PEDS Flashcards
The oxyhemoglobin dissociation curve of the newborn is shifted to the left or the right? Why?
Left. Fetal Hgb does not bind with 2,3 DPG. Thus, the newborn’s oxyhe- moglobin dissociation curve will be shifted to the left. This gives the fetus the advantage ofloading more oxygen at low fetal oxygen partial pres- sures (fetal arterial PCh of20-30 mmHg). [Ped. Anesthesia, George Greg- ory, M.D., Vol!, p52j
What happens to the oxyhemoglobin disso- ciation curve during the first few months of life1 Why?
The oxyhemoglobin dissociation curve shifts right. As fetal Hgb is re- placed by adult Hgb (at 3-4 months of age, infants have increased levels of2,3 DPG as compared to adults), the infants l\0 increases (the curve shifts right) to approximate that of the adult, enhancing 0 2 delivery. [Gregory, Ped. Anesthesia, Vol!, p52]
An infant is considered premature if born before what gestational age and has what weight? In what five ways is the premature infant different from the full-term neonate?
Prematurity is defined as less than 38 weeks gestation and less than 2500 gm at birth. As compared to the term infant, the premature infant is less able to: (1) suck, (2) maintain body temperature, (3) swallow, (4) eat, and (5) sustain ventilation. [Gregory, Ped. Anes., pp30-31]
At what conceptual age is surfactant devel- oped?
Surfactant appears initially between 23 and 24 weeks gestational age and increases in concentration during the last 10 weeks of gestational life. [Miller, Anesthesia, 1994, p2451]
What pressure is needed to open airways at birth?
Inspiratory pressures more negative than 25-40 mm Hg are required to overcome the surface tension when opening the alveoli for the first time. [Guyton, TMP, 1996, pp1049-1050; Barash, Clinical Anesthesia, 1997, pl082]
Identify the two limitations of kidney func- tion in the newborn. What is the significance of these limitations?
GFR at birth is 15-30% of the normal adult on a weight basis, and the ability to concentrate the urine is diminished. Hence, infants do not toler- ate large volumes of water and salts because oflow GD\ and decreased tubular concentrating ability. [Davison, Eckhardt, and Perese, Mass Gen- eral, 1993, p387]
When do liver enzymes become completely functional in the neonate?
During the first week oflife the liver functions poorly and is incapable of conjugating significant quantities of bilirubin with glucuronic acid. Re- duced quantities of blood clotting factors are also synthesized. The cyto- chrome P450 enzyme system isfully functional at one month ofage. Sum- mary: Liver metabolism is decreased in the neonate until one month of age.[Guyton, TMP, 1996, ppl052-1053; Morgan and Mikhail, Clinical Anesthesiology, 1996, p730]
Where does the spinal cord end in the neo- nate?
The spinal cord of the newborn ends at the lower border of L3. [Ellis & feldman, Anatomyfor Anaesthetists. 8e. 2004 pp126]
What are the angles of the left and right bronchi in a child less than three years of age?
Left, 55 degrees. Right, 25 to 70 degrees. [Smith, Anes. for Infants and Children, p12, Adriani and Griggs]
Why is subglottic stenosis potentially more severe in the pediatric patient than in the adult?
The pediatric airway has a relatively small cross-sectional area in a nor- mal pediatric patient. With the presence of a subglottic stenosis, which may be congenital or acquired, even a small amount of swelling can rapid- ly occlude the opening. [Rasch and Webster, Clinical Manual of Ped. Anes., 1994, p19; Steward, Manual ofPed. Anes., 1995, p246; Authors]
What factors contribute to the decreased functional residual capacity (FRC) in the neonate and infant during general anesthe- sia?
The chest wall in infants is less rigid (more compliant) because ribs are cartilaginous and not bony. In addition, the boxlike configuration of an infant’s thorax permits less elastic recoil than the dorsoventrally flattened thoracic cage of the adult does. Additionally, an infant is more vulnerable to muscle fatigue, which may further decrease the stability of the chest wall. As a result of all these factors, an infant’s chest wall is extremely compliant. The net effect of the compliant chest wall and the poorly com- pliant lungs is a reduced functional residual capacity (FRC). [Miller, Anesthesia. 6e. 2005 pp2842; Davis & Motoyama, Smith’s Anes. for In- fants and Children. 7e. 2006 pp34; Cote, PA1C. 3e. 2001 pp13]
In newborns, the closing capacity is higher than FRC. What does this mean?
