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|Year : 2007
: 10 | Issue : 2 | Page
|Anaesthesia for neonatal cardiac surgery
Suresh Chengode, Priya R Menon
Department of Anaesthesia, Amrita Institute of Medical Sciences, Kochi., India
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Keywords: Cardiac surgery, Neonatal, Anaesthesia
|How to cite this article:|
Chengode S, Menon PR. Anaesthesia for neonatal cardiac surgery. Ann Card Anaesth 2007;10:158-67
| Introduction|| |
Significant progress has been made in neonatal cardiac surgery over the last two decades owing to major advances in paediatric cardiology, anaesthesia, cardiopulmonary bypass (CPB) techniques and perioperative cardiac intensive care. ,, The mortality and morbidity after paediatric cardiac surgery has decreased considerably, especially in the neonates following biventricular repair, although, the management of neonates before and after complex single ventricle repair is still an ongoing challenge. , Furthermore, cardiac surgery may be performed in the low birth weight and premature neonates with good early and midterm results,  however, the same does not hold true for those undergoing surgical palliation for complex single ventricle lesions. 
Advances in the field of diagnostic modalities, monitoring options, treatment, and our understanding of the pathophysiology of various congenital cardiac lesions has led to improved outcome with every aspect of periopereative management in neonatal cardiac surgery. In this article, the authors have tried to review the anaesthetic management relevant to the management of neonates with congenital heart disease presenting for cardiac surgery in the neonatal period. Sound knowledge regarding the pathophysiology of congenital heart diseases is absolutely necessary for the appropriate anaesthetic management.
| General Considerations|| |
Immaturity of myocardium, transitional circulation, natural physiological changes in the pulmonary and systemic vascular beds in the neonatal period, specific pathology related changes in the pulmonary vasculature, abnormal intracardiac and extra-cardiac mixing of oxygenated and deoxygenated blood along with the altered blood flow patterns and loading conditions present unique challenges during anaesthetic management for either palliative or corrective surgical procedures in this subset of patients.
Clinical examination and history would help to know the functional status of the cardio-respiratory system. One should specifically look for the adequacy of systemic circulation, degree of cyanosis and respiratory distress.
Reviewing the echocardiographic findings and cardiac catheterisation data help to plan an appropriate anaesthetic management based on the pathophysiology. Quantification of the pulmonary to systemic blood flow ratio (Qp:Qs), intra-cardiac and great vessel pressures and oxygen saturation data and changes in these following various interventions such as inhaled nitric oxide (NO), ventilation with 100% oxygen, balloon occlusion of shunts etc. are useful in deciding the appropriate perioperative manipulations to alter pulmonary vascular resistance (PVR) and blood flow.
Laboratory investigations would throw light on the functional maturity of organs such as liver and kidney. Preoperative polycythaemia with haematocrit more than 60% might need blood letting and haemodilution during the intra and postoperative period to reduce the viscosity, especially for palliative shunt procedures. Arterial blood gas (ABG) analysis and serum lactate levels will help to assess the adequacy of pulmonary and systemic perfusion and any imbalance between them.
Preoperative fasting of 2 to 3 hours for clear glucose containing fluids and 4 hours for milk is followed in many centres for elective surgical procedures in neonates. , Psychological counselling of the parents is more important and premedication can be omitted or restricted to intramuscular atropine 10 µg/kg or glycopyrrolate 5 µg/kg intramuscularly.  Neonates with ductus dependant circulation who are on prostaglandin infusion should have the infusion continued till the CPB is initiated. 
In addition to the recommended routine minimum monitoring, most of the procedures require invasive arterial pressure and central venous pressure monitoring. Some procedures need extra monitoring or modifications. A 5 lead electrocardiogram (ECG) with lead II and V5 is of great use in arterial switch operation. Site of pulse oximeter probe placement is dictated by the pathophysiology and the surgical procedure planned. Arch hypoplasia/atresia may show lower arterial oxygen saturation (SpO 2 ) in lower limbs because of patent ductus arteriosus (PDA) supplying the descending aorta. Transposition of great arteries (TGA) with a large PDA and restricted patent foramen ovale and intact ventricular septum shows higher SpO 2 in the lower limbs - reverse differential cyanosis. Near infra-red spectrophotometry (NIRS) and the regional oxygen saturation help to detect critical cerebral hypoxia, especially during hypothermic circulatory arrest. 
A femoral arterial line better monitors invasive arterial pressure, if an extended CPB run is anticipated because of the changes that can happen in the systemic vascular resistance (SVR) and thus the arterial waveform trace following prolonged CPB. Both right radial and femoral arterial lines are preferred in arch reconstruction and coarctation repair to assess the gradient across the lesion, pre and post repair.
