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  • Pathophysiology of Cyanotic CHD

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    Lodi Palle
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    Central cyanosis is caused by desaturated blood and is a hallmark of cyanotic congenital heart disease (CHD). The degree of cyanosis varies depending on factors like pulmonary blood flow, pulmonary vascular resistance, right ventricular outflow tract obstruction, and the presence and size of septal defects. Conditions with low or no pulmonary blood flow, like transposition of the great arteries or pulmonary atresia, result in severe cyanosis. Cyanotic CHD can also lead to congestive heart failure if pulmonary blood flow is too high. The document discusses the pathophysiology of specific cyanotic lesions and how they relate to oxygen saturation and clinical presentation.

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    Central cyanosis is caused by desaturated blood and is a hallmark of cyanotic congenital heart disease (CHD). The degree of cyanosis varies depending on factors like pulmonary blood flow, pulmonary vascular resistance, right ventricular outflow tract obstruction, and the presence and size of septal defects. Conditions with low or no pulmonary blood flow, like transposition of the great arteries or pulmonary atresia, result in severe cyanosis. Cyanotic CHD can also lead to congestive heart failure if pulmonary blood flow is too high. The document discusses the pathophysiology of specific cyanotic lesions and how they relate to oxygen saturation and clinical presentation.

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    276 views32 pages

    Pathophysiology of Cyanotic CHD

    Uploaded by

    Lodi Palle
    Central cyanosis is caused by desaturated blood and is a hallmark of cyanotic congenital heart disease (CHD). The degree of cyanosis varies depending on factors like pulmonary blood flow, pulmonary vascular resistance, right ventricular outflow tract obstruction, and the presence and size of septal defects. Conditions with low or no pulmonary blood flow, like transposition of the great arteries or pulmonary atresia, result in severe cyanosis. Cyanotic CHD can also lead to congestive heart failure if pulmonary blood flow is too high. The document discusses the pathophysiology of specific cyanotic lesions and how they relate to oxygen saturation and clinical presentation.

    Copyright:

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    Download as PDF, TXT or read online from Scribd
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    of 32

    PATHOPHYSIOLOGY OF

    CYANOTIC CHD

    BY
    J. A. AL-ATA
    COSULTANT & ASSISTANT
    PROFESSOR OF PEDIATRIC
    CARDIOLOGY
    CYANOSIS
    • BLUISH discoloration of SKIN & MM due
    to doxyhemoglobin.
    • Desaturated arterial blood Central
    cyanosis.
    • Peripheral cyanosis Normal Art. Sat.
    • Detected; clinically ( sat below 85% ), pulse
    oximetry, or ABG.
    CAUSES OF CYANOSIS
    • Central cyanosis:
    • Respiratory
    • CNS
    • Muscular
    • Cardiac
    • Peripheral cyanosis:
    • CHF
    • Shock
    • Acrocyanosis
    • Abnormal hemoglobin
    Types of Cyanotic CHD
    • With pulmonary blood flow;
    • D-TGA
    • Truncus arteriosus
    • TAPVD
    • DORV
    • Single ventricle no ps.
    • With pulmonary blood flow;

    • TOF
    • Critical pulmonary stenosis
    • Pulmonary Atresia
    D-TGA
    • Parallel circulation not in series
    • Body----RA----RV----AO----Body

    • Lungs---LA----LV----PA----Lungs
    • Poor mixing
    • Hypoxia & Acidemia
    • Hyperventilation
    • Increased pulmonary flow
    • CHF
    • Myocardial depression
    TRUNCUS ARTERIOSUS
    • Complete mixing so cyanosis is minimal
    • VSD always present
    • Identical pressures in both ventricles
    • Systemic saturation is proportional to pulmonary
    blood flow ( PBF )
    • PVR & PA.s caliber determine PBF
    • CHF is a usual presentation
    • Eisenmenger syndrome may develop
    • AS & AI are complicating factors
    TAPVR

    • NON-Obstructed TAPVR
    • Similar hemodynamics to a large ASD
    • Lt to Rt shunt magnitude is determined by RV
    compliance & ASD size
    • Rt heart & pulmonary volume overload
    • Complete mixing at RA level
    • Minimal cyanosis due to large PBF
    • Slight PA pressure elevation
    TAPVR, CONT;
    • Obstructed TAPVR
    • Pulmonary venous hypertension & secondary PA &
    RV hypertension
    • Less RV & PA volume overload
    • Pulmonary venous oedema
    • More cyanosis & respiratory distress
    • Complete mixing
    TRICUSPID ATRESIA

    • Increased RA pressure & size


    • Dependant on the ASD or PFO
    • Dilated LA & LV
    • Complete mixing in LV
    • With TGA PBF & SAT.
    • Variable degree of cyanosis
    EBSTEIN ANOMALY
    • Variable degrees of cyanosis depending on
    amount of Rt to Lt shunt across ASD or
    PFO
    • Hugely dilated RA
    • Incompetent TV
    • Atrialized & small poorly functional RV
    • RVOTO & PS can be associations
    • SVT ( WPW ) can be associated
    TETRALOGY OF FALLOT
    • Decreased PBF & Amount of RT to LT
    shunt determine degree of cyanosis
    • PBF is mainly determined by RVOTO & PS
    • Pink TOF = mod RVOTO & balanced
    shunting across the VSD
    • Increased PBF can result from PDA or
    MAPCAS
    • Equal ventricular pressures
    HYPERCYANOTIC SPELL
    PULMONARY ATRESIA
    • With VSD
    • An extreme form of TOF
    • Early cyanosis when PDA closes
    • Ductal dependant
    • CHF with MAPCAS / PDA
    • Balanced form
    PULMONARY ATRESIA
    CONT;
    • Without VSD
    • Early marked cyanosis ( extremely decreased PBF )
    • Ductal dependant
    • RV sinusoids
    • RV decompression by TR
    • ASD or PFO mandatory
    SUMMARY
    • Central cyanosis is the hallmark of cyanotic CHD
    • Cyanosis is a serious symptom or sign
    • Variable degrees of cyanosis occur due to
    variability in PBF, PVR, RVOTO, presence & size
    of shunting site e.g. ASD and hemoglobin
    concentration
    • CHF can occur in cyanotic CHD due to increased
    PBF
    • Pulmonary AVMs & Methemoglobinemia are
    non-cardiac causes of central cyanosis.
    Thank You

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