Some airways close during the expiratory phase of normal tidal breathing. [Barash, Clinical Anesthesia, 1997, pp1095-1097]
How is the in children calculat- ed? What is the dead-space of a 30 kg child?
Dead-space is 2.0-2.5 mL/kg. Multiply patient weight by 2.0 or 2.5 to get dead-space. The dead-space of a 30 kg child is 30 kg x 2 mL!kg = 60 mL. [Davison, Eckhardt, and Perese, Mass General, 1993, p568; Barash Hand- book, Clinical Anesthesia, 1997, p407; Barash, Clinical Anesthesia, 1997, p1097]
What is the tidal volume of a neonate in mL/kg?
A neonate should have a ventilator setting for tidal volume of7 mL!kg (6-8 mL/kg is the normal range). This is the same as the adult range. [Barash, Clinical Anesthesia, 1997, p1097]
What is the minute volume per kg for the neonate?
Tidal volume in the neonate is 7 mL/kg and respiratory rate is 30-50 per minute. Ventilation “” tidal volume x respiratory rate. An estimate of minute ventilation in the neonate is: minute ventilation::::: 7 mL!kg x 30- 50 per minute= 210-300 mL!kg/min. 250 mL!kg!min is a reasonable nwnber to remember. Minute ventilation is 250 mL!kg. [Barash, Clinical Anesthesia, 1997, p1097; Authors]
Calculate the minute volume of a newborn who weighs 3 kg and has a respiratmy rate of 40 breaths per minute?
Minute volume::::: respiratory rate (breaths per minute) x tidal volume. Tidal volume is 7 rnL!kg (tidal volume is the same in the adult and the infant). If respiratory rate is 40 and the newborn weighs 3 kg, minute ventilation is 40 x (3 kg) x (7 mL!kg) = 840 mL/min. [Clinical Anesthesia, 2e, 1992, Barash, p1314]
How does chest wall compliance and pul- monary (lung) compliance differ in the in the neonate compared with the young, healthy adult’
In the neonate, chest wall compliance is increased and pulmonary coiTt- pliance is decreased. This means the chest wall is easier to distend (it is less rigid) but the lung is more difficult to distend (it is more rigid). [Bell and Kain, Peel. Anes. Handbook, 1997, p113]
What is the length of the infant trachea from the cords to carina?
The length of the trachea (vocal cords to carina) in infants and neonates and children up to one year of age varies from 5-9 em. [Cote, PAIC. 3e. 2001 pp92]
What is the distance from the teeth (alveolar ridge) to midtrachea in the newborn? In the infant who is six month to one-year-old? In the two-year-old, three-year-old, and four- year-old?
Newborn::::: 10 cm;6 mo to 1yr = ll cm; 2yr= 12 cm; 3yr::: 13-14 cm; 4 yr = 15 cm; 5 yr = 15-16 cm. [Cote, PAlC. 3e. 2001 pp93t]
lis the infant larynx located higher, at the same, or at a lower level in the neck com- pared to the adult larynx? Identify the level of the infant larynx.
The infant larynx is located higher in the neck, at the level of C3-4 than in the adults, where the larynx is located at the level of C4–5. Author’s com- ment: I find these text statements somewhat misleading-as you know, the cricoid cartilage-certainly part of the larynx-lies at C6, and many texts (Miller, for example) state that the adult larynx ranges from C3-C6. Perhaps the more accurate statement is: the thyroid cartilage is located at C3–4 in infants compared to C4-5 in adults. [Miller & Stoelting, Basics. 5e. 2007 pp233; Cote, PAIC. 3e. 2001 pp81; Authors]
How does the longue differ in the child compared with the adult?
A child’s tongue is relatively larger in proportion to the rest of the oral
cavity, compared to the adult tongue. [Cote, PAlC. 3e. 2001 pp81 I
Why are infants more prone to airway ob- struction?
Infants have a proportionately larger tongue than adults. [Gregory, Ped.
Anes., 2002, p223]
What part of a child’s airway has the small- est diameter?
The cricoid cartilage is the narrowest part. [Davison, Eckhardt, and Perese, Mass General, 1993, p434; Morgan and Mikhail, Clinical Anesthe- siology,1996,p730;Miller,AHesthesio, 1994,p2l01]
What is the blood volume (mL!kg) of the preterm neonate, term neonate, infant, child, and adult? What is the estimated blood volume of a 3.5 kg neonate?
