Pediatrics

Question 1

Aspiration in CXR finding in kids vs adults? Why right sided aspiration is far less common in kids than adults?

Answer 1

Hyperinflation and air trapping on the LEFT lung with mediastinal shift towards the RIGHT

To figure out this question you need to make an educated guess between TWO possible answers (answers B & C), as answers A & D are nonsensical. Aspiration of foreign bodies result in two common lung pathologies: 1) air-trapping with resultant hyperinflation distal to the foreign body (a bit more common in children) or no air flow past the foreign body with resultant atelectasis and lung volume loss (a bit more common in adults). Since this patient had diffuse wheezing (indicative of obstructive air movement), air trapping is more likely. If the lung is hyperinflated, then the mediastinum will be pushed away towards the right (answer B). If the lung is atalectatic with volume loss, the mediastinum will be pulled towards the left (answer C). Also of note, children’s right mainstem takeoff tends to be more acute than adults making the mantra of right sided aspiration less common.

Question 2

Post extubation croup?

Answer 2

Following multiple episodes of trauma to the glottis (from the repeated direct bronchoscopy) the patient is having glottis oedema and essentially post-intubation croup, which responds well to racaemic epinephrine (see question 9). Peanuts, especially when fragmented, can lead to a chemical pneumonitis and ARDS (answer A), with hypoxia and high oxygen needs, but not stridor. Peanut fragements also would not cause stridor, more likely diffuse wheezing. Heliox might help in some situations of stridor (see Resp8), but answer C is clearly a better choice as it treats the underlying problem.

Question 3

17 year old girl with scoliosis has a Cobb angle of 65 degrees, which of the following co-morbidities are most likely:

Answer 3

Pulmonary hypertension

Pulmonary hypertension is secondary to restrictive lung disease which is due to an abnormal constricted, rotated thorax, due to scoliosis. The Cobb angle is a radiologic method to measure the severity of scoliosis (you will not be asked to calculate one, but its based on the greatest angle between any two vertebrae). Above 10 degrees, the spine appears scoliosed, but usually does not cause cardiopulmonary pathology until the angle is at least 60 degrees. Long-standing pulmonary hypertension can lead to cor pulonale. Surgical repair is often very bloody and has an increased risk of neurologic sequelae, mostly related to the spinal cord, not the brain (answers A & B). Answers C & D are completely unrelated as well. Mitral valve prolapse, not stenosis, has increased frequency in children with thoracic skeletal disorders (as well as a multitude of other associations).

Question 4

What’s the concern with retake back for bleeding post-tonsillectomy’s

Answer 4

Pulmonary aspiration on induction

The patient with the bleeding tonsil swallows massive amounts of blood and are essentially a full stomach. Aspiration of blood is not as dangerous as food or acidic stomach contents (see GI question 3), but can still lead to life threatening hypoxia depending on the volume. Patient cooperation (answer A) could be a problem due to both age and possibly anaemia. The other answers are unlikely a problem. As a side note, some authors recommend not to give patients undergoing tonsillectomy anti-emetics as this will delay the diagnosis of bleeding (since the patient may vomit blood, alerting the caregivers to a bleeding problem at that time.

Question 5

What tube type you should use if CO2 laser for laryngeal polyp excision?

Answer 5

Metal ETT

This is a question about airway fire risk. CO2 laser can ignite highly flammable gases such as oxygen and nitrous oxide, therefore either a metal ETT is preferred or no ETT at all (intermittent intubation and ventilation, for example). Metal tape can also be used, but is not as reliable as a metal ETT. The red rubber ETTs have the advantage of having a less irritating reaction in the setting of a fire.

Question 6

A 9 year old boy with a remote family history of malignant hyperthermia (MH) has masseter muscle spasm (MMS) after succinylcholine administration. Which of the following is the BEST answer:

A. Discontinue surgery and observe the patient for 6 hours
B. Discontinue surgery and observe the patient for 24 hours
C. Send a stat creatinine kinase (CK) level
D. Administer dantrolene
E. Administer cisatracurium

Answer 6

Administer dantrolene

MMS can occur in response to succinylcholine administration in up to 1% of pediatric patients and is discussed in detail in Neonatal question 30. MMS is reason to cancel elective surgery (and observe) or use clean technique for an emergent one. Patients with MMS should be tested for MH susceptibility (caffeine-halothane contracture test). A patient with a high pretest probability of MH (family history, personal history, etc) in which MMS occurs should be considered an MH episode until proven wrong; therefore, emergency therapy should begin. In this setting, further diagnostic tests (answer C) will only delay treatment. Non-depolarizing muscle relaxants will not break the MMS (answer E), see question 35.

