Effect of anaesthetic agents on cardiovascular system
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EFFECT OF ANAESTHETIC AGENTS ON CARDIOVASCULAR SYSTEM. www.anaesthesia.co.in [email protected] 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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Effect of anaesthetic agents on cardiovascular system

EFFECT OF ANAESTHETIC AGENTS ON CARDIOVASCULAR SYSTEM

www.anaesthesia.co.in

[email protected]


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 anaesthetics2

Inhalational anaesthetics


Inhalational anaesthetics3

 Sympathetic activity

Direct effect on SAN

Baroreceptor reflex

Inhalational anaesthetics

HR

  • Halothane   HR

  •  withIsoflurane > Desflurane (dose – dependent)

  • Unchanged with Sevoflurane


Inhalational anaesthetics4

Inhalational anaesthetics


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 anaesthetics coronary autoregulation

Inhalational anaesthetics: Coronary autoregulation


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


Intravenous induction agents

Intravenous Induction Agents


Intravenous induction agents1

Intravenous Induction Agents


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


Opioids3

Opioids


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 succinylcholine1

Neuromuscular Blockers - Succinylcholine


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


Neuromuscular blockers nondepolarizers2

Neuromuscular Blockers - Nondepolarizers


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


Effect of anaesthetic agents on cardiovascular system

Thank you !

www.anaesthesia.co.in

[email protected]


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