Pre term neonate) 95-100 mL!kg; term neonate, 85-90 mL/kg; infant, 80 mL!kg; child, 75 mL!kg; adult, 65-75 mL!kg. The estimated blood volume of a 3.5 kg term neonate is: 85-90 mL!kgx 3.5 kg= 297.5-315 mL. [Da- vison, Eckhardt, and Perese, Mass General, 1993, p387; Morgan and Mikhail, Clinical Anesthesia, 1996, p7281
What is the hemoglobin (Hgb) concentra- tion at 2 weeks of 2-3 months of age? 2 years of age?
At 2 weeks, Hgb is !3-19 gllOO mL blood; at 2-3months, Hgb is less than !O-Il g/100 mL blood; at 2 years, Hgb is less than 12.5 gllOO mL blood. [Bell and Kain, Ped. Anes. Handbook, 1997, pp16, 2811
Describe the physiological anemia of the neonate and pediatric patient.
Normal hemoglobin levels in the full-term newborn infant range between 14-20 g/dL. The hemoglobin concentration progressively “bottoms out” during the 9th to 12th week reaching a minimum of 10-ll g/dL, with a hematocrit of 33%. Afler the third month ( 12 weeks) the hemoglobin levels stabilize at 11.5-12.0 gldL until about 2 years of age. After 2 years of age, the hemoglobin levels gradual increase to reach adult levels of 14.0- 15.5 gldL by puberty. [Cote, PA/C, 2001, ppl9-20; Gregory, Ped. Anes., 2002, p124]
Compare the physiological anemia in the preterm neonate to the full-term neonate.
In preterm infants, the decrease in hemoglobin levels is greater and earli- er, reaching the minimum hemoglobin concentration of8 g/dL by 4-8 weeks (hemoglobin “bottoms out” earlier and lower). At about l year old, the preterm and full-term infants hemoglobin levels are comparable and pre term infants following the same progression, reaching normal adult levels at puberty. [Cote, PAIC, 200l, pp19-20; Gregory, Ped. Anes., 2002, p124]
Below what hemoglobin concentration is anemia sufficient to jeopardize oxygen carrying capacity (and hence cause you to cancel elective surgery) in the neonate? Infant older than three months?
Less than I3 g/dL in the newborn and less than 10 g/dL in the pediatric patient older than three months.(Steward, Manual ofPed. Anes., 1995, p3IS; Stoelting and Miller, Basics, 1994, p381 I
A three-month-old infant, who is scheduled for surgery, has a hemoglobin of 10.5 mg/dL. What action should be taken?
None; this hemoglobin level is normal for this age. At three months of age, hemoglobin concentration normally decreases to this level. “It is rare for infants to develop any clinically significant symptoms from physiolog- ic anemia of the newborn.” [Bell and Kain, Ped. Anes. Handbook, 1997, p282l
During the preoperative evaluation of a 6- month-old surgical candidate, you note physiologic anemia. What is a likely cause for the physiologic anemia?
he infant with physiologic anemia at 6 months of age is most likely a formerly premature infant (expremie). “Even at several months of age,
expremies remain anemic because of poor nutrition and delayed hemato- poiesis that is induced by earlier transfusions.” Reminder: the nadir (low point) of physiologic anemia typically occurs at 2-3 months for full-term infants. [Gregory, Ped. Anes., 4e, 2002, p373; Cote, PAIC, 3”1 ed., 2001, p20; Yemen, Ped. Anes. Handbook, 2002, p139]
How are maintenance fluid requirements calculated for the pediatric patient?
4 mL!kg/hr. for first 10 kg; 2 mL!kg/hr. for second 10 kg; 1 mL!kg/hr. for each additional kg. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p728]
For a 3-week-old, 4 kg newborn undergoing prolonged surgery, maintenance fluids should be delivered at how many mL!hr.?
Maintenance fluid delivery rate for a 4 kg newborn is: 4 mL/kg/hr. x 4 kg = 16 mL!hr. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p728]
What is the fluid deficit of a normal66lb child NPO for 5 hours? Hint: first calculate the weight of the child in kg.
