Pulmonary Function and Physiology Flashcards
Infant PFT: Formula for R interruptor
Rint = Pmo/V
Pmo = mouth pressure V = tidal flow Rint = interrupter resistance
How many acceptable maneuvers needed for PFT?
minimum of 3
What is the largest difference between FEV1 or FVC allowed?
> 6yr: <0.150L
<6yr: <0.100L
Acceptability criteria for forced maneuvers (8)
1) Must have Best Expiratory Volume ≤ 5% of FVC or 0.100L (whichever is greater)
2) No evidence of faulty zero-flow setting
3) No cough in 1st second of expiration
4) No glottic closure within or after 1st second
5) Must achieve 1 of 3 End of Forced Expiration indicators
6) No evidence of obstructed mouthpiece
7) No evidence of leak
8) FIVC - FVC ≤0.100 or 5% of FVC
What is the Anaerobic Threshold?
The point above which lactate production exceeds removal
Change to anaerobic metabolism after anaerobic threshold
**At AT, VCO2 increases relative to VO2, changes the slope of the line
Indications for exercise test
- Evaluation of exercise tolerance
- Evaluation of undiagnosed exercise intolerance
- Evaluation of CV disease
- Evaluation of respiratory disease
- Specific clinical scenarios:
- Pre-op eval
- Exercise eval and pulmonary rehab
- Eval for impairment and disability
- Eval for transplant
Absolute contraindications for CPET
- Acute MI (3-5 days)
- Unstable angina
- Uncontrolled arrhythmias
- Syncope
- Endocarditis, Myocarditis, Pericarditis
- Heart failure
- Thrombosis of lower extremity
- Pulmonary edema
- RA desat <85%
- Respiratory Failure
Relative contraindications for CPET
- Left main coronary stenosis
- Moderate stenotic valvular heart disease
- Severe HTN
- Tachy/bradyarrhythmias
- Hypertrophic cardiomyopathy
- Pulmonary HTN
- Advanced or complicated pregnancy
- Electrolyte abnormalities
- Orthopedic impairment
Indications for Spirometry
1) Diagnosis
2) Monitoring
3) Disability/Impairment evaluation
4) Other
- Research
- Surveys
- Derivation of reference values
- Pre-employment
- Health assessment pre-physical activity
Relative contraindications for spirometry
1) Increase in myocardial demand or changes in BP (MI 1 week)
2) Increase in intracranial/intra-ocular pressure (Brain surgery 4 weeks, eye surgery 1 week)
3) Increase in sinus or middle ear pressures
4) Increase in intrathoracic and intra-abdominal pressure
5) Infection control
Indications for Methylcholine challenge
Help determine if current respiratory symptoms may be due to asthma or to make that diagnosis much less likely
Contraindications to methylcholine challenge
1) Airflow limitation (FEV1 <60%)
2) Spirometry quality
3) Cardiovascular problems
4) Cant perform any testing maneuvers properly
5) Pregnant/nursing mothers
6) Use of cholinesterase inhibitor medication
Medications to hold prior to skin testing
1) Anti-histamines (1st = 72 hours, 2nd = 7 days)
2) Topical steroids: 3 weeks
3) TCAs: 7-14 days
4) Benzos: 7 days
5) H2 blockers: 2 days
6) Omalizumab: 6 mos
7) Topical CNI: 7 days
No effect: short term PO steroids (1 week), leukotriene receptor antagonists
What is Aerobic threshold?
60% aerobic capacity + 70% max HR, 80% lactate threshold
Aerobic capacity = VO2 max (plateau where increased work but no change in oxygen uptake)
DLCO2 relative to VO2
VO2 = (HR x SV) x (CaO2 -CvO2)
DLO2 = VO2/AaDO2
What is the forced oscillation technique?
Application of an external pressure (small amplitude oscillations) signal superimposed on spontaneous breathing and measurement of the flow response of the respiratory system
Optimal frequency for forced oscillation technique?
4-8 Hz
Limiting factor for forced oscillation technique
- potential influence of upper airway compliance on respiratory system
- non-cooperation: refusal to use mouthpiece, inability to breathe without leak, difficulty breathing against oscillations
- wide range of health reference data
What is the respiratory exchange ratio?
Ratio of CO2 output to O2 consumption (VCO2/VO2)
Rest = 0.8-0.9
Increased exercise: increased carb utilization = larger fraction of metabolic fuel = increased R
Rapid rise after ventilatory threshold with increased VCO2, also increased after stopping exercise due to decreased VO2
What happens to end-tidal oxygen concentration during hyperventilation phase of exercise?
PETO2 remains relatively constant until the ventilatory threshold (AT) then it increases due to increase in minute and alveolar ventilation
What is the role for NO in the airways?
NO regulates vascular and bronchial tone (dilation), facilitates the coordinated beating of cilia and is a neurotransmitter for non-adrenergic and non-cholinergic neurons in the bronchial wall
Why is nasal NO increased in asthma?
Dual purpose:
1) relaxes bronchial smooth muscle and inhibits pro-inflammatory signaling events
2) can contribute to airway inflammation/injury through formation of toxic reactive nitrogen species
What is the amino acid precursor for NO?
What enzyme produces NO?
Amino acid: L-arginine
Enzyme: nitric oxide synthase
Advantages of allergy skin testing
- more sensitive
- rapid results
- able to visualize reaction
- wider variety of allergens
3 components to a diagnosis of an IgE-mediated allergic disorder
1) Identification of possible culprit through history
2) Demonstration of IgE-specific to the allergens by skin testing or in-vitro testing
3) Determination that exposure to the allergen results in sx
Advantages of RAST testing
- No risk of anaphylaxis
- No need to withhold medications
- Not affected by skin integrity or skin disease
Definitions of Acceptability, Usability and Reproducibility with PFTs
Acceptability: objective technical parameters for a maneuver to decide if there was maximal effort and FEV1/FVC are acceptable
Usability: If not acceptable, it may be best effort and they may be clinically usable
Reproducible: comparing between maneuvers
What is back extrapolated volume?
= volume of gas exhaled before time 0
Found by drawing a line with a slope equal to peak flow through the point of peak flow on the volume-time curve and setting time 0 to the intersection of time access
<5% FVC or <0.100L (whichever is greater)
too high = not max effort
In spirometry, does coughing in the first second affect FEV1, FVC or both?
FEV1 only
3 criteria for end of forced expiration (need 1)
1) Plateau < 0.025L/s change x 1 sec (most reliable)
2) Forced exhalation time of 15 seconds
3) If no plateau, judge if same FVC consistently achieved (FVC ≥ to repeatability tolerance of largest FVC within same testing)
What aspects of quality control are needed for a PFT lab?
- Daily calibration verification at low, medium, high flows
- Recalibrate often
- Daily inspection for displacement of piston stop
- Daily check of smooth operation of syringe
- Accuracy of ± 0.015L
- Monthly syringe leak test
- Documentation
PFT coaching for children
- Enthusiastic
- Detailed, simple instructions
- No intimidation
- Visual feedback
- May be ok to do more than 8 manuevers
- May benefit from practicing each step
- < 6, may be able to get acceptable FEV0.75
4 ways to look for Anaerobic Threshold
Point at which lactic acid production > lactic acid removal
1) VCO2/VO2: VCO2 increases faster and crosses VO2 line
2) VCO2/VO2: slope becomes steeper
3) RER >1
4) VEqO2 suddenly increases
Equation for Residual Volume (RV)
TLC - VC
What is Functional residual capacity?
How much volume is left after a normal breath, dependent on chest recoil and lung recoil
Normal resting volume of the respiratory system
What are the 2 opposing forces that make up FRC?
1) Lung elastic recoil
2) Chest wall recoil
What is lung elastic recoil?
Static recoil (stiffer requires more pressure), gets worse with age (FRC increases with age)
What is chest wall recoil?
