Deliberate Hypotension Flashcards
deliberate hypotension is
controlled, induced, elective
deliberate hypotension is a reduction of systolic BP to
80-90 mmHg
deliberate hypotension is a decrease in MAO to
50-65 mmHg in normotensive patients
deliberate hypotension is a __ reduction in MAP
30%
benefits of deliberate hypotension
- reduced blood loss
- facilitation of surgical dissection
- reduction of oozing beneath skin flaps
- prevention of aneurysmal rupture (intracranial, aortic)
- reduction in intravascular tension (coarctation of the aorta)
benefits of deliberate hypotension- reduced blood loss
- conserve blood supply
- avoidance of transfusion reactions
- decreased transmission of blood-borne disease
benefits of deliberate hypotension- facilitation of surgical dissection
- microscopic surgical (ENT, intracranial AV malformation)
- identification of malignant versus nonmalignant tissue, vital structures
- reduction of amount of cauterized tissue, debris and wound infection
- reduction in operative time
benefit of deliberate hypotension- reduction of oozing beneath skin flaps
better plastics outcome, improved wound healing
indications for deliberate hypotension
- neurosurgery- cerebrovascular
- large orthopedic procedures- total hip arthroplasty, spinal fusions
- surgery on large tumors- pelvic
- surgery on the head and neck- maxilla-facial, middle ear
- plastic surgery
- patient in whom transfusion is undesirable
deliberate hypotension contraindications- improved drugs and monitoring have allowed patients who previously would have been excluded __
eligible for DH
deliberate hypotension contraindications- relative
H/) cerebrovascular disease, renal dysfunction, liver dysfunction, severe peripheral claudication, myocardial infarction or angina
deliberate hypotension contraindications- __volmeia
hypo
deliberate hypotension contraindications- __ anemia
severe
deliberate hypotension contraindications- untreated
hypertension- increased risk of death and morbidity during DH (treatment of HTN returns cerebral autoregulation toward normal- DH safe for medically-controlled HTN)
influences of bleeding perioperatively-
- arterial
- capillary
- venous
influences of bleeding perioperatively- arterial
related to MAP; abolished by tourniquet, reduced by decreased MAP, HR
influences of bleeding perioperatively- capillary
dependent on local flow in the capillary bed- reduced be decreased BP and local vasoconstriction (infiltration)
influences of bleeding perioperatively- venous
related to venous return, venous tone and dependent on posture- abolished by spinal or epidural and direct acting vasodilators
methods to achieve hypotension- body positioning
operative side above the level of the heart (for each 2.5 cm of vertical height above the heart, the local material pressure is reduced by 2mmHg)
aiding the venous pooling in vasodilator capacitance vessels; head-up position
methods to achieve hypotension- PPV
decreased venous return, and thus CO
methods to achieve hypotension- PEEP
decreased venous return
methods to achieve hypotension- __ SV and HR
decreased
methods to achieve hypotension- tourniquets, monitor duration
60 min upper limb and 90 min for lower limb, ischemia can occur in less time than this
methods to achieve hypotension- tourniquets, monitor pressure
250mmHg in arm; 300mmHg in leg
methods to achieve hypotension- don’t use tourniquet on
sickle cell patients
methods to achieve hypotension- local infiltration with epi
local vasoconstriction; concentration 1:200,00 to 1:400,000
methods to achieve hypotension- pharmacologic
- volatile anesthetic agents
- sympathetic ganglionic blockers
- alpha-adrenergic blockers
- beta-adrenergic blockers
- vasodilators
- spinal and epidural anesthesia
isoflurane- minimal effect on
myocardial contractility at low concentrations
isoflurane- __ effect is readily adjusted
vasodilation
isoflurane- great for
moderate reduction in BP
isoflurane- less of an effect
on ICP than halothane
isoflurane- depresses
cerebral metabolism (CMRO2)
isoflurane- minimizes
reflex vasoconstriction or tachycardia (CNS depressant)
CO- inhaled agent
maintained
CO- IV agent (sodium nitroprusside)
maintained
tachycardia- inhaled agent
rare
tachycardia- IV agent (sodium nitroprusside)
frequent
pulmonary shunting- inhaled agent
unchanged
pulmonary shunting- IV agent (sodium nitroprusside)
increased
cerebral blood flow- inhaled agent
maintained
cerebral blood flow- IV agent (sodium nitroprusside)
maintained
cerebral metabolism- inhaled agent
decreased
cerebral metabolism- IV agent (sodium nitroprusside)
unchanged
cerebrovascular CO2 reactivity- inhaled agent
