Cardiorespiratory System

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Following birth, the function of gas exchange is transferred from the placenta to the lungs. Oxygen supply to the newborn infant depends upon the establishment of rhythmic breathing, expansion of the lungs with air, adequate pulmonary blood flow to pick up oxygen from the lungs, and systemic blood flow to transport oxygen to the tissues.

Normal respiration requires that the central and peripheral nervous systems involved in breathing are appropriately developed, that respiratory muscle function, especially of the diaphragm, is normal, and that the bony chest cage is normal both in size and stability. The airways are filled with fluid before birth, and this fluid must be effectively cleared to allow entry of air into the lungs. The presence of pulmonary surfactant is essential to reduce alveolar surface tension and facilitate lung expansion.

Oxygen is predominantly transported in the blood through its attachment to hemoglobin. Hemoglobin deficiency due to blood loss or hemolysis of red cells may thus reduce oxygen transport. Oxygen transport may also be reduced due to hemoglobin abnormalities, such as methemo-globinemia, which impair the oxygen-carrying capacity of the blood.

The proper circulatory pathways must also be established following birth in order to ensure adequate pulmonary blood flow. The normal increase in pulmonary blood flow after birth may be prevented by a failure of pulmonary vascular resistance to fall, as in persistent pulmonary hypertension of the newborn, or in congenital heart disease, where there is an obstruction of systemic venous blood flow into the lungs as occurs in pulmonary atresia. Furthermore, oxygen transport to the tissues may be inadequate because systemic arterial supply is reduced by myocardial failure, or by congenital heart lesions in which left ventricular output is impaired, as with severe aortic stenosis or aortic atresia.

Despite the complexity of these systems, the adaptations to birth usually occur uneventfully. The purpose of the resuscitation team is to prepare for those unusual occasions when the normal transition from intrauterine to extrauterine life does not proceed smoothly.

Pithed Frog Position

Figure 1.1. Acrocyanosis is the blue discoloration of the distal extremities noted in many normal infants, but it can be observed in older babies with cold stress, infection, or heart failure. Peripheral cyanosis of the hands and feet is a common clinical finding in normal infants in the first 24 hours of life, but may be a nonspecific sign of illness. This finding is the result of a combination of high fetal hemoglobin concentrations and relatively sluggish peripheral circulation from arteriolar vasoconstriction. Note that the infant's face, lips, and trunk appear pink. Spontaneous improvement always occurs. Gentle stroking induces a rapid vasomotor reaction resulting in the sudden dispersal of peripheral cyanosis.

Figure 1.2. This infant's trunk, face and extremities are cyanotic, indicating a reduced hemoglobin oxygen content of at least 5 g/dL. Cyanosis is easier to detect in infants with polycythemia dian in those with anemia, although oxygen saturation may be higher in the former and reduced in the latter.

Methemoglobinemia

Figure 1.3. Methemoglobinemia is a condition which results in oxidized iron in hemoglobin being rendered unable to carry oxygen. Though the partial pressure of oxygen may be normal, oxygen content is low. Compare the color of the normal infant on the left with the typical slate grey color of the methemoglobinemic infant on the right. Distress may not be evident in infants until methemoglo-bin is 50% of the total hemoglobin. Methemoglobinemia is most commonly caused by postnatal exposure to toxins, such as nitrates or aniline dyes, but can also be congenital.

Figure 1.4. Methemoglobinemia occurred in this infant after the administration of intravenous nitrofurantoin. Methemoglobin was 45% of the total hemoglobin, resulting in the slate grey color. Poor oxygen delivery can lead to severe metabolic acidosis. Treatment is intravenous methylene blue or ascorbic acid.

Figure 1.5. Differential cyanosis in an infant with congenital heart disease. Note the line of demarcation in the midabdomen showing the pink body proximally and the cyanosis distally (this infant had pink hands and blue feet). This occurs in infants with aortic obstruction (coarctation of the aorta, interrupted aorta) with a patent ductus arteriosus supplying the descending aorta.

Aorta Coarctation Infant

Figure 1.5. Differential cyanosis in an infant with congenital heart disease. Note the line of demarcation in the midabdomen showing the pink body proximally and the cyanosis distally (this infant had pink hands and blue feet). This occurs in infants with aortic obstruction (coarctation of the aorta, interrupted aorta) with a patent ductus arteriosus supplying the descending aorta.

Figure 1.6. Differential cyanosis in an infant with congenital heart disease. Note the demarcation line in the mid-abdomen, and that the proximal part of the body is cyanotic, but the distal portion is pink (this infant had blue hands and pink feet). In this infant, this was due to aortopulmonary transposition, coarctation of the aorta, patent ductus arteriosus and pulmonary arterial hypertension. Well-oxygenated blood from the pulmonary artery passes through the ductus to the descending aorta, but the ascending aorta receives poorly-oxygenated blood from the right ventricle.

Blood Red Cyanosis Blue

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Differential Cyanosis

Figure 1.7. The same infant as in Figure 1.6 showing the differential cyanosis at the mid-abdomen as well as the blue hands and pink feet.

