CONTROLLED HYPOTENSION

Moderator: Dr V. Y. Srinivas
Presenter: Dr. Ann Susan Mathew
 HISTORY
• The concept of intentionally decreasing arterial
blood pressure to hypotensive levels was first
proposed by Cushing in 1917 and was introduced
into clinical practice by Gardner in 1946
• Gained popularity in Britian after Griffith and Gillies
advocated “hypotensive spinal technique in 1948”.
• Enderby, in 1950, introduced ganglion blockade
using pentamethonium to decrease arterial blood
pressure.
 Pharmacological techniques
Spinal and Volatile Directly acting
Epidural Anaesthetic vasodilating
Anaesthesia Agents drugs

Autonomic
Alpha adrenergic Beta adrenergic
ganglion
receptor blockers receptor blockers
blocking drugs

Combined alpha
and beta
blockers
CCBs PGE1
 Spinal and epidural anaesthesia
• Pharmacologic sympathectomy with LA is a effective
way of inducing hypotension.
• Epidural/spinal anaesthesia produce arteriolar and
venous dilation and hypotension.
• These effects are enhanced by pooling of blood in the
venous system  decreases venous return  reduces
CO.
• If block is extended to mid-thoracic , innervation of
heart is also affected thereby preventing
compensatory tachycardia.
• The unpredictable degree of hypotension and
the necessity for large infusions of fluids are
principal drawbacks of these techniques.
• It was recently demonstrated that if
hemodynamic stability is maintained by IV
infsuion of low dose epinephrine (1-
5mcg/min), this technique can be used safely.
 Inhalational agents
• Clearly one can decrease MAP by increasing
the inspired concentration of inhaled
anaesthetic.
 CVS effects
• Hypotension after halothane results primarily
from myocardial depression that produces a
dose dependant decrease in arterial BP, CO
and SV plus a dose dependant increase in right
heart filling pressure.
• SVR does not decrease significantly as skeletal
muscle tone increases. Also renal vascular
resistance increases
• The intravascular volume status of the patient before
induction of hypotension affects the degree of reduction
in cardiac output during isoflurane anaesthesia.
• In healthy young people 2-3% Iso decreases MAP by
decreasing SVR.
• In older or chronically hypertensive patients, similar
concentration may also decrease cardiac output. Hence
in such patients it is more prudent to use a moderate
concentration of Iso along with agents that tend to
maintain CO than using high concentrations of Iso alone
 Cerebrovascular effects
• Halothane decreases cerebral vascular
resistance and increases CBF in a
concentration related manner, provided auto-
regulatory limits are not exceeded. Cerebral
autoregulation is lost when concentration of
halothane increases.
• Enflurane increases ICP by increasing the
normal production of CSF.
• It also induces seizure activity in some
patients especially during hypocapnia.
• Administration of low concentration of Iso
produces controllable decrease in MAP and
concentration related depression of cerebral
metabolism while preserving physiological
relationships b/w flow and pressure and b/w
flow and metabolism.
• With higher concentrations, the direct
vasodilatory effects predominate, CBF
increases and autoregulation is impaired.
• In the presence of cerebral vasodilation,
cerebral edema is more likely to occur if
systemic blood pressure is allowed to
increase.
• Therefore the possibility of secondary
neurologic injury exists
• Volatile anesthetics should not be used as sole agent
but only as an adjuvant to induce hypotension in
patients with intracranial disease because the high
concentrations required can worsen the edema.
• Such a technique can also increase ICP before dura is
opened and may affect autoregulation.
• The combination of increased ICP and decreased
MAP can reduce CPP to less than 40mm Hg and can
induce brain ischemia.
• Sevo and desflurane appear to be superior to
iso when used as an agent to faciltate
deliberate hypotension.
 Sodium Nitroprusside
• Vasodilating drug most commonly used to induce
hypotension during surgery.
• Onset is rapid, has short duration and is readily
controllable.
• Acts primarily on arteriolar tone
• Fluid balance is an important determinant of
cardiovascular response to sodium nitroprusside.
It decreases CO during hypovolemia and not
during normovolemia.
• Because the intact drug contains 5 cyanide
groups, toxicity is a concern.
• Cyanide diffuses rapidly into the tissue where
it binds with high affinity to cytochrome
oxidase. Such binding causes interference with
electron transport and produces tissue
hypoxia
• Also tachyphylaxis is a concern.
 Nitroglycerin
• Directly dilates venous capacitance vessels.
• Has a short half life and no clinically significant
toxic metabolites.
• Result depends on volume status of the patient.
Cardiac output may decrease if preload is
compromised.
• Although both resistance and capacitance vessels
are dilated, NTG has its major effect on the latter.
• However the effect of reduced preload would be
offset by an increased HR and myocardial
contractility due to an increased sympathetic activity
illicted by baroreceptor reflex.