It is our practice to avoid placement of central venous multilumen catheter in the internal jugular vein (IJV) vein in a patient with obstructed total anomalous pulmonary venous return (TAPVR). Instead, we prefer to insert a short single lumen cannula in the IJV to monitor central venous pressure (CVP) and a multilumen catheter in the femoral vein. This is to avoid inadvertent right ventricular stimulation and ventricular fibrillation (VF) with the guide wire or the long catheter. The myocardium is highly sensitive and resuscitation following VF can be difficult in this subset of patients.
Both nasopharyngeal and rectal/bladder temperature monitoring is preferred where moderate hypothermia is planned, and is mandatory when deep hypothermia and circulatory arrest or low flow techniques are employed. Neonates loose body heat relatively faster than older children and this decrease in body temperature can by itself trigger arrhythmias. They should be kept warm by active means till the institution of CPB and also after separation from the CPB.
Induction of Anaesthesia
Inhalational induction with sevoflurane until the time of securing an intravenous catheter is well tolerated by most patients. Myocardial depression and a decrease in SVR are the major drawbacks, if higher concentrations are used. Intramuscular induction with ketamine (3 -5 mg/kg) alone or in combination with succinlycholine is preferred when induction needs to be faster in the absence of intravenous lines.  Addition of glycopyrrolate 5-10 µg/kg gives adequate antisialogogue effect.
Intravenous induction of anaesthesia is preferred, if an intravenous cannula is already present. High dose narcotics, especially fentanyl (25-100 µg/kg) or sufentanil (2.5-10 µg/kg)  help to maintain myocardial contractility and haemodynamic stability without significant alterations in PVR. Ketamine in a dose of 1- 2 mg/ kg can also be used intravenously for induction. If normocarbia and adequate oxygenation are ensured, ketamine does not have significant effect on PVR.  Intravenous administration of benzodiazepines such as midazolam (0.05-0.2 mg/ kg) also provides haemodynamic stability, however, in combination with high dose narcotics can decrease SVR significantly. Muscle relaxants such as pancuronium (0.1 mg/kg) help endotracheal intubation without decreasing heart rate, especially in combination with high dose narcotics.
Maintenance of Anaesthesia
Inhalational anaesthetics such as isoflurane (0.5-1.2%) with air - oxygen mixture can safely be used to maintain anaesthesia. Fractional inspired oxygen concentration (FiO 2 ) needs adjustments depending upon the pathophysiology of the lesion. Fentanyl as a continuous infusion (5 - 10 µg/kg/ hr) can be used for maintenance of analgesia. Propofol infusion (2-6 mg/kg/hr) as a part of total intravenous anaesthesia has been described in neonates. , In the presence of high-dose catecholamine infusion and prolonged usage, this can lead to a rare condition of propofol infusion syndrome.  Unlike vecuronium, pancuronium does not produce bradycardia when combined with high dose narcotics. , Benzodiazepine such as midazolam when combined with fentanyl for maintenance of anaesthesia can provide amnesia, sedation and good analgesia with little pulmonary vascular reactivity. Nitrous oxide as an adjuvant during induction of anaesthesia is well tolerated by neonates with compensated heart disease. It is criticized for its effect of expansion of air embolism in patients with shunt lesions. It is a mild myocardial depressant and can cause elevation of PVR, which may be undesirable in patients with pre-existing pulmonary hypertension.
Pre-cardiopulmonary bypass management
Once adequate level of analgesia and amnesia is ensured with the choice of pharmacological agents mentioned earlier, the balance between the pulmonary and systemic blood flow should be addressed depending on the pathophysiology. Controlled ventilation with adjustments in rate, tidal volume and FiO 2 is a strategic way of manipulating the PVR : SVR and also Qp : Qs. 
Although there is no consensus on the benefit, methylprednisolone in low dose (10 mg/kg) or high dose (30 mg/kg) can be administered so as to modify the inflammatory and immunological response to CPB, especially if long CPB run or deep hypothermic circulatory arrest (DHCA) is anticipated or planned. 
Aprotinin in a high dose of 30,000-50,000 kallikrein inhibiting units (KIU) /kg to the patient and same dose in the CPB followed by an infusion of 20,000 - 30,000 KIU/kg/hr is beneficial to modify the inflammatory response and also to decrease the postoperative blood loss and total blood product usage in the post-CPB period. 
Adequate anticoagulation with heparin at a dose of 3 mg/kg and an activated clotting time (ACT) > 480 seconds should be ensured before aortic cannulation. Depending upon the relative size of arterial cannula to the aorta, there will be a reduction in systemic pressure, as monitored peripherally, and an increase in left ventricular (LV) afterload. This might necessitate immediate institution of CPB.