The fluid deficit is 350 mL. There are 2.2lb per kg. 66lb divided by 2.2 Jb/kg = 30 kg. Maintenance fluid for 30 kg child = (4 mL!kg/hr. x 10 kg) + (2mL/kg/hr. x 10 kg)+ (1 mL!kg/hour x IO kg)= 40 mi./hr.+ 20 mL!hr. + 10 mL!hr. = 70 mL!hr. 70 mi./hr. x 5 hrs. = 350 mL deficit. [Rasch and Webster, Clin. Manual ofPed. Anes., 1994, pl49]
Pediatric fluid replacement for blood loss is best determined by which method of moni- toring?
Hematocrit. Blood loss is typically replaced with crystalloid (3 mL of lactated Ringer’s per mL of blood loss) or colloid (1 mL of 5% albumin per mL of blood loss) until hematocrit falls to a pre-determined level. [Mor- gan and Mikhail, Clinical Anesthesiology, 1996, p728; Pediatric Anes., pp475-476]
Why is the cardiac output in infants de- pendent on heart rate and not stroke vol- ume?
Infants cannot alter stroke volume, so the only way to alter cardiac output is to change heart rate. Stroke volume cannot be altered because of the low contractile mass per gram of cardiac tissue, which results in limited ability to increase myocardial contractility, and also because left ventricu- lar compliance is reduced which makes ventricular fil!ing difficult. [Ba- rash, Clinicnl Anesthesia, 1997, p1097]
What is the normal heart rate of the term infant?
Heart rate of the term infant is reported to be 100-180 beats per minute {Mass General). Bell and Kain indicate that the normal heart rate of the neonate is greater than 120 beats per minute. 120-180 beats per minute might be considered an appropriate range for the term infant. [Davison, Eckhardt, and Perese, Clinical Procedures of the Massachusetts General Hospital, 1993, p.438; Bell and Kain, Ped. Anes. Handbook, !997, p420; Authors]
List two ways the physiology ofthe cardio- vascular system of the neonate differs from that of the adult.
In the neonate: (1) cardiac output is heart-rate-dependent, and (2) left ventricular compliance is decreased. [Morgan and Mikhail, Clinical Anes- thesiology, 1996, p726]
At what age is basal metabolic rate normally the highest?
Basal metabolic rate (BMR) peaks somewhere between 6-12 months old. In a full-term infant, BMR rises progressively during the first 10 days of life. After the first few weeks of life, BMR decreases nearly linearly throughout life (Nagelhout & Zag!aniczny). However, if you look at calor-ic requirements, infants under 1year old require about 100 cal!kg/day, whereas older infants require 75 cal/kg/day, and adults require 35 cal!kg/day. [Nagelhout and Zaglaniczny, NA, 2001, p397; Gregory, Ped. Anes., 2002, p87]
Give four reasons why it is so difficult to keep newborns warm?
(l) Newborns readily lose heat because of their greater surface area to body weight ratio. (2) They cannot compensate by shivering. (3) They have limited subQ fat for insulation. (4) They have limited stores of brown fat and unstable thermoregulatory systems. [Davison, Eckhardt, and Perese, Mass General, 1993, pp387,512]
By what route do infants lose most of their body heat?
Most heat loss is lost by radiation. [Davison, Eckhardt, and Perese, Mass General, 1993, p389; Barash Handbook, Clinical Anesthesia, 1997, p330; Stoelting, PPAP, 1987, p638]
Newborns produce heal primarily by what mechanism?
Newborns produce heat by non-shivering thermogenesis by metabolism of brown fat. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p727; Steward, Manual ofPed. Alles., 1995, p37]
What is the significance of brown fat? Where is brown fat located?
Infants respond to cold stress by increasing norepinephrine production, which enhances metabolism of brown fat and increases body heat, i.e., chemical thermogenesis. Brown fat is located in the interscapular space and around large blood vessels, around the neck, behind the sternum, and around the kidneys and adrenals. [Steward, Manual ofPed. Anes. 4e. 1995 pp37]
What controls non-shivering thermogenesis in infants?
The autonomic nervous system activates non-shivering thermogenesis in infants. [Steward, Manual ofPed. Anes., 1995, p37]
INon-shivering (cellular) thermogenesis is a crucial heat -generating mechanism in the neonate and infant, as you know. At approx- imately what age does non-shivering ther- mogenesis cease to be clinically significant?
