Ravilya_Pediatrics_ Cardiology Pathphys

Front 1

Preload, afterload in different cardiac diseases

Back 1

Preload, afterload in different cardiac diseases (very important for Board examination): Preload (volume work) is increased in valvular insufficiency (e.g., aortic insufficiency, mitral insufficiency, tricuspid insufficiency) and in left-to-right shunt (e.g., VSD). Cardiac chambers are dilated. Management: reduce preload Afterload (pressure work) is increased in valvular stenosis (e.g., aortic stenosis, mitral stenosis) andcoarctation oftheaorta. Management: reduce afterload. Afterload is decreased in high-output failure (e.g., large systemic arteriovenous fistualas) which has normal myocardial function, decrease peripheral vascular resistance, and increase myocardial contractility

Front 2

Maximum decline of pulmonary pressure a

Back 2

Maximum decline of pulmonary pressure after birth:first 2-3 days of life,decline occurs mostly in first hour of birth.

Front 3

Which organ gets maximum blood supply in fetal life from cardiac output?

Back 3

Which organ gets maximum blood supply in fetal life from cardiac output? Placenta (65%). All other organs get 35%.

Front 4

Most important factor causing pulmonary vasoconstriction?

Back 4

Most important factor causing pulmonary vasoconstriction? Hypoxia. Other factors are acidosis, sepsis (group B Strep,
which releases thromboxane A2, which causes puhnonary vasoconstriction

Front 5

Time to close functionally:

Back 5

Time to close functionally:
Foramen ovale: by 3 months ofage.
Ductus arteriosus: by10-15 hours, but anatomic obliteration ofductus does not occur until after first week oflife

Front 6

Most important factor in ductal closure of neonate:

Back 6

Most important factor in ductal closure of neonate: oxygen. (Hyperoxia closes duct, hypoxia opens it.)

Front 7

Factors closing duct

Back 7

Factors closing duct indomethacin, hyperoxia, alkalosis.

Front 8

Factors opening duct:

Back 8

Factors opening duct: hypoxia, prostaglandin E1, S, acidosis.

Front 9

Which heart disease is most common in high altitudes

Back 9

Which heart disease is most common in high altitudes? PDA.

Front 10

When first child has congenital heart disease, what is chance that 2nd child will also?

Back 10

When first child has congenital heart disease, what is chance that 2nd child will also? 2-6%.

Front 11

When two siblings have congenital heart disease, what is chance that 3rd child will also?

Back 11

When two siblings have congenital heart disease, what is chance that 3rd child will also? 20-30%.

Front 12

Most common cause of congenital heart disease

Back 12

Most common cause of congenital heart disease: unknown, but genetics factor play animportant role.

Front 13

Which heart disease is most common in high altitudes?

When first child has congenital heart disease, what is chance that 2nd child will also?

Back 13

Which heart disease is most common in high altitudes? PDA.

When first child has congenital heart disease, what is chance that 2nd child will also? 2-6%.

Front 14

Oxygen saturation and pressure gradient in different cardiac diseases:

Back 14

Front 15

Back 15

normal

Front 16

Back 16

AS

Front 17

Back 17

TAPVR (Total anomalous pulmonary venous return)

Front 18

Back 18

vsd

Front 19

Back 19

tof

Front 20

Back 20

ps

Front 21

Back 21

PDA

Front 22

Back 22

TRANSPOSITION OF GREAT VESSELS

Front 23

Back 23

TRUSCUS

Front 24

Back 24

Front 25

Which organ gets maximum blood supply in fetal life from cardiac output?

Back 25

Which organ gets maximum blood supply in fetal life from cardiac output? Placenta (65%). All other organs get 35%.

Front 26

Maximum decline of pulmonary pressure after birth:

Back 26

Maximum decline of pulmonary pressure after birth: first 2-3 days of life,decline occurs mostly in first hour of birth.

Front 27

Most important factor causing pulmonary vasoconstriction?

Back 27

Most important factor causing pulmonary vasoconstriction? Hypoxia. Other factors are acidosis, sepsis (group B Strep,
which releases thromboxane A2, which causes pulmonary vasoconstriction).