Condiopulmonary bypass management
Deleterious effects of CPB can be ameliorated to a great extent by minimising the non-biological contact surface area of the CPB circuit. Using 3/16 inch arterial line, reducing the overall length of all the tubing used, use of vacuum assisted venous drainage, especially when employing 3/16 tubing for venous line and use of low priming volume oxygenators help to achieve this goal.
Acid-base management on CPB during cooling and rewarming, especially when DHCA is planned is still a debatable issue. Adequate vasodilatation before and during the cooling and rewarming period ensures uniform cooling and when combined with alpha-stat strategy of ABG management (temperature uncorrected), can prevent the uncoupling of metabolism and blood flow to the brain and the disadvantages associated with the luxury perfusion. It is a practice in many centres to administer phenoxybenzamine , in a dose of 0.5-1 mg/kg at the time of aortic cannulation, especially in neonates with severe pulmonary artery hypertension (PAH). This, along with the administration of sodium nitroprusside,0.5-1 µg/kg/min infusion on CPB allows adequate vasodilatation and ensures uniform cooling and brain protection. The pH-stat technique (temperature corrected with carbon dioxide administration) of ABG management during cooling and rewarming definitely ensures uniformity of brain cooling and favourable results, at least in the immediate postoperative neurological recovery.  Isoflurane, desflurane or sevoflurane administered throughout the period of CPB has been shown to have favourable cardiac and brain protective effects. . Administration of all pharmacological agents are discontinued from the CPB circuit during the period of DHCA and restarted when circulation is re-established.
In a study conducted at the author's institute, (unpublished data) addition of 20% albumin in the blood prime in a dose of 2-4 gm/kg showed negligible post-CPB weight gain even after 6 - 8 hrs of CPB run. Lung mechanics and gas exchange were better maintained in the postoperative period when compared with the addition of 5% albumin at 1gm/kg in the prime solution. No hyperosmolar state, hypernatraemia or increased blood product usage were noted in the postoperative period.
With the improvisations in the circuit technology and cannula designs, the need for DHCA has decreased. Bicaval cannulation and hypothermic low flow techniques are employed in those situations where DHCA was the norm earlier. But continuous low flow perfusion techniques are not devoid of complications. Cerebral odema, damage to neuronal Golgi apparatus, soft tissue oedema and deterioration in lung function are some of the reported after-effects of low flow CPB. These complications are not apparent, if short duration of DHCA (15-20 mins) with intermittent cerebral perfusion for 2-3 mins is employed. Following precautions and modifications are recommended during DHCA. 
- Pre-CPB steroids and aprotinin.
- Hyper-oxygenation before DHCA.
- Longer time for cooling (1-2 mins for each degree centigrade of cooling).
- Using pH-stat technique during cooling and rewarming, especially in neonates with multiple aorto- pulmonary collaterals.
- Maintaining a haematocrit of 30.
- Intermittent cerebral perfusion for 2-3 mins at 15 - 20 mins interval.
- Modified ultrafiltration (UF) after CPB.
- Postoperative cerebral protection strategies such as avoiding hyperthermia, hyperglycaemia, and maintaining adequate cardiac output and thus cerebral perfusion.
Ultrafiltration and CPB
Removal of fluid from the circuit by UF during CPB helps to maintain adequate haematocrit, removal of extra fluid added while on CPB and the inflammatory mediators to a certain extent.
Continuous ultrafiltration (CUF) should produce haemoconcentration while on CPB. The results are inconsistent in neonates mainly because of the difficulty in maintaining adequate reservoir volume, especially when low prime volume circuits are used.  Loss of reservoir volume due to CUF necessitates addition of extra fluid in the form of blood, plasma, crystalloid or colloid solutions offsetting the primary goal of CUF. When reservoir volume is sufficient, CUF can be employed in neonatal CPB to remove the extra fluid.
Dilutional ultrafiltration (DUF) and zero balance ultrafiltration (ZBUF) are high volume UF during CPB. Continuous replacement with crystalloid fluid equal to the amount of ultrafiltrate, helps to maintain the reservoir volume. Although not useful to haemoconcentrate during CPB, these techniques help to remove inflammatory mediators.
Modified ultrafiltration (MUF) is designed to continue UF even after weaning from the CPB. The circuit could be an arterio-venous or a venovenous. MUF can be used exclusively or can be combined with CUF, DUF or ZBUF. This technique allows greater degree of haemoconcentration, reduces total body water, attenuates dilutional coagulopathy and reduces blood product requirements, improves pulmonary gas exchange, improves ventricular compliance and function and also arterial pressure.  MUF is effective in removing both the anti-inflammatory and proinflammatory mediators generated during CPB.  Some of the reported negative aspects of MUF are air embolism, reduction in plasma concentration of drugs, (especially opioids, benzodiazepines, and aprotinin), hypothermia, and increase in plasma heparin concentration.
