Anaesthesia for congenital heart disease

Anesthesia for Congenital Heart Disease

INCIDENCE• 7 to 10 per 1000 live births• Premature infants 2-3X higher incidence• Most common form of congenital disease• Accounts for 30% of total incidence of all

congenital diseases• 10% -15% have associated congenital

anomalies of skeletal, RT, GUT or GIT• Only 15% survive to adulthood without

treatment

CLASSIFICATION OF CHD

• L - R SHUNTS INCLUDE :– ASD →7.5% of CHD– VSD → COMMONEST CHD – 25%– PDA → 7.5% of CHD

• Common in premature infants

– ENDOCARDIAL CUSHION DEFECT - 3%• Often seen with trisomy 21

– AORTOPULMONARY WINDOW

CLASSIFICATION OF CHD

• R – L SHUNTS– Defect between R and L heart– Resistance to pulmonary blood flow → ↓ PBF →

hypoxemia and cyanosis

• INCLUDE :– TOF – 10% of CHD, commonest R-L shunt– PULMONARY ATRESIA – TRICUSPID ATRESIA– EBSTEIN’S ANOMALY

R – L SHUNTS

• GOAL → ↑ PBF to improve oxygenation– Neonatal PGE1 (0.03 – 0.10mcg/kg/min)

maintains PDA → ↑ PBF– PGE1 complications → vasodilatation,

hypotension, bradycardia, arrhythmias, apnea or hypoventilation, seizures, hyperthermia

– Palliative shunts → ↑ PBF, improve hypoxemia and stimulate growth in PA → aids technical feasibility of future repair

Almost any anesthetic technicmay be used in any CHD patient

if

the anesthesiologist understands

•the pathophysiology of the lesion and

•the pharmacology of the drugs employed.

ANESTHETIC MANAGEMENT

• Perioperative management requires a team approach

• Most important consideration is necessity for individualized care

• CHD is polymorphic and may clinically manifest across a broad clinical spectrum


• 50% Dx by 1st week of life; rest by 5 years• Child’s diagnosis & current medical condition

will determine preoperative evaluation• Understand the anatomic and hemodynamic

function of child’s heart• Discuss case with pediatrician and cardiologist• Review diagnostic & therapeutic interventions• Above will estimate disease severity and help

formulate anesthetic plan

HISTORY & PHYSICAL

• Assess functional status – daily activities & exercise tolerance

• Infants - ↓ cardiac reserve → cyanosis, diaphoresis & respiratory distress during feeding

• Palpitations, syncope, chest pain• Heart murmur (s)• Congestive heart failure• Hypertension

HISTORY & PHYSICAL

• Tachypnea, dyspnea, cyanosis

• Squatting

• Clubbing of digits

• FTT d/t limited cardiac output and increased oxygen consumption

• Medications – diuretics, afterload reduction agents, antiplatelet, anticoagulants

• Immunosuppressants – heart transplant

LABORATORY EVALUATION

• BLOODWORK• Electrolyte disturbances 2° to chronic diuretic therapy

or renal dysfunction

• Hemoglobin level best indicator of R-L shunting magnitude & chronicity

• Hematocrit to evaluate severity of polycythemia or iron deficiency anemia

• Screening coagulation tests

• Baseline ABG & pulse oximetry

• Calcium & glucose - newborns, critically ill children


• 12 LEAD EKG– Chamber enlargement/hypertrophy– Axis deviation– Conduction defects– Arrhythmias– Myocardial ischemia


• CHEST X - RAY– Heart size and shape– Prominence of pulmonary vascularity– Lateral film if previous cardiac surgery for

position of major vessels in relation to sternum


• ECHOCARDIOGRAPHY– Anatomic defects/shunts– Ventricular function– Valve function– Doppler & color flow imaging direction of

flow through defect/valves, velocities and pressure gradients


• CARDIAC CATHERIZATION– Size & location of defects– Degree of stenosis & shunt

– Pressure gradients & O2 saturation in each chamber and great vessel

– Mixed venous O2 saturation obtained in SVC or proximal to area where shunt occurs

– Low saturations in LA and LV = R – L shunt– High saturations in RA & RV = L – R shunt


