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Anesthesia in adults with congenital heart disease : Current Opinion in Anesthesiology
Norwood-Sano B. Aortic Valvuloplasty C. Coarctation of the Aorta Repair D. Tetralogy of Fallot Repair with Transannular Patch If you are human, leave this field blank or you will be considered spam: archives. Discuss your thoughts in the Forum. Dolly D. Hansen, "the Mother of Pediatric Cardiac Anesthesia", devoted her entire career to the life of children with congenital heart disease CHD. Hansen graduated from Copenhagen University Medical School in , and later completed a fellowship in pediatric anesthesia at Boston Children's Hospital in By default, Dr.
Hansen became the only pediatric cardiac anesthesia attending at BCH in , and for the next 30 years Dr. Hansen worked in the pediatric cardiac anesthesia division at BCH. In addition to being one of the first women in the field Dr. Hansen has been a CHD anesthesia pioneer.
Congenital Heart Disease
Hansen was the first anesthesiologist to routinely care for children undergoing surgical repair with deep hypothermic cardiac arrest and to provide anesthesia in the hyperbaric chamber. Improvements in medical and surgical management in recent decades have resulted in significantly more children with CHD surviving to adulthood.
The aim of this article is to focus on broad classification of CHD and to provide an updated review on the current perioperative anaesthetic management of CHD patients in different settings such as a interventional cardiac procedures that have dominated the field, b uncorrected patients for non-cardiac surgery and c corrected patients for non-cardiac surgery. The complexity of the defects along with a variety of non-cardiac surgery makes it impossible to have one single-anaesthesia technique.
Congenital heart disease CHD is a structural and functional heart disease, which is present at birth.
The prevalence of CHD in India reported in was around 2. In adults, it was 2. Improvements in medical and surgical management have resulted in significantly more children with CHD surviving into adulthood. Anaesthesia-related cardiac arrest during non-cardiac surgery is more common in these patients.
This review article emphasises the early recognition of the risk, understanding the physiology, advantages of a multidisciplinary approach and utility of newer modalities in anaesthetic management of these patients. It will focus on anaesthesia for diagnostic and therapeutic cardiac catheterisation, uncorrected CHD for non-cardiac surgery, grown up congenital heart disease GUCHD and adult patients with corrected congenital cardiac lesions presenting for non-cardiac surgery. Congenital heart disease is broadly classified as a cyanotic and acyanotic CHD and b conditions with shunt and without shunt[ 7 ] [ Table 1 ].
Recent advances in cardiac surgery and availability of newer palliative procedures have contributed to increased survival of patients with cyanotic heart disease and with single ventricle. This has resulted in subset of patients who have undergone corrective or palliative surgery, and have some limitations, including: a Blalock-Taussig BT shunt, b Norwood procedure, c Fontan procedure with single ventricle, d TGA with complete correction, e intracardiac repair for double outlet right ventricle DORV and ToF, f corrected total anomalous pulmonary venous connection TAPVC and g corrected with device closure or stenting.
Cardiac surgery can correct CHD by way of either biventricular repair complete repair or univentricular repair palliative. It is important to know the physiology of circulation in patients with CHD[ 5 ] that can be divided into A normal circulation or series circulation, B parallel or balanced circulation and C single ventricle circulation.
The systemic and pulmonary circulations work together in series. Occasionally, surgeons deliberately keep fenestrations, similar to patent foramen ovale PFO or small VSD as a pressure release mechanism, which leads to some shunting. Left-to-right shunts result in increased pulmonary blood flow PBF and potentially decreased systemic blood flow; right-to-left shunts cause deoxygenated blood to flow into the systemic circulation, causing cyanosis and reduced PBF.
Changes in systemic vascular resistance SVR and pulmonary vascular resistance PVR as a result of anaesthesia, including the administration of oxygen, impact on the behaviour of the shunt depending on its size. Here, the systemic and pulmonary circulations are connected by some means and physiologically work in parallel. High pulmonary blood flow leads to pulmonary oedema and desaturation and reduced systemic perfusion. Lower PBF leads to desaturation and acidosis.
