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Effects of Inhalation Anesthetic Agents

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Mean arterial pressure (MAP)

  • Halothane, isoflurane, desflurane, and sevoflurane all produce similar and dose-dependent decreases in MAP.
  • N2O produces either no change or modest increase in MAP

Mechanism

  • Halothane reduce MAP by decreases in myocardial contractility (and cardiac output)
    * No effect on SVR
  • Isoflurane, desflurane, and sevoflurane reduce MAP by decrease in systemic vascular resistance

Heart rate (HR)

  • Isoflurane, desflurane, and sevoflurane increase HR
    * Sevoflurane increase HR only at >1.5 MAC
    * Isoflurane and desflurane increase HR at lower concentration
  • Halothane does not cause reflex HR (secondary to decreased BP)
    * Due to depressed carotid sinus reflex and depressed sinus node depolarisation

This increase in HR is prevented by a small dose of opioid

Isoflurane vs desflurane

  • At 0.5 MAC, isoflurane and desflurane produce similar decrease in MAP
  • At 0.5 MAC, isoflurane increase HR, but desflurane does not
  • With isoflurane, the increase in HR is:
    * Blunted in elderly
    * More likely to occur in younger patients

Cardiac output and stroke volume

  • All inhalational anaesthetic agents (except N2O) decrease cardiac output by 15-30%
  • Increase in HR tend to compensate for the decrease in cardiac output
  • N2O causes mild increase in cardiac output
    * Possibly due to mild sympathomimetic effect of N2O

Right atrial pressure (RAP)

–> Indicator of central venous pressure

  • Halothane, isoflurane, and desflurane all increase RAP
    * Due to myocardial depression
    * Peripheral vasodilating effect may minimise the increase in RAP
  • N2O increases RAP
    * Possibly due to increased pulmonary vascular resistance due to sympathomimetic effect

Systemic vascular resistance (SVR)

  • Isoflurane, desflurane, and sevoflurane decrease SVR
  • Halothane and N2O does not affect SVR

Blood flow distribution with isoflurane

  • Isoflurane increases blood flow in skeletal muscle and skin
     beta agonist effect
  • Implications include:
    Excess perfusion relative to O2 requirement
    * Loss of body heat
    * Enhanced drug delivery to neuromuscular junctions

Cutaneous blood flow

  • Halothane does not increase overall SVR
    * But increase blood flow to brain and skin
  • All inhalational anaesthetic agents (except for N2O) increase cutaneous blood flow
    * Most likely due to inhibition on temperature regulating mechanisms
  • N2O may produce cutaneous vasoconstriction

Clinical relevance

Peripheral vasodilation:

  • Undesirable in aortic stenosis
  • Beneficial in mitral or aortic regurgitation

Pulmonary vascular resistance (PVR)

  • All inhalational anaesthetic agents (except for N2O) exert little effect on PVR
  • N2O causes pulmonary vasoconstriction
    * Exaggerate pulmonary hypertension
    * Increase magnitude of right-to-left intracardiac shunting of blood

Duration of administration

  • After 5 hours, cardiac output recovers from the cardiac depressant effects of inhalational anaesthetic agents
  • HR is increased and SVR is decreased
    –> BP unchanged

This recovery is

  • Most pronouced in halothane
  • Least in isoflurane
    * Isoflurane caused minimal drop in cardiac output anyway

Cardiac dysrhythmias

  • Alkane derivative (e.g. halothane)
    –> Decreases the dose of epinephrine necessary to evoke ventricular cardiac arrhythmia
  • Ether derivatives (e.g. ENF, isoflurane, desflurane, sevoflurane)
    –> Minimal effect
  • Both halothane and isoflurane
    * Slow the rate of SA node discharge
    * Prolong His bundle and ventricular conduction time
  • Both halothane and isoflurane prolong QTc

Accessory pathway and ablation procedures

  • Isoflurane increases refractory of accessory pathways
    –> Interfer with postablation studies
  • Sevoflurane has almost no effect on AV or accessory pathways
    –> Acceptable for ablation procedures

Spontaneous breathing

Spontaneous breathing during anaesthesia has 2 effects relevant to CVS

  • Accumulation of CO2
     Sympathetic stimulation
    Direct relaxing effect on peripheral vascular smooth muscles
  • Better venous return
    * Due to less pressure on pulmonary vessels

Thus, During spontaneous breathing

  • Cardiac output is higher
  • HR is higher
  • MAP is higher
  • Total peripheral resistance is lower

Coronary blood flow

  • Inhalational anaesthetic agents causes coronary vasodilation
    * Preferentially dilates vessels with diameters from 20 microm to 50 microm

However,

  • Coronary steal syndrome is not clinically significant
    * All inhalational anaesthetic agents (including isoflurane) are cardioprotective
    * [SH4:56]

Neurocirculatory response

  • Abrupt increase in isoflurane and desflurane (from 0.55 to 1.66 MAC)
    –> Sympathetic stimulation and increase renin-angiotensin activity
    –> Increased HR and MAP
    * Greater increase with desflurane
    * Blunted by fentanyl, esmolol, and clonidine
  • Abrupt increase in sevoflurane
    –> No neurocirculatory response

Effect of pre-existing disease

  • In patients with coronary artery disease,
    * N2O produce myocardial depression which doesn’t occur in patients without cardiac disease
  • Calcium channel blockers
    –> Myocardial depression
    –> More vulnerable to direct depressant effect of inhalational anaesthetic agents

Cardiac protection

Ischaemic preconditioning

  • Brief episodes on myocardial ischaemia
    –> Offers protection against subsequent longer periods of ischaemia and infarct

Two phases

  • First phase last for 1-2 hours
  • Second phase occurs after 24 hours, lasting up to 3 days

Mechanism of ischaemic preconditioning

Release of adenosine
–> Binds to adenosine receptors
–> Increase protein kinase C activity
–> Phosphorylation of ATP-sensitive K+ channel (KATP)
–> Less sensitive to inhibition by ATP
–> More K+ current
–> Less Ca2+ accumulation and more hyperpolarization
–> More relaxation and mild negative inotropic effect

Anaesthetic preconditioning

  • Brief exposure to isoflurane, sevoflurane, and desflurane
    –> Activate KATP channel
    –> Cardioprotection identical to ischaemic preconditioning
  • Cardiac surgical patients receiving sevoflurane has less troponin I release in the first 24 hours than patients receiving propofol
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