Case Introduction Division of Pulmonary and Critical Care Medicine, Albany Medical Center, Albany, New York Diagnosis of Intra-Operative Pulmonary Embolism using End-tidal CO2 and Arterial Blood Gas Kristoffer P. Neu MD, Anwar Mohammad Haque MD REFERENCES: 1Patel et al. Changes in End Tidal CO2 and Arterial Blood Gas Level After Release of Tourniquet. SMJ1987 vol.80, No2, 213 Kam et al. The Arterial Tourniquet: Pathophysiological Consequences and Anaesthetic Implications . Anaes thesia, 2001, 56, 534-545 Lee et al. Oxygen Consumption and Car bon Dioxi ode Eliminatio n After Release of Unilateral Lower Limb Pneuma tic Tourniquets. Anesth Analg 1992 ; 75:113-7. Wes t J. Respiratory Physiology: T he Essentials 8th edition. 2008 A 44-year-old male presented to the emergency room after a fall and suffered a stage 4 tibial plateau fracture. The patient was taken to the operating room (OR) for an external fixation of patient’s left leg to stabilize the fracture and two days later went back to the OR for internal fixation of the fracture. During the case, the patient had an intra- operative tourniquet placed over the left knee for hemostasis during the repair. Immediately after the tourniquet release, the patient’s saturations had dropped to 83%. The patient’s heart rate went from 85 to 115 beats per minute however the blood pressure remained stable. The oxygen saturation was increased by bag mask ventilation and increasing the FiO2 from 40% to 100%. The patient was then placed back on volume control ventilation with settings of tidal volumes of 800 mL, a rate of 12, PEEP of 5, and FiO2 40%. There was continuous EtCO2 monitoring throughout the case, which was 35 mmHg prior to tourniquet release. After release, the EtCO2 decreased to 23 mmHg instead of increasing, as would be expected. An ABG was obtained and found the patient had an initial pH of 7.24, PCO2 of 61, PO2 of 85, bicarbonate of 26, and saturation was 95% On 100% FiO2 with an A-a gradient of 552. Based on the large A-a gradient and a decrease in end-tidal CO2, an acute physiologic dead space occurred and a PE was suspected. A CT angiogram was performed and confirmed multiple large proximal segmental PE’s. Discussion Normal physiologic changes with tourniquet release show that EtCO2 and PaCO2 increase within one minute and do not return to normal for 13 minutes. The blood pH decreases maximally in 4 minutes due to an increase in PCO2 as well as a metabolic acidosis from lactic acid formation. In an area of lung that does not have adequate perfusion, the measured alveolar CO2 would be low and alveolar O2 concentrations would be high, thus creating a physiologic dead space. In our patient, we see an acute formation of physiologic dead space with his EtCO2 decreasing instead of increasing and he has a large A-a gradient which left only one possible explanation in such an acute setting, a large PE. Conclusion The combined use of EtCO2 and an ABG was able to demonstrate an acute physiologic dead space quickly narrowing the diagnosis to an acute PE. Intra-operative Pulmonary Embolism (PE) is reported with tourniquet use in lower extremity orthopedic surgeries. Routinely, end-tidal CO2 (EtCO2) is used in these cases to monitor gas exchange. Presented is a case of acute PE following tourniquet release in which the diagnosis was made using EtCO2 monitoring and arterial blood gas (ABG) sampling. This case reminds us how important it is to have an understanding of basic physiology of ventilation and perfusion in order to make correct clinical diagnosis. pH Over Time 7.1 7.15 7.2 7.25 7.3 7.35 7.4 7.45 7.5 11:45 12:30 13:00 13:30 17:30 Time pH pCO2 Over Time 0 10 20 30 40 50 60 70 11:45 12:30 13:00 13:30 17:30 Time pCO2 EtCO2 Over Time 0 5 10 15 20 25 30 35 40 9:00 9:30 10:00 10:30 11:00 11:30 12:00 Time EtCO2 Images 1 & 2 : CTA scan of the chest confirming large bilateral PE’s (Red arrows pointing to the emboli). Image 1 Image 2 Figure 1: A- Shows EtCO2 over time. The arrow is the time the tourniquet was released. B & C- demonstrate pCO2 and the pH shortly after the tourniquet was released. Figure A: shows the PO2 and PCO2 in a unit of normal V/Q ratio. Figure B: shows a V/Q ratio of zero (no ventilation). In this scenario, the PCO2 increases in both intravascular and in the alveolar space. Figure C: Demonstrates a V/Q ratio of infinity (no perfusion, only ventilation) similar to what occurs in a PE. As demonstrated with no perfusion the PCO2 will decrease in the alveolar space but will increase in the serum. #1089
