I. Cardiovascular System

SECTION I. Cardiovascular System


A Ablation Procedures



MAZE AND MINI-MAZE PROCEDURES


The MAZE procedure is offered to patients at high risk for stroke who have unsuccessful attempts at chemical treatment. It is an “open-heart” cardiac surgery procedure intended to eliminate atrial fibrillation (AF). The name refers to the series of incisions arranged in a maze-like pattern in the atria. The Cox Maze III procedure is now considered to be the “gold standard” for effective surgical cure of AF. It may be performed concomitant with mitral valve repair (MVR) or replacement for patients who also have mitral valve disease. MAZE is performed employing pulmonary vein isolation and a number of incisions in the right and left atria. These incisions or cryoablations ultimately form scar tissue thereby mechanically interrupting transmission of triggering impulses of atrial fibrillation. For MAZE, it is necessary for the patient to have a sternotomy and cardiopulmonary bypass (CPB). All of the monitoring and medication necessary for CPB is required for the MAZE procedure. In addition to the lesions made in the atria, the left atrial appendage is often removed as it is thought to be a culprit in the stasis of blood flow, thereby increasing the possibility of stroke should it remain. The term mini-MAZE is still sometimes used to describe an open-heart procedure requiring cardiopulmonary bypass, but it more commonly refers to minimally invasive epicardial procedures not requiring cardiopulmonary bypass.

The mini-MAZE procedure is performed utilizing thorocoscopy on a beating heart. No CPB is required in this situation; it is utilized where there is mitral valve repair or replacement. “Keyhole” incisions are employed for the mini-MAZE, and the patient is placed in the lateral position. Routine monitoring with the addition of an arterial line and one lung ventilation (OLV) are adjuncts of this procedure.


PULMONARY VEIN ISOLATION AND CATHETER ABLATION FOR PERSISTENT ATRIAL FIBRILLATION


Surgical management of rate-related cardiac rhythm anomalies has historically been provided by catheter ablation of the offending right atrial conduction pathways. For conditions such as Wolff-Parkinson-White syndrome, right atrial flutter, or supraventricular tachycardia, catheter ablation to permanently block impulses has been performed by groin catheterization much like cardiac angiograms. Until recently, atrial fibrillation has not been addressed in this manner.

Research on the contributing triggers for atrial fibrillation has illuminated the possibility that pulmonary vein isolation and ablation of offending fibers is an alternative when chemical means fail. Catheter ablation for atrial fibrillation has been performed with patients under general anesthesia. Groin catheterization continuing with a catheter puncture across the atrial septal wall and advancement of the catheter into the left atrium is performed. A lesion is created with the catheter tip and a specified energy. The lesion then prevents transmission of offending impulses that trigger the atrial fibrillation.

General anesthesia management includes an endotracheal tube, an arterial line, and resuscitative drugs. Multiple arrhythmias and blood pressure swings are evident during this procedure. These are often short-lived and resolve spontaneously without any intervention or with very little intervention on the part of the anesthesia provider.






B Automatic Internal Cardioverter Defibrillator



DEFINITION


Automatic implantable cardioverter defibrillators are surgically implanted to prevent sudden cardiac death from malignant ventricular tachyarrhythmias. These are self-contained diagnostic devices that continuously monitor the patient’s heart rate and electrocardiographic activity. They sense potentially lethal ventricular arrhythmias and treat them with electrical discharges. Whereas pacemakers use low-energy impulses measured in microjoules, these defibrillators release an electrical discharge of approximately 30 J after sensing periods of fibrillation lasting approximately 20 seconds. Most devices now can be programmed to reconfirm ventricular tachycardia or ventricular fibrillation after charging to prevent inappropriate shock therapy.


INDICATIONS


Patients considered for implantation are those who have had minimal success with standard antiarrhythmic drug therapy. The majority of patients have severe coronary artery disease with reduced left ventricular function, ischemic cardiomyopathy, or idiopathic cardiomyopathy.


