Effect of intracardiac shunts on inhalation induction

Published on 13/02/2015 by admin

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Effect of intracardiac shunts on inhalation induction

David J. Cook, MD and Eduardo S. Rodrigues, MD

Intracardiac shunts may alter the rate of induction of inhaled anesthetic agents. This alteration depends on the direction and size of the shunt and on the solubility of the anesthetic agent used.

Induction of anesthesia is a function of the equilibration of three factors: the rate of anesthetic inflow into the lungs and equilibration with alveolar gas (as determined by tidal volume, respiratory rate, inspired fraction of anesthetic agent, and functional residual capacity), the rate of transfer of the anesthetic agent from lungs to arterial blood, and the rate of transfer of the anesthetic agent from blood to brain:

< ?xml:namespace prefix = "mml" />PA ↔ Pa ↔ Pb

image

where PA equals the alveolar partial pressure of the inhaled anesthetic agent; Pa, the arterial partial pressure of the inhaled anesthetic agent; and Pb, the brain partial pressure of the inhaled anesthetic agent. Pimage equals the mixed venous partial pressure of the inhaled anesthetic agent.

Cardiac shunts primarily alter the effect of the uptake of the anesthetic agent by pulmonary arterial blood. The determinants of anesthetic uptake from alveoli are the blood-gas partition coefficient of the anesthetic agent, the cardiac output (CO), and the alveolar to mixed venous partial pressure difference of the anesthetic agent (PA – Pimage).

The blood-gas partition coefficient is the distribution ratio of the anesthetic agent between blood and alveolar gas at equilibrium (relative solubility). For a highly soluble agent, it usually takes several passes of the blood volume through the lung before enough of the agent is absorbed that the blood is saturated to the point that the necessary Pa of the agent to achieve anesthesia is reached. A highly soluble agent, then, has a much slower induction time, compared with an agent that is not soluble (see following discussion). Assuming no change in ventilation or inspired fraction of anesthetic agent and normal tissue perfusion, the rate of induction is determined primarily by anesthetic solubility and the effective pulmonary blood flow.

Right-to-left shunt

With a right-to-left shunt, a portion of the CO bypasses the lung, slowing induction because less anesthetic agent can be transferred from the alveoli to systemic blood per unit of time. The rate of induction for an insoluble agent is proportional to the degree of shunting (i.e., the greater the shunt, the slower induction). The impact of the shunt is less pronounced for a soluble anesthetic agent. Using ether as an example, with a blood-gas partition coefficient of 12, 1 L of blood would have to absorb 12 times more ether than 1 L of gas. If ventilation were 5 L/min with 10% ether, then 500 mL of ether would be delivered to the alveoli per minute. At equilibrium, the entire blood volume would have to absorb 6 L of ether before equilibrium was reached. In this scenario, ventilation slows induction because only 0.5 L of ether is delivered to the alveoli; it would take 12 min for 6 L to be delivered to the alveoli. If there were a 50% right-to-left shunt and pulmonary blood flow was only 2.5 L (half of the “normal” 5 L/min), pulmonary blood flow would still take up the 0.5 L of ether.

However, for a poorly soluble anesthetic agent (e.g., N2O, with a blood-gas partition coefficient of 0.47), if ventilation is 5 L/min with 50% N2O, then 2.5 L of N2O is delivered to the alveoli per minute. The entire blood volume would have to absorb approximately 1.25 L of N2O before equilibrium was reached. If the patient had a 50% shunt, the 2.5 L of blood flowing through the lungs would absorb 1.25 L of N2O but would then mix with the 2.5 L of blood that bypassed the lung, resulting in a concentration of only 0.625 L of N2O. Induction time would take at least twice as long.

These examples demonstrate that, with highly soluble agents, such as ether, uptake is limited primarily by ventilation. With poorly soluble agents, such as N2O, uptake is limited primarily by blood flow. Subsequently, the impact of shunting is greater with agents of lower solubility (Figures 63-1 and 63-2).

image
Figure 63-1 Decrease in arterial-to-inspired concentration ratio caused by a 50% right-to-left shunt from control for three anesthetic agents of different solubility (ether, halothane, and N2O). (From Tanner G. Effect of left-to-right, mixed left-to-right, and right-to-left shunts on inhalation induction in children: A computer model. Anesth Analg. 1985;64:101-107.)
image
Figure 63-2 Decrease in arterial-to-inspired concentration ratio from control for two anesthetic agents (halothane and N2O) caused by a 20% right-to-left shunt. (From Tanner G. Effect of left-to-right, mixed left-to-right, and right-to-left shunts on inhalation induction in children: A computer model. Anesth Analg. 1985;64:101-107.)

Left-to-right shunt

With a left-to-right shunt, no significant change occurs in the speed of induction, assuming that systemic blood flow is normal. If tissue perfusion is decreased because of the left-to-right shunt, then induction will initially be slowed because less anesthetic agent will be delivered to the brain per unit of time. CO usually increases to compensate for the shunting, and local control of vasculature maintains cerebral perfusion and minimizes the effect of the shunt (Figure 63-3).

image
Figure 63-3 Arterial-to-inspired concentration (FA/FI) ratio for N2O modeled with and without a 50% left-to-right shunt and normal tissue perfusion. For the normal simulation, imageBC = 3.0 L/min, imageT = 3.16 L/min, imageLR = 0.16 L/min, and imageS = 0.16 L/min. For the left-to-right shunt simulation, imageBC = 3.0 L/min, imageT = 6.0 L/min, imageLR = 3.0 L/min, and imageS = 0.3 L/min. imageBC, Blood flow perfusing body compartments; imageLR, left-to-right shunt; imageS, right-to-left shunt; imageT, total cardiac output. (From Tanner G. Effect of left-to-right, mixed left-to-right, and right-to-left shunts on inhalation induction in children: A computer model. Anesth Analg. 1985;64:101-107.)

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