Massive CO2 embolism in cardiopulmonary bypass circuit – a near miss
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《血管的通路杂志》
Department of Cardiothoracic Surgery, Royal Infirmary Edinburgh, Edinburgh, EH16 4SA, UK
Abstract
Objectives: We report a case of massive air embolism in the cardiopulmonary bypass (CPB) circuit to highlight the principle of its immediate management and its preventive measures. Methods: The air embolism was caused by the accidental connection of carbon dioxide (CO2) supply to the monitoring arm of the retrograde cardioplegia delivery system. The CPB ceased, resulting in cardiac arrest requiring immediate internal cardiac massage. Cerebral protective measures were also instituted instantaneously and the air embolism was purged from the CPB circuit. The cause of air embolism was identified after high initial arterial CO2 concentration was detected in the blood gas analysis. The CO2 supply was disconnected, and CPB was restarted. Spontaneous cardiac activities resumed shortly after, and the operation was completed uneventfully. Results: The patient had no immediate post-operative sequel and remained well at 6 weeks follow-up. Conclusion: Massive air embolism in cardiopulmonary bypass (CPB) circuit is a life-threatening emergency. Immediate cerebral protective manoeuvres and rectification of the cause of air embolism are vital for favourable outcome. However, high degree of vigilance and cooperation amongst all teams involved are paramount to prevent its occurrence in the first place.
Key Words: Cardiopulmonary bypass; Carbon dioxide; Air embolism
1. Introduction
Carbon dioxide (CO2) insufflation has been shown to reduce the risk of air embolism during open cardiac surgery [1]. CO2 delivery through a blower has also been used to improve visualisation during off-pump coronary artery bypass grafting (CABG) [2]. We described a case of massive CO2 embolism in cardiopulmonary (CPB) circuit due to an accidental delivery of CO2 via the retrograde cardioplegia system.
2. Case report
A 62-year-old male, with triple vessel disease and poor left ventricular function, was admitted for CABG. The procedure was performed on cardiopulmonary bypass (CPB) via aortic root arterial cannulation and right atrial two-staged venous cannulation, under moderate systemic hypothermia (28 °C). Myocardial protection was undertaken by delivering multiple doses of blood cardioplegia through antegrade and retrograde routes.
After the insertion of the 14F retrograde cardioplegia cannula (Edwards Lifesciences, USA), the monitoring side-arm of the retrograde cannula was attached to a monitoring line for connection to a pressure transducer circuit. As similar monitoring lines have also been used for CO2 delivery in our unit, this was unknowingly attached to CO2 supply instead. In this instance, the three-way tap on the retrograde cannula side-arm was also not turned off (Fig. 1).
A large quantity of air bubbles were noted within seconds in the venous circuit, and the venous cannulation site, prior to the priming of monitoring line. The air bubbles were initially thought to be due to problems with the venous cannulation purse-string. Despite two further reinforcement purse strings, air bubbles persisted to exude under pressure around the venous cannula. By this stage, the right atrium was distended, with air bubbles resulting in a massive air embolism in the venous circuit, and eventual cessation of CPB. Subsequent asystolic arrest required immediate internal cardiac massage. Simultaneously, the patient was placed in the Trendenleburg position. As there was no air embolism in the arterial circuit, the venous circuit air embolism was eliminated by removing the venous cannula, and priming the venous line with normal saline.
Despite a methodical initial check, the cause of the air embolism was not immediately obvious, until a high arterial pCO2 of 12.6 kPa was detected on his arterial blood gas at the onset of the event (pH 7.41, pO2 11.2, pCO2 12.6, HCO 27.6, and base excess –1.2). Iatrogenic CO2 introduction was suspected, and the wrong connection was quickly identified. CO2 supply was disconnected from the sidearm of the retrograde cannula so that the correct pressure transducer could be connected.
After systemic de-airing of the heart, CPB was resumed. The heart also regained its sinus activities. The patient was ventilated with 100% oxygen to speed up the removal of CO2 from the body. The rest of the CABG was completed uneventfully, and the blood CO2 level eventually normalised. The patient was extubated twelve hours after his surgery without any neurological deficit, and was discharged five days later. There were no problems at a follow-up period of 6 weeks.
3. Discussion
Massive air embolism during CPB can cause significant neurological morbidity and fatality. The immediate management strategies are directed to: optimise cerebral protection, and remove air embolism from the heart, peripheral circulation and the CPB circuit. These measures include: (a) immediate cessation of CPB and placement of the patient in Trendelenburg position, (b) making a stab in aorta or removing the aortic cannula to allow retrograde drainage of air from the cerebrovascular bed if arterial air embolism is present, (c) temporary retrograde perfusion via superior vena cava, if necessary with temporary compression of carotids to allow retrograde purging of air through the vertebral system, (d) purging of perfusion lines to remove air from the circuit, (e) systemic deairing of all heart chambers, massage of air out from coronaries, and (f) mechanical ventilation of lungs to evacuate pulmonary venous air [3]. Steroid administration, ventilating with 100% oxygen, and the use of barbiturate anaesthesia may also be beneficial [3]. Concurrently, the cause of the air embolism should be identified and rectified in order to resume CPB rapidly.
