Respiratory Flashcards
A four year old male with severe status asthmaticus has required intubation secondary to fatigue and progressive dyspnea. He is adequately oxygenated, but he is severely hypercarbic because the restricted airflow and prolonged expiratory phase has limited the ventilator rate to only eight breaths per minute to prevent further air trapping. Which of the following statements MOST accurately describes the response of the body to the hypercarbia?
A. Cerebral blood flow will decrease in response to the hypercarbia.
B. Chemoreceptors in the brainstem and in the carotid body will not respond to the elevated PaCO 2 because he is well oxygenated.
C. Deoxygenated hemoglobin molecules will bind hydrogen ions and carbon dioxide to form carbaminohemoglobin and buffer the pH.
D. The kidneys will decrease the excretion of ammonium ion and chloride while retaining HCO − 3 and sodium to buffer the pH.
E. There will be increased responsiveness of the adrenergic receptors to circulating catecholamines.
C. Deoxygenated hemoglobin molecules will bind hydrogen ions and carbon dioxide to form carbaminohemoglobin and buffer the pH.
(Lucking Ch. 1)
A twelve year old male with acute respiratory distress syndrome has required intubation for progressive hypoxemia. His initial ventilator settings are as follows: Fraction of inspired oxygen: 1.0 Peak inspiratory pressure: 35 cm H 2 O Peak end expiratory pressure: 12 cm H 2 O Mean airway pressure: 22 cm H 2 O Ventilator rate: 14 breaths per minute His most recent arterial blood gas result revealed a pH 7.37, PaCO 2 40 mm Hg, PaO 2 100 mm Hg, and SaO 2 96%. The barometric pressure is 760 mm Hg, the partial pressure of water vapor is 47 mm Hg, and the respiratory quotient is assumed to be normal (0.8). Which of the following values most closely approximates the alveolar oxygen gradient?
A. 538 mm Hg
B. 563 mm Hg
C. 573 mm Hg
D. 610 mm Hg
E. 663 mm Hg
B. 563 mm Hg
(Lucking Ch. 1)
A two month old infant with hypoplastic left heart syndrome status post Stage I Norwood Procedure is developing pulse oximetry evidence of increasing hypoxemia. Point of care arterial blood sampling reveals pH 7.38, PaCO 2 44 mm Hg, PaO 2 35 mm Hg, SaO 2 75%, and a hemoglobin 12.0 g/dL. Which of the following values best estimates the arterial oxygen content of this infant?
A. 10.5 mL O 2 /dL.
B. 11.2 mL O 2 /dL.
C. 12.2 mL O 2 /dL.
D. 14.2 mL O 2 /dL.
E. 16.8 mL O /dL.
C. 12.2 mL O 2 /dL.
(Lucking Ch. 1)
A two year old male presents with profuse watery diarrhea and tachypnea. He is tachycardic and tachypneic on clinic exam with pulse oximetry readings of 85% and a good waveform which correlates with the heart rate. He is placed on increasing concentrations of oxygen, but he appears dusky and his pulse oximetry readings and clinical exam remain essentially unchanged. Consequently, an arterial blood gas is performed which reveals pH 7.28, PaCO 2 34 mm Hg, PaO 2 189 mm Hg, and base deficit (–7). Which of the following diagnoses is most likely?
A. Carboxyhemoglobinemia
B. Malfunctioning pulse oximeter
C. Methemoglobinemia
D. Sickle cell disease
E. Ventilation perfusion mismatch
C. Methemoglobinemia
(Lucking Ch. 1)
A sixteen year old trauma victim with a pulmonary contusion has developed evidence of acute respiratory distress syndrome. He currently is receiving mechanical ventilator support in the pressure regulated volume control mode with the following settings: Fraction of inspired oxygen: 0.80 Inhaled tidal volume: 500 mL / exhaled tidal volume: 475 mL Peak end expiratory pressure: 10 cm H 2 O Mean airway pressure: 16 cm H 2 O Ventilator rate: 16 breaths per minute His pulse oximeter reading is 92% and his end tidal carbon dioxide is 30 mm Hg. An arterial blood gas reveals a pH 7.35, PaCO 2 45 mm Hg, PaO 2 65 mm Hg, and oxygen saturation 90%. The best estimate of the percent dead space ventilation is which of the following?