Outward recoil (negative pressure relative to the lung, more chest wall expands, stretches the lung)
What is PAlv equal to at FRC?
0
How do the lungs change with respect to elastic recoil in pulmonary fibrosis?
Increased elastic recoil (stiff lungs) -> FRC goes down
How do the lungs change with COPD?
Increased compliance, decreased elastic recoil - FRC increased
What is compliance?
Measure of distensibility of matter and specifies the ease with which matter can be stretched or distorted
Equation for pulmonary compliance?
Lung Compliance (C) = Change in Lung Volume (V) / Change in Transpulmonary Pressure {Alveolar Pressure (Palv) – Pleural Pressure (Ppl)}
What happens to the lungs and chest wall with a pneumothorax?
The lung and chest wall go to their relaxation volumes
Lung = ~0% TLC
Chest wall = ~66% of TLC
Equation for trans-respiratory system pressure
Ptcw + Ptp = Ppl + Pst = Palv
Equation for trans-pulmonary pressure
Palv-Ppl = Pst (static recoil pressure, always positive)
(Pst+Ppl) - Ppl = Pst
Equation for trans-chest wall pressure
Ppl-Patm = Ppl (pleural pressure)
The compliance of the respiratory system intersects the 0 pressure line at which point?
FRC
Factors that determine compliance
1) Tissue composition
2) Surface tension forces and fluid lining the alveoli
How does age affect FRC?
FRC increases with age
How does obesity affect FRC
FRC decreases with obesity
What is dead space?
Ventilation of lung areas which are unable to exchange gases with the blood
What is anatomical dead space?
Ventilation of airways which are anatomically unsuited for exchanging gases with the blood
What is alveolar dead space?
Ventilation of alveoli which have no capillary blood flow thus they cannot exchange gases
What is physiological dead space?
All dead space in the lungs (anatomical + alveolar)
Equation for minute ventilation
Tidal volume x resp rate
Equation for alveolar ventilation
Total ventilation - anatomic dead space
What happens to PaCO2 if alveolar ventilation is halved?
alveolar and arterial CO2 will double
What is the normal volume for anatomic dead space
150 mls
What changes the anatomic dead space
Increases with large inspirations because of traction/pull exerted on the bronchi by surrounding lung parenchyma
Changes depending on size and posture of the subject
What is the Bohr equation?
VD/VT = (FACO2 - FECO2)/FACO2
What is the Bohr equation for alveolar dead space?
VD/VT = (PaCO2-PETCO2)/PaCO2
What is the partial pressure of a gas equal to?
Fraction of the gas x pressure (barometric-water)
eg. PACO2 = FACO2 (PB-47)
What is the alveolar ventilation equation?
PACO2 = (VCO2/VA) x 0.863
What happens to anatomical, alveolar, and physiological dead space during exercise, compared to rest?
Anatomical: no change
Alveolar: less (exercise = capillary recruitment)
Physiological: less
What happens to anatomical, alveolar, and physiological dead space when going from sitting to supine position?
Anatomical: less (presses on airway and makes it narrow)
Alveolar: less
Physiological: less
What is the equation for Reynolds number and what does it mean?
RN = [2 (radius) (density of gas) (velocity of gas)]/viscosity of gas
Determines is flow is laminar or turbulent (larger the number, the more likely to be turbulent)
Where within the lung would you be most likely to get turbulent flow?
The larger airways
What is the equation for airway resistance?
AR = [ 8(Viscosity) (length)]/pi (radius^4)
If you increase the radius, you dramatically reduce the resistance (smaller airways = sum of each part of the generation)
What is the role of surfactant protein A, B, C and D? (R)
A and D: innate immune function
B and C: enhance adsorption (how all the components are organized to form a thin film) and organizes lipids (which are also a component of surfactant
Is ABCA3 a component of surfactant? If not, what is it’s role? (R)
ABCA-3 is NOT a component of surfactant.
It’s literally part of the membrane of lamellar bodies, which are the organelle in which all surfactant components (so protein like SP-B, lipids and phospholipids) are stored before they make their way to the cell surface and then alveoli. ABCA-3 also helps with transporting phospholipids into lamellar bodies (recall that phospholipids make up 80% of surfactant)
What is a lamellar body? (R)
A storage organelle for surfactant components
What components are involved in clearing surfactant? (R)
Surfactant is degraded in both alveolar epithelial cells AND macrophages. On macrophages, GM-CSF attaches to it’s corresponding receptor (2 subunits: CSF2RA, CSF2RB). (There is also recycling of surfactant in the alveolar epithelial cells–especially important for infants with RDS who get exogenous surfactant, which they recycle, before endogenous surfactant production kicks in)
In which cells is surfactant produced? (R)
Type 2 alveolar epithelial cells
Is NKX2.1 a component of surfactant? If not, why does it cause surfactant disorders? (R)
No, it’s not a component of surfactant. It is a transcription factor that is needed for transcription of ABCA3, SP-B, SP-C. It’s also expressed in other tissue like thyroid and CNS (basal ganglia)
What is the purpose of surfactant? (R)
- Reduces surface tension at the air liquid interface and prevents collapse of alveoli at the end of expiration
- Less surface tension means less work of breathing
- Innate host defence and injury response
What are potential complications of high fiO2? (R)
- Absorptive atelectasis
- Bad for patients with hypoventilation–>decrease hypoxic respiratory drive
- Reactive oxygen species, so very bad for preterm infants and can get more lung injury, retinal injury
How does work of breathing change in moderate obstructive disease
Normal elastic work
Increased inspiratory resistive work
Markedly increased expiratory resistive work
Active expiratory work
Work of breathing in severe asthma
Increased elastic work due to hyperinflation
Increased inspiratory resistive work
++++++ Expiratory resistive work
Active expiratory work
Work of breathing in pulmonary fibrosis
Increased elastic work
Normal inspiratory and expiratory resistive work
No expiratory work
Why do patients with stiff lungs (ie. pulmonary fibrosis) breathe with lower tidal volumes?
Decreasing the tidal volume drops the elastic work (dropping TV by half drops work by 1/4) but you increase the dead space so need to breathe faster to keep up alveolar ventilation
3 jobs of the pulmonary circulation
1) Gas exchange (maximize diffusion)
2) Filtration (only other organ that gets all the blood pumped from the heart)
3) Blood reservoir
List 5 factors that affect diffusion as per Fick’s law
Diffusion= (surface area/thickness) x diffusion coefficient x (P1-P2)
- Surface area
- Thickness of the alveolar-capillary diffusion barrier
- Solubility of the gas
- Molecular weight of the gas
- Partial pressure difference
Which zone do you get the most blood flow?
The bottom (least resistance)
At which point in the breathing cycle is pulmonary vascular resistance at its lowest?
At FRC (decreases from RV to FRC and increases after to TLC) Capillary thins out and artery gets bigger with bigger lung volumes
Where is relation to the airways are the pulmonary arteries?
Parallel to the airways (also the lymphatics)
What is the purpose of hypoxic pulmonary vasoconstriction?
Acts to divert blood away from hypoxic regions to ventilated regions to improve V/Q matching
Which area of the lung is least compliant?
Top (due to gravity)
More expanded already at the top - when you breathe in, air wants to go to more compliant zones - bottom distends more than the top
Which area of the lung is the most ventilated?
Bottom (plus more perfused down there too)
How does the V/Q matching change within the lung?
The V/Q ratio increases from bottom to top (top has lots of ventilation but limited perfusion)
What is an ideal V/Q relationship?
1
How does a nitrogen washout work?
Used to test uniformity of gas distribution. Greater slope = greater inhomogeneity
The subject inspires a single breath of pure oxygen from RV to TLC (inspiratory VC maneuver). At end-inspiration, the dead space is filled with oxygen that has just been inspired.
