The causes of severe metabolic
acidosis in the post-cardiac surgical patient fall into two categories-Hypoperfusion
and deranged glucose metabolism. Hypoperfusion can also be defined as impaired
oxygen delivery . When the tissues have an insufficient oxygen supply, they
switch from aerobic (mitochondrial) ATP production to anaerobic ATP production,
a much less efficient means of generating ATP and one which generates lactic
acid as a by-product. This form of lactic acidosis is Type A . Lactic and
pyruvic acids are important normal precursors for the synthesis of glucose by
the liver .
Where severe liver disease is
present, inadequate glucose synthesis may occur, resulting in low blood glucose
levels and high levels of these acidic gluconeogenic precursor molecules. This
type of lactic acidosis is called Type B. It may occur in the absence of hypoperfusion
but often hypoperfusion is an added complication in the clinical context . Furthermore,
certain catecholamines, principally adrenaline but also isoprenaline,
accelerate hepatic glycogenolysis and switch off hepatic gluconeogenesis thus
promoting high blood sugar levels and high levels of lactic acid . They also
have a direct effect on cells in general to activate glycolytic energy
production. This may also occur in the absence of hypoperfusion .
Unchecked, the high blood sugar levels that may ensue would result in greatly increased blood viscosity and subsequent impaired oxygen delivery due to increased capillary transit time . Hypoperfusion can be cardiac, macro circulatory or microcirculatory in nature. Often there are combinations of aetiologies in any one patient . The various causes of hypoperfusion in the cardiac surgical patient are worth considering in some detail but before doing so it will first be necessary to review some elementary cardiovascular physiology.
To investigate and identify mechanisms which are conducive to metabolic acidosis in post-heart surgery patients. Study the consequences of postoperative metabolic acidosis and how this can be corrected.
A comprehensive search of
electronic databases (PubMed, Science Direct and Google scholar) using the key
words “metabolic acidosis”, “heart surgery”, “post-operative” was used.
The references in the identified articles were hand-searched for additional studies which were missed by the search strategy. Evidence from these data were critically analysed and summarised to produce this article. The studies consisted of non-randomised retrospective studies, case reports, and review articles.
The circulation of blood is analogous
to the movement of electricity. The latter is governed by Ohm’s law which
states that V=IR . The equivalent equation for blood circulation is the
following: mean blood driving pressure is equal to the product of blood flow
(cardiac output) and systemic vascular resistance (MAPs-CVP=CO x SVR or for the
pulmonary circulation MAPp-LAP=CO x PVR). CVP is central venous pressure and
LAP is left atrial pressure. Since it is the MAP, CVP, LAP and CO that can be
directly measured, the resistances are always derived values . If the
pressure measurements are in mmHg and the CO is in litres per minute, then the
resistance units are called Wood units after the famous British pioneer of
invasive Cardiology, Paul Wood. The more commonly used unit is when International
units are obtained by multiplying the value in Wood units by 80. For blood to
flow through the capillary bed a driving pressure from arteriole to venule of
at least 25 mmHg is required .
Normal circulating blood volume
is 5 litres of which red cells constitute around 40% and plasma 60% . Blood
volume is principally held in the venous system . Venous channels outnumber
arterial channels in a ratio of at least 5 to 1 in all tissues. When general
vasodilation occurs the storage capacity of the venous system increases .
The pressure exerted by the blood returning to the heart is important and is
designated the preload. Optimal cardiac function occurs with filling pressures
in the range 5-15 mmHg. Within this pressure range, increasing the filling
pressure increases cardiac output . The pressure against which the heart
has to eject blood is also an important variable which is called the afterload
When severe hypertension is
present or there is some other increased resistance to outflow of blood from
the ventricle cardiac output is diminished . During passage of blood
through the capillary bed around 10% of the plasma leaks through pores in the
capillary wall into the extravascular extracellular space. Most of this fluid is
reabsorbed into the circulation by venules but some returns to the central
veins via the lymphatic system . The resistance to flow of fluid in a
tubular conduit is given by Poiseuille’s equation: R= (k x length of tubing x
viscosity)/radius4. It is to be noted that vascular resistance is
inversely proportional to the fourth power of the radius of the vessel and that
it is directly proportional to viscosity . Both blood viscosity and
arteriolar tone show considerable variation in the post cardiac surgical
patient and need to be considered in the management of hypoperfusion .
