Pathophysiologic Consideration In Patients With Congenital Heart Disease
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Transcript of Pathophysiologic Consideration In Patients With Congenital Heart Disease
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Pathophysiologic Pathophysiologic Consideration Consideration
In Patients With In Patients With Congenital Heart Congenital Heart
DiseaseDisease
Professor Of Anaesthesia .. Ain Shams UniversityProfessor Of Anaesthesia .. Ain Shams University
SAMIA SHARAF .MDSAMIA SHARAF .MD
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Classification Of Congenital Heart Classification Of Congenital Heart LesionsLesions
1) Obstructive lesions eg.
Aortic stenosis – coarctation of aorta
1) Increased pulmonary blood flow eg.
ASD – VSD – PDA
1) Decreased pulmonary blood flow lesions eg. Tetralogy of fallot – tricuspid atresia – pulmonary atresia
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Classification Of Congenital Heart LesionsClassification Of Congenital Heart Lesions
Left To Right Shunt Atrial Level : ASD 5% , TAPVC Ventricular Level : VSD 33%Great Artery Level : PDA 10%Truncus Arteriosus : 1%Coronary Level : ALCAPA
Right To Left Shunt TOF : 9%TGA : 1%
Left Heart Obstructive Lesions Mitral StenosisAortic Stenosis : 8%Coarctation : 5%Hypoplastic Left Heart Syndrome
Right Side Obstructive Lesions Pulmonary Stenosis / Atresia : 10%Tricuspid Stenosis Hypoplastic Right Heart
Single Ventricle
Others Vascular Rings Venous Anomalies Arteriovenous Fistula
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Clinical Presentation Of Children Clinical Presentation Of Children With CHDWith CHD
1) Cyanosis ( due to hypoxia )
2) Respiratory system abnormalities
3) Cardiac failure
4) Arrhythmias
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Cyanosis Cyanosis Pathophysiologic Effects of HypoxiaPathophysiologic Effects of Hypoxia (1) Growth (2) Heart Exercise intolerance :
myocardial dysfunction ventricular compliance and contractility
Irreversible myocardial damage . Increased sympathetic tone
down regulation of beta receptors cardiomyopathy
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(3) Hematology A major adaptive response to chronic hypoxia Red cell mass
Polycythemia Secondary Spherocytosis Blood viscosity Risk of thromboembolic events
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Hemostasis : PolycythemiaPolycythemia
DICDIC
Primary fibrinoly
sis
Coagulation abnormalities
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Mechanism of coagulation abnormalities
Increased blood viscosity
Fibrin depositio
n&
platlet aggreg.
Thrombocytopenia
& Low Fibrinogen & Other
Factor Level
Increase intravasc
ular strains
DIC Hypercoag. blood
& tendency to bleed
Consumpution of
platlets , fibrinogen , factor V ,
VIII
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Chronic hypoxia causes impairment of neurologic development and increase risk of neurologic damage .
Brain abscess : Rt. – Lt. shunt Cerebrovascular thrombosis and hemorrhage .
(4) CNS(4) CNS
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Respiratiry System AbnormalitiesRespiratiry System Abnormalities
Anatomical abnormalities of airway Pulmonary abnormalities associated with or
pulmonary blood flow .
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Anatomical Abnormalities Of Anatomical Abnormalities Of AirwayAirway
1) Short trachea eg. interrupted aortic arch 2) large airway obstruction : ( trachea & bronchi ) Compression by enlarged aorta or
pulmonary artery . Upwards displacement and increase angle of
bifurcation of trachea by enlarged LA .
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3) Small airway obstruction : • Compression of lung parenchyma by
enlarged heart and vessels .• Pulmonary hypertension .
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Pulmonary Changes Associated Pulmonary Changes Associated With Pulmonary Blood FlowWith Pulmonary Blood Flow
Patients with chronic hypoxia1) Slight of alveolar ventilation 2) pulmonary venous PO2 is high 3) V/Q mismatch alveolar –
pulmonary venous O2 gradient 4) Physiological dead space end tidal
CO2 is lower than arterial PaCO2
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Pulmonary Changes Associated Pulmonary Changes Associated With Pulmonary Blood FlowWith Pulmonary Blood Flow
Obstruction of small airway Pulmonary congestion pulmonary
compliance , lung water & Impaired gas exchange
Progressive of pulmonary vascular resistance due to hypertrophy in muscular layer of pulmonary arteries reverse of left to right shunt
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Cardiac FailureCardiac Failure
Causes of limited cardiac reserve : (1) Increased cardiac workload Pressure overload :
ventricular outflow tract obstruction SVR blood viscosity
Volume overload : * Valvular insufficiency * Single ventricle * Left – right shunt
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(2) Myocardial contractility:
Prolonged workload of myocardium Vascular supply to ventricles Blood hyperviscosity Chronic hypoxia
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Compansatory MechanismCompansatory Mechanism
Ventricular hypertrophy Adrenergic system changes
Activation of B receptors Renal system compansation
*Salt & water retention
*Renin secretion
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Types :Types :
* Congenital
* Acquired
Etiology :Etiology : Intrinsic electrophysiology abnormalities Damage from chronic hypoxia – hemodynamic stress Surgical injury eg. F4 , Fontan operation , atrial
correction of TGA
ArrhythmArrhythmiasias
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Congenital Conduction System Congenital Conduction System AbnormalitiesAbnormalities
Congenital complete atrioventricular block Wolf – Parkinson white syndrome Supraventricular tachycardia Arrhythmias associated with Ebstien anomaly
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Acquired Conduction System Acquired Conduction System AbnormalitiesAbnormalities
Non surgical : rare Surgical by :
* cardioplegia
* mechanical retraction
* ischemia
* metabolic abnormalities
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Anaesthetic Risk factors affecting anaesthetic risk in congenital
heart disease
Cyanotic heart Cyanotic heart diseasedisease
Cardiovascular Cardiovascular impairmentimpairment
Pulmonary Pulmonary diseasedisease
Myocardial Myocardial dysfunctiondysfunction
Arrhythmias Arrhythmias
Magnitude Magnitude of surgeryof surgery
Anaesthetic riskAnaesthetic risk
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How To Reduce Anaesthetic Risk ??