Phase 1: 0% nitrogen (gas is from conducting airways)
Phase 2: sigmoid curve upwards - gas from dead space and alveoli
Phase 3: slope indicates almost constant nitrogen concentration in alveolar gas. Expect horizontal in healthy lung with evenly distributed oxygen/nitrogen
Phase 4: small spike as bottom airways close (closing volume)
Equation for PiO2
PiO2 = FiO2 x (PB -47)
Sea level, PB = 760
Abbreviated Alveolar Gas Equation
PAO2 = PIO2 - [PACO2/R]
Full Alveolar Gas Equation
PAO2 = PIO2 - [PACO2/R] + FiO2 X PACO2 x (1-R/R)
5 causes of hypoxemia
1) Low inspired FiO2
2) Hypoventilation
3) Shunt
4) V/Q mismatch
5) Diffusion limitation
Definition of a shunt
Perfusion without ventilation
Blood that enters the arterial system without going through ventilated areas of the lung - drops arterial PO2, cannot be fixed with 100% O2
Normal physiologic shunt value
1-2%
Do shunts increase PCO2 in arterial blood?
No, even though the shunted blood has lots of CO2, the chemoreceptors sense the elevation of arterial CO2 and respond by increasing ventilation (reduces the CO2 of unshunted blood until the level is normal)
Most common cause of hypoxemia?
V/Q mismatch
With airway obstruction, how does the V/Q ratio change?
O2 will fall and CO2 will rise and the O2 and CO2 of the alveolar gas and end-capillary blood will be the same as mixed venous blood (decreased V/Q)
With obstruction in blood flow, how does the V/Q ratio change?
O2 rises and CO2 falls, eventually reaching the composition of inspired gas when blood flow is abolished (O2 is the same as inspired gas - increased ratio)
How does distribution of lung blood flow change with exercise?
Distribution of blood flow becomes more uniform and the apex assumes a larger share of O2
What part of the lung has the higher PO2?
The apex
The major share of the blood comes from the lower zones, thus it lowers the overall PO2
The expired alveolar gas comes more uniformly from apex and base because differences in ventilation are much less than those for blood flow
What is the arterial-alveolar gradient?
The difference between ideal alveolar PO2 (PAO2) and the arterial PO2 (PaO2)
PAO2 - PaO2 (normal ~12)
Causes of elevated Aa gradient
Shunt
V/Q mismatch
DIffusion
Causes of normal Aa gradient
Hypoventilation
Low inspired FiO2
What is the role of surfactant protein A, B, C and D? (R)
A and D: innate immune function
B and C: enhance adsorption (how all the components are organized to form a thin film) and organizes lipids (which are also a component of surfactant
Is ABCA3 a component of surfactant? If not, what is it’s role? (R)
ABCA-3 is NOT a component of surfactant.
It’s literally part of the membrane of lamellar bodies, which are the organelle in which all surfactant components (so protein like SP-B, lipids and phospholipids) are stored before they make their way to the cell surface and then alveoli. ABCA-3 also helps with transporting phospholipids into lamellar bodies (recall that phospholipids make up 80% of surfactant)
What is a lamellar body? (R)
A storage organelle for surfactant components
What components are involved in clearing surfactant? (R)
Surfactant is degraded in both alveolar epithelial cells AND macrophages. On macrophages, GM-CSF attaches to it’s corresponding receptor (2 subunits: CSF2RA, CSF2RB).
In which cells is surfactant produced? (r)
Type 2 alveolar epithelial cells
Is NKX2.1 a component of surfactant? If not, why does it cause surfactant disorders? (r)
No, it’s not a component of surfactant. It is a transcription factor that is needed for transcription of ABCA3, SP-B, SP-C. It’s also expressed in other tissue like thyroid and CNS (basal ganglia)
What is the purpose of surfactant? (r)
- Reduces surface tension at the air liquid interface and prevents collapse of alveoli at the end of expiration
- Less surface tension means less work of breathing
- Innate host defence and injury response
What are potential complications of high fiO2? (r)
- Absorptive atelectasis
- Bad for patients with hypoventilation–>decrease hypoxic respiratory drive
- Reactive oxygen species, so very bad for preterm infants and can get more lung injury, retinal injury
Predicted PaO2/PAO2 equation
0.96-0.003 (age)
Expect to get worse with age because V/Q mismatch gets worse with age
What is the shunt equation? What assumptions are typically made? (R)
(CcO2 - CaO2)/(CcO2 - CvO2)
CcO2 = alveolar (ideal scenario)
CaO2 = arterial
CvO2 = venous. Can assume at saturation of 75% and PvO2 of 45 mmHg
What is the respiratory exchange ratio - R (R)
VCO2/VO2 (ratio of CO2 production to oxygen consumption. Usually is 0.8 (we actually consume more oxygen than we produce CO2). This ratio depends on diet.
What is the difference between hypoxemia and hypoxia? (R)
Hypoxemia = insufficient oxygenation = low PaO2
Hypoxia = insufficient oxygen for a tissue or organ
Can have hypoxia without hypoxemia with ischemic hypoxia, cyanide poisoning, anemia, CO poisoning
Equation for VO2 (Fick Equation)
O2 delivered - O2 returned
= CO x (CaO2 - CvO2) = (HR x SV) (CaO2 - CvO2)
Equation for oxygen delivery
CO x CaO2
= (HR x SV) x (1.34 x Hgb x SaO2)
How does exercise affect diffusing capacity?
Increases surface area = increases diffusion
How do you increase the driving pressure for diffusion?
Increase FiO2 (increase PaO2) Driving pressure = (alveolar pressure - capillary pressure)
What is the extraction ratio?
VO2/DO2
consumed/delivered
Equation for predicted A-a DO2
0.3Age + 4 (when breathing room air only)
What is the critical oxygen extraction ratio?
The max you can extract from the blood at any time
0.65-0.7
What is the ratio of PaO2/PAO2 good for?
To compare between scenarios to see if the lungs are improving or not
Causes of low SvO2
Anemia (hemorrhage)
Hypoxemia (lung disease/impaired diffusion, decreased ventilation, low inspired FiO2)
Stagnant flow (low preload, decreased contractility)
Increased VO2 (fever, sepsis, burn, trauma)
Where is the breathing cycle is diffusion at its maximum?
TLC (directly related to lung volume)
What happens when the oxygen dissociation curve shifts to the right?
More unloading of O2 at an given PO2
“exercising muscle is acid, hypercarbic, and hot and benefits from unloading of oxygen from its capillaries”
Increase temp, increased 2-3 DPG, increased (H+), decreased pH
What happens when the oxygen dissociation curve shifts to the left?
Less unloading of O2 at a given PO2
Decreased temp, decreased DPG, CO, increased pH (decreased H+)
Equation for VO2
O2 delivered - O2 returned
= CO x (CaO2 - CvO2) = (HR x SV) (CaO2 - CvO2)
Equation for oxygen delivery
CO x CaO2
= (HR x SV) x (1.34 x Hgb x SaO2)
What can increase oxygen demand?
Fever, catabolic stress, infection, agitation, seizures, increased WOB, positive inotropes
What can decrease oxygen demand?
Sedation, mechanical ventilation, muscle paralysis, barbiturates, hypothermia
What is the extraction ratio?
VO2/DO2
consumed/delivered
How does anemia affect the oxygen dissociation curve?
Shifts to the right - easier to unload as it’s harder to hang on
What is the critical oxygen extraction ratio?
The max you can extract from the blood at any time
0.65-0.7
What does a low SvO2 mean?
1) low SaO2
2) Increased VO2
3) Decreased CO
4) Decreased Hgb
Causes of low SvO2
Anemia (hemorrhage)
Hypoxemia (lung disease/impaired diffusion, decreased ventilation, low inspired FiO2)
Stagnant flow (low preload, decreased contractility)
Increased VO2 (fever, sepsis, burn, trauma)
How can you increase oxygen delivery?
1) Increase cardiac output (best way)
2) Increase Hgb
3) Increased FiO2
What are the pulmonary complications of diving (R)?