Hypoperfusion could be due to
severely impaired systolic or diastolic cardiac function. Where the heart is
unable to sustain a cardiac output sufficient for life, progressive lactic
acidosis occurs due to inadequate oxygen delivery. Severely impaired systolic
function may exist pre-operatively or may be a new feature of an operation that
has been unsuccessful or where serious complications have occurred. The lactic
acidosis in these cases is countered with catecholamines to try and boost
cardiac output and systemic vascular resistance. Secondary hyperglycaemia is
treated with an intravenous infusion of insulin . Sodium bicarbonate
solution can also be given to directly buffer the acids, but this has the
limiting factor of increasing plasma sodium level . Usually after using
NaHCO3 for 24 hours the plasma sodium level has increased
noticeably. When it exceeds 145 mmol/L it is generally considered unacceptable
to continue using it to treat metabolic acidosis. Severe hypernatremia can have
serious neurological consequences and must be avoided . Intra-aortic
balloon pumping is also used in the presence of severely impaired systolic
cardiac function. A sausage shaped balloon is inserted through a delivery
system into the descending thoracic aorta, usually via the femoral artery. This
allows a helium bladder to drive sequential inflation and deflation cycles of
the balloon in the aorta.
The cyclical (diastolic) volume
displacement that balloon inflation causes acts as an auxiliary pump and
usually supplements cardiac output by around 30%. Severely impaired diastolic
cardiac function usually indicates the presence of a pathological collection of
blood in the pericardial sac, a condition called cardiac tamponade . The
clinical features usually include raised CVP, decreased blood pressure,
impaired urine output, increasing oxygen requirements and metabolic acidosis.
It is treated by immediate re-opening of the chest and the release of the pressurized
collection of blood. It is the collection of blood and clot around the heart
which prevents the chambers of the heart from filling adequately during
There is a linear relationship
between oxygen delivery and haemoglobin concentration. In the event that
non-fatal massive post-operative haemorrhage occurs, hypoperfusion could occur
due to lack of circulating blood volume and a low haemoglobin concentration .
Such situations are treated with blood transfusion and measures to correct the
cause of the haemorrhage which usually means re-opening the chest in the
operating theatre. Hypoperfusion is an invariable ramification of being on
cardiopulmonary bypass if maintained for a long enough duration. . This is
because of activation of a systemic inflammatory response to the extracorporeal
circulation wherein blood is directly exposed to the foreign surfaces of the
cardiopulmonary bypass machine . Such inflammatory activation results in an
opening up of pores in the capillaries of the body such that plasma proteins
change their volume of distribution and become distributed in the entire
extracellular space, a space that is many times larger than plasma volume .
The plasma protein that is
routinely measured is albumin. Its concentration day by day following cardiac
surgery is inversely proportional to the degree of capillary leak present .
Capillary leakage expands the extravascular extracellular space which leads to
increased inter-capillary gap at tissue level which in turn results in
microcirculatory hypoperfusion. Microcirculatory hypoperfusion is also
contributed to by inflammatory mediators and cellular elements of the blood
adhering to the inner lining of microcirculatory blood vessels thus reducing
their calibre. In patients with diabetes glycosylated haemoglobin gives an
indication of average blood glucose levels over the preceding 3 months .
Glycosylated haemoglobin cannot
carry oxygen. When expressed as a percentage of total haemoglobin the value
gives a measure of the average blood glucose concentration over the preceding 3
months. In normal patients and well-controlled diabetics, levels will be below
7g%. Levels above 12g% pre-operatively can be associated with metabolic acidosis
due to inadequate oxygen carrying capacity of the blood. Whilst glycosylated
haemoglobin is a convenient marker for systemic protein glycosylation, all the
body proteins are glycosylated to some extent in diabetic patients which means
that glucose has become covalently bonded to them. It is likely that this
process affects basement membranes of capillaries and could impair oxygen
diffusion between cells thus contributing to hypoperfusion at the molecular
Capillary architecture is also
relevant to microcirculatory hypoperfusion . Capillaries branch off from
arterioles at a range of angles from acute to perpendicular to obtuse. Acutely
branching capillaries give rise to antegrade flow (in the same general
direction as the systolic arterial blood flow) whilst obtusely angled
capillaries give rise to retrograde flow, i.e., blood flows into them
preferentially during diastole . It is believed that the acute and
perpendicularly angled capillaries continue to be perfused during non-pulsatile
cardiopulmonary bypass but the retrograde capillaries, which are normally
perfused during diastole are relatively under-perfused during CPB as there is
then no diastolic flow phase. At a macroscopic level the coronary arteries are
examples of blood vessels in which flow occurs principally in diastole .
Patients cannot be maintained on cardiopulmonary bypass for prolonged periods
of time. Due to the above mechanisms, irreversible and terminal decline would
occur if a healthy adult was placed on conventional cardiopulmonary bypass for
48 hours. In clinical practice the limit for a bypass run would be 24 hours in
the average adult cardiac surgical patient although times of 1-3 hours are the
normal duration for the vast majority. Longer periods on CPB can be sustained
by using special extracorporeal life support systems which are not routinely
used in clinical cardiac surgery.
