Termination of CPB
Discontinuation of bypass is accomplished by a series of necessary procedures and conditions:
· Rewarming must be completed.
· Air must be evacuated from the heart and any bypass grafts.
· The aortic cross-clamp must be removed and the heart must beat.
· Lung ventilation must be resumed.
The surgeon’s decision about when to rewarm is important; adequate rewarming requires time, but rewarming too soon removes the protective effects of hypothermia. Rapid rewarming often results in large temperature gradients between well-perfused organs and peripheral vasoconstricted tissues; sub-sequent equilibration following separation from CPB decreases core temperature again. An excessive gradient between the infusate temperature and the patient’s core temperature can result in deleterious brain hyperthermia. Infusion of a vasodilator drug (nitroprusside, isoflurane, or phentolamine [primar-ily in children]) by allowing higher pump flows often speeds the rewarming process and decreases large temperature gradients. Some believe that allowing some pulsatile flow (ventricular ejection) may also speed rewarming. Excessively rapid rewarming, however, can result in the formation of gas bubbles in the bloodstream as the solubility of gases rapidly decreases. If the heart fibrillates during rewarm-ing, direct electrical defibrillation (5–10 J) may be necessary. Administration of lidocaine, 100–200 mg, and magnesium sulfate, 1–2 g, prior to removal of aortic cross-clamping is a common protocol and may decrease the likelihood of fibrillation. Many clinicians advocate a head-down position while intracardiac air is being evacuated to decrease the likelihood of cerebral emboli. Lung inflation facili-tates expulsion of (left-sided) intracardiac air by compressing pulmonary vessels and returning blood into the left heart. TEE is useful in detecting resid-ual intracardiac air. Initial reinflation of the lungs requires greater than normal airway pressure and should generally be done under direct visualization of the surgical field because excessive lung expansion can interfere with internal mammary artery grafts.
General guidelines for separation from CPB include the following:
· The core body temperature should be at least 37°C.
· A stable rhythm must be present. Atrioventricular pacing is often used and confers the benefit of a properly timed atrial systole. Persistence of atrioventricular block should prompt measurement of serum potassium concentration. If hyperkalemia is present, it can be treated with calcium, NaHCO3, furosemide, or glucose and insulin.
· The heart rate must be adequate (generally 80–100 beats/min). Slow heart rates are generally treated by pacing. Many inotropic agentswill also increase heart rate. Supraventricular tachycardias generally require cardioversion.
· Laboratory values must be within acceptable limits. Significant acidosis (pH < 7.20), hypocalcemia (ionized), and hyperkalemia (>5.5 mEq/L) should be treated; ideally the hematocrit should exceed 22%; however, a hematocrit <22% should not by itself trigger transfusion of red blood cells at this time. When CPB reservoir volume and flow are adequate, ultrafiltration may be used to increase the hematocrit.
· Adequate ventilation with 100% oxygen must have been resumed.All monitors should be rechecked for proper function and recalibrated if necessary.
CPB should be discontinued as systemic arterial pressure, ventricular volumes and filling pressures, and cardiac function (on TEE) are assessed. Central aortic pressure may be measured directly and should be compared with the radial artery pressure and cuff pressure (if there is a disparity). A reversal of the normal systolic pressure gradient, with aortic pressure being greater than radial pressure, is often seen immediately postbypass. This has been attrib-uted to opening of arteriovenous connections in the hand as a consequence of rewarming. Central aortic root pressure can also be estimated by palpation by an experienced surgeon. Right ventricular volume and contractility can be estimated visually, whereas filling pressures are measured directly by central venous, pulmonary artery, or left atrial catheters. Cardiac output can be measured by thermodilution. TEE can define adequacy of end-diastolic volumes, right and left ventricular contractility, and valvular function.
Weaning is typically accomplished by pro-gressively clamping the venous return line (tub-ing). As the beating heart fills, ventricular ejection resumes. Pump flow is gradually decreased as arterial pressure rises. Once the venous line is completely occluded and systolic arterial pressure is judged to be adequate (>80–90 mm Hg), pump flow is stopped and the patient is evaluated. Some surgeons wean by clamping the venous line and then progressively “filling” the patient with arte-rial inflow.
Most patients fall into one of four groups when coming off bypass ( Table 22–2). Patients with good ventricular function are usually quick to develop good blood pressure and cardiac out-put and can be separated from CPB immedi-ately. Hyperdynamic patients can also be rapidly weaned. These patients emerge from CPB with a very low SVR, demonstrating good contractility and adequate volume, but have low arterial pres-sure; their hematocrit is often reduced (<22%). Diuresis (off CPB) or red blood cell transfusions increase arterial blood pressure.