- Pulmonary barotrauma
- Decompression sickness
- Nitrogen narcosis
What are the respiratory problems with air travel and typical barometric presssure? (R)
- Decreased PaO2 due to decreased Pb, which is often pressured to 560 mmHg
- Expansion of contained gases
- Low humidity
What is the Henderson hasselbach equation (R)
pH = 6.1 + log (HCO3)/0.03PCO2
(it’s just the log of HCO3)
this equation is used by blood gas machine to figure out HCO3
PcO2 and pH are directly measured
How is CO2 transported in blood (R)
- Majority as HCO3- either in plasma (majority) or within RBC
- Smaller amount as part of hemoglobin or dissolved in plasma. (Recall that the CO2 dissociation curve shows a very linear relationship of PaCO2 to dissolved CO2)
Difference between static and dynamic compliance?
- static = no flow. Vt/Pplateau - PEEP
- dynamic compliance = flow. Vt/PIP-PEEP. Airway resistance and RR influence dynamic compliance. High RR = lower dynamic compliance in patients with airway obstruction
Equation for DLCO
[(VA) (Pulmonary cap blood volume) (HB)] / [(alveolar-capillary membrane thickness) (COHb)]
How does Mueller maneuver affect DLCO?
Mueller: inhalation against closed glottic, decreases intrathoracic pressure and increases blood return to the lungs
= Increased DLCO
How does PH affect DLCO?
Decreased DLCO
How does lobar resection affect DLCO?
Decreased VA = decreased DLCO (normal if DLCO is corrected for volume)
How does hemorrhage affect DLCO?
Decreased (normal if corrected for Hgb)
Pulmonary hemorrhage = increased DLCO (increased blood in the space)
How does smoking affect DLCO?
Smoking increases carboxyhemoglobin = decreased DLCO
Equation for oxygenation index
(Mean airway pressure x FiO2)/100
Obesity changes on PFT
Classically - no changes on PFT except MVV until VC becomes reduced in extreme cases
- Decreased FRC/ERV
- Decreased TLC
- Increased RV
What can affect Peak Expiratory Flow?
Effort!!!
Numbers can be artificially high with tongue thrusts or spitting
May be low due to poor effort or technique
3 reasons for poor 6 second plateau in children less than 6yrs
1) High elastic recoil = exhalation of FVC prior to 6 seconds
2) Require coaching specific to developmental level with possible incentive display
3) Restrictive lung disease
Blood gas findings if bubble in venous sample
1) pH: unchanged
2) pO2: increased
3) pCO2: decreased
4) HCO3: unchanged
Starling equation
Qf = Kf[(Pc − Pis) − σ(πpl − πis)]
Qf = net flow of fluid Kf = capillary filtration coefficient Pc = capillary hydrostatic pressure Pis = hydrostatic pressure of the interstitial fluid σ = reflection coefficient πpl = colloid osmotic (oncotic) pressure of the plasma πis = colloid osmotic pressure of the interstitial fluid
How does extra fluid in the interstitial removed?
Removed by lymphatic drainage of the lung - the pulmonary lymphatic vessels are mostly located in the extra alveolar interstitium
What can happen as a result of increased capillary permeability?
ARDS, oxygen toxicity, inhaled/circulating toxins
What can happen as a result of increased capillary hydrostatic pressure?
Increase LA pressure resulting from LV infarction or MS
Too much IV fluids
What can happen as a result of decreased interstitial hydrostatic pressure?
Too rapid evacuation of pneumo or hemothorax, upper airway obstruction
What can happen as a result of decreased colloid osmotic pressure?
Protein starvation, dilution of blood products by IV solutions, renal problems resulting in urinary protein loss (proteinuria)
3 reasons why PEF is not use in paediatrics
1) It is effort dependent
2) It has high variability
3) PEF is less sensitive than standard spirometry in detecting reversibility of airflow obstruction after bronchodilator administration as well as worsening of airflow limitation in response to inhalational challenge
Medical student asking about CPAP and BiPAP, mention2 conditions in which you will prefers BiPAP over CPAP and why?
Central sleep apnea – can provide rate so ventilation will occur despite central apnea
Neuromuscular disorder – inspiratory pressure required to provide ventilation
What is P50?
P50 is the PO2 at which 50% of the hemoglobin present in the blood is in the deoxyhemoglobin state and 50% is in the oxyhemoglobin state.
(At a temperature of 37C, a pH of 7.4 and PCO2 of 40mmHg, normal human blood has a P50 or 26 or 27mmHg. If the oxyhemoglobin dissociation curve is shifted to the right, the P50 increases. If it is shifted to the left, the P50 decreases).
3 causes that shifts the Hb -Sat curve to the right
Increased temperature Reduced pH Increased 2,3 DPG Increased PCO2 Memory tool: think of exercising muscles--hot, acidosis, high CO2
Obesity, what do you expect in PFT?
Reduced FVC Reduced TLC Reduced ERV, FRC Normal FEV1 and FEV1/FVC (although increased risk of asthma) Reduced MIP/MEP Increased DLCO
HHT calculate the shunt, what is a normal shunt?
Equation = (CcO2 - CaO2)/(CcO2-CvO2)
Normal shunt: ~ 2-5 %
General mechanism/stages of airway clearance:
- Get air behind mucous to open up lungs
- Loosen/unstick secretions from small airways
- Mobilize secretions through the airways to larger airways
- Clear secretions from the central airways
Key points about Positioning for airway clearance
Supine less beneficial unless muscle weakness with diaphragmatic sparing
- Prone positioning can improve respiratory function
- reduction in GER
- In unilateral disease, if affected lung is upwards, this may cause rapid
decompensation, as typically the upper lung is preferentially ventilated
Key points about manual hyperinflation for airway clearance
Aim: enhance mobilization of secretions by increasing expiratory flow, re-inflation of atelectatic areas and improve gas exchange
- Generally, do not exceed 10cmH2O above vent pressures
- Contraindications: HD instability, undrained pneumothorax, cystic/bullous lung
disease, severe bronchospasm, high PEEP
Key points about Intermittent Positive Pressure Breathing for airway clearance
Augments tidal volumes via Positive pressure delivered through mouthpiece or mask
- Utilized contralateral ventilation to get air behind secretions to allow for mobilization
- Precautions: O2 sensative children, post-op air leak, HD instability, Pneumo, Lung abscess, bronchial tumor, severe bronchospasm
3 component to Active Cycle of Breathing for airway clearance
1) Breathing control: resting period of relaxed breathing at patients own depth/pace
2) Thoracic expansion exercises: 3-5 deep breaths with emphasis on inspiration
3) Forced expiration “huff”: combines 1 to 2 forced expirations followed by regular breathing
Key points about PEP for airway clearance
Mouthpiece or mask
- Thought to have effect on peripheral airways and collateral channels of
ventilation
- Increase in lung volumes may allow air to get behind secretions and mobilize
- Mask with one way valve where expiratory resistance is added (manometer
measures/sets)
- Contraindications/precautions: HD instability, pneumo, bronchospasm
Key points about Intrapulmonary Percussive Ventilation for airway clearance
Modified IPPB, with superimposed high frequency mini-bursts of air on intrinsic breathing pattern, creating internal vibration
- Postulated to promote sputum clearance
- Contraindications/precautions: HD instability, pneumo, bronchospasm, Lyells
syndrome (Toxic Epidermal necrolysis)
Key points about Maximum Insufflation for airway clearance
Breath stacking, IPPB, glossopharyngeal breathing
- Can use NIV (volume mode) or Bag/mask
- Creates greater VC than spontaneous
- Improves cough strength and airway clearance
- Contraindications/precautions: HD instability, pneumo, bronchospasm
Key points about Mechanical Insufflation/Exsufflation for airway clearance
Apply positive pressure, then rapid shift to negative pressure - Creates high expiratory flow, simulating a cough
- Most effective when child can command a cough
- Contraindications/precautions: Increased ICP, prem, abdo distention, pneumo
3 components of a cough
Deep inspiration (85-90% of TLC)
- Glottic closure (requires intact bulbar function)
- Effective contraction of expiratory muscles (abdo and intercostal)
- Generate pleural pressures of 190cm H20
Conditions NOT amenable to physiotherapy
Croup
Pertussis
- Can precipitate paroxysmal cough
Foreign body
- Consider PT after removal if issues with retained secretions
Pulmonary edema
- CPAP/NIV may be used to treat edema
Lobar pneumonia/empyema
- Healthy children can cough out secretions independently
- Consider if there is pneumonia in a child with underlying high risk condition
Bronchiolitis
- No reduction in LOS, Oxygen requirement, severity score
Difference in children’s anatomy that make them more susceptible to upper airway narrowing
Larynx of neonate is more superior (higher in neck)
Epiglottis is narrow, omega shaped, vertically positioned Narrowest segment of the pediatric airway is subglottic region
● Encircled by the rigid cricoid cartilage ring
● Non-fibrous mucosa is easily obstructed with edema
● Cartilage is soft and compliant → allows for dynamic collapse of airways
Large heads, lax neck support → increases obstruction when supine Large tongues relative to oropharynx
What is capillary hydrostatic pressure?