Sepsis is another form of
hypoperfusion. Its characteristic is the release of lipid soluble bacterial
endotoxins into the bloodstream . As the liver normally filters lipid
soluble toxins from the blood, it is usually affected early on in the clinical
picture of sepsis. As noted earlier, liver dysfunction itself is a potent cause
of type B lactic acidosis . Adequate perfusion of the tissues requires a
driving pressure between the heart and the capillaries. The driving pressure is
provided by the heart contracting but also by the arterioles maintaining a tone
which resists the flow of blood to some extent. In this way normal blood flow is
distributed to the tissues that need it most by selective arteriolar
vasodilation. The endotoxins in sepsis paralyse the arterioles so that they
lose their tone and no longer restrict blood flow into the capillary beds they
supply. This causes a severe drop in blood pressure which in turn leads to
hypoperfusion. To make matters worse, the endotoxins can have a direct effect
on the heart to depress its function.
Where blood pressure falls to
dangerously low levels due to endotoxin mediated arteriolar vasodilation, we
call the clinical picture septic shock. It can be present without any
impairment of cardiac function. Severe allergic reactions can cause a very
similar clinical picture of circulatory shock in which case it is generally
called anaphylactic shock . It is distinguished from septic shock by its
sudden onset associated with drug administration. When sepsis is suspected it
is treated with antibiotics directed against the known or likely infecting
bacterium and with vasoconstrictor medication, most commonly noradrenaline, by
intravenous infusion. In cardiac surgery we deal with septic patients either
because they have had endocarditis pre-operatively or they become septic
following routine cardiac surgery, for instance due to infarction of the intestines.
In the latter condition metabolic
acidosis is a usual feature. The gravity of the situation can be gauged by
whether or not renal failure has supervened as well . Where there is a
metabolic acidosis and the patient continues to pass satisfactory volumes of
urine he will likely survive. Where the urine output tails off or stops in MA
survival become much more of an issue and concerned vigilance in optimizing all
aspects of care needs to be strictly enforced. Even when that is done the likelihood
of mortality for this type of patient is at least 50% . Mesenteric
infarction is one of the more common causes of death following cardiac surgery
and occurs as a result of thrombotic or embolic occlusion of mesenteric
arteries. In patients who remain in the ITU for several weeks following
surgery, other causes of sepsis are often seen typically in the form of
pneumonia, sternal wound infection and central line sepsis.
In metabolic acidosis, there is
an excess of hydrogen ions in the blood which is reflected in the base deficit.
In order to get early warning of the direction of travel, the MA can be
temporarily corrected by administering 8.4% sodium bicarbonate. Each millilitre
of this solution contains 1meq of hydroxyl ions. The dose (in mls) required to
correct a MA is given by the formula: (Body weight x BD)/6. After the
corrective dose is administered the BD will rise to a new level in keeping with
the speed of recovery. In the favorable situation it will not rise back to the
level it was at before administering bicarbonate. Where the outcome is going to
be fatal the BD keeps rising back to its previous level or higher despite
multiple attempts at correction. The only exception to this is in the case of
catecholamine induced metabolic acidosis which generally responds to high dose
IV insulin by infusion along with minimisation or withdrawal of intravenous
Other Causes of
Acute or chronic renal failure is
associated with the build-up of fixed acids in the blood such as sulphate,
phosphate chloride and urate . The hydrogen salts of these anions are
acidic to a variable degree and may contribute to MA where cardiac surgical
patients have co-existing renal failure. The healthy kidneys are able to
secrete hydrogen ions in exchange for re-absorbing potassium into the blood
stream so that the hydrogen salts are excreted in the urine while those in the
bloodstream are generally potassium or sodium salts . Normal urine is
acidic in reaction .
Biochemistry textbooks are keen on the idea of the anion gap as a measure of MA. It is given by formula: AG=[Na] – [(Cl) + (HCO3)] . It can be useful in non-surgical settings such as in the evaluation of a variety of types of poisoning, such as with salicylic acid but is of very little use in clinical cardiac surgery .
In clinical cardiac surgery, severe metabolic acidosis (defined as a base deficit of 6 mmol/L or more) is invariably a finding which demands serious consideration and attention. The magnitude of base deficit is a good marker of the severity of metabolic derangement and can help to prioritise the need for urgent senior medical input when the base deficit exceeds 10 mmol/L . Lactic acidosis is the principal cause of MA in post cardiac surgical patients . Type A lactic acidosis is treated by attending to the underlying cause of hypoperfusion. Type B lactic acidosis is treated with supportive measures including repeated correction of the MA with sodium bicarbonate . When due to liver failure, the outcome is unfortunately frequently fatal. Catecholamine induced lactic acidosis always responds well to withdrawal of adrenaline or substitution with noradrenaline coupled with intravenous insulin by infusion .
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Jeevan Francis, Department
of Medicine, University of Edinburgh, 39 Summerhill Rd, Aberdeen AB15 6HJ, United
Kingdom, Email: email@example.com
Francis J, Prothasis
S, Varghese R, Jomon M, Roy R, et al. Management of
metabolic acidosis in the post-cardiac surgical patient (2020) Clinical Cardiol Cardiovascular Med 4: 11-15.
Metabolic acidosis, Cardiac surgery, Post-operative.