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105 Cards in this Set

  • Front
  • Back
When does cardiogenisis start
3 weeks
When is the heart done develping
7 weeks
In utero what is the 02 saturation
85%
Congenital heart defects are only known Why in
10% of babies
Prenatal environmental and genetic risks
rubella, diabetes, alcoholism, PKU, hypercalcemia,
Drugs, chromosome aberrations
Heart defect complications
CHF
Hypoxemia
Cyanosis
L to R shunt
Patent ductus arteriosus
Atrial septal defect
Ventricular septal defect
will cause
increase fatigue, murmur, Risk of endocarditis, CHF, Growth retardation.
(this is much worse than a right to left shunt)
PDA (Patent Ductus Arteriosus)
Oxygen rich blood flowing to the pulmonary artery, causing a left to right shunt. easy to fix.
ASD (atrial septal defect)
Increase pulmonary blood flow, (left to right shunt)
In utero the right side has
higher pressure and transitions to having the left side with higher pressure.
VSD ( Ventricular septal defect)
Most common type of congenital heart lesions, Between bentricle wall, More work on heart. needs patch and open heart surgery.
what is looked for in evaluation for surgery in congenital heart surgery.
they need the child to be as big as possible before there are serious signs or symptoms.
R to L shunt
Squatting
Cyanosis
syncope
Coarctation of the Aorta
restriction on the Aorta
Transposition
aorta and pulmonary arterie are switched in position
Acquired cardiovascular disorders
Kawasaki disease, 2nd leading cause of heart disease in children. starts as vascularitis, and effects the heart muscle and cause damage to the heart.
Systemic hypertension
in children it often has an underlining disease. (Renal and coarctation of the aorta)
- A cause of the hypertension is amost always found.
Hypoplastic left ventricle
two ways to treat,
-norwood procedure 50% mortality rate
-heart transplant
Cardiomyopathy
causes unknown in most cases
may need valve replacement or valve replacement
Dilated cardiomyopathy
the entire heart muscle expands and the valvs do not close,
hypertrophic cardiomyopathy
heart muscle is very thick which lowers ejection,
Restrictive cardiomyopathy
muscle does not expand or contract
Marphans syndrome
can cause anurysm on aorta
-disorder of the connective tissue characterized by disproportionately long limbs, long thin fingers, a typically tall stature, and a predisposition to cardiovascular abnormalities, specifically those affecting the heart valves and aorta. The disorder may also affect numerous other structures and organs
Cardiomyopathy
is any disease of the heart muscle in whick the heart loses its ability to pumb blood effectiviely. could be from bad heart rhythms or viral infections and sometimes the cause is not known
Congenital heart defects
problems with the heart at birth,
when do fetal heart contractions start
the 28th day
Postnatal Development changes
The heart changes position
there is an increase in systemic vascular resistance
heart range is 100 to 180 bpm
Dialated type of cardiomyopaty
DCM
the heart has a globular shape and the largest circumference of the left ventricle is not at its base but midway between apex and base.
Hypertrophic cardiomyopathy
HCM
In the hypertrophic type the wall of the left ventricle is greatly thickened; the left ventricular cavity is small, but the left atrium may be dilated because of poor diastolic relaxation of the ventricle
Restrictive cardiomyopathy
RCM
the left ventricular cavity is of normal size, but again, the left atrium is dilated because of the reduced diastolic compliance of the ventricle.
What is cardiomyopathy
The cardiomyopathies are a diverse group of diseases that primarily affect the myocardium itself. Most are the result of underlying cardiovascular disorders, such as ischemic heart disease or hypertension. Cardiomyopathies also can be secondary to infectious disease, exposure to toxins, systemic connective tissue disease, infiltrative and proliferative disorders, or nutritional deficiencies. Despite this large number of possible causes, most cases of cardiomyopathy are idiopathic; that is, their cause is unknown.
What are the problems with DCM
(dilated cardio myopathy)
The basic problem is diminished myocardial contractility, which is reflected in diminished systolic performance of the heart. Dilated cardiomyopathy causes decreased ejection fractions, increased end-diastolic and residual volumes, decreased ventricular stroke volume, and biventricular failure.
What are the problems with HCM
(hypertrophic cardiomyopathy)
The thickening of the septum results in a hyperdynamic state, especially with exercise. Diastolic relaxation also is impaired and ventricular compliance is decreased. Obstruction of left ventricular outflow can occur when heart rate is increased and intravascular volume is decreased.218 Individuals complain of angina, syncope, palpitations, and symptoms of myocardial infarction and left heart failure.
What are the problems with restrictive cardiomyopathy
RCM
The myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole. The overall clinical and hemodynamic picture mimics and may be confused with that of constrictive pericarditis.