Optimisation of heart rate, rhythm, preload, afterload and contractility is essential for successful weaning from CPB. Neonatal myocardium is immature and has under-developed cellular organelles like sarcoplasmic reticulum. This results in suboptimal calcium handling by myocytes and thus their excitation contraction coupling. Neonatal heart is dependant on adequate extra-cellular calcium to maintain contractility. The process of re-sequestration of calcium is also immature and thus neonatal ventricular diastolic compliance is suboptimal. Disorderly arranged myofibrils and under-developed sympathetic innervations also result in myocardial dysfunction following CPB in neonates.
Sinus rhythm and a heart rate of 140 - 160 /min are desirable. Higher rates would result in decreased diastolic filling and coronary perfusion. While weaning from CPB, neonatal hearts benefit from atrial pacing or sequential pacing in the presence of conduction defects or low heart rates.
LV preload can be assessed by measuring the left atrial (LA) pressure. Preload recruitable stroke volume is limited in neonates, therefore, LA pressure greater than 12 mm Hg does not offer greater advantage. Neonatal LV and right ventricle (RV) do not tolerate increased afterload. Output of both ventricles improves following a reduction in the respective vascular resistances, which contribute to the afterload. Systemic vasodilators such as sodium nitroprusside and phenoxybenzamine would help to decrease the SVR and also PVR. Persistence of high PVR should be addressed by adjusting the ventilation to ensure complete expansion of lungs, low airway pressure, high FiO 2 and low PaCO 2 . Further reduction in PVR can be achieved by using inhaled NO at a dose of 10 - 40 parts per million (ppm).
Inotropes help to improve the cardiac output by increasing the contractility once the afterload, preload, heart rate and rhythm are optimised. The choice of ionotrope to be used after CPB depends on the pathophysiology of the lesion, degree of impairment of ventricular function, myocardial protection on CPB, and haemodynamic end points. Dopamine is useful in mild ventricular dysfunction, but should be used with caution in patients with increased PVR. Phosphodiesterase inhibitors improve cardiac output in the setting of reduced contractility and high SVR or PVR with RV dysfuction. Shunt dependent pulmonary blood flow requires adequate systemic pressure head. Therefore adrenaline is preferred to correct hypotension following Blalock-Taussig (BT) shunt.
Difficulty in weaning from CPB or instability following surgery should prompt for a reevaluation of the repair. Epicardial or transoesophageal echocardiography helps to determine the presence of residual defects or abnormal blood flow patterns. Intra-cardiac chamber and great artery pressure data and oxygenation data also help to assess the completeness of the repair.
| Lession Specific Issues|| |
Transposition of great arteries
These patients present either for palliative procedure or definitive repair in the neonatal period. Palliative procedures may be Rashkind's septostomy, Blalock Hanlon septectomy or pulmonary artery banding. Definitive repair is arterial switch operation. In ductus dependent patients, prostaglandin E1 (PGE 1 ) in a dose of 0.05 - 0.1 µg/kg/min should be started and continued till CPB is instituted. Most of the neonates presenting for palliative procedures or arterial switch operation do not require sedative premedication. Induction of anaesthesia is usually with high-dose fentanyl or sufentanil, if intravenous access is available. Intramuscular ketamine or inhalational induction with sevoflurane can be used, if intravenous access is not available.
Ventilatory strategies to decrease the PVR should be employed in TGA patients with high PVR, decreased pulmonary blood flow and poor intercirculatory mixing. Hypercarbia, hypoxia, and acidosis should be avoided in this subset of patients. Reduction in SVR should be avoided because this can increase the recirculation of systemic venous blood and further decrease arterial saturation. Reduction in PVR may be counterproductive in TGA with ventricular septal defect patients already in failure, as this might compromise systemic perfusion.
Phenoxybenzamine administered after aortic cannulation helps to reduce pulmonary vascular reactivity and also allows uniform cooling during induced hypothermia on CPB. DHCA or low flow CPB may have to be employed during the surgical repair. MUF in conjunction with CUF helps to minimise fluid retention following CPB and also helps to haemoconcentrate.
A mean arterial pressure of 25-35 mm Hg is beneficial and better tolerated in the initial period following weaning from CPB. Milrinone with a small dose of adrenaline ensures adequate ionotropy, vasodilation and lusitropy following successful surgical repair.