Most of the massive air emboli are caused by either mechanical faults in the CPB circuitry or human errors, which has been described in detail along with their prevention measures by Mills et al. [3].
In this case, the CO2 used for minimising air embolism in open-heart surgery [1], ironically caused the massive air embolism, when it was accidentally delivered through the retrograde cardioplegia pressure monitoring line. When the CO2 accumulation rate exceeded that of CO2 absorption and drainage via the venous cannula, a massive column of air embolism rapidly developed on the venous circuit. The cause was not apparent until a very high arterial CO2 concentration was detected.
To prevent such recurrence, blood should be aspirated from the monitoring arm of the retrograde cannula after its insertion to remove any residual air. The three-way tap should then be closed off. Alternatively, the monitoring arm can be primed with normal saline and the three-way tap turned off before its insertion. This can only be connected and opened when the rest of the monitoring circuit is flushed through with normal saline. The appropriate coronary sinus pressure trace must also be confirmed on the monitor.
When CO2 is used to flood the operative field, a different colour-coded delivery line should be used. Regular monitoring of blood CO2 is also necessary, as profound systemic hypercarbia and acidosis can occur, by the potential absorption of CO2 via cardiotomy suction in the operative field [4]. In our case, it had aided us in the identification of the cause of CPB air embolism.
A high degree of vigilance and co-operation amongst all teams involved remain the key elements in the prevention, and management of massive air embolism during CPB. Should the inevitable occur, immediate cerebral protection, and removal of air embolism methodically will ensure optimal outcome.
References
Svenarud P, Persson M, van der Linden J. Effect of CO2 insufflation on the number and behavior of air microemboli in open-heart surgery: a randomized clinical trial. Circulation 2004; 109:91127–1132.
Roy A, Stanbridge RL, O'Regan D, Salerno G, Saldanha C, Griselli M, Cherian A. Progression to 100% off-pump coronary artery bypass with the Octopus 1 dual holder. Heart Surg Forum 2001; 4:2174–178.
Mills NL, Ochsner JL. Massive air embolism during cardiopulmonary bypass: causes, prevention and management. J Thorac Cardiovasc Surg 1980; 80:708–717.
O'Connor BR, Kussman BD, Park KW. Severe hypercardia during cardiopulmonary bypass: a complication of CO2 flooding of the surgical field. Anesth Analg 1998; 86:264–266.(Dharmendra Agrawal, Keng-)
Abstract
Objectives: We report a case of massive air embolism in the cardiopulmonary bypass (CPB) circuit to highlight the principle of its immediate management and its preventive measures. Methods: The air embolism was caused by the accidental connection of carbon dioxide (CO2) supply to the monitoring arm of the retrograde cardioplegia delivery system. The CPB ceased, resulting in cardiac arrest requiring immediate internal cardiac massage. Cerebral protective measures were also instituted instantaneously and the air embolism was purged from the CPB circuit. The cause of air embolism was identified after high initial arterial CO2 concentration was detected in the blood gas analysis. The CO2 supply was disconnected, and CPB was restarted. Spontaneous cardiac activities resumed shortly after, and the operation was completed uneventfully. Results: The patient had no immediate post-operative sequel and remained well at 6 weeks follow-up. Conclusion: Massive air embolism in cardiopulmonary bypass (CPB) circuit is a life-threatening emergency. Immediate cerebral protective manoeuvres and rectification of the cause of air embolism are vital for favourable outcome. However, high degree of vigilance and cooperation amongst all teams involved are paramount to prevent its occurrence in the first place.
Key Words: Cardiopulmonary bypass; Carbon dioxide; Air embolism
1. Introduction
Carbon dioxide (CO2) insufflation has been shown to reduce the risk of air embolism during open cardiac surgery [1]. CO2 delivery through a blower has also been used to improve visualisation during off-pump coronary artery bypass grafting (CABG) [2]. We described a case of massive CO2 embolism in cardiopulmonary (CPB) circuit due to an accidental delivery of CO2 via the retrograde cardioplegia system.
2. Case report
A 62-year-old male, with triple vessel disease and poor left ventricular function, was admitted for CABG. The procedure was performed on cardiopulmonary bypass (CPB) via aortic root arterial cannulation and right atrial two-staged venous cannulation, under moderate systemic hypothermia (28 °C). Myocardial protection was undertaken by delivering multiple doses of blood cardioplegia through antegrade and retrograde routes.
After the insertion of the 14F retrograde cardioplegia cannula (Edwards Lifesciences, USA), the monitoring side-arm of the retrograde cannula was attached to a monitoring line for connection to a pressure transducer circuit. As similar monitoring lines have also been used for CO2 delivery in our unit, this was unknowingly attached to CO2 supply instead. In this instance, the three-way tap on the retrograde cannula side-arm was also not turned off (Fig. 1).