The most common clinical manifestation of restrictive cardiomyopathy is congestive heart failure, particularly right heart failure. Cardiomegaly and dysrhythmias are common. In most cases there is no therapy for restrictive cardiomyopathy other than treating the underlying disease process. Death occurs as a result of congestive failure or dysrhythmias.
What is the usuall cause of valvular dysfunction
The usual cause of acquired valvular dysfunction is inflammation of the endocardium secondary to acute rheumatic fever or infective endocarditis (see p. 1124). Structural alterations of the heart valves lead to stenosis, incompetence, or both.
what is the ductes venouses and when does it close
closes within the first 7 days of life
-located between the placenta and the liver, when cord is clamped this ends placental curculation and become the Ligamentum venosum,,,
What is the foraman ovalle
closes within the first month of life.
-located at the atrial septal wall allowing blood to go directly to the left atriam to bypass the lungs in utero
what is the ductes arterioses and when does it close
closes within 10 to 21 days
-connects the pulmonary vein directly to the aorta allowing blood to bypass the lungs in utero
Describe postnatal hymodynamics
the systolic pressure is low in the full-term newborn (approximately 39 to 59 mmHg), reflecting the decreased LV strength. As the left ventricle becomes more developed, the systolic pressure rises steadily until it equals adult levels once the child reaches puberty.

The heart rate of the newborn ranges from 100 to 180 beats/min, which gradually decreases as the child grows. Similarly, the newborn's cardiac output is high, which is a reflection of the fetal circulation described earlier. Oxygen consumption doubles at birth; to maintain adequate oxygen delivery, the cardiac output also remains high. These changes, however, cause minimal cardiac reserve in the newborn. Additional stressors could increase oxygen demands and result in acute deterioration. By 2 months of age, oxygen consumption decreases by half. As the newborn grows, stroke volume steadily increases while the heart rate decreases.3
what happens by th 4th week of embyology cardiac development
By the fourth week of gestation, cardiovascular septation, ventricular development, aortic arch evolution, and circulation begin.
what is the placental cord made up of
two arteries non o2
one vein carry 02 to the fetus
when do fetal heart contracitons begin
28 days
what are the causes of CHD
 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
circulation route of blood through the heart
Desaturated blood returning from the superior vena cava, inferior vena cava, and coronary veins enters the right atrium and is pumped to the right ventricle through the tricuspid valve. The right ventricle then pumps the blood through the pulmonic valve to the pulmonary artery; the blood flows to the lungs, where it is oxygenated. The oxygenated blood returns from the lungs through the pulmonary veins and enters the left atrium. The left atrium pumps blood to the left ventricle through the mitral valve. The left ventricle then pumps blood through the aortic valve and into the aorta. The coronary arteries receive the saturated blood along with delivery to the systemic circulation.
How does hypoxemia arise from CHD (congenital heart defects
 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
• L to R shunts-pathophysiology, characteristics, defects involved.
Defects Increasing Pulmonary Blood Flow (L to R Shunt)
 Patent ductus arteriosus (PDA)
 Failure of the ductus arteriosus to close
 PDA allows blood to shunt from the pulmonary artery to the aorta
Patent Ductus Arteriosus (PDA)

Defects Increasing Pulmonary Blood Flow (L to R shunt)
 Atrial septal defect
 Abnormal communication between the atria
 Three major types
 Ostium primum defect
 Ostium secundum defect
 Sinus venosus defect

Atrial Septal Defect

Defects Increasing Pulmonary Blood Flow (L to R Shunt)
 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

Ventricular Septal Defect (VSD)

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
Atrioventricular Canal Defect
• R to L shunts-pathophysiology, characteristics.
Defects Decreasing Pulmonary Blood Flow (R to L Shunt)
 Tetralogy of Fallot
 Syndrome represented by four defects
 Ventricular septal defect (VSD)
 Overriding aorta straddles the VSD
 Pulmonary valve stenosis
 Right ventricle hypertrophy
Tetralogy of Fallot