preserved
cerebrovascular CO2 reactivity- IV agent (sodium nitroprusside)
impaired
monitoring of EEG and SSEP- inhaled agent
may not be possible
monitoring of EEG and SSEp- IV agent (sodium nitroprusside)
no interference
hepatic blood flow- inhaled agent
maintained
hepatic blood flow- IV agent (sodium nitroprusside)
maintained
prolonged recovery- inhaled agent
possible, dose and duration-related
prolonged recovery- IV agent (sodium nitroprusside)
none
effective- inhaled agent
yes
effective- IV agent (sodium nitroprusside)
yes
administration- inhaled agent
simple
administration- IV agent (sodium nitroprusside)
requires infusion pump and setting up solution
control- inhaled agent
easy
control- IV agent (sodium nitroprusside)
variable, may be unstable if patient response not carefully gauged
fine tune- inhaled agent
imprecise
fine tune- IV agent (sodium nitroprusside)
more precise
onset time- inhaled agent
4-5 min
onset time- IV agent (sodium nitroprusside)
variable (1-5 min); quick onset at the expense of possible overshoot
recovery time- inhaled agent
5-7 time
recovery time- IV agent (sodium nitroprusside)
very short, 1-2 min
rebound HTN- inhaled agent
none
rebound HTN- IV agent (sodium nitroprusside)
yes, can be treated effectively with beta-blockers
toxic metabolics- inhaled agent
none
toxic metabolics- IV agent (sodium nitroprusside)
rarely cyanide and thiocyanate toxicity
tachyphylaxis- inhaled agent
rare
tachyphylaxis- IV agent (sodium nitroprusside)
rare
sevoflurane- shown to minimize
the HR fluctuation that occur with use of nitroglycerin, nicardipine, or alprostadil (PGE) to achieve hypotension (decreased sympathetic activity; study looked at combination with nitrous oxide)
sympathetic ganglionic blocker- trimethaphan (Arfonad)- interruption of
sympathetic outflow, vasodilation
sympathetic ganglionic blocker- trimethaphan (Arfonad)- causes
urinary retention, mydriasis (mistaken for cerebral ischemia), tachycardia due to parasympathetic block (bleeding), tachyphylaxis
clonidine, dexmedetomidine- pretreatment with clonidine po reduced
the required infusion of PGE 1 needed to maintain DH and reduces the blood loss by 45%
clonidine, dexmedetomidine- use of dexmedetomidine combined with remifentamil
to provide controlled hypotension during posterior spinal fusion
alpha adrenergic blockers- phentolamine (Regitine), droperidol-
vasodilation, increased HR and myocardial oxygen demand due to beta stimulation
beta adrenergic blockers- propranolol, atenolol, esmolol, (labetalol): big advantage is
decreased HR and CO
beta adrenergic blockers- propranolol, atenolol, esmolol, (labetalol): used along with
vasodilators
beta adrenergic blockers- propranolol, atenolol, esmolol, (labetalol): prevents
wide variations in BP (vasospasm re: SAH)
beta adrenergic blockers- propranolol, atenolol, esmolol, (labetalol): labetalol is
not as potent, no increase in ICP
beta adrenergic blockers- propranolol, atenolol, esmolol, (labetalol): labetalol maskes
the adrenergic response to acute blood loss (long duration lasts in postop period)
beta adrenergic blockers- propranolol, atenolol, esmolol, (labetalol): propranolol pretreatment reduced
the dose of SNP and the rebound HTN upon discontinuation
beta adrenergic blockers- propranolol, atenolol, esmolol, (labetalol): esmolol reduced
plasma renin activity- improved stability; greater reduction in CO
sodium nitroprusside-
“dial-a-pressure”
sodium nitroprusside- good for
short procedures
sodium nitroprusside- caution
increased ICP
sodium nitroprusside- cyanide toxicity, monitor
acid/base balance
sodium nitroprusside- no adverse effect on
myocardial contractility
sodium nitroprusside- pretreat with
propranolol or captopril to reduce dose of SNP and avoid rebound HTN (or enalapril 2.5mg 60 min p)
nitroglycerin- less dramatic
decrease in BP
nitroglycerin- decreases __ more rapidly than _
systolic BP
diastolic (maintains flow)
nitroglycerin- less rapid
recovery
nitroglycerin- coronary artery perfusion __
better
nitroglycerin- __ in some patients
less effective
nitroglycerin- __ in ICP- caution
increase
nitroglycerin- 3-in NTG transdermal: reduced blood loss by
almost 50% and reduced the need for transfusion of patients having ORIF of femora fractures; “induction of moderate hypotension”
spinal and epidural anesthesia- vasodilation of
both arterial and venous due to sympathectomy
spinal and epidural anesthesia- if T1-T4 are blocked,
tachycardia is prevented
spinal and epidural anesthesia- used in __ surgery
lower abdominal and pelvic; pelvic venous plexuses
spinal and epidural anesthesia- if epinephrine is added to the local, the ___ might be counteracted