The pressure exerted by blood against the wall of a capillary = capillary hydrostatic pressure (CHP), and is the same as capillary blood pressure. CHP is the force that drives fluid out of capillaries and into the tissues.
What is interstitial hydrostatic pressure?
As fluid exits a capillary and moves into tissues, the hydrostatic pressure in the interstitial fluid correspondingly rises. This opposing hydrostatic pressure is called the interstitial fluid hydrostatic pressure (IFHP).
Generally, the CHP originating from the arterial pathways is considerably higher than the IFHP, because lymphatic vessels are continually absorbing excess fluid from the tissues. Thus, fluid generally moves out of the capillary and into the interstitial fluid. This process is called filtration.
What is osmotic pressure?
The net pressure that drives reabsorption—the movement of fluid from the interstitial fluid back into the capillaries—is called osmotic pressure (sometimes referred to as oncotic pressure).
Whereas hydrostatic pressure forces fluid out of the capillary, osmotic pressure draws fluid back in. Osmotic pressure is determined by osmotic concentration gradients, that is, the difference in the solute-to-water concentrations in the blood and tissue fluid.
What is the blood colloidal osmotic pressure?
The pressure created by the concentration of colloidal proteins in the blood
Its effect on capillary exchange accounts for the reabsorption of water. The plasma proteins suspended in blood cannot move across the semipermeable capillary cell membrane, and so they remain in the plasma. As a result, blood has a higher colloidal concentration and lower water concentration than tissue fluid. It therefore attracts water.
How is the interstitial colloidal osmotic pressure different from the blood colloidal osmotic pressure?
The blood colloid osmotic pressure is higher than the interstitial fluid colloidal osmotic pressure (IFCOP), which is always very low because interstitial fluid contains few proteins.
Thus, water is drawn from the tissue fluid back into the capillary, carrying dissolved molecules with it. This difference in colloidal osmotic pressure accounts for reabsorption.
Primary chest muscles responsible for breathing at rest
- Diaphragm = principal muscle of respiration; Accessory Ms = stabilize rib cage
- Failure to fixate rib cage → paradoxical breathing
- Expiratory muscles inactive
Primary chest muscles responsible for breathing with increased demands
-Accessory Ms recruited for inspiration → upward motion of the rib cage
-Expiratory muscles activated → end expiratory volumes decr below FRC
-Therefore: Any decr in expiratory muscle = ↑RV, ↓VC
-Sleep associated with ↓FRC, ↓Tone which can lead to
paradoxical breathing, hypoventilation
-Thus nocturnal hypoventilation / blood gas abn often the first sign of progressive NMD
Anatomy of the Pleural Space
The pleural space is 10 to 24 μm wide, filled with thin liquid film.
- The parietal pleura covers the inner aspect of the chest wall and diaphragm.
- The visceral pleura is tightly adherent to the surface of the lungs and to interlobar fissures.
Characteristics of the Parietal Pleura
Consists of a single layer of flat, cuboidal mesothelial cells, supported by loose connective tissue.
Blood vessels, nerves, and lymphatic vessels invest the connective tissue. The arterial supply is derived from the intercostal and internal mammary arteries. Venous blood drains to the systemic circulation.
Innervated with the sensory branches of the intercostal and phrenic nerves.
Has direct connection to the lymphatic vessels. The surface of the parietal pleura contains stomas that are 2 to 12 μm in diameter and exhibit preferential caudal distribution. They exhibit as much as a 10-fold increase in size with inspiratory maneuvers.
Stomas are clearing fluid and particle accumulations via the lymphatic glands. Lymphatic vessels are located in the submesothelial layer of the parietal pleura.
The anterior parietal pleura drains to the internal intercostal lymph nodes, and the posterior parietal pleura drains to the lymph nodes located along the internal thoracic artery.
Characteristics of the Visceral Pleura
Consist of a single mesothelial layer of cuboidal cells overlying the basement membrane, and there are multiple submesothelial layers of connective tissue.
Microvilli, are evident on the apical surfaces of the visceral mesothelial cells. The microvilli participate in the homeostasis of the pleural fluid and contribute to transmembrane solute and fluid movement.
Further, vesicles contained within the microvilli trap particles and glycoproteins, thereby reducing friction between the visceral and parietal pleurae.
Blood supply to the visceral pleura is via the bronchial arteries, with a minor contribution from the pulmonary circulation. The connective tissue underlying the mesothelial layer is richly endowed with type 1 collagen and provides much of the tensile strength of the pleura.
The lymphatic glands drain to the mediastinal nodes, following the course set by the pulmonary veins and arteries.
The visceral pleura has no sensory innervation, but it is supplied by branches of the vagus and sympathetic trunks.
How is the pleural fluid formed and absorbed?
Normally, the influx and outflow of pleural fluid is in steady state and results in (0.1 to 0.2 mL/kg) of sterile, colorless liquid.
The pleural liquid is thickest over dependent areas of the thorax, it provides union and prevents friction between the visceral and parietal pleurae.
There is a balance among production of pleural fluid, competence of the pleural membrane, and absorption of pleural fluid via microvilli, capillary membranes, and lymphatic stomas.
Fluid influx and outflow are described by Starling forces and also are determined by clearance via lymphatic stomas.
Nearly 90% of pleural liquid filtered out of the arterial end of the capillaries is re-absorbed at the venous end. The remainder of the filtrate (10%) is returned via the lymphatic glands.
The balance between filtration and re-absorption forces determines the direction of liquid movement.
Net liquid absorption from the pleural space occurs because absorption pressure is slightly greater than filtration pressure.
What are the forces acting on the pleural fluid?
There is a net pressure of 9 cm H2O (filtration pressure) at the parietal pleural capillary level, tending to drive liquid into the pleural space.
In contrast, a net driving pressure of -10 cm H2O (absorption pressure) is acting on the visceral pleural capillaries, driving liquid from the pleural space into the capillaries.
Starling equation
Qf = Kf[(Pc − Pis) − σ(πpl − πis)]
Qf = net flow of fluid Kf = capillary filtration coefficient Pc = capillary hydrostatic pressure Pis = hydrostatic pressure of the interstitial fluid σ = reflection coefficient πpl = colloid osmotic (oncotic) pressure of the plasma πis = colloid osmotic pressure of the interstitial fluid
What can augment pleural fluid absorption?
Intercostal and diaphragmatic activity (e.g., deep breathing exercises), which results in increased vascular and lymphatic uptake owing to dilation of the lymphatic stomas and the dehiscences formed between mesothelial cells of the visceral pleura.
