Patho 2.mod 2.chd

Front 1

Developmental Anatomy of the CV System: When does Cadiogenesis begin?

Back 1

3 weeks gestation, complete at 7 weeks, important to realize that this formation takes place prior to many women knowing that they are pregnant. Take Floic acid and don't take drugs.

Front 2

Where does the heart arise?

Back 2

Mesenchyme, develops as an enlarged blood vessel w/large lumen and muscular wall, middle grows faster than the ends
-creates "bulboventricular loop
-contractions start at the 28th day

Front 3

Developmental Anatomy of the CV System: Cardiac septation, Formation, seperates

Back 3

-endocardial cushions, (formation of chambers)
-Septum primum and secundum
-Ostium primum and secondum
-Foramen ovale
-ductus arteriosis

Front 4

Trans. circulation,

Back 4

 Circulatory changes take place that affect blood flow, vascular resistance, and oxygen tension
Closure of fetal shunts
Ductus venosus (VSD)(7days)(vent)
Foramen ovale (PFO)(atrium)
Ductus arteriosus (ASD)(Atrium)(15hrs-1021 days)

Front 5

Postnatal Development

Back 5

Changes in the position of the heart
Changes in the size of the right ventricle
Hemodynamics
Decreased pulmonary vascular resistance
Increased systemic vascular resistance
Heart rate ranges from 100 to 180 beats per minute
Newborns have a high oxygen demand

Front 6

How does Blood Circulate
Congenital Heart Defects?

Back 6

Underlying cause is known in only 10% of defects
Prenatal, environmental, and genetic risk factors
Maternal rubella, insulin-dependent diabetes, alcoholism, PKU, and hypercalcemia
Drugs
Chromosome aberrations

Front 7

Complications of Congenital Heart Defects

Back 7

Congestive heart failure
Hypoxemia-
Heart defects that allow desaturated blood to enter the system without passing through the lungs result in hypoxemia and cyanosis
Cyanosis-a blue discoloration of the mucous membranes and nail beds

Front 8

Defects Increasing Pulmonary Blood Flow (L to R Shunt)

Back 8

Patent ductus arteriosus (PDA)
Failure of the ductus arteriosus to close(ASD)
PDA allows blood to shunt from the pulmonary artery to the aorta

Front 9

Defects Increasing Pulmonary Blood Flow (L to R shunt)

Back 9

Atrial septal defect
Abnormal communication between the atria
Three major types
Ostium primum defect
Ostium secundum defect
Sinus venosus defect

Front 10

Acyanotic congenital heart defects L->R defects

Back 10

-PDA (aorta to pulmonary artery) easy surgery! shows up with failure to thrive, SOB, etc.)
-VSD
-incr. fatigue, heart murmur, incr. endocarditis, CHF,Growth retardation

Front 11

Acyanotic congenital heart defects L->R defects:
-ASD (atrial septal defect):

Back 11

Atrial septal defect
Abnormal communication between the atria
-fix with patch, or balloon

Front 12

Acyanotic congenital heart defects L->R defects
Ventricular Septal Defect (VSD)

Back 12

Defects Increasing Pulmonary Blood Flow
Atrioventricular canal defect (AVC)
Results from nonfusion of the endocardial cushions
Demonstrates abnormalities in the atrial and ventricular septa and atrioventricular valves
Complete, partial, and transitional AVCs

Front 13

Defects Increasing Pulmonary Blood Flow (L to R Shunt)

Back 13

Ventricular septal defect (VSD)
Abnormal communication between the ventricles
Most common type of congenital heart lesion
Types
Perimembranous VSD
Muscular VSD
Supracristal VSD
AV canal VSD

Front 14

Defects Increasing Pulmonary Blood Flow: Atrioventricular canal defect (AVC)

Back 14

-Results from nonfusion of the endocardial cushions
Demonstrates abnormalities in the atrial and ventricular septa and atrioventricular valves
Complete, partial, and transitional AVCs

Front 15

Defects Decreasing Pulmonary Blood Flow (R to L Shunt: Tetralogy of Fallot

Back 15

Syndrome represented by four defects
Ventricular septal defect (VSD)
Overriding aorta straddles the VSD
Pulmonary valve stenosis
Right ventricle hypertrophy

Front 16

PFO (Patent ovale foramen, when does it close normally?

