Transesophageal echocardiogram (mid-esophageal, left ventricular outflow tract view) showing the heart during de-airing following aortic valve surgery. Air is seen as white speckles throughout the left heart. Of note, there is no air seen in the right heart. AA = ascending aorta; ECG = electrocardiogram; LA = left atrium; LV = left ventricle; MV = mitral valve (arrowed); RVOT = right ventricular outflow tract.
Epicardial pacing
Epicardial pacing is commonly required in the immediate and early post-CPB period. Atrial pacing may be used alone to increase heart rate in patients in sinus rhythm or in a junctional rhythm where atrio-ventricular (A-V) conduction is intact. When possible atrial pacing is preferable to A-V or ventricular pacing. Ventricular pacing may be employed in isolation when there is no effective atrial contraction (e.g. in chronic atrial fibrillation). In cases where A-V synchronization is likely to be helpful and effective sinus rhythm is not yet established, atrial and ventricular epicardial leads should be placed to facilitate sequential A-V pacing.
Appropriate epicardial pacing modes are specifically intended to improve cardiac performance to enable effective weaning from CPB. Commonly pacing is usually set at around 80–90 bpm immediately post-CPB. However, the pacing rate should be determined by patient requirement and not by protocol. When using dual chamber pacing, the standard preset atrio-ventricular interval is 150 ms; however, where increased heart rates are required, the A-V delay should be adjusted accordingly.
If cardiac function and rhythm are satisfactory after weaning from CPB, pacing may not be necessary.
Mechanics of separation from CPB
As soon as cardiovascular, respiratory, and metabolic parameters are within acceptable limits and the patient is adequately re-warmed and ventilated, the perfusionist commences weaning, initially by incrementally occluding the venous return to the CPB circuit, thus allowing the heart to fill with and hence eject blood. The CPB arterial pump flow is simultaneously gradually reduced. As cardiac stroke volume progressively increases to a level suitable for physiological circulation, the venous return pipe is completely occluded, the arterial flow reduced to “off,” and the transition from CPB to “normal” circulation completed.
Ideally at this stage the heart should be relatively “relaxed” and the chambers empty with left and right atrial filling pressures low (2–5 mmHg). Circulating volume can be increased as required by infusion of fluid via the aortic cannula (in adults usually in 100-ml aliquots). Current convention tends towards the heart being weaned from CPB with low filling pressures, allowing the ventricles time to adjust to working under the increasing ventricular end-diastolic pressures associated with changes in pre- and afterload.
Weaning from CPB may take just a few seconds in a patient with vigorous cardiac activity who might typically be taken to “half-flow” and then off CPB. In patients with less promising cardiac function, the weaning process may need to be protracted, requiring a period of “partial bypass,” that is, low-flow CPB, during which time titration of ventricular volume loading and optimization of inotropes, vasoconstrictors, and cardiac rhythm can be undertaken.
Assessment and adjustment of preload
Central venous pressure is used to reflect and guide the filling volume of the heart. Perfusionists rarely have the opportunity to inspect the heart under direct vision and it may provide considerable information to the surgeon and anesthetist. Normally, only the right ventricle is visible: a relaxed and slightly underfilled right ventricle typically displays inward dimpling of its anterior surface during systole. In patients with impaired left ventricular function, or if weaning from CPB is proving difficult, direct left atrial pressure or pulmonary artery/pulmonary capillary wedge pressure measurements are helpful. In some centers, all patients presenting for cardiac surgery have both central venous and pulmonary artery catheters placed perioperatively.
TEE helps to assess preload and volume status of the chambers and may be particularly useful in the presence of restrictive ventricular physiology, when higher filling pressures may be encountered at lower ventricular cavity volumes.
Assessment of contractility and inotropic support
Myocardial contractility can be estimated from observing the heart both directly and with TEE looking for coordinated muscle contraction generating an acceptable aortic pulsation and arterial blood pressure. Additionally, a sharp upstroke in the monitored arterial wave (dp/dt) and wide area under the arterial waveform curve may also reflect contractility, but are dependent on pre- and afterload. Quantitative measures of contractility include assessment of cardiac output with thermodilution or alternative techniques; these provide an estimation of stroke volume. The information that TEE can provide about ventricular function may be observational and qualitative, but evolving technology can provide readily interpretable quantitative echocardiographic analysis of cardiac output and myocardial contractility.
Inotropic support should be adjusted using all the information available about the patient’s cardiovascular function. The strategies employed are considered below and generally guided by institutional and local team practice. Inotropic support should, if possible, be optimized prior to weaning from CPB, thus presenting the patient with borderline cardiac function with optimal conditions for a successful transition from CPB.
