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EFFECT OF ANAESTHETIC AGENTS ON CARDIOVASCULAR SYSTEM

EFFECT OF ANAESTHETIC AGENTS ON CARDIOVASCULAR SYSTEM. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. CARDIOVASCULAR SYSTEM. Cardiac output (Stroke volume x Heart rate) Systemic vascular resistance (B.P. / C.O.) Coronary blood flow & autoregulation Arrhythmogenicity.

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EFFECT OF ANAESTHETIC AGENTS ON CARDIOVASCULAR SYSTEM

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  1. EFFECT OF ANAESTHETIC AGENTS ON CARDIOVASCULAR SYSTEM www.anaesthesia.co.in anaesthesia.co.in@gmail.com

  2. CARDIOVASCULAR SYSTEM • Cardiac output (Stroke volume x Heart rate) • Systemic vascular resistance (B.P. / C.O.) • Coronary blood flow & autoregulation • Arrhythmogenicity

  3. Direct myocardial depressant   C.O.  sympathetic N.S. activity  peripheral vasoconstriction Minm change in BP Inhalational anaesthetics – N2O •  catecholamines,  plasma Nep,  SVR •  baroreceptor-mediated tachycardia

  4.  influx of Ca++ through slow channels  binding of Ca++ by plasma membrane  uptake & release of Ca++ by SR Inhalational anaesthetics Contractility  by halothane   BP,  SV,  RAP  due to alterations in Ca++ metabolism

  5. Inhalational anaesthetics Contractility •  by isoflurane in isolated hearts  C. O. maintained in vivo with minimal myocardial depression till 2 MAC ;  SV,  HR, Normal C. O. • Sevoflurane dose-dependent myocardial depression through direct effect on Ca++ channels • Desflurane dose-dependent myocardial depression

  6. Inhalational anaesthetics

  7.  Sympathetic activity Direct effect on SAN Baroreceptor reflex Inhalational anaesthetics HR • Halothane   HR •  withIsoflurane > Desflurane (dose – dependent) • Unchanged with Sevoflurane

  8. Inhalational anaesthetics

  9. Inhalational anaesthetics Arrhythmogenicity Halothane Sensitizes heart to Epi  automaticity of SAN Slows myocardial conduction

  10. Inhalational anaesthetics Coronary steal phenomenon Coronary stenosis +  coronary perfusion pressure  Detrimental redistribution of coronary blood flow with Isoflurane  Contractile dysfunction; more in region distal to a critical coronary stenosis  Avoided if CPP restored

  11. Inhalational anaesthetics: Coronary autoregulation

  12. Inhalational anaesthetics • Protection against myocardial ischemia  All except Des • Interaction with CCBs  En > Halo > Iso • Rapid  in concentration of Des & Iso   HR &  BP

  13. Xenon • Good haemodynamic stability • Little change in BP • No change in LV function with 65% Xe (MAC – 71%) • Slight  in HR

  14. Intravenous Induction Agents- Thiopentone sodium • Venodilation   preload • Direct myocardial depression at high doses • SVR  relatively unaltered after normal induction dose in healthy adults • HR   due to baroreceptor reflex • Myocardial O2 consumption  

  15. Intravenous Induction Agents- Propofol •  BP •  SVR -  sympathetic activity + direct  in vascular S.M. tone •  / unchanged HR •  coronary perfusion pressure • Unchanged global O2 supply-demand ratio

  16. Intravenous Induction Agents - Etomidate • Unchanged myocardial function • Minm effect on haemodynamic stability • No effect on symp N. S. & baro-R fncn •  coronary vascular resistance,  coronary perfusion  well-maintained myocardial O2 supply-demand ratio

  17. Intravenous Induction Agents - Ketamine • HR, BP, CO, SVR, PVR • Can be attenuated by prior BDZs, other inhal or i/v anaes agents, adrenergic ATs • Centrally mediated  symp tone, not dose dependent; overrides direct myocardial depressant effect except at high doses