• CARDIAC CATHERIZATION– Determine shunt direction: ratio of pulmonary to

systemic blood flow : Qp / Qs– Qp / Qs ratio < 1= R – L shunt– Qp / Qs ratio > 1= L – R shunt

Congenital Cardiac Surgery

• Preoperative medication– D/C diuretics and digoxin unless heart failure is

poorly controlled or digoxin is being used primarily for rhythm

– Continue inotropes– Continue prostaglandin infusions

MONITORING

• Routine CAS monitoring

• Precordial or esophageal stethoscope

• Continuous airway manometry

• Multiple - site temperature measurement

• Volumetric urine collection

• Pulse oximetry on two different limbs

• TEE

MONITORING

• PDA– Pulse oximetry right hand to measure pre-ductal

oxygenation– 2nd probe on toe to measure post-ductal

oxygenation

• COARCTATION OF AORTA– Pulse oximeter on right upper limb– Pre and post - coarctation blood pressure cuffs

should be placed


• GENERAL PRINCIPLES

Where:

Q = Blood flow (CO)

P = Pressure within a chamber or vessel

R = Vascular resistance of pulmonary or systemic vasculature

Ability to alter above relationship is the basic tenet of anesthetic management in children with CHD

RP

Q


P manipulate with positive or negative inotropic agents

Q hydration + preload and inotropes

However, the anesthesiologist’s principal focus is an attempt to manipulate resistance, by dilators and constrictors


• GENERAL CONSIDERATIONS– De-air intravenous lines air bubble in a R-L shunt

can cross into systemic circulation and cause a stroke

– L-R shunt air bubbles pass into lungs and are absorbed

– Endocarditis prophylaxis– Tracheal narrowing d/t subglottic stenosis or

associated vascular malformations


– Tracheal shortening or stenosis esp. in children with trisomy 21

– Strokes from embolic phenomena in R-L shunts and polycythemia

– Chronic hypoxemia compensated by polycythemia → ↑ O2 carrying capacity

– HCT ≥ 65% → ↑ blood viscosity → tissue hypoxia & ↑ SVR & PVR → venous thrombosis → strokes & cardiac ischemia


– Normal or low HCT D/T iron deficiency → less deformable RBCs → ↑ blood viscosity

– Therefore adequate hydration & decrease RBC mass if HCT > 65%

– Diuretics → hypochloremic, hypokalemic metabolic alkalosis

Air Bubble precautions

• To prevent paradoxical air embolism• Remove all bubbles from iv tubing• Connect the iv tubing to the venous cannula while there is free flowing

in fluid .• Eject small amount of solution from syringe to clear air from the needle

hub before iv injection• Aspirate injection port before injection to clear any air• Hold the syringe upright to keep bubbles at the plunger end• Do not leave a central line open to air• Use air filters• ? No N2O.

PREMEDICATION

a) Omit for infants < six months of ageb) Administer under direct supervision of

Anesthesiologist in preoperative facilityc) Oxygen, ventilation bag, mask and pulse

oximetry immediately availabled) Oral Premedication

• Midazolam 0.25 -1.0 mg/kg• Ketamine 2 - 4 mg/kg• Atropine 0.02 mg/kg

PREMEDICATION

e) IV Premedication• Midazolam 0.02 - 0.05 mg/kg titrated in small

increments

f) IM Premedication• Uncooperative or unable to take orally• Ketamine 1-2 mg/kg• Midazolam 0.2 mg/kg• Glycopyrrolate or Atropine 0.02 mg/kg

ANESTHETIC AGENTS

• INHALATIONAL AGENTS– Safe in children with minor cardiac defects– Most common agents used are halothane and

sevoflurane in oxygen– Monitor EKG for changes in P wave retrograde

P wave or junctional rhythm may indicate too deep anesthesia

INHALATIONAL ANESTHETICS

• HALOTHANE– Depresses myocardial function, alters sinus

node function, sensitizes myocardium to catecholamines

MAP + HR CI + EF

• Relax infundibular spasm in TOF

• Agent of choice for HOCM


SEVOFLURANE

• No HR

• Less myocardial depression than Halothane

• Mild SVR → improves systemic flow in L-R shunts

• Can produce diastolic dysfunction


ISOFLURANE

• Pungent not good for induction

• Incidence of laryngospasm > 20%


• Vasodilatation leads to SVR → MAP HR which can lead to CI


DESFLURANE

• Pungent not good for induction; highest incidence of laryngospasm

• SNS activation → with fentanyl HR + SVR



NITROUS OXIDE

• Enlarge intravascular air emboli

• May cause microbubbles and macrobubbles to expand obstruction to blood flow in arteries and capillaries

