Anesthesia-related morbidity and mortality is higher in infants than adults, as well as in younger compared to older children. In particular, airway complications are more likely in very young infants. Critical events are highest in infants < 2 kg [Tay et. al. Paediatr Anaesth 11: 711, 2001]. The newborn period is defined as the first 24 hours after birth, and the neonatal period is defined as the first 30 days. The most critical period of time in a neonate’s life is from 24-72 hours

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Preoperative Checklist

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• Warm the room
• Peds Bear hugger
• Overhead warming lights
• Age appropriate headrest and monitors
• IV setup in room
• See patient early to determine need for premedication needs
• For latex precautions, use latex free gloves, black bag on circuit, latex-free IV setup (clear masks are OK, as are ETT, LMA, and tape

Cardiac[edit]

Neonates have reduced ventricular compliance and less ability to increase contractility [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 1202, 2006], thus are relatively dependent on heart rate to increase cardiac output. In fact, according to Barash, the neonatal heart is only capable of increasing CO by about 30% (the adult, by contrast, can increase CO by 300%). Bradycardia is thus particularly dangerous in the neonate. Hypoxemia, which can precipitate bradycardia, should be vigorously avoided. Neonates also have a diminished baroreceptor response to hypotension, and have difficulty mounting a tachycardiac response [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 1202, 2006]

Pulmonary[edit]

Neonatal oxygen consumption (per kg) is 2-3 times that of the adult. Unfortunately, their closing volume (the volume at which alveoli begin to close, producing a shunt) is within the range of normal tidal volumes, thus small changes in lung volume (ex. laryngospasm) can lead to shunting and desaturations. Desaturation in the infant can be EXTREMELY rapid

N.B.: alveolar closing can occur even while intubated. If a neonate drops its lung volume enough to lead to alveolar closing, it may appear that the infant has been extubated or main-stemmed, because resistance to ventilation will be so high. In fact, the infant remains intubated – the only successful treatment is often either lidocaine (do not exceed 1.5 mg/kg) or paralysis

Infant tidal volume is actually the same as adults (7 cc/kg),it is their respiratory rate that makes up for a high VO2. As RR is 30-50, infant induction and recovery are much more rapid than with adults. Infants also fatigue more quickly than adults because they have a lower fraction of Type 1 muscle in their diaphragm, and their chest walls, which are highly compliant, are less efficient

Airway[edit]

Neonates are obligate nose breathers, thus choanal atresia can be life-threatening. The large tongue of the neonate obscures DL and can make ETT placement more difficult. Note also that the neonatal glottis is at C4 (as opposed to C5 in adults), thus the angle between the oropharynx and the laryngopharynx is more acute, making visualization more difficult – whether or not the glottis is truly more “anterior” is irrelevant, as the only thing which matters is the angle of visualization. The narrowest portion of the airway conduit is at the cricoid cartilage, which can lead to long-term ventilatory problems if damaged. The infant’s occiput is also problematic, as it makes direct visual alignment more difficult (attempt to rectify with a neck roll)

Neonatal Endotracheal Tube Size[edit]

Neonatal Endotracheal Tube Depth[edit]

For preemies and neonates (cm) = weight (in kg) + 6

Miller Blades

• < 32 weeks: 00
• Term: 0 (< 3 kg)

Neonatal LMA Size[edit]

LMA sizes ~ weight (kg) / 20 + 1 (round to nearest 0.5)

Cardiovascular[edit]

Fetal circulation is made of three shunts: 1) foramen ovale 2) ductus arteriosus and 3) placenta. Oxygenated placental blood travels up the IVC and once in the right atrium hits the crista dividends (CD) – the CD directs this oxygenated blood through the foramen ovale, into the left atrium, ventricle, and into the brain and upper extremities. Less-oxygenated blood returns via the SVC, and is directed by the crista dividends (CD) into the right ventricle, to the pulmonary artery and through the ductus arteriosus (pulmonary vascular resistance is high because of low pO2, low pH, and filled with fluid) where it then travels towards the lower extremities