Co-arctation of aorta
General anaesthesia with controlled ventilation is the technique of choice. Invasive arterial pressure measurement in right radial artery and femoral artery allows assessment of gradient across the lesion both pre- and post-repair, and also helps in appropriate blood pressure management during cross clamping of the aorta. Normocarbia should be maintained as hypocarbia can decrease brain and spinal cord blood supply. Incidence of paraplegia is 0.5 - 1.5% following aortic cross clamp and spinal cord hypoperfusion.  Left heart bypass, mild hypothermia, low dose anti-coagulation, normocarbia etc. are some of the strategies to be employed for spinal cord protection in the event of persisting lower body hypoperfusion. Inhalational agents such as isoflurane with neuroprotective and vasodilating properties are preferred for maintenance of anaesthesia. High dose opioid anaesthesia is recommended in neonates with cardiac failure. Thoracic epidural with morphine as an adjunct might be beneficial to avoid or modify spinal cord ischaemia. 
Interrupted aortic arch
This is a classical ductus dependent lesion. If the child is receiving PGE 1 , it should be continued till cross clamping. Surgical repair usually requires CPB or even DHCA. Radial and femoral artery pressures should be monitored. High dose narcotic anaesthesia is recommended, as most of these neonates present in a critical state with severe acidosis and low cardiac output state. Renal perfusion and urine output should be monitored and optimised with judicious use of ionotropes and diuretics. LV failure may persist even after repair necessitating pharmacological support for the heart.
In the neonatal period these patients present with high pulmonary blood flow, PAH and congestive failure. Narcotic based anaesthesia is the technique of choice. Ventilatory manipulations to maintain normocarbia, low FiO 2 and positive pressure ventilation are employed to decrease pulmonary blood flow. Increase in SVR should be avoided. Associated anomalies such as DiGeorge syndrome and facial dysmorphism may make tracheal intubation difficult. Hypocalcaemia should be identified and corrected. Irradiated blood is recommended for transfusion purpose, if thymic aplasia is present.
Patent ductus arteriosus
Neonates with PDA present with pulmonary over-circulation. Invasive arterial pressure monitoring cannula should ideally be placed in the right hand. Femoral arterial line helps to confirm that it is the PDA which is test clamped and not the aorta, the possibility of which is not unknown. At least two large venous accesses should be secured for volume replacement in the rare event of acute blood loss, which again is a possibility, if the PDA tears. Sick neonates tolerate narcotic based anaesthesia better than inhalational technique. Controlled hypotension with a systolic pressure of around 50 - 60 mm Hg helps to prevent accidental tear while dissecting, clamping or clipping the PDA. This can be achieved with short acting vasodilators such as sodium nitroprusside or with inhalational agents alone in patients with good LV function.
Adequate postoperative analgesia would allow early extubation and adequete breathing, thus minimising pulmonary complications. Intercostal blocks, epidural opioids either by caudal or thoracic route, intra-pleural local anaesthetics, intravenous narcotics and nonsteroidal anti-inflammatory agents through oral or per-rectal routes are some of the effective means to provide postoperative analgesia.
Neonatal palliative shunt procedures
BT shunt (subclavian to pulmonary artery) and central shunt (aorta to pulmonary artery) are the commonly performed palliative shunt procedures in the neonatal period.
Central shunts with or without augmentation of branch pulmonary arteries are usually performed through median sternotomy with CPB support. Modified BT shunts (Gore-Tex shunt between subclavian and pulmonary arteries) are performed through thoracotomy. Most of these children will be already on PGE 1 infusion and this will have to be continued till the flow through the shunt conduit is established. Desaturation may worsen, once the lung is collapsed during thoracotomy. Collapsed lung may need expansion and ventilation intermittently in these situations. Communication between the anaesthetist and the surgeon is the key factor here. Hypotension should be avoided; infact pressures should be kept slightly higher to allow pulmonary perfusion through the PDA or collaterals, especially when the PVR can increase following lung collapse. Ionotropes and/or vasopressors such as phenylephrine infusion may have to be started to maintain myocardial contractactility and arterial pressure. Any untoward incident (severe hypoxia, hypotension) after clamping and opening of pulmonary artery should be treated and simultaneously the pulmonary arterial end anastomosis should be completed as fast as possible. Even mild hypothermia with a temperature of 34 - 35 °C and icepacks around the head helps to minimize neurological damage.  Heparinisation prior to clamping may not be required in neonates, infact this can lead to bleeding into the lung parenchyma following lung handling during the procedure. Post-procedure, the haemoglobin should be kept around 15 gm % and heparin infusion started in a dose of 2.5 to 5 units/Kg/hr to allow shunt flow and prevent spontaneous shunt blockade.
