Mean arterial blood pressure (MAP)

An acceptable MAP on CPB is that which provides adequate tissue perfusion. Adequate tissue perfusion is, however, also influenced by the pump flow rate and the core body temperature. MAP is determined by flow rate and arteriolar resistance. In general, higher pressures should be maintained in the presence of known cerebrovascular disease, in particular carotid stenosis, renal dysfunction, coronary disease or left ventricular hypertrophy.

On commencement of CPB there is a transient drop in systemic pressure. This is due to vasodilatation associated with the sudden decrease in blood viscosity resulting from hemodilution by the CPB prime solution and, secondarily, from the systemic inflammatory response (SIRS) associated with CPB. However, as CPB continues there is a gradual increase in perfusion pressure due to increasing vascular resistance. This is a result of equilibration of fluid between the vascular and tissue “compartments,” hemoconcentration from diuresis, the increase in blood viscosity seen with hypothermia, and the progressive increase in circulating levels of catecholamines and renin as part of the stress response to CPB.

It is important to emphasize that manipulation of MAP alone is not sufficient to guarantee adequate organ perfusion. Neither a low MAP with a high flow nor a high MAP with a low flow are sufficient in themselves. Whole body DO₂ must firstly be optimized and secondly, vascular resistance altered to bring the MAP into the autoregulatory range for critical organ beds, with due consideration to underlying pathophysiology.

Pulmonary artery (PA) and left atrial (LA) pressure

On CPB the PA and LA pressures should be close to zero. PA or LA pressure monitoring is useful during CPB to assess left ventricular distension, in particular in cases where increase in blood flow back to the left heart is expected (cyanotic heart disease, large bronchial flow in chronic lung disease or aortic regurgitation). Care must be taken with PA catheters to ensure that migration of the catheter tip does not occur, leading to “wedging” and subsequent PA rupture or infarction of the lung.

Central venous pressure (CVP)

On CPB, CVP is expected to be close to zero and no more than in single digits. An increase in CVP indicates impaired venous drainage to the reservoir. The causes of an increase in CVP are inadequate cannula size, obstruction to the line or cannula tip, and insufficient height difference between the patient and the reservoir to enable gravity siphon drainage. The consequence of an increase in CVP during bypass is to reduce effective perfusion of critical organs with resultant edema. The liver is particularly sensitive to reduced flow as nearly three-quarters of hepatic blood flow occurs at near venous pressure. If a persistently high CVP, uncorrected by attention to the factors mentioned above, is noted during CPB the patient’s head and eyes should be closely observed for signs of engorgement and consideration given to altering the venous cannulation to improve drainage.

Electrocardiogram

The ECG must be recorded throughout CPB to ensure that it remains isoelectric during cardioplegic arrest. Following removal of the aortic clamp and resumption of myocardial activity persistent ST segment changes may be related to ischemia resulting from inadequate re-vascularization, coronary ostial obstruction, e.g. by an incorrectly seated aortic valve prosthesis, or air/particulate embolization. Additionally, the ECG is useful in guiding the postoperative management of epicardial pacing.

Temperature

The principal reason for hypothermic CPB is to protect the heart and other organs by reducing metabolic rate and thus oxygen requirements. In the myocardium, hypothermia sustains intracellular reserves of high-energy phosphates and preserves higher intracellular pH and electrochemical neutrality. Myocardial cooling can be achieved with cold cardioplegia, pouring cold topical solution on the heart and cooling jackets, as well as by systemic hypothermia. Systemic hypothermia is not uniform due to different blood flow to different vascular beds. High blood flow rates and slow cooling ensures less variation in systemic hypothermia. Temperature should be measured at multiple sites and the advantages and limitations of each site needs to be recognized. During cardiac surgery temperature can be measured in the following locations: nasopharynx, tympanic membrane, pulmonary artery, bladder or rectum, arterial inflow, water entering heat exchanger, and venous return.

Nasopharyngeal temperature probes underestimate, but approximate to brain temperature, with the mixed venous temperature on the CPB circuit being an approximation of average body temperature. Bladder and rectal temperatures give an indication of core body temperature, but these can be erroneous due to interference from varying urine production and fecal matter, respectively. These low blood flow sites tend to underestimate temperature so are particularly valuable following deeper levels of hypothermia. On re-warming the aim is to achieve uniform normothermia. To avoid rebound hypothermia after cessation of CPB, which occurs if too great a temperature gradient is allowed to develop between peripheral and core temperatures, vasodilators can be used to promote more uniform re-warming by distributing greater blood flow, and therefore heat, from the core to peripheries. The process of re-warming must be controlled to avoid rapid changes in temperature, or excessive blood temperatures, which can result in microbubble formation due to the reduced solubility of gases in blood as the temperature increases, denaturing of plasma proteins, hemolysis, and cerebral injury. As a general guide for every 1°C drop in temperature there is an associated 7% drop in oxygen demand, i.e. a 7°C reduction in temperature results in a 50% drop in oxygen demand (see Table 5.6).

At < 15°C oxygen is too tightly bound to hemoglobin and is therefore unavailable to tissues. In addition, the viscosity of the blood can be too high for effective flow through the CPB circuit.

Urine volume

Urine volume on CPB is monitored as an indicator of renal perfusion. Indications for diuretic use during CPB include hyperkalemia, hemoglobinuria, and hemodilution. Furosemide is used for treatment of hyperkalemia and mannitol is used to generate alkaline urine to treat hemoglobinuria.

Transesophageal echocardiography (TEE)

TEE is applied increasingly as a routine part of surgery when intracardiac cavities are opened. It is a useful tool to assess adequacy of de-airing of the heart. In addition, TEE can be used to assess intracardiac structures (valves, prostheses, septal walls, left and right ventricular outflow tracts), the position of cannulae and regional wall motility.

Laboratory investigations

This is discussed in detail in Chapter 6. Minimal monitoring during CPB requires measurement of PO₂, PCO₂, base excess (BE), hemoglobin, HCT, pH, potassium, glucose, and coagulation status using ACT.

Termination of CPB

Table 5.7 provides a checklist of the basic conditions that need to be fulfilled before weaning can be attempted. Terminating CPB is a gradual process with constant communication between surgeon, anesthetist, and perfusionist. The first step is for the perfusionist to restore the blood volume to the heart by gradual occlusion of the venous return. The patient is partially supported by the CPB machine with blood passing through both the heart and the lungs. The heart begins to eject blood when a critical volume is reached. The perfusionist continues to return blood from the venous reservoir to the patient while continuing to occlude the venous line until the patient is weaned from CPB. Termination of CPB is achieved by complete occlusion of the arterial and venous lines.

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