permanent
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.
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
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
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.
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.
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
with a rapid ventricular response can compromise the
heart's ability to deliver an adequate CO.
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
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
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
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.
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
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
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
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.
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.
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
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
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
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
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.
Manipulation of the carotid sinus can contribute to
postoperative hypertension, which is associated with
a higher risk of postoperative bleeding, stroke, and
can be effectively managed by the intravenous
administration of labetalol, nicardipine,
hydralazine, or, if severe, SNP.
Acute TBI with hypotension
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
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
2. Positive inotropic drugs or vasoconstrictors can
be used for rapid restoration of the MAP to an
acceptable level until intravascular volume is
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.
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.
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.
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.