Clinically and physiologically significant non-shivering thermogenesis persists up to the age of 2 years. Non-shivering thermogenesis may con- tinue into adulthood, but generally is not a relevant and significant source of heat generation in the adult. [Davis & Motoyama, Smith’s Anes.Jor Infants and Children. ?e. 2006 pp162; Gregory, Pediatric Anes. 4e. 2002 pp67]
What is the best way to maintain an infant’s body heat? What is the best way to warm an infant in the operating room?
The best way to maintain an infant’s body heat is to maintain high ambi- ent temperature. Increasing operating room temperature is the best way to warm an infant. [Cote, PAIC. 3e. 2001 pp628]
Premature infants may require what ambi- ent temperature to maintain a normother- mic state?
26’C. [Cote, PAlC. 3e. 2001 pp628]
At what rate do infants consume oxygen? How does this compare with the adult?
Resting 0 2 consumption in healt-hy infants is 7 mL!kg/min (twice that of the adult). [Davison, Eckhardt, and Pcrese, Mass General, 1993, p387]
To what do preductal or postductal coarcta- tion of the aorta refer?
Coarctation of the aorta refers to a discrete narrowing of the aorta imme- diately distal to the origin of the left subclavian artery. A preductal coarc- tation refers to a coarctation in a neonate or infant in which the narrow- ing occurs proximal to the opening of the ductus arteriosus. Postductal coarctations supposedly present in adulthood long after closure of the ductus arteriosus. [Rasch and Webster, Clin. Manual ofPed. Anes., p435; Morgan and Mikhail, Clinical Anesthesiology, 1996, p402]
Should upper extremity blood pressure be monitored in the neonate with preductal coarctation of the aorta on the right or the left side?
Monitoring of blood pressure is best achieved in a patient with a preduc- tal coarctation by placing a catheter in the right radial artety. [Stoelting, Co-Existing, 1993, p52; Bell, Kain, and Hughes, Ped. Anes. Handbook, 1997, pp158-159]
Blood shunts through what two structures in the neonate with persistent fetal circulation?
Blood shunts through the ductus arteriosus and the foramen ovale. [Mor- gan and Mikhail, Clinical Anesthesiology, 1996, p702]
What causes the foramen ovale to close in the newborn?
The closure of the foramen ovale is due to the decrease in pulmonary vascular resistance and increased pulmonary flow that occurs as the infant takes his/her first breaths and the alveoli expand. The decrease in pulmo- nary vascular resistance is accompanied by constriction of the ductus arteriosus secondary to oxygenation. This results in an increase in pul- monary blood flow and an increase in left atrial pressure. The increased ptessureintheleftatriumshutstheflap, locatedontheleftsideofthefo- ramen ova/e. [Barash, Clinical Anesthesia, 1997, pl09I; Guyton, TMP, 1996, pl05l]
Name the physiologic factor most responsi- ble for closure of the ductus arteriosus after birth.
Nonnal closure of the ductus arteriosus occurs in response to increased arterial oxygen tension (PnOJJ, as well as to reduction in circulating pros- taglandins that follow separation of the placenta. (Realize that a number ofother substances such as eicosanoids and factors such as PaC02 and pH have been implicated, but that increased oxygen tension seems to be the major factor precipitating ductus arteriosus closure.) [Cot, PAIC, yd ed. 2001, p356; Gregory, Ped. Anes., 4th eel. 2002, p424]
What is a patent ductus arteriosus? When does the ductus arteriosus normally close?
Patent ductus arteriosus is the abnormal persistence in the newborn of blood flow through the ductus arteriosus, an opening between the pulmo- nary artery and aorta. Normally, the ductus closes within a few hours to a few days after birth due to changes in the pressures of the pulmonary vasculature. [Guyton, TMP, 1996, p1051]
Is the shunt of a patent ductus arteriosus right-to-left or left-to-right?
The shunt is left-to-right. [Stoelting, Co-Existing, 1993, p40]
With a patent ductus arteriosus, what cardi- ovascular changes occur?
A patent ductus arteriosus allows blood to flow from the aorta into the pulmonary artery. The additional blood is reoxygenated in the lungs and returned to the left atrium and left ventricle and this causes increased workload on the left side of the heart and left ventricular hypertrophy, and increased pulmonary vascular congestion and resistance. Most pa- tients are asymptomatic. [Stoelting, Co-Existing, 1993, p41]
hat hemodynamic alteration may wors- en (increase flow through) a left-to-right intracardiac shunt?