Note that while earlier animal data suggested that cardiac output changes occur ONLY in response to changes in heart rate, other animal data suggests that the Frank-Starling mechanism is in fact intact in the neonate [Kirkpatrick SE et. al. Am J Physiol 231: 495, 1976]. Thus, LVEDP, while possibly not as significant as heart rate in the neonate, still may play a role in determining cardiac output

Pulmonary[edit]

At birth, air-filled lungs decrease PVR rapidly, and oxygenated blood closes the ductus arteriosus (which shunts RV blood into the lungs and LA, thereby increasing LA pressure and closing the foramen ovale. Normalization of PVR is a gradual process, however, and takes a full 3-4 days to complete. Anatomic closing of the DA/FO actually takes months. An autopsy study of 965 patients showed that 20% of people aged 30 and older actually still have a PFO [Hagen PT et. al. Mayo Clin Proc 59: 17, 1984]

Pulmonary normalization occurs rapidly – normal tidal ventilation is established within 10 minutes, and normal FRC is achieved by 20 minutes. In preterm infants (< 28 weeks), normalization of cardiopulmonary status can be accelerated by a single dose of dexamethasone within 2 hours of delivery [Kopelman AE et. al. J Pediatr 135: 345, 1999]

95% of infants should have a closed DA by 4 days of life. According to Reller et. al., prematurity is not a risk factor for a PDA, although asphyxia and respiratory distress syndrome are. Surprisingly, Reller’s group only found an 11% incidence of PDA in premature infants with RDS and no history of asphyxia [Reller MD et. al. J Pediatr 122: S59, 1993]

Another common respiratory pathology is persistent pulmonary hypertension, which can occur spontaneously or develop secondary to meconium aspiration, sepsis, pneumonia, RDS, or congenital diaphragmatic hernia. Note that the neonatal respiratory smooth muscle is extremely sensitive to low pO2, low pH (constricts), and nitrous oxide (dilates). Treatment goals are a pO2 > 50 mm Hg and a pCO2 < 60 mm Hg, which may entail surfactant, high frequency ventilation, ECMO, or inhaled N2O.

One relatively new mode of ventilation is Proportional Assist Ventilation (PAV). Available on Drager Evita 4, in PAV delivered flow and volume is proportional to patient demand and impedance. There is some evidence that once respiratory muscles are fatigued, giving too much support may retard recovery, as may too little support (muscle fatigue). By constantly adjusting the level of pressure support to cover abnormally increased loads caused by increased resistance or reduced compliance, we can allow the ventilator to do the “excess” work and let the patient do a normal amount of work. In PAV, the goal is to maintain a constant fraction of work per breath done by the ventilator. A study by Schulze et. al. suggested that in VLBW infants with RDS, PAV maintains similar arterial oxygenation with lower airway and transpulmonary pressures [Schulze A et. al. J Pediatr 135: 339, 1999]

Intrauterine hypoxemia is a serious threat to the newborn’s pulmonary system, as it causes smooth muscle proliferation [Murphy JD et. al. J Pediatr 104: 758, 1984] and leads to meconium passage in utero, with subsequent obstruction. Previously, the standard of care was to intubate all infants with meconium at birth, but current recommendations are to suction the infant and only intubate infants with low Apgar scores (ex. < 7) [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 1185, 2006]

Summary of Pulmonary Differences[edit]

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Summary of Pulmonary Differences With Adults

1. Higher O2 consumption
2. Higher closing volume
3. Higher MV:FRC (ie have to maintain elevated RR)
4. Compliant ribs and less Type 1 muscle in the diaphragm

FEN/Renal[edit]

Neonatal kidneys experience increased blood pressure at birth, as well as decreased renal vascular resistance, which increase GFR over the course of 3-4 days. Still, at 1 month the kidneys are only ~ 60% mature. Neonates are called “obligate sodium losers” because they cannot fully respond to aldosterone and thus excrete less than 20-25 mEq/L of sodium in their urine (adults can dilute their urine down to 5-10 mEq/L)

Metabolic[edit]

