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HYPOTENSIVE ANESTHESIA

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

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HYPOTENSIVE ANESTHESIA

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  1. HYPOTENSIVE ANESTHESIA PRESENTED BY: Dr CHITTRA MODERATED BY: Dr GIRISH

  2. WHAT IS INDUCED HYPOTENSION?? 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

  3. FACTORS AFFECTING BLOOD LOSS • 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

  4. PHYSIOLOGICAL METHOD OF CONTROLLED HYPOTENSION • 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

  5. TECHNIQUES 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 anesthesticconc • Further dec will be done by hypotensive drugs

  6. INHALATION AGENTS 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

  7. 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

  8. 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 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

  9. HYPOTENSIVE DRUGS • 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

  10. GANGLIONIC BLOCKING DRUGS • Compete with Ach for nicotinic receptors on autonomic postjunctionalganglionic membrane • Overall effect of autonomic blockade depends on predominance of one or other system • Produces vasodilation, ↑ed venous capacitance and hypotension

  11. DIRECT- ACTING VASODILATOR DRUGS • Mainly acts through NO • NO diffuses into vascular smooth muscle , stimulates c-GMP ,causing vascular relaxation • SNP and NTG provide exogenous NO

  12. SODIUM NITROPRUSSIDE 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: • Conversion to cyanomethemoglobin: 1 of every 5 CNˉ ions is converted • Binding to cytochromeoxidase: inhibiting oxidative phosphorylation • Conversion to cyanocobalamin: in presence of adequate hydroxocobalamin • Conversion to thiocyanate: catalyzed by enzyme rhodenase

  13. 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

  14. DETECTION OF CYANIDE TOXICITY: • Impending CNˉ intoxication • Requirement for high doses of SNP >10µg/kg/min • Resistance apparent within 5-10 min after start of infusion • 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

  15. CLINICAL FEATURES OF CYANIDE TOXICITY • 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

  16. PREVENTION 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 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

  17. TREATMENT OF CYANIDE TOXICITY • Sodium thiosulfateis 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

  18. ADENOSINE • Endogenous vasodilator • Acts on specific adenosine receptors located in several vascular beds and on AV node • Activation of adenylatecyclase 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

  19. ↑ 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

  20. HYDRALAZINE • 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

  21. PROSTAGLANDIN E1 • 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

  22. PHENTOLAMINE • 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

  23. β-ADRENERGIC BLOCKING DRUGS • 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

  24. α+β BLOCKERS 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

  25. CALCIUM CHANNEL BLOCKERS • Verapamil and nicardipine decreases SVR • Verapamil produces myocardial depression and delays AV conduction- not recommended for induced hypotension • Nicardipinevasodilates 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.

  26. TECHNIQUES TO PREVENT TACHYPHYLAXIS • Use of inhalational anesthetics • Avoid fluid overload • Preop sedation and opioids • Use of βblockers • Adequate analgesia and muscle relaxation • Pretreatment with ACE inhibitors • Combining drugs/dexmedetomidine /clonidine

  27. SAFETY FACTORS 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

  28. MAINTENANCE OF NORMAL ACID- BASE BALANCE • 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

  29. OXYGENATION 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

  30. 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

  31. CONTRAINDICATIONS 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

  32. COMPLICATIONS OF INDUCED HYPOTENSION • Cardiac arrest and hypotension • Temporary or permanent neurologic deficits • Reactionary hrg • Failure of technique

  33. THANKS

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