• In shunts, potential for bubbles to be shunted into systemic circulation


NITROUS OXIDE

• At 50% concentration does not affect PVR and PAP in children

• Mildly CO at 50% concentration

• Avoid in children with limited pulmonary blood flow, PHT or myocardial function

IM & IV ANESTHETICS

KETAMINE• No change in PVR in children when airway

maintained & ventilation supported• Sympathomimetic effects help maintain HR,

SVR, MAP and contractility• Greater hemodynamic stability in

hypovolemic patients• Copious secretions → laryngospasm →

atropine or glycopyrrolate

IM & IV ANESTHETICS

KETAMINE• Relative contraindications may be coronary

insufficiency caused by:– anomalous coronary artery– severe critical AS– hypoplastic left heart syndrome with aortic atresia– hypoplasia of the ascending aorta

• Above patients prone to VF d/t coronary insufficiency d/t catecholamine release from ketamine

IM & IV ANESTHETICS

IM Induction with Ketamine:• Ketamine 5 mg/kg • Succinylcholine 5 mg/kg or Rocuronium 1.5 – 2.0

mg/kg • Atropine or Glycopyrrolate 0.02 mg/kg IV Induction with Ketamine:• Ketamine 1-2 mg/kg • Succinylcholine 1-2 mg/kg or Rocuronium 0.6-1.2

mg/kg• Atropine or Glycopyrrolate 0.01 mg/kg

IM & IV ANESTHETICS

OPIOIDS• Excellent induction agents in very sick children• No cardiodepressant effects if bradycardia avoided• If used with N2O - negative inotropic effects of

N2O may appear• Fentanyl 25-100 µg/kg IV• Sufentanil 5-20 µg/kg IV• Pancuronium 0.05 - 0.1 mg/kg IV offset

vagotonic effects of high dose opioids

IM & IV ANESTHETICS

ETOMIDATE• CV stability• 0.3 mg/kg IV

THIOPENTAL & PROPOFOL• Not recommended in patients with severe cardiac

defects• In moderate cardiac defects:

– Thiopental 1-2 mg/kg IV or Propofol 1-1.5 mg/kg IV– Patient euvolemic


ANESTHESIA INDUCTION

• Myocardial function preserved IV or inhalational techniques suitable

• Severe cardiac defects IV induction

• Modify dosages in patients with severe failure

ANESTHESIC MANAGEMENT

ANESTHESIA MAINTENANCE

• Depends on preoperative status

• Response to induction & tolerance of individual patient

• Midazolam 0.15-0.2 mg/IV for amnesia


• L - R SHUNTS :• Continuous dilution in pulmonary

circulation may ↑ onset time of IV agents

• Speed of induction with inhalation agents not affected unless CO is significantly reduced

• Degree of RV overload and/or failure underappreciated – careful induction


• L-R SHUNTS :– GOAL = SVR and ↑ PVR → L-R shunt

• PPV & PEEP increases PVR• Ketamine increases SVR• Inhalation agents decrease SVR


• R-L SHUNTS :– GOAL : PBF by SVR and ↓ PVR

PVR & ↓ SVR → ↓ PBF – Hypoxemia/atelectasis/PEEP

– Acidosis/hypercapnia HCT

– Sympathetic stimulation & surgical stimulation

– Vasodilators & inhalation agents → ↓ SVR


• ↓ PVR & SVR → PBF– Hyperoxia/Normal FRC– Alkalosis/hypocapnia– Low HCT– Low mean airway pressure– Blunted stress response– Nitric oxide/ pulmonary vasodilators– Vasoconstrictors & direct manipulation→ SVR


• R –L SHUNTS :– Continue PE1 infusions

– Adequate hydration esp. if HCT > 50%– Inhalation induction prolonged by limited

pulmonary blood flow– IV induction times are more rapid d/t bypassing

pulmonary circulation dilution– PEEP and PPV increase PVR


• COMPLEX SHUNTS :• Manipulating PVR or SVR to PBF will:

• Not improve oxygenation• Worsen biventricular failure• Steal circulation from aorta and cause

coronary ischemia

• Maintain “status” quo with high dose opioids that do not significantly affect heart rate, contractibility, or resistance is recommended


• COMPLEX SHUNTS :– Short procedures slow gradual induction with low

dose Halothane least effect on +ve chronotropy & SVR

– Nitrous Oxide limits FiO2 & helps prevent coronary steal & ↓ Halothane requirements


• OBSTRUCTIVE LESIONS• Lesions with > 50 mmHg pressure gradient +

CHF opioid technique• Optimize preload improves flow beyond

lesion• Avoid tachycardia ↑ myocardial demand & ↓

flow beyond obstruction• Inhalation agents -ve inotropy & decrease

SVR worsens gradient & flow past obstruction


• Cardiopulmonary Bypass– Differences from adult

• Lower temperatures (15-20 degrees C)

• Lower perfusion pressure (20-30mmHg)

• Very significant hemodilution (3-15 times greater)

• Pump flows range from 200ml/kg/min to zero!

• Different blood pH management (alpha-stat vs pH stat)

• Tendency to hypoglycemia

• Cannula placement is much more critical

Anticoagulation and haemostasis during CPB

Anticoagulation

Heparin

• time of administration

• Route – central line

Current clinical protocol • Heparin – 300 units/kg i.v.• Draw arterial sample for ACT in 3-5 min.• Give additional heparin to achieve

ACT >300 (normothermic CPB)

ACT > 400 (hypothermic CPB)• Prime extracorporial circuit with heparin 3 units/ml•

• Monitor ACT every 30 min. during CPB

• If ACT decreases below desired minimum value – supplemental dose of 50-100 units/kg

Haemostasis

At conclusion of CPB

• Protamine – mainstay of heparin neutralization

• Dosage – 1.3 mg to neutralise 100units of heparin

• ACT after administration

if more then baseline – additional bolus (25 -50mg)

of protamine

protamine reaction

• Increase in PAP & CVP

• Decrease in LAP & SAP

Precaution

• via peripheral line

• Administer slowly < 5mg/min.

• Test bolus dose 25-50 mg – look for haemodynamics

• Careful with pt. having food allergy

Treatment

• Stop protamine

• Administration of fluids and epinephrine

• Steroids

• Pulmonary vasodialators - NTG, SNP


• Deep hypothermic circulatory arrest (DHCA)– Neonates and small infant usually < 10 kg– Oxygen consumption falls 2-2.5 times per 10

degree fall in temperature– Allows more controlled complex surgery in a

bloodless field– Often total CPB time is actually shortened by this

technique


• Weaning from CPB– Heart assessed by direct visualization and right or

left atrial filling pressure, central cannula or TEE– Pulse oximetry is also very helpful– Problems weaning are due to:

• Inadequate repair, • pulmonary hypertension • And/or left or right ventricular dysfunction


• Weaning from CPB– Problems weaning diagnosed by

• Intraoperative cardiac catheterization

• Echo-doppler

– Leaving the operating room before correcting the problem leads to a significant INCREASE in morbidity

Postoperative care

• Observation on a monitored bed in ICU/HDU for 24 hours or overnight atleast because of their predisposition to develop ventricular/ supraventricular tachycardia, bradyarrhythmia and myocardial ischemia

• Meticulous attention to fluid balance to prevent hypovolumia• Monitoring of blood pressure preferably invasive, Oxygen saturation and

CVP• Position slowly- risk of postoperative postural hypotension with secondary

increase in right to left shunting • Prevention of venous stasis by early ambulation and by applying effective

elastic stocking or periodic pneumatic compression.• Adequate pain management – adverse hemodynamics and possibly

hypercoagulable state

Post op pain management

• Opioid analgesia

• Regional analgesia

• Alternative and supplementary analgesia


• Selected Specific Conditions/Procedures:– Tetralogy of Fallot– Patent Ductus Arteriosus(PDA)– ASD– VSD

TETRALOGY OF FALLOT

TETRALOGY OF FALLOT

• 10% of all CHD

• Most common R – L shunt

• 4 anomalies:– RVOT obstruction ( infundibular, pulmonic or

supravalvular stenosis )– Subaortic VSD– Overriding aorta– RVH

CXR IN TOF

• Normal heart size

• Pulmonary oligemia

• Upturned cardiac apex

• Rt aortic arch

TOF : Coagulation Abnormalities

• Thrombocytopenia

• Platelet functional defects

• Hypofibrinogenemia

• Elevated PT, APTT.