What can augment pleural fluid generation/ decrease absorption?
Markedly negative intrapleural pressures throughout the respiratory cycle (e.g.,atelectasis or with continuous suction on closed thoracostomy tubes).
Hypoventilation decreases absorption of particulate matter from the pleural space.
How is extra pleural fluid cleared?
The rate of fluid transport from the pleural space through the lymphatic glands increases in a linear fashion to exceed the usual rate of fluid production by almost 30-fold, that is crucial to prevent and clear fluid accumulation.
How does the pleural space maintain the air-free environment?
The pleural membranes are permeable to gas, yet the pleural space is free of air. The difference between total gas pressure in the venous system and that in the pleural space accounts for this fact.
Because total gas pressure in venous blood is approximately 73 cm H2O subatmospheric, and intrapleural pressure at resting lung volume is approximately 5 cm H2O subatmospheric, there is a pressure gradient of approximately 68 cm H2O, favouring continuing absorption of gas from the pleural space into the circulation.
The partial pressure of nitrogen in the capillary and venous blood is the major contributor to the total partial pressure of gas in the pleural space.
The clinical practice of using O2 to reduce the PN2 and speed resorption of pneumois based on this principle, 100% oxygen breathing can increase the rate of absorption of loculated pleural air by six-fold.
Pathogenesis of Accumulation of Excess Pleural Fluid
It is an equilibrium between pleural liquid formation (filtration) and removal (absorption).
Effusion happen whenever filtration exceeds removal as a result of:
(1) increased filtration associated with normal or impaired absorption,
(2) normal filtration associated with inadequate removal,
(3) addition of exogenous fluid (peritoneal cavity or intravenous fluid extravasation).
Thus, disequilibrium may be caused by disturbances in the Starling forces that govern filtration and absorption, alterations in lymphatic drainage, or both.
How does inflammation affect the balance of the pleural fluid?
Inflammation (e.g., pleural infection, rheumatoid arthritis, systemic lupus erythematosus, pulmonary infarction) or direct toxic damage to the endothelium may:
a- increase the filtration coefficient which allows protein loss from the capillaries and accumulation in the pleural cavity, thereby increasing oncotic pressure in the interstitial space.
b-Local blood flow may increase in response to inflammation, resulting in an increase in capillary hydrostatic pressure.
→The net consequence of these changes is increased liquid and protein transudation into the pleural cavity that exceeds the normal capacity of lymphatic drainage.
In all conditions that result in pleural effusion caused by abnormality in the pleural membrane, there will be an excess of protein or other large molecules in the pleural fluid.
What can enhance pleural fluid formation?
→increased capillary hydrostatic pressure or more negative hydrostatic pressure in the interstitial space.
Hydrostatic pressure increases with:
A- systemic venous hypertension (e.g., pericarditis, right-sided heart failure caused by overinfusion of blood or fluid, superior vena cava syndrome).
B- because of pulmonary venous hypertension (e.g., Congestive heart failure).
The resulting increased accumulation of pleural liquid (hydrothorax) is caused by increased driving pressure in the systemic capillaries.
Markedly subatmospheric pleural pressure (e.g., persistent high negative pressures occasionally used during tube thoracostomy drainage), contribute to effusions that occur after pneumonectomy, recurrence of effusion after repeated thoracenteses.
What can impede Lymphatic drainage?
(1) systemic venous hypertension
(2) mediastinal lymphadenopathy (e.g., lymphoma or fibrosis)
(3) fibrosis of the parietal pleura (e.g., tuberculosis)
(4) obstruction of the thoracic duct (e.g., chylothorax)
(5) developmental hypoplasia of the lymphatic channels (e.g., hereditary lymphedema).
Results of a pleural effusion on the respiratory system
- Limited lung inflation and decrease in vital capacity.
- Lung and chest wall are uncoupled, and function may not be coordinated.
- Elastic resistance to lung distention increases, thereby limiting lung expansion.
- Compressive atelectasis contribute to decreased lung expansion, V\Q mismatch, and hypoxemia.
- Pleural inflammation is associated with pain that worsens with deep breathing, limiting full lung expansion. Pleuritic pain may resolve as pleural fluid increases because contact between the irritated pleural membranes is reduced.
- The chest wall may bulge outward, with downward displacement of the ipsilateral hemidiaphragm. Inspiratory muscles are then placed at a mechanical disadvantage, compromising inspiratory efforts.
- Rarely, a large pleural effusion will produce mediastinal shift, decreasing venous return and compromising cardiac output.
Therapy→ may also contribute to ongoing pulmonary compromise.
- Pain caused by thoracentesis or indwelling chest tubes may limit full inspiration.
- Ongoing use of suction for chest tube drainage may promote continued development and removal of pleural fluid. Chronic loss of protein or lipids as a result of chest tube drainage may result in malnutrition.
Signs/Symptoms of Pleural Effusions
Pleural effusion is usually secondary to other disease, look for them.
Small volume→ asymptomatic, as volume increase → cardiorespiratory difficulties.
Chest tightness, and dyspnea, orthopnea. Older children may have sharp pleuritic pain on inspiration or a cough that is caused by stretching of the parietal pleura.
Pain may be felt in the chest overlying the site of inflammation or may be referred to the ipsilateral shoulder if the central diaphragm is involved or
to the abdomen if the peripheral diaphragm is involved.
Physical Exam findings for Pleural Effusions
Pleural rub caused by roughened pleural surface, as the volume increase, it disappears.
Diminished thoracic wall excursion, fullness of the intercostal spaces, dull or flat percussion, decreased tactile and vocal fremitus, diminished whispering pectoriloquy, and decreased breath sounds are easily demonstrated over the involved site in an older child with moderate effusion.
Displacement of the trachea and cardiac apex toward the contralateral side and splinting of the involved hemithorax, resulting in scoliosis concave to the affected side.
What is the earliest radiologic sign of pleural liquid accumulation?
Obliteration of the C-P angle
PA film is relatively insensitive in detecting pleural effusion.
When effusion increases:
- Uniform water density.
- Widened interspaces on the affected side
- Displacement of the mediastinum to the contralateral hemithorax.
How much fluid is required on an upright CXR to required to be visualized?
400mL
Role of Lateral decubitus CXR for pleural effusions
Thin, mobile (nonloculated) pleural fluid will layer out on the dependent side
Lateral decubitus views with the unaffected side inferior may enhance visualization of the underlying parenchyma on the affected hemithorax.
Placing the unaffected side superior can detect as little as 50 mL; this liquid is seen as a layering of liquid density in the dependent portion of the thoracic cavity.
A decubitus film demonstrating more than 10 mm of pleural fluid between the inside of the chest wall and the lung indicates an effusion of sufficient volume for thoracentesis. Decubitus films may also demonstrate infrapulmonary pleural effusion
Failure of the liquid to shift from the upright to the decubitus view indicates loculation, as commonly seen in staphylococcal empyema
Best imaging test for pleural effusions
U/S
Can differentiate pleural thickening from effusion, and identify the best site for thoracentesis, or chest tube and detect loculations.
Demonstrable multiple echogenic foci indicate an exudate or an empyema.
With an empyema, there may be accentuation of the visceral pleura caused by thickening of the visceral pleura, compressive atelectasis, or consolidation of the adjacent parenchyma. Thus, the border between the pleural fluid and the parenchyma may be accentuated.
Role of CT in pleural effusions
CTs are helpful in the evaluation of:
- pleura and the underlying parenchyma in large loculated effusions
- Pleural thickening or a mass is readily apparent
- The parietal pleura readily enhances in the presence of an empyema
-A loculated parapneumonic effusion is differentiated from a lung abscess by the angle made between the fluid-filled mass and the chest wall. An empyema usually creates an obtuse angle where it meets the chest wall, in contrast to the acute angle produced by an abscess.
What imaging can detect a bronchopleural fistula?