ANESTHETIC CONSIDERATIONS






1. Anesthetic management is best handled by general anesthesia because of testing that is necessary to properly place and program this device.


2. Prolonged periods of asystole are at times encountered and can cause cerebral and myocardial ischemia.


3. Vasoactive drugs are helpful for blood pressure stabilization.


4. If ventricular tachycardia occurs before clinical induction, lidocaine treatment should be avoided because it may result in the inability to induce ventricular tachycardia on demand during testing.


5. Minimal monitoring includes ECG leads II and V 5 along with an arterial line.


6. IV sedation or general anesthesia may be used for these patients. Due to the stress associated with testing and the amount of sedation necessary for the procedure, some practitioners advocate that general anesthesia with a controlled airway is the best choice.






C Surgery for Coronary Artery Disease



INTRODUCTION


Coronary artery disease is the predominant cause of death in patients in the fourth and fifth decades and the most common cause of premature death in men aged 35 to 45 years. Annually approximately 1.5 million individuals endure some level of myocardial insult. The most recent data show that there are more than 1,285,000 inpatient angioplasty procedures, 427,000 inpatient bypass procedures, 1,471,000 inpatient diagnostic cardiac catheterizations, 68,000 inpatient implantable defibrillators, and 170,000 inpatient pacemaker procedures performed in the United States.

Coronary artery disease alters coronary blood flow, decreases coronary reserve, and increases the incidence of coronary artery vasospasm. Risk factors associated with the progression of coronary artery disease include age, gender, genetic predisposition, obesity, hyperlipidemia, hypertension, stress, diabetes mellitus, and smoking. Exacerbating the effects of coronary artery disease are combinations of peripheral vascular disease, carotid disease, and a compromised pulmonary system.

Patients with atherosclerotic coronary disease become symptomatic when 75% of the coronary vessel is occluded, resulting in a decrease in coronary blood flow. Ischemia depresses myocardial function and causes severe chest pain referred to as angina pectoris. In addition to pain, cells are subject to increased irritability and become increasingly vulnerable to fibrillation, alterations in the conduction pathways, and thrombus formation.


ANESTHESIA CONSIDERATIONS






1. The goals of anesthetic management for coronary revascularization are directed toward producing analgesia, amnesia, and muscle relaxation; abolishing autonomic reflexes; maintaining physiologic homeostasis; and providing myocardial and cerebral protection.


2. The avenues available to accomplish these goals include an effective preoperative evaluation, administration of modest doses of sedation and pain medication before any attempt at line placement is made; and use of O 2 in the preoperative setting.


3. Administration of a balanced anesthetic with opioid, inhalation agents, sedative-hypnotics, and muscle relaxant provides a stable hemodynamic state for the difficult cardiovascular patient.


4. The inhalation agents offer the additional advantage of anesthetic preconditioning, which is cardioprotective.


Preoperative Assessment


A thorough preoperative assessment of the patient should include comprehensive review of systems, airway status, and laboratory data; physical examination; review of surgical history; and review of current medications. Actual reports of diagnostic procedures such as cardiac catheterization, echocardiogram, and Doppler studies should be reviewed by the anesthesia provider.


Hemodynamic Status






1. Evaluation of cardiovascular status includes a discussion with the patient regarding his or her functional status.


2. Cardiac catheterization may be used for diagnostic assessment, electrophysiologic evaluation, or direct intervention for patients in cardiogenic shock. The catheterization evaluation provides information about pressures and oxygen saturations of the four chambers of the heart, PA pressure, systemic pressure, body surface area, CI (liters/min/m 2), stroke index (mL/beat/m 2), left ventricular ejection fraction (EF), degree of stenosis in coronary vessels, and coronary dominance. The normal values are listed in the table below.