Question 7

A 5 year old boy with a confirmed episode of malignant hyperthermia (MH) one year ago has a successful “clean” anesthetic and is in the PACU at this time with no evidence of MH. The patient is otherwise ready for discharge 30 minutes after being admitted to the PACU. The best next step is to:

A. Discharge the patient home, inform the parents about signs and symptoms of MH
B. Observe the patient in the PACU for 30 more minutes, then discharge home as above (answer A)
C. Observe the patient in the PACU for 6 hours, then discharge home
D. Admit the patient overnight for observation
E. Administer one dose of prophylactic dantrolene and discharge home

Answer 7

Observe the patient in the PACU for 6 hours, then discharge home

This is not based on evidence, only “expert” opinion. MH can occur both intra-operatively and post-operatively, and a 6 hour observational period would encompass the overwhelming majority of all MH episodes, yet have the practicality of outpatient discharge. Overnight observation is not recommended if the patient is asymptomatic. There is no place for prophylactic dantolene, and as a muscle relaxant itself, should not be given prior to discharge.

Question 8

A hyperthermic, tachycardic 16 year old bipolar patient with a mixed respiratory and metabolic acidosis has a mixed venous oxygen saturation (MVO2 sat) of 77%. Which of the following conditions are most likely:

A. Malignant hyperthermia (MH)
B. Serotonin syndrome
C. Thyroid storm
D. Sepsis
E. Neuroleptic malignant syndrome (NMS)

Answer 8

D: Sepsis

Of the following, only in sepsis would one expect the MVO2 sat to increase, not decrease. Sepsis is classically associated with increased MVO2 sat despite an increase in oxygen consumption (VO2) (see ICU question 12). The reasons for this is unclear, but may have to do with increased oxygen delivery (DO2) secondary to increased cardiac output. All of the above answers can be confused with MH in certain circumstances. The primary thing each one has in common is an increased VO2, leading to acidosis, haemodynamic instability, and electrolyte disorders. NMS (answer E) is the only one other than MH to have associated rigidity (which is the one of the most specific signs for MH) and is due to withdrawal* of neuroleptic medicines (more specifically, depletion of dopamine in the basal ganglia leading to rigidity…sound familiar: Parkinsons). Unlike MH, NMS’s rigidity responds to muscle relaxation and succinylcholine is not contraindicated. Although textbooks love to give a MH differential, only NMS closely resembles MH.

*NMS can be seen with both withdrawal and titration (up) of neuroleptic drugs and withdrawal of dopaminergic drugs. Classically one thinks of situations where there is an abrupt decrease in dopamine agonism, but this is overly simplified and has exceptions. Becoming an expert in NMS outside of the classic causes and ways it mimics MH is likely not worth your efforts. Both MH and NMS can be treated with dantrolene. Bromocriptine and amantadine will only work with NMS.

Question 9

Thiopental and pancuronium and relation to MH?

Answer 9

Both thiopental and pancurionium appear to be mildly protective in that they may increase the triggering threshold for MH.

Question 10

The halothane-caffeine contracture test (HCCT) is:

Answer 10

Is a highly sensitive test for MH

HCCT is highly sensitive, as most people susceptible to MH will have a positive test. However, it is not very specific, in that many of the people who test positive on the HCCT do not have MH. HCCT remains a more sensitive test as compared to genetic testing (of the ryanodine alleles).

Question 11

Would NDNMB work for rigidity caused by MH?

Answer 11

The patient is likely in the early stages of malignant hyperthermia (MH), as rigidity is the single most specific sign. Both non-depolarizing and depolarizing muscle relaxants such as rocuronium and answers A & C act at the muscle end plate. Acetycholine signals do not result in action potentials under blockade, therefore voltage gated calcium channels do not open, and calcium induced release of calcium (CIRC) does not occur (resulting in sarcoplasmic release of calcium and muscle contraction). However, in MH, the muscle endplate is circumvented as CIRC continues without any input from neuron signaling. Therefore, MH is unaffected by muscle relaxants (answer D). Nitrous oxide is not a triggering agent for MH (answer E), only succinylcholine and halogenated volatile agents.

Question 12

Is there a rule treating dysarrythmias in MH?