An increase in systemic vascular resistance (SVR) may increase left-to- right intracardiac shunt flow, such as occurs in atrial septal defect. Avoid interventions that may increase SVR in the patient with an ASD. [Mor- gan, Mikhail, and Murray, Clinical Anesthesiology, 4e, 2006, p481]
What is the probable problem if the pediat- ric patient has a systolic and diastolic murmur?
Patent ductus arteriosus. A continuous systolic and diastolic murmur is often the only manifestation of patent ductus arteriosus. [Stoelting and Miller, 1994, p260; Guyton, TMP, 1996, pp276-277]
Where are pulse oximeters placed on the neonate to monitor preductal and postductal oxygenation?
Preductal oxygenation should be measured with a pulse oximeter on the right hand orfinger. Postductal oxygenation should be measured with a pulse oximeter on the left foot or a left toe. [Cote, PAIC, 2001, p395; Duke, Secrets, 2000, p302]
What is the purpose of a preductal pulse oximeter in the neonatal patient undergoing cardiac surgery?
Measurements of arterial oxygen saturation taken at a preductallocation (right hand/finger) are a better index of neonatal cerebral oxygenation than are those taken at a postductallocation (left foot/toes). The right-to- left shunt at the ductus arteriosus persists for some time after birth and this shunt may affect oxygen saturation readings, thus preductal place- ment of the pulse oximeter is preferred. A postductal pulse oximeter may be used in addition to the preductal pulse oximeter to quantitate the severity of the right-to-left shunt. [Birnbach, Textbook Ob. Anes., 2000, p7l4; Norris, Ob. Anes., 1999, pp680-68l; Duke, Secrets, 2000, pp301- 302]
Where should arterial blood pressure be measured in a patient undergoing repair of a patent ductus arteriosus (PDA)?
The catheter for measuring blood pressure should be placed in a periph- eral artery such as the femoral. [Stoelting, Co-Existing, 1993, p 42; Au- thors]
Identify the best site to obtain arterial blood gases from in the neonate.
Arterial blood gases in the neonate are best obtained from the radial arte1y.ln additional to ease of access, this site will reflect preductal oxy- gen saturation, which better reflects cerebral oxygenation. [Gregory, Peel. Anes., 2002, p257]
Which two sites are to be avoided when obtaining arterial blood gases in the neo- nate? Why?
Arterial blood gases samples are usually not obtained from the brachial or femoral arteries. Obtaining blood samples from a brachial artery has been associated with nerve damage. Obtaining blood samples from a femoral artery has been associated with femoral head necrosis and limb shorten- ing. The artery of first choice for obtaining arterial blood gas samples is the radial artery. [Gregory, Ped. Anes., 2002, p257]
Identify 4 factors that may cause a neonate/infant to return to fetal circulation.
Persistent fetal circulation (or a return to fetal circulation) is common in pre term infants and infants with metabolic derangements (asphyxia, sepsis, meconium aspiration, congenital diaphragmatic hernia). Hypox- emia, acidosis, pneumonia, and hypothermia are 4 primary precipitating factors in persistent fetal circulation. The pathologic mechanism common to all4 factors is increased pulmonary vascular resistance (PVR) and to-left shunting. [Nagelhout and Zaglaniczny, NA, 2”’ eel. 2001, pll35; Gregory, Ped. Anes., 4th ed. 2002, pp424-425]
What is the usual cause of persistent pulmo- nary hypertension (persistent fetal circula- tion)? Is the shunt associated with persistent pulmonary hypertension left-to-right or right-to-left?
Hypoxia, acidosis, and other factors cause a high pulmonary vascular resistance; the resulting pulmonary hypertension causes blood to shunt from right-to-left. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p702; Barash, Clinical Anesthesia, 1997, p1092)
List three congenital defects in which there isaright-to-leftshunt.
(1) Tetralogy ofFallot; (2) pulmonary atresia with ventricular septal defect;and(3)patentforamenovale.[Miller,Anesthesia, 1994,pp1815- 1816)
What is the anesthetic concern for the pedi- atric patient undergoing repair of a ventricu- lar septal defect (VSD) without significant pulmonatyhypertension?