3. An EF of 50% or greater in a patient with normal valve function is acceptable. If the patient has mitral regurgitation, an EF of 50% to 55% is considered to indicate left ventricular dysfunction. An EF of less than 50% reflects a moderate reduction of ventricular function. Poor cardiac function relates to an EF below 30% and may stem from ventricular hypokinesis, akinesis, or dyskinesis.


4. Echocardiography is used to evaluate ventricular function by measuring wall motion during systole. It can permit a qualitative and quantitative assessment and reflects the four types of abnormal wall function described previously.


5. Single photon emission computed tomography (SPECT) scan is another diagnostic tool used in the preparation of patients for cardiac surgery. It is a noninvasive procedure that makes use of a radionuclide tracer to provide a three-dimensional picture of heart structures and function. It is capable of producing a measurement of rate and volume of blood flow, size and location of blockages or narrowing of vessels, and more accurate diagnosis of heart disease in women.









































Normal Intracardiac Pressures


Notation Range (mm Hg)
Central venous pressure CVP 0-8
Right atrial pressure RAP 0-8
Right ventricular end-systolic pressure RVESP 15-25
Right ventricular end-diastolic pressure RVEDP 0-8
Pulmonary artery pressure (systolic) PAP systolic 15-25
Pulmonary artery pressure (diastolic) PAP diastolic 8-15
Pulmonary artery pressure (mean) PAP 10-20
Pulmonary capillary wedge pressure; pulmonary artery occlusion pressure PCWP; PAOP 6-12


Laboratory Data


Laboratory examinations for patients with ischemic heart disease involving two or more associated risk factors (diabetes, obesity, family history, and smoking) should include complete blood count; electrolytes; cardiac enzymes (including enzyme fraction for creatinine phosphokinase), serum creatinine, cholesterol; and coagulation screening profile.

Coagulation function studies are used to monitor patients receiving heparin therapy and warfarin products. Platelet inhibitors are often part of the drug regimens of patients who need cardiac surgery. These agents are associated with the risk of excess bleeding. However, no evidence suggests that surgery is contraindicated in this situation. It is recommended that 24 to 48 hours elapse before surgery is performed after these drugs are discontinued. The platelet inhibitors (glucoprotein IIb/IIIa receptor inhibitors) in use at this time include abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). It should be emphasized that long-term heparin therapy results in prolonged bleeding times and may affect calculations of loading doses of heparin required for CPB. Other issues related to the cause and treatment of adverse bleeding are discussed later in this chapter.


Long-Term Use of Medications






1. Prevention of rebound hypertension and reduction of perioperative hemodynamic stress are primary considerations for continuation of antihypertensive therapy until the morning of surgery. Potential drug interactions with anesthetic agents should be anticipated and evaluated, and treatment should proceed accordingly.


2. Calcium-channel blockers are used widely to control hypertension, angina, and arrhythmias in patients with cardiovascular disease. Their continued use up to the day of surgery is a common practice and provides the advantage of controlling dysrhythmias and preventing coronary spasm. Potential hazards associated with continued therapy include a reduction in patient responses to inotropes and vasopressors and atrioventricular conduction problems.


3. β-Adrenergic receptor–blocking agents play an important role in the therapy of cardiovascular patients and must be continued up to and during the preinduction period. β‑Blockers allow for reduction in myocardial oxygen consumption by providing an overall decrease in sympathetic stimulation and catecholamine release. Because the heart rate is slowed, diastolic filling is improved. These drugs are helpful in controlling anginal symptoms, hypertension, tachycardia, and myocardial ischemia. Bronchospasm and decreased inotropic response to β stimulants in conjunction with greater vasoconstriction in response to sympathomimetics are potential disadvantages to continuation of β-blockade up to the time of surgery.


4. Digitalis therapy may be continued until the morning of surgery if it is used to treat rapid ventricular response to atrial fibrillation or flutter; otherwise, it may be discontinued, because other inotropes with greater efficacy may be given preoperatively if needed. If potassium is used, its effects must be carefully monitored.


