Neonatal - M5

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Increases in neonatal heart rate (HR) lead to a near linear increase in cardiac outputneonate has very limited (if any) ability to augment stroke volume in relation to volume status (preload),therefore making cardiac output essentially relative to heart rate.Neonates have limited myocardial contractile protein (especially in the left ventricle which was not pumping against much resistance (afterload) up until birth due to a low SVR in the fetus.In other words, increased preload (end-daistolic LV volume) does not result in an increased stroke volume, which is called "limited preload reserve")An increased parasympathetic response in relation to the sympathetic responseThe autonomic nervous system goes into high gear in response to hypoxia. Both the sympathetic and parasympathetic system responds. In adults, the sympathetic response is more pronounced with resultant tachycardia and hypertension. In neonates, and even small infants, the parasympathetic response is more pronounced due to two main reasons.First, the sympathetic nervous system is far less developed than the parasympathetic system. Secondly the neonatal myocardium and baroreceptor reflexes are less responsive than adultslow FRC/VO2 ratio as compared to adultsWhatever the case it seems that it is the increased oxygen consumption more than a possible decreased FRC that is the primary driver of rapid desaturations.Type 1 fibers are fatigue (twitch) resistant and responsible for endurance and less likely to fatigue.The lower proportion of these fibers in the diaphragm (and intercostals) puts neonates at a disadvantage (as compared to adults) when dealing with respiratory distress, as they are (more) prone to tire out.In neonates, the compliance of the lungs is low (due to incomplete alveolar development), which can be thought of it having a greater affinity to collapse upon itself (in other words, takes a higher air pressure to expand). On the other hand, the chest wall compliance is increased because the rib cage is cartilaginous (and flimsy).Why does this matter: with a lung that has a strong tendency to collapse upon itself and a chest wall that is too weak to effectively prevent the lung from pulling inward there are lower residual volumes (RV) at the end of expiration. This means that FRC (residual volume + expiratory reserve volume) is decreased (depending on the source you read!)*.Therefore, the more compliant the chest wall is, the less well it can prevent the lung from 'collapsing' at end expiration (low RV);therefore, the greater the decrease in FRC.both hypoxic and hypercarbic drives are immature at birthNeonates have less ability to autoregulate flow through multiple vascular beds including the cerebral system. This inability is more pronounced with prematurity. The loss of autoregulation means that increased blood pressure (as with intubation or surgical stress) leads to proportionately more blood flow to the brain.High flow through the germinal matrix (a highly vascularized and fragile portion of the brain) can lead to bleeding and thus IVH.nonshivering thermogenesisinhibited by volatile anestheticsnormal neonatal glucose for a full-term infant can range as low as 30 mg/dLAfter 1 day of life, hypoglycaemia of the neonate is defined under 45 mg/dL, but this infant being 4 hours old, treatment should be heldAn infant born to a diabetic mother should be monitored carefully for hypoglycaemia(due to large amounts of glucose that crossed the placenta prior to birth stimulating excessive fetal insulin production)0.5 grams of dextroseAdminister 1 cc of D50 IV," Administer 2 cc of D25 IV Administer 5 cc of D10 IV"In newborns, the spinal cord ends at about L3after 1 year (and onward) ends at L1*.The dural sac ends at S4 in neonates and at S2 for 1 year olds and adults.Dexamethasone (and steroids in general) have numerous side effects including increasing blood glucose levels, especially in diabetics.The increased glucose which crosses the placenta, leading to hyperinsulinaemia of the newborn and thus neonatal hypoglycemia when the supply of glucose is interrupted after birth.The two most common strategies of neonatal ventilation for respiratory distress syndrome (RDS) are high frequency oscillatory ventilation (HFOV) and a pressure or volume limited synchronized mode of ventilation such as SIMV or AC.Inability to oxygenate newborns is an indication for ECMO so long as the course of ventilation has been relatively short (less than 2 weeks), the child is big enough (usually correlating to a gestational age of 34, which this child is), and a treatable, reversible course.HFJV has been shown to worsen neurologic outcome (intraventricular haemorrhage) in newborns with RDS.After 28 days RDS is called BPD. BPD is essentially a long-term sequelae of RDS and mechanical ventilation.Essentially, the inflammation, barotrauma, and high oxygen tensions lead to scarring and other dysplastic changes leading to chronic lung disease and often pulmonary hypertension.L/S of 2 is indicative of sufficient surfactant production by the fetal lung,while and L/S of 1.5 (or less) is notNeonates have a higher total water content and less proportionate muscle massA lipid soluble agent such as fentanyl and