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ConsultatiConsultationon
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Role Of Surgeon
Case discussion :
Pts. with CHD may not tolerate :
Abdominal laparoscopic procedures ( eg. stenotic valvular lesions , single ventricle )
Absorption of CO2 ( C.O.P dependant low PVR) . One lung ventilation Prone position ( Fontan pt. )
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Role Of Pediatric Cardiologist
Preoperative consultation Preoperative consultation sometimes add a little sometimes add a little
benefit to benefit to anesthiologist !!!!!anesthiologist !!!!!
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Efficacy Of Repairs For CHD LesionsEfficacy Of Repairs For CHD Lesions
CURED CORRECTION PALLIATION
PDAASD
VSDTFOCoarctation of aortaPulmonary or aortic stenosisAV Canal repair
ConduitsPA bandingModified Glenn shunt
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How To Look To Patient Data
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History Taking
o Growtho Exercise Intoleranceo Recurrent Chest Infection o Syncopal Attacks o Squatting
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ECG , Echo & Cardiac Cath.
Systolic & Diastolic Dysfunction
Reduced Fractional Shortening
Systolic Dysfunction
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Diastolic Dysfunction
Ventricular Hypertrophy
Obstructive Volume
Before Repair
e.gvalvular
& outflow
obst.
After Repair
e.g Homograft conduit
Before Repair
e.gLt . to Rt.
shunt
After Repair
e.g•Pulmonary valve regurge ( F4 )•MV repair
Concentric Eccentric
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Anaesthetic considerations :
Consider determinants of coronary perfusion & myocardial oxygen balance
• Heart rate changes • Hypotension • Myocardial contractility
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Anaesthetic considerations
increase wall
thickness
coronary filling become
s diastoli
c
coronary perfusion
depends on bl. p. & hr
Maintain heart rate to
decrease regurgitant
fraction
Syst. DysfunctionIn Dialted
type
RV LVanaesthet
ic myocardia
l depressio
nDecrease driving filling
pressure of coronary arteries
Coronary ischemia
Diast. Dysfunction
In Hypertrophi
c & restrictive
type
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Residual Shunts :
o Occasionally present after repair of ASD , VSD & F4
o Small patch leaks are hemodynamically benign
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Dysrhythmias :Atrial & ventricular types increase mortality and morbidity
Arrhythmias Associated With Specific Arrhythmias Associated With Specific Surgical ProceduresSurgical Procedures
Ostium secondum ASD :• P-R interval is prolonged in 20-30% of patients • AF , atrial flutter with advancing age
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VSD : •RBBB•Atrial ectopic , junctional beats , premature ventricular
beat •Late onset of complete heart block or ventricular arrhythmias are rare
Repair of F4 :•RBBB & complete heart block
Mustard or Senning operation : •Sinus nodal dysfunction •Bradycardia•A-V block , AF
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Severity of hypertension of base line PAH correlated with the incidence of major complications ( pulmonary hypertensive crisis or cardiac arrest )
Pulmonary hypertension
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Cardiovascular risk of PAH
Major perioperative hemodynamic deterioration mainly pulmonary hypertensive crisis and acute right ventricular failure and cardiac arrest .
Data to look for : o Mean pulmonary artery pressure > 25 mmHg o Severity of base line PH : Subsystemic PAP < 70% of syst. bl. pressure Systemic PAP = 70 – 100 of syst. bl. pressure Suprasystemic PAP > 70 of syst. bl. pressure
( based on mean pressures )
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ANAESTHETIC CONSIDERATIONS
Avoid Factors Rapidly Increasing PVR
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Laboratory dataHematocrit value
Increase More Blood ViscocityIncrease More Blood Viscocity
Hyperviscosity Hyperviscosity symptomssymptoms
Decreased oxygen Decreased oxygen deliverydelivery
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Blood Indicies :
Increase Blood Increase Blood Viscosity Viscosity
Increase Blood Increase Blood Viscosity Viscosity
Hyperviscosity Symptoms At Hyperviscosity Symptoms At Lower Hematocrit ValueLower Hematocrit Value
Hyperviscosity Symptoms At Hyperviscosity Symptoms At Lower Hematocrit ValueLower Hematocrit Value
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Phlebotomy
Done to relieve hyperviscosity symptoms with hematocrit > 65 % in absence of iron deficiency anaemia or signs of dehydration
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Hemostatic values
•Prolonged PT , PTT , APTT values most frequently seen in cyanotic patients
•Thrombocytopenia is related to degree of polycythemia .
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SummaryGeneral associated risk factors in CHD
Severe form of isolated lesion
Complex lesions
Concurrent infectious disease
Congestive heart failure
Acute hemodynamic deterioration
Previous palliative or corrective procedures
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SummaryRisk criteria of hemodynamic critical impairment
in perioperative period in CHD
• Arterial saturation < 75 %• Hematocrit > 65 %• Qp / Qs > 2 : 1• LV outflow tract gradient > 50 mmHg• RVOT gradient > 50 mmHg• PVR > 6 wood units
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