5. It is recommended that antidysrhythmics be continued until the day of surgery except for disopyramide, encainide, and flecainide, which should be discontinued except in the presence of the most life-threatening dysrhythmias. These agents have been associated with increased mortality, and postbypass MI has been noted with their continuance. Disopyramide has been noted to cause difficulty in termination of CPB.


6. Antidepressants provide no advantage if continued up to the day of surgery and may interact negatively with sympathomimetics. However, as noted previously, it is important to give sedation and anxiolysis to these patients during the preoperative phase.


ANESTHESIA MONITORING






1. Electrocardiography and Noninvasive Blood Pressure

Leads II and V 5 can help in the diagnosis of dysrhythmias, ischemia, conduction defects, and electrolyte disturbances. None of the standard leads can detect posterior wall ischemia. The noninvasive blood pressure cuff must be placed on the same side as the arterial line to allow for correlation of blood pressure.


2. Radial Arterial Line

Sternal retraction may play a role in distorting the radial artery waveform. The right radial artery is usually selected in cases in which the left internal mammary artery is dissected for anastomosis and because radial arterial line monitoring may show a false low number because of compression of the subclavian artery at the retractor. The brachial artery is contraindicated because it is an end artery of the arm.


Other Arterial Line Sites


Use of the brachial artery for monitoring is most commonly dismissed because it provides the bulk of circulation for the lower arm and is considered an end artery. The femoral artery is superficial and offers access to the central arterial tree. It also provides appropriate access should intraaortic balloon pump (IABP) placement be necessary. However, if the femoral artery is used, it should be noted that an alternative site may become necessary if use of IABP is instituted.




1. Central Venous Pressure

Use of the right internal jugular (IJ) vein is recommended, as cannulation of the left IJ vein increases the risk of laceration of the left brachiocephalic vein. Central venous pressure (CVP) lines may be used for monitoring, to provide a central line for fluid and drugs, and in situations in which a PA catheter is not used.


2. Pulmonary Artery Catheter

The PA catheter was historically used for all coronary artery bypass graft (CABG) procedures, but it is associated with complications and now has a more narrow range of uses. It is indicated for use in high-risk patients with an EF of less than 40%.


3. Transesophageal Echocardiography

Transesophageal echocardiography (TEE) allows continuous monitoring of the chambers of the heart, ascending and descending aorta, valvular function, chamber filling, and wall contractility and motion. Detection of gaseous or particulate emboli, identification of intracardiac shunting, diagnosis of aortic dissection, evaluation of saphenous vein graft flow, and confirmation of left ventricular dimension (filling) during weaning are other potential applications for this monitoring method. TEE may predict or suggest myocardial ischemia as defined by regional wall motion abnormalities, valve replacement procedures, cardiac aneurysms, intracardiac tumors, aortic dissection, and repair of complex congenital lesions.

Relative contraindications to the use of TEE include dysphagia, mediastinal radiation, upper GI surgery or bleeding, esophageal stricture, tumor, varices, and recent chest trauma. In conjunction with the increased use of TEE, certain complications have been reported to occur during open-heart surgery. Cardiac arrhythmias, bronchospasm, and esophageal laceration are rare. The common cardiac formulas are listed in the following table.









































