Answer 12

Yes but not as ppx.

Procainamide should be used in the setting of dysrhythmias associated with MH, but is not given prophylactically, and certainly not immediately. Dealing with an MH episode should be the easiest question on your boards and you KNOW it’s coming, and not just once. The following initial steps should be performed if MH is suspected: Discontinue triggering agents, hyperventilate with 100% O2, alert surgeons and staff, call for help, administer dantrolene 2.5 mg/kg, and repeat every 5 minutes until the patient starts to stabilize. Other important measures (once the above has been done) is cooling the patient with ice, administering bicarb (for hyperkalaemia and acidosis), draw labs, treat labs, get good lines and arterial line. Also important is adding additional mannitol to keep urine output > 2 cc/kg/hr (to avoid renal tubular obstruction due to myoglobin).

Question 13

Electrolytes abnormalities with MH

Answer 13

MH leads to increased oxygen consumption and CO2 production leading to a mixed respiratory and metabolic acidosis. With myocyte death, potassium, creatine kinase and myoglobin are released leading to hyperkalaemia, increased creatinine kinase (answer B), and myoglobinuria (not answer C, haemoglobinuria). Hyponatraemia is commomly seen in MH, not hypokalaemia (answer D). Tissue thromboplastin release leads to disseminated intravascular coagulation (DIC) with resultant thrombocytopaenia (answer E). See Haematology questions 9 & 10 for more detail on DIC. Increased creatine kinase and myoglobin are essentially universally seen with MH, but neither are very specific.

Question 14

Which of the following describes the pathophysiology of malignant hyperthermia (MH):

A. Potassium release from membrane channels stuck in the open position
B. Inability to re-uptake calcium into the sarcoplasmic reticulum (SR)
C. Abnormalities in calcium induced release of calcium (CIRC)
D. Inability of calcium to enter the cell
E. Abnormalities in actin causing prolonged actin myosin contraction

Answer 14

Your Notes:

Expand/Contract Explanation
The correct answer is: C: Abnormalities in calcium induced release of calcium (CIRC)

CIRC is the MH buzzword I think you will have to know for the boards (also described as ECRC = excitation calcium release coupling). Multiple genes have been identified leading to MH, with many of them involving the ryanodine receptor. Normally, extra-cellular calcium enters the myocyte through the dihydropyrodine receptors on the T-tubule, which is adjacent to the SR. The calcium from the dihydropyrodine receptors open the ryanodine receptor, allowing a very large calcium release from the SR, resulting in muscle contraction. In MH, the ryanodine receptor is essentially stuck in the open position where calcium is continually released and leads to contraction (see Cardiology Physiology question 3 for description of contraction). This unopposed contraction (hyperthermia, oxygen consumption, increased CO2 production) leads to ATP depletion, and muscle breakdown (thus rhabdomyolysis, hyperkalaemia, increased creatinine kinase). Therefore the abnormal CIRC signaling underlies the pathology. Answer B is somewhat correct in an abstract way, but answer C is definitely correct. The other answers I just completely made up.

Question 15

A 2 year old child received caudal anesthesia with 15 ml of 0.5% ropivicaine under general anesthesia just prior to a 15 minute inguinal hernia repair. At the end of the case, the patient is found to be completely apneic even though no opioids were administered and the end tidal sevoflurane concentration is 0.01%. What is the most likely cause:

A. The angiocath penetrated the spinal cord
B. The angiocath penetrated the dural sac
C. The angiocath punctured the sacrococcygeal membrane
D. The patient has an epidural haematoma
E. Intravascular injection of ropivicaine

Answer 15

B: The angiocath penetrated the dural sac

The patient has a high spinal from dural puncture. Just like in adults large volumes of local anesthetics can lead to respiratory collapse. Also, just like adults, dural puncture can lead to post-dural puncture headaches, although probably less frequently in children. Epirdural blood patches can be used for children and adults for this complication. Damage of spinal elements (answer A) is very rare with caudal approach, and presents with nerve distribution specific injuries (not apnea). The puncture of the sacrococcygeal membrane is the distinct pop felt when placing a caudal anesthetic properly (answer C). An epidural haematoma would more likely result in bladder/ bowel dysfunction and sensory/ motor loss of the lower extremities (answer D). Intravascular injection of ropivicaine or bupivacaine can lead to bradycardia, heart block, and cardiovascular collapse unresponsive to epinephrine, defibrillation, and chest compressions. Intralipid is given in this situation to bind ropivicaine (answer E).

