Pulmonology Flashcards
Define: Hyperpnea/ hypopnea Dyspnea/Tachypnea Hyperventilation/Hypoventilation Hypoxia/Hypoxemia Hypercapnia Apnea Periodic breathing
Hyperpnea/ hypopnea- increased/decreased breathing
Dyspnea- awareness of breathing, uncomfortable breathing
Tachypnea-increased frequency of breathing
Hyperventilation/Hypoventilation- Breathing in excess or insufficient for metabolism resulting in increased/decreased PaCO2
Hypoxia- reduced O2 in inspired air
Hypoxemia- reduced oxygen in arterial blood
Hypercapnia- increased inspired or arterial blood CO2
Apnea- stop breathing
Periodic breathing- periods of increased or decreased breathing
Gases in the environment
mainly Nitrogen, and O2 and the rest including CO2 is 1%
The percentages of gases are the same in high elevations, but there is less atmospheric pressure that drives the O2 into our lungs
Ideal Gas law
PV=nRT (pressure, volume, amount of gas, R, temperature)
Each gas in a mixture does not affect another, so they are considered in terms of partial pressures
Partial pressure (PO2) provides the driving force for O2 into the blood
Atmospheric Po2= 150
Alveolar Po2= 100 (arterial O2 is the same but a small dip)(drop is due to dead space, FRV/FRC, O2 utilization)
Mixed venous Po2= 50
It is the gradient of O2 that favors diffusion of O2
Atmospheric PCO2= 0
Alveolar PCO2= 40 (arterial is the same)
Mixed venous PCO2= 45
Expiratory Reserve and FRV= FRC
4 Steps of the pathway for gas exchange between the atmosphere and the tissues for O2
Step 1: Air moved from environment-> alveoli (Active process)
Step 2: Oxygen diffuses into the lung capillaries (passive process
Step 3: O2 is moved from the lungs to the heart and tissues (active process)
Step 4: O2 diffuses to tissues down concentration gradient
4 Steps of the pathway for gas exchange between the atmosphere and the tissues for CO2
Step 1: CO2 diffuses to from tissues to capillaries (passive)
Step 2: CO2 is moved from the Tissues to the lungs and heart (active)
Step 3: Oxygen diffuses into the alveoli (passive process
Step 4: CO2 is expelled from alveoli (typically passive due to mechanical recoil, but can be active)
Oxygen content in blood
Dissolved (active)+ bound to Hb
Dissolved O2= PaO2 x solubility coefficient (.3ml/100ml Blood)
Bound= Hb concentration x 1.34 x O2 saturation
usually 19.7
Content= 20 ml/100 ml Blood
Healthy lungs= normal dissolved O2
Anemia= low bound, and therefore low content
But anemics have very low PvO2 because you use up more of the arterially dissolved O2. Breathig frequency doesnt change bc chemoreceptors sense dissolved arterial O2
Respiratory structures
Cunducting zone (no gas exchange): trachea, bronchi, bronchioles, terminal bronchioles
Respiratory zone (site of gas exchange): respiratory bronchioles, alveolar ducts and sacs
Muscles of inspiration: external intercostals and diaphragm
Muscle of expiration: mainly elastic recoil, but also abdominal and internal intercostals
Lung volumes and capacities
Tidal volume: resting breath
Functional Residual Capacity: air left over after tidal expiration (sum of Expiratory Reserve volume (air we can breath out and residual volume (air in alveoli)
Inspiratory capacity: If we inspire from FRC point to our max lung volume, sum of tidal and inspiratory reserve volume
Vital capacity: Exp/Insp reserve volumes and tidal volume
How do we move air
In order for there to be airflow in or out of the lungs, there must be a pressure differential between alveoli and the atmosphere
There needs to be a negative Palv relative to Patm
Pleural pressure (Ppl) is the pressure in the intrapleural space and is usually negative
Transpulmonary/transmural pressure is the difference between Palv and Ppl. Cannot be measured but describes eleastic recoil pressure of the lungs.
The negative Ppl counterbalances the tendency of the alveoli to want to collapse
The lung wants to collapse and at RV, there is a small recoil pressure, as you inflate the lungs, there is an increased recoild pressure, which becomes highest at TLC
The Recoil pressure is due partially to surface tension which is decreased by surfactant (produced by type 2 epithlial cells). Lung tissue is also elastic which gives another portion of the elastic recoil pressure.
Atelectasis and alveolar interdependance
Atelectasis is the slow collapse of alveoli. Surfactant reduces atelectasis and periodic sighs reinflate the the alveoli.
