Download hypotensive anesthesia

PRESENTED BY: Dr CHITTRA
MODERATED BY: Dr GIRISH
Concept of intentional induction of hypotension to
decrease blood loss was first proposed by Cushing in
1917
 Use of circulatory adjustments to achieve desirable
hemodynamic state in order to decrease blood loss
associated with surgery
 Controlled lowering of arterial blood pressure
 Light anesthesia
 Coughing, bucking, airway obstruction, PEEP, improper
positioning, fluid overload - ↑central venous pressure
 General vs regional
 Posture : parts above heart are perfused at lower pressures
 For every 1 inch of vertical height 2mmHg decrease in
pressure
 Head –up tilt favours arterial hypotension in upper parts
 Positioning of surgery above the heart improves
drainage of blood and local tissue flow
 Dec venous and capillary bleeding
 Maintain low intrapulmonary pressure during
controlled ventilation
 Tourniquiet application-pressure 100mm above
systolic… 1.30hrs max allowable time
 i.v. line and basic monitoring should be established
 Invasive BP monitoring is must
 After intubation controlled ventilation is preferred
 Hypotension is induced gradually by hypotensive drug
given at least 10 min before surgery commences
 Patient is then tilted to decrease arterial pressure
 Further decrease in arterial pressure can be obtained by
gradual increase in anesthestic conc
 Further dec will be done by hypotensive drugs
HALOTHANE:
 Dose dependent depression of myocardial contractility
 more pronounced myocardial depression in ischemic
myocardium
 Do not alter diastolic fxn
 decreases LV mechanical efficiency
 attenuates baroreceptor reflex responses
 Decreases in arterial pressure produced by halothane
are attributed to reductions in myocardial contractility
and cardiac output, there is no change in SVR
 It is a potent cerebral vasodilator
 Cerebral blood flow and volume are inc
 At more than 1 MAC obtunds cerebrovascular
vasoconstriction in response to hypocapnia
 Elective hypocapnia is used to dec cerebral blood
flow,ICP during neurosurgery. Hence CI in these
surgeries
ISOFLURANE:
 More rapid induction of hypotension, easy control
and prompt recovery
 Incerased HR, CO and Stroke volume are
maintained upto MAC×2
 Dec in SVR
 Direct acting myocardial depression also happens
but at MAC× 2.5
 In presence of moderate reduction of PaCo2 3035mmhgCMRO2 is decreased and cerebral blood
flow is unchanged despite decrease in cerebral
vascular resistance
 At more than 1 MAC vasodilatory effects become
prominent
 Reduction in CO or decrease in SVR
 Precapillary arterioles are major determinants of resistance
CLASSIFICATION:
GANGLIONIC BLOCKERS: pentolinium, trimethaphan
DIRECT ACTING VASODILATORS: SNP,NTG,Hydralazine ,
adenosine, PGE1
α- ADRENERGIC BLOCKING DRUGS: phentolamine,
urapidil,nicergoline
Β-ADRENERGIC BLOCKING DRUGS: propranolol,esmolol
α+β BLOCKING DRUGS: Labetalol
CALCIUM CHANNEL BLOCKERS: Verapamil, nifedipine
 Compete with Ach for nicotinic receptors on autonomic
postjunctional ganglionic membrane
 Overall effect of autonomic blockade depends on
predominance of one or other system
 Produces vasodilation, ↑ed venous capacitance and
hypotension
 Mainly acts through NO
 NO diffuses into vascular smooth muscle , stimulates c-
GMP ,causing vascular relaxation
 SNP and NTG provide exogenous NO
SODIUM NITROPRUSSIDE
NITROGLYCERINE
Onset of
action
Rapid onset, rapid recovery
Rapid , moderately slow recovery
Duration
Evanescent action
Short acting
Route
i.v. drip
i.v. drip
Mode of action Direct effect on both resistance
and capacitance vessels
Direct effect on capacitance
vessels mainly
Tachycardia
May occur in children
Very common
Cardiac output Unchanged,↑,↓,depending on
posture preload,afterload,other
depressant drugs
,
Metabolism
Cynaide and thiocyanate
Degraded rapidly
Stability
Available as powder,unstable
when reconstituted,protect from
