Respiratory Physiology Flashcards
Inspiration Muscles
Diaphragm & external intercostals
Inspiration ACCESSORY Muscles
Sternocleidomastoid
Anterior/middle/posterior scalenes
What law applies to breathing & inspiration?
Boyle P1V1 = P2V2
Expiration Muscles
PASSIVE
Driven by chest wall recoil
Active Expiration Muscles
Transverse abdominis
Internal & external oblique
Internal intercostals
How many functional airway divisions are present?
23 divisions/generations
What are the 3 respiratory zones?
Conducting
Transitional
Respiratory (gas exchange)
Conducting Zone
Trachea, bronchi, & bronchioles
Ends w/ terminal bronchioles
Function to facilitate bulk gas movement
DEAD SPACE 150 mL or 2 mL/kg
Trachea
Conducting zone
Generation 0
Cilia present
Smooth muscle present
Cartilage present
Bronchi
Conducting zone
Generation 1-3
Cilia present
Smooth muscle present
Cartilage patchy
Bronchioles
Conducting zone
Generation 4
Cilia present
Smooth muscle present
NO cartilage
Transitional zone
Respiratory bronchioles
Duel function - air conduit & gas exchange
Respiratory Bronchioles
Transitional zone (sometimes noted as respiratory zone)
Generation 17
Some cilia & smooth muscle present
NO cartilage
Respiratory Zone
Gas exchange
Alveolar ducts & sacs
How does gas exchange occur?
Gas exchange occurs across the flat epithelium (type 1 pneumocytes) via diffusion
Alveolar Ducts
Generation 20
Some smooth muscle
NO cilia or cartilage
Alveolar Sacs
Generation 23
NO cilia, smooth muscle, or cartilage
What airway structures are susceptible to external compression?
Bronchioles & alveolar ducts
Do NOT contain cartilage
What keeps the airways open?
Positive (+) transpulmonary pressure Ptp
Minute ventilation
VE = Tidal volume (VT) x RR
Volume gas patient inhales & exhales over 1 minute
Inversely r/t PaCO2
Reference adult value = 4 L/min
Alveolar ventilation
VA = (Tidal volume - dead space) x RR
OR
= CO2 production / PaCO2
1° determinant CO2 elimination
Only measures VE available to participate in gas exchange
Directly proportional to CO2 production
Inversely proportional to PaCO2
Anatomic Dead Space
Air confined to the conducting airways
Alveolar Dead Space
Alveoli that are ventilated, but not perfused
Physiologic Dead Space
= Anatomic Vd + Alveolar Vd
Calculated w/ Bohr equation
Vd/Vt = (PaCO2 - PeCO2) / PaCO2
Apparatus Dead Space
Vd added by equipment
Facemask or HME
Circle system
Dead Space to Tidal Volume Ratio
= Vd/Vt %
Fraction tidal volume that contributes to dead space
Reference adult value 33% during spontaneous ventilation
Normal 150 mL / 450 mL = 0.33
50% during mechanical ventilation
↑Dead Space
Facemask, HME, PPV
Atropine (anticholinergic) bronchodilation ↑conducting airway volume
Old age
Neck extension opens the hypopharynx
HoTN, ↓CO, COPD, PE (thrombus, air, amniotic fluid) ↓pulmonary blood flow
↓Dead Space
- ETT, LMA, trach
- Neck flexion
- ↑CO
- Position (supine or Trendelenburg)
Compliance
Compliance = ∆V / ∆P
Alveolar Compliance Curve
Normal Upright Awake Adult
Non-dependent APEX
↑PAO2
↓PACO2
↑V/Q ratio (V>Q)
↓compliance ↓alveolar ventilation
↓pulmonary blood flow ↓alveolar perfusion
Dependent BASE
↓PAO2
↑PACO2
↓V/Q ratio (V<Q)
↑compliance ↑alveolar ventilation
↑pulmonary blood flow ↑alveolar perfusion
Normal Va/Q Ratio
= 0.8
Ventilation = 4 L/min
Perfusion = 5 L/min
Ventilation / Perfusion Mismatch
↑A-a gradient
Bronchioles constrict to minimize zone 1
HPV minimizes shunt
Blood passing through under ventilated alveoli tends to retain CO2
What is the most common cause of hypoxemia in the PACU?