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Case
Introduction
Division of Pulmonary and Critical Care Medicine, Albany Medical Center, Albany, New York
Diagnosis of Intra-Operative Pulmonary Embolism using End-tidal CO2 and Arterial Blood GasKristoffer P. Neu MD, Anwar Mohammad Haque MD
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A 44-year-old male presented to the emergency room after a fall and suffered a stage 4 tibial plateau fracture. The patient was taken to the operating room (OR) for an external fixation of patient’s left leg to stabilize the fracture and two days later went back to the OR for internal fixation of the fracture. During the case, the patient had an intra-operative tourniquet placed over the left knee for hemostasis during the repair. Immediately after the tourniquet release, the patient’s saturations had dropped to 83%. The patient’s heart rate went from 85 to 115 beats per minute however the blood pressure remained stable. The oxygen saturation was increased by bag mask ventilation and increasing the FiO2 from 40% to 100%. The patient was then placed back on volume control ventilation with settings of tidal volumes of 800 mL, a rate of 12, PEEP of 5, and FiO2 40%. There was continuous EtCO2 monitoring throughout the case, which was 35 mmHg prior to tourniquet release. After release, the EtCO2 decreased to 23 mmHg instead of increasing, as would be expected. An ABG was obtained and found the patient had an initial pH of 7.24, PCO2 of 61, PO2 of 85, bicarbonate of 26, and saturation was 95% On 100% FiO2 with an A-a gradient of 552. Based on the large A-a gradient and a decrease in end-tidal CO2, an acute physiologic dead space occurred and a PE was suspected. A CT angiogram was performed and confirmed multiple large proximal segmental PE’s.
DiscussionNormal physiologic changes with tourniquet release show that EtCO2 and PaCO2 increase within one minute and do not return to normal for 13 minutes. The blood pH decreases maximally in 4 minutes due to an increase in PCO2 as well as a metabolic acidosis from lactic acid formation. In an area of lung that does not have adequate perfusion, the measured alveolar CO2 would be low and alveolar O2 concentrations would be high, thus creating a physiologic dead space. In our patient, we see an acute formation of physiologic dead space with his EtCO2 decreasing instead of increasing and he has a large A-a gradient which left only one possible explanation in such an acute setting, a large PE.
ConclusionThe combined use of EtCO2 and an ABG was able to demonstrate an acute physiologic dead space quickly narrowing the diagnosis to an acute PE.
Intra-operative Pulmonary Embolism (PE) is reported with tourniquet use in lower extremity orthopedic surgeries. Routinely, end-tidal CO2 (EtCO2) is used in these cases to monitor gas exchange. Presented is a case of acute PE following tourniquet release in which the diagnosis was made using EtCO2 monitoring and arterial blood gas (ABG) sampling. This case reminds us how important it is to have an understanding of basic physiology of ventilation and perfusion in order to make correct clinical diagnosis.
pH Over Time
7.17.157.2
7.257.3
7.357.4
7.457.5
11:45 12:30 13:00 13:30 17:30
Time
pH
pCO2 Over Time
0
10
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11:45 12:30 13:00 13:30 17:30
TimepC
O2
EtCO2 Over Time
05
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11:00
11:30
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Time
EtCO2
Images 1 & 2 : CTA scan of the chest confirming large bilateral PE’s (Red arrows pointing to the emboli).
Image 1 Image 2
Figure 1: A- Shows EtCO2 over time. The arrow is the time the tourniquet was released. B & C- demonstrate pCO2 and the pH shortly after the tourniquet was released.
Figure A: shows the PO2 and PCO2 in a unit of normal V/Q ratio. Figure B: shows a V/Q ratio of zero (no ventilation). In this scenario, the PCO2 increases in both intravascular and in the alveolar space. Figure C: Demonstrates a V/Q ratio of infinity (no perfusion, only ventilation) similar to what occurs
in a PE. As demonstrated with no perfusion the PCO2 will decrease in the alveolar space but will increase in the serum.
#1089
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