• The baroreceptor reflex mechanism would also
counteract the decrease in SVR resulting in a biphasic
response.
• Because adrenergic response will be partially blocked
by anesthesia, CVS effects of NTG will be different in
anaesthetized patients.
• Acute termination of NTG produces prolonged
period of vasodilation.
• As with sodium nitroprusside, low intracranial
compliance contradicts use of NTG.
 Hydralazine
• Smooth muscle relaxant.
• Significantly reduces SVR without changing
CO, pH or venous admixture.
• Rebound hypertension does not occur and ICP
increases significantly.
 Purine derivatives
• Adenosine, derived from ATP
• Hypotension occurs rapidly owing to marked
dilation of resistance vessels.
• Recovery is more rapid and no rebound
hypertesnion occurs.
• Dilates cerebral vessels and increases CBF,
increase ICP when intracranial compliance is
low and impair cerebral autoregulation
• Adenosine is a potent coronary vasodilator that can
produce an unfavorable redistribution of coronary
blood flow leading to ischemia.
• Administration through central line advocated as partial
breakdown can occur before it reaches the arteriolar
smooth muscle vasculature . Hence drug requirements
are 40% higher. It can be decreased by adding
dipryridamole which inhibits adenosine uptake into cell.
• Adenosine also has disadvantage of causing heart block
 Trimethaphan
• Ganglion blockade has long been the mainstay of inducing
deliberate hypotension
• Hypotension results from occupation of receptor sites and
stabilisation of post-synaptic membrane, both of which
will block neural transmission through autonomic ganglia.
• Lacks sensitivity and hence both parasympathetic and
sympathetic activity depressed
• Parasympathetic depression- tachycardia, mydriasis,
cycloplegia, reduced GI tone and motility and urinary
retention.
• Has a short half life (1-2 min) owing to rapid
inactivation by plasma cholinesterase.
• Causes histamine release, bronchospasm,
tachyphylaxis and potentiation of Sch induced
myoneural blockade.
• Generally does not affect cerebral circulation.
 phentolamine
• Decreases MAP by blockade of alpha
adrenergic receptors within 2 min of IV
administration.
• Does not affect cerebral circulation
significantly.
 Esmolol
• Short acting cardioselective IV beta blocker
having a very rapid onset of action.
• In contrast to sodium nitroprusside plasma
renin activity was slightly decreased which
improved the stability of hypotension.
• Because of its potential for marked myocardial
depression, it seems prudent to combine
esmolol with other drugs or used it when only
modest reduction in BP is required.l
 labetolol
• Produces hypotension by blocking alpha nd beta blockers .
• Decreases cardiac output and SVR
• Peak effect occurs within 5 min and has a relatively long (4
hours) half life compared to sodium nitroprusside or NTG.
• An important advantage of labetolol is the absence of any
increase in ICP even when intracranial compliance is low.
• Labetolol masks the adrenergic response to acute blood
loss and because of its relatively long half life, this effect
lasts through early post-op period.
 nicardipine
• Calcium channel blocker that dilates
peripheral, coronary and cerebral vessels
while maintaining myocardial contractility and
cardiac output without tachycardia.
• Careful titration of nicardipine infusion (10-
250mcg/kg/hr) is mandatory as nicardipine
induced hypotension resists conventional
treatment such as phenylephrine.
 PGE1
• Naturally occuring substance that has been
evaluated as apossible hypotensivedrug
• It appears to be a mildly hypotensive agent
that may not be able to produce profound
hypotension in all patients.
Effect of hypotension on organ function
• Deliberate hypotension decreases arterial BP by
decreasing CO or SVR or both. However a
reduction in CO may not be be the most
appropriate method because keeping CO stable
is crucial for maintaining blood flow to tissues.
• CO should remain suuficiently high not only to
provide adeqaute oxygen and energy susbstrates
but also to remove metabolic wasts before their
accumulation causes tissue damage.
• Because deliberate hypotension is clearly
designed to decrease arterial BP but still
preserve organ blood flow and function, it
must be emphasised that decreasing BP by
haemorrhage also decreases organ blood flow.
• The use of deliberate hypotension requires
constant assesmentof intravascular fluid
volume throughout surgery, to ensure optimal
organ function
 CNS effects
• Because ischemia of the brain and myocardium
are the principal hazards of deliberate
hypotension, the effects of arterial hypotension
on cerebral circulation are particularly important.
• The current rationale for setting the “safe” lower
limit for MAP at 50 to 55 mmHg in normothermic
patients is based on the belief that this range
represents the lowest MAPat which
autoregulation of CBF is still in force.
• For chronically hypertensive patients the
curve for autoregulation shiftsto the right, that
is, the lowest BP at which autoregulation of
CBF is still in force is higher than for
normotensive patients.
• With effective hypertensive therapy, however,
the curve for autoregulation moves back to its
normal position.
• The factor most important to cerebral autoregulation is
CPP and not BP as such.
