The heart-lung machine diverts blood away from the heart and lungs, adds oxygen to the blood, then returns the blood to the body—all without the blood having to go through the heart. Perfusionists are also responsible for measuring selected laboratory values such as blood cell count and monitoring circulation. Under the direction of the anesthesiologist and surgeon, perfusionists may also administer medicines through the cardiopulmonary bypass circuit.
Monitoring of aortic line pressure, blood temperature and integrity of gas supply to the oxygenator is essential. Volatile anaesthetics provide cardioprotective effects through preconditioning. Nitrous oxide is avoided during CPB to prevent an increase in the size of air emboli. Anaesthetic requirements are reduced with hypothermia, however drug pharmacokinetics are also altered due to haemodilution and altered metabolism leading to variable effect.
Hypothermia is frequently used during CPB for its presumed organ protective effects. Blood viscosity increases with hypothermia and allows maintenance of a higher perfusion pressure despite haemodilution. However, hypothermia reversibly inhibits the clotting factors and platelets.
Currently, the data are inconclusive regarding the superiority of hypothermic over the normothermic bypass. Core temperature monitoring sites include the rectum, urinary bladder, oesophagus and pulmonary artery. Nasopharyngeal temperature gives an estimate of cerebral temperature. With cooling, CO 2 becomes more soluble in the blood partial pressure decreases causing alkalosis. The constancy of the charge state of this ring is important in the regulation of pH-dependent cellular processes.
In alpha-stat, pH is not corrected, and PaCO 2 is allowed to fall with hypothermia. Alpha-stat maintains limits microemboli by maintaining cerebral autoregulation. Inhomogeneous cerebral cooling is the disadvantage of alpha-state management.
CO 2 is added to the oxygenator causing increased cerebral blood flow and cooling. Prolonged pH-stat management can lead to severe acidosis, so a switch to conventional alpha-stat during the rewarming phase is required. In adults with moderate hypothermia, alpha-stat is beneficial. This maximises cerebral cooling and avoids severe acidosis with prolonged pH-stat. Ultrafiltration during and after CPB removes inflammatory mediators and excess fluid thereby producing haemoconcentration.
Conventional ultrafiltration uses a haemofilter inserted into the bypass circuit. Modified ultrafiltration MUF is used after completion of the surgical repair before protamine administration, with blood removed from the arterial line and returned to the venous line after passing through the haemofilter. It was first described by Naik et al.
Weaning is the process where extracorporeal support is gradually withdrawn as the heart takes over the circulation. Several steps are required for successful completion of weaning. The use of hypothermia requires a period of rewarming.
Rapid rewarming and hyperthermia are associated with cerebral injury. The high gradient between core and peripheral temperature can lead to after drop in temperature. Use of vasodilators can help in homogenous rewarming and to increase venous capacitance during transfusion of circuit blood. Supplemental doses of anaesthetics are administered; acid-base balance, electrolytes, PaO 2 , PaCO 2 , sugar and haematocrit are kept within normal limits.
Serum potassium of 4. After open-heart procedures, deairing of the heart is done. TOE is useful to assess the adequacy of deairing. Air embolism, frequently involving the right coronary artery due to its anterior location, can cause arrhythmias, ST-elevation and myocardial dysfunction.
It is treated by increasing the perfusion pressure and maintaining pulsatile perfusion by partially clamping the venous line. Heart rate, rhythm and contractility are assessed. Removal of the aortic cross-clamp can be associated with ventricular fibrillation, especially in conditions causing left ventricular hypertrophy like severe aortic stenosis.
Defibrillation is achieved using internal paddles with the biphasic energy of 5—20 J. Antiarrhythmics such as amiodarone, lidocaine and magnesium[ 33 ] can be added for persistent dysrhythmias.
Mechanical ventilation is started, and the perfusionist gradually occludes venous return and fills the heart while incrementally reducing pump flows. Difficulties in weaning manifested by systemic hypotension may be due to either hypovolaemia, ventricular dysfunction or low SVR.
Hypovolaemia is treated by giving controlled boluses of blood from the circuit. Low SVR is treated with vasopressors such as phenylephrine, noradrenaline or vasopressin.
The need for inotropes should be evaluated by visually assessing contractility and with TOE. Prior left ventricular dysfunction, severe pulmonary hypertension, inadequate myocardial protection and prolonged cross-clamp time are factors to consider in determining the post-bypass use of inotropes.