Contrast Sinography
Radiopaque contrast injected into the affected pleural space through a needle or an existing chest tube.
As the patient coughs, the contrast material opacifies the fistula and spreads throughout the bronchial tree. This is the procedure of choice for peripherally situated small fistulas. Selective bronchography is used to delineate multiple centrally located fistulas.
Physical and Chemical Characteristics of Chyle
Sterile Ingested lipophilic dyes stain the effusion Predominantly lymphocytes Sudan stain shows fat globules Total fat content > plasma Protein content = half or same as plasma Lytes, BUN, glucose same as plasma
Different appearance of pleural fluid
Transudate = pale, clear, yellow
Exudate = purulent, sometimes milky with fatty degeneration of pus if long standing infection
Chyle = milky white and opalescent, chylomicrons after feeding
Chyliform = if no fat, chylomicrons or a turbid supernatant
Bloody = vascular erosion from a malignant tumour
Chocolate brown = fluid or anchovy paste appearance = amebiasis
Putrid odour fluid = anaerobic pleural infections
Light’s criteria
(1) Pleural fluid to serum protein level is >0.5.
(2) Pleural fluid to serum lactate dehydrogenase (LDH) level is >0.6.
(3) Pleural fluid to serum LDH level is greater than two thirds of the upper limit of normal for serum levels
Absence of all three criteria indicates that the pleural fluid is a transudate, and the presence of any one of the three criteria indicates an exudate.
Minor criteria suggest an exudate include elevated pleural liquid cholesterol (>45 mg/dL, 1.16 mmol/L) and a pleural liquid protein level >30 g/L.
Tests to run on pleural fluid
Min = Total protein, LDH, glucose
Other: albumin, bacterial culture, cell count/differential, pH
Definition of Eosinophilic pleural effusion
Greater than 10% eosinophils
Pleural ( hemothorax or pneumothorax, pulmonary infarction), parasitic or fungal infection, and drug hypersensitivity reactions
Cell count differential for pleural fluid
Hemothorax is present if the hematocrit of the pleural fluid is more than 50% of the hematocrit of the peripheral blood. Usual causes include trauma, malignancy, lung infarction, and postpericardiotomy syndrome.
80% of transudates have WBC of up to 1000/μL. Monocytes, lymphocytes, and macrophages are the predominant white blood cells in a transudate.
WBC counts of <10,000/μL, of which approximately 85% are lymphocytes is characteristic for Lymphoma and TB.
Lymphs also commonly seen in the pleural fluid of patients with sarcoidosis, chronic rheumatoid arthritis, chylothorax, and yellow nail syndrome.
WBC counts are usually >10,000/μL in patients with parapneumonic effusion, empyema, acute pancreatitis, and lupus pleuritis.
pH abnormalities in pleural fluid
PH >7.45 or greater than blood pH is consistent with a transudate.
PH <7.30 occurs in the presence of increased carbon dioxide production (e.g., infection), acid leak into the pleural space (e.g., esophageal rupture with high amylase in PF), or a decrease in normal hydrogen ion transport from the pleural space (e.g., pleuritis, pleural fibrosis).
What is considered to be a parapneumonic effusion?
Pleural effusions with pH <7.10, an LDH level >1000 IU/L, and a glucose level <50% of blood glucose
What does isolated high LDH in pleural fluid mean?
High LDH in the face of normal or near-normal levels of pleural fluid protein suggests malignancy or pleural infection.
What does glucose value in pleural fluid mean?
<50% of blood values in cases of decreased transport to the pleural space or increased uptake.
Empyema, tuberculosis, rheumatoid arthritis, lupus pleuritis, pancreatitis, malignancy, and esophageal rupture reduce pleural fluid glucose levels.
Characteristics of Chylous effusions
- Normal pleural fluid/serum glucose concentration ratio (>0.5)
- Presence of chylomicrons, the presence of triglycerides, and an abundance of T lymphocytes.
- The pleural fluid pH is normal.
What is an extravasated infusate or effusion?
Secondary to peritoneal dialysis -> characteristic biochemical picture:
Milky appearance or color may be similar to that of the infusate. The pleural liquid glucose level is greater than the blood glucose level.
Pleural liquid LDH levels are low and the fluid may have a neutrophilic predominance or may be hemorrhagic, as shown by cell counts.
When is a pleural biopsy indicated?
Indicated in patients with unexplained inflammatory pleural effusion.
This typically occurs in the context of malignancy—either as a primary cause or 2ry to infection.
How can air get into the pleural space?
- Pleural space and atmosphere have free communication (defect in chest wall, parietal pleura, alveolar rupture)
- During assisted ventilation (pneumomediastinum, PIE, subcutaneous emphysema, pneumopericardium)
Components of the pressure-volume curve
The lung volume at any given pressure during deflation is larger that during inflation (hysteresis)
The lung without any expanding pressure has some air inside it -> even if atm pressure increases, small airways close trapping gas in the alveoli (this lung closure occurs at high lung volume with increasing age and in some types of lung disease)
Transpulmonary pressure: the pressure around the lung when the alveolar pressure is atmospheric
The pressure needed to open a lung unit is related to the radius of curvature and surface tension of the meniscus of fluid in the airspace leading to the lung unit. The units with larger radii and lower surface tensions will “pop” open first because, with partial expansion, the radius increases and the forces needed to finish opening the unit decrease.
Surfactant decreases the opening pressure from greater than 20 to 15cm H2O.
Because surfactant does not alter airway diameter, the decreased opening pressure results from surface adsorption of the surfactant to the fluid in the airways. The inflation is more uniform as more units open at lower pressures, resulting in less overdistention of the open units.
The pressure needed to open a lung unit depends on what factors?
- The radius of curvature
- Surface tension of the meniscus of fluid in the airspace leading to the lung unit.
The units with larger radii and lower surface tensions will “pop” open first because, with partial expansion, the radius increases and the forces needed to finish opening the unit decrease.
What is the equation for compliance?
Compliance (= the slope of the pressure-volume curve)
change in volume/change in pressure
What happens with reduced compliance?
Reduced compliance -> caused by an increase of fibrous tissue in the lung (pulmonary fibrosis) and by alveolar edema (prevents some inflation of alveoli).
Also falls if the lung remains unventilated for a long period (esp if volume is low) -> atelectasis and increased surface tension
Falls if pulmonary venous pressure is increased and the lung is full of blood
What happens with increased compliance?
Increased compliance -> pulmonary emphysema and in the normal aging lung.
Alteration in the elastic tissue in the lung
Also occurs with asthma (since at a higher volume on the curve)
Mechanism of surfactant
Reduces surface tension - molecules of phosphatidylcholine are hydrophobic at one end and hydrophilic at the other, align themselves in the surface. Intermolecular repulsive forces oppose normal attracting forces (greater when compressed).
This:
1) Increases compliance of lung, reduces work of expanding each breath
2) Stabilizes alveoli (small surface area = small tension = pressure lower allowing flow into smaller alveoli)
3) Prevents edema
Pulmonary surfactant = mixture of specific lipids and proteins that reduces surface tension at the air-liquid interface, thereby preventing alveolar collapse at end expiration. Critical function requires tight regulation of alveolar surfactant composition and quantity.
Components of Surfactant
Surfactant = complex mixture of phospholipids, neutral lipids and specific proteins that is produced by the alveolar type II epithelial cells (AEC2) stored in intracellular organelles (lamellar bodies) and secreted by exocytosis into the alveolar lumen
80% phospholipids, ~8% protein, ~8% neutral lipids (primarily cholesterol)
Major lipid = phosphatidylcholine (PC) → needed for surfactant to function in reducing surface tension
4 proteins: A, B, C, D
On the hemoglobin dissociation curve at what PO2 does a hemoglobin saturation of 90% occur
90% -> 60mmHg
60% -> 30mmHg
50% -> 28mmHg (P50)
Normal patient: Saturation of 90% corresponds to PaO2 of about 65 mmHg
Other useful anchor points:
o PaO2 = 100, SaO2 = 97% (arterial blood)
o PaO2 = 40, SaO2 = 75% (venous blood)
o P50 = PaO2 at which there is 50% haemoglobin saturation. This is generally at PaO2 of 27 mmHg.