Atelectasis
Shunt V/Q = 0
Blood retains CO2 ↑PaCO2
What indicates severe V/Q mismatch?
Retained CO2 ↑PaCO2
Dead Space
Vd
V/Q = ꝏ
Ventilation but no perfusion
Overventilated alveoli give off an excessive amount CO2
CO2 diffuses 20x faster than oxygen
Apex V > Q Zone 1
Shunt
Shunt or venous admixture
V/Q = 0
Perfusion but no ventilation
Under-ventilated alveoli retains CO2 and unable to take in enough oxygen
Base V < Q Zone 3
What law applies to alveolar surface tension?
Law of LaPlace
P = (2 x T) / r
P = pressure
T = tension
r = radius
What equalizes surface tension effects?
Surfactant
↓radius ↑surfactant concentration
When does surfactant production begin & peak?
Begins at 22-26 weeks gestation
Peaks at 35-36 weeks
West Zones
- Dead space
- Ventilation matched to perfusion V/Q = 1
- Shunt
West Zone 1
Alveolar pressure PA > arterial pressure Pa > venous pressure Pv
Bronchioles constrict to minimize ventilation to poorly perfused alveoli
West Zone 1
Causes
HoTN, PE, excessive airway pressure (PPV or PEEP)
West Zone 2
Pa > PA > Pv
Blood flow directly proportional to Pa-PA difference
West Zone 3
Pa > Pv > PA
Any venous blood that empties directly into L side heart or bypasses the lungs
HPV ↓pulmonary blood flow to poorly ventilated alveoli
Where to place the PA catheter tip?
West zone 3
Capillary pressure > alveolus
Vessel always open & blood moving through
What are 3 anatomic shunt sites?
Thesbian, bronchiolar, & pleural veins
West Zone 4
Pa > Pis > Pv > PA
Pulmonary edema
West Zone 4
Causes
↑capillary hydrostatic pressure
- Fluid overload, mitral stenosis, and sever pulmonary vasoconstriction
Profound reduction in pleural pressure
- Laryngospasm or inhalation against closed glottis → negative pressure pulmonary edema
Alveolar Gas Equation
Used to estimate partial pressure O2 in the alveoli
PAO2 = FiO2 x (PB − PH2O) − (PaCO2 / RQ)
Respiratory Quotient
= CO2 production / O2 consumption
= 200 mL/min / 250 mL/min
= 0.8
Hypoxemia
Low O2 concentration in the blood
PaO2 < 80 mmHg
Hypoxia
Insufficient O2 to support the tissues
Hypoxemia Causes
- Hypoxic mixture
- Hypoventilation
- Diffusion limitation
- V/Q mismatch
- Shunt
Hypoxic Mixture
Causes
O2 pipeline failure
High altitude
Hypoxic Mixture
Presentation & Treatment
Normal A − a gradient
Administer supplemental FiO2
Hypoventilation
Causes
Opioid overdose
Residual anesthetic agent
Residual NMB
Neuromuscular disease
Obesity hypoventilation
Hypoventilation
Presentation & Treatment
Normal A − a gradient
Fix underlying cause
- Narcan
- Adequate NMB reversal
Supportive ventilation CPAP/BiPAP
Administer supplemental FiO2
V/Q Mismatch
Causes
COPD
One-lung ventilation
Impaired HPV
Embolism - air, gas, amniotic fluid
V/Q Mismatch
Presentation & Treatment
↑A − a gradient
Resume 2-lung ventilation
Decrease/discontinue drugs that inhibit HPV
Identify & treat embolism
Administer supplemental FiO2
Diffusion Impairment
Causes
Pulmonary fibrosis
Emphysema
Interstitial lung disease
Diffusion Impairment
Presentation & Treatment
↑A − a gradient
Administer supplemental FiO2
Shunt Causes
R→L shunt
Atelectasis
Pneumonia
Bronchial intubation
Intracardiac shunt
Shunt
Presentation & Treatment
↑A − a gradient
Supplemental FiO2 does NOT help
A − a Gradient
PAO2 − PaO2
Normal < 15 mmHg (physiologic shunt)
How much does shunt increase A − a gradient?