A. 2%
B. 5%
C. 15%
D. 20%
E. 33%
E. 33%
(Lucking Ch. 1)
A five year old male is found unresponsive in a smoke-filled room at the scene of a house fire. He is intubated at the scene and transported to the Emergency Department being ventilated with 100% oxygen. Upon arrival to the Emergency Department, he is found to have a pulse oximeter reading of 100%. Which of the following statements provides the best interpretation of the pulse oximetry reading?
A. Although the pulse oximetry reading accurately reflects a well oxygenated patient, the 100% oxygen should be continued to treat potential carboxyhemoglobinemia.
B. It is difficult to determine if the pulse oximetry value represents effective oxygenation because the pulse oximeter will inappropriately interpret carboxyhemoglobin to be oxyhemoglobin.
C. The ability to effectively oxygenate the patient with supplemental oxygen via conventional ventilation as reflected by the pulse oximeter reading obviates the need for hyperbaric oxygen.
D. The patient is well oxygenated and should have his fraction of inspired oxygen weaned to maintain a pulse oximetry level of 94 – 99% to minimize potential oxygen toxicity.
E. The pulse oximetry value likely overestimates the degree of oxygenation because the methemoglobin formed as a result of smoke inhalation has a very similar light absorption as oxyhemoglobin at 660 nm.
B. It is difficult to determine if the pulse oximetry value represents effective oxygenation because the pulse oximeter will inappropriately interpret carboxyhemoglobin to be oxyhemoglobin.
(Lucking Ch. 1)
The capnogram depicted in the figure most likely represents which of the following clinical conditions?
A. Acute respiratory distress syndrome
B. Asthma
C. Compromised cardiac output
D. Pneumothorax
E. Pulmonary edema
B. Asthma
(Lucking Ch. 1)
The saccular stage of lung development continues the development of alveoli and is the initiating phase of surfactant production. At what point in gestation does the saccular stage begin?
A. 4 weeks
B. 17 weeks
C. 26 weeks
D. 36 weeks
E. 40 weeks
C – 26 weeks. The saccular stage begins around gestational age 26 weeks. This is when respiratory bronchioles and alveoli develop in the acini and type II pneumocytes begin to produce surfactant. Disruption of gestation in the canalicular period (which precedes saccular) and saccular period leads to RDS. What results is pulmonary hypoplasia because of acinar and vascular immaturity as well as surfactant deficiency. Surfactant is critically important for maintenance of normal lung compliance. At 4 weeks gestation, the ven- tral groove of the foregut buds to initiate respiratory tree formation. By 17 weeks, the majority of airways have been formed. At 36 weeks begins the alveolar phase when alveoli develop and mature into adolescence.
(Lucking Ch. 7)
What level of the airways presents the least resistance to airflow in healthy lungs?
A. Nose
B. Oropharynx
C. Trachea
D. Large airways
E. Small airways
E – small airways. The cross-sectional area of all the small airways is cumulatively larger than either trachea, bronchi, or upper airways. Therefore, the overall resistance to airflow at the level of small airways (generally believed to be the 11th generation and beyond) is lower than that of the nose, oropharynx, trachea, or bronchi.
(Lucking Ch. 7)
Which of the following acini in the diagram below would have the shortest time constant (shortest time to inflate with air)?
Image contains airway with 3 alveoli.
1. Normal compliace and normal resistance.
2. Lower resistance x low compliance (small alveoli with normal diameter bronchiole)
3. High resistance x high compliance (narrow bronchus, large alveolus)
A. 1
B. 2
C. 3
D. 1 and 3
E. 2 and 3
B – 2. A lobule/acinus with poor compliance (low compliance) and low air- ways resistance will have the shortest filling time (RC time constant). This is because airways resistance is low allowing for faster transit time through the airway, and lung compliance is low causing rapid filling of the airspace. Both airways resistance and lung compliance being low lead to a short time constant. In ARDS, which is a heterogeneous lung disease, there are varying resistances and compliances (RC time constants) throughout the lung. This makes treating ARDS with mechanical ventilation a challenge.
(Lucking Ch. 7)
A 14-year-old with history of BPD is admitted to Floating Children’s Hospital in Boston with a right lower lobe pneumonia. He has an oxyhemoglobin saturation of 86% breathing room air. His respiratory rate is 44, and he has nasal flaring. You obtain an arterial blood gas while he is breathing room air, and the values are pH 7.42, PaCO2 40, PaO2 50. What is his A-a gradient?