Ventricular septal defect (VSD) without significant pulmonary hyperten- sion should be managed to avoid arrhythmias, RV dysfunction, pulmo- nary vascular obstructive disease, and paradoxical embolus. [Kaplan, CardiacAnesthesia, 1999,pp809-810)
What is the anesthetic concern for the pedi- atric patient undergoing repair of a ventricu- lar septal defect (VSD) with significant pulmonary hypertension?
The patient with an unrepaired VSD and irreversible pulmonary hyper- tension often displays right-to-left shunting through the VSD (Eisen- menger’s physiology). Manipulations that may increase PVR can cause rapid deterioration and include hypoxia, hypercarbia, acidosis, hypo- thermia, atelectasis, sympathetic stimulation and polycythemia. Early closure ofVSD before I year old results in normal ventricular function and ejection fraction. [Kaplan, Cardiac Anesthesia, 1999, pp809-810)
A right-to-left intracardiac shunt is pre- sent in the patient with a ventricular septal defect (VSD with Eisenmenger’s syndrome). What hemodynamic alterations may worsen (increase shunt Oow) the right-to-left shunt ofVSD with Eisenmenger’s syndrome?
An abrupt increase in pulmonary vascular resistance (PVR) or a decrease in systemic vascular resistance (SVR) is poorly tolerated in the patient with ventricular septal defect {VSD). Avoid interventions that may increase PVR or decrease SVR in the patient with a right-to-left intracardiac shunt. [Nagelhout & Zaglaniczny, NA, 3’’ ed., 2004, p432)
List three conditions that increase right-to- left shunt (tetralogy ofFallot).
Acidosis, hypercarbia, and hypotension {decreased SVR) increase right-to- left shunt. In general, increases in pulmonary vascular resistance or de- creases in systemic vascular resistance (caused by acidosis or hypercarbia) increase right-to-left shunt. Volatile anesthetics and histamine release decrease SVR. [Stoelting and Mil!er, Basics, 2000, p258; Hurford, Bailin, Davison, Haspel, Rosow, Mass Gen Handbook, 1998, p411; Morgan and Mikhail, Clinical Anesthesia, 1996, p370)
List four congenital heart defects involved with tetralogy of Fallot (cyanotic heart dis- ease).
(1) Ventricular septal defect, {2) right ventricular outflow tract obstruc- tion (pulmonary stenosis), (3) right ventricular hypertrophy, and
(4) dextroposition (to the right) of the aorta with overriding of the ven- tricular septal defect. [Morgan, Clinical Anesthesiology, 1996, p370)
Does blood shunt right-to-left or left-to- right through the ventricular septal defect in tetralogy of Fallot (cyanotic heart disease)?
Blood shunts right-to-left, permitting unoxygenated blood to mix with oxygenated blood, resulting in cyanosis. [Morgan and Mikhail, Clinical Anesthesiology, !996, p370)
An infant has Tetralogy of Fallot (cyanotic heart disease). Which of the following arte- rial blood gas parameters will not typically be changed: 1’,02, pH, P,CO,?
pH and P.C02 are likely to be in the normal range. P,02 is usually marked- lydecreased (
What are the goals of anesthetic
management for the patient who has tetralogy of Fallot (cyanotic heart disease)?
The goals of anesthetic management should be to maintain intravascular volume and systemic vascular resistance (SVR). Increases in pulmonary vascular resistance also should be avoided. [Morgan and Mildlail, Clinical Anesthesiology, 1996, pp370-371]
What change in systemic vascular resistance and in pulmonary vascular resistance in- crease shunt in the patient with tetralogy of Fallot? What drugs increase shunt in the patient with tetralogy of Fallot by altering systemic vascular resistance or pulmonary vascular resistance?
Shunt increases when systemic vascular resistance decreases or pulmo- nary vascular resistance increases. Volatile anesthetics, drugs that cause histamine release, ganglionic blockers, alpha blockers, or other vasodila- tors (nitroprusside) decrease systemic vascular resistance, increase right- to-left shunt, and worsen arterial hypoxemia. Increased pulmonary vascu- lar resistance increases shunt in a child with cyanotic heart disyase. N20 increases pulmonary vascular resistance, which is detrimental to children with right-to-left shunts. [Greg01y, Pediatric Anes., 2e, p857; Stoelting, Co-Existing, 1993, p44]
What pharmacologic agent decreases a right to left shunt?