↑1% every 20 mmHg
Lung Volumes
IRV
Vt
ERV
RV
*Based on healthy 70 kg male
Lung Capacities
2+ lung volumes
IC
VC
FRC
TLC
*Based on healthy 70 kg male
What are lung volumes & capacities based on?
IBW
Healthy 70 kg male
How do lung volumes & capacities differ in females?
↓25%
IRV mL
3,000 mL
Tidal Volume mL
Vt = 500 mL
OR
6-8 mL/kg IBW
ERV mL
1,100 mL
RV mL
Unable to measure
1,200 mL
Closing Volume
Variable
Lung volume above RV when small airways begin to close/collapse
Closing Volume % TLC
30% TLC at 20 yo
55% TLC at 70 yo
IC mL
Inspiratory capacity
IRV + Vt = 3,500 mL
Lung Capacities
2+ lung volumes = capacity
VC mL
Vital capacity
IRV + Vt + ERV = 4,600 mL
OR
65-75 mL/kg
FRC mL
Functional residual capacity
ERV + RV = 2,300 mL
OR
35 mL/kg
Volume at end-expiration
TLC mL
IRV + Vt + ERV + RV = 5,800 mL
Closing Capacity
RV + CV = variable
Absolute lung volume when small airways begin to close/collapse
What patients & scenarios does CC = FRC?
Neonate
30 yo under GA
Supine 40 yo adult
Standing or sitting 65 yo
What happens when CC ≥ FRC?
Airway closure during normal tidal volume breaths → intrapulmonary shunting & hypoxemia ↑WOB
Unable to measure w/ spirometry
How to measure CV or CC?
Nitrogen or Xenon
Define FRC
Lung volume when inward elastic recoil (lung) balanced by the outward recoil (chest wall) = static equilibrium
O2 reserve that prevents hypoxemia during apnea
What formula represents the time until an apneic patient desaturates?
= FRC / VO2
VO2 = oxygen consumption
↑FRC
COPD
Advanced age elasticity ↑air trapping
PEEP
Position:
- Sitting
- Lateral
- Prone
↓FRC
General anesthesia 50% reduction
NMBs
Obesity, pregnancy, and neonates
Fluid overload or pulmonary edema
↑FiO2 → absorption atelectasis
Position:
- Supine
- Lithotomy
- Trendelenburg
Oxygen Content
CaO2 = (Hgb x SaO2 x 1.34) + (PaO2 x 0.003)
O2 forms reversible bond w/ Hgb 97%
O2 dissolved in the blood plasma 3%
Normal Hgb/Hct
Hgb 13-15 g/dL
Hct 39-45%
What law applies to O2 dissolved in the blood plasma?
Henry’s law = gas concentration in a solution α gas partial pressure above the solution
Oxygen 20x less soluble than CO2
Normal CaO2
20.4 mL O2 per dL
Oxygen Delivery
DO2 = CaO2 x CO x 10
How fast O2 delivered to the tissues
What mechanism/factor drives O2 delivery?
Cardiac output
What converts dL → L?
Conversion factor = 10
Normal DO2
1,000 mL O2 per minute
Oxygen Consumption
VO2 = CO x (CaO2 − CvO2) x 10
Difference b/w O2 that leaves the lungs & O2 amount that returns
What law/principle applies to O2 consumption?
Fick
Normal VO2
250 mL/min
OR
3.5 mL/kg
How does temperature affect VO2?
↓core body temp ↓O2 consumption
VO2 ↓5-7% every 1°C
FICK PRINCIPLE
Vgas = [Diffision coefficient x (P1 − P2) x Surface area] / Membrane thickness
Vgas = (D ∗ ∆P ∗ SA) / T
ΔP = partial pressure gradient
Oxyhemoglobin Dissociation Curve
P50
PaO2 when Hgb 50% saturated by O2
P50 = 26.5 mmHg
SpO2 90% : PaO2
90% = PaO2 60 mmHg
80% = PaO2 50 mmHg
75% = PaO2 40 mmHg
60% = PaO2 30 mmHg
What causes the carboxyhemoglobin dissociation curve to shift to the LEFT?
