Question 18 from the second paper of 2006 asked about the causes of post-bypass hypoxia. Prior to this, and subsequently, there have been no questions directly addressing this topic. However, it is an interesting and important topic.
Ruesch and Levy divide the causes into aetiological categories:
- Mechanical problems
- Pulmonary oedema
- Intrapulmonary shunt
- Intracardiac shunt
Mechanical problems
- Pneumothorax
- Haemothorax
- Endotracheal tube migration
- Mucus plugging the bronchus
- Blood clot plugging the bronchus
- Phrenic nerve palsy
Pneumothorax due to unusual drain placement is an infrequently encountered complication. Usually, the skill of the surgeon is equal to the task of placing the drains without this happening.
Pulmonary oedema
- Post-bypass ARDS (as a circuit-related SIRS complication)
- Poor LV function (the patient may already have been in pulmonary oedema pre-operatively)
- Anaphylaxis-associated increase in pulmonary vascular permeability
ARDS no longer plagues the post-bypass community quite as much as it used to. Back in the day, cruelly primitive bypass circuits used to activate complement and set up a systemic inflammatory response. Now, we have nicer circuits; but ARDS in still not out of the question
Intrapulmonary shunt
- Atelectasis (due to surgical handling, or incomplete reinflation of the left lung)
- There will very likely (70% chance) be some atelectasis, particularly of the left lower lobe. And there can be a pleural effusion. Usually, but not always, the drains should take care of this.
- Furthermore, the chest wall is not especially compliant now that there are sternal wires. This is going to be counterproductive when you try to take a deep full breath (as it will hurt).
- The bog-standard means of managing this are well known to everybody and I will do no more than list them here:
- Adequate analgesia
- PEEP (including NIV)
- Incentive spirometry
- Chest physiotherapy
- Sitting out of bed in a chair
- Early mobility
- Inhibition of hypoxic pulmonary vasoconstriction(the GTN or nitroprusside are usually to blame for this - they inhibit the normal pulmonary arterial behaviour)
Intracardiac shunt
- The increase of right sided pressures can unveil a hitherto silent septal defect, thereby shunting venous blood into the left circulation. This is not "freakishly rare", as a patent foramen ovale exists in about 10% of the population. This flap-like opening, normally shut, gets opened by an increase in right sided pressures (associated with post-bypass pulmonary hypertension) and shunts venous blood into the systemic circulation. Hilarity ensues, as you try to work out why your patient is hypoxic in spite of essentially normal X-ray findings.
Investigations
- Assessment of the pain level and adequacy of analgesia
- Assessment of the trends in ventilator pressures (i.e. has the peak pressure suddenly increased?)
- Auscultation and percussion
- ABG
- CXR
- TTE and TOE