Defects Decreasing Pulmonary Blood Flow (R to L Shunt)
 Tricuspid atresia
 Imperforate tricuspid valve
 Lack of communication between the right atrium and right ventricle
 Additional defects
 Septal defect
 Hypoplastic or absent right ventricle
 Enlarged mitral valve and left ventricle
 Pulmonic stenosis
Tricuspid Atresia
what is coarctation of the aorta
 Narrowing of the lumen of the aorta that impedes blood flow
 Coarctation of the aorta is almost always in a juxtaductal position, but it can occur anywhere between the origin of the aortic arch and the bifurcation of the aorta in the lower abdomen
what is hypoplastic left heart syndrome
 Abnormal development of the left-sided cardiac structures
 Obstruction to blood flow from the left ventricular outflow tract
 Under development of the left ventricle, aorta and aortic arch, and mitral atresia or stenosis
what is a tet squat
Squatting is a spontaneous compensatory mechanism used by older children to alleviate hypoxic spells. Squatting and its variants increase systemic resistance while decreasing venous return to the heart from the inferior vena cava. The decrease of systemic return makes relatively more oxygenated blood available to the body. The increase of systemic resistance also reverses the shunt through the VSD to a left-to-right shunt, which has the effect of increasing pulmonary blood flow. Through both of these mechanisms, squatting decreases the degree of hypoxemia temporarily.
Kawaski disease as it relates to heart and coronary arteries
Small capillaries, arterioles, and venules become inflamed, as does the heart itself.

Stage II (days 12 to 25): Inflammation spreads to larger vessels, and aneurysms of the coronary arteries develop.

Stage III (days 26 to 40): Medium-size arteries begin granulation process, causing coronary artery thickening; inflammation resolves in the microcirculation; and there is increased formation of thrombi.

Stage IV (day 40 and beyond): Vessels develop scarring, intimal thickening, calcification, and stenosis of coronary arteries.
S/S of Kawaski disease
The child must exhibit five of the following six criteria, including fever:

1. Fever for 5 or more days (often diagnosed with shorter duration of fever if other symptoms are present)

2. Bilateral conjunctival infection without exudation

3. Changes in the oral mucous membranes, such as erythema, dryness, and fissuring of the lips; oropharyngeal reddening; or “strawberry tongue”

4. Changes in the extremities, such as peripheral edema, peripheral erythema, and desquamation of palms and soles, particularly periungual peeling

5. Polymorphous rash, often accentuated in the perineal area

6. Cervical lymphadenopathy
o Systemic HTN-differential between children and adults
 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
summery review of congenital heart defects
Development of the Cardiovascular System

1. The heart arises from the mesenchyme and begins as an enlarged blood vessel with a large lumen and a muscular wall. By approximately the eighth week of gestation, all structures of the fetal heart and vascular system are present.

2. The endocardial cushions are instrumental in closing the atrial septum, dividing the atrioventricular canals into the right and left atrioventricular orifices, and closing the septum.

3. In the fetus the pulmonary and systemic circulatory systems are connected by the foramen ovale, an opening between the atria; by the ductus arteriosus, a fetal vessel that joins the pulmonary artery to the aorta; and by the ductus venosus, a fetal vessel that connects the inferior vena cava to the umbilical vein.

4. Fetal circulation is different from postnatal circulation because of the presence of fetal shunts and altered metabolic needs of the various organs.

5. Fetal blood flow depends on resistance for its distribution through the body. Resistance in the pulmonary circulation is higher than resistance in the systemic circulation, so myocardial thickness is about the same in the right heart and the left heart.

6. After birth, systemic resistance increases and pulmonary resistance decreases.

7. Pulmonary vascular resistance drops suddenly at birth because the lungs expand and the pulmonary vessels dilate. It continues to decrease gradually during the first 6 to 8 weeks after birth. Decreased resistance causes the right myocardium to thin out.

8. Systemic vascular resistance increases markedly at birth because severance of the umbilical cord removes the low-resistance placenta from the systemic circulation. Increased systemic resistance causes the left myocardium to thicken.

9. Changes in resistance cause the fetal connections between the pulmonary and systemic circulatory systems to disappear. The foramen ovale closes functionally at birth and anatomically several months later; the ductus arteriosus closes functionally 15 to 18 hours after birth and anatomically within 10 to 21 days; and the ductus venosus closes within 1 week after birth.

10. At birth a series of circulatory changes occur that affect blood flow, vascular resistance, and oxygen tension. The most important change is the shift of gas exchange from the placenta to the lungs.

11. After birth, significant postnatal changes occur, including thinning of the right ventricular myocardium as the pulmonary vascular resistance drops. As the systemic vascular resistance increases, the left ventricular myocardium becomes thicker.

