EFFECT OF ANAESTHESIA ON MYOCARDIAL OXYGEN CONSUMPTION AND CORONARY CIRCULATION

1. EFFECT OF ANAESTHESIA ON MYOCARDIAL OXYGEN CONSUMPTION AND CORONARY CIRCULATION University College of Medical Sciences & GTB Hospital, Delhi

2. DETERMINANTS OF MYOCARDIAL OXYGEN CONSUMPTION • Resting O2 consumption by heart = 9mL/100g/min • HEART RATE • WALL TENSION- Law of Laplace- LV wall tension = Pr/w where P = Transmural pressure, r = radius of hollow organ w = wall thickness • CONTRACTILE STATE

3. REGULATION OF CORONARY BLOOD FLOW • RESTING CBF = 225 mL/min = 5% of total cardiac output • Peak CBF – early diastole ( after isovolumic relaxation) • According to PoiseuilleHegan formula – • Blood flow (Q) = ∆P∏r4/8Lᶯ where ∆P = coronary perfusion pressure r = radius , L = length of vessel ᶯ = fluid viscosity

4. REGULATION OF CBF • CBF remains constant when coronary perfusion maintained between 50 – 120 mmHg by autoregulation • Local regulation by – Adenosine, O2, CO2, NO, endothelin, PGs • Sympathetic – α1 – vasoconstriction β - ↑ HR and contractility • Parasympathetic

5. EFFECT ON MYOCARDIAL OXYGEN CONSUMPTION AND CORONARY CIRCULATION • General anaesthesia – intubation/extubation intravenous agents inhalational agents opioids neuromuscular blockers • Regional/local anaesthesia • Positioning • I V Fluids

6. EFFECT OF INTUBATION/LARYNGOSCOPY • Noxious stimulus – hypertension and tachycardia occurs • Response proportional to – - force - duration of laryngoscopy • Increase in B.P starts in 5 sec peaks in 1-2 mins settles in 5 mins • Can result in myocardial ischaemia

7. INTUBATION/ LARYNGOSCOPY • Ways to reduce this response : • Increase the depth of anaesthesia • Narcotics ( like fentanyl) • Aerosol application of topical anaesthetic agents • Labetalol/ esmolol • Direct arterial B.P monitoring in high risk patients

8. EFFECT OF EXTUBATION • Increase in B.P , HR • Increase myocardial oxygen consumption (MVo2) • Narcotics , beta adrenergic agents , Ca channel blockers - protective

9. EFFECT OF INTRAVENOUS AGENTS Propofol • HR – not much effect - may reset or inhibit baroreceptor reflex - ↓parasympathetic tone ( dose dep.) • Wall tension – vasodilatation due to – - ↓ intracellular smooth muscle Ca mobilization - inhibition of PGI2 synthesis - ↓ angiotensin II synthesis - activation of K-ATP channels - stimulation of NO

10. I.V. AGENTS- PROPOFOL • Contractility - ? Myocardial depression • Net effect - CBF and MVo2 - decrease • Global myocardial O2 demand to supply ratio preserved

11. I.V.AGENTS Barbiturates • HR – ↑ • Wall tension - ↓ in preload (↑ in venous capacitance) • Contractility – dose related ↓ availability of Ca to myofibrils , ↓ in sympathetic outflow from CNS

12. BARBITURATES • Net effect- increased MVo2 • Proportional decrease in coronary artery resistance and and increased CBF. • Avoid in hypovolemic, CAD, ventricular hypertrophy, HF patients ( Lowers C.O )

13. I.V AGENTS Ketamine • HR - ↑ (centrally mediated sympathetic stimulation) • Inotropic state – no effect ( sympathetic stimulation overrides direct myocardial depressant action - caution in shock and critically ill

14. I.V AGENTS –Ketamine • ↑ work and myocardial oxygen consumption • ↑ C.O, ↓ coronary vascular resistance - ↑ O2 supply • Undesirable increase in HR and BP – - α and β adrenergic antagonists - vasodilators - clonidine - benzodiazepines - propofol

15. I.V AGENTS Etomidate • Lacks effect on sympathetic and baroreceptor function • Coronary vascular resistance ↓ perfusion↑ • Myocardial O2 demand supply ratio maintained