LEFT = LOVES
- Alkalosis ↑pH ↓H+
- Hypocarbia ↓CO2
- Hypothermia
- ↓2,3 DPG
- Fetal hemoglobin FHgb α + γ
- Benzocaine overdose → methemoglobin MetHgb
- Carboyxhemoglobin (smoke inhalation) COHgb
- Normal physiology = lungs
What causes the carboxyhemoglobin dissociation curve to shift to the RIGHT?
RIGHT = RELEASE
- Acidosis ↓pH ↑H+
- Hypercarbia ↑CO2
- Hyperthermia (MH, neuroleptic malignant syndrome, or serotonin syndrome)
- ↑2,3 DPG
- Normal physiology = tissue level
Cellular Energy Currency
ATP
Adenosine triphosphate
What is the 1° substrate used for ATP synthesis?
Glucose
Aerobic Metabolism
- Glycolysis
- Krebs cycle
- Oxidative phosphorylation
Glycolysis
Convert 1 glucose to 2 pyruvic acid molecules
Net gain 2 ATP
Krebs Cycle
Occurs in the mitochondria matrix
Produces H+ ions as NADH to be used in the electron transport chain
Net gain 2 ATP
Oxidative Phosphorylation
Electron transport chain
Goal to produce ATP (energy)
Net gain 34 ATP
Anaerobic Metabolism
Pyruvate acid → lactic acid → lactic acidosis
Anion gap metabolic acidosis
When oxygen supply reestablished intracellular lactate converted back to pyric acid inside the cell
What clears serum lactate?
Liver
CO2 Buffer System
H2O + CO2 ↔ H2CO3 (carbonic acid) ↔ H+ + HCO3¯
Reaction requires carbonic anhydrase enzyme
CO2 Transportation
Bicarbonate HCO3¯ 70%
Hgb bound 23%
Dissolved in plasma 7%`
Bohr Effect
O2 offloading from Hgb
CO2 + ↓pH ↑H+ → erythrocyte releases O2
L shift at the tissue level
Haldane Effect
CO2 loading onto Hgb
↑O2 → erythrocyte releases CO2
R shift at the lungs
Hypercapnia
Definition & Equation
Respiratory acidosis PaCO2 > 45 mmHg
PaCO2 = (CO2 production) / (Alveolar ventilation)
Hypercapnia Causes
- ↑CO2 production
- ↓CO2 elimination
- Rebreathing
What consequences are associated w/ hypercapnia?
↑CO2 displaces alveolar O2 → arterial hypoxemia
↓oxygen carrying capacity
Oxyhemoglobin curve shifts R ↑P50 releases more O2 to the tissues
Myocardial depressant & directly dilates the peripheral vasculature ↑HR ↑MVO2
↑Pulmonary vascular resistance PVR
Respiratory stimulant ↑minute + alveolar ventilation
Hyperkalemia H+/K+ pump activation buffers CO2
Acidosis → plasma proteins buffer H+ & release Ca2+ → ↑Ca2+
↑ICP CO2 freely diffuses across the blood-brain barrier ↓CSF pH ↓cerebrovascular resistance ↑CBF & volume
Acute Respiratory Acidosis
Predicted pH
Every 10 mmHg > 40 mmHg → pH ↓0.08
Chronic Respiratory Acidosis
Predicted pH
Every 10 mmHg > 40 mmHg → pH ↓0.03
CO2 Ventilatory Response Curve
Describes the relationship b/w PaCO2 & minute ventilation VE
What causes the CO2 ventilatory response curve to shift to the LEFT?
Respiratory center ↑sensitivity to CO2
Hypoxemia
Metabolic acidosis
Surgical stimulation
Intracranial HTN ↑ICP
Fear & anxiety
Salicylates, Aminophylline, Doxapram, & NE
What causes the CO2 ventilatory response curve to shift to the RIGHT?