Front 28

Time to close functionally:

Back 28

Time to close functionally:
Foramen ovale: by 3 months ofage.
Ductus arteriosus: by10-15 hours, but anatomic obliteration of ductus does not occur until after first week oflife.

Front 29

Most important factor inductal closure of neonate:

Back 29

Most important factor inductal closure of neonate: oxygen. (Hyperoxia closes duct, hypoxia opens it.)

Front 30

Factors closing duct

Back 30

Factors closing duct indomethacin, hyperoxia, alkalosis.

Front 31

Factors opening duct

Back 31

Factors opening duct: hypoxia, prostaglandin E1, S, acidosis.

Front 32

A newborn has cyanosis and respiratory distress. Initially, how do you differentiate cardiac from pulmonary disease?

Back 32

A newborn has cyanosis and respiratory distress. Initially, how do you differentiate cardiac from pulmonary disease? (Very
important) hyperoxia test. (Give 100% oxygen.) IfP02 is more than 150, then it is probably a pulmonary disease. IfP02is
less than 150, then it isprobably a cardiac disease.
DEFINITIVE DIAGNOSIS: echocardiogram

Front 33

A full-term newborn has hypoxia and severe respiratory distress, low apgar and history of fetal distress, and is on ventilator with
very high setting (100% oxygen). This may be due to

Back 33

A full-term newborn has hypoxia and severe respiratory distress, low apgar and history of fetal distress, and is on ventilator with
very high setting (100% oxygen). This may be due to: persistent pulmonary hypertension (PPHN

Front 34

The most useful measure of systolic function of the left ventricle:

Back 34

The most useful measure of systolic function of the left ventricle: left ventricular ejection fraction (LVEF) (stroke volume/end-diastolic volume) Normal LVEF: above 55 %
...--Mildly reduced LVEF: 40-50 %
Moderately reduced LVEF: 30-40 %
Severely reduced LVEF: less than 30 %
Please remember, cardiac output is a poor measure of systolic function

Front 35

The effect of diastolic dysfunction of the left ventricle (important):

Back 35

The effect of diastolic dysfunction of the left ventricle (important): rise of left ventricular filling pressure, rise of left atrial pressure, pulmonary congestion, reduce cardiac output if ventricular filling is impaired. Ventricular relaxation (or diastole) is energy dependent. Increased interstitial fibrosis and poor cardiac relaxation: occurs in ischemia or hypoxemia, myocardial hypertrophy, and chronic volume overload

Front 36

A patient appears with heart failure and increased preload. The drug used to reduce the preload and to improve the clinical condition (very important):

Back 36

A patient appears with heart failure and increased preload. The drug used to reduce the preload and to improve the clinical condition (very important): diuretics or venodilating agent that reduces the venous return.

Front 37

Preload is characterized by

Back 37

Preload is characterized by end-diastolic volume or pressure.
(i)
Normal heart with increased preload: improves systolic function.
(ii)
Failing heart with increased preload: does not improve systolic function but further worsen pulmonary congestion.
(iii) Normal heart with decreased preload; decreases systolic function and pressure.
(iv) Failing heart with decreased preload: little effect on left ventricular pressure.

Front 38

Ventricular afterload:

Back 38

Ventricular afterload: directly proportional to systemic pressure; inversely proportional to thickness of the ventricle.
arterial pressure x the radius of the left ventricle
Afterload = (arterial pressure X radius
of the left ventricle Increased)/2 X thinkness of left ventricle

Afterload: occurs in dilated thin ventricle at any given arterial pressure.
Decreased afterload: occurs in smaller or thicker ventricle at any given arterial pressure.
A patient appears with increased afterload resulting in reduced cardiac performance,
Next step in management afterload should be reduced

Front 39

The most common cause of right ventricular pressure overload (important):

Back 39

The most common cause of right ventricular pressure overload (important): left-sided heart dysfunction resulting in
pulmonary hypertension.

Right-sided heart failure: due to either chronic right ventricular pressure overload (e.g., pulmonary hypertension due to cor
pulmonale or pulmonary vascular disease) or to intrinsic dysfunction of right ventricle or its valves.