Congenital Heart Defects

1. Most congenital cardiovascular defects have begun to develop by the eighth week of gestation, and most have many causes, both environmental and genetic.

2. Environmental risk factors associated with the incidence of congenital heart defects typically are maternal conditions. Among these are viral infections, diabetes, drug intake, alcohol intake, metabolic disorders, and advanced maternal age.

3. Genetic factors associated with congenital heart defects include but are not limited to Down syndrome, trisomy 13, trisomy 18, cri du chat syndrome, and Turner syndrome. It now appears, however, that most genetic mechanisms of causation are multifactorial.

4. Classification of congenital heart defects is based on whether they (a) cause blood flow to the lungs to increase or decrease, (b) obstruct ventricular blood flow patterns, or (c) cause mixing of unoxygenated and oxygenated blood.

5. Congestive heart failure is usually the result of congenital heart defects that increase blood volume and pressure in the pulmonary circulation. Clinical manifestations are almost the same as the manifestations of congestive heart failure in adults. Unique manifestations in children include failure to thrive and periorbital edema.

6. Cyanosis, a bluish discoloration of the skin, indicates that the tissues are not receiving adequate oxygenated blood. Cyanosis can be caused by defects that (a) restrict blood flow into the pulmonary circulation; (b) overload the pulmonary circulation, causing pulmonary hypertension, pulmonary edema, and respiratory difficulty; and (c) cause large amounts of unoxygenated blood to shunt from the pulmonary to the systemic circulation.

7. Congenital defects that maintain or create direct communication between the pulmonary and systemic circulatory systems cause blood to shunt from one system to another, mixing oxygenated and unoxygenated blood and increasing blood volume and pressure on the receiving side of the shunt.

8. The direction of shunting through an abnormal communication depends on differences in pressure and resistance between the two systems. Flow is always from an area of high pressure to an area of low pressure.

9. Acyanotic congenital defects that increase pulmonary blood flow consist of abnormal openings (patent ductus arteriosus, atrial septal defect, ventricular septal defect, atrioventricular canal defect, or truncus arteriosus) that permit blood to shunt from left (systemic circulation) to right (pulmonary circulation). Cyanosis does not occur because the left-to-right shunt does not interfere with the flow of oxygenated blood through the systemic circulation.

10. If the abnormal communication between the left and right circuits is large, volume and pressure overload in the pulmonary circulation leads to congestive heart failure.

11. In truncus arteriosus the main trunk fails to divide longitudinally into the aorta and pulmonary artery. All blood from both ventricles enters the truncus, so that mixed blood is delivered by both circulatory systems, causing cyanosis and CHF.

12. In heart defects that decrease pulmonary blood flow (tetralogy of Fallot, tricuspid atresia), myocardial hypertrophy cannot compensate for restricted right ventricular outflow. Flow to the lungs decreases, and cyanosis is caused by an insufficient volume of oxygenated blood.

13. Obstruction of ventricular outflow commonly is caused by pulmonary stenosis, aortic stenosis, coarctation of the aorta, interrupted aortic arch, or hypoplastic left heart syndrome.

14. Despite obstruction, ventricular outflow remains normal because of compensatory ventricular hypertrophy stimulated by increased afterload and, in postductal coarctation of the aorta, development of collateral circulation around the coarctation.

15. Left heart failure can develop as a result of right ventricular obstruction if afterload backs up into the pulmonary circulation. Congestive heart failure can result from left ventricular obstruction in preductal coarctation of the aorta, in which left-to-right shunting through the patent ductus arteriosus greatly increases blood flow into the pulmonary circulation.

16. Complex congenital defects that depend on mixing of the pulmonary and systemic circulations for survival during the postnatal period include complete transposition of the great arteries, total anomalous pulmonary venous connection, and double-outlet right ventricle. This mixing results in desaturated systemic blood flow and cyanosis.

17. In complete transposition of the great vessels, the circulatory systems are not connected serially or through a shunt, so that oxygenated blood remains permanently in the pulmonary circulation and unoxygenated blood remains permanently in the systemic circulation. Survival depends on patency of the ductus arteriosus; after that, surgical intervention is mandatory.

18. Total anomalous pulmonary venous connection is caused by the persistence of the fetal common pulmonary artery and the lack of pulmonary venous return to the left atrium. All blood from the pulmonary and systemic circulations enters the right atrium. Mixed blood enters the left atrium through an atrial septal defect; it then flows into the systemic circulation and causes cyanosis. Obstruction in the common pulmonary vein causes pressure to back up into the lungs, leading to congestive heart failure.