Total anomalous pulmonary venous return
Preoperative general condition of the patient depends on the type of TAPVR and degree of obstruction to pulmonary venous drainage. Severely obstructed neonates would have been already on ventilator and ionotropic support. An intravenous synthetic narcotic in moderate doses is well tolerated for induction of anaesthesia. Intravenous line can be secured with inhalational agents or intramuscular ketamine in not so sick neonates. Maintenance of anaesthesia can be successfully performed with a combination of volatile anaesthetic and narcotic drugs. Ventilatory strategies with high F1O 2 , hypocarbia and low airway pressure helps to decrease PVR and improve oxygenation. Sympathetic response, especially to pain, should be adequately suppressed. It is our practice to insert a short single lumen central venous line in the IJV and multilumen catheter in the femoral vein. Care should be taken while placing central venous lines, not to stimulate the RV with the catheter or the guide wire for the fear of inducing fatal arrhythmias. For the same reason, hypothermia should also be avoided during induction of anaesthesia and line placement.
Surgical procedure might require DHCA or low flow CPB. Weaning from CPB is facilitated by hyperventilation, ionotropes and vasodilators such as phenoxybenzamine. Sick neonates with obstructed physiology and severe PAH will benefit from inhaled NO at 5 to 80 ppm.
Methhaemoglobinaemia is a side effect when using high dose NO for long duration and should be suspected when the arterial oxygen tension (PaO 2 ) and saturation shows high values with relatively fixed SpO 2 of 85-88% on the pulse oximeter. Pulmonary artery pressures and rarely LA pressures need to be monitored continuously for proper haemodynamic management. A fenestration in the inter-atrial septum and an open chest prevents low cardiac output state and deterioration in RV function.
Hypoplastic left heart syndrome and stage 1 repair
Stage 1 repair is palliative and allows definitive Fontan procedure as a second stage correction. This involves the creation of a non-restrictive ASD, a neoaorta with the native proximal pulmonary trunk and a systemic to pulmonary shunt, which can be either a central or modified BT shunt. Most of these neonates are sick and acidotic because of compromised systemic oxygen delivery. The prostaglandin infusion which they might be already receiving for maintaining ductal patency, should be continued until CPB is established. High dose fentanyl induction helps to maintain the myocardial contractility and also to reduce the stress during induction .Airway should be secured recognizing the need for prolonged postoperative ventilation. Maintenance of anaesthesia should aim at good analgesia and amnesia, thus ameliorating the operative and CPB induced stress. Narcotic based anaesthesia with low dose of volatile anaesthetics / or benzodiazepines helps to meet this goal.
Maintaining a balance between the PVR and SVR is crucial for adequate oxygenation and systemic perfusion. Ventilatory strategies with low FiO2, arterial carbon dioxide tension between 40-50 mm Hg and positive end-expiratory pressure would help to prevent a decrease in PVR. In an inherently inefficient parallel circuit and univentricular physiology, an increase in PVR would increase systemic blood flow and decrease pulmonary blood flow. Decrease in pulmonary blood flow can lead to hypoxia, myocardial depression and subsequently low cardiac output. On the other hand, a decrease in PVR would result in an increased pulmonary blood flow. The flow through the PDA then decreases leading to inadequate systemic and coronary perfusion resulting in metabolic acidosis and myocardial depression. Addition of 2-4% carbon dioxide in inspired gas helps to maintain normal tidal volume and minute ventilation, while achieving a high PaCO 2 . This will allow normal functional residual capacity and adequate oxygenation without reduction in PVR. , SVR and myocardial contractility may need manipulation with appropriate use of vasodilators and/or ionotropes to maintain systemic perfusion. Alpha adrenergic blockers such as phenoxybenzamine administered at the initiation of CPB in a dose of 0.25 - 0.5 mg/kg as bolus, helps to ameliorate the vasoconstriction response to hypothermia and stress. Selective infusion of the same in a dose of 0.25 - 1 mg/kg/ day in the post-CPB period helps patients demonstrating reactive SVR. In view of the anticipated long CPB time and the need for profound hypothermia with or without circulatory arrest, aprotinin administration is recommended, which would help to decrease the systemic inflammatory response following CPB and also reduce postoperative blood loss.
Selecting the site for placement of invasive arterial blood pressure monitoring cannula is important, if an innominate artery to pulmonary artery shunt is planned. It is better to avoid right radial artery for this purpose because blood flow may be affected following the shunt. MUF is beneficial because of the prolonged CPB and profound hypothermia, which these patients are subjected to, during the stage 1 repair.
