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Metabolic management during cardiopulmonary bypass. Oxyhemoglobin dissociation curve. Pump flow rate must be adjusted with due consideration to temperature if the metabolic demands for oxygen are to be matched by delivery. Typical flow rates over a range of temperatures are shown in Appendix 5.1. Does anyone know how to bypass the serial key prompt? Everytime i open up serum it asks me for the serial. Straight after when i input it and change a preset my DAW crashes =/ level 2. 1 point 4 years ago. Would like to know this too!:D. 1 point 4 years ago.

Pump flow rate must be adjusted with due consideration to temperature if the metabolic demands for oxygen are to be matched by delivery. Typical flow rates over a range of temperatures are shown in Appendix 5.1.

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Deep hypothermic circulatory arrest

Deep hypothermic circulatory arrest (DHCA) is discussed in detail in Chapter 10, but is briefly mentioned here for completeness. Certain cardiac procedures require DHCA, rather than just conventional mild to moderate hypothermia, usually because the aorta cannot be cross-clamped or total absence of blood flow is required to enable surgical access. DHCA is used to dramatically lower the body’s metabolic demand while protecting organs, particularly the brain, during a period in which perfusion is suspended. This technique utilizes severe to deep hypothermia, with or without the use of aortic cross-clamping and delivery of cardioplegia, to facilitate surgery to the left ventricular outflow tract, aortic valve, ascending aorta or great vessels. Pediatric palliative and corrective surgical procedures also frequently necessitate periods of DHCA. Procedurally dictated, intermittent “low-flow” (5–15 ml/kg/minute) states may be employed during DHCA to deliver oxygenated blood to the brain via antegrade cerebral perfusion (ACP) and retrograde cerebral perfusion (RCP). During ACP in adult patients, mean arterial pressure (MAP) should be 65 mmHg, and during RCP the central venous pressure (CVP) should be 25 mmHg.

pH and acid–base metabolism

The normal pH of arterial blood is 7.4 (± 0.05). Bicarbonate and non-bicarbonate systems play important roles in buffering pH changes.

Bicarbonate system

The bicarbonate buffer system (carbonic acid H2CO3 and bicarbonate HCO3) is considered to be the most important mechanism for physiological regulation of pH. It possesses approximately 53% of the total buffering capacity of body fluids. Exogenous sodium bicarbonate is easily administered during CPB. It should be noted that bicarbonate’s molecular weight is small enough to allow its passage across the semipermeable fibers of hemofilter systems and may thus be removed with the effluent product or “plasma water waste” if hemofiltration is used during CPB. The simple formula [(body weight (kg) × 0.3)/2] × base deficit = mmol NaHCO3 needed to yield base excess equal to 0 is often used when treating persistent acidosis.

Non-bicarbonate buffers

  • Inorganic phosphate buffers are important in regulating pH in the intracellular and renal tubular fluids. Inorganic phosphates are removed during hemofiltration.

  • Plasma proteins possess significant buffering capacity because of the ionic nature of their amino acid structure and because of their high plasma concentrations. Plasma proteins are not removed during hemofiltration because of their larger molecular size.

  • Hemoglobin and oxyhemoglobin play a major role in buffering hydrogen ions at the tissue level. Considered the most important of the non-bicarbonate pH buffers, hemoglobin is not removed during hemofiltration because of the size of the red blood cell.

Metabolic acidosis and alkalosis

Metabolic acidosis is usually due to systemic O2 delivery (DO2) during bypass not meeting systemic O2 demand (VO2). The options to address this are to increase pump flow or HCT, thereby increasing DO2, or to reduce VO2 by decreasing temperature or possibly by increasing depth of anesthesia. Failing this, administration of sodium bicarbonate, or the use of hemofiltration (ultrafiltration) may correct the acidosis.

CPB-related metabolic alkalosis may be due to a reduction in serum potassium levels (e.g. due to increased urine output or hemofiltration) and is best treated by titrated administration of potassium chloride.

Respiratory acidosis and alkalosis

Respiratory acidosis is the result of insufficient removal of CO2 from the patient’s blood by the membrane oxygenator. Increasing the sweep gas rate through the membrane oxygenator will facilitate the transfer or elimination of excess CO2 from the patient’s blood. Conversely, respiratory alkalosis is the result of excessive CO2 removal.

Alpha-stat and pH-stat strategies for blood gas management

The optimal pH management strategy during hypothermic CPB is as yet undetermined. The two main strategies utilized clinically, alpha-stat and pH-stat, differ in their approach to the acid–base alterations that occur with hypothermia. As blood temperature falls, gas solubility rises and the partial pressure of carbon dioxide decreases (PCO2 decreases 4.4% for every °C drop in temperature). With alpha-stat management, arterial gas samples are not corrected for sample temperature and the resulting alkalosis remains untreated during cooling; with pH-stat management, arterial blood gas samples are temperature corrected and carbon dioxide is added to the gas inflow of the CPB circuit so that the PCO2 and hence pH, is corrected to the same levels as during normothermia. The advocates of alpha-stat point to potential benefits in terms of the function of intracellular enzyme systems and the advantage of preserving cerebral autoregulation. Proponents of pH-stat, which results in cerebral vasodilation, cite, as advantages, higher levels of oxygen delivery to the brain and enhanced distribution of blood flow. However, the higher cerebral blood flows associated with pH-stat also have the potential to carry more gaseous or particulate emboli to the brain.

