BSA, Body surface area; CVP, cardioventricular pacing; DIA BP, diastolic blood pressure; EDV, end-diastolic volume; ESV, end-systolic volume; HR, heart rate; LVEDP, left ventricular end-diastolic pressure; PAP, peak airway pressure; PCWP, pulmonary capillary wedge pressure; SI, stroke index; SYS BP, systolic blood pressure.
Perfusion principles
The goal of CPB is to provide a motionless heart in a bloodless field while the vital organs continue to be adequately oxygenated. The CPB pump provides respiration (oxygenation and elimination of CO2), circulation (maintenance of perfusion pressure), and regulation of temperature (hypothermia to preserve myocardium). Initiation of CPB subjects the circulating blood of the patient to significant physiologic and physical changes.
Anesthetic and perfusion management must address the impact of low flow indices, reduced metabolic requirements, changing viscosity of the patient’s circulating volume, and postoperative inflammatory response. Multiple factors interact to create a substantially new environment for physiologic homeostasis.
Hemodynamic abnormalities that occur during CPB include endothelial dysfunction (“total body systemic inflammatory response”), which causes symptoms similar to those in patients with sepsis or trauma. Other abnormalities include persistent heparin effect, platelet dysfunction or loss, coagulopathy, fibrinolysis, and hypothermia.
Rapid recirculation of the total blood volume during CPB subjects blood and tissue components to a foreign environment that invites cellular trauma. The patient experiences tremendous alterations in core temperature, hematocrit (in the form of hemodilution), the coagulation cascade, and perfusion pressures (nonpulsatile perfusion).
As a result of excessive hemodilution, the platelet count decreases rapidly to 50% of the preoperative level but usually remains above 100,000 per microliter. Bleeding time is greatly prolonged, and platelet aggregation and function are impaired. Reductions occur in the plasma concentrations of coagulation factors II, V, VII, IX, X, and XII and are attributed to hemodilution.
Extracorporeal circuit
The CPB (pump) circuit consists of separate disposable components bioengineered to interface with perfusion pumps, fluid-based thermoregulating systems, air-oxygen blenders, anesthetic vaporizers, pressure transducers, temperature monitors, and in-line oxygen and blood-gas analyzers. The pump components include venous cannulas from the right atrium or vena cava, which are usually fenestrated at the tip and reinforced. Venous tubing includes the venous return for the blood drained to the machine from the LV.
The venous drainage to the venous reservoir depends on gravity, patient intravascular volume, and the position of and resistance from the venous cannula. The table height can affect venous drainage to the pump. Drainage collects in the venous reservoir, where air bubbles are removed and drainage from other reservoirs is mixed together. If a low volume is allowed here, air can be entrained into the arterial circulation.
Blood suctioned from the heart, pericardium, and pleural spaces drains to the cardiotomy reservoir. The CPB circuit pushes blood forward and returns blood under pressure to the patient by means of either rollers (most common) or a centrifugal (vortex) pump.
Prime
A significant factor is the amount of crystalloid solution required to prime the tubing, reservoir, filters, and oxygenator. Establishment of an air-free circuit is essential for unimpaired fluid volume transport and prevention of air embolism.
Most circuits require at least 2000 mL of a solution such as Normosol, Plasmalyte A, or Isolyte S, with pH and electrolytes closely matching the composition of whole blood. Added to this base solution are heparin, sodium bicarbonate, mannitol, hetastarch, albumin, and possibly corticosteroids or antihyperfibrinolytic agents. This addition can result in priming volumes in excess of 2000 mL, which, when transfused to the patient at the onset of CPB, can cause a hemodilutional bolus of 30% to 50% of the patient’s circulating blood volume.
Vascular transport
The heart and lungs are isolated and bypassed from systemic blood flow. This function is accomplished by right atrial or vena caval cannulation with subsequent diversion of venous blood that is returning to the heart.
The venoatrial cannulas are connected to polyvinyl chloride tubing that extends from the surgical field to the venous reservoir situated at a level well below the patient’s heart to facilitate gravity exsanguination.
Blood from the reservoir is propelled by roller or centrifugal pump to the oxygenator, where it becomes arterialized by interfacing with a membrane oxygenator.