Question 16

What’s dose of free morphine preservative epidural for children

Answer 16

0.1 mg/kg is a safe and effective dose in pediatric patients.

Question 17

What’s the doses of 0.25% bupivacaine with epinephrine is the minimum dose administered to cover post-operative pain for perineal surgery

Answer 17

O.5 cc/kg of a dose of bupivicine greater than 0.175% will cover perineal surgery pain. Upper abdominal surgery can be covered with 1.25 ml/ Kg dose.

Question 18

4. An otherwise healthy 6 month old child is to undergo surgery for craniosynostosis in the supine position with Mayfield head support. Physical exam and head CT show no evidence of high intercranial pressure (ICP). The anesthetic plan is induction with propofol, lidocaine, fentanyl, and succinylcholine followed by propofol and remifentanyl infusion. Which of the following is the greatest anesthetic concern for this patient:

A. Bleeding
B. Venous air embolism (VAE)
C. Brain herniation
D. Malignant hyperthermia (MH)
E. Propofol infusion syndrome (PRIS)

Answer 18

The correct answer is: A: Bleeding

Craniostenosis (premature fusion of skull sutures) surgery involves dividing the skull along the suture lines, just above the cerebral venous sinuses, which can bleed quickly and profusely (answer A). These structures are typically avoided with routine intracranial surgery. VAE (answer B) can occur with open venous sinuses as they are tented open, but in the supine position where venous pressure is nearly always higher than atmospheric pressure it is less of a concern (see Neurosurgery questions 21 & 22 for more on VAE). Brain herniation should not occur with normal ICP (answer C). MH (answer D) is increased in children (although especially rare under 1 years of age), but still rare altogether. PRIS (answer E) is more likely to occur with much longer propofol infusions (48 hours +) and is described in detail in Neonatology question 27.

Question 19

A 1 year old child with DiGeorge syndrome undergoing late cleft palate repair has two distinct episodes of laryngospasm following extubation. After the patient is in the PACU stabilized, which of the following blood tests would be most helpful:

A. Haemoglobin (Hb)
B. Potassium (K)
C. Interferon
D. Calcium (Ca)
E. Glucose

Answer 19

D: Calcium (Ca)

There are two clues that Ca is the right answer. First, DiGeorge syndrome has a very high incidence of hypoparathyroidism with hypocalcaemia; and second, hypocalcaemia can increase the incidence of laryngospasm. Tetany (involuntary contraction of muscles) is a common sign of hypocalacaemia and one that every medical student knows. So it should make sense that if facial muscles are predisposed to spasm (Chvostek sign), why shouldn’t the muscles that control the glottis? You will see this issue also come up on the boards in the setting of a thyroidectomy where the parathyroids were not spared with resultant hypocalcaemia. The other answers are pure distractors. DiGeorge is remembered by CATCH-22: Cardiac (tetralogy of Fallot), Abnormal facies, Thymic aplasia (increased infections), Cleft palate, and Hypocalcaemia, due to a deletion on chromosome 22.

Question 20

Which of the following IS NOT associated with difficult intubation:

A. Pierre-Robin syndrome
B. Treacher-Collins syndrome
C. Carpenter syndrome
D. Crouzon disease
E. Niemann-Pick

Answer 20

E: Niemann-Pick

The boards love to ask you about rare congenital disease that are difficult to intubate. The most commonly seen are Pierre-Robin and Treacher-Collins which both have micrognathia and cleft palate. Other conditions you might run into is Carpenter, Crouzon, Freeman-Shldon, Goldhenar, Anderson, Apert, Cri du chat, and many, many others. Neiman-Pick is a lysosomal storage disease.

Question 21

Flow volume lops for following

1	Laryngomalacia
2	Tracheomalacia
3	Mediastinal mass
4	Choanal atresia
5	Laryngeal polyps
6	Epiglotitis
7	Obstructive sleep apnea

Answer 21

Flow volume lops are represented with the inspiratory portion below the line and expiratory above. Lesions with variable obstructions that are extrathoracic have limited ability to pull air on inspiration and intrathoracic lesions have limited ability to push air out on expiration.

Think of laryngiomalacia where the larynx collapses when air is being pulled in (negative pressure inside the larynx), but does not obstruct on expiration (when laryngeal pressures are positive and pushing the laryngeal walls away from each other).