Alpha-stat management is based on the concept that the dissociation constant, pK, of the histidine imidazole group changes with temperature in a manner nearly identical to physiological blood buffers. Hence, the ionization state (α) of this group stays the same, irrespective of temperature. As the imidazole group’s ionization state is a key determinant of intracellular protein function, advocates of alpha-stat management contend that this strategy promotes normal protein charge states and function, even at low temperatures.

The pH-stat approach requires increases in the total carbon dioxide content of the blood as the temperature falls in order to maintain fixed temperature-corrected pH values. The optimal pH of most enzymatic reactions does vary with hypothermia, mostly in accordance with the predictions of the alpha-stat hypothesis. Hence, the relative acidosis of pH-stat would be expected to lower enzymatic reaction rates. Whether this is beneficial in reducing energy consumption, or harmful by impairing key cellular homeostatic mechanisms, is unclear.

Differences in alpha-stat and pH-stat management become progressively greater as temperature is reduced. The effect is quite profound below 25°C, but above 32°C the change in CO2 solubility is small and of much less clinical and physiological relevance. This is further evident when one appreciates how little CPB time most adult cardiac surgical patients spend at hypothermic temperatures. Most cases are conducted with mild hypothermia and in those much of CPB time is spent transitioning to, or from, those temperatures; the actual time on CPB spent below 32°C may only be 25% of the total CPB time. Thus, although frequently discussed, alpha-stat versus pH-stat management is of little actual relevance in most adult cardiac surgery.

Potassium (K+)

Hyperkalemia is the most common electrolyte disturbance during CPB. Potassium levels can be lowered using diuretics, insulin, and dextrose administration, or hemofiltration. The treatment of choice is dictated by the potassium level, the persistence of rise in potassium levels, and the presence or absence of electrophysiological disturbances. Serum potassium levels transiently rise with the administration of cardioplegia and this will usually correct without treatment within a short period after ceasing delivery of cardioplegia. Potassium levels in the range 5.5–6.5 mmol/l can be treated with administration of a diuretic, usually furosemide 20–40 mg. In some centers, levels between 6.5 and 7 mmol/l are treated using insulin and dextrose infusions. Levels above 7 mmol/l or persistently raised potassium levels can be lowered using “zero balance hemofiltration.” A crystalloid solution, typically normal saline, is added to the CPB circuit to maintain circulatory volume and then removed by hemofiltration causing concomitant removal of potassium. As this technique can result in the loss of significant amounts of bicarbonate through the hemofilter, it should be replaced using sodium bicarbonate titrated to blood bicarbonate levels.

The urgency or need to treat hyperkalemia should in part be determined by the presence or absence of electrophysiological disturbance. In the absence of ECG changes, moderate hyperkalemia may not require treatment. If treatment is chosen, its effect should not be longer than the anticipated period of hyperkalemia. It is important to note that during CPB extracellular potassium may rise but typically, even untreated, increases in K+ levels are nearly always transient, as the extracellular potassium concentration in the plasma is quite small relative to the intracellular capacity for its uptake. Rapid shifts to the intracellular space and urinary excretion often correct K+ levels quite quickly after CPB.

Hypokalemia, usually less than 4.5 mmol/l, is treated by administration of potassium chloride, normally in 10–20 mmol boluses. It is worth bearing in mind that rapid bolus administration of potassium during CPB may cause transient vasodilatation. Potassium levels alter with temperature. Treatment should thus be undertaken in the context of:

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  • temperature;

  • the rate of rise of the potassium level;

  • the persistence of that level; and

  • the point during surgery at which it is occurring.

Ideally, potassium is finally corrected before separation from CPB using results of electrolyte measurements taken at a body temperature of not less than 35°C.

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Calcium (Ca2+)

Calcium levels are reduced by hemodilution, chelation by preservatives in bank blood or by hemofiltration. Significantly low serum Ca2+ levels are generally corrected close to the termination of CPB, when the aortic cross-clamp has been removed, a cardiac rhythm has been established, and the temperature is approaching normothermia. One gram (or 3–5 mg/kg) of calcium chloride is usually all that is required to normalize serum ionized calcium levels (1–1.5 mmol/l). Administration of Ca2+ may exacerbate reperfusion injury and should be avoided immediately before or after cross-clamp removal. Timing of administration can be guided by normalization of cardiac conduction indicating adequate reperfusion.

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Magnesium (Mg+)

Magnesium depletion occurs during CPB if hemofiltration is used or if there is high volume diuresis, particularly with loop diuretics. In these situations, a 2 mg bolus of Mg+ may be added empirically into the circuit after the core temperature has reached 34°C and the aortic cross-clamp has been removed. Ideally, if Mg+ levels are available, Mg+ administration should be titrated according to blood levels.

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