A heat exchanger mounted on the oxygenator provides for control of blood temperature. Oxygenated blood passes through an arterial filter and an in-line arterial gas monitoring device.
Aortic cannula placement is distal to the sinus of Valsalva and proximal to the brachiocephalic (innominate) artery. The arterial line pressure of the extracorporeal circulation (ECC) depends on flow and resistance but usually is maintained below 300 mmHg.
Myocardial protection techniques
Injury to the myocardium is a complex occurrence and may result from numerous physiologic events. Tachycardia, hypertension or hypotension, and ventricular distention can all play a role in the events that produce an oxygen supply–demand imbalance.
Contractile function deteriorates rapidly after the initial insult of ischemia. Rapid cardioplegia-induced cardiac arrest, decompression of the ventricles, and hypothermia are the underlying techniques used to ensure myocardial protection during CPB.
The duration of aortic cross-clamping time, collateral coronary blood supply, frequency of cardioplegia delivery, and composition of cardioplegia are factors that influence the extent of reperfusion injury. Intermittent doses of cold crystalloid cardioplegia help to maintain cardiac arrest, hypothermia, and pH; counteract edema; wash out metabolite; and provide oxygen and substrate for aerobic metabolism.
Administration of inhalation anesthetics has been shown to produce protection against myocardial ischemia and reperfusion injury. This phenomenon is termed anesthetic-induced preconditioning (APC) and derives from positive effects on mitochondria, potassium adenosine triphosphate channels, reactive oxygen species, calcium overload, and inflammation. APC reduces myocardial necrosis and improves postoperative cardiac performance.
Cardioplegia
Cardioplegia is a potassium solution administered into the coronary circulation to provide diastolic arrest. It is composed of potassium (15–30 mEq/L), calcium to prevent ischemic contracture (stone heart), albumin or mannitol for osmolarity correction, and glucose or simple amino acids as a metabolic substrate.
The cardioplegia delivers oxygen and nutrients, removes waste products, and cools or rewarms the heart. It is administered in an antegrade manner into the aortic root, from which it distributes to the coronaries and into the myocardium. It may also be administered in a retrograde fashion into the coronary sinus, from which it distributes through veins, venules, and capillaries of the myocardium.
The cardioplegia composition is blood or crystalloid based. Blood-based cardioplegia is oxygenated blood that is diluted with fluid at a 4:1 ratio. It has a hematocrit of 16% to 18% and is given at 4° to 14° C.
Crystalloid-based solutions do not contain hemoglobin; therefore, they deliver dissolved O2 only. Because of this, crystalloid solutions can be used only with myocardial hypothermic techniques. Intracellular cardioplegia has a low sodium content to produce loss of membrane potential by eliminating the sodium gradient across the membrane.
Extracellular solutions produce diastolic arrest by depolarization of the membrane with high potassium concentrations.
Anticoagulation
Initiation of CPB requires systemic heparinization to establish a safe level of anticoagulation. The currently accepted regimen is 300 units of heparin per kilogram of patient weight.
The heparin dose is usually calculated to maintain an activated clotting time (ACT) of 400 sec (the normal range is 130 sec or less).
Heparin is administered IV through the central venous port. Its peak effect occurs within 2 minutes, and verification is based on the ACT, which should be established 5 to 10 minutes after administration.
Special circumstances such as long-term heparinization, antithrombin III deficiency, heparin-induced thrombocytopenia (HIT), and excessive hemodilution may cause “heparin resistance,” which alters the algorithm for calculating the loading dose.
Management of a patient with heparin-associated thrombocytopenia and thrombosis (HATT) presents a particular challenge. HIT is evident after exposure to heparin because the platelet count suddenly falls. The onset can be as soon as 2 days or as long as 5 days after institution of heparin therapy. Surgery should be postponed if at all possible, and heparin must be eliminated from the patient’s medication regimen until the platelets are normal and do not aggregate in response to heparin. A polysulfated glycosaminoglycan (danaparoid) as well as a thrombin inhibitor (hirudin) have been used safely for CPB.
Prophylaxis and treatment of coagulopathy
Antifibrinolytics
Patients for CABG procedures on CPB receive an antifibrinolytic. First-time patients are treated with aminocaproic acid.