hypotensive effect of the block
hypotension- organ function- it might be best to reduce BP by
decreasing SVR rather than CO so blood flow to tissues can be maintained
hypotension- organ function- __ and __ are the principle hazards of deliberate hypotension
ischemia of the brain and myocardium
hypotension- organ function- CNS: principle of __ is key
autoregulation
hypotension- organ function- CNS: “safe” lower limit is __ in normotensive patients because that is the lowest pressure at which autoregulation of CBF is maintained
50-55 mmHg
hypotension- organ function- CNS: during normotension, CNF changes linearly with __ when __; when the MAP fall below 50mmHg, CBF __
PaCO2 when PaCO2 is 20-70mmHg
no longer responds to changes in PaCO2
hypotension- organ function- heart:
maintain balance between myocardial oxygen supply and demand
hypotension- organ function- heart: AVOID
tachycardia, myocardial depression, coronary artery perfusion alteration
hypotension- organ function- lungs: increased PaCO2 due to
increased dead space; must maintain CO with fluid replacement
hypotension- organ function- lungs: decreased PaO2 due to
increased shunt (seen with use of Nipride, but not with iso; seen with normal lungs, but not with COPD**)
hypotension- organ function- lungs: necessitates
controlled ventilation, increased oxygenation
hypotension- organ function- kidneys: GFR is reduced with
MAP falls below 75 mmHg
hypotension- organ function- kidneys: metabolic needs of kidneys still met but
oliguria occurs
hypotension- organ function- kidneys: normovolemia patients
have rapid recovery of urine production when hypotension is discontinued (strict maintenance of urine output during deliberate hypotension is not necessary)
hypotension- organ function-kidneys: renal function was better preserved with
combination of iso and labetalol than with higher concentrations of iso alone
hypotension- organ function- splanchnic circulation: liver perfusion is altered due to
limited autoregulation for the hepatic artery and no autoregulation for the portal venous circulation
hypotension- organ function- splanchnic circulation: increased sympathetic outflow (baroreceptor mediated in response to decrease BP) causes
splanchnic vasoconstriction and decreased blood flow to the liver and the intestine
hypotension- organ function- eye: decreased blood flow to the eyes causes
blurring of vision and rarely blindness
hypotension- organ function- eye: position carefully to avoid
increased intraocular pressure which would oppose blood flow even further (external pressure; venous congestion- neutral position)
hypotension- organ function- eye: maintain
Hgb
hypotension- organ function- eye: colloid versus crystalloid
minimize edema
monitoring: ECG
signs of inadequate myocardial perfusion like ST depression and ectopic beats
monitoring: pulse ox
signs of decreased oxygenation and peripheral perfusion
monitoring: temp
body heat lost more rapidly from vasodilation
monitoring: art line
beat to beat measurement of BP (allows sampling of ABGs, place transducer at level of internal carotid)
monitoring: EtCO2
not complete accurate due to increased dead space, decreased CO, and changes in body metabolism
monitoring: EtCO2 sudden decrease may indicate
pulmonary embolism
monitoring: EtCO2 use as guide to
avoid hyperventilation which would further decrease CBF
monitoring: central venous line
fluid replacement and monitor CVP
monitoring: UOP
especially long cases
monitoring: other options
evoked potentials, EEG, serum electrolytes, ABGs, Hct
complications- __ is not different from that of all anesthetics
mortality
complications- nonfatal complications
- CNS related- dizziness, prolonged awakening, cerebral artery thrombosis
- retinal thrombosis
- anuria, oliguria
- postop bleeding
complications- __ hypotension
inadequate; use second agent
complications- __ hypotension
excessive
type of DH
- slow onset, sustained moderate hypotension with slow return to normal (plastic, maxilla-facial, ear, nose, throat)
- moderate sustained hypotension with reduced HR (when massive blood loss is anticipated)
- profound hypotension with short periods of excessively small pressures (clipping cerebral aneurysm)
background anesthesia of DH
- balanced anesthesia
- omit atropine
- use generous sedation or analgesia
- NMB
- during hypotension, increase FiO2
- continue in PACU- avoid CO2 retention, hypoxia, use patient’s position
don’t reduce the systolic BP during the operation to less than
preop DBP
avoid the severe head-up tilt unless
arterial pressure is being measured at the level of the Circle of Willis