FRCA Notes

Advantages	Disadvantages
Secured gas exchange	Abnormal blood flow distribution Greater flow to muscle than GI or hepatic circulations
Guaranteed cardiac ouput	Inflammatory pathway activation
MAP control by changing flow & vascular resistance	Embolic damage
Can provide pulsatile or continuous flow	Coagulopathy
Allows control of body temperature	Errors e.g. mechanical or human (rare)

The circuitry itself

Modern CPB often involves the use of minimised circuits (MiECC), characterised by:

Small priming volumes (e.g. approx. 600ml vs. historic 1800ml)
Tip-to-tip coating of the contact surfaces
Closed systems
Use of centrifugal pumps (instead of roller pumps)
Avoidance of cardiotomy suction and vents, using mechanical salvage of red blood cells

Contact of blood with the circuit induces a systemic inflammatory response and coagulation system activation involving leucocytes, platelets and complement
Said response is reduced by coating the circuit and oxygenator with a biocompatible material such as heparin, phosphorylcholine or PMEA

Gas emboli within the circuitry contribute to neurological complications of CPB
The circuitry is thus completely de-aired before surgery, e.g. with a CO₂ flush, in order to reduce neurocognitive impairment from such gaseous microemboli

The circuitry is also primed prior to use
Use of crystalloid and colloid solutions is associated with haemodilution, coagulopathy and extravasation of fluid
Minimising the circuit-prime volumes, and using autologous priming, helps reduce the haematological impact of priming

Venous side

Deoxygenated blood drains from the right heart, by gravity, into the venous reservoir
Inadequate venous flow risks air entrainment, and may be due to air locks, kinks in or clamps on the tubing, or poor cannula placement

Shed blood describes blood taken from cardiotomy suction, pleural or pericardial vents/drains, or the wounds

Historically it was pumped into a cardiotomy (shed blood) reservoir before being mixed into the venous reservoir and thus into the CPB machine
This blood is, however, highly activated by the negative pressure on the suction lines and blood-air interfaces
This state is associated with activation of both the clotting cascade and inflammatory pathways
Reinfusion is shed blood is associated with neurological injury, cognitive decline and acute lung injury

Therefore in modern CPB shed blood is handled using a cell salvage machine, reducing the pathological activation of the blood, before returning it

In the venous reservoir, deoxygenated blood is mixed with filtered shed blood
This mixed blood is pumped through a heat exchanger, and then into the oxygenator (gas exchanger)

Oxygenator (gas exchanger)

A hollow-fibre, microporous membrane system is used to oxygenate blood from the venous side of the circuit
The system has a relatively high intrinsic resistance, hence requiring blood to be pumped through
Modern oxygenators have a reduced area of blood-gas interface (a source of inflammatory response) and are extremely efficient

Gas exchange occurs according to Fick's law of diffusion:

Rate ∝ KA(ΔC)/D

K = diffusion constant
A = area for diffusion
ΔC = concentration gradient
D = distance of diffusion

Compared to the lungs, oxygenators have a lower surface area (3.5m²vs. 100m²) and greater distance of diffusion (200μm vs. 10μm)
As such, they rely on higher pressure gradients (e.g. up to 760mmHg i.e. 100kPa) to ensure gas exchange

Arterial side

Oxygenated blood leaves the gas exchanger and passes through an aortic filter
A combination of screen filtration and depth filtration is used to minimise:

Embolic load (solid, gaseous and fat), which is associated with organ injury including cognitive dysfunction
Inflammatory response by using a leucocyte-depleting filter

Oxygenated blood then passes into the aorta, distal to the aortic cross-clamp, and is thus pumped through the systemic circulation

Monitoring

Perfusionists rely on a range of monitoring and safety devices:

Monitoring and safety devices during CPB

Mixed venous blood saturation monitors (S_vO₂)

Real-time (continuous) in-line blood gas analysers both pre- and post-oxygenator

Oxygenator arterial outlet temperature monitoring

Regional cerebral tissue oxygenation using NIRS

Line pressure monitors

Emergency bypass routes

Manual control of rotary pumps

Ports facilitating sampling and addition of fluids/components

Opening of the venous line allows passive flow to the venous reservoir
As venous flow increases, the aortic flow will be gradually increased to ∽2.5L/min