light,use within 12 hrs
Stable,colorless,absorbed by
plastics,use high density
polyethylene drips
Dose
0.5-10µ/kg/min
0.5-10µ/kg/min
ICP
↑ in early stages
↑
Rebound HTN
Occurs in absence of β blockade
Does not occur
CYANIDE TOXICITY
 Molecular formula of SNP Na2{Fe(CN5)NO}×2H2O
 Cyanide released from SNP is transformed into nontoxic
products
 Disposal of free CNˉ through:
1. Conversion to cyanomethemoglobin: 1 of every 5 CNˉ ions
is converted
2. Binding to cytochrome oxidase: inhibiting oxidative
phosphorylation
3. Conversion to cyanocobalamin: in presence of adequate
hydroxocobalamin
4. Conversion to thiocyanate: catalyzed by enzyme
rhodenase
 Mechanism of cyanide toxicity is interference with
aerobic metabolism
 Free CNˉinhibits electron transport system
 Decreased oxygen utilisation, decreased CO2
production, increased production of anaerobic
metabolites
 Metabolic acidosis and deterioration of CNS and CVS
occurs
 HALLMARK of cytotoxic hypoxia is tissue hypoxia
with normal or elevated PaCO2
DETECTION OF CYANIDE TOXICITY:
 Impending CNˉ intoxication
a. Requirement for high doses of SNP >10µg/kg/min
b. Resistance apparent within 5-10 min after start of
infusion
c. Tachyphylaxis apparent 30-60/min after start of
infusion
 Severity of acidosis proportional to CNˉ level
 Lethal blood CNˉ level in humans is 500µg/dl
 Lethal blood thiocyanate level is 340µg/dl
 Increased requirements of SNP
 Metabolic acidosis
 Progressive hypotension with narrow pulse pressure
 Refractory hypotension unresponsive to vasopressors
and fluids ,responsive to thiosulfate
 CVS collapse
 Bright venous blood
 Increased SpO2 and PaO2
 Total projected dose should not exceed 1.5mg/kg for
short duration or 0.5mg/kg/hr for long duration
 Infusion rate should not exceed 10µ/kg/min
 Initial rate should be 0.5-1µ/kg/min
 Frequent arterial acid base determinations should be
done
 Antidote therapy should be available
 If high dose is needed other drugs should be added
 If still resistance is detected infusion should be
abandoned
 Sodium thiosulfate is DOC
 3 times more than CNˉ should be present
 Provides adequate supply of sulfhydryl radicals to form
thiocyanate from CN ˉ
 Bolus inj of 30mg/kg ,cont infusion of 60 mg/kg/h
 Hydroxycobalamin (vit B12) prevents inc in CNˉ conc
in RBC’s when given with SNP
 50mg/kg bolus,infusion 100mg/kg/h
 Acidosis correction and fluid replacement
 Endogenous vasodilator
 Acts on specific adenosine receptors located in several
vascular beds and on AV node
 Activation of adenylate cyclase and depression of action
potentials
 Selectively affects resistance vessels, with little effect on
venous capacitance
 Because of very short half-life (< 10 s), continuous
infusion (60–120 g/kg/min) is required for controlled
hypotension
 Hypotension is short lasting, not accompanied by rebound
hypertension when discontinued
 ↑ coronary blood flow ,↓ afterload
 Unfavorable changes in distribution of regional coronary
blood flow may led to myocardial ischemia in patients
with CAD
 Inhibits renin release and prevents activation of RAS
 Dilates cerebral vessels, ↑ ICP, impairs cerebral
autoregulation
 Direct arteriolar vasodilator
 ↓ SVR ,no change in CO ,reflex tachycardia
 ↑ ICP but no rebound HTN
 i.v. dose is 2.5 to 10 mg-effect begin within 10 to 20 minutes
and last 3 to 6 hours max dose 20 mg
 Parenteral administration of hydralazine is not advisable in
patients with coronary artery disease, patients with multiple
cardiovascular risk factors, or in older patients of possibility of
precipitation of myocardial ischemia due to reflex tachycardia
FENOLDOPAM
 Pure D1 antagonist with selective renal , mesentric, &
peripheral vasodilator action
 Maximal response in 10-20 min
 Cont infusion 0.1- 0.6µg/kg/min
 Potent vasodilator effect on pulmonary and systemic
vascular beds
 100-150ng/kg/min used to induce hypotension