Assessment of afterload
Commonly systemic vascular resistance (SVR) is assumed to be low following CPB because of the systemic inflammatory response accompanying CPB and hemodilution. Patients at risk of a profound inflammatory response include those with long CPB times, long aortic cross-clamp times, complex cardiac surgery, and previous exposure to CPB. Commonly short-acting vasoconstrictors (e.g. metaraminol, phenylephrine) are administered during CPB and in the weaning phase. Similarly, infusions of noradrenaline (norepinephrine) or vasopressin may be used to maintain SVR in the weaning and post-CPB periods.
An estimate of systemic vascular resistance can be obtained while on CPB using the equation:
This is accurate unless there is additional native cardiac output, in which case the equation will overestimate the SVR, since the denominator will be falsely low. Wood units of vascular resistance are converted to more commonly used international units (dyn.s cm−5) by multiplying the Wood unit value by 80.
Normal values for SVR are 900–1200 dyn.s cm−5. Units of SVR are sometimes indexed to body surface area.
Optimal SVR for weaning from CPB needs to be considered according to individual pathophysiology. However, the following considerations generally apply:
patients with dilated, poorly functioning left ventricles exhibiting a low ejection fraction (< 30%) are thought to benefit from lower range SVR values;
patients with coronary disease with residual, flow-limiting lesions or with left ventricular hypertrophy with small cavity size, but normal cardiac outputs, are thought to benefit from SVR values higher than normal; and
coexisting disease in other organs, particularly cerebral or renal, may also dictate the requirement for higher SVR in order to maintain adequate perfusion pressures to these organs.
Consideration must also be given to the anesthesia regimen used. Use of volatile anesthetic agents, prior to and during extracorporeal circulation, may result in a dose-dependent reduction in SVR (700–900 dyn.s cm−5). Total intravenous anesthesia, e.g. using propofol infusion, may also exert a dose-dependent effect on SVR, similar to that seen with volatile agents.
The role of TEE in weaning from CPB
There is a wide variation in the use of TEE in adult cardiac surgery, ranging from routine to highly selective. TEE can be an extremely valuable tool informing decision making if difficulties are encountered when weaning from CPB.
In the event of failed weaning from CPB, TEE is also a useful real-time modality for guiding the placement of mechanical support devices. The tip of an intra-aortic balloon pump can be visualized directly with TEE, as can the placement of ECMO cannulae. The effectiveness of ventricular assist devices can be assessed and adjustments to therapy made under TEE guidance.
A detailed discussion of the role of TEE is beyond the scope of this chapter. A summary of the key benefits of TEE in weaning from CPB is given in Table 8.2.
| Confirm adequate de-airing |
| Guide filling of heart and manipulation of preload |
| Confirm valve position and function |
| Identify paraprosthetic leaks |
| Identify patient–prosthesis mismatch |
| Identify outflow tract obstruction, e.g. systolic anterior motion of mitral valve (SAM) |
| Identify coronary artery obstruction, e.g. secondary to atheromatous embolism/complication of surgery |
| Display aortic dissection following aortic decannulation |
| Identify intracardiac shunts |
| Identify regional wall motion abnormalities |
| Diagnose ventricular systolic and diastolic dysfunction |
| Guide inotropic support |
| Identify pericardial and pleural collections |
| Guide placement of mechanical support devices |
Reversal of anticoagulation
Protamine is used to reverse heparin anticoagulation after successful transition from CPB to physiological circulation. Practice of heparin reversal varies among centers:
The venous cannulae are removed prior to protamine administration and the arterial cannula is removed before, during or after protamine delivery according to local practice. Preload can be supported during protamine administration by titrating fluid administration from the extracorporeal circuit while the arterial cannula is still in situ.
Protamine administration may be associated with cardiovascular instability. This is generally limited to mild or moderate vasodilatation and mild negative inotropic effects, which are usually attenuated by slow administration of protamine over 5–15 minutes. More severe adverse reactions to protamine may be seen in patients with existing pulmonary hypertension, due to pulmonary vasoconstriction or in those with previous exposure to protamine. In a small number of patients adverse hemodynamic responses may be unexpectedly severe due to anaphylactoid or, in extreme cases, anaphylactic responses to protamine or the protamine–heparin complex. These rare but severe responses will require escalation of inotropic and vasoconstrictor support. Use of pulmonary vasodilators may be necessary and, in exceptional cases, re-heparinization and return to CPB may be the only course of action available to support cardiorespiratory function and allow time for recovery from this reaction.
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