• CPP= MAP- ICP
• An important consequence is that patients with
increased ICP should never undergo deliberate
hypotension before dura is opened unless measurement
of ICP is available before surgical procedure.
• Autoregulation may be absent in the tissue surrounding
brain tumor in the acute phase of a SAH and after brain
trauma.
• PaCO2 is an important consideration during
deliberate hypotension. During normotension,
CBF changes linearly with paCO2 b/w 20-70 mm
Hg. An increase in 1mm Hg in paCO2 produces a
2.65% increase in CBF. However when a
progressive degree of hypotension is induced,
this relationship becomes progressively flatter
so that when MAP falls below 50 mm Hg, CBF
no longer responds to changes in paCO2.
 Effects on heart
• During deliberate hypotension, maintenance of
oxygen supply sufficient for metabolic needs of
myocardium is of importanc.
• The intact coronary circulation undergoes a high
degree of pressure-flow autoregulation that is mildly
dirupted by volatile anaesthetic agents.
• However, progressive systemic hypotension gradually
depletes coronary vasodilatory reserve and diminishes
ability of heart to cope with stresses that increase
myocardial oxygen demand.
• Arterial hypotension obtained with direct vasodilating drugs
such as sodium nitroprusside and with CCBs frequently
incurs reflex tachycardia.
• In addition to increasing oxygen demand, tachycardia
decreases diastolic filling time and may thus reduce
myocardial perfusion.
• Many drugs have been used to decrease tachycardia. The
cardioselective Beta 1 receptor antagonist, Esmolol,
decreases HR but also supresses myocardium.
• Labetolol and Urapidil don’t incur reflex tachycardia.
• Adenosine directly depresses sinus node.
• A a general rule, patients with known or
suspected IHD should not undergo deliberate
hypotension unless appropriate monitoring is
used.
 Effect on lungs
• With sodium nitoprusside, arterial
oxygenation decreases, shunt fraction
increases and dead space too if CO decreases.
• Because of changes in oxygenation and
possibly CO2 elimination, controlled
ventilation is preffered.
 Effect on kidneys
• RBF= 20-25% CO
• Renal circulation is characterised by a well
functioningautoregulatory mechanism.
• Reanl arterioles have low resting vascular tone and hence
limited ability to dilate further in response to hypotension.
• GFR is maintained until MAP falls below 75 mm Hg. At this
level, perfusion is sufficient to meetthe metabolic needs of
kidney cells.
• Because renal dysfunction is not a frequent complication of
deliberate hypotension, short periods of decreased RBF are
apparently not detrimental.
 Effects on splanchnic circulation
• Because pressure-flow autoregulation is
limited in the hepatic arterial bed and
probably absent in the portal venous
circulation, profound changes in liver perfusion
may occur during deliberate hypotension.
• Increased sympathetic nervous outflow
following baroreceptor stimulation induces
splanchnic vasoconstriction.
 Effect on eye
• IOP decreases as arterial BP decreases.
• Eye has 2 separate systems of blood vessels- uveal and
retinal.
• Uveal vessels are peculiar in possesing both pre-
capillary sphincters and hence having a steady blood
flow.
• Because uveal system carries most of the blood
supplying the eye, sudden decreases in MAP are
transmitted to the eye as decrease in IOP manifesting
as blurring of vision.
 monitoring
• Beat to beat measurement of arterial BP is mandatory for patients
underoing clinically significant decrease in BP. The usual practice iis to
insert an arterial for the continuous montoring of BP. The catheter
also allows for intermittent sampling of blood for blood gas analysis.
• ECG monitoring essential to detect signs of inadequate myocardial
perfusion (ectopics, ST segment changes)
• EtCO2- a sudden decrease would indicate sudden decrease in CO ( as
in pulmonary embolism) or by disconnection of breathing system.
• Capnography may help to avoid hyperventilation which could be
harmful as decrease in paCO2 would further decrease CBF.
• Pulse oximetry and temperature monitoring as body heat is lost more
rapidly due to peripheral vasodilation.
 complications
• Usually related to CNS such as dizziness,
prolonged awakening and cerebral
thrombosis.
• Other potential complications include anuria
and oliguria.
 summary
• Deliberate hypotension is effective in decreasing
blood loss and providing better visibilty in the
surgical field.
• Many drugs and techniques have been successful in
lowering arterial BP. The mechanism of action of
these drugs differ and produce complex changes in
reflexes and subsequently blood flow to various
organs. Because deliberate hypotension is not
without risk, the advantages and disadvantages
must be considered.
• For the healthy young patient, complications are rare.
• The elderly and those with underlying organ
dysfunction are probably at higher risk.
• Therefore the anaesthesiologist must assess each
patient carefully so that the decision to use deliberate
hypotension is based on reason.
• The intelligent use of deliberate hypotension has
distinct advantages for certain procedures and may
promote surgical success.