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