Hypovolemic patients include those with nor-mal ventricular function and those with varying degrees of impairment. Those with preserved myo-cardial function quickly respond to 100-mL aliquots of pump blood infused via the aortic cannula. Blood pressure and cardiac output rise with each bolus,
and the increase becomes progressively more sus-tained. Most of these patients maintain good blood pressure and cardiac output with a left ventricular filling pressure below 10–15 mm Hg. Ventricular impairment should be suspected (when definitive diagnosis using TEE is not available) in hypovolemic patients whose filling pressures rise during volume infusion without appreciable changes in blood pres-sure or cardiac output or in those who require filling pressures above 10–15 mm Hg. Ventricular dysfunc-tion is easily diagnosed by TEE.
Patients with pump failure emerge from CPB with a sluggish, poorly contracting heart that pro-gressively distends. In such cases, CPB may need to be reinstituted while inotropic therapy is initi-ated; alternatively, if the patient is less unstable, a positive inotrope (epinephrine, dopamine, dobu-tamine) can be administered while the patient is observed for improvement. If the patient does not respond to reasonable doses of one of these three agents, milrinone can be added. In patients with poor preoperative ventricular function milrinone may be administered as the first-line agent prior to separation from CPB. In the rare instance that SVR is increased, afterload reduction with nitroprus-side or milrinone can be tried. The patient should be evaluated for unrecognized ischemia (kinked graft or coronary vasospasm), valvular dysfunction, shunting, or right ventricular failure (the distention is primarily right sided). TEE will facilitate the diag-nosis in these cases.
If drug therapies fail, intraaortic balloonpump (IABP) counterpulsation should be initiatedwhile the patient is “rested” on CPB. The efficacy of IABP depends on proper timing of inflation and deflation of the balloon ( Figure 22–15). The bal-loon should inflate just after the dicrotic notch is seen on the intraaortic pressure tracing to aug-ment diastolic blood pressure and coronary flow after closure of the aortic valve. Inflation too earlyincreases afterload and exacerbates aortic regur-gitation, whereas late inflation reduces diastolic augmentation. Balloon deflation should be timed just prior to left ventricular ejection to decrease its afterload. Early deflation makes diastolic augmen-tation and afterload reduction less effective. Use of a left or right ventricular assist device (LVAD or
RVAD, respectively), may be necessary for patients with refractory pump failure. If myocardial stun-ning is a major contributor or there are areas of hibernating myocardium, a delayed improvement in contractile function may allow complete wean-ing from all drugs and support devices only after 12–48 h of therapy. Circulatory assist devices, such as the Abiomed and HeartMate, can be used as a bridge to cardiac transplantation; the former can be used for several days whereas the latter device can be left in place for months to years.
Many clinicians believe that positive inotropes should not routinely be used in patients coming off CPB because they increase myocardial oxy-gen demand. The routine use of calcium similarly may worsen ischemic injury and may contribute to coronary spasm (particularly in patients who were taking calcium channel blockers preoperatively). Nevertheless, there are centers that administer cal-cium salts or a positive inotrope (eg, dobutamine), or both, to every patient at the conclusion of CPB. Commonly used positive inotropes and vasopres-sors are listed in Table 22–3. Epinephrine, dopa-mine, and dobutamine are the most commonly used agents. Clinically, epinephrine is the most potent inotrope and is often effective in increasing both cardiac output and systemic blood pressure when others agents have failed. In lower doses, it
has predominantly β agonist activity. Dobutamine, unlike dopamine, does not increase filling pres-sures and may be associated with less tachycardia than dopamine; unfortunately, cardiac output often increases without significant changes in blood pres-sure. On the other hand, dopamine may improve renal blood flow (at reduced doses) and is often more effective in increasing blood pressure than in increasing cardiac output. Interestingly, when infused to increase cardiac output to similar extents, epinephrine is associated with no more increase (and perhaps less) in heart rate than dobutamine. Inamrinone and milrinone, both selective phos-phodiesterase type III inhibitors, are inotropes with arterial and venous dilator properties; milrinone may be less likely than inamrinone to decrease the platelet count. In studies of patients with chronic heart failure these two inodilators, unlike other inotropes, did not appreciably increase myocardial oxygen consumption. The combination of an ino-dilator (usually milrinone) and a β-adrenergic agonist results in at least additive (and possibly synergistic) inotropic effects. Norepinephrine is useful for increasing SVR but may compromise splanchnic and renal blood flow at increased doses. Some clinicians use norepinephrine in combina-tion with phosphodiesterase inhibitors to prevent excessive reductions in systemic arterial pressure. Arginine vasopressin may be used in patients with refractory hypotension, a low SVR, and resistance to norepinephrine. Inhaled nitric oxide and pros-taglandin E1 may also be helpful for refractory pul-monary hypertension and right ventricular failure (Table 22–4); nitric oxide has the added advantage of not decreasing systemic arterial pressure. Studies have not confirmed outcome benefits to the use of nesiritide, a human B-type natriuretic peptide, thy-roid hormone (T 3), or glucose–insulin–potassium
infusions for vasoactive/inotropic support after CPB.
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