16. I.V AGENTS Dexmeditomidine • HR- ↓ • Contractility ↓ • Decrease in O2 consumption and redistribution of CBF from non ischaemic to ischaemic zones after acute brief occlusion

17. I.V AGENTS

18. INHALATIONAL AGENTS Halothane • HR - ~ or ↓ (reduction in sympathetic activity or rate of discharge from SA Node) • Contractility - ↓ ( decreases intracellular Ca) • Coronary blood flow - ↓ due to - - reduced perfusion pressure - reduced Mvo2 ( sec. to↓ contractility)

19. INHALATIONAL AGENTS Enflurane • HR - ↑ • Contractility – dose dep. Negative inotropic effect • SVR ↓ • Net effect - protective • CBF↑

20. INHALATIONAL AGENTS Isoflurane • HR - ↑ • Contractility – minimal upto 2 MAC • SVR- ↓ • Myocardial O2 consumption decreases • O2 demand supply ratio improved • Coronary vasodilator • Coronary steal ( in animal models)

21. INHALATIONAL AGENTS Sevoflurane • HR – minimal effect • Contractility - ↓ ( effect on Ca channels) • Net effect - protective • Coronary vasodilator

22. INHALATIONAL AGENTS Desflurane • HR- ↑ ( dose dep.) • Contractility - ↓ • Wall tension - ↓ (peripheral vasodilatation) • Coronary vasodilator - ↓ cardiac work • Net effect – ↓ MVo2

23. INHALATIONAL AGENTS N2O • Contractility - ↓ • SVR - ↑↑ • Minimal change in B.P

24. INHALATIONAL AGENTS

25. OPIOIDS

26. OPIOIDS • Cardiovascular effects 1/α potency • Meperidine>morphine>fentanyl>sufentanil • Opiod induced hypotension – main concern • Volume status of the patient • Can be treated by i.v fluids, alpha adrenergic agonists (phenyephrine)

27. NMBs

28. LOCAL ANAESTHETICS • Decrease in action potential duration and relative refractory period • Dose dependent negative inotropic effect (Ca influx and release from SR affected) • ↓contractility α conduction blocking potency Bupivacaine > lidocaine • CV Toxicity – slowing of conduction in myocardium, peripheral vasodilatation

29. NEURAXIAL BLOCKS- TECHNIQUES • Spinal/epidural/caudal • ↓ in HR and B.P • Sympathectomy that accompanies the technique depends on height of block • HR – Block of cardio accelerator fibres • Fall in right atrial filling pressure • B.P – Vasodilatation ( veno > arteriolar)

30. NEURAXIAL BLOCK TECHNIQUES • Healthy patients – TPR ↓ by 15-18% C.O - SAME • Cardiac disease – SVR ↓ by 25% C.O ↓ by 10%

31. EFFECT OF POSITIONING • Supine - ↑ in venous return • ↑ in preload , ↑ SV , ↑ C.O • Reflex baroreceptor activation → compensatory decrease in HR/SV/CO • Trendelenberg position - ↑ venous return→ baroreceptor reflex response→ vasodilatation and bradycardia • Lithotomy - ↑ preload • Prone - ↓ preload ( venous return impeded)

32. INTRA OPERATIVE I.V FLUIDS • Effect of anaesthesia – venodilatation and cardiac depression • Goal of fluid therapy – sustained adequate oxygen delivery in relation to oxygen consumption • Fluids administered to expand blood volume (as a compensation for venodilatation)→ increase preload→ increase stroke volume

33. LAPAROSCOPIC SURGERY • EFFECT OF PNEUMOPERITONIUM • ↓ C.O (α to IAP) – due to decreased venous return • ↑SVR,PVR (↑ arterial pressures) – mediated by mechanical and neurohumoral factors • Deleterious in cardiac disease patients • HR same or increased

34. LAPAROSCOPIC SURGERY • ↓ in venous return and C.O can be prevented by- • Fluid loading • Head down before peritoneal insufflation • Intermittent sequential pneumatic compression devices

35. REFERENCES • Wylie and Churchill-Davidson’s A Practice Of Anesthesia; 7th edition • Miller’s Anesthesia; Ronald D.Miller. 7th edition • Pharmacology and Physiology in Anesthesia Practice; Robert K.Stoelting , Simon C.Hillier. 4th edition • Kaplan’s Cardiac Anesthesia; 5th edition

36. THANK YOU