Now extrapolate to polyps (negative pressure brings them close together) or epiglottitis – it’s the same overall principle, but less likely to produce the above flow volume loop in real life (low specificity).

Mediastinal mass on inspiration is brought up and away from the bronchus due to expansion of the thoracic cavity. On expiration, the mass is brought back down towards the airways and obstruction occurs.

With tracheomalacia, the answer depends where the lesion primarily exists and in the majority of cases it is the distal trachea which is intrathoracic, therefore one would expect in the majority of cases that it will have an obstruction seen on expiration, although both have been described. In fact, I have seen references for both flow-volume loops, but considering the prevalence of proximal versus distal tracheomalacia, we choose loop C as the correct answer (and I hope the ABA would too).

In choanal obstruction, the obstruction is fixed therefore either a normal pattern will be seen or a fixed obstruction on both inspiration and expiration.

OSA is an exception to the above rules, where one would expect to see the lesion of flow volume loop on inspiration. However, with OSA, the problem is with expiration (in reality, figure C is not an accurate graph of OSA, it instead looks more like COPD with a scooped pattern (but with “sawtoothing”), but the point remains its effect on morphology is on the expiratory loop).

Question 22

3 year old with a peritonsilar abcess presents for surgery. On exam the patient is uncooperative and you are unable to examine the abscess. The patient has normal vital signs and no respiratory distress or obstruction in the upright or recumbent position. The patient has a functioning IV. The CRNA suggest oral versed and an a inhalational induction, you respond:

A. Inhaled induction is contraindicated
B. Oral versed should not be used as it may lead to bursting of the abcess
C. Oral versed should not be used as it may lead to airway obstruction
D. IV ketamine is the only safe option for this case
E. IV midazolam would be ok, but oral versed should be avoided

Answer 22

C: Oral versed should not be used as it may lead to airway obstruction

Peritonsilar abcess is one of many very dangerous airway cases in pediatrics. There are two major concerns. First, the abscess can obstruct the glotic opening (sound familiar, kinda like epiglottitis?) leading to complete obstruction. Therefore, spontaneous breathing throughout induction is paramount. Forcing positive pressure (by way of mask ventilation) has a fairly high chance of being impossible. Second, rupture of the abscess can lead to copious amounts of puss being expressed in the airway so intubation should be carried out carefully and meticulously. The issue with midazolam is not so much the route (although why give oral versed when a IV is present?) but the concern for airway obstruction once sedated. Therefore, answer C is correct and answers B & E are incorrect. There are multiple possibilities regarding intubating this patient and ketamine is an option (I wouldn’t use it, but I would not say its necessarily incorrect), but not the only option by any means

Question 23

17 year old girl with scoliosis has a Cobb angle of 65 degrees, which of the following co-morbidities are most likely:

A. Seizure disorder
B. Mental retardation
C. Hirtuism
D. Mitral valve stenosis
E. Pulmonary hypertension

Answer 23

E: Pulmonary hypertension

Pulmonary hypertension is secondary to restrictive lung disease which is due to an abnormal constricted, rotated thorax, due to scoliosis. The Cobb angle is a radiologic method to measure the severity of scoliosis (you will not be asked to calculate one, but its based on the greatest angle between any two vertebrae). Above 10 degrees, the spine appears scoliosed, but usually does not cause cardiopulmonary pathology until the angle is at least 60 degrees. Long-standing pulmonary hypertension can lead to cor pulonale. Surgical repair is often very bloody and has an increased risk of neurologic sequelae, mostly related to the spinal cord, not the brain (answers A & B). Answers C & D are completely unrelated as well. Mitral valve prolapse, not stenosis, has increased frequency in children with thoracic skeletal disorders (as well as a multitude of other associations).

Question 24

Normal VS for term

Answer 24

Age	HR	Systolic BP	Diastolic BP	Respiratory rate
Preterm	160	50	30	50
Term	130	60	40	50
1 yr	120	80	60	25
Toddler	90	100	60	20

Following the toddler age, I think of children’s vitals the same as a healthy adult, except they breathe a little bit faster. In general, a newborn has a high HR (since they can not augment stroke volume) and it falls as this ability develops. They also have blood pressures that would be dangerously low for adults until they are a toddler. The high oxygen consumption (VO2) requires a high respiratory rate (delivery of oxygen (DO2)). If these terms (VO2 & DO2) are the least bit confusing, please read the ICU section before proceeding, I am not going to re-detail the concepts of oxygen consumption in this section. Also, of note, if you look at 10 sources for this table you will find 10 different ranges.

