Cardiac Structural Defects



Cardiac Structural Defects









PERINATAL AND NEONATAL CIRCULATION

Labor benefits the fetus’ impending transition to life by moving fluid present in the alveoli during fetal development into the interstitial space and speeding up its absorption. In addition, by 34 weeks of gestation surfactant is produced, which prevents the alveoli from collapsing with expiration.

The first breath is taken in response to hypoxia at birth, reexpansion of the chest when vaginal delivery is complete, and changes in skin temperature when the neonate emerges from the womb. This initial breath causes the pulmonary artery blood flow to increase and the pulmonary vascular resistance to decrease. As the pulmonary vascular resistance falls below that of the systemic circulation, blood flow across the ductus arteriosus shifts from left to right. This initiates the functional closure of the ductus arteriosus. By the time the neonate is 8 hours old, right-to-left shunting has stopped, and the vessel closes completely by the time the infant is 1 to 3 weeks old.


During fetal life a one-way valve, the foramen ovale, permits shunting of blood from the inferior vena cava through the right atrium to the left atrium. At birth, left atrial pressure rises above right atrium pressure and closes the foramen ovale flap.

By 2 months of age the infant’s pulmonary artery has reverted from a thick-walled vessel to a thin-walled vessel and pulmonary artery pressure drops. If the infant continues to have left-to-right shunting, causing pulmonary overload, the signs and symptoms become apparent by 2 months of age.

Table 25-1 lists assessments and their significance for cardiac structural defects in the newborn.


CONGENITAL HEART DISEASE

Approximately 1% of neonates have congenital heart disease, the most common structural malformation observed. Maternal diabetes, alcohol use, excessive smoking, teratogen exposure, progesterone use, and maternal viral infections (rubella) are some of the causes of congenital heart disease.









Table 25-1 Assessments and Significance for Cardiac Structural Defects in the Newborn

























































Assessment


Significance


Left precordial bulge


Cardiomyopathy


Thrills


Murmur


Palpable fourth heart sound


Hypertrophic cardiomyopathy


Bounding pulse


Patent ductus arteriosus


Aortic regurgitation


Arteriovenous malformation


Fever


Anemia


Shock


Thready pulse


Reduced cardiac output


Severe aortic stenosis


Absent, weak, delayed femoral pulse


Coarctation of the aorta


Cyanosis (Assess lips, nail beds, and mucous membranes)


Low cardiac output


Hypothermia


Systemic venous congestion


Pulmonary obstruction


Acrocyanosis (bluish discoloration around the mouth)


Normal finding until skin has been exposed to the sun; does not mean cyanosis


Clubbing of fingers and toes


Cyanotic congenital heart disease


Usually appears after 12 months of age


Infective endocarditis


Chronic liver disease


Inflammatory bowel disease


Chronic pulmonary disease


Benign genetic variant


Dependent edema


High right heart pressure-tricuspid valve malfunction


Right-sided heart failure


Hepatomegaly (infant and child)


Right heart failure


Pulmonary edema related to left-to-right shunting (pulmonary congestion = hyperexpansion = pushing liver further below the costal margin )


Splenomegaly


Congestive heart failure


Infective endocarditis


Ascites


Congestive heart failure


Dextrocardia (heart on right side of chest)


Situs inversus totalis (all organs “switch” sides Heart shift alone = heart defects


Blue color on room air and on 100% O2


Heart disease (lung disease = color changes from blue to pink when on 100% O2)


60-62% pulse oximetry on room air and on 100% O2


Heart disease (lung disease = pulse oximetry changes from 60% to 99% when on 100% O2)


35-38 Pao2 (mm Hg) on room air and on 100% O2


Heart disease (lung disease = Pao2 changes from 35 to 120 when on 100% O2)

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Oct 17, 2016 | Posted by in NURSING | Comments Off on Cardiac Structural Defects

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