Hypoglycemia can be problematic in SGA infants and infants of diabetic mothers, both of whom should have glucose monitored. There is, unfortunately, no consensus on what truly constitutes hypoglycemia in these patients [Cornblath et. al. Pediatrics 85: 834, 1990]. A study of 171 infants undergoing heart surgery with at least 8 years of follow up showed that in those undergoing circulatory arrest, higher glucose was not correlated with worse outcomes [de Ferranti S et. al. Anesthesiology 100: 1345, 2004]

Prematurity[edit]

Respiratory distress syndrome, apnea, hypoglycemia, hypocalcemia, hypomagnesemia, hyperbilirubinemia

Small for Gestational Age[edit]

Hypoglycemia, immature temperature control, thrombocytopenia, viral infection, congenial abnormalities

Large for Gestational Age[edit]

Hypoglycemia, birth trauma, hyperbilirubinemia, transposition of the great arteries

Anticholinergic Premedication[edit]

The decision re: whether or not to routinely premedicate neonates with anticholinergics is controversial – Jöhr, in a 1999 editorial, claims that he abandoned routine premedication for over a decade, with no negative consequences. Supporters of Jöhr point out that bradycardia is almost always due to hypoxemia, for which the appropriate treatment is oxygen, not medication. Proponents of routine premedication, however, point out that as delivery of IV medication is delayed in the face of bradycardia [Zimmerman G and Steward DJ. Anesthesiology 65: 320, 1986], anticholinergics must necessarily be given in advance [Jöhr M. Paediatr Anaesth. 9: 99, 1999]

Succinylcholine[edit]

Because SCh in neonates has such a high volume of distribution, the recommended dose is 3 mg/kg in neonates (and 2 mg/kg in children). Be VERY careful with a second dose, as the cholinergic effects can lead to bradycardia and arrest. Note that despite the blackbox warning, the incidence of hyperkalemic arrest in boys < 8 who receive SCh is 1:250,000 (mortality is 50%). According to Barash, the first treatment is epinephrine at 5-10 ucg/kg, as it stimulates the Na-K pump [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 1189, 2006], after which consider calcium, magnesium, bicarbonate, insulin, Kayexelate, and furosemide

Non-Depolarizing NMBDs[edit]

Rocuronium behaves similarly in the neonate as compared to the adult. Vecuronium, because it is metabolized by the liver (which is immature in the neonate), actually behaves more like a long-acting NMBD – in neonates and infants, vecuronium at 0.1 and 0.15 mg/kg maintains paralysis for 59 and 110 min, respectively [Meretoja OA. Br J Anaesth 62: 184, 1989]. It has no effect on blood pressure [Miller RD et. al. Anesth 61: 444, 1984], as opposed to pancuronium, also long-acting, which can lead to hypertension and tachycardia [Cabal LA et. al. Pediatrics 75: 284, 1985]

Reversal[edit]

If edrophonium is used, because of its rapidity (peak effect in ~ 2 mins), atropine must be given prior. Neostigmine, by contrast, peaks at 10 mins, thus it is acceptable to give glycopyrrolate at the same time

Opiates[edit]

Morphine is generally avoided in neonates because of the potential for prolonged respiratory depression. Fentanyl at high doses (25-50 ucg/kg) can also produce postoperative respiratory depression. From a cardiovascular standpoint, opiates are thought to be relatively benign, but in the neonate, two considerations must be taken into account – first, fentanyl has cholinergic side effects which can lead to bradycardia, and second, all opiates are mild vasodilators. This does not mean that fentanyl should be avoided, only that it should be administered carefully – Yasterman’s study of 10-12.5 ucg/kg (in 2.5 ucg/kg boluses) showed that both heart rate and SBP decreased, but according to Barash not outside the realm of stability [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 1190, 2006]

Three major considerations are 1) hemodynamic control required [if the neonate requires resuscitation, consider using opiates and ketamine (as opposed to volatile anesthetics or propofol) to protect cardiac output] 2) postoperative pain relief [strongly consider a combined regional/general technique] and 3) postoperative respiratory function [extubated vs. intubated, if an attempt at extubation will be made, take this into account when selecting anesthetic agents]

All things being equal, endotracheal intubation is preferred as it can be difficult to accomplish in an emergency. Note that awake intubations run the risk of intracerebral hemorrhage (which neonates are already at relatively high risk for).

