Cold versus Warm Cardioplegia
The cardioplegic solution for myocardial protection can be delivered at
either cold (≈4-10⁰C) or warm (≈35-37⁰C) temperatures and there is still
much debate regarding the optimal cardioplegic
temperature(19). Since the 1950s, cold crystalloid
solutions were used to maintain the arrested state of the heart due to
it lowering the myocardial oxygen demand and reducing the risk of
ischaemic damage(20). Potassium-induced
electromechanical arrest lowers the oxygen demand of the myocardium by
90%. Lower temperatures of cardioplegic solution reduce this oxygen
demand by a further 5-20% which is done by reducing the myocardial
basal metabolic rate(19).
Lower temperatures of cardioplegia may cause membrane rupture,
denaturalisation of proteins, inhibition of
Na+-K+ and Ca2+ATP systems in the sarcolemma and sarcoplasmic reticulum, and lead to
oedema and calcium sequestration(21). A longer period
of time is needed to rewarm the heart by reperfusion, increasing the
risk of reperfusion injury and arrhythmias(19).
Hypothermia also leads to right shift of the oxyhaemoglobin
dissociation curve, causing lower oxygen availability for the myocardium
in cold blood cardioplegia. At 20⁰C only 50% of the total oxygen
content in blood cardioplegia is available, falling to a further 30%
when temperature is decreased to 10⁰C(19). Other
disadvantages of cold cardioplegia include inadequate delivery of the
cardioplegic solution due to sludging, cold agglutinin activation
and rouleoux formation, leading to myocardial ischaemia and a delay
in recovery of myocardial metabolism and function
postoperatively(19).
To avoid these side-effects of cold cardioplegia, warm blood
cardioplegia was brought in in the 1970s(20). Giving
continuous warm cardioplegia prevents hypothermic ischaemia and
also minimises reperfusion injury(19). A meta-analysis
by Fan et al. found that warm cardioplegia was associated with improved
postoperative cardiac index reduced cardiac markers (cTn and CK-MB)
indicating less cardiocyte injury(20).
Lichtenstein et al. observed the outcomes in two groups of patients
undergoing CABG post-MI. The warm group had lower 30-day mortality rate
and a reduced need for postoperative IABP(19). An
Emory University study however found a significantly higher rate of
postoperative neurological complications in warm versus cold
cardioplegia (4.5% versus 1.4%), along with more perioperative strokes
with warm cardioplegia (3.1% versus 1.0% with cold). They hypothesised
this was due to use of blood cardioplegia in the warm group which had
higher glucose level and caused hyperglycaemia, absence of
neuroprotective benefits of hypothermia, and embolic events leading to
stroke(19).
With warm cardioplegia there is need for larger total volumes of
cardioplegic solution, increased use of high potassium cardioplegia to
eliminate episodes of electric activity, higher risk of systemic
hyperkalaemia, reduced systemic vascular resistance, as well as
increased use of crystalloid and alpha-agonists to maintain perfusion
pressures(19).
Kuhn et al. looked at the amount of endothelial injury with each
technique, quantified by measuring circulating endothelial cells (CECs),
von Willebrand factor (vWF) and soluble thrombomodulin (sTM).
Concentrations of all these factors were much higher with warm
cardioplegia, reflecting greater endothelial injury compared to cold
cardioplegia(22). The advantages and disadvantages of
each technique is summarised in Table 2.