Patho

Front 1

continuous murmur during systole and diastole and signs of pulmonary hypertension. If this condition is severe, permanent pulmonary hypertension may result if condition not corrected by two years of age

blood is shunted from the high pressure aorta to the low pressure pulmonary arteries. This results in pulmonary hypertension

Back 1

patent ductus arteriosus

Front 2

Blood normally shunts from the left atrium to the right, but may shunt from the right to left during periods of high venous return (for example exercise or stress).

There is little clinical manifestations of this condition unless the condition is severe. However, this condition markedly increases the probability of strokes because clots can easily be shunted into the systemic blood that goes to the brain.

Back 2

atrial septal defect

Front 3

blood is shifted from the high pressure left ventricle to the low pressure right ventricle (figures C moderate size defect and D large defect).

Clinical manifestations is pulmonary hypertension, insufficient systemic blood flow, harsh murmur throughout systole, left ventricular hypertrophy, and congestive heart failure due to excess venous return to the left ventricle. Note that in the large VSD right and left ventricular pressure become identical (normally right is lower than left)

Back 3

ventricular septal defect

Front 4

failure of the atrial and ventricular septum to properly form.


clinical manifestation including pulmonary hypertension, congestive heart failure, and systemic insufficiency are highly variable.
This condition is very common in children with trisomy 21 (Down syndrome) .

Back 4

atrioventricular canal defect

Front 5

large amounts of blood to shift from the high pressure right ventricle (because of the pulmonary stenosis and hypertrophy) to the lower pressure left ventricle. Therefore, the systemic arterial blood is not fully saturated with oxygen (decreases from 98% to 75% saturated).

Clinical manifestations: Sever cyanosis of the infant (blue color) because of the poor oxygen content of arterial blood. This permanently appears when the ductus arteriosus closes. Before, this time, brief periods of cyanosis may appear during crying and feeding. Systolic heart murmur present.

Back 5

tetratology of fallot

Front 6

failure of the right AV valve to form or only a small AV valve to form.

there is little or no blood flow from the right atrium to the right ventricle. Generally, a vetricular septal defect permits some blood to enter the right ventricle.
This results in mild to severe cyanosis depending on the amount of pulmonary blood flow. This condition becomes worse upon closure of the ductus arteriosus

Back 6

tricuspid atresia

Front 7

is failure of the aortic arch to properly form.
This results in narrowing of the aorta.

Back 7

coarctation of the aorta

Front 8

narrowing of the aorta is after the left subclavian, left common carotid, and brachiocephalic trunk (arteries that provide blood to the upper body) branches from the aortic arch and before the ductus arteriosus joins aorta.


Before, the ductus arteriosus closes the infant has high blood pressure and blood flow to the upper body (strong pulse in the carotid arteries and arms), but low pressure (weak pulse in groin area) to the lower body. Although the oxygen content of the blood to the lower body is low, it is sufficient to maintain function of these tissues.
After the ductus arteriosus closes, the lower body becomes very hypoxic because of the very low blood flow (no pulse of a very weak pulse in groin). This results in a metabolic acidosis (due to the lactic acid) and very high blood pressure in the upper body (exaggerated pulse in carotid arteries) because of the reflex initiated by the acidosis. The lower body often turns blue and cold because of the lack of blood flow.

Back 8

preductal coarctation

Front 9

The lower body becomes very hypoxic because of the very low blood flow (no pulse of a very weak pulse in groin). This results in a metabolic acidosis (due to the lactic acid) and very high blood pressure in the upper body (exaggerated pulse in carotid arteries) because of the reflex initiated by the acidosis. The lower body often turns blue and cold because of the lack of blood flow.

Back 9

postductal coarctation

Front 10

Failure of the left heart and aorta to properly develop. The left heart is very small and often deformed.
Clinical manifestations are severe hypoxemia, acidosis, and shock shortly after the closing of the ductus arteriosus.

Back 10

hypoplastic left heart syndrome

Front 11

Condition in which aorta arises from the right ventricle and pulmonary arteries arise from the left ventricle.

Severe cyanosis, hypoxia, and acidosis that develops when the ductus arteriosus closes (allows some mixing of blood). Before, closure of the ductus arteriosus the hypoxia may be mild.

Back 11

Transposition of the Great Arteries

Front 12

Pulmonary vein either directly or indirectly empties into the right ventricle. An atrial septal defect is also present. The results of this defect is excess pulmonary blood flow with greatly decreased aortic blood flow.

Clinical manifestations are mild to moderate cyanosis due to the mixing of oxygenated and unoxygenated blood and the low blood flow in the systemic system. Because of the high blood flow, the right heart can go into congestive heart failure.

Back 12

Total Anomalous Pulmonary Venous Connection

Front 13

there is only one artery leaving the heart. This artery then branches to form the pulmonary artery and aorta. A large ventricular septal defect is also present. In these conditions, the heart functions as a single unit (no right or left heart).
Clinical manifestations are mild to severe cyanosis dependent on the amount of pulmonary blood flow. Several days after birth the infant develops congestive heart failure.

Back 13

Persistent Truncus Arteriosus