Aminocaproic acid and tranexamic acid
Aminocaproic acid (Amicar) was initially proposed for the treatment of fibrinolysis associated with prostate and cardiac surgery. Tranexamic acid is considered to be more potent than aminocaproic acid. Antifibrinolytics are hemostatic agents given as an IV loading dose and then by continuous infusion before CPB.
The loading dose of aminocaproic acid is 100 to 150 mg/kg followed by an infusion dose of 10 to 15 mg/kg/hr. The dose of tranexamic acid is 10 to 15 mg/kg loading with an infusion of 1 to 1.5 mg/kg/hr. The drug has renal excretion and a plasma half-life of approximately 80 minutes. These drugs have proven effective in reducing bleeding after bypass.
Desmopressin
Desmopressin acetate (DDAVP) is a synthetic analog of vasopressin, which releases a variety of hemostatically active substances from the vascular endothelium. It is administered in doses of 0.3 mcg/kg intravenously, intranasally, or subcutaneously.
It has a half-life of 55 minutes (with clinical effects lasting from 5 to 6 hours) and results in an approximately fourfold increase in circulating levels of factor VIII, prostacyclin, tissue plasminogen activator, and von Willebrand factor.
The overall effect of desmopressin is hemostatic. DDAVP has also been used to treat uremia, cirrhosis, platelet disorders, and mild or moderate cases of hemophilia A (von Willebrand disease). Current evidence does not support the broad administration of DDAVP to cardiac surgical patients as prophylaxis for bleeding.
Pharmacologic approaches to blood pressure control
Blood pressure control during the perioperative phase may be accomplished with the use of pharmacologic agents independently or in combination. Vasodilators such as hydralazine, nitroglycerin, and nitroprusside are useful for control of blood pressure and improving peripheral blood flow.
α-Adrenergic agonists (e.g., clonidine) reduce stress-mediated neurohumoral responses to induction and CPB. They decrease heart rate and blood pressure and have sedative and antinociceptive characteristics, which may reduce opioid requirements without respiratory depression. They can be used independently or in conjunction with IV induction agents and opioids; they help to reduce the amount of agent required.
Careful use of β-blockers can decrease heart rate, contractility, and blood pressure, which works to reduce oxygen use. These drugs increase the duration of diastole to allow for a more complete oxygenation of the LV. They act synergistically with nitroglycerin and blunt tachycardia and decrease ischemia of the myocardium. They have the ability to reduce catecholamine-induced ventricular arrhythmias. The disadvantage associated with β-blockers is that they may precipitate bradyarrhythmias, heart block, or bronchospasm. β-Blockers available in IV form for use during cardiac surgery include esmolol, labetalol, metoprolol, and propranolol. Reversal of the effects of β-blockers can be achieved through use of β-agonists (isoproterenol) and cardiac pacing (unless emergent CPB initiation is possible).
Vasodilator therapy includes direct vasodilators (hydralazine, nitroglycerin, or nitroprusside), α-adrenergic blockers (labetalol, phentolamine), angiotensin-converting enzyme inhibitors (enalaprilat IV), central α-agonists (clonidine), or calcium channel blockers (nicardipine IV, verapamil, or diltiazem). Disadvantages include a slow onset of action or long duration of action, reflex tachycardias, and toxicity reactions. The drug therapy is to be selected individually for each patient and situation and administered judiciously for the desired effect.
Vasopressor therapy includes agents with selective direct effects (methoxamine, phenylephrine), α1-agonist mixed agents (dopamine, ephedrine, epinephrine, noradrenaline), or vasopressin (direct peripheral vasoconstriction with no β-adrenergic effects).
Other drugs that work indirectly to increase blood pressure include the positive inotropic drugs (e.g., dobutamine, dopamine, and milrinone). Calcium reverses hypotension associated with the use of halogenated agents, calcium channel blockers, hypocalcemia, β-blockers, and CPB. When administered intravenously by central line, it can increase blood pressure as well as reverse the cardiac effects of toxicity resulting from hyperkalemia.
Preoperative period
Considerations during the preoperative period include sedation and monitoring of the patient while placement of appropriate invasive monitoring lines ensues.
All equipment should be available and invasive lines inserted before the patient is brought to the operating room.
Invasive monitors are useful during induction and should be placed before induction except in emergency situations such as ruptured aneurysms, cardiac tamponade, or ventricle rupture.
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