Figure 1.8. This infant developed venous congestion and numerous petechial hemorrhages as a result of a nuchal cord, which is the cause of the red or plethoric face and head. Subconjunctival hemorrhages are also present.

Figure 1.9. Tight nuchal cords can cause excess venous pressure in the head, and result in the rupture of small capillaries in the face causing petechiae and suffusion. These findings typically resolve spontaneously in a few days.

Figure 1.10. Following a difficult breech extraction, there was injury to the spinal cord at C7. This resulted in marked hypotonia (the infant is lying in the "pithed frog" position). Note that the infant is crying, and that a normal infant would usually flex extremities when disturbed. The abdominal disten-tion is due to lack of abdominal muscle tone and an enlarged, paralyzed bladder.

Figure 1.10. Following a difficult breech extraction, there was injury to the spinal cord at C7. This resulted in marked hypotonia (the infant is lying in the "pithed frog" position). Note that the infant is crying, and that a normal infant would usually flex extremities when disturbed. The abdominal disten-tion is due to lack of abdominal muscle tone and an enlarged, paralyzed bladder.

Cardiorespiratory System

Figure 1.11. Erb's palsy is the result of trauma to the upper brachial plexus (nerve roots C4-7) at delivery. The infant's left arm is flaccid with the shoulder adducted and the arm internally rotated. The extended elbow follows down to a pronated forearm and flexed wrist. Spontaneous resolution is seen in 70 to 90% of cases within 30 days. Rarely is the injury permanent. Infants with Erb's palsy should have a chest radiograph taken to check for involvement of the ipsilateral diaphragm due to paralysis of the phrenic nerve (C3, 4 and 5).

Figure 1.12. Lack of fetal movement in utero can result in positional deformities of the chest wall. Positional deformities, per se, do not cause respiratory distress, but if the changes are due to neuromuscular or osseous problems, respiratory distress may occur.

Thoracic Dystrophy

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Phrenic Nerve Palsy

Figure 1.13. In the same infant as in Figure 1.12, note how the folded arm compressed the chest causing this change in the chest wall. Decreased fetal movement should alert one to neuromuscular conditions such as spinal muscular atrophy or myotonic dystrophy.

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Figure 1.14. This is an infant with asphyxiating thoracic dystrophy, an autosomal recessive condition which severely restricts chest growth. The congenital deformity of the chest due to the short ribs results in a small chest which limits pulmonary expansion and severely restricts respiration. Because of the small thorax, the whole liver lies in the abdomen, producing the rounded and enlarged appearance seen in this infant.

Figure 1.15. In the anteroposterior and lateral radiograph of an infant with asphyxiating thoracic dystrophy, note the thin, abnormally short, straight ribs and small chest wall with protuberant abdomen. This bell-shaped appearance occurs in a variety of conditions because of prenatal weakness of the muscles or a neurologic abnormality.

Figure 1.14. This is an infant with asphyxiating thoracic dystrophy, an autosomal recessive condition which severely restricts chest growth. The congenital deformity of the chest due to the short ribs results in a small chest which limits pulmonary expansion and severely restricts respiration. Because of the small thorax, the whole liver lies in the abdomen, producing the rounded and enlarged appearance seen in this infant.

Glioma Nasal
Figure 1.16. Nasal obstruction by a glioma in the left nostril caused respiratory distress in this infant. This neural tissue typically comes through the cribriform plate.
Nasal Obstruction Newborn

Figure 1.17. Choanal atresia results from blockage of one or both choanae and may present shortly after birth with cyanosis which is relieved when the infant cries. Unilateral choanal atresia may present later in life with the inability to breathe through one side of the nose. Narrowing occurs to some degree within the choanae of many infants. In this radiograph, contrast medium instilled into the nasal cavity did not reach the nasopharynx, indicating obstruction of the choana, most likely from atresia. Atresia is unilateral in 90% of cases (twice as frequent on the right side), and is more common in female infants. Associations occur with facial anomaly syndromes such as Apert's and Treacher-Collins, and with the CHARGE sequence (coloboma, heart disease, atresia of the choanae, retarded postnatal growth and development, genitourinary anomalies, and ear anomalies and deafness).

Ear Anomaly

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Figure 1.18. Macroglossia can result from trauma, hypothyroidism, storage diseases (such as Pompe's), Beckwith-Wiedemann syndrome, hemangiomas, and lymphangiomas, but occurs most often as an idiopathic finding. In the Pierre Robin sequence, the large tongue is exaggerated because of the mandibular hypoplasia.

Pierre Robins Picture Big Tongue

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Apert Syndrome

Figure 1.19. A lateral radiograph of die head and neck in an infant with Beckwith-Wiedemann syndrome shows the macroglossia which encroaches on the oropharynx with resulting respiratory distress. (Singleton, E., Wagner, M.)

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Responses

  • asmara hagos
    Is coarctation of the aorta cyanotic?
    8 years ago
  • Norberto
    What is the circulatory system(venous) of a frog?
    8 years ago
  • derek
    Is it normal for breast discoloration during pregnancy?
    8 years ago
  • sebastian
    What is frog position in new born?
    2 years ago

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