  18. Intravenous Induction Agents

  19. Intravenous Induction Agents

  20. Opioids HR • Fent analogs   HR by vagomimetic action; severe bradycardia /asystole possible with Fent analogues; usually have favourable effect on myocardial O2 supply-demand ratio in CAD patients • Pethidine  HR by anticholinergic action • Morphine  / 

  21. Opioids • Histamine release HR, MBP; Peth > Morph (less with slower administration); negligible with Fent analogues •  contractility of isolated cardiac muscle, but blood concn insufficient; Morph & Fent both cardiostable at clinical concns • Minor  in BP with Fent analogs  possibly by a centrally mediated  in sympathetic tone

  22. 1 Potency Cardiovascular side effects  Opioids Potency : Sufent > Fent > Morph > Peth C.V. S/Es : Peth > Morph > Fent > Sufent

  23. Opioid AG - ATs • Nalbuphine, Pentazocine  HR, BP, SVR, PAP, LVEDP • Butorphanol  Small  in PAP • Newer agents  Minimal effects, except meptazinol, dezocine

  24. Opioids

  25. Benzodiazepines • Mild, transient, dose-related fall in ABP, associated with  catecholamine concn and  sympathetic tone • Dangerously exaggerated fall in BP with concurrent hypovolemia, coadministered i/v or inhaln anaesthetics or opioids

  26. Interactions • Opioids / BDZs + Ketamine  sympathomimetic effects • Opioids + BDZs   MBP due to  SVR, probably due to  sympathetic tone • Propofol / Opioids + NMBs fent analogs + vec  bradycardia & asystole, no change in HR with pancuronium

  27. Neuromuscular Blockers - Succinylcholine • Low doses  negative inotropism & chronotropism • Large doses  tachycardia • Arrhythmias

  28. Neuromuscular Blockers - Succinylcholine

  29. AUTONOMIC EFFECTS Not reduced by slower injection Dose – related Additive over time in case of divided doses Seen with d-TC, Pan, Roc HISTAMINE RELEASE Reduced by slower injection rate Can be prevented by A/Bs, NSAIDs Tachyphylaxis occurs Neuromuscular Blockers - Nondepolarizers

  30. Neuromuscular Blockers - Nondepolarizers HISTAMINE RELEASE • Erythema of face, neck, torso; moderate  BP, HR; rarely bronchospasm; degranulation of serosal mast cells in skin, conn. tissue & near blood vessels & nerves. • Mainly with mivacurium, atracurium, doxacurium, d-TC, metocurine

  31. Neuromuscular Blockers - Nondepolarizers

  32. Local Anaesthetics •  rate of depolarization in fast-conducting tissue of Purkinje bundle & ventricular myocardium ( fast Na+ conductance  depresses rapid phase of depolarization) •  contractility,  BP,  HR, asystole  resistant to pacing

  33. Local Anaesthetics • Prolonged PR-interval,  duration of QRS - complex •  spontaneous pacemaker activity in SAN  sinus bradycardia, sinus arrest • Dose dependent (-)ive inotropic action on heart

  34. Local Anaesthetics • Biphasic action on vascular smooth muscle (low concn – vasoconstriction; high concn – vasodilation) • Indirect action – due to autonomic blockade • CC / CNS ratio– Lignocaine > Etidocaine > Bupivacaine

  35. LIGNOCAINE Recovery of Na+ channels from lignocaine is complete, even at high HRs BUPIVACAINE Depresses rapid phase of depolarization more Rate of recovery from use-dependent block slower Incomplete restoration of Na+ channels available between action potentials, esp at high HRs Anti - arrhythmic Arrhyth-mogenic Local Anaesthetics

  36. Local Anaesthetics Bupivacaine : R- bupi more cardiotoxic. Prolonged PR-interval & QRS complex, predisposition to re-entrant arrhythmias, VT / VF / Heart blocks / CHF (due to loss of contractility)  resistant to defibrillation

  37. Cardiovascular stability • Careful selection of agent • Titrated doses *To patient & comorbid conditions * To surgery • Slow rate of administration • Knowledge of cardiovascular effects • Prompt recognition & appropriate treatment in case of problems

  38. Thank you ! www.anaesthesia.co.in anaesthesia.co.in@gmail.com

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