Abstract
Failure of tissue oxygenation represents an emergency during CPB. The principal causes are gaseous embolism, inadequate oxygenation and inadequate CPB flow.
Failure of tissue oxygenation represents an emergency during CPB. The principal causes are gaseous embolism, inadequate oxygenation and inadequate CPB flow.
Massive Air Embolism
Massive air embolism (AE) is defined as the witnessed or likely entry of air into the circulation. The quoted incidence is 1:1,000 cases, which is probably an underestimate. In 25% of recorded cases, massive AE leads to permanent injury or death.
Air can enter the circulation from the surgical field, from the CPB circuit and via indwelling venous and arterial cannulae. A degree of venous AE probably occurs in all patients undergoing CPB and appears to have few obvious consequences.
Surgical Field Entrainment
This is by far the most common source of significant AE. Air enters the circulation when the heart is opened or when a loose suture allows air to be entrained via the venous cannula. The inadvertent delivery of air with cardioplegia solutions may lead to coronary embolism. An aortic root or pulmonary vein venting at high negative pressure can draw air into the ventricle via a coronary arteriotomy. Valveless centrifugal pumps may allow retrograde siphoning of arterial blood and air entrainment via the arterial cannula.
Cardiopulmonary Bypass Air
The maintenance of an adequate volume in the CPB venous reservoir is a fundamental principle of perfusion. Advances in CPB circuit design, monitoring and alarm systems have dramatically reduced the likelihood of this event. Nowadays, CPB equipment includes venous- and arterial-line bubble detectors, and a system that automatically shuts off the pump when the reservoir volume falls below a critical level.
The transition from bubble to membrane oxygenators has significantly reduced the amount of gas deliberately added to the circulation during oxygenation. Punctured or misconnected lines and the loss of membrane integrity may, however, lead to significant gas embolism.
Anaesthetic Sources
Unprimed monitoring and IV infusion lines, and the use of pressurized infusion devices, may result in the inadvertent delivery of significant quantities of air. The practice of re-connecting partially used infusion bags greatly increases the risk of AE and should be avoided.
Physical Principles
An understanding of the gas laws and the properties of air bubbles within the circulation are the keys to successful management (Box 27.1). Nitrogen and oxygen are the main constituents of air. As oxygen is readily absorbed, the challenge is the enhancement of nitrogen elimination. Hypothermia tends to reduce the bubble size (Charles’ law) and increase blood nitrogen solubility (Henry’s law). Barometric and hydrostatic pressures (Boyle’s law) prevent dissolved nitrogen leaving solution, while the partial pressure dictates any tendency to bubble formation (Henry’s law). Self-contained underwater breathing apparatus (‘scuba’) divers know that too rapid an ascent can lead to the formation of nitrogen bubbles, causing decompression illness (the bends).
Box 27.1 The gas laws
- Charles’ law
States that at a constant pressure the volume of a given mass of gas varies directly with the absolute temperature
- Boyle’s law
States that at constant temperature the volume of a given mass varies inversely with the absolute pressure
- Henry’s law
States that at a particular temperature the amount of a given gas dissolved in a given liquid is directly proportional to the partial pressure of the gas in equilibrium with the liquid
The institution of hyperoxia (PaO2 ≫13 kPa) gradually leads to nitrogen displacement (denitrogenation). The arteriovenous oxygen difference (i.e. PaO2 – PvO2) reflects the gradient favouring nitrogen absorption. A nitrogen bubble, 4 mm in diameter (i.e. 0.025 ml), takes more than 10 hours to be absorbed while breathing air, but less than 1 hour while breathing 100% oxygen. As with anaesthetic gas elimination, the rate of denitrogenation is CO dependent.
Management
As massive AE is rare, it is essential that anaesthetists are aware of the possibility and the goals of management before they encounter the problem for the first time. For this reason, many centres have developed their own management protocols, with action plans for the anaesthetist, surgeon and perfusionist. Such plans should be developed after consideration of local practice (e.g. whether or not retrograde coronary sinus cardiac protection is practised). The clinical scenario also lends itself well to simulation (Box 27.2 and Table 27.1). The fundamental principles of good management are early diagnosis, good communication and rapid institution of measures of proven or likely benefit.
Box 27.2 Basic principles of the management of massive AE during CPB
Make the diagnosis
Communicate the diagnosis
Prevent further AE
Identify the source of the AE
Limit organ damage
Clear the CPB circuit of air
Expel air from the major arteries
Re-establish circulation
Table 27.1 The roles of surgeon, perfusionist and anaesthetist in the management of massive AE during CPB
| Perfusionist | Surgeon | Anaesthetist |
|---|---|---|
| Stop CPB pump and clamp lines | Clamp aortic cannula | Carotid compression |
| Cut aortic cannula | Steep head-down position | |
| Ventilate with 100% O2 | ||
| Add cold fluid to reservoir | Prevent cardiac ejection | Cerebroprotectants? |
| Refill arterial line | Connect arterial line to RA | |
| RCP at 1–2 l min-1 | Initiate RCP at 20 °C | |
| Vent air from aortic cannula | ||
| Stop RCP | Reconnect arterial line to aorta | |
| Restart CPB and cool | Complete surgery | Maintain MAP ~ 80 mmHg |
| Slow partial rewarm | Consider hyperbaric O2 |
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