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Full anatomic correction biventricular repair is not possible in some congenital defects such as hypoplastic left heart syndrome or double-outlet right ventricle. In single ventricle physiology, only one ventricle works as a systemic ventricle and the other is rudimentary. The pulmonary blood flow is passive based on pressure gradient between the pulmonary artery PA and left atrium.
Usually, these patients have three-staged surgical palliation; BT shunt or PA band in infancy; Glenn or hemi-Fontan superior vena cava connected to PA at 1 st or 2 nd year of life and then a Fontan procedure — both inferior and superior vena cava connected to PA. However intermittent positive pressure ventilation IPPV may be needed to avoid hypercapnoea and hypoxia, and minimal peak inspiratory pressures and inspiratory times may optimise PBF.
A point system for the risk stratification of a CHD patient before undergoing a procedure was developed by Mossad.
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Risk classification of children with congenital heart disease undergoing non-cardiac surgery. The patients at highest risk are infants with a functional single ventricle and patients with suprasystemic pulmonary hypertension PHT , left ventricular outflow tract obstruction, and cardiomyopathy.
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The usual procedural risks during various catheterisation laboratory interventions are coronary ischaemia, cardiac arrest, low cardiac output, RV failure, pulmonary hypertensive crisis, arrhythmias, cardiac perforation and tamponade. Good preoperative assessment is essential to determine the physiological status of the patient. This includes recording the height and weight, thorough examination of the cardiovascular and respiratory systems and the presence of cyanosis, clubbing or squatting episodes.
Signs and symptoms of poor cardiac output and heart failure include difficulty in feeding, poor growth, sweating in infants or reduced exercise tolerance with fatigue in older children. Increased respiratory rate, chest retraction, nasal flaring, use of accessory muscles of respiration, pedal oedema, jugular venous distention, enlarged liver and rales suggest cardiac failure.
Peripheral pulses and blood pressure in all extremities should be measured abnormal findings in coarctation of the aorta and BT shunt. Similarly, oxygen saturation by pulse oximetry should be measured in all limbs differential cyanosis. Oxygen saturation after exercise can give some idea about heart function. Association with Down's syndrome is common and hence atlantoaxial subluxation should be kept in mind.
The child with history of prolonged intubation can have subglottic stenosis. The current medications should be reviewed and administered unless there are any contraindications on the day of surgery [ Table 3 ]. Need for a cardiology review depends on the complexity of the lesion. CHD patients who have had complete repair do not need a cardiology reference if they are fit and healthy. A standard pre-anaesthetic visit without cardiology consultation is acceptable.
For complex lesions and major surgeries, cardiology reference is advocated, and especially if patient's condition has changed recently. However, clearance must always be given by an anaesthesiologist as the cardiologist will not have full knowledge of anaesthetic effects and surgical procedures. In adult patients coming to surgery, one should look for long-term problems that vary with the disease condition [ Table 4 ].
Congenital heart diseases and anaesthesia
Left-to-right shunt causes increased pulmonary blood flow. The amount of flow determines the response of pulmonary vasculature.
In the initial period, the pulmonary vasculature will accommodate the flow unless heart failure occurs due to left ventricular overload e. This PHT[ 8 ] can present as follows:.
Reactive - is the difficult variety, and challenging to control in perioperative periods. The first variety can be part of balanced circulation physiology and should be looked after during anaesthetic management of left-to-right shunts. Reactive PHT occurs in older children or adults with untreated shunts. It may be still responsive to oxygen, but also increases with stimuli that cause pulmonary vasoconstriction.
Eisenmenger syndrome is shunt reversal due to suprasystemic pulmonary arterial pressures and conversion of acyanotic left-to-right shunt to cyanotic right to left shunt. Generally, atrial level shunts will take more time than ventricular level shunts for development of pulmonary arterial hypertension. Adult patients with Eisenmenger syndrome are most challenging for anaesthetic management.
The signs and symptoms in the advanced stages include central cyanosis, dyspnoea, fatigue, haemoptysis, syncope and right-sided heart failure. As a consequence of chronic slow progressive hypoxaemia with central cyanosis, adult patients suffer from multiple system problems including coagulation disorders bleeding complications and paradoxical embolism , renal dysfunction, hypertrophic osteoarthropathy, heart failure, reduced quality of life and premature death.
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