A decrease in the magnitude of a righHo-left shunt (tetralogy of Fallot is a right-to-left shunt) occurs if systemic vascular resistance (SVR) increas- es. Phenylephrine increases SVR and decreases a right-to-left shunt. [Stoelting and Miller, Basics, 2000, p258; Hurford, Bailin, Davison, Haspel, Rosow, Mass Gen Handbook, 1998, p411]
During the case, oxygen saturation decreas- es, apparently because of increased shunt* ing. The patient has tetralogy ofFallot. What agents might be selected to decrease shunt and increase oxygen saturation?
Intravascular fluid volume must be maintained with IV fluid
administration since acute hypovolemia will tend to increase the magnitude of the righHo-left intracardiac shunt. A n alpha- agonist drug such as phe- nylephrine must be promptly available to treat an undesirable decrease in systemic blood pressure caused by a decrease in SVR. [Stoelting, Co- Existing, 1993, pp44-45]
Will a intracardiac shunt theo- retically slow or accelerate inhalation induc- tion? Is the effect be clinically significant?
A right-to-left intracardiac shunt will theoretica!ly slow inhalation induc- tion, because less anesthetic is absorbed from the lung, and mixing will further dilute blood passing to the left, decreasing the arterial concentra- tion of the blood going to the brain, especially the less soluble agents. This effect is rarely problematic. [Fleisher, Anesthesia and Uncommon Disease, 5e, 2006 p91]
Will a intracardiac shunt theo- retically slow or accelerate intravenous induction?
An intravenous induction will be theoretically accelerated with a
right to left intracardiac shunt. [Fleisher, Anesthesia and Uncommon Disease, 5e, 2006 p91]
Will a intracardiac shunt theo- retically slow or accelerate inhalation indue· Lion? Why is this phenomenon rarely evi- dent clinically?
A inlracardiac shunt shou!d accelerate the speed of inhalation induction because the rate of transfer of anesthetic agent from the lungs to the blood is increased. However, this effect is rarely clinically evident because decreased delivery of anesthetic to the target tissues negates the increased uptake of agent with a left -to-right inlracardiac shunt. [Fleisher, Arwsthesia and Uncommon Disease, 5e, 2006 p9l; Barash, Clinical Anes- thesia, Se, 2006, pp1209-1210]
Will a intracardiac shunt theo· retically slow or accelerate intravenous induction? Why is this phenomenon rarely evidentclinically?
Intravenous induction should be slowed by a lefHo-right shunt; however, unless cardiac output is very poor, the effect is clinically irrelevant. [Fleisher, Anesthesia and Uncommon Disease, Se, 2006 p91; Barash, ClinicalAnesthesia,Se, 2006,pp1209-1210]
Where is the fistula usually located in a patient with a tracheal-esophageal fistula?
In 90% of tracheal-esophageal fistulas, the lower segment of the esopha- gus inserts just above the carina onto the posterior wall of the trachea. [Barash, Clinical Anesthesia, 1997, p1107; The Physiologic Basis ofSur- gery, 1993, p63; Yao and Artusio, Problem Oriented Patient Management, 1993]
Where is the proper placement of the endo- tracheal tube in a patient with a tracheal- esophageal fistula? Describe the procedure for intubating the patient with a tracheal- esophageal fistula.
The tip of the endotracheal tube can be placed just distal to the tracheal- esophageal fistula (between the fistula and the carina). The endotracheal tube can be inserted until it enters one or the other mainstem bronchi. Look for unilateral expansion of the chest and unilateral breath sounds. The endotracheal tube is then slowly withdrawn until bilateral breath sounds are present. [Barash, Clinical Anesthesia, 1997, pll07; Morgan and Mikhail, Clinical Anesthesiology, 1996, p735]
What is trachea malacia (also known as tracheobronchomalacia)? What patients are at risk for developing tracheomalacia?
Malacia” means abnormal softening of tissue, therefore tracheomalacia would be softening of the tracheal tissue, especially the cartilaginous rings. Tracheoma!acia is sometimes seen in neonates/infants, often in association with esophageal atresia (e.g., tracheoesophageal fistula, TEF) or with extrinsic compression by vascular anomalies or mediastinal mass- es. Tracheomalacia may also be associated with hyperthyroidism. [Bissonnette, Ped. Anes., 2002, p1203; Barash, Clinical Anesthesia, 4th ed. 2001, p1188; Barash, Handbook, 4th ed. 2001, p596; Authors]