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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