A variety of inotropes are available, but the evidence base to advocate one inotrope over another is lacking. Inodilators such as milrinone, dobutamine and levosimendan can be used in the setting of ventricular dysfunction with increased afterload. Use of levosimendan may be associated with a reduction in mortality. In spite of all measures, if the patient fails to wean, mechanical support devices like intra-aortic balloon pump, ventricular assist device or extracorporeal membrane oxygenation should be considered.
After separation from CPB, heparin is reversed with protamine in a ratio of — Protamine is administered over 10—15 min. Protamine can cause various reactions, namely type I hypotension, due to fast infusion , type II anaphylaxis and type III pulmonary hypertensive crisis.
Once protamine administration is complete, ACT is checked to confirm normalisation. Additional protamine should be given if circuit blood containing heparin is transfused.
High doses of protamine also cause anticoagulation. Residual re-heparinisation may also occur as the drug emerges out of poorly perfused compartments, especially in obese patients heparin rebound. The final step is arterial decannulation. Post CPB, radial arterial catheters may underestimate central aortic systolic pressure but mean pressure is equivalent , due to vasodilation and arteriovenous shunting in the upper limb.
Arterial cannulation can be associated with bleeding, cannula malposition causing selective cerebral perfusion, plaque dislodgement and dissection. It can be diagnosed with TOE. Repair of the dissection is necessary under DHCA. Massive air embolism is due to pumping from an empty reservoir. Treatment is cessation of the pump and commencing retrograde cerebral perfusion.
Other complications include oxygenator failure, pump malfunction, clotting in the circuit, tubing rupture, gas supply failure and electrical failure due to which hand cranking must be available at all times.
CPB causes qualitative and quantitative platelet dysfunction. The concentration of pro-coagulants decreases due to haemodilution.
Inflammatory, coagulation, complement and fibrinolytic pathways are activated. Thromboelastography can help in knowing the cause of bleeding diathesis. Bleeding is greater with prolonged bypass time, redo-surgery and preoperative use of anticoagulants. Studies have shown decreased blood loss and transfusion requirement in cardiac surgery patients with prophylactic anti-fibrinolytics.
Inflammatory response and hypotension can cause acute kidney injury AKI. Risk factors are prolonged bypass time, sepsis and diabetes. Treatment includes maintenance of high perfusion pressure, use of early biomarkers to detect AKI and dialysis.
The spectrum of cerebral injury ranges from cognitive dysfunction to stroke. The strategy includes maintenance of higher perfusion pressure, adequate HCt, and alpha stat management. Contact of blood with artificial surfaces, ischaemia-reperfusion injury, endotoxaemia and operative trauma can cause systemic inflammatory response after CPB. Acute phase reaction is initiated by the release of complement, cytokines, endotoxins and NO leading to increased capillary permeability.
Rewarming can cause stress response and release of inflammatory mediators. The role of steroids is controversial in view of the lack of adequate benefit and flaring of postoperative infection. Subclinical myocardial injury can occur due to cross clamping of the aorta in spite of cardioplegia. Stunning of the myocardium is responsible for immediate dysfunction. Factors include metabolic acidosis, preoperative ventricular function, reperfusion injury and inflammatory mediators.
Optimisation of electrolytes, temperature and pH helps to reduce arrhythmias. Acute respiratory distress syndrome can be present due to the effects of CPB. Anaesthesia-induced atelectasis and reduced mucociliary clearance further contribute to acute lung injury. As a result atelectasis and pleural effusions are common pulmonary abnormalities after cardiac surgery.
Therefore, lung protective lung strategies are required in the pre- and post-operative periods of cardiac surgery. Vasoplegia is characterised by severe, vasopressor-resistant vasodilation due to activation of nitric oxide synthase, vascular smooth muscle ATP-sensitive potassium channels and relative deficiency of vasopressin. Treatment includes fluid resuscitation and vasopressors such as phenylephrine, norepinephrine and vasopressin.
Use of the heart-lung machine in cardiac surgery is called cardiopulmonary bypass. Cardiopulmonary bypass provides patients with cardiac and pulmonary support, while bypassing the heart and lungs. Cardiopulmonary bypass artificially provides patients three physiologic processes or functions:. Once the cannulas from the patient have been connected to the cardiopulmonary bypass circuit, the blood is drained from the veins into the heart-lung machine while the blood is pumped into an artificial lung oxygenator , which adds oxygen and removes carbon dioxide.
The oxygenated blood is pumped back to the aorta to provide oxygen to the tissues and organs of the patient. The person responsible for performing cardiopulmonary bypass is called a cardiovascular perfusionist.
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