Question 25

Blood volume for Peds

Answer 25

Newborn: 90 cc/kg Infant 75 cc/kg Toddler 70 cc/kg.

Question 26

3. Match the arterial blood gas with the correct age ``` pH paO2 paCO2 1 7.20 50 50 2 7.40 70 35 3 7.40 95 40 A Immediately after birth B 1 week after birth C Toddler ```

Answer 26

The correct answer is: A: 1=A; 2=B; 3=C Think of babies as being born acidotic and retaining CO2. This corrects itself within a week, where they generally live at a normal pH and a slightly low CO2 tension. Think of a toddler as an adult

Question 27

Which of the following is a normal umbilical artery blood gas: ``` pH paO2 paCO2 1 7.20 50 50 2 7.30 20 50 3 7.35 30 40 4 7.40 95 40 ```

Answer 27

B: 2 The boards will not be this easy, but this is set up so you can use the table to get these principles down. Answer 2 is a normal umbilical artery blood gas and answer 3 is a normal umbilical venous blood gas. Note how the venous blood gas’s pH is higher than the arterial: this is because of the fetal circulation (placenta -> vein -> heart -> arterial -> placenta) is backwards (compared to adults), with the most oxygenated blood (from the placenta) being venous. The ABA loves arterial blood gas questions and seems to always have one that involves umbilical values.

Question 28

Which of the following is correct regarding fetal haemoglobin: A. It is right shifted, compared to adult hemoglobin B. It is replaced by the adult form by 1 month of age C. It has an increased affinity for 2,3-DPG D. It has an increased affinity for oxygen E. It is prone to sickling at low oxygen tensions Expand/Contract Explanation

Answer 28

D: It has an increased affinity for oxygen Fetal haemoglobin (F-Hb) is present at birth and is replaced by adult Hb starting around 3 months and completely at 6 months. F-Hb is unable to bind to 2,3-DPG which causes a left shift on the oxygen saturation curve, increasing its affinity for oxygen (the p50 of F-Hb is 19, whereas adult Hb is 27). Fetal Hb is an adaptive response for fetuses due to the low oxygen tensions provided by the placenta (see the blood gas values in the question above!), which is why the high oxygen affinity (left-shift) is beneficial. F-Hb does not sickle at low O2 tensions, making its upregulation (with hydroxyurea) a treatment for sickle cell anaemia.

Question 29

Which of the following is true regarding the transition from fetal to neonatal circulation following birth: A. The ductus arteriosis contracts and closes over the first 1 hour B. Pulmonary vascular resistance (PVR) decreases precipitously C. Type II pneumocytes begin surfactant production after spontaneous ventilation begins D. The foramen ovale typically closes (anatomically) in 2-3 weeks in most cases E. The primary pacemaker of the heart switches from the AV node to the SA node

Answer 29

Your Notes: Expand/Contract Explanation The correct answer is: B: Pulmonary vascular resistance (PVR) decreases precipitously Following birth, the circulatory physiology of the newborn changes drastically. Prior to birth, placental oxygenated blood is delivered to the fetus via the umbilical vein, through the liver (and ductus venosus), to the IVC and into the right atrium. Blood from the IVC has high (relatively speaking) oxygen tensions whereas SVC blood has low oxygen tensions. IVC blood is preferentially directed through the foramen ovale into the left ventricle where it is pumped out the aorta (look at a diagram of this as you read along). From the aorta, highly oxygenated blood is delivered to the first three branches off the aorta (brachocephalic, left carotid, & left subclavian) before it is mixed with deoxygenated blood from the ductus arteriosis. Where does the blood from the ductus arteriosus come from? Blood from the SVC is preferentially directed down into the right ventricle, out the pulmonary artery and due to HIGH PULMONARY VASCULAR RESISTANCE (PVR), it is directed up the ductus arteriosis into the aorta. Once the lung is filled with air, the high oxygen tensions reduces PVR and pulmonary arterial blood preferentially flows through the pulmonary circulation and not the ductus arteriosis. After a couple weeks of disuse, the ductus arteriosis is anatomically closed (not the foramen ovale). The foramen ovale is functionally closed in this circulatory setting (as it is lower resistance for right atrial blood to flow into the pulmonary circulation than cross the foramen ovale into the left atrium), but is not anatomically closed for months (and, in fact, in 25%+, never closes at all).