After the stage 1 repair, the circulation still remains parallel but with a restrictive element in the size and the length of the shunt. Balance between Qp and Qs is crucial for maintaining adequate blood oxygenation and systemic oxygen delivery. In the post-CPB state, signs of poor oxygen delivery such as low mixed venous oxygen saturationpersistent hypotension, high serum lactate, low NIRS value of tissue oxygen content etc. should prompt active manipulation of PVR, SVR, their balance, and ionotropic support to improve blood oxygen saturation and tissue oxygen delivery. In the event of failure to achieve adequate systemic oxygen delivery, even after trying above mentioned strategies, the need for extra- corporeal membrane oxygenation should be actively considered and should be instituted before hypoxic end organ damage sets in.
During pre-CPB period, fluids are administered for maintaining intravascular volume, renal function and to replace blood or fluid loss. Multi electrolyte solution with lowest effective glucose concentration is preferable in neonates as the maintenance fluid. Usual maintenance dose in cardiac patients, following induction of anaesthesia and controlled ventilation, is about 2 ml /kg/hr. Blood glucose and electrolytes should be monitored at regular intervals and deficits and excesses should be actively treated. Clinically significant blood loss should be replaced with whole blood, red cell concentrate or colloids such as human albumin and plasma depending upon the preoperative haematocrit and the repair planned. In patients with high haematocrit, colloids can be used to replace volume loss and also to achieve haemodilution and thus reduction in viscosity. This is useful for maintaining flow through shunt conduits and prevent thrombosis following systemic to pulmonary artery shunt procedures.
It is better to restrict crystalloid administration at least for the first couple of hours after weaning from CPB. This helps to prevent extravascular fluid accumulation resulting from the loss of capillary integrity after CPB. Intravascular volume is maintained with blood products or human albumin solution. Starch preparations are also being used now-a-days in neonates. 
Intraoperative anaesthetic management is part of a continuum in the perioperative care of neonates undergoing surgery for congenital cardiac defects. Active involvement in the preoperative and postoperative management by the concerned anaesthesiologist helps in better understanding of the response to various therapeutic interventions and also planning monitoring modalities.
| References|| |
|1.||Chang AC. Pediatric cardiac intensive care: current state of the art and beyond the millennium. Curr Opin Pediatr 2000; 12: 238-246. |
|2.||Ravishankar C, Tabbutt S, Wernovsky G. Critical care in cardiovascular medicine. Curr Opin Pediatr 2003; 15: 443-453. |
|3.||Laussen PC. Neonates with congenital heart disease. Curr Opin Pediatr 2001; 13: 220-226. |
|4.||Gaynor JW, Mahle WT, Cohen MI, et al. Risk factors for mortality after the Norwood procedure. Eur J Cardiothorac Surg 2002; 22: 82-89. |
|5.||Mahle WT, Spray TL, Wernovsky G, Gaynor JW, Clark BJ, 3rd. Survival after reconstructive surgery for hypoplastic left heart syndrome: A 15-year experience from a single institution. Circulation 2000; 102: III136-141. |
|6.||Oppido G, Napoleone CP, Formigari R, et al. Outcome of cardiac surgery in low birth weight and premature infants. Eur J Cardiothorac Surg 2004; 26: 44-53. |
|7.||McMahon CJ, Penny DJ, Nelson DP, et al. Preterm infants with congenital heart disease and bronchopulmonary dysplasia: postoperative course and outcome after cardiac surgery. Pediatrics 2005; 116: 423-430. |
|8.||Cote C. NPO after midnight for children: a reappraisal. Anesthesiology 1990; 72: 589-592. |
|9.||Delphin E, Seckin AI, Moore RA. Preoperative evaluation and preparation of the pediatric patient with cardiac disease. In: Lake CL, ed. Pediatric Cardiac Anesthesia, 4th ed. Norwalk: Appleton & Lange, 2005; 96-110. |
|10.||Hensley F. Premedication for children with congenital heart disease - beneficial or harmful? J Cardiothorac Anesth 1990; 4: 423-424. |
|11.||Sakamoto T, Hatsuoka S, Stock UA, et al. Prediction of safe duration of hypothermic circulatory arrest by nearinfra red spectroscopy. J Thorac Cardiovasc Surg 2001; 122: 339-350. |
