Abstract
Failure to wean a patient from CPB at the first attempt after routine cardiac surgery is a relatively uncommon occurrence. Following prolonged, complex or emergency surgery, however, failure to wean is relatively common. In the majority of cases, weaning difficulty can be attributed to myocardial ischaemia secondary to a prolonged AXC time, inadequate myocardial protection, frank MI or coronary embolism. Less common causes include extremes of prosthetic valve malfunction, anastomotic strictures, extremes of vascular resistance and cardiac compression from retained surgical swabs.
Failure to wean a patient from CPB at the first attempt after routine cardiac surgery is a relatively uncommon occurrence. Following prolonged, complex or emergency surgery, however, failure to wean is relatively common. In the majority of cases, weaning difficulty can be attributed to myocardial ischaemia secondary to a prolonged AXC time, inadequate myocardial protection, frank MI or coronary embolism. Less common causes include extremes of prosthetic valve malfunction, anastomotic strictures, extremes of vascular resistance and cardiac compression from retained surgical swabs.
The key to successful termination of CPB in this situation is the recognition that there is a problem, the identification of the cause or causes and the timely institution of remedial therapy accompanied by effective communication (Box 6.1). In order to prevent ventricular distension and inadequate coronary perfusion, the surgical team must act before the situation escalates. In certain scenarios the reinstitution of CPB, insertion of an IABP or institution of ECMO should be considered. Generally speaking, conditions impeding successful weaning can be considered as either correctable or non-correctable by the anaesthetist (Box 6.2).
Box 6.1 Diagnosing a post-CPB low CO state
Box 6.2 Causes of failure to wean from CPB
Correctable by the anaesthetist or perfusionist
Impaired myocardial function
Air embolism
Dysrhythmia
Hypothermia
Metabolic/acid–base
Preload
Respiratory/airway
Extremes of SVR and PVR
Profound haemorrhage
Gross anaemia
Monitoring artefact
Not correctable by the anaesthetist or perfusionist
Acute MI
Inadequate surgical correction
New anatomical defect
Prosthetic valve malfunction
Correctable Causes
Impaired Ventricular Function
Dysfunction may be systolic or diastolic, can affect the LV or RV and may be regional or global. TOE is invaluable in assessing the extent and severity of ventricular dysfunction and the response to intervention. Myocardial stunning secondary to prolonged myocardial ischaemia, or inadequate myocardial protection or revascularization, usually responds to a further period of CPB and inotropes; however, more frequently, ECMO can be used over a 24–48-hour period to allow cardiac function to recover. Preceding any attempt to wean from CPB, a minimum period of 10–15 minutes of coronary reperfusion following removal of the AXC should be observed. A spasm of native coronary arteries or arterial bypass conduits, which may cause significant ventricular dysfunction, usually responds to nitrates.
Air Embolism
The incidence of air embolism is increased following procedures in which the left heart is opened (e.g. aortic, MV, AV and LV aneurysm surgery). The right coronary artery (RCA) is more commonly affected as its ostium lies superiorly in the supine patient. RV distension and conduction abnormalities may be the first clinical indications of air embolism. TOE may reveal a regional wall motion abnormality (RWMA) and myocardial ‘air contrast’ (increased echo reflectivity) in the RCA territory. In practice, vasopressors are used to treat mild myocardial dysfunction, whereas allowing the heart to eject while on partial CPB may be necessary if myocardial dysfunction is severe. Ventilation of the lungs with an FiO2 of 1.0 should, at least in theory, accelerate the absorption of nitrogen from intravascular air.
Dysrhythmia
It is futile to attempt to terminate CPB in the presence of untreated asystole, bradycardia, VT or VF. Atropine and epicardial pacing are the first-line treatments for bradydysrhythmias. Persistent ventricular dysrhythmias require electrical cardioversion in the first instance. An underlying physical or metabolic cause should be actively sought before resorting to antidysrhythmics (e.g. lidocaine, amiodarone). New-onset AF or other SVT may respond to synchronized transatrial cardioversion, whereas unstable nodal rhythms may be converted to sinus rhythm by isoproterenol.
Hypothermia
Ventricular irritability, dysrhythmias and contractile dysfunction are more common at temperatures <34 °C. Deep hypothermic circulatory arrest (DHCA) is necessary for some complex procedures, affecting the patient blood flow requirements and subsequent complete rewarming both bladder and nasopharyngeal temperatures are necessary if DHCA is utilized. See Table 6.1 for details.
Table 6.1 Effect of hypothermia on patient flow index requirements
| Hypothermia | Temperature (°C) | Flow Index (l min–1 m–2) |
|---|---|---|
| Normothermia | 34–37 | 2.4 |
| Moderate hypothermia | 32–34 | 2.2 |
| Hypothermia | 28–32 | 1.8–2.0 |
| Profound hypothermia | <28 | 1.6 |
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