Exam #4_Semester 2 Flashcards
partial pressure - definition
amount of pressure that a gas exerts in a mix of other gases
- fraction of barometric pressure
- only gases that are in solution (not bound)
partial pressure - key values
Pb = 760mmHg (sea level) PH20 = 47mmHg (constant) PIO2 = 150 PICO2 = 0 PAO2 = 102 PACO2 = 40 PaO2 = 40 (pulm art) PaCO2 = 46 (pulm art) PvO2 = 102 / 95 (pulm vein) PvCO2 = 40 (pulm vein)
respiratory quotient (R)
ratio of CO2 produced relative to O2 consumed
- function of fuel being used (carbs=1, fats=0.7, mixed=0.8)
- variable in alveolar gas equation
what is the driving force between the liquid/air interface at the alveolar/capillary border
diffusion - Ficke’s Law
flux = -DA (ΔC/ΔX)
cardiovascular and respiratory system interactions
ventilatory pump: musculature that drives ventilation changes in lung
- chemoreceptors (carotid body) detect changes in partial pressure of key gases (O2, CO2, and pH) and primarily effect this
circulatory pump: heart (pumps blood)
- baroreceptors (carotid sinus) detect pressure changes (MAP) and primarily effect this
chemo-receptors
detect changes in chemicals (pH, O2, CO2) in blood (key blood gases) and send signals to respiratory neural centers which influence activity of respiration
- carotid body
minute ventilation
volume of air moved in and out of the lungs per unit time (minute)
alveolar ventilation
volume of air at level of alveoli available to diffuse across alveolar/capillary interface
- fraction of minute ventilation
why is albuterol an effective rescue medication
target is specific to beta 2 adrenergic receptors of the SM surrounding the respiratory system (conducting portion and respiratory bronchioles of the gas exchange portion)
- albuterol binds beta 2 receptors, causing CA++ extrusion from SM cells and relaxation (inc. air flow)
why are isoproterenol and epi (in over the counter inhalers) not ideal
although there target is beta-2 adrenergic receipts, they are non-specific and also bind beta-1 and alpha-1 which can cause contraction of SM
pleurisy
painful pathologic rubbing of visceral lining of lung and parietal lining of inside of thoracic cavity
- normally pleural space between these 2 linings has fluid to reduce friction
pleural space
space between visceral lining of lung and parietal lining of thoracic cavity
- pressure here is sub-atmospheric (key to maintain this negative pressure)
- becomes even more negative when chest expands - draws air in
muscles of inspiration
diaphragm: passive breathing
external intercostals: active breathing
muscles of expiration
passive recoil of lungs: passive breathing
internal intercostals: active breathing
what happens to pleural pressure when you inhale / expand chest cavity
it becomes more negative - pulls air in
negative pressure breathing
during inhalation, pressure in alveoli becomes more negative (pressure at airway opening stays the same)
- increase in pressure difference causes air to flow into alveoli
note: positive pressure breathing occurs when on ventilator
hysteresis
prior state dictates what will occur
- In lung: prior state will dictate pressure/volume relationship that is observed (esp. w.out surfactant)
- lungs behave differently depending on state of inflation
- In lung: surface tension varies with area of alveoli (ST increases as area (radius) increases)
compliance
change in volume that accompanies a change in pressure
surface tension
phenomenon of differences in attractive forces at the air/liquid interface (cells are filled with liquid and alveoli with air)
- large attractant forces between adjacent molecules at air-liquid interface compared with molecules lower down in body of fluid
- typically: surface tension increases as volume decreases - but not in lung b/c of surfactant!
surfactant
complexmixture of phospholipids and proteins that play key immunological and biophysical roles
- amphipathic (hydrophobic and hydrophilic ends)
causes surface tension to increase proportionately with radius of alveoli, keeping pressure constant (prevents collapse of smaller alveoli)
produced at 32-34 weeks in utero (septal cells) - why premature infants can have respiratory distress syndrome (hyaline membrane disease)
hyaline membrane disease of the newborn
infants born with insufficient surfactant in lungs; alveoli can collapse (atelectasis) since pressure b/t large and small alveoli is unequal and air moves to larger alveoli and small alveoli collapse
babies first breath
birth: very small alveoli with high surface tension (require huge negative pressure to combat surface tension and open alveoli)
- use substantial inspiratory muscles to expand thoracic cavity and create large negative pleural pressure
- this initial effort is same with of without surfactant
Second breath: surfactant coats alveoli (type 2 cells) and subsequent inhalations become easier due to decreases surface tension
- radius of alveoli doubles and effort is 1/4th that of first breath
pneumothorax
integrity of pleural space is disrupted (breached) ad lung and chest wall behave how they want to (seperately)
- negative intrapleural pressure is wiped out (air from atmosphere rushes in), lung recoils, and chest wall expands out to 70% of TLC
- chest tube is used to re-establish pressure - lung will naturally re-expand
transmural pressure
difference between pressure inside a vessel / conduit and that which exists outside
• As lung volume decreases, transmural pressure becomes negative (outside higher than inside), radius of the airway decreases, leading to an increase in resistance
• As lung volume increases, transmural pressure in the airway is positive (inside pressure greater than outside), radius of airway increases, leading to less resistance to flow
chemical / pharmacological factors causing SM contraction
Chemoreceptor mediated – irritants
Acetylcholine (muscarinic receptors)
Histamine (endogenous substance released by mast cells)
chemical / pharmacological factors causing SM relaxation
Epinephrine - receptors in SNS – beta 2 mediated effect
- physiological antagonist of acetylcholine
Isoproterenol: pure beta agonist, non-specific
- useful rescue medication
Beta 2 agonists (albuterol, terbutaline)
- selective beta-2 agonist (best rescue)
obstructive lung disease
problem is getting air out: asthma, chronic bronchitis, COPPD, emphysema
Lung recoil is not as strong / lungs loose elasticity (not able to push as much air out - RV increases)
Compliance (change in volume with pressure changes) actually increases
restrictive lung disease
problem is getting air in: pulmonary fibrosis
Lungs become very stiff - problem is getting the air in - reduction in TLC
respiratory gases - what we breath in
oxygen
carbon dioxide
water
nitrogen
Note: total pressure will always be 760mmHg, but components change (see table in notes)
hypoventilation
causes dropping PO2 levels within the system (at both level of alveoli and subsequently tissues)
- does not just mean breathing too slowly
why is PO2 leaving lungs (94-96mmHg - PaO2) not equal to PO2 in alveoli (102mmHg - PAO2)
PaO2 is a reflection of the cumulative input from every segment of the lung in terms of V/Q ratio (some high, some low, some zero - vary!!)
