Cardiopulmonary bypass (also known as extracorporeal circulation) was first used clinically in surgery at Thomas Jefferson University Hospital in 1954 by Dr. John Gibbon, Jr.
It has been used literally millions of times since this first “pump run” to allow the circulation to be temporarily shunted outside the body to allow the heart to be drained and stopped during heart surgery to repair defective valves and to perform coronary artery bypass grafting (CABG or in the vernacular “cabbage.”)
Because of the inherent complications in supporting the circulation in this non-physiologic way, the trend in cardiac surgery in the last several years has been to perform “off pump” heart surgery whenever possible.
However, in a seeming contradiction, a large study published in the New England Journal of Medicine in October of 2009 reported worse outcomes in patients that are operated on without cardiopulmonary bypass
Listed below are some of the complications that can occur with coronary pulmonary bypass (CPB.)
Machine Complications
As with any piece of mechanical equipment, bypass machines can fail or become defection. During bypass the pump is operated by a trained bypass perfusionist who is in attendance throughout the pump run. Possible machine problems include:
Rupture of the hoses and tubes carrying the blood
Defective tubing stopcocks or dislodgement
Power interruption to the machine
Electrical shortage
Inadvertent introduction of air into the circuit
Failure of oxygenator
Pump flow reversal
Lung Complications
Injury to the lungs occurs more than any other serious complication of cardiopulmonary bypass and tends to amplify. some known risk factors for developing pulmonary dysfunction are smoking, length of bypass, older age, obesity, pulmonary hypertension, COPD (emphysema and chronic bronchitis), poor heart function preoperatively, and emergency surgery.
Possible lung injury secondary to bypass includes:
Acute respiratory distress syndrome (ARDS)- this is the most severe manifestation of the physiologic insult to the lungs during bypass, which is multifactorial.
Leukoembolization – results from activation of complement.
Atelectasis (lung collapse)
Ventilation-perfusion mismatch – since the blood is not being pumped through the heart, there is no blood being sent through the pulmonary arteries. The only blood supply that the lung receives is from the bronchial arteries, which results in ischemia to the lungs.
Interstitial edema (fluid in the lung tissue) – affects post-bypass oxygenation. Results from neutrophils clumping in the microvasculature and releasing oxygen free radicals.
Neurological complications
These complications are among the most feared and have been characterized by practitioners as “pump head.” Up to half of patients undergoing cardiopulmonary bypass experience cognitive deficits.
Some preoperative risk factors include age, diabetes mellitus, peripheral vascular disease, hypertension, impaired kidney function, previous stroke, and an ejection fraction < 40%.
Intraoperative risk factors include length of bypass, atherosclerosis of the aorta, need to return to cardiopulmonary bypass, use of an intraaortic balloon pump, and calcified mitral and aortic valves.
Possible complications and sequelae include:
Global or regional hypoperfusion – this occurs when not enough blood and oxygen reaches the brain. Risks factors for global hypoperfusion are carotid artery disease and hypertension (high blood pressure).
Emboli – this occurs when a blot clot, particle of matter, or air travels to the brain and occludes an artery. The origin of emboli include aortic cannulation and aortic clamping where atherosclerotic plaque can be dislodged, bone marrow, particles for the tubing, and blood and fibrin clots.
The number or microemboli is known to increase with manipulation of the tubing and circuit by the perfusionist when injecting drugs or drawing blood samples.
Air emboli to the brain occur when there is a break in the lines, inadequate removal of air from the lines and empty heart chambers, malfunction of the oxygenator, and air moving through a patient foramen ovale (i.e., congenital hole in the middle heart wall) from an intravenous line.
Stroke – the incidence ranges from 1% to 7%.
Encephalopathy – the incidence is estimated to be about 7%
Delirium and confusion
Agitation
Memory Deficit
Seizure
Drug and Immune Reactions
Protamine reaction – this drug is used to reverse heparin which is given to prevent clotting of the blood as it passes through the tubing of the bypass machine. Protamine adminstration causes a temporary hypotension (a drop in blood pressure) which can be treated by the use of vasopressors (drugs which constrict the arteries and raise the blood pressure) and by a slower rate of administration.
Very rarely, the administration of protamine causes a severe and life-threatening reaction that is marked by severe and untreatable hypotenison, massive pulmonary arterial constriction, and right heart failure.
Often the only course left open to clinicians to save the patient’s life is reheparinization and emergent return to the bypass as a supportive measure until rescue medical therapy can be initiated. This includes use of steroids, antihistamines, aminophylline, pulmonary vasodilators such as PGE and inhaled nitric oxide, and vasopressors such as epinephrine and phenylephrine.
Systemic inflammatory response syndrome – this occurs when the blood plasma enzyme systems are activated by heparin/protamine complexes, mechanical shear stress of the blood cell components, and blood contact with the noncoated surfaces of the bypass circuit. Higher levels of inflammation have been correlated with worse outcomes.
Hematological Complications
Heparin-induced thrombocytopenia (i.e., low platelets) – this condition arises when the heparin used to prevent clotting of the blood in the tubing of the bypass machine binds platelet factor 4 and results in the production of immunoglobulin G type antibodies. This causes activation of the clotting cascade and the subsequent consumption of platelets.
Not all decreases in platelet count post bypass are related to HIT. The mild form of HIT is self-contained and does not require treatment. Type 2 HIT requires heparin to be stopped immediately and the initiation of thrombin inhibitors such as argatroban, lepirudin, or bivalirudin to be started to prevent life-threatening clots from forming.