MAC requirement[edit]

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MAC requirements in the newborn are identical to those in mature adults, however they increase by ~ 50% at 6 months of age according to Barash [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 1191, 2006]. Data from halothane experiments based on 24 infants suggests that the MAC of neonates is 25% less than that of infants [Lerman J et. al. Anesthesiology 59: 421, 1983]. In contrast to the above, metanalysis of isoflurane, sevoflurane and desflurane requirements show no peak at 6 months of age, but decreasing MAC requirement from birth onwards. Br. J. Anaesth. (2003) 91 (2): 170-174. doi: 10.1093/bja/aeg132 . The theoretical, non-clinical study by Mazoit is frequently cited, including by Barash, but appears to be in conflict with clinical data. (Paediatr Drugs. 2006;8(3):139-50. Pharmacokinetic/pharmacodynamic modeling of anesthetics in children: therapeutic implications. Mazoit JX)

Extubation[edit]

When deciding whether or not to extubate, check for signs of being awake (crying [must be visualized, cannot be heard when ETT in place], eyes open, grasping for tube)

Extubation Criteria in Infants

1. Crying (must be visualized, cannot be heard when ETT in place)
2. Eyes open
3. Grasping for tube

Regional techniques are becoming more popular. Interestingly, infants do not develop hypotension following spinal anesthesia (mechanism not fully understood), but rather develop respiratory depression and hypoxemia

Caudal blocks are particularly popular, and can provide 6-8 hours of analgesia. 0.25% bupivacaine is approved in infants, and 0.25% ropivacaine is used off-label, both with 5 ucg/mL epinephrine. Clonidine is not routinely added to infants because there is some debate about whether or not it contributes to post-operative apnea [Fellman C et. al. Pediatr Anaesth 12: 637, 2002; Breschan C et. al. Pediatr Anaesth 9: 8, 1999]

Post-Operative Apnea[edit]

Post-operative apnea is a serious concern in the neonate, particularly if there is a history of prematurity, prior apneic episodes, bradycardia, congenital defects, anemia, or chronic lung disease (ex. respiratory distress syndrome). Infants have a lower percentage of type I fibers and are at risk for fatigue. Residual anesthetic agents may also contribute.

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Treatment may be as simple as tactile stimulation with blow-by oxygen, although if this is not adequate caffeine may be required. Caffeine is an adenosine-inhibitor, and can increase central respiratory drive, increase sensitivity to CO2, and improve muscle contractility [McNamara DG et. al. Paediatr Anaesth 14: 541, 2004]. A Cochrane Database Review of methylxanthines for the prevention of apnea in prematurity (five studies) suggests that methylxanthines are effective at reducing post-operative apnea from days 2-7 after initiating treatment [Henderson-Smart DJ et. al. Cochrane Database Review, CD000140, 2001]. Caffeine appears to be slightly less effective than theophylline but with a better side effect profile (note, also, that the utility of methylxanthines for non-premature infants is still a matter of debate [McNamara DG et. al. Paediatr Anaesth 14: 541, 2004]). As a last resort, endotracheal intubation and mechanical ventilation are used.

Consider a spinal or regional technique in these infants – one prospective, randomized study of 36 former premature infants showed a reduction in apnea from 36% to 0% [Welborn LG et. al. Anesthesiology 72: 838, 1990]. A smaller study of 18 ex-premature infants showed no change in central apnea in spinal vs. GA, but the GA cohort had lower minimum HR and SpO2 values [Krane EJ et. al. Anesth Analg 80: 7, 1995]. Note that the addition of sedation (ketamine) to spinal anesthesia in the Welborn study significantly worsened the incidence of apnea [Welborn LG et. al. Anesthesiology 72: 838, 1990].