Cardiac Formulas

Parameter Notation Formula Normal Range
Stroke volume SV SV = CO ÷ HR 60-90 mL/beat
Stroke index SI SI = SV ÷ BSA 40-60 mL/beat/m 2
Cardiac output CO CO = SV × HR 5-6 L/min
Cardiac index CI CI = CO ÷ BSA 2.5-4 L/min/m 2
Mean arterial pressure MAP MAP = diastolic pressure + one third pulse pressure 80-120 mmHg
Systemic vascular resistance SVR SVR = (MAP – CVP) ÷ (CO × 80) 700-1400 dyne/sec/cm 5
Pulmonary vascular resistance PVR PVR = (PAP – PCWP) ÷ (CO × 80) 50-300 dyne/sec/cm 5
Left ventricular stroke work index LVSWI LVSWI = 0.0136 × (MAP – PCWP) × SI 40-60 g × m/beat/m 2
Coronary perfusion pressure CPP CPP = DIA BP – LVEDP mm/Hg
Ejection fraction EF EF = (EDV – ESV) ÷ EDV 55%-70%
Rate-pressure product RPP RPP = SYS BP × rate >15,000
Triple index TI TI = SYS BP × rate × PCWP >180,000
BSA, Body surface area; DIA BP, diastolic blood pressure; EDV, end-diastolic volume; ESV, end-systolic volume; HR, heart rate; LVEDP, left ventricular end-diastolic pressure; PCWP, pulmonary capillary wedge pressure; SI, stroke index; SYS BP, systolic blood pressure; CVP, cardioventricular pacing; PAP, peak airway pressure.




4. Monitoring of Core Temperature

Accurate monitoring of core temperature is essential in order to control target hypothermia as well as to reestablish normothermia. The most accurate indicator of core temperature is at the thermistor of the PA catheter. Brain temperature is reflected in nasopharyngeal measurement, but a lag time occurs on rewarming. The probe should be inserted before heparinization to a depth of 7 to 10 cm through the nares. Tympanic temperature may also lag behind brain rewarmed temperature and is no better for monitoring of this parameter. Bladder or rectal temperature measurement is today considered inaccurate when renal and splanchnic blood flow is decreased. Brain temperature should not drop below 20° C, as profound hypothermia (15° to 20° C) appears to cause a loss of cerebral autoregulation.


5. Cerebral Monitoring

In addition to the monitoring of brain temperature, electrophysiologic monitoring is often employed. EEG is not an effective method for monitoring subtle changes, but any asymmetric EEG activity is considered a problem. Bispectral analysis (BIS) monitoring may correlate with the depth of anesthesia; it is actually a derived parameter to assess the degree of wakefulness.


PERFUSION PRINCIPLES






1. 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 CO 2), 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.


2. 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.


3. 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.


4. 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).


5. 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






1. 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 left ventricle.


2. 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.


3. 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






1. 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.


2. 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






1. 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.


2. 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.


3. Blood from the reservoir is propelled by roller or centrifugal pump to the oxygenator, where it becomes arterialized by interfacing with a membrane oxygenator.


4. 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.


5. 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 mm Hg.


Myocardial Protection Techniques






1. Injury to the myocardium is a complex occurrence and may result from numerous physiologic events.


2. Tachycardia, hypertension or hypotension, and ventricular distention can all play a role in the events that produce an oxygen supply-demand imbalance.


3. 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.


4. 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.


5. 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 ATP channels, reactive oxygen species, calcium overload, and inflammation. APC reduces myocardial necrosis and improves postoperative cardiac performance.


Cardioplegia






1. Cardioplegia is a potassium solution administered into the coronary circulation to provide diastolic arrest. It is composed of potassium (15 to 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.


2. 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.


3. 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.


4. Crystalloid-based solutions do not contain hemoglobin; therefore they deliver dissolved O 2 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.


5. Extracellular solutions produce diastolic arrest by depolarization of the membrane with high potassium concentrations.


Anticoagulation






1. 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.


2. The heparin dose is usually calculated to maintain an ACT of 400 seconds (the normal range is 130 seconds or less).


3. Heparin is administered intravenously 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.


4. 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.


5. 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. Patients undergoing subsequent surgeries, those with renal failure, those at high risk of bleeding, and Jehovah’s Witnesses are occasionally treated with aprotinin.


Aminocaproic Acid and Tranexamic Acid






1. 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.


2. 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.

Only gold members can continue reading. Log In or Register to continue

May 31, 2016 | Posted by in ANESTHESIA | Comments Off on I. Cardiovascular System

Full access? Get Clinical Tree

Get Clinical Tree app for offline access