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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

EFFECT OF ANAESTHETIC AGENTS ON CARDIOVASCULAR SYSTEM

www.anaesthesia.co.in

anaesthesia.co.in@gmail.com

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

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
inhalational anaesthetics

 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

inhalational anaesthetics1
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
inhalational anaesthetics3

 Sympathetic activity

Direct effect on SAN

Baroreceptor reflex

Inhalational anaesthetics

HR

  • Halothane   HR
  •  withIsoflurane > Desflurane (dose – dependent)
  • Unchanged with Sevoflurane
inhalational anaesthetics5
Inhalational anaesthetics

Arrhythmogenicity

Halothane

Sensitizes heart to Epi

 automaticity of SAN

Slows myocardial conduction

inhalational anaesthetics6
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

inhalational anaesthetics7
Inhalational anaesthetics
  • Protection against myocardial ischemia  All except Des
  • Interaction with CCBs  En > Halo > Iso
  • Rapid  in concentration of Des & Iso   HR &  BP
xenon
Xenon
  • Good haemodynamic stability
  • Little change in BP
  • No change in LV function with 65% Xe (MAC – 71%)
  • Slight  in HR
intravenous induction agents thiopentone sodium
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  
intravenous induction agents propofol
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
intravenous induction agents etomidate
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
intravenous induction agents ketamine
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
opioids
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  / 
opioids1
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
opioids2

1

Potency

Cardiovascular side effects 

Opioids

Potency : Sufent > Fent > Morph > Peth

C.V. S/Es : Peth > Morph > Fent > Sufent

opioid ag ats
Opioid AG - ATs
  • Nalbuphine, Pentazocine  HR, BP, SVR, PAP, LVEDP
  • Butorphanol  Small  in PAP
  • Newer agents  Minimal effects, except meptazinol, dezocine
benzodiazepines
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
interactions
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
neuromuscular blockers succinylcholine
Neuromuscular Blockers - Succinylcholine
  • Low doses  negative inotropism & chronotropism
  • Large doses  tachycardia
  • Arrhythmias
neuromuscular blockers nondepolarizers
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
neuromuscular blockers nondepolarizers1
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
local anaesthetics
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
local anaesthetics1
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
local anaesthetics2
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

local anaesthetics3
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
local anaesthetics4
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

cardiovascular stability
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
slide39

Thank you !

www.anaesthesia.co.in

anaesthesia.co.in@gmail.com