hypotensive anesthesia
DESCRIPTION
HYPOTENSIVE ANESTHESIA. PRESENTED BY: Dr CHITTRA MODERATED BY: Dr GIRISH. WHAT IS INDUCED HYPOTENSION??. Concept of intentional induction of hypotension to decrease blood loss was first proposed by Cushing in 1917 - PowerPoint PPT PresentationTRANSCRIPT
PRESENTED BY: Dr CHITTRAMODERATED BY: Dr GIRISH
HYPOTENSIVE ANESTHESIA
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
WHAT IS INDUCED HYPOTENSION??
Light anesthesiaCoughing, bucking, airway obstruction, PEEP, improper
positioning, fluid overload - ↑central venous pressureGeneral vs regional Posture : parts above heart are perfused at lower pressuresFor every 1 inch of vertical height 2mmHg decrease in
pressureHead –up tilt favours arterial hypotension in upper parts
FACTORS AFFECTING BLOOD LOSS
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 ventilationTourniquiet application-pressure 100mm
above systolic… 1.30hrs max allowable time
PHYSIOLOGICAL METHOD OF CONTROLLED HYPOTENSION
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
TECHNIQUES OF CONTROLLED HYPOTENSION
HALOTHANE:Dose dependent depression of myocardial
contractilitymore pronounced myocardial depression in
ischemic myocardiumDo not alter diastolic fxndecreases LV mechanical efficiencyattenuates baroreceptor reflex responsesDecreases in arterial pressure produced by
halothane are attributed to reductions in myocardial contractility and cardiac output, there is no change in SVR
INHALATION AGENTS
It is a potent cerebral vasodilatorCerebral blood flow and volume are incAt more than 1 MAC obtunds cerebrovascular
vasoconstriction in response to hypocapniaElective 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 recoveryIncerased HR, CO and Stroke volume are
maintained upto MAC×2Dec in SVRDirect acting myocardial depression also happens
but at MAC× 2.5In presence of moderate reduction of PaCo2 30-
35mmhgCMRO2 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, trimethaphanDIRECT ACTING VASODILATORS: SNP,NTG,Hydralazine ,
adenosine, PGE1α- ADRENERGIC BLOCKING DRUGS: phentolamine,
urapidil,nicergolineΒ-ADRENERGIC BLOCKING DRUGS: propranolol,esmolol α+β BLOCKING DRUGS: LabetalolCALCIUM CHANNEL BLOCKERS: Verapamil, nifedipine
HYPOTENSIVE DRUGS
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
GANGLIONIC BLOCKING DRUGS
Mainly acts through NONO diffuses into vascular smooth muscle , stimulates c-
GMP ,causing vascular relaxationSNP and NTG provide exogenous NO
DIRECT- ACTING VASODILATOR DRUGS
SODIUM NITROPRUSSIDE
NITROGLYCERINE
Onset of action
Rapid onset, rapid recovery Rapid , moderately slow recovery
Duration Evanescent action Short actingRoute i.v. drip i.v. dripMode of action
Direct effect on both resistance and capacitance vessels
Direct effect on capacitance vessels mainly
Tachycardia Very common May occur in children
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 converted2. Binding to cytochrome oxidase: inhibiting oxidative
phosphorylation3. Conversion to cyanocobalamin: in presence of
adequate hydroxocobalamin4. Conversion to thiocyanate: catalyzed by enzyme
rhodenase
SODIUM NITROPRUSSIDE
Mechanism of cyanide toxicity is interference with aerobic metabolism
Free CNˉinhibits electron transport systemDecreased 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 intoxicationa. Requirement for high doses of SNP
>10µg/kg/minb. Resistance apparent within 5-10 min after
start of infusionc. 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 SNPMetabolic acidosisProgressive hypotension with narrow pulse
pressureRefractory hypotension unresponsive to
vasopressors and fluids ,responsive to thiosulfate
CVS collapseBright venous blood Increased SpO2 and PaO2
CLINICAL FEATURES OF CYANIDE TOXICITY
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 doneAntidote therapy should be available If high dose is needed other drugs should be
added If still resistance is detected infusion should be
abandoned
PREVENTION OF CYANIDE TOXICITY