19. Treatment for all congenital defects is surgical correction of the anomaly and management of cyanosis and left heart failure.

Acquired Cardiovascular Disorders

1. The most common acquired cardiovascular disorders of childhood are Kawasaki disease, rheumatic heart disease, and hypertension.

2. Kawasaki disease is an acute systemic vasculitis that also may result in the development of coronary artery aneurysms and thrombosis.

3. Primary hypertension in children is the same as that in adults, except that it is more likely to be in an early, asymptomatic stage.
what does a fibronis plaq cause
hemorhage to occure and clotting
what is the cause of atherosclerosis
inflamation of the inner lining of the vessel will cause monocytes and macrophages to attack causing a place for plaqe to form
Mean arterial pressure
is what is keeping one side of the vessel away from the other
how do you figure MAP
S plus 2 times diastolic
--------------------------
3
MAP
CO (HR times SV) times prepherial vascular resistance
Stroke volume
end diastolic volume or amount of voluem that is in the ventricle after all valves closed equal to preload
end diastolic volume - end systolic volume equals
ejection fx
Heart rate controled by
sympathetic
parasymathetic
temp
neural
chemical
prepherial resistance is equal to
blood viscosity/ by number an size of blood vessels
what is blood viscosity due to
RBC concentraiton
tempreture
fluids
blood vessel intrinsic factor is
lg to small to lg which has to due with pressure
what can cause blood vessel size to change
tempreture
neruo
pressure
chemical
and intrinsic factors like size
what is the pressure when it dropes into the right atrium
7 to 10 mmhg
map
holding one side of the arota away from the other
Diastolic pressure
equal to MAP close acutally a little higher
Systolic pressure is equal to
diastolic plus pulse pressure
pule pressure is equal to
systemic vascular resistance divided by arterial capacity
map
systolic minus diastolic
decresa map
vessels collapse
increase map
stretching and killing vessel
Mean arterial pressure
is what is keeping one side of the vessel away from the other
how do you figure MAP
S plus 2 times diastolic
--------------------------
3
MAP
CO (HR times SV) times prepherial vascular resistance
Stroke volume
end diastolic volume or amount of voluem that is in the ventricle after all valves closed equal to preload
end diastolic volume - end systolic volume equals
ejection fx
Neuro and blood pressure
efferent system, afferent system and medula ///
remember that you can have an electricle impulse without a mechanical result
pulmonary vascular resistance
example pulmonary hypertension
leading to corpulmonaly
control of blood pressure
renin
antidiuretic
baro receptors
Renin angiotensins alsdosterone
stops the renin conversion
Primary hypertension
we dont know what is causing it (esential or idopathic)
Secondary hypertension
caused by another factor (we know what is causeing it)
Risk factors for hypertension
Family HX
Patients whose parents hav htn have a risk
92 to 95 % of hypertension cases are what
primary HTN
causes hypertension
Gender
Race (black)
Age
High sodium intake
glucose intolerance
smoking
obesity
alcohol
low in K mg c
problems with pressure signals
Secondary hypertension
remove problem and the hypertension is gone
when can primary htn start
30 to 50
pheochromocytoma
tumer on the adrenal / big cause of secondary htn
what does insulin resistance cause
vasoconstriction
complicated hypertension
complications start
malignant hyperension
rapid progression when diastolic goes above 140 and systolic is 210 but this can be either or
120 over 80
pre hypertension
peripheral vascular disease
conditions resulting in interference in blood flow to or from extremities
Deep vein thrombosis
starts with a clot that forms around a valve or and infection on the vein itself. this thrombosis sits there and stops curculation
orthostatic hyotension
-when you stand the heart can not keep up with the body demand
starts with venous pooling..
-decrease sv and cardiac output
-increase sympethetic activity
-heart tries to increase myocardial activity
-vasoconstriciton and arterial constriciton occure
corotic sinis syncope
increased parasympothetic system when you press on your corotic
vaso vagal syncope
push too hard which causes, vaso dilitation by the parasympathetic system, causing brady cardia from activaiton of the vegas nerve
cardiovascular shock
septic shock
neuro shock
anafilactic shock
types of shock
cardiovascular shock
get a hole in our closed system
septic shock and allergy
ruin high low system, dilate the vessels and create hypotension
biggest problems with shock
getting O2 to the cells and getting co2 away from cells
exam notes
cardiac and vessels
we do not need formulas
35 for mary aby
blue pron