The target flow is historically estimated using BSA and temperature, although lean body mass may be a more sensitive estimate of systemic metabolic requirements
Measurements of DO₂ provided by the CPB machine need to incorporate [Hb] and S_aO₂, which may help further determine the requisite pump flow

Once suitable pump flow is acheived, CPB is fully established and ventilation of the lungs can cease
The heart is usually completely emptied by CPB, but this mayn't occur until after aortic cross-clamping e.g. in severe AR or presence of shunts

Even pulsatile CPB flow leads to a low pulse pressure, so MAP is a more accurate variable to monitor
Target MAP is usually 50-80mmHg

Hypotension

Blood pressure inevitably falls at the onset of CPB due to:

Loss of venous return
Vasoplegic syndrome

Vasoplegic syndrome describes a reduced SVR due to pro-inflammatory mediator release, anaesthetic drugs and other perioperative drugs e.g. calcium channel blockers
Prolonged vasoplegia is less common than previously owing to advances in CPB circuit technology and techniques

This period of low pressure is often short-lived, and MAP can be maintained through:

Vasoconstrictors e.g. perfusionists will use higher-strength phenylephrine (500μg - 1mg doses) to increase vascular resistance
Alterations of pump flow, which are a more rapid way of temporarily reducing MAP for surgical needs
Use of goal-directed haemodynamic therapy once off CPB to maintain DO₂

Hypertension

Hypertension on CPB may derive from:

Inadequate anaesthesia/analgesia
Catecholamine release
Hypothermia-induced vasoconstriction

Management is with treatment of the underlying cause and use of arterial vasodilators

Temperature control

Hypothermia is often instigated
The beneficial effect comes from reduced systemic and cerebral oxygen consumption
This increases tolerance to the low-flow/low-MAP state during CPB
Deep hypothermic cardiac arrest (DHCA) is sometimes used for complex aortic or congenital cardiac surgery

See: dedicated page on temperature management during CPB

Acid-base and electrolytes

Acid-base status, electrolytes and blood sugar are monitored on a continuous (or at least half-hourly) basis during CPB

Metabolic acidosis risks tissue injury and organ dysfunction
It arises due to:

Tissue hypoxia
Electrolyte imbalance
Excessive use of 0.9% NaCl or unbalanced colloids

In order to reduce post-operative complications associated with acid-base and electrolyte disturbance, recommendations are:

In cases of mild-moderate hypothermia (i.e. not DHCA), interpretation of acid-base status using alpha-stat blood gases
Maintain pH 7.35-7.45
Consider use of magnesium sulphate for arrhythmia prophylaxis

Severe metabolic injury and deranged kidney function may benefit from intra-operative haemofiltration

Blood products

Haematological variables including ACT, Hb and haematocrit are measured on a half-hourly basis
See: dedicated page on anticoagulation during CPB

Anti-fibrinolytics are often given, either:

Tranexamic acid e.g. 5-6g in divided doses - often for lower risk or elective cases
Aprotinin e.g. up to 5,000,000units in divided doses - often for high bleeding risk cases, dissections etc. as the benefit outweighs the risks from aprotinin

pRBCs are recommended for:

Hb <60g/L or if inadequate DO₂ in conjunction with indices of oxygenation (such as S_vO₂ and O₂ extraction ratio)
Hct <25% and inadequate tissue oxygenation

Patients will have cell-saved blood returned to them at the end of bypass

Patients often require clotting factors or other products at the end of bypass, which are titrated according to point of care tests including TEG/ROTEM
These include:

Prothrombin complex concentrate such as octaplex (factors II, VII, IX and X, protein C and protein S) e.g. 500-1500IU
Fresh frozen plasma (factors II, V, VIII, IX, X, and XI, and antithrombin III)
Others such as cryoprecipitate less commonly

Although systemic hypothermia is cerebro-protective, the myocardium is typically not part of the bypass circuit and requires protection via different means
The main techniques used are:

