1 / 39

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.

aglaia
Download Presentation

EFFECT OF ANAESTHETIC AGENTS ON CARDIOVASCULAR SYSTEM

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related