Question 30

Which of the following neonatal disorders can ‘lead’ to patent ductus arteriosis (PDA): A. Persistent pulmonary hypertension of the newborn (PPHN) B. Exposure to 100% oxygen within the first 2 days of life C. Indomethacin exposure D. Gastroschisis E. Cyanide toxicity Expand/Contract Explanation

Answer 30

The correct answer is: A: Persistent pulmonary hypertension of the newborn (PPHN) PDA is a complex disease where the ductus arteriosis does not close. In most cases, the cause is unknown and thought to be due to intrauterine events and genetic abnormalities. Other causes of PDA include prematurity, especially in association with hypoxia, low oxygen tensions, high altitudes, and cardiac defects. PPHN is a special case where due to high pulmonary pressures, blood is directed away from the pulmonary outflow tract and through the patent foramen ovale, to the left atrium, then left ventricle, then aorta. Life would not be possible unless there was flow through the PDA (but backwards, that is from the aorta to the pulmonary artery and through the pulmonary circulation)…read that sentence again, slowly. Therefore the PDA is a necessary adaptive response to PPHN. Closure of the PDA could be fatal, so prostaglandins (prostaglandin E1 analogs) may be administered to keep the PDA open. Indomethacin (and ibuprofen) inhibits the synthesis of prostaglandins and lead to PDA closure. PPHN treatment is directed towards the underlying cause, usually some form of ventilatory failure. Exposure to 100% O2 may contribute to undesirable neonatal effects such as retinopathy of prematurity, but would not contribute to PDA (since hypoxia is a major risk factor). Answers "Gastrschisis" & "Cyanide toxicity" are completely unrelated.

Question 31

Which of the following statements are true: A. Neonatal stroke volume is more sensitive to changes in preload than adults B. Increases in afterload in the neonate lead to significant increases in stroke volume C. Neonates lack a sympathetic nervous system at birth D. Increases in neonatal heart rate (HR) lead to a near linear increase in cardiac output E. Systemic vascular resistance is decreased in the neonatae compared to the fetus

Answer 31

D: Increases in neonatal heart rate (HR) lead to a near linear increase in cardiac output This is a hard question, in that you need to know that the neonate 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. You also have to not overthink the question and imagine heart rates in the upper 200’s in which filling time would be a major issue, decreasing stroke volume. 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”). Additionally, unlike adults, increased afterload does not increase myocardial contractility, which is called “afterload mismatch. “ Neonates do have a sympathetic system functioning at birth as discussed in Neo9.

Question 32

A 2 week full term infant undergoing G-tube placement becomes hypoxic after mask ventilation becomes impossible. The anesthesiologist notes that the pulse oximeter reading rapidly falls along with the heart rate 20 seconds after this occurs. The most likely reason for the patient’s bradycardia is: A. Ischaemia of the SA node during the episode of hypoxia B. Ischaemia of the AV node during the episode of hypoxia C. An increased parasympathetic response in relation to the sympathetic response D. A paradoxical response to a normal sympathetic outflow (increased due to hypoxia) commonly seen in newborns E. Absence of beta-1 receptors on the neonatal myocardium Expand/Contract Explanation

Answer 32

The correct answer is: C: An increased parasympathetic response in relation to the sympathetic response The 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 adults. It is not due to complete absence of beta 1 receptors nor a paradoxical response.

Question 33

A 4 week old infant is being induced for pyloric stenosis surgery with a rapid sequence induction. The child was crying and the CRNA felt it was cruel to place the oxygen mask on the infant’s face pre-induction as it was making the crying worse. Following induction, the child nearly immediately starts to desaturate because: A. Pyloric stenosis causes a restrictive lung disease picture B. Silent aspiration occurred C. Malignant hyperthermia D. Relatively low FRC/VO2 ratio as compared to adults E. Relatively low tidal volume as compared to adults Expand/Contract Explanation

Answer 33

The correct answer is: D: Relatively low FRC/VO2 ratio as compared to adults Neonates, but not children in general, may have a decreased functional reserve capacity (FRC) compared to adults* as well as high oxygen consumption (VO2), which leads to rapid desaturation. Let's break it down to the two components and see how this affects things we already understand. A decreased FRC means that during the apneic period, the oxygen available to the pulmonary circulation to pick up and distribute to the body is very low (those alveoli that are filled with oxygen but do not participate in tidal volumes are, by definition, reduced with decreased FRC). When that oxygen is utilized (released from Hb) and no new oxygen is available, the Hb saturation decreases rapidly. The high VO2 means that the oxygen delivered is quickly consumed. The neonate’s high VO2 needs are also, in part, why the respiratory rate (minute volume) is so high (both tidal volume and FRC oxygen is rapidly used). This simple concept can get very tricky in a hurry…see below. *Many sources say that neonatal FRC is the same as adults, others say it's less (with a variety of magnitudes). Some explain FRC in terms of ml/kg while others are referring to %TLC. Even taking these into consideration, the sources are inconsistent. Whatever 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.