Cardioplegic arrest
Cross-clamp-fibrillation

Cardioplegic arrest

A solution of predominantly potassium, as well as other elecltrolytes, is used to arrest the heart in diastole, improving operative conditions
It is typically cooled to 4°C but may be warmed
It can be administered anterogradely or retrogradely

See: dedicated page on cardioplegia

Cross-clamp-fibrillation

Intermittent cross-clamping of the aorta and subsequent myocardial ventricular fibrillation (spontaneous on cross-clamping or by use of a DC fibrillating device)
Fibrillation can only be safely tolerated for 10 - 15mins so only suitable for quick procedures
At the end of the period, the cross-clamp is removed and the heart defibrillated into sinus rhythm

At decreased temperature, such as during CPB, there is an increased solubility of gases in blood, most notably CO₂
Therefore measurement of CO₂ and pH at low temperature requires caution
This leads to two methods for measuring blood gases during CPB: pH-stat and ɑ-stat

pH-stat

In pH-stat, the pH is kept constant at 7.4 by addition of CO₂ to the oxygenator and blood gas parameters are corrected by temperature
The pH is measured at the actualy patient temperature, giving a relative hypercarbia

Using pH-stat blood gas management increases CO₂ content during cooling

As cerebral blood flow is controlled by PCO₂, pH-stat tends to lead to cerebral vasodilation and an increase in CBF
Autoregulation, however, is lost and CBF becomes pressure-dependent

This leads to better cerebral cooling but risk of increased micro-emboli load

ɑ-stat

ɑ-stat measures blood gas variables inc. pH at a constant 37°C, without the addition of CO₂, and alkalosis is permitted during cooling
ɑ-stat blood gas readings are interpreted uncorrected for body temperature

Using ɑ-stat may normalise, or reduce, the CBF with the consequence of reduced efficiency of cerebral cooling

In most centres the ɑ-stat is used, as the majority of post-operative neurological injury is caused by micro- and macro-emboli
In the paediatric population, however, the pH-stat is often used as the hypoperfusing effect is more dominant with regards to neurological outcome
Some centres use pH-stat on cooling but ɑ-stat on re-warming

A multi-disciplinary effort requiring adequate communication between the perioperative team
Use of a checklist is recommended

Criteria for CPB weaning

Criteria	Notes
Lung ventilation re-established	Re-expansion & resumption of ventilation
De-airing of cardiac chambers & grafts (particularly LA/LV)	Aided by TOE
Aortic cross-clamp removed	Restores coronary artery (and graft) blood flow
HR and rhythm compatible with weaning	May require epicardial pacing esp. if prolonged CPB or existing conduction defects
Need for inotropy/IABP considered	Target MAP >60mmHg, no one inotrope known to be superior
Normothermia (36 - 37°C)	Both hypothermia and hyperthermia are harmful
Normal electrolytes and acid-base balance	May necessitate use of bicarbonate
Adequate Hb and Hct	Should be maintained throughout CPB

Haemodynamic instability post-CPB

As the aortic cross-clamp is removed, may need vasoactive support to combat ventricular dysfunction or vasoplegia, both of which are common following CPB
Low cardiac output states are associated with:

↑ morbidity
Higher short-term and long-term mortality
↑ resource utilisation

Management is to correct the cause (e.g. graft dysfunction, hypovolaemia) and use of positive inotropy, or vasopressors, as indicated

Predictors of requiring vasopressor support	Predictors of requiring inotropic support
Use of ACE-I or other vasodilators pre-operatively	Poor LVEF or known heart failure
Septic patient	Symptoms of heart failure e.g. SOBOE, oedema
High intra-operative phenylephrine requirement	Multiple heart failure medications
↑ duration of CPB (as greater SIRS response)	↑ duration of cross-clamping
	Residual ischaemic heart disease e.g. not possible to undertake all planned grafts
	MVR for mitral regurgitation; the sudden ↑ in LV afterload may precipitate failure

Options for vasopressor support include noradrenaline (1^st line), vasopressin, methyline blue or high-dose hydroxycobalamin
Options for inotropic support include dopamine, milrinone, low-dose adrenaline or IABP

Principles of Cardiopulmonary Bypass