EFFECT OF ANAESTHETIC AGENTS ON CARDIOVASCULAR SYSTEM

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EFFECT OF ANAESTHETIC AGENTS ON
CARDIOVASCULAR SYSTEM
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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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Inhalational anaesthetics N2O

• ? catecholamines, ? plasma Nep, ? SVR
• ? baroreceptor-mediated tachycardia

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Inhalational anaesthetics

• Contractility
• ? by halothane ? ? BP, ? SV, ? RAP ? due to
  alterations in Ca metabolism

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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

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Inhalational anaesthetics
HALO ISO SEVO DES
SVR -- ?? ? ?
Splanchnic blood flow ? ?? (-) till 1 MAC (-) till 2 MAC
Coronary blood flow ? ?? ? ?
Blood flow relative to myocardial O2 demand ? ? ? ?
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Inhalational anaesthetics

• HR
• Halothane ? ? HR
• ? with Isoflurane gt Desflurane (dose dependent)
• Unchanged with Sevoflurane

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Inhalational anaesthetics
HALO ISO SEVO DES
HR ? ? - ?
BP ? ? ? ?
Cardiac Index ? - ? ? / ?
Conduction system slowing Min -
Sensitization to Epi Min - -
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Inhalational anaesthetics

• Arrhythmogenicity

Halothane
Sensitizes heart to Epi
? automaticity of SAN
Slows myocardial conduction
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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

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Inhalational anaesthetics Coronary
autoregulation
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Inhalational anaesthetics

• Protection against myocardial ischemia ? All
  except Des
• Interaction with CCBs ? En gt Halo gt Iso
• Rapid ? in concentration of Des Iso ? ? HR ?
  BP

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Xenon

• Good haemodynamic stability
• Little change in BP
• No change in LV function with 65 Xe (MAC 71)
• Slight ? in HR

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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 ? ?

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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

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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

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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

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Intravenous Induction Agents
Thio. Prop. Keta. Etom.
HR ? -/? ? -
BP -/? ?? ? -
Preload ? ? ? -
Afterload - ?? ? -
Myocardial fncn ? at high doses ? ?/? -
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Intravenous Induction Agents
Thiopentone ? hypotension in limited cardiovascular reserve ie. Hypovolemia, CAD etc.
Propofol Compromised cor BF in severe CAD Carefully in hypovolemia, critical CAD, ventricular hypertrophy, CHF.
Etomidate Drug of choice in pre-existing cardiovascular disease
Ketamine C.I. in IHD, vascular aneurysms Avoided in shock, critical illness
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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 ? ?/ ?

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Opioids

• Histamine release ? ?HR, ?MBP Peth gt 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

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Opioids

• Potency Sufent gt Fent gt Morph gt Peth
• C.V. S/Es Peth gt Morph gt Fent gt Sufent

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Opioid AG - ATs

• Nalbuphine, Pentazocine ? ?HR, ?BP, ?SVR, ?PAP,
  ?LVEDP
• Butorphanol ? Small ? in PAP
• Newer agents ? Minimal effects, except
  meptazinol, dezocine

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Opioids
Morph Peth Fent ( analogs)
HR ?/ ? ? ?
Contractility - - / ? -
BP ? / - Minor ?
Hist release -
Cholinomimetic action - -
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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

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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

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Neuromuscular Blockers - Succinylcholine

• Low doses ? negative inotropism chronotropism
• Large doses ? tachycardia
• Arrhythmias

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Neuromuscular Blockers - Succinylcholine
Sinus bradycardia Children, in adults after 2nd dose, prevented by thio, atr, precurarization
Nodal / jncnal rhythms More after 2nd dose, prevented by precurarization
Ventri dysrhythmias Potentiated by intubation, hypoxia, hypercarbia, surg stimulation
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APPROXIMATE AUTONOMIC MARGINS OF SAFETY OF NONDEPOLARIZERS APPROXIMATE AUTONOMIC MARGINS OF SAFETY OF NONDEPOLARIZERS APPROXIMATE AUTONOMIC MARGINS OF SAFETY OF NONDEPOLARIZERS APPROXIMATE AUTONOMIC MARGINS OF SAFETY OF NONDEPOLARIZERS
DRUGS VAGUS SYMP. GANGLIA HIST. RELEASE
Benzylisoquinolinium compounds Benzylisoquinolinium compounds Benzylisoquinolinium compounds Benzylisoquinolinium compounds
Mivacurium gt 50 gt 100 3.0
Atracurium 16 40 2.5
Cisatracurium gt 50 gt 50 None
d-Tubocurarine 0.6 2.0 0.6
Steroidal compounds Steroidal compounds Steroidal compounds Steroidal compounds
Vecuronium 20 gt 250 None
Rocuronium 3.0 5.0 gt 10 None
Pancuronium 3.0 gt 250 None
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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

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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

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Neuromuscular Blockers - Nondepolarizers
Panc. Vec. Atrac. Roc.
HR ? - ? ?
BP ? - ? -
Autonomic effects - -
Histamine release - - -
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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

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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

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Local Anaesthetics

• Biphasic action on vascular smooth muscle (low
  concn vasoconstriction high concn
  vasodilation)
• Indirect action due to autonomic blockade
• CC / CNS ratio
• Lignocaine gt Etidocaine gt Bupivacaine

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Local Anaesthetics
Anti - arrhythmic
Arrhyth-mogenic

• 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

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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

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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

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Atropine

• Anticholinergic M1, M2, M3
• Effects Tachycardia, fever, increased BMR
• Dose
• Uses Treatment of bradycardia, premedication,
  reversal, antisialogogue, mydriasis, motion
  sickness

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• Mephenteramine
• Indirectly acting ?, ? agonist
• Synthetic

• Ephedrine
• Indirectly acting ?, ? agonist Direct action on
  adrenergic receptors
• Does not reduce uterine blood flow

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Dopamine

• Receptors D1, D2, ?, ? Rs
• Actions D1- postsynaptically ? vasodilation
  D2- presynaptic, inhibit Nep reuptake, N V ?-
  vasoconstriction ?- stimulation of heart
• Clinical uses low BP, low U/O
• S/Es- Tachycardia, dysrhythmias, interferes with
  ventilatory response to hypoxemia

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Dobutamine

• Receptors ?1 Rs, weak ?2 effect
• Actions stimulation of heart
• Clinical uses low C.O. in CHF in increased SVR
• S/Es- Mild tachycardia, dysrhythmias

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