• Laboratory data– Cyanosis leads to polycythemia

• May consider phlebotomy esp if no CPB

• Leads to coagulation problems

– Anemia may be “relative” and need transfusion– Newborn infant has immature systems including

renal/hepatic/coagulation– Hypoglycemia is much more common

Airway Abnormalities in TOF

• TOF with pulmonary atresia: tracheomalacia, bronchomalacia

• Associated syndromes – DiGeorge syndrome, CHARGE, Goldenhar’s syndrome, Down’s syndrome.

TETRALOGY OF FALLOT

• Hypercyanotic ( “tet” ) spells occur D/T infundibular spasm, low pH or low PaO2

• In awake patient manifests as acute cyanosis & hyperventilation

• May occur with feeding, crying, defecation or stress

• During anesthesia D/T acute dynamic infundibular spasm

Triggers

• ↑O2 demand

• crying feeding defecation

• Hypovolemia

• Relative anemia

• Anxiety

• Hypoxia hypercarbia acidosis

TETRALOGY OF FALLOT

• Treatment of Hypercyanotic Spells– High FiO2 → pulmonary vasodilator → ↓ PVR– Hydration (fluid bolus) → opens RVOT– Morphine (0.1mg/kg/dose) → sedation,↓ PVR– Ketamine → ↑ SVR, sedation, analgesia → ↑ PBF– Phenylephrine (1mcg/kg/dose) → ↑ SVR– β-blockers (Esmolol 100-200mcg/kg/min)

→ ↓HR,-ve inotropy → improves flow across obstructed valve &↓ infundibular spasm

Volatile Esmolol Propranolol ↑ depth of ↓ HR & anesthesia contractility

↑ pre load ↓ infundibular spasm

↓ acidosis TREATMENT (NaHCO3)

↑SVR ↓ PVR

Phenylnephrine norepinephrine posture1-10µg/kg 0.01µg/kg


• Tetralogy of Fallot– Preoperative Preparation

• Heavy premedication

– Consider IM ketamine or inhalation induction but get rapid control of airway.

– Keep SVR up and PVR down, maintain heart rate– Intraoperative TEE


• Tetralogy of Fallot– Weaning from CPB, ratio RV:LV pressure should

be < 0.8– May need to keep PVR low with NTG, milrinone,

dobutamine phentolamine, PGE1

– May need RV inotrope post op– May need temporary pacing wire


• Tetralogy of Fallot– Perioperative concerns

• Increase in PVR or decrease in SVR leading to Right to Left shunt

• Tet Spells pre induction (crying/anxiety)

• Polycythemia and bleeding

• Air embolus

• RV failure

PALLIATIVE SHUNTS IN TOF

• Blalock-Taussig shunt [anastomosis of

subclavian artery and pulmonary artery]

• Modified B-T shunt [Goretex graft used]

• Pott’s shunt [descending aorta left pulmonary

artery]

• Waterston’s shunt [ascending aorta right

pulmonary artery]

Patent Ductus Arteriosus

• Ductus Arteriosus connects the descending aorta to the main pulmonary trunk near the origin of the left subclavian

• Normal postnatal closure results in fibrosis- which becomes the ligamentum arteriosum.

• Small PDA does not increase risk for heart failure- but does carry a risk for bacterial endocarditis.


• PATENT DUCTUS ARTERIOSUS– 1/8000 live births, associated with prematurity

and female predominance of approx 3:1– Left to right shunt causes pulmonary edema– Occasionally right to left cause lower body

cyanosis– SpO2 probe on Right hand and lower limb

• Confirms correct vessel ligated

– Vagal reflex is pronounced by lung traction– Antibiotics required to prevent endocarditis

• Confirmation of crossmatched blood in OT.

• Radial arterial line preferably on opposite side of aortic arch.

• At the time of PDA ligation SBP reduced to 80-90 mm of hg with Halothane/SNP

• Watch for haemorrhage due to rupture.

Thank you!!

Anaesthesia for congenital heart disease

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