A large quantity of air bubbles were noted within seconds in the venous circuit, and the venous cannulation site, prior to the priming of monitoring line. The air bubbles were initially thought to be due to problems with the venous cannulation purse-string. Despite two further reinforcement purse strings, air bubbles persisted to exude under pressure around the venous cannula. By this stage, the right atrium was distended, with air bubbles resulting in a massive air embolism in the venous circuit, and eventual cessation of CPB. Subsequent asystolic arrest required immediate internal cardiac massage. Simultaneously, the patient was placed in the Trendenleburg position. As there was no air embolism in the arterial circuit, the venous circuit air embolism was eliminated by removing the venous cannula, and priming the venous line with normal saline.
Despite a methodical initial check, the cause of the air embolism was not immediately obvious, until a high arterial pCO2 of 12.6 kPa was detected on his arterial blood gas at the onset of the event (pH 7.41, pO2 11.2, pCO2 12.6, HCO 27.6, and base excess –1.2). Iatrogenic CO2 introduction was suspected, and the wrong connection was quickly identified. CO2 supply was disconnected from the sidearm of the retrograde cannula so that the correct pressure transducer could be connected.
After systemic de-airing of the heart, CPB was resumed. The heart also regained its sinus activities. The patient was ventilated with 100% oxygen to speed up the removal of CO2 from the body. The rest of the CABG was completed uneventfully, and the blood CO2 level eventually normalised. The patient was extubated twelve hours after his surgery without any neurological deficit, and was discharged five days later. There were no problems at a follow-up period of 6 weeks.
3. Discussion
Massive air embolism during CPB can cause significant neurological morbidity and fatality. The immediate management strategies are directed to: optimise cerebral protection, and remove air embolism from the heart, peripheral circulation and the CPB circuit. These measures include: (a) immediate cessation of CPB and placement of the patient in Trendelenburg position, (b) making a stab in aorta or removing the aortic cannula to allow retrograde drainage of air from the cerebrovascular bed if arterial air embolism is present, (c) temporary retrograde perfusion via superior vena cava, if necessary with temporary compression of carotids to allow retrograde purging of air through the vertebral system, (d) purging of perfusion lines to remove air from the circuit, (e) systemic deairing of all heart chambers, massage of air out from coronaries, and (f) mechanical ventilation of lungs to evacuate pulmonary venous air [3]. Steroid administration, ventilating with 100% oxygen, and the use of barbiturate anaesthesia may also be beneficial [3]. Concurrently, the cause of the air embolism should be identified and rectified in order to resume CPB rapidly.
Most of the massive air emboli are caused by either mechanical faults in the CPB circuitry or human errors, which has been described in detail along with their prevention measures by Mills et al. [3].
In this case, the CO2 used for minimising air embolism in open-heart surgery [1], ironically caused the massive air embolism, when it was accidentally delivered through the retrograde cardioplegia pressure monitoring line. When the CO2 accumulation rate exceeded that of CO2 absorption and drainage via the venous cannula, a massive column of air embolism rapidly developed on the venous circuit. The cause was not apparent until a very high arterial CO2 concentration was detected.
To prevent such recurrence, blood should be aspirated from the monitoring arm of the retrograde cannula after its insertion to remove any residual air. The three-way tap should then be closed off. Alternatively, the monitoring arm can be primed with normal saline and the three-way tap turned off before its insertion. This can only be connected and opened when the rest of the monitoring circuit is flushed through with normal saline. The appropriate coronary sinus pressure trace must also be confirmed on the monitor.
When CO2 is used to flood the operative field, a different colour-coded delivery line should be used. Regular monitoring of blood CO2 is also necessary, as profound systemic hypercarbia and acidosis can occur, by the potential absorption of CO2 via cardiotomy suction in the operative field [4]. In our case, it had aided us in the identification of the cause of CPB air embolism.
A high degree of vigilance and co-operation amongst all teams involved remain the key elements in the prevention, and management of massive air embolism during CPB. Should the inevitable occur, immediate cerebral protection, and removal of air embolism methodically will ensure optimal outcome.
References
Svenarud P, Persson M, van der Linden J. Effect of CO2 insufflation on the number and behavior of air microemboli in open-heart surgery: a randomized clinical trial. Circulation 2004; 109:91127–1132.
Roy A, Stanbridge RL, O'Regan D, Salerno G, Saldanha C, Griselli M, Cherian A. Progression to 100% off-pump coronary artery bypass with the Octopus 1 dual holder. Heart Surg Forum 2001; 4:2174–178.
Mills NL, Ochsner JL. Massive air embolism during cardiopulmonary bypass: causes, prevention and management. J Thorac Cardiovasc Surg 1980; 80:708–717.
O'Connor BR, Kussman BD, Park KW. Severe hypercardia during cardiopulmonary bypass: a complication of CO2 flooding of the surgical field. Anesth Analg 1998; 86:264–266.(Dharmendra Agrawal, Keng-)