A. 18
B. 36
C. 50
D. 100
E. 110
C – 50. If breathing room air, the fraction of inspired oxygen is 0.21. Barometric pressure at sea level would be 760 mmHg and partial pressure of H20 47 mmHg. Using the alveolar gas equation, this child has a PAO2 of 100 (PAO2 = 0.21(760–47) – 40/0.8). If his PAO2 is 100 and his PaO2 is 50, then his A-a gradient is 50.
Remember the alveolar gas equation:
PAO2 = (FiO2)(Patm-PH20) - PaCO2/0.8
* IN = FiO2 x (Patm-PH20) = 0.21 x (760-47) = 150
* OUT = PaCO2/0.8
* THEREFORE: PAO2 = 150 - PaCO2/0.8
And the A-a gradient equation:
A-a gradient = PAO2 - PaO2
IA 14-year-old with history of BPD is admitted to Floating Children’s Hospital in Boston with a right lower lobe pneumonia. He has an oxyhemoglobin saturation of 86% breathing room air. His respiratory rate is 44, and he has nasal flaring. You obtain an arterial blood gas while he is breathing room air, and the values are pH 7.42, PaCO2 40, PaO2 50.
You supplement oxygen with 50% face mask via venturi valve. His oxyhemoglobin saturation improves to 96%, and you obtain another arterial blood gas. The values are pH 7.44, PaCO2 36, PaO2 296. In this scenario, what is the most probable cause of his hypoxemia?
A. Hypoventilation
B. Decreased inspired oxygen tension
C. Anatomic right→left shunt
D. Diffusion defect
E. Ventilation/perfusion mismatch
E – ventilation/perfusion mismatch. V/Q mismatch is the most common cause of hypoxemia in children with lung disease (acute and chronic). In this case, V/Q mismatch is most likely because of a widened A-a gradient that improves oxygenation with supplemental oxygen. Diffusion defect is also a possibility for someone with a widened A-a gradient that improves with oxygen, but in this clinical scenario, with a child who has a lobar pneumonia, ventilation and perfusion mismatch is more likely because of regional disruption of ventilation accompanied by preserved or diminished perfusion.
Normal A-a gradients range = 3 to 8 mmHg
- An Elevated A-a gradient indicates that there is poor oxygen delivery to the vascular bed at the level of the acini/alveoli.
- Repeat A-a gradient is: PAO2 = 150 - 36/0.8 = 105, A-a = 150 - 296.
Consider the five main causes of hypoxemia (Table 7.2):
1. ventilation/per- fusion (V/Q) mismatch
2. anatomic shunt
3. diffusion defect
5. hypoventilation
6. altitude (or decreased ambient air pressure).
One can further narrow down the cause of hypoxemia by supplementing oxygen and assessing for a response. In the case of anatomic shunt, oxygen supplementation will have little to no effect on improving oxygenation.
What are main differences in pediatric airway compared to adult?
Larger tongue
More anterior larynx
Omega/floppy epiglottis
Funnel shaped larynx
Why does resistance in pediatric airway increase significantly with small change in caliber?
Poiseulle’s Law
Resistance = 8nl / pi*radius^4
If turbulent, raise to 5th power
What determines how turbulent flow is in an airway?
Reynolds Number
Re = diametervelocitydensity / viscosity
Higher diameter, velocity, or density leads to more turbulence (why heliox - less dense - can reduce turbulence)
What is transmural pressure?
The pressure across the wall of a structure, inside - outside
(e.g. transmural pressure in extrathoracic upper airway = airway - atmosphere, slightly negative on inspiration)
What causes dynamic collapse in the setting of upper airway obstruction? E.g. croup
Increased effort leads to VERY negative transmural pressure and airway collapse
What does this flow pattern (solid line) represent?
DYNAMIC extrathoracic obstruction (e.g. croup) - limitation primarily to inspiration due to dynamic collapse with generation of significantly negative transmural pressure, some limitation to exhalation only because inspired tidal volume is smaller
What does this flow pattern (solid line) represent?
FIXED intra- or extrathoracic obstruction, e.g. complete tracheal rings, does not vary with inspiration vs. exhalation
What does this pattern represent?