|12.||Dinardo JA. Anesthesia for congenital heart disease. In: DiNardo JA, ed. Anesthesia for Cardiac Surgery, 2nd ed. Stamford: Appleton & Lange, 1998; 158-159 |
|13.||Hickey PR, Hansen DD. Fentanyl- and sufentanil-oxygenpancuronium anesthesia for cardiac surgery in infants. Anesth Analg 1984; 63: 117-124 |
|14.||Hickey PR, Hansen DD, Cramolini GM, Vincent RN, Lang P. Pulmonary and systemic hemodynamic responses to ketamine in infants with normal and elevated pulmonary vascular resistance. Anesthesiology 1985; 62: 287-293 |
|15.||Lim EH, Tan S, Lim SL. Anesthesia for a neonate with persistent buccopharyngeal membrane and unilateral choanal atresia. Paediatr Anaesth 2005; 15: 509-511 |
|16.||Golden S. Combination propofol-ketamine anaesthesia in sick neonates. Paediatr Anaesth 2001; 11: 119-122. |
|17.||Wooltorton E. Propofol: contraindicated for sedation of pediatric intensive care patients. CMAJ 2002; 167: 507. |
|18.||Gravlee GP, Ramsey FM, Roy RC, Angert KC, Rogers AT, Pauca AL. Rapid administration of a narcotic and neuromuscular blocker: a hemodynamic comparison of fentanyl, sufentanil, pancuronium, and vecuronium. Anesth Analg 1988; 67: 39-47. |
|19.||Salmenpera M, Peltola K, Takkunen O, Heinonen J. Cardiovascular effects of pancuronium and vecuronium during high-dose fentanyl anesthesia. Anesth Analg 1983; 62: 1059-1064. |
|20.||Lawrenson J, Eyskens B, Vlasselaers D, Gewillig M. Manipulating parallel circuits: the perioperative management of patients with complex congenital cardiac disease. Cardiol Young 2003; 13: 316-322. |
|21.||Varan B, Tokel K, Mercan S, Donmez A, Aslamaci S. Systemic inflammatory response related to cardiopulmonary bypass and its modification by methyl prednisolone: high dose versus low dose. Pediatr Cardiol 2002; 23: 437-441. |
|22.||Shen I, Giacomuzzi C, Ungerleider RM. Current strategies for optimizing the use of cardiopulmonary bypass in neonates and infants. Ann Thorac Surg 2003; 75: S729-S734. |
|23.||Ogawa K, Yamamoto T, Asada S, et al. The effect of phenoxybenzamine on the pulmonary vascular bed in surgically corrected ventricular septal defect associated with pulmonary hypertension. Jpn Heart J 1979; 20: 157-161. |
|24.||Motta P, Mossad E, Toscana D, Zestos M, Mee R. Comparison of phenoxybenzamine to sodium nitroprusside in infants undergoing surgery. J Cardiothorac Vasc Anesth 2005; 19: 54-59. |
|25.||DiNardo JA. Profound hypothermia and circulatory arrest. In: Lake CL, ed. Pediatric Cardiac Anesthesia, 4th ed. Norwalk: Appleton & Lange, 1998; 253-257. |
|26.||Kurth CD, Priestley M, Watzman HM, McCann J, Golden J. Desflurane confers neurologic protection for deep hypothermic circulatory arrest in newborn pigs. Anesthesiology 2001; 95: 959-64. |
|27.||Elliott MJ. Ultrafiltration and modified ultrafiltration in pediatric open heart operations. Ann Thorac Surg 1993; 56: 1518-1522. |
|28.||Davies MJ, Nguyen K, Gaynor JW, Elliott MJ. Modified ultrafiltration improves left ventricular systolic function in infants after cardiopulmonary bypass. J Thorac Cardiovasc Surg 1998; 115: 361-369, discussion 369-370. |
|29.||Naik SK, Knight A, Elliott MJ. A successful modification of ultrafiltration for cardiopulmonary bypass in children. Perfusion 1991; 6: 41-50. |
|30.||Park SC, Neches WH. The neurologic complications of congenital heart disease. Neurol Clin 1993; 11: 441-462. |
|31.||Rosen DA, Rosen KR. Anomalies of the aortic arch and valve. In: Lake CL, ed. Pediatric Cardiac Anesthesia, 4th ed. Norwalk: Appleton & Lange, 2005: 397-398. |
|32.||Nussmeier NA. Management of temperature during and after cardiac surgery. Tex Heart Inst J 2005; 32: 472-476. |
|33.||Jobes DR, Nicolson SC, Steven JM, Miller M, Jacobs ML, Norwood WI, Jr.: Carbon dioxide prevents pulmonary overcirculation in hypoplastic left heart syndrome. Ann Thorac Surg 1992; 54: 150-151. |
|34.||Bradley SM, Simsic JM, Atz AM. Hemodynamic effects of inspired carbon dioxide after the Norwood procedure. Ann Thorac Surg 2001; 72: 2088-2093; discussion 2093-2094. |
|35.||Liet JM, Bellouin AS, Boscher C, Lejus C, Roze JC. Plasma volume expansion by medium molecular weight hydroxyethyl starch in neonates: a pilot study. Pediatr Crit Care Med 2003; 4: 305-307. |
Department of Anaesthesia, AIMS, Elamakkara, Kochi, Kerala Pin. 682026.
Source of Support: None, Conflict of Interest: None