• Volatile anaesthetics produce dose-dependent increases in cerebral blood flow (CBF).

• Volatile anaesthetics administered during normocapnia in concentrations of >0.6 MAC produce

• Cerebral vasodilation

• Decreased cerebral vascular resistance

• Drug induced increase in CBF occurs despite concomitant decreases in cerebral metabolic
requirements

Cerebral Hemodynamic Response in Form of active arteriolar Vasomotion to maintain a constant CBF to
wide range of Changes in CPP (Cerebral Perfusion Pressure) independent to metabolic coupling

Lower limit -50-70mmhg

Upper -130-150mmhg

• ISOFLUORANE maintains auto regulation of cbf compared to halothane

• Increase in systemic blood pressure produce smaller increase in brain protrusion during
administration of ISOFLUORANE and enfluorane

• Halothane –loss of auto regulation is responsible for greater brain swelling in animals

• SEVOFLUORANE and DESFLUORANE – do not alter auto regulation

Inhaled anesthetics produce dose-dependent decreases in cerebral metabolic oxygen requirements

Decrease in CMRO2 is greater during the administration of Isoflurane than with an equivalent MAC
Concentration of Halothane

Desflurane and Sevoflurane decrease cerebral metabolic oxygen requirements similar to Isoflurane

Inhaled anesthetics produce increase in ICP due to increase in CBF

Patients with space –occupying intracranial lesions (SOL) are most vulnerable to these drug-induced
increases in ICP

Hyperventilation of the lungs to decrease the PaCo2 to about 30mmhg opposes the tendency for inhaled
anesthetics to increase ICP

Enflurane : sustained increase in ICP by increasing

rate of production of CSF

 resistance to reabsorption of CSF

Isoflurane : mild increase in ICP

does not alter production of CSF

decreases reabsorption

Nitrous oxide : increase in ICP due to increase in CBF

• Mean arterial pressure

• Heart rate

• Cardiac output

• Right atrial pressure

• Systemic vascular resistence

• Pulmonary vascular resistence

• Cardiac dysrhythmias

• Coronary blood flow

• Inhaled Anesthetics Decrease Arterial Pressures

• Halothane, isoflurane, Desflurane, and Sevoflurane produce dose dependent decrease in MAP

• Nitrous oxide produces either no change or modest increase in systemic blood pressure

MECHANISM:

• Halothane and Enflurane decreases in myocardial contractility and cardiac output.

• Isoflurane, Desflurane and Sevoflurane decrease the systemic vascular resistance. (decrease in
SVR >>than decrease in myocardial contractility)

• Decrease In Cardiac Output By Majority Agents

• Halothane produces dose-dependent decreases in cardiac output

• Isoflurane, desflurane – no effect d/t better maintainance of HR

• Sevoflurane causes a- decrease in cardiac output @ MAC 1,1.5

 which stabilizes @MAC 2

• Nitrous oxide causes modest increase in cardiac output due to mild sympathomimetic effects of
this drug

• Halothane: weak coronary vasodilator

• Isoflurane: greater vasodilatation, increase in coronary blood flow of small coronary vessel (not
accompanied by epicardial vessel dilatation)

• Desflurane and Sevoflurane: coronary vasodilatation

Note: coronary vasodilator reserve:

Ratio of peak coronary blood flow after brief coronary occlusion to baseline flow.

Isoflurane >>halothane.

• Pattern of breathing

• Response to co2

• Response to hypoxemia

• Bronchial tone

• Mucociliary function

• Surfactant

• Hypoxic pulmonary vasoconstriction

• Include Effect On – Tidal Volume

Respiratory Rate

TIDAL VOLUME: decreased

RESPIRATORY RATE: increased

MECHANISM: Volatile anesthetics acting on central respiratory chemoreceptor neurons through

activation of THIK-1 receptors.
Factors affecting Ventilatory response to PaCO 2

• Bronchodilatation

• Mechanism: direct action on bronchial smooth muscle

indirect: inhibition of reflex neural pathway

Halothane: maximum

• Halothane and isoflurane- transiently reduce phosphatidyl choline synthesis

• Mechanism: increase in hydrogen peroxide mediated reduction of phosphatidyl choline content

in type 2 cells by affecting cell energitics

• Hepatic blood flow

• Drug clearance

• Liver function test

• Hepatotoxicity

• Effect on renal Blood Flow, GFR,Urine output

• Fluoride induced nephrotoxicity

• Vinyl induced nephrotoxicity

• Prolonged administration of nitrous oxide –interference with dna synthesis- megaloblastic

anemia (exposure to anesthetic concentration of n20 for 24hrs)

• Also causes agranulocytosis on >4 days exposure

• Chronic inhalation of n20 –peripheral neuropathy

• Also inhaled anesthetics particularly n20- dose dependent inhibition of polymorphonuclear
leucocytes.

• Stoelting’s Pharmacology and Physiology 5th Edition

• Millers Anesthesia 8th Edition

• Morgan and Mikhail’s Clinical Anesthesiology 5th Edition