Respiratory Physiology Flashcards
Hypoxic Pulmonary Vasoconstriction
local reaction that occurs in response to a reduction in alveolar oxygen tension (not arterial PO2)
* The pulmonary vascular bed is the only region in the body that responds to hypoxia with vasoconstricion
* HPV selectively increases the pulmonary vascular resistance in poorly ventilated areas to minimize shunt flow to these regions. The response begins within seconds and achieves its full effect in about 15 minutes.
* HPV is a protective mechanism that minimizes shunt flow during atelectasis or one lung ventilation
Factors that impair HPV
Drugs:
Volatile Anesthetics >1.5 MAC
*Vasodilators, phosphodiesterase inhibitors (sildenafil, milrinone), dobutamine, and some calcium channel blockers increase shunt flow by inhibiting HPV
*Vasoconstrictive drugs such as phenylephrine, epi, and dopamine may constrict well-oxygenated vessels and increase shunt flow
*(induction drugs do NOT affect HPV)
Altered physiology:
*Hypervolemia (LAP>25) and elevated CO may distend constricted vessels and increase shunt flow, although hypovolemia may cause pulmonary vasoconstriction to well ventilated alveolar units. Therefore, euvolemia is best.
*Excessive PEEP or high tidal volumes increase dead space (zone 1) and reduce optimal V/Q matching
Muscles of inspiration
*Sternocleidomastoid (accessory muscle)
*Anterior Scalene (Accessory muscle)
*Middle Scalene (accessory muscle)
*Posterior Scalene (Accessory muscle)
*External Intercostals (increase the anterior- posterior diameter)
*Diaphragm (increases in the superior-inferior dimension of chest)
*Contraction of the inspiratory muscles reduces thoracic pressure and increases thoracic volume. This is an example of Boyle’s law.
Muscles of expiration
- Transversus Abdominis
- Internal intercostals
- Rectus abdominis
- External Oblique
- Internal oblique
- Exhalation is usually passive. The process is driven by the recoil of the chest wall.
- Active Exhalation is carried out by the abdominal musculature (rectus abdominis, internal obliques, and external obliques), preset when MV increases or pt has lung disease like COPD.
- Forced exhalation to cough VC-15mL/kg required for it to be effective
- Mnemonic: I let the air out (exhale) of my TIREs (Transverse abdominis, Internal oblique, Rectus abdominis, External oblique)
Functional divisions of the airway
Three zones:
*Conduction Zone (bulk gas movement): Trachea, bronchi, bronchioles (anatomic dead space, starts with nose/mouth)
* Transitional Zone- (Bulk gas movement): Respiratory bronchioles (air conduit and gas exchange)
*Respiratory Zone (Gas Exchange): Alveolar Ducts, Alveolar Sacs (Gas exchange across flat epithelium (type 1 pneumocytes) by diffusion)
Airway patency
To keep airway patent down to bronchioles that don’t have cartilage the pressure inside the airway must be greater that the pressure outside of the airway.
* Alveolar pressure is the pressure inside the airway
* Intrapleural pressure is the pressure outside of the airway
* Transpulmonary pulmonary pressure (TPP) is the difference between the pressure inside the airway and the pressure outside of the airway
*TPP=Alveolar pressure-intrapleural pressure
* if value is positive= airway stays open
* if negative=airway collapses
Tidal Breathing
Transpulmonary pressure (TPP) is always positive (keeps airway open)
intrapleural pressure is always negative (keeps lungs inflated)
Alveolar pressure becomes slightly negative during inspiration and slight positive during expiration
there is no airflow at FRC or end-inspiration
Aside from pneumo, the only time intrapleural pressure becomes positive is during forced expiration
what is the most common cause of increased Vd/Vt under general anesthesia?
reduction in CO.
If the EtCO2 acutely decreases, you should first rule out hypotension before considering other causes of increased dead space.
how does an LMA, atropine and neck extension affect Vd?
an LMA reduces Vd because it bypasses much of the anatomic Vd between the mouth and the glottis
Atropine increase Vd, because its bronchodilator action increases the volume of the conduction airway
Neck extension increases Vd, because it opens the hypopharynx and increases its volume
List of increases to Vd and decreases
Increased: facemask, HME, PPV, anticholinergics, old age, extension, Decreased CO, COPD, PE, sitting
Decreased- ETT, LMA, tracheostomy, flexion, supine, trendelenburg
in the circle system, dead space begins at the y-piece. If Vd increased MV must increase to maintain normal PaCO2
Bohr Equation
This equation compares the partial pressure of CO2 in the blood vs the partial pressure of CO2 exhaled. The greater difference=the greater amount of dead space.
Vd/Vt= (paco2-PeCO2)/PaCO2….EtCO2 can be used instead of PeCO2
Where is ventilation greatest?
Ventilation is greatest at the lung base due to higher alveolar compliance. Perfusion is greatest at the lung base due to gravity.
Alveoli with greater volumetric change during a breath is going to be better ventilated.
Dead space and shunt ratios, what is the clinical correlation
Dead space=VQ= Infinity- good ventilation, no perfusion
Shunt= V/Q=0- good perfusion, no ventilation
V/Q mismatch (specifically atelectasis) is the most common cause of hypoxemia in the PACU
As FRC becomes smaller (the result of anesthesia and surgery), There is less radial traction to hold the airways open. The result is atelectasis, right to left shunt, V/Q mismatch, and hypoxemia.
