Role of Pulse Oximetry and Capnography in Induced Hypotension Essay Study

Abstract

Induced hypotension is a deliberate reduction of the arterial blood pressure by at least 20% of the baseline of the mean arterial blood pressure. It has many benefits to facilitate the surgical technique and control of bleeding that will improve the operative conditions in some types of operations as during microsurgery (e.g. middle ear, endoscopic sinus surgery and spine surgery) (Donald, 1982). Induced hypotension has certain physiological effects on ventilation and perfusion of lung alveoli and increased dead space ventilation (Miller, 2000). That means that there is increase in the number of the alveoli that are ventilated but not perfused which results in decrease in the end tidal carbon dioxide tension. Still, in the induced hypotensive techniques we institute increase in the minute ventilation by increasing the tidal volume and respiratory rate and this will lead also to a decrease in the arterial carbon dioxide tension.. Normally, the arterial to end tidal carbon dioxide difference (Pa-ET CO2) gradient is less than 5 mmHg (approximately 3.6-4.6 mmHg) in healthy awake patients (Shankar, Moseley, Kumar, 1991). Under general anesthesia in adults it has been evaluated as 4.7±2.5 mmHg and with controlled ventilation the gradient reached a mean of and 2.2 mmHg at large tidal volumes (Nunn, Hill, 1980) and 4.5 mmHg at small tidal volumes (Ramwell, 1988). So, When ventilation and perfusion function normally, PETCO2 should read 2-5 mmHg lower than the PaCO2. This natural CO2 gradient (PaCO2-PETCO2) exists between the level of CO2 in the artery and the end-tidal point because every alveoli varies in its own rate of ventilation and perfusion (Ahrens, Wijeweera, Ray, 1999). During induced hypotension there is abnormal clinical state that cause a widened gradient (> 5 mmHg) which is alveolar hypoperfusion (Ogrady, Egstorm, Fisher, 1993). Alveolar Hypoperfusion means alveolar perfusion that is significantly less than alveolar ventilation in a large number of alveolar/capillary units which impairs CO2 transfer from the blood to the lungs. This higher ventilation (V) than perfusion (Q) ratio (V/Q) results in a lower measured PETCO2 (Ahrens, Wijeweera, Ray, 1999). Global hypoperfusion of the lung (i.e, cardiac arrest and shock) can cause the patient’s PETCO2 to read less than the patient’s true PaCO2 (Ward, Yealy, 1998). Global hypoperfusion states can cause a disparity between the patient’s PETCO2 and PaCO2. Inadequate perfusion reduces alveolar CO2 gas exchange. In the setting of low perfusion and normal ventilation, a high V/Q ratio results. Ventilation that dramatically exceeds lung perfusion dilutes the overall concentration of exhaled CO2. In this setting, the CO2 detector once again reports a lower PETCO2 concentration than the patient’s true arterial CO2. That means that the end tidal carbon dioxide tension in this case is not representative for the actual arterial carbon dioxide tension (Jin, Weil, Tang, et al, 2000). That means that PETCO2 is not reliable for determining the adequacy of ventilation during low cardiac output because of the changes in the arterial to end tidal carbon dioxide gradient which occur in these conditions (Ward, Yealy, 1998). In this direction, adequacy of ventilation must be continually evaluated, and quantitative monitoring of carbon dioxide tension and volume of expired gas are strongly encour¬aged. And the values must be co related with concomitant readings of serial blood gases analysis (Ahrens, Wijeweera, Ray, 1999). We can conclude that, during anesthesia, once normocapnia is achieved with normal arterial blood pressures, there is hardly any need to decrease ventilation after induction of controlled hypotension. That means that ETCO2 does not reflect changes in PaCO2 because as P (a-ET) CO2 gradient is increased, PaCO2 remains in the clinically acceptable range the larger decrease in ETCO2 during controlled hypotension is mainly due to the increase in the Vd phys/Vt and V/Q ratios. The value of our essay is to guard against the false impression of the patient hyperventilation that may accompany the decrease in the level of end tidal carbon dioxide which occurs usually during hypotensive anesthesia. That false impression may lead the anesthetist to erroneously reset the ventilator parameters to maintain the normal value of the end tidal carbon dioxide tension and this resetting leads to increase in the value of the arterial carbon dioxide tension (hypoventilation). End tidal carbon dioxide tension must be co related to the arterial carbon dioxide tension to avoid hypercarbia that may lead to harmful effects on the patient e.g. (delayed recovery, increased intracranial tension and hypertension and tachycardia that lead to increased bleeding during surgery). And those effects are unwanted during microsurgery. So, we must limit the values of the capnography clinically as an estimation of arterial carbon dioxide tension (PaCO2) during deliberate hypotensive anesthesia. And must be used as positive indicator of endotracheal tube placement, disconnection alarm, presence of venous air embolism and even as a cardiac output monitor (Carol, Frank, 2002).