Flow limitation – effort (esophageal pressure continues to change) without a continued increase in flow; e.g. croup or other extrathoracic airway obstruction
Also causes increased afterload on LV, pulsus paradoxus
What happens to cross-sectional area of central vs. peripheral airways as patient goes from infant to adult?
Central airway conductance (1/resistance) stays relatively constant while cross sectional area and therefore conductance of periphery increases significantly starting at about 5 years old
Why pediatric patients struggle with lower airway obstruction more than adults
When in end tidal CO2 waveform does inspiration begin?
ETT size equation
Uncuffed ETT (age/4)+4
Cuffed ETT is above -0.5
age 0-1: 3.0 or 3.5
age 2-4: 4.0
age 4-6: 4.5
age 6-8: 5.0
age 8-10: 5.5
age 10-12: 6.0
age 12+: 6.5 or 7.0
What happens to transalveolar pressure with lower airway obstruction?
Generate very positive pleural pressure with forced exhalation against air trapping, very positive alveolar pressure, so proximal to the obstruction have negative transmural pressure (airway-pleural) and get dynamic collapse proximal to obstruction
What does this flow pattern represent?
Lower airway obstruction
What is the time constant?
Time required for a system to change (inflate or deflate) by 63% of total
T = airway resistance x compliance
Inverse of the slope of the flow-volume curve during passive exhalation
Takes 4*Time constant (4RC) to fully empty, so max rate is 60/4RC
With ARDS, compliance decreases, resistance only slightly increased so time constant decreases slightly and max rate is high; with bronchiolitis, resistance very high, compliance only slightly down, so time constant long and max rate very low
Why does NiPPV work for increased work of breathing in asthma?
Air trapping, positive alveolar pressure, to breathe in, have to lower the alveolar pressure below atmospheric pressure so need VERY negative pleural pressure (wasted effort); if add PEEP to airway, only have to generate pressure in alveolus less than the airway pressure (CPAP)
Match compliance/resistance with restrictive/obstructive pathophysiology
Restrictive lung disease = poor compliance (e.g. ARDS)
Obstructive lung disease = high airway resistance (e.g. bronchiolitis, asthma)
Lung volumes
Describe pleural pressure, transpulmonary pressure, trans-chest wall pressure, etc. at FRC
Transmural pressure = inside-outside
Transpulmonary pressure = alveolar (0) - pleural (-5 because lung wants to collapse) = +5, why alveoli don’t collapse
Trans chest wall pressure = pleural (-5) - atmosphere (0) = -5 (chest wall wants to expand)
Trans respiratory system pressure = alveolar - atmospheric = 0 at FRC (positive transpulmonary and negative trans-chest wall pressures balanced)
What happens to pressure-volume loop as compliance worsens?
Compliance is delta V / delta P so less compliant curve has lower slope
Show optimal PEEP/Vt on pressure volume loop
What is closing volume of lung?
Normally FRC (all alveoli open) > CV > RV (all alveoli collapsed)
At young age and old age, closing volume may actually be higher than FRC/end expiration, so very prone to atelectasis especially supine
Infants also lack collateral ventilation from adjacent alveoli
Show elastic and dynamic work on pressure volume loop
Work = force*distance
Work of breathing = delta P * delta V
What are static and dynamic compliance?
Static (0 flow) = elastic work
Dynamic = resistive work
Cstat = VT/(Plateau pressure - PEEP)
Cdyn = VT/(PIP - PEEP)
What happens to respiratory rate relative to normal to minimize work of breathing in disease states?
Poor compliance: increased rate
High airway resistance: decreased rate
How do we measure transpulmonary pressure (matters most for injury) at end exhalation?
Transpulmonary pressure = Palveolar - Ppleural
Alveolar ~ airway
Pleural ~ esophageal
Normal = 0 - -3 = +3 atm
Increased pleural pressure (e.g. obesity) will give negative transpulmonary pressure and promote collapse, so can apply PEEP to normalize it
Why do we care about transpulmonary pressure at end inspiration? ~stress on lung
Driving pressure of lung = plateau pressure - PEEP
True transpulmonary pressure at end inspiration (alveoli/airway - pleural/esophagus) = plateau pressure - esophageal plateau
The TPP plateau is less than the driving pressure, implying that some of that driving pressure is used to move the chest wall and thus is not really “seen” by the lung
What is different in diaphragm between infants and adults?