Factors external to the red blood cell that will cause shifting of the hemoglobin curve
Decreased pH, increased CO2, increased temperature will cause rightward shift–>so think about shift in a patient with sepsis, infection
Carbon monoxide–>left-ward shift, so difficult to unload oxygen. In addition, CO has a much higher affinity for Hb than oxygen does so small amounts of CO can occupy large amounts of Hb
What does rightward shift of the hemoglobin curve mean?
Rightward shift means that for the same PO2, there is a lower percent saturation–>less affinity and more unloading of oxygen
What does leftward shift of the hemoglobin curve mean?
Leftward shift means higher affinity and decreased unloading of oxygen
Factors Factors internal to the RBC that will cause shifting of the hemoglobin curve
Increased DPG (which happens in chronic hypoxia such as high altitude, chronic lung disease)–>rightward shift
Fetal haemoglobin–>high oxygen affinity, which makes sense since the fetus is in a hypoxic environment
Hemoglobin S (sickle cell)–>decreased affinity for oxygen and rightward shift
Methhemoglobin occurs when ferrous ion (Fe2+ is oxidized to the ferric form (Fe3+). Fe3+ heme groups irreversibly bind oxygen and cause the remaining normal Fe2+ groups to have high affinity for oxygen.
Explain the mechanism in which 100% oxygen treats a pneumothorax.
Providing 100% oxygen will “wash out” nitrogen in the intrapleural air, causing faster resolution of pneumothorax
Presence of 100% oxygen in alveoli will cause nitrogen to diffuse out of the pleural space
–>Inhale 100% oxygen to alveoli–>no nitrogen in blood, only oxygen–>blood in pleura contains oxygen not nitrogen. So there is a gradient for nitrogen to move from pleural space to blood vessel. Nitrogen is the main component of air, so when the nitrogen is gone, the air is reabsorbed too.
The theoretical basis is that oxygen therapy reduces the partial pressure of nitrogen in the alveolus compared with the pleural cavity, and a diffusion gradient for nitrogen accelerates resolution
Pneumothorax will resolve 4x faster
This method can be used for a small, primary pneumothorax, stable patient, no severe symptoms
Size: several ways to estimate size, >3 cm to apex of lung or >2 cm to lateral edge is considered large
Normal oxygen content in the blood (ml of oxygen/dL)
normal is 17-20 mL/dL
Equation for oxygen delivery (DO2)
DO2 = CO x [ 1.39 x Hgb x SaO2] + 0.003 x PaO2
Assuming there was no cardiorespiratory disorders, what would result in the single largest improvement in patient’s oxygenation status: increasing the FiO2 or transfusing with packed red blood cells?
Transfusion will have a greater impact on oxygenation status
Each unit of packed red blood cells (PRBCs) is expected to raise circulating hemoglobin (HGB) by approximately 1 g/dL
Normal predicted A-a gradient
(Age + 10)/4
What is the best way to increase oxygen delivery?
Increase cardiac output
If you transfuse the patient, what would happen to the oxygen saturation?
The percent saturation would not change, though the oxygen content of the blood would increase (by increasing hemoglobin)
What complication is most likely after 24 hours of administration of 100% oxygen
Absorptive Atelectasis
The absorption of atmospheric air will take place within hours, whereas oxygen is absorbed within minutes.
Atelectasis therefore occurs more rapidly during ventilation with an increased inspired oxygen fraction and especially with 100% oxygen, compared with breathing normal air.
Pulmonary Consequences of Supplemental O2
Absorptive atelectasis Accentuation of hypercapnia Airway injury BPD Parenchymal injury Extrapulmonary toxicity Mortality
Alveolar gas equation and explain.
PAO2 = PiO2 - PCO2/R
= (Pb-PH20) FIO2 - PCO2/R
As alveolar ventilation increases, the alveolar PCO2 decreases, bringing the alveolar PO2 closer to the inspired PO2. The alveolar PO2 obtained using the alveolar air equation is a calculated idealized average alveolar PO2. It represents what alveolar PO2 should be, not what it is.
The alveolar gas equation is used to calculate alveolar oxygen partial pressure as it is not possible to collect gases directly from the alveoli. The equation is helpful in calculating and closely estimating the PaO2 inside the alveoli.
What is the assumption for pulmonary end-capillary O2 content?
Generally held to be the same as the alveolar O2 content
also assume that SvO2 = 75% and PvO2 = 45
What happens to the alveolar equation at high altitude
When you go to high altitude , PAO2 falls and you get hypoxic (lower PiO2)
Henderson Hasselbach equation
pH = PkA +log (HCO3)/CO2
turns into:
pH = PkA + log (HCO3)/0.03x PCO2
Compensation for respiratory acidosis
Hoc3 compensation is in the same direction as PaCO2
1,2,3,4
Acute: (up 10, up 1), (down 10, down 1)
Chronic (up 10, up 3), (down 10, down 4)
Compensation for metabolic process
Compensatory change in CO2 is always in the same direction as change in HCO3
In metabolic acidosis - expected CO2= 1.5 x HCO3 + 8+/-2 -Winter’s equation
In metabolic alkalosis - CO2 goes up by 0.7 for every mmol increase in HCO3
Bronchiolitis with hyperinflation/atelectasis (vignette)
Mechanisms of atelectasis ?
Bronchiolitis occurs when viruses infect the terminal bronchiolar epithelial cells,causing direct damage and inflammation in the small bronchi and bronchioles. Edema, excessive mucus, and sloughed epithelial cells lead to obstruction of small airways and atelectasis.
Is there a role for chest physio in bronchiolitis?
No
8 month wheeze, tachypnea; what happens to Vd (dead space) with:
A. Increased Vt
B. Bronchodilation
A. Increased Vt : Increased Vd
B. Bronchodilation : Increased Vd
The anatomic dead space can be altered by bronchoconstriction, which decreases VD; bronchodilation,which increases VD; or traction or compression of the airways, which increases and decreases VD, respectively.
Bronchodilation = increased airway calibre due to relaxation of airway smooth muscle (thus increases anatomical dead space present at any given time)
What can change the anatomic dead space?
Increases with large inspirations due to traction or pull exerted on the bronchi by the surrounding lung parenchyma.
Its volume depends on the size and posture of the subject
Blood supply to the lung?
Lung gets blood from 2 separate systems:
1) Bronchial
○ High pressure/low volume
○ Bronchial arteries come form aorta or a branch from that
○ Provides blood to conducting airways -> mainstem bronchi to terminal bronchioles
○ Bleeding -> profuse, can result in massive hemoptysis
2) Pulmonary ○ Low pressure/high capacitance ○ Comes from RV ○ Supplies acinar units (gas exchange) ○ Alveolar hemorrhage -> low grade, chronic, diffuse
Causes of pulmonary hemorrhage in children
Infection Abscess Pneumonia Trauma Vascular disorders Coagulopathy Congenital Lung Malformations Miscellaneous: Catamenial, Factitious, Malignancy DAH syndromes
Causes of DAH syndromes
1) Immune mediated
- Idiopathic pulmonary capillaritis
- GPA
- MPA
- Anti-GBM disease
- SLE
- HSP
- Behcets
- Cryoglobulinemia vasculitis
- JIA
- COPA syndrome
2) Non-immune mediated
- IPH
- Acute idiopathic pulmonary hemorrhage of infancy
- Heiner’s syndrome
- Asphyxiation/abuse
- CV causes
- Pulm vein atresia/stenosis
- TAPVR
- Mitral stenosis
- Left sided failure
- PCH
- Pulm telangiectasia
