Cardiac Advanced Life Support

• Deterioration following cardiac surgery often occurs in the immediate post-operative hours
• It usually manifests as a deviation from the normal pattern of correctable physiological abnormalities that occur post-surgery

• Hypovolaemia is common, most commonly due to haemorrhage
• Risk factors for post-operative haemorrhage include:
• Pre-operative anti-platelet or -coagulant treatments
• Existing bleeding diathesis
• Emergency or re-do surgery
• Prolonged bypass times


• 'Medical' bleeding arises due to correctable post-CPB coagulopathy, including the residual effects of residual heparinisation
• FBC, VHA, clotting screens and blood gases for Hb/haematocrit should identify issue and guide correction
• Hb >80g/L, haematocrit >25% are suitable targets


• 'Surgical' bleeding arises due to excessive blood loss
• Common bleeding sites include: into chest drains | sternal wire sites | anastomotic leaks | occult internal collections (pleural/pericardial)
• CXR and TOE form part of diagnostic assessment
• Should prompt consideration of surgical re-exploration

• Cardiac tamponade is a surgical emergency


• Tamponade can be difficult to diagnose as the 'classical' signs of hypotension, reduced CO, rising filling pressures and tachycardia may be obscured
• Often the first sign is rising vasoactive infusion requirements i.e. hypotension


• Both TTE and TOE can be used to diagnose tamponade
• They may miss small volumes of blood which can still cause cardiac compression and haemodynamic instability
• TOE is a superior modality for tamponade; TTE can miss blood in certain positions and may be obscured by drain placements


• Cases of suspected tamponade will require re-sternotomy and surgical drainage
• There is a risk of massive increase in preload at the time of re-sternotomy
• This risks graft suture rupture
• Should stop vasoactive treatment at the time of re-sternotomy to avoid this

• CPB often causes a fall in ventricular function, even in the absence of pre-operative dysfunction
• This usually resolves within 72hrs, but this may be delayed
• Perioperative TOE identifies LV dysfunction and the need for either pharmacological (inotropy) or mechanical (IABP) support
• RV failure accounts for 20% of post-operative low CO states

• Early graft dysfunction (3%) and valve failure (uncommon) can lead to myocardial ischaemia
• Myocardial ischaemia following coronary revascularisation may be masked in the immediate post-operative period by epicardial pacing
• Features of myocardial ischaemia include new ECG changes, persistent low CO state and RWMA on TOE

• Arrhythmia, particularly AF


• Prolonged vasodilation and relative hypovolaemia can occur post-CPB
• Commonly this is from re-warming, but anaphylaxis, sepsis, adrenal insufficiency and use of inodilators can also cause vasodilation

• The priority is to correct reversible causes of arrest in a timely manner (typically VF, bleeding or tampoande)
• If these measures fail then immediate chest re-opening should occur to preserve cerebral function
• The CALS protocol should be activated in the presence of cardiac arrest, indicated by lack of pulsatile waveforms and clinical cardiac arrest

• External compressions can cause cardiac/graft injury, which may be fatal
• Basic life support should therefore be delayed for up to 1 minute to allow initial management of:


1. VF or pulseless VT → expeditious defibrillation with three stacked shocks at 150J


2. Asystole → institution of external pacing, e.g. DDD pacing at 80-100bpm and maximum current (no atropine or adrenaline)


3. PEA → turn off pacing box, as pacing may disguise underlying rhythm e.g. VF (no adrenaline)


• In addition to the above, one should instigate some ventilatory changes:
• Switch F_iO₂ to 1.0 and PEEP off [optimises preload]
• Change to BVM ventilation
• Treat tension pneumothorax if present


• Other changes to support the ailing cardiovascular system include:
• If an IABP is present, it should be changed to a pressure trigger and 1:1 ratio with maximal augmentation
• Stop sedation as it may contribute to haemodynamic compromise and there is unlikely to be awareness with such poor cerebral perfusion


• If the patient remains in cardiac arrest despite the above, modified ALS should be started and preparations for re-sternotomy made

• The initial VF/pulseless VT overall responds to defibrillation in 50% of cases
• The efficacy of each of the 'stacked' 150J shocks decreases in time:
• First shock: 78%
• Second shock: 35%
• Third shock: 14%
• Any subsequent stacked shocks: negligible success rate


• If these fail, commence CPR and prepare for re-sternotomy
• The patient should also receive 300mg IV amiodarone (or 1mg/kg IV lidocaine) immediately
• CPR should be continued in 2min cycles, with a DC shock every 2mins, until re-sternotomy

• If the asystole/bradycardia hasn't responded to pacing, or turning the pacing box off reveals the patient is in actual PEA, then start CPR
• Do not give adrenaline (see below) or atropine
• Prepare for re-sternotomy

• External compressions are performed in a similar way to standard ALS e.g. 100-120bpm
• Effectiveness of compressions should be judged against a systolic impulse of >60mmHg
• An inability to achieve this suggests either:
• Inadequate technique
• Inadequate pre-load secondary to hypovolaemia | tamponade | tension pneumothorax

• 50% of post-operative cardiac arrests require re-sternotomy, although the overall risk for patients undergoing cardiac surgery is 2.7%
• Emergent re-sternotomy should occur within 5mins to facilitate internal cardiac massage or internal defibrillation


• Internal cardiac massage is associated with a 2x increase in cardiac index vs. external massage (e.g. 1.3 vs. 0.6L/min/m²)
• Internal defibrillation requires much smaller energies; use 20J

• Adrenaline should be avoided during cardiac ALS if possible, certainly in the standard 1mg dose during cardiac arrest
• Its use can cause large surges in blood pressure, especially once ROSC is acheived, potentially leading to:
• Exacerbating bleeding
• Catastrophic disruption at surgical sites e.g. tearing or rupture of anastamotic grafts


• If needed, lower doses are recommended e.g.≤50μg
• This should provide enough support to treat aetiologies such as anaphylaxis or peri-arrest hypotension, but reduce the risk of iatrogenic injury

• ECMO-CPR may appropriate in some patients with refractory cardiac arrest
• Good neurological outcomes occur in 40 - 50% of E-CPR cases
• The primary determinant of outcome is time from cardiac arrest to ECMO flow and is optimally <30mins

• Cardiac arrest is rarely sudden, always witnessed, rapidly diagnosable and often readily reversible owing
• CPR should be delayed by up to 1min to allow electrical management first
• Three stacked 150J DC shocks given for VF/pulseless VT
• Amiodarone 300mg IV is given immediately after the three stacked shocks for those in shockable rhythms
• Either do not use adrenaline, or give small doses e.g. 50μg
• Re-sternotomy is the final common pathway for all rhythms/aetiologies and should occur within 5mins