 BP returns to 15% of normal 15min after infusion is
stopped
 ↑ in plasma renin activity
 Phentolamine produces transient nonselective α-
adrenergic blockade
 Administered intravenously, phentolamine produces
peripheral vasodilation and decrease in systemic blood
pressure that manifests within 2 minutes and lasts 10
to 15 minutes
 Decreases in blood pressure elicit baroreceptormediated increases in sympathetic nervous system
activity, manifesting as cardiac stimulation
 30 to 70 µg/kg IV
 Prevents ↑ in HR, CO, plasma renin activity,
catecholamine levels & blocks rebound HTN after
stoppage of SNP infusion
 Esmolol is more effective than SNP in producing better
operative conditions
 Rapid onset, short duration ,cardioselectivity
DRUG
DOSE
CARDIOSELEC
TIVITY
ELIMINATION
HALF- LIFE
PROPRANOL
OL
0.06mg/kg
0
4 hrs
Metoprolol
0.15mg/kg
+
3-4 hrs
Esmolol
Loading dose: 0.5
mg/kg/min,
0.3mg/kg/min infusion
+
10 min
Labetalol
0.2-0.4 mg/kg
0
3.5-4.5 hrs
LABETALOL
 α1 , β1 , β2 blocker& partial agonist at β2 receptor,
inhibition of neuronal uptake of norepinephrine
 Potency for β blockade is 1/5th to 1/10th of α blockade
 With inhalation agents ↓es BP by decreasing SVR with
either no change or ↓ HR & slight or no ↓ in CO
 Preferred when prolonged hypotension is required
 Absence of tachycardia, ↑ in CO ,rebound HTN , ICP
 bolus dose is 20 mg initially (over 2 min), followed by
20 to 80 mg every 10 minutes to total dose of 300 mg
 Infusion rate is 0.5 to 2 mg/min
 Verapamil and nicardipine decreases SVR
 Verapamil produces myocardial depression and delays AV
conduction- not recommended for induced hypotension
 Nicardipine vasodilates peripheral, coronary, cerebral
vessels while maintaining CO without tachycardia
 The peripheral vasodilation and resulting decrease in
systemic blood pressure produced by nifedipine activate
baroreceptors, leading to increased peripheral sympathetic
nervous system activity manifesting as increased heart rate
 This increased sympathetic nervous system activity
counters the direct negative inotropic, chronotropic, and
dromotropic effects of nifedipine.
 Use of inhalational anesthetics
 Avoid fluid overload
 Preop sedation and opioids
 Use of β blockers
 Adequate analgesia and muscle relaxation
 Pretreatment with ACE inhibitors
 Combining drugs/dexmedetomidine /clonidine
ONSET AND DEGREE OF HYPOTENSION:
 Hypotension should be induced slowly within 10-15
min
 BP should not be lowered to predetermined level
 Depends on age,condition, posture, surgical
requirement
 Very dry operative field and dark venous blood reqires
increase in BP
 Central venous oxygen tension below 30 mmHg
indicates tissue hypoxia
 Near normal PaCo2 should be maintained
 Hypocapnia decreases CO, coronary, cerebral and spinal
cord blood flows ,cause leftward shift of oxyhemoglobin
dissociation curve, inhibit HPV
 Increase in alveolar dead space is of significance only in
elderly patients or when both PEEP and head up tilt are
used
Increase in diff b/w alveolar and arterial oxygen tensions
{P (A-a)O2}
 Increased intrapulmonary shunt
 Blunting of HPV reflex is seen with inhalation
anesthetics and vasodilators
 More with SNP than with NTG
 Decrease in PVR and pulmonary artery pressure
,increased shunt fraction
 Decrease CO
 Increased extraction of oxygen by tissues
 Portion of blood with decreased mixed venous
oxygenation that passes through hypoventilated areas
have more dec in PaO2
 High FiO2 is recommended
 Compensates for venous admixture due to V-Q
imbalance
RELATIVE CONTRAINDICATIONS
 Inexperience
 Pregnancy
 Significant reduction in oxygen delivery
 Renal,cerebral or CAD
 Children with cardiac shunts
 Patients with sickle cell disease
 Uncorrected polycythemia
 Ganglionic blocking drugs in patients with narrow
angle glaucoma
 Cardiac arrest and hypotension
 Temporary or permanent neurologic deficits
 Reactionary hrg
 Failure of technique