Treatment includes humidified O2 and maneuvers designed to reopen the airways (mobility, coughing, deep breathing, and IS)
Compensation of V/Q mismatch
The body responds to these imbalances by attempting to match ventilation to perfusion.
* To combat dead space (zone1), the bronchioles constrict to minimize ventilation of poorly perfused alveoli
* To combat shunt (zone 3), hypoxic pulmonary vasoconstriction reduces pulmonary blood flow to poorly ventilated alveoli
the Law of Laplace
the relationship between pressure, radius, and wall tension.
cylinder shape Tension= pressure x radius ie blood vessels, cylindrical aneurysms
spherical shape Tension = pressure x radius/2 ie alveoli, cardiac ventricles, saccular aneurysm
lung zones greatest to lowest
Zone 1 PA>Pa>Pv Dead Space
There is ventilation but no perfusion, does not occur in normal lungs, increased by hypotension, pulmonary embolus, or excessive pressure. Alveoli constrict to reduce dead space
Zone 2 Pa>PA>Pv Waterfall
VQ=1, blood flow is directly proportional to the difference in Pa-PA, the greater the difference the greater the blood flow
Zone 3 Pa>Pv>PA Shunt
V/Q=0, TO combat zone 3 hypoxic pulmonary vasoconstriction reduces pulmonary blood flow to underventilated units, tip of pulmonary artery catheter should be placed here
Zone 4 Pa>Pist>Pv>PA pulmonary edema
pulm edema occurs when the rate of fluid entry into the pulm interstitium exceeds the rate of fluid removal by the lymphatic system
Alveolar gas equation
Alveolar oxygen= FiO2 x (Pb-PH2O) - (PaCO2/RQ)
FiO2= Fraction of inspired O2
Pb= barometric pressure (760, 1 atm)
PH20= humidity of inhaled gas ( assumed to be 47mmhg)
RQ= Respiratory quotient (assumed to be 0.8)
RQ= carbon dioxide production/ oxygen consumption
A-a gradient
Difference between alveolar oxygen and arterial oxygen. Allows for diagnosis of the cause of hypoxemia by indicating the amount of venous admixture.
When breathing room air, the normal A-a gradient is less than 15mmhg due to normal physiological shunt: thebesian, bronchiolar, and pleural veins bypass the alveolar-capillary interface and deliver deoxygenated blood to the left heart.
A large difference implies a significant degree of shunt, V/Q mismatch, or diffusion defect across the alveolar-capillary membrane
What increases A-a gradient
Aging (closing capacity increases relative to FRC)
Vasodilators (decreased hypoxic pulmonary vasoconstriction)
Right-to-left shunt (atelectasis, pneumonia, bronchial intubation, intracardiac defect)
Diffusion limitation (alveolocapillary thickening hinders O2 diffusion)
Estimation of % shunt to A-a gradient
shunt increases 1% for every 20mmhg of A-a gradient
example A-a gradient is 218 then 218/20 shunt of 11%
normal A-a gradient is 5-10mmHg
lung volumes
all numbers based on 70kg male
Inspiratory reserve volume - 3000mL- volume of gas that can be inhaled after a tidal inhalation
Tidal volume- 500 - volume of gas that enters and exits the lungs during tidal breathing
Expiratory reserve volume -1100 - volume of gas that can be forcibly exhaled after tidal exhale
Residual volume - 1200- gas that remains in lungs after complete exhalation, can’t be exhaled, provides oxygen reservoir during apnea
Closing volume - variable around 30% at age 20, 55% at age 70 - the volume above residual volume where the small airways begin to close
Lung capacities
Total lung capacity -5800 - IRV+TV+ERV+ RV
vital capacity 4500- IRV+ TV+ERV
Inspiratory capacity 3500- IRV+TV
FRC 2300- RV+ERV it is the lung volume at end-expiration
Closing Capacity- Variable - RV+CV the absolute volume of gas contained in the lungs when small airways close
Key facts on volumes
- TV is 6-8 mL/kg
- VC is 65-75 m:/kg
- FRC is 35 mL/kg
- All are calculated on IBW
- Lung volumes are 25% smaller in females
- Lung volumes change with body position- larger when sitting and smaller when supine
- Patients with obstructive lung disease such as asthma, emphysema, and bronchitis have an increased residual volume, closing capacity, and TLC
- spirometry cannot measure residual volume, therefore it also can’t measure total lung capacity or FRC, CV, CC
How is FRC measured?
Nitrogen washout
helium wash-in
body plethysmography
what affects FRC and what can restore it
What zone increases
Some conditions can reduce outward lung expansion and or reduce lung compliance
when FRC is reduced, intrapulmonary shunt (west zone 3) increases
Alveolar recruitment maneuvers and PEEP act to restore FRC by reducing West zone 3
What decreases FRC
General anesthesia, obesity, pregnancy, neonates, neuromuscular blockade, light anesthesia, excessive IV fluids, High FiO2 (absorption atelectasis), reduced pulmonary compliance (acute lung injury, pulm edema, pulm fibrosis, atelectasis, effusion), positions: supine, lithotomy, trendelenburg
What increase FRC
Advanced age- decreased lung elasticity causes air trapping which increases RV and FRC
Positions: prone, sitting, lateral, Obstructive lung disease-air trapping, PEEP, Sigh breaths
Factors that increase Closing volume (CV)
COPD, LV failure, obesity, surgery, extremes of age, and pregnancy Mnemonic CLOSE-P