Question 34

Which of the following factors explain why infants experience (on average) a quicker inhalation induction than adults: ``` A. Increased minute ventilation (MV) per Kg of body weight B. Decreased MV/ FRC ratio C. Increased MV/ FRC ratio D. Decreased MV/ VO2 ratio E. Increased MV/ VO2 ratio ```

Answer 34

Your Notes: Expand/Contract Explanation The correct answer is: C: Increased MV/ FRC ratio This is a subject that I have yet to read an explanation that "makes sense," so let me give it a try. Volatile agents are not like oxygen (see above Neo10) that is rapidly metabolized and has a never-ending sink; instead they reach a certain alveolar partial pressure (which correlates to its partial pressure in the brain) and essentially stays the same until you turn the dial. The lung’s alveoli begin induction filled with air, not sevoflurane. The higher the minute volume, the more sevoflurane is delivered to the lungs, and the quicker induction occurs (inhaled induction is sped by increased ventilation – you already knew that!). To simplify things, lets say that for alveolar volatile concentration to reach a steady state (a certain partial pressure which correlates with an anesthetized patient) we must not only fill the alveoli that participate in tidal volumes but also those in the FRC. The higher the FRC, the longer it takes to reach that steady state…. follow with me, we’re almost there…. therefore if the MV here high (lots of sevoflurane delivered) and FRC were low (fewer alveoli that need to reach a steady state), induction would be hastened. Realize that this is a gross oversimplification (if not an outright lie), but it hopefully helps make sense why "Increased MV/ FRC ratio" is correct. The MV/FRC ratio in neonates is 5:1 and its about 1.5:1 in adults. Why is MV so high? It is because oxygen consumption is higher with a same or lower FRC, requiring the neonate to breath more to deliver more oxygen.

Question 35

The neonatal diaphragm contains 25% type 1 muscle fibers as opposed to 55% in adults, the significance of this is: A. Neonates are more likely to suffer from respiratory fatigue B. Neonates are less likely to suffer from respiratory fatigue C. Neonates have a larger tidal volume (per kg) than adults D. Neonates have a smaller tidal volume (per kg) than adults

Answer 35

Expand/Contract Explanation The correct answer is: A: Neonates are more likely to suffer from respiratory fatigue 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. Tidal volumes between neonates and adults are proportionately about the same; whereas minute volume is significantly increased in babies.

Question 36

Which of the following is true: A. Neonates are obligate nose breathers B. Lung compliance is increased as compared to adults C. Chest wall compliance is increased as compared to adults D. Functional reserve capacity (FRC) increases as chest wall compliance increases E. Hypoxic, but not hypercarbic, drives are fully developed in terms

Answer 36

The correct answer is: C: Chest wall compliance is increased as compared to adults There is A LOT of information in this question, and do not jump onto the next question until you deal with the reason the other answers are incorrect. In all humans, the lung has a tendency to collapse upon itself and the chest wall has a tendency to expand (see Respiratory Questions 3 & 5 for more description on this important respiratory principle) creating a negatively pressured pleural space. 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); and, therefore, the greater the decrease in FRC. Therefore, answer "Functional reserve capacity (FRC) increases as chest wall compliance increases" is wrong. Answer "Hypoxic, but not hypercarbic, drives are fully developed in term neonates" is incorrect because both hypoxic and hypercarbic drives are immature at birth. "Neonates are obligate nose breathers" is some BS that overly brainy academics without common sense (or children!) dreamt up and is still found in text books to this day. Wait till your infant has a cold and see how poorly worded this piece of dogma is**. *FRC can be thought of as the point at which the outward elastic recoil of the chest matches the inward inward recoil of the lung (at end-expiration). In neonates both of these factors are decreased as compared to adults. Whether this results in a decreased FRC depends on the source. **In reality, some neonates will convert to oral breathing later than others (following a nose pinch) and are termed "obligate" for some reason.