Alveolar interdependance: alveoli are interconnected, so when some alveoli inflate, they pull on others to help open them and allow further inflation. Natural inspiration causes a more negative Ppl which causes the peripheral alveoli to inflate first
elastic properties of the chest wall
The chest wall has a natural tendency to want to expand, which is at equilibrium at 60% VC. At residual volume (0% VC), there is a large pressure for the chest wall wanting to expand. At 100% Vc or TLC the chest wall wants to collapse
The point at which the Chest wall wanting to expand and the alveoli wanting to collapse is equilibriated is at The FRC which is why at tidal breathing its the recoil that expels air from our lungs
At FRC (end expiration), There is no air flow (Alveolar pressure=atm pressure= 0) And the lungs are tugging on the intrapleural space. Intrapleural pressure= alveoar presure- Ppl= 0- -5= +5
During inspiration: Diaphragm causes an even more negative Ppl, and it creates a slight -1 alveolar pressure
-1 - -8= +7 (transmural pressure)
Lung compliance
measurement of distensibility in the lung dV/dP
Ptp (transpulmonary pressure)= Palv-Ppl
When there is no airflow (at the begining and end of inspiration) and Palv =0, so Ptp=Ppl
Compliance= dV/dPpl
Emphysema= decreased Elasticity (increased compliance), obstructive
Fibrosis= decreased compliance, restrictive
Airway resistance
depends on total cross sectional area, airway resistance is highest at the large airways (there are less of them)
Also lung volume, at higher lung volumes, airway resistance is lower
Airflow
Flow = (Palv-Patm)/ airway resistance
Expiration happens in two phases: effort dependent and effor independent
Effort Dependent: where how hard you push correlates to how fast (flow, L/sec) air leaves
effort independent: the airway resistance gets so high at the end of expiration, that no matter how hard you push, there is a limit to how fast air leaves
Distribution of air in lungs in healthy vs diseased states
In restrictive/fibrotic disease, all of the various volumes are reduced because lung compliance us reduced
In obstructive (leads to dynamic compression), TLC is larger, RV is huge, ERV is small
Regional distribution of air during inspiration
Gravity pulls the lungs down, making pleural pressure more negative at the top than the bottom, From FRC air goes to the bottom first where there is greater compliance, all regions simultaneously inflate but more air goes to the bottom than the top
Dead space in the pulmonary system and alveolar ventilation
anatomic Dead space: is in the conducting zone, of the tidal volume (500 ml), 150 remains in the dead space and does not contribute to alveolar gas exchange
Minute volumes: volume of each breath x breaths/minute
12 breaths/minute:
Total minute ventilation= Vt (tidal volume) x frequency= 6000 ml
Total alveolar ventilation= frequency x (Vt-Vd)= 12 x 350= 4200
Changing breathing frequency/pattern affects alveolar ventilation.
Changes in carbon dioxide and oxygen throughout the respiratory cycle
At the onset of expiration: you are breathing out dead space, so the air is like fresh air, its not until the end of expiration that the air is actually alveolar air that has participated in alveolar ventilation (CO2 is high)
dead space volume calculation:
Vd= Vt x (FACO2 - FECO2)/FACO2
F= fraction, E=expired
We can also estimate the arterial gas partial pressures by using the end tidal fractions mulitplied by the difference in barometric and water pressure
alveolar hypo/hyper ventilation
Hypoventilation: when PaCO2> 45, alveolar ventilation is not sufficient to eliminate CO2 relative to CO2 production, and PaO2 also is lower (natural sleep, anesthesia, drug overdose, COPD,
Hyperventilation: decreased PaCO2, usually due to low atmospheric O2 levels, chemoreflex increases ventilation
Pulmonary blood vessels vs Systemic blood vessels
Pulmonary circulation is a low pressure system. lowere pressures, more compliant, less thick, carry 10% of blood
Pulmonary vascular resistance depends upon lung volume, it is lowest at FRC
Alveolar vessels get squished during inspiration, and extra alveolar get stretched during inspiration, the opposite is true regarding expiration
Increasing pulmonary blood flow during exercise
blood flow isnt evenly distributed throughout the lung and can be increased mainly with distension and recruitment, and to some extent increased pulmonary pressure. when cardiac output is increased, distension and recruitment increase blood flow and decrease resistance
Distribution of blood flow in the lung, effects of alveolar pressure
Zone 1: no blood flow (PA> Pa >Pv)
