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1440 PART 5 ■ Anesthetic, Surgical, and Interventional Procedures: Considerations TABLE 86-3. Disorders Frequently Associated With Persistent Neonatal Pulmonary Hypertension Diagnosis Symptoms and Signs Investigations Treatment Congenital diaphragmatic hernia Meconium aspiration syndrome Birth asphyxia Septicemia Respiratory distress Displaced cardiac sounds, usually shifted to the right No breath sounds over one hemithorax, usually left side Scaphoid abdomen “Honeymoon” period History of intrauterine fetal distress Meconium stained amniotic fluid Meconium in pharynx and trachea Respiratory distress Chest wall retractions History of intrauterine fetal distress or difficult delivery Low APGAR scores Hyper- or hypotonicity Seizures Cardiovascular compromise Poor peripheral circulation Poor urine output Respiratory distress not always present Hypo- or hyperthermia Hypotonicity Cardiovascular compromise with poor peripheral circulation Poor urine output Respiratory distress not always present initially Chest x-ray diagnostic Meconium present at tracheobronchial suctioning Chest X-ray shows pachy bilateral infiltrates Cardiac and cerebral ultrasonography Cerebral function monitoring Elevation of liver enzymes Computed tomography on day 3 for prognostic reasons C-reactive protein White blood cell count Bacterial cultures Chest x-ray may show fine granular infiltrates iNO inhaled nitrous oxide; HFOV high frequency oscillatory ventilation; ECMO extracorporeal membrane oxygenation. In more severe cases: Intubation Mechanical ventilation Analgo-sedation Vigorous acid-base correction Surfactant replacement iNO, HFOV, ECMO No emergency surgery! If possible thorough tracheobron - chial suctioning Possible indication for partial liquid ventilation (For further treatment please see Congenital diaphragmatic hernia) Endotracheal intubation Mechanical ventilation Inotropic support Diuretics Acid-base correction Pharmacologic seizure control Avoidance of hyperglycemia Adequate antibiotics Respiratory support as needed Volume replacement Inotropic support Diuretics Myocardial Function The neonatal cardiac myocyte contains more noncontractile ele - ments, has a disorganized intracellular arrangement of the con - tractile proteins, and its shape is less elongated than in the adult. 29 This leads to a reduced capability of the neonatal myocardium to generate force. 30 The sarcoplasmatic reticulum and the T-tubular system are also immature, which leads to an increased dependence on extracellular calcium for contraction. 31 Developmental changes both in the cytoskeleton and the extracellular matrix make the neonatal myocardium less compliant, and both early diastolic relaxation and late diastolic filling are reduced compared to the adult. 32,33 While the overall number of ventricular myocytes is still increasing (hyperplasia) during the neonatal period, after that period further increase in ventricular mass depends only on physiologic hypertrophy. 34 Compared to adults, the neonatal myocardium is metabolically less effective in handling fatty acids, which makes carbohydrates and lactate its primary energy substrates. 35 It is also more resistant to hypoxia, 36 which might be explained by increased myocardial glycogen stores and higher rates of anaerobic glycolysis in the neonatal myocardium com pared to the adult. Better myocardial performance is also observed following an ischemic insult in the immature heart, 37 something which might be explained by less pronounced increase in resting tension during the ischemic insult compared to the adult myocar dium, thus, resulting in better preservation of myocardial energy stores. The parasympathetic innervation of the neonatal heart is considered to be more mature compared to the sympathetic system 38 and the expression of cholinergic receptors is maximal at birth and remains high during the neonatal period. 39 The time course for the maturation of the sympathetic nervous system is associated with great interindividual variability. At 3 months of age, the sympathetic nervous system can often be regarded as functionally developed but final maturation can be delayed until 1 year of age in certain individuals. The adrenergic plexus system is less developed, 40 which might explain the pronounced response to norepinephrine simulating denervation supersensitivity. 41 Circulating catecholamines are, thus, relatively more important for inotropic and chronotropic function in the neonate. The b- adrenergic receptors and the adenylate cyclase system are well developed in the neonate 38 but the coupling between the two might be reduced since direct activation of adenylate cyclase will produce a larger increase in inotropic response compared to b-receptor stimulation. 42 Birth is associated with very high levels of circulating catecholamine levels, 43 which most likely results in
CHAPTER 86 ■ Management of the Neonate: Anesthetic Considerations 1441 Figure 86-1. Progressive reduction in cardiac output during the first days of life. LVO (n 16), SV(n 16), and ICBFV (a .20) in the first 72 h after birth in healthy term infants. Mean and 1 SD. Reproduced from Winberg 61 with permission. near maximal adrenergic stimulation of the myocardium imme - diately after parturition. During this time, the functional reserve of the myocardium is limited and the myocardium responds poorly to further increases in demand. 44 During the first days of life, there is a progressive reduction in cardiac output (Figure 86–1) leading to an increase in functional reserve and an increased response to inotropic stimulation. 45 Reactions to Changes in Preload, Afterload, Inotropy, and Heart Rate Recent scientific evidence has demonstrated that cardiac output is not unaffected by changes in preload. 46–48 A direct relationship between neonatal stroke volume and cardiac output exists already immediately following birth, whereas changes in heart rate does not appear to have the major influence on cardiac output in this setting as previously believed (Figure 86–2). 46 The increase in stroke volume in response to volume loading exists already immediately after birth but will be more prominent towards the end of the neonatal period. 45 The inflection point of the Frank– Starling relationship might be at a lower filling pressure (8 mmHg) compared to adults (12–15 mmHg). Because of the limited ability to generate force by the neonatal myocardium and the reduced compliance the neonatal heart tolerates increases in afterload poorly 46,49 (Figure 86–3). This is most pronounced regarding the right ventricle but applies to the left ventricle as well. Right ventricular strain often cause leftward interventricular septal shift, which can limit the filling of the left ventricle. 50 With the possible exception of the immediate period following parturition, the neonatal myocardium responds to inotropic stimulation with an increase in cardiac output. However, the response is usually less pronounced compared to adults. The choice of the optimum inotrope can be debated but, according to clinical experience, dopamine, dobutamine, epinephrine, isoproterenol, and norepine - phrine all increase cardiac output. Choosing agents with less effects on afterload might have a theoretical advantage since the neonatal myocardium tolerates increases in afterload poorly. Heart rate has previously been perceived as the major factor affecting cardiac output in the neonate. This is, as described above, only Figure 86-2. Left ventricular stroke volume (SV) versus left ventricular output (LVO) in 16 term infants during the first 72 h after birth. partially true. 46 Relative bradycardia obviously reduces cardiac output, but increases in heart rate above approximately 180 to 190 bpm do not cause an increase in output, since higher rates limit diastolic filling time; hence, the stroke volume is reduced. Even at heart rates below 180 bpm, the supposed tight relationship between heart rate and cardiac output can be questioned in the early neonatal period (Figure 86–4). The optimal heart rate with regard to optimizing the hemodynamic situation will of course Figure 86-3. Left ventricular stroke volume (SV) versus systemic vascular resistance (SVR) in 16 term infants during the first 72 h after birth.
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Chapter 86

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