Prenatal Cocaine Exposure[edit]

A study of 16 neonates exposed to cocaine in utero suggested that cardiac output was reduced on the first day of life, but returned to normal on day 2 [van de Bor M et. al. Pediatrics 85: 30, 1990]. A study of 214 infants exposed to cocaine in utero showed a 3.7-fold relative risk of cardiovascular abnormalities [Lipshultz SE et. al. J Pediatr 118: 44, 1991]. Thus, in neonates exposed to cocaine, consider delaying surgery to the second day of life, if possible, and have a high suspicion for cardiovascular abnormalities.

Cote combined data from eight prospective studies (255 patients) to develop an algorithm based on gestational age, post-conceptual age, apnea at home, size at gestational age, and anemia [Cote CJ et. al. Anesthesiology 82: 809, 1995]. Cote’s data showed that the incidence of apnea following inguinal hernia repair did not fall below 5% until gestational age reached 35 weeks and post-conceptual age reached 48 weeks, and that the incidence of apnea following inguinal hernia repair did not fall below 1% until gestational age reached 32 weeks and post-conceptual age reached 56 weeks (or post-gestational 35 weeks with post-conceptual 54 weeks). Any infant that exhibits apnea, has a history of apnea, or is anemic, should not undergo outpatient surgery

Sudden Infant Death Syndrome[edit]

Most common cause of death in infants from 1 to 12 months of age. Risk factors for SIDS include low birth weigiht, maternal smoking or cocaine use, young maternal age, and low socioeconomic status [Gibson E et. al. Pediatrics 96: 69, 1995]. There is no relationship between apnea of prematurity and SIDS [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 1193, 2006], and there is no evidence that general anesthesia plays a role in SIDS [Steward DJ. Anesthesiology 63: 326, 1985]. The American Academy of Pediatrics recommends that infants be placed on their back or side while sleeping [Kattwinkel J et. al. Pediatrics 93: 814, 1992]

Retinopathy of Prematurity (ROP)[edit]

Incidence has increase as survival rate for extremely premature infants rises. Repair may require several procedures under general anesthesia. As hyperoxic vasoconstriction of retinal vessels may be a contributing factor, the anesthesiologist is faced with the decision of what FiO2 is acceptable – Flynn’s study of 101 premature infants showed that the OR for ROP was 1.9 for every 12 hours that transcutaneous O2 was > 80 mm Hg [Flynn JT et. al. NEJM 326: 1050, 1992], thus 50-80 mm Hg tcPO2 are often recommended [Phelps DL NEJM 326: 1078, 1992] – this corresponds to an SpO2 of 90-95%

Maintenance Requirements in Children[edit]

Replacement of Losses[edit]

Intraoperative Glucose[edit]

Infants: 4 mg/kg/min = 240 mg/kg/hr maintenance requirements
D5 = 50 mg/mL
Delivery of D5 @ > 4 mL/kg/hr may lead to hyperglycemia

Medications for Children[edit]

Preoperative Medication in Children[edit]

Resuscitation Medication in Children[edit]

• Epinephrine = 10-100 ucg/kg for arrest (100 ucg/kg in ETT), 1-4 ucg/kg for hypotension
• Atropine = 0.01 – 0.02 mg/kg (0.3 mg/kg in ETT) – actual dose 0.1 – 1 mg
• Adenosine = 0.1 mg/kg (max dose 6 mg)
• Lidocaine = 1-1.5 mg/kg
• SCh = 2-3 mg/kg
• Rocuronium 1 mg/kg
• Calcium chloride = 10-20 mg/kg (dilute to 10 mg/cc or else veins will sclerose, try to give centrally if possible)
• Bicarbonate = 1 mEq/kg (dilute to 1 mEq/cc or else veins will sclerose)
• Naloxone = 0.1 mg/kg
• DEFIBRILLATION = 2 J/kg (can increase up to 4 J/kg)

Preoperative Medication in Children[edit]

• Midazolam 0.05-0.1 mg/kg IV (0.5-1 mg/kg PO, 15 mg max)
• Methohexital 1-2 mg/kg IV (25-30 mg/kg PR, 500 mg max)
• Ketamine 1-2 mg/kg IV, 10 mg/kg IM, 5-8 mg/