Sodium thiosulfate is DOC3 times more than CNˉ should be presentProvides adequate supply of sulfhydryl
radicals to form thiocyanate from CN ˉBolus inj of 30mg/kg ,cont infusion of 60
mg/kg/hHydroxycobalamin (vit B12) prevents inc in
CNˉ conc in RBC’s when given with SNP50mg/kg bolus,infusion 100mg/kg/hAcidosis correction and fluid replacement
TREATMENT OF CYANIDE TOXICITY
Endogenous vasodilatorActs on specific adenosine receptors located in several
vascular beds and on AV nodeActivation of adenylate cyclase and depression of action
potentialsSelectively affects resistance vessels, with little effect on
venous capacitanceBecause 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
ADENOSINE
↑ coronary blood flow ,↓ afterloadUnfavorable changes in distribution of regional coronary
blood flow may led to myocardial ischemia in patients with CAD
Inhibits renin release and prevents activation of RASDilates 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
HYDRALAZINE
Potent vasodilator effect on pulmonary and systemic vascular beds
100-150ng/kg/min used to induce hypotensionBP returns to 15% of normal 15min after infusion is
stopped ↑ in plasma renin activity
PROSTAGLANDIN E1
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 baroreceptor-mediated increases in sympathetic nervous system activity, manifesting as cardiac stimulation
30 to 70 µg/kg IV
PHENTOLAMINE
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
β-ADRENERGIC BLOCKING DRUGS
DRUG DOSE CARDIOSELECTIVITY
ELIMINATION HALF- LIFE
PROPRANOLOL
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
LABETALOLα1 , β1 , β2 blocker& partial agonist at β2 receptor,
inhibition of neuronal uptake of norepinephrinePotency for β blockade is 1/5th to 1/10th of α blockadeWith inhalation agents ↓es BP by decreasing SVR with
either no change or ↓ HR & slight or no ↓ in COPreferred when prolonged hypotension is requiredAbsence of tachycardia, ↑ in CO ,rebound HTN , ICPbolus 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
α+β BLOCKERS
Verapamil and nicardipine decreases SVRVerapamil produces myocardial depression and delays AV
conduction- not recommended for induced hypotensionNicardipine vasodilates peripheral, coronary, cerebral vessels
while maintaining CO without tachycardiaThe 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.
CALCIUM CHANNEL BLOCKERS
Use of inhalational anestheticsAvoid fluid overloadPreop sedation and opioidsUse of β blockersAdequate analgesia and muscle relaxationPretreatment with ACE inhibitorsCombining drugs/dexmedetomidine /clonidine
TECHNIQUES TO PREVENT TACHYPHYLAXIS
ONSET AND DEGREE OF HYPOTENSION:Hypotension should be induced slowly within
10-15 min BP should not be lowered to predetermined
levelDepends on age,condition, posture, surgical
requirementVery dry operative field and dark venous
blood reqires increase in BPCentral venous oxygen tension below 30
mmHg indicates tissue hypoxia
SAFETY FACTORS
Near normal PaCo2 should be maintainedHypocapnia 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
MAINTENANCE OF NORMAL ACID- BASE BALANCE
Increase in diff b/w alveolar and arterial oxygen tensions {P (A-a)O2}
Increased intrapulmonary shuntBlunting of HPV reflex is seen with inhalation
anesthetics and vasodilatorsMore with SNP than with NTGDecrease in PVR and pulmonary artery
pressure ,increased shunt fraction
OXYGENATION
Decrease COIncreased extraction of oxygen by tissuesPortion of blood with decreased mixed venous
oxygenation that passes through hypoventilated areas have more dec in PaO2
High FiO2 is recommendedCompensates for venous admixture due to V-
Q imbalance
RELATIVE CONTRAINDICATIONS InexperiencePregnancySignificant reduction in oxygen deliveryRenal,cerebral or CADChildren with cardiac shuntsPatients with sickle cell diseaseUncorrected polycythemiaGanglionic blocking drugs in patients with
narrow angle glaucoma
CONTRAINDICATIONS
Cardiac arrest and hypotensionTemporary or permanent neurologic deficitsReactionary hrgFailure of technique
COMPLICATIONS OF INDUCED HYPOTENSION
THANKS