Zone 2: blood flow only during systole (Pa>PA>Pv)
Zone 3 Continuous blood flow (Pa> Pv> PA)
this is because Gravity pulls the lungs down causing a more negative Ppl at the top and inflates the alveoli all the time squishing alveolar vessels
Active influences on pulmonary vascular resistance
alvolar hypoxia, alveolar hypercapnia, low pH-> increased resistance so that blood flows to areas of that lung that are well ventilated
Passive influences that increase vascular resistance: Increased lung volume (compression of alveolar vessels), Decreased lung volume (compression of extra alveolar vessels)
Passive influences that decrease vascular resistance:
(increased pressure)
As pulmonary pressure goes up, edema will start to form because lymphatics get overwhelmed
Ventilation/perfusion ratios
V/Q ratio is low at the bottom of the lung and high at the top of the lung, because perfusion is relatively greater than ventilation in the bottom. At the top ventilation is realtively greater than perfusion at the top of the lung
V/Q matching:
Normal: alveolus is being both perfused and ventilated (matched)
Airway blocked: low V/Q
No perfusion: high VQ
Pathway for diffusion of O2
- Gas dissolves into alveolar surfactant
goes through alveolar epithelium, basement membrane, interstitial fluid space, capillary basement membrane, capillary epithelium, then into plasma and RBC membrane to bind to Hb. Alveolar/capillary membrane is only .5 microns thick (increased with disease and edema and leads to a decrease in diffusion)
Solubility of O2 and CO2 calculation of Henry’s Law
Amount dissolved= Partial pressure x solubility coefficient
CO2 is 20x more soluble than O2
Factors that determine rate of diffusion across membrane
Diffusion rate= dP x A x Solubility / (distance x MW)
disease makes it take longer for O2 to dissolve. CO2 takes longer to equilibrium
Exercise limits the time blood spends in the lungs so people with disease have real issues with diffusing gasses
Oxygen-Hb dissociation curve
Shifts in O2 (left increases O2 affinity, Right decreases O2 affinity)
Decrease in pH/ increase in CO2 causes a right shift (Bohr effect)
Increase in temp/ increase in 23 BPG cause right shifts
Right shifts enhance O2 unloading
Effects of Anemia and carbon monoxide
CO2 transport in the blood
most of CO2 travels in the bound form to bicarbonate and a little to Hb
there is a small (albeit more than O2) bound to Hb
CO2 comes into the erythrocyte, carbonic anhydrase makes the CO2 into bacarb and H+ causing the Hb to release O2 and the bicarb leaves the cell through CL counter exchange
The CO2 leaves in the lungs and the carbonic anhydrase makes more CO2 from bicarb causing there to be less H and O2 attaches
Intrapulmonary shunt
Intrapulmonary shunt causes hypoxemia due to the Hb dissociation curve, even if V/Q ratio is increased in one lung due to the shpe of the Hb-dissociation curve
If the hypoxemia is due to diffusion limitations, increasing PO2 will increase PaO2
If the hypoxemia is due to shunt, PaO2 wont do shit with extra O2
When PAO2 is much different than PaO2 then you know there is a alveolar-capillary exchange problem which can be attributed to one of three things:
- Increased Right to left shunt
- Increased ventilation to perfusion mismatch (V/Q mismatch)
- impaired diffusion
Controller of breathing in the brainstem
Pontine Respiratory Group- inhibits inspiration
Dorsal Respiratory Group- contains inspiratory neurons and integrates peripheral senses
Ventral respiratory group- contains both inspiratory and expiratory neurons, home of the pre Botzinger complex that creates the respiratory rythym generator
The signals send to spinal nerves to control muscles of breathing
Timing is controlled by rhythm generator, Shaping is controlled by the pattern, integration in the pre motor
Post I neurons activate airway muscles to inhibit fast expiration
Non respiratory functions of respiratory - CPGs hijack brainstem to do stuff other than breath
Chemo receptors
Cells that alter discharge due to PCO2, PO2, pH found in the carotid and aortic bodies and the CNS
Central for CO2 and pH
peripheral for O2
Glomus type 2 cells are in the carotid and oartic bodies and sense O2 and when O2 decreases they release ACh and cause APs, hypoxemia causes carotid body activity and stimulates ventilation
Carotid bodies are also CO2 and pH sensitive, hypercapnia and acidosis stimulates ventilation
Central chemoreceptors detect CSF CO2 and/or pH
BBB prevents arterial H from diffusing, but CO2 diffuses in and creates acidosis to stimulate chemoreceptors and will increase central receptor firing
