The pharmacodynamics of inhaled anesthetics is discussed here in detail. The action of inhalation agents are as follows:
I. Pulmonary effects
2. Cardiovascular effects
For pharmacodynamics of inhaled anesthetics , the pulmonary effects of inhalation agents are many and important as this is the portal of entry. There are effects on the following parameters:
1. Pulmonary ventilation: All volatile anaesthetics (except xenon) reduce the tidal volume, minute volume and increase the respiratory rate. As an index of respiratory depression, the rise in Paco2 is caused by Entlurane> Desflurane or Isoflurane> Sevoflurane or Halothane. Xenon decreases respiratory rate and increases tidal volume.
In pharmacodynamics of inhaled anesthetics , the central respiratory control mechanisms are initiated by chemoreceptors and mechanoreceptors in the upper airways, lungs and chest wall with signal transmitted by the vagus and spinal nerves. The laryngeal and pulmonary irritant receptors and pulmonary stretch receptors are affected by inhalation agents. Pulmonary stretch receptors are located in the small airway smooth muscle and respond to changes in stretching or changes in lung volume. Afferents from these receptors (with a high concentration of receptors at the carina) inhibit further inspiration. In pharmacodynamics of inhaled anesthetics , this is known as the Herring-Breuer reflex; activation of this may produce tachypnoea and low tidal volume.
For determining the pharmacodynamics of inhaled anesthetics we observe that Inhalation agents reduce the FRC subsequent to their action on inspiratory and expiratory muscles due to their effect on motor neurons. There is a depression of ventilatory responses to hypercarbia and hypoxia by all inhalation agents due to depression of central and peripheral chemoreceptor function in a dose-dependent manner.
2. Bronchomotor tone: Volatile anaesthetics are potent bronchodilators by a direct depressant effect on the bronchial smooth muscle. Halothane and ether have a significant effect. This action takes place because of a decrease in intracellular calcium concentration and reduction in calcium sensitivity in the presence of a bronchoconstricting agent. Inhaled agents preferentially dilate distal airways than proximal airways. They also increase baseline pulmonary compliance.
3. Mucociliary function: Pharmacodynamics of inhaled anesthetics reduce the rate of mucus clearance by decreasing ciliary beat frequency, metachronism (wave of motion produced by cilia towards the trachea) as well as altering the characteristics of mucus.
4. Pulmonary vascular resistance: is affected by many factors like cardiac output, autonomic activity and local vasoactive substances. Hypoxic pulmonary vasoconstriction (IJPV) is a phenomenon by which pulmonary blood flow is preferentially redistributed away from poorly ventilated lung regions (e.g., atelectatic units) to more adequately ventilated regions in determining pharmacodynamics of inhaled anesthetics
While the pharmacodynamics of inhaled anesthetics are under study the Inhalation agents exert inhibitory effects on HPV, shunting or oxygenation
5. Pulmonary surfactant: Normally pulmonary surfactant reduces the work of breathing by reducing the alveo lar surface tension Volatile anaesthetics produce progressive yet reversible reductions in phosphatidyicholine the main lipid component of surfactant and also affect type II alveolar cell function.
The pharmacodynamics of inhaled anesthetics were explained in detail above.