Type I muscle fibers increase after age 2, infants susceptible to diaphragm disease
What causes thoraco-abdominal dysynchrony?
Intercostal muscle weakness – when diaphragm contracts, normally the intercostal muscles contract and thoracic cage moves out
Phase shift between abdomen and rib cage can occur with weakness of one – collapse of rib cage with diaphragm contraction; can be common in neonates even during normal sleep
Infants may be more prone to develop hypoxemic respiratory failure than young adults for all of the following reasons
Lower baseline PaO2
Relative lack of collateral sources of ventilation
Critical closing capacity closer to FRC
Increased elastic recoil of the chest wall
More horizontal orientation of ribs
Equation for Peak Inspiratory Pressure based on contribution of airway resistance and static compliance?
Paw = (flow * resistance) + volumechest elastance
Paw = (deltaV/deltaT * 8nl/pir^4) + VE
delatV/deltaT = inspiratory flow rate, must be constant to measure
If flow rate = 0, no airway resistance contribution, see only plateau pressure or static compliance, that’s what the alveoli see
What is required to perform an inspiratory hold?
Volume control (constant/square flow pattern) and paralysis
What contributes to more ventilator associated lung injury, barotrauma or volutrauma?
Volutrauma
Grading of subglottic stenosis
Cotton-Myer staging system
Grade 1 through grade 4
Subglottic diameter 4mm or less in term neonate is significantly narrowed (normal 4.5-5.5mm)
Narrowest portion of airway in neonates vs. adults
Neonate: cricoid
Adult: vocal cords
List four factors that increase the risk of subglottic stenosis after intubation?
Large ETT
Prolonged intubation
GERD
Concurrent NG tube
Most common causes of croup?
Parainfluenza
COVID
adenovirus, flu, RSV, rhino, entero
What are the benefits of HFNC?
- Provides oxygen
- Washout of exhaled CO2 to prevent rebreathing
- Warm humidification - decreases metabolic work needed to do this, improves mucociliary clearance
- Some CPAP (5-6 cm H2O?)
Actual benefit is less escalation of care; no difference in LOS, O2 duration
Better tolerated than nasal CPAP without change in duration of treatment of LOS
normal range for lung compliance?
10-15 mL/cm H2O
ABCA3 mutation
surfactant deficiency
What is normal Vd/Vt?
25-35%
Management of pulmonary contusion
Fluid restriction
Higher incidence than in adult trauma patients because of higher compliance of chest wall, greater transmission of energy to intrathoracic structures
If <20% of lung impacted, unlikely to need mechanical ventilation; >30% high risk of intubation
Initial management of tracheoinnominate artery fistula?
Immediate control of hemorrhage in a suspected tracheoinnominate artery fistula often requires replacement of the tracheostomy tube with a larger size and inflation of the cuff to apply pressure and tamponade the bleeding
usually develops in first 3 weeks after trach
Risk factors: steroids, prolonged intubation, low trach or high innominate, overinflated cuff, tracheitis/stomal infection
Neural control of respiration
3 parts:
1. dorsal respiratory group in nucleus tractus solitarius (inspiratory)
2. ventral respiratory group in the medulla (expiratory); also pre-Botzinger complex connection between
3. pontine respiratory group (depth/frequency)
*Rostral medulla = rhythm generation
- Chemoreceptors at midbrain sense pH change: slow deep breathing (diver holding breath … eventually brain becomes unconscious in attempt to protect itself from further pH drop)
- Peripheral chemoreceptors also at common carotid and aortic arch (CN IX and X) mostly sense hypoxemia but also pH and CO2
- Thoracic neural receptors given info on stretch and irritants in airway (CN IX)
Diving reflex
Ice/water and breathhold cause trigeminal nerve to signal brainstem, signals via vagus nerve to reduce HR and increase peripheral vasoconstriction reducing oxygen consumption and ensuring supply of O2 to vital organs
First line treatment for hypersensitivity pneumonitis
Removal of antigen exposure
Pediatric lung transplant outcomes
Median survival still only 4.9 years
Bronchiolitis obliterans responsible for almost half of deaths after 5 years
PAH greatest indication for transplant
At what level of elevation does hypoxia become a driver for respiration?
10,000 feet, Patm of 523 mmHg