Respiratory center ↓sensitivity to CO2
Metabolic alkalosis
Volatile anesthetics
Opioids
NMBs
Post carotid endarterectomy
Natural sleep
What receptors are the 1° PaCO2 monitor?
Central chemoreceptors in the medulla
Respond INDIRECTLY to PaCO2
Where is the respiratory control center located?
Reticular activating system RAS in the medulla & pons
Respiratory Control Center
1° Function
1° job to determine how fast & deep patient breathes
Regulate PaCO2 & PaO2
Where does the respiratory control center receive inputs from?
Central & peripheral chemoreceptors
AND
Stretch receptors in the lungs
Where are central chemoreceptors located?
Medulla
Where are peripheral chemoreceptors located?
Carotid bodies at the common carotid artery bifurcation
AND
Transverse aortic arch
Outline the central respiratory center
Medulla
- DRG/VRG
- Central chemoreceptors
Pontine
- Pneumotaxic (upper pons)
- Apneustic (lower pons)
Cerebral cortex - conscious breathing control able to modify responses
DRG
Dorsal respiratory group or center (DRC)
Located in the nucleus tractus solitarius (medulla)
Respiratory pacemaker
Dorsal = inspiration
VRG
Ventral respiratory group or center (VRC)
Located in the medulla
1° responsible for expiration
Ventral = active expiration
More important during exercise or stress
Pneumotaxic center
Located in the upper pons
Inhibits the DRG (pacemaker)
Triggers END inhalation
Apneustic Center
Located in the lower pons
Stimulates the DRG (pacemaker)
Triggers INhalation
Define Apneic Threshold
The highest PaCO2 where the patient will NOT breathe
How do central chemoreceptors respond to PaCO2?
INDIRECT response to PaCO2
Sends stimulatory impulses to the DRG
What 1° stimulates the central chemoreceptors?
CSF pH or H+ ion concentration
What receptors are the 1° PaO2 monitor?
Peripheral chemoreceptors
Monitor hypoxemia PaO2 < 60 mmHg
What do peripheral chemoreceptors 2° monitor?
1° PaO2
2° PaCO2, H+, & perfusion pressure
What cells sense & transduce PaO2 into an AP?
Type 1 glomus cells
Mediate hypoxic ventilatory drive
What serve as the peripheral chemoreceptors afferent limb?
Hering’s nerve & glossopharyngeal nerve IX
Terminates in the inspiratory center in the medulla
How does carotid endarterectomy impair peripheral chemoreceptors?
Severs the afferent limb on the surgical side
Pulmonary Reflexes
- Hering-Breuer inflation reflex
- Hering-Breuer deflation reflex
- J receptors
- Paradoxical head reflex
What transduces pulmonary reflexes?
Stretch receptors in the smooth airway muscle transduce pressure conditions in the airway
Information transmits along the Vagus → DRG
Efferent response via phrenic nerve
Hering-Breuer Reflex
INFLATION
- When lung inflation > 1.5 L above FRC (3x Vt) reflex turns off the DRG
- Stops further inspiration; helps to avoid overinflation
- Reflex not active during normal inspiration
DEFLATION
- Stimulates patient to take a deep breath
- Prevents atelectasis
J Receptors
Pulmonary C-fiber receptors
Stimulation causes tachypnea in response to pulmonary embolism or CHF
Paradoxical Head Reflex
Newborn baby stimulus to take 1st breath
HPV
Hypoxic pulmonary vasoconstriction
Local response to ↓alveolar oxygen tension PAO2 → minimizes shunt
Pulmonary vascular bed the only region in the body that responds to hypoxia with vasoconstriction
How long to initiate the HPV response?
When is the peak effect achieved?
Only seconds to initiate
Achieves peak effect ≈ 15 minutes
What inhibits HPV?
Volatile anesthetics > 1.5 MAC
Phosphodiesterase inhibitors
Dobutamine
Hypervolemia
Excessive PEEP
↑Vt
How do volatile agents affect HPV?
Impair HPV
↑shunt fraction & ↓PaO2
What preserves HPV?
IV anesthetic agents
- Ketamine
- Propofol
- Opioids