Back 16

-1 month functionally
-3 months physically
hole between muscle flaps in the atrium, pressure from Left closes it post-partum

Front 17

Defects Decreasing Pulmonary Blood Flow (R to L Shunt): Tricuspid Atresia

Back 17

-Imperforate tricuspid valve
-lack of communication between R atrium and ventricle
--Septal defect
--hypoplastic or absent R ventricle
-enlarged mitral valve &left ventricle
--Pulmonic stenosis

Front 18

Tetralogy of Fallot:S/s

Back 18

-Squatting, reduces area that need circulation
-Cyanosis
-Clubbing
-Sycope

Front 19

Obstructive Defects: Coarctation of the aorta

Back 19

-Narrowing of lumen of aorta, decreases blood flow (Distal to the L subclavian)
-malformation of fusion of the cusps
-causes an increased workload on the L ventricle

Front 20

Obstructive Defects: Aortic stenosis

Back 20

 Narrowing of the aortic outflow tract
 Caused by malformation or fusion of the cusps
:Causes an increased workload on the left ventricle

Front 21

Mixed Defects:
Transposition of the great arteries

Back 21

Aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle
Results in two separate, parallel circuits
Unoxygenated blood circulates continuously through the systemic circulation
Oxygenated blood circulates continuously through the pulmonary circulation
Extrauterine survival requires communication between the two circuits

Front 22

Congenital heart defects Symptoms:

Back 22

-inc. pulse
-inc. resp
-retard drowth
-dyspnia, orthopenia
-Fatigue
-URI

Front 23

Acquired Cardiovascular Disorders
 Kawasaki disease

Back 23

AKA mucocutaneous lymph node syndrome
Acute, self-limiting systemic vasculitis that may result in cardiac sequelae

*Stages(not on test)
One (0-12 days): capillaries, venules, arterioles, and the heart become inflamed
Two (12-35 days): inflammation of larger vessels; coronary aneurysms appear
Three (26-40 days): medium-sized arteries begin granulation process; small vessel inflammation decreases
Four (day 40 and beyond): scarring of vessels, thickening of tunica intima, calcification, coronary artery stenosis
Diagnosis (5 of 6 major findings)
Fever for 5 or more days (unresponsive to antibiotics)
Bilateral conjunctivitis without exudation
Erythema of oral mucosa (strawberry tongue)
Changes in the extremities, such as peripheral edema and erythema with desquamation of palms and soles
Polymorphous rash
Cervical lymphadenopathy

Front 24

Acquired Cardiovascular Disorders: Systemic hypertension

Back 24

Hypertension in children differs from adult hypertension
Often have an underlying disease
Renal disease or coarctation of the aorta
A cause of the hypertension in children is almost always found
Children with hypertension are commonly asymptomatic, silent killer
-promote Lifestyle changes first then meds second

Front 25

Acquired Cardiovascular Disorders: Childhood obesity

Back 25

*Multivariable and multidimensional
*Risk factors
Race, socioeconomic status, and lack of health insurance
Childhood nutrition, level of physical activity, and engagement of sedentary activities (TV, computer use, etc.)
Association with parental obesity

Front 26

Terms: Acyanotic:

Back 26

-lacking cyanosis, no blue

Front 27

Coarctation:

Back 27

Narrowing or constriction of a lumen

Front 28

Hypoplastic left Heart Syndrome

Back 28

Under-developed left side,
-need transplant

Front 29

Dilated Cardiomyopathy

Back 29

-most common
-arrythmias
-impair
-Dilated cardiomyopathy (congestive cardiomyopathy)(DCM)

Front 30

Hypertrophic Cardiomyopathy

Back 30

-genetic component
- Hypertrophic cardiomyopathy (HCM)
 Asymmetrical septal hypertrophy
Hypertensive (valvular hypertrophic) cardiomyopathy

Front 31

Restrictive

Back 31

Fiberous, no exspansion

Front 32

Causes of Cardiomyopathy

Back 32

 Unknown in most cases.
 DCM result of metabolic disorders, persistant arrhythmias can weaken heart.
 HCM can run in families-genetic component.
 Few cases directly treatable, therapy mostly aimed at secondary effects.

Front 33

S/S of Cardiomyopathy

DCM: CHF

Back 33

Infants: rapid, labored respirations & sweating with feedings. Lethargy, inactivity, & FFT.
 Older children: exercise intolerance, abn heart beats, dizziness, weight loss due to nausea or decreased appetite

Front 34

S/S of Cardiomyopathy:
HCM: presents in many ways.

Back 34

Infants: CHF,
Older Children: exercise intolerance, chest pain with activity, palpations, dizziness, passing out.
 Some children have no symptoms-dx by presence of murmur from ventricular outflow

Front 35

RCM: increased work of breathing, freq respiratory infections

Back 35

Fatigue, dizziness & fainting. May have enlarged abdomen due to pressure on the R side of the heart-causing liver engorgement and ascities.

Front 36

Diagnostics

Back 36

Chest x-ray
EKG
Echocardiogram
Cardiac Catheterization

Front 37

Treatment-Immediate

Back 37

 Initial trx may require critical care such as ventilators, IVfluids & IV meds to improve BP and heart function.
 May be sick enough to require ECMO.
 Commons meds are diruetics & beta blockers.

Front 38

Treatment-Longterm

Back 38

 May need valve replacements.
 May need heart transplants.
Long-term prognosis
 Occurs with a wide spectrum of severity & outcome.
 Depends on cause and degree of irreversible damage to the heart.

Front 39

Downs syndrome has a high incidence of?

Back 39

PDA, VSD's