thiopental will redistribute to the muscle (and other major sinks) slower (because there is less muscle to redistribute to, which is responsible for much of the fast redistribution of these drugs).Propofol, another lipophilic drug does not seem to follow this pattern. A single dose of propofol redistributes faster in neonates due to the increased blood volume, and considerations for a smaller lipid-soluble sink do not seem to play as large a role for this drug, thus answer choice "Has a shorter duration due to faster redistribution".Because the blood volume of neonates is larger, a larger dose (mg/kg) is given which results in a duration of action identical to adults. (Confused yet, my head is spinning just writing this stuff!)A hydrophilic drug like muscle relaxants would require a larger initial dose as the water content is high in neonates, but since clearance of these drugs rely less on redistribution and more on actual drug metabolism.(So answer "Has a shorter duration due to faster redistribution" would not be correct for muscle relaxants in case you're wondering).With PRIS, propofol is assumed to inhibit proteins which allow the transfer of fatty acids into the mitochondria so that the mitochondria are essentially starved of its energy source. In non critically ill patients there is enough free glucose and amino acids available for energy in the absence of fatty acids (this is an oversimplification, but it'll get you through the boards).With PRIS, the decreased energy sources result in lactic acidosis and eventually when all energy sources are depleted, necrosis develops. That is why there is a metabolic acidosis in PRIS. For completeness, the free fatty acids increase an inflammatory and catecholamine (sympathetic) response leading to arrhythmias, and organ dysfunction. Muscle necrosis (which have a lot of mitochondria) leads to rhabdomyolyisis and renal failure.Infants are more sensitive to opioids, benzodiazepines, and barbiturates, in general, than older children and adults.This might be due to a more permeable blood brain barrier, smaller lipid soluble sink, or liver clearance and inactivation.Thiopental and propofol's decreased sensitivity is likely due to the increased blood volumerequiring an increased initial dose (although propofol metabolism is also probably increased in children too)For unknown reasons, higher doses of ketamine are needed in infants.First is volume of distribution (of the hydrophilic compartment) in which infants have a larger volume of distribution than older children, which, themselves, have a larger volume of distribution than adults. This means that the larger the volume of distribution, the larger the dose required would be (yet "All of the above" is incorrect - why? Keep reading). The other principle is that infants, for the most part, are more sensitive than older children to muscle relaxants, meaning a smaller dose is required.The exception to this last rule is succinylcholine which affects infants and older children about the same, yet because of the larger volume of distribution, infants require an increased dose.Masseter muscle spasm (MMS) following succinylcholine may represent MH in up to 30% (probably fewer) episodesindication to delay elective surgery (because of the high morbidity and mortality of MH).Masseter spasm is a self-limited phenomenon, and when ventilation is possible, it should be continued until the episode has passed.In the can-not-ventilate scenario of masseter spasm, the last thing one should do is give a long acting paralytic as the spasm may break before hypoxia ensues (otherwise an invasive airway should be placed).right hand is PRE-ductal.The ductus arteriosis in fetal circulation supplies non-oxygenated blood into the aorta prior to the left subclavian take-off of the aorta. This means that all circulation post-ductal (left hand and feet) can have a mixture of oxygenated blood from the left ventricle and unoxygenated blood from the ductus arteriosis.retinopathy of prematuritypathophysiology of the disease involves retinal artery constriction, followed by proliferation of abnormal vessels resulting in scar tissue and haemorrhage causing retinal detachment.For otherwise healthy infants,most authors suggest delaying elective surgery (particularly where the patient is discharged home) until the infant is 44-60 weeks (most favor above 50).For patients with apneic spells, or pulmonary disease (such as bronchopulmonary dysplasia),surgery should be delayed until the patient is at least 6 months oldPost-anesthetic apneic episodes are defined ascessation of breathing for 15 or more seconds, or apnea of any duration resulting in desaturation or bradycardia.There is no distinct time cut-off following surgery to when an apneic spell would be attributed to anesthesia, but large metanalyses have not looked past 24 hours, .so answer chic "55 week post gestational age infant with apneic spells 1 day after surgery" is likely to have consensus not to be due to anesthesiaIn the past non-non-vigerous newborns would have tracheal suctioning immediately. More recent guidelines (2015) state that the neonate should have positive pressure ventilation first.The reason for this is routine tracheal suctioning delays the intervention that is known to work (PPV) versus the one that has rather poor evidence (tracheal suctioning).Meconium aspiration can often lead to a chemical pneumonitis presenting withpulmonary oedema, hypoxia, and pulmonary hypertensionFor newborns, bradycardia is assumed to be oxygen deprivation.Therefore, for hypoxia without bradycardia (less than 100 beats/min), it is assumed the hypoxia is not as severe and supplemental oxygen (blow-by) is administered. When the heart rate is less than 100, positive pressure ventilation should be administered. When the heart rate is less than 60, chest compressions at 120/ minute should be started...BUT, the FIRST thing that should be done is mask ventilation.The chest compression to ventilation ratio is 90:30Tracheal epinepherine can be given at 10 times the IV doseTracheal epinephrine has been clearly demonstrated to be less reliable than the IV as a route.epinephrine doses are now recommended to be 0.01-0.03 mg/ kg.Because the tracheal route does have less predictability, guidelines allow for increased (0.1 mg/kg) doses to still be used in the tracheal routereview APGARNECBy far the most common pressor used in this situation has been dopamine, which is thought not to restrict blood flow to the gutVACTERLV: vertebral anomalies; A: anal defects; C: cardiac defects (especially VSD, ASD, TOF); T: TEF; E: esophageal atresia; R: Renal and radial atresia; L: other limbs.Intentional main-stem intubation, then backing the ETT out until bilateral breath sounds are heard, but not in the stomachCDHImmediate tracheal intubation is routine and usually done awake immediately after birth (without induction), as positive pressure ventilation should be avoidedCDHHFOVCDHPTX contralateral to herniaCDHpulmonary hypertension and ultimately right ventricular failureChoanal atresiaCHARGEABG 4 is the classic presentation of pyloric stenosis with a metabolic alkalosis and electrolyte deficiency (hypochloraemia and hypokalaemia) due to vomiting.This patient has multiple signs of hypovolaemic shock that is seen when patients present late and, therefore, chances are this patient is acidotic (do to decreased cardiac output and therefore oxygen delivery, forcing anaerobic metabolism with lactic acid production). Therefore, one would expect a metabolic acidaemia (with underlying metabolic acidosis and alkalosis).Pyloric stenosis is a medical not surgical emergencyOnce the patient is stabilized, an awake or RSI intubation is preferred as aspiration risk is very high. Some authors advocate orogastric suctioning (awake) prior to induction.No opioids should be given due to the patient's metabolic alkalosisPyloric stenosis results in metabolic alkalosis due to frequent vomiting (as described in Neo50). Respiratory compensation for metabolic alkalosis (with alkalaemia and alkalotic CSF) is decreased minute ventilation and retention of CO2. Administration of opioids following pylorotomy has an increased risk of respiratory failure by decreasing the drive to breath even further (dissolved CO2 in the CSF crosses into the medullablalock taussig shuntessentially acts as a surrogate for a patent ductus arteriosis (PDA) with left-to-right sided flowThe primary issue the BT-shunt addresses with TOF is the pulmonary (infundibular) stenosis which greatly limits blood flow to the lungs (through the pulmonary artery (PA)). Patients with very severe or total occlusion of pulmonary outflow rely on a PDA, as blood from the aorta will spill through the PDA and perfuse the pulmonary arteries (finally coming back to the left atrium as oxygenated blood).The BT-shunt creates a shunt ("a new PDA") from the right subclavian artery (or brachiocephalic) to the pulmonary artery, accomplishing the same thing I described for the PDA. This allows the patient to increase pulmonary flow and oxygen delivery so that growth can occur.Later on (2 months to 18 months) definite surgery is undertaken.For definite surgery the pulmonary outflow tract is resected to relieve obstruction and the VSD is closed.Glenn procedureIt is the anastomosis of the superior vena cava (SVC) to the pulmonary artery" is a Glenn procedure, which is used for some single ventricle pathologies, which also establishes pulmonary flow, except its venous to PA (SVC to PA) instead of arterial to PA (BT-shunt). The Fontan procedure often follows the Glenn later on and is where the IVC flow is dealt with to also feed the pulmonary artery."A new aorta is constructed utilizing resected pulmonary artery" is part of the Norwood procedure where patients with small aortas secondary to hypoplastic left heart syndrome (for example) have a new aorta formed out of the PA (now the RV is responsible for systemic arterial flow) and a BT-shunt is used for pulmonary flowraise the Hb by 1 g/dl,4 cc/kg of PBRCsMeningomyelocele is the most severe form spina bifida where both the meninges and spinal cord protrude through a vertebral defect and present with a meningeal sac with spinal cord elements within.These patients are very prone to infection with resultant meningitis therefore great care should be given to keep the meningeal sac clean and intact. Surgery should be performed within 48 hours to cover the exposed meninges.other associated concerns of meningomyelocelehydrocephalus posterior herniation with Arnold-Chiari