- anatomic venous shunts: areas in lung where blood flows but never interacts with alveolar surface
what happens when you hold your breath
alveolar ventilation decreases, PACO2 increases as does PaCO2
- increasing degree of acidosis
value to use for tidal volume
500 ml (0.5 liters)
value to use for anatomic dead space
150ml
anatomic dead space -air
air exists but no gas exchange occurs (approx. 150ml)
- note: this air has properties of inspired air (PO2=150mmHg, no CO2, water vapor present)
alveolar ventilation
rate at which gas exchange can occur
- reflection of tidal volume adjusted for dead space
- fraction of minute ventilation
- two equations (simple and more precise - see notes)
- exclusively about CO2!!
increase alveolar ventilation (hyperventilate)
decrease PACO2 ("blowing off CO2") - recall, PACO2 is a reflection of PaCO2
anatomic venous shunts - blood
areas in the lung where blood flows but never interacts with alveolar surface
• Blood in anatomic venous shunts will have a V/Q ratio of zero (blood is not re-oxygenated at all)
Note: blood will have partial pressures identical to when it entered lung (PO2=40 and PCO2=46mmHg)
three types of shunts
Anatomic: portion of CO bypasses the lung
Alveolar: perfusion passes through alveolar save with no ventilation
Physiologic: due to very low V/Q ratios in some areas of lung
anatomic shunt
portion of CO (cardiac output) bypasses lung
– Intracardiac right to left shunt (septal defect - pathologic condition)
• Mixing venous blood with arterial blood results in decreased PaO2
– Lung vasculature that doesn’t interface with alveoli – normal condition
alveolar shunt
perfusion that passes through an alveolar interface with no gas exchange
– Collapsed alveoli (atelectasis)
– Pus-filled or edematous alveoli (increase thickness or distance = reduction in flux)
physiologic
due to very low V/Q ratios of some areas in the lungs (essentially no gas exchange)
– Venous admixture (wasted blood flow)
– Clinically - most common cause is atelectasis (mucus, edema, tumor, foreign body)
V/Q ratio
ratio of air reaching the alveoli to the amount of blood reaching the alveoli
- unites value
- varies depending on lung location and body position (gravity has effect)
- average for healthy lung = 0.84
oxygen content
total amount of oxygen in the blood
- total dissolved oxygen plus oxygen associated with other molecules (Hgb)
- ml oxygen / deciliter blood
- normal: 19.5 ml O2 per 100 ml blood
note: very different than partial pressure which only included free O2 (not bound)
factors that determine oxygen content
- Amount of gas dissolved (PO2)
- Amount of Hgb and its saturation
- Amount of MetHgb
why is there only 6mmHg difference b/t PaO2 (40mmHg) and PaCO2 (46mmHg) in pulmonary artery
this small difference in partial pressure corresponds to a large difference in the volume of these two gases in the blood of the pulmonary artery (CO2 high O2 low)
- CO2 is WAY more soluble that O2 in liquid
goal of oxygen therapy
elevate PO2 and drive Hgb to 100% saturation
key roles of Hgb
Oxygen transport to tissues (through binding with ferrous iron – Fe+2)
Buffing capability – Bohr effect
CO2 transport molecule – key for transport from periphery (loading it up) to the lungs (offloading it)
Bohr effect
Hgb gains a proton (acts as weak base) when oxygen dissociates from Hgb
form of CO2 in blood
Large amount as HCO3- (HCO3- is a transport mechanism for CO2)
Small amount is dissolved
Small amount is carbamino (bound to proteins, such as Hgb)
forms of O2 in blood
Bound to Hgb = 98.6% - reversibly associated with Hgb
Dissolved O2 (PO2) = 1.4%
what determines the volume of a gas in a liquid (2 factors)
- partial pressure of the gas
- solubility coefficient (O2=0.024, CO2=0.57)
Note: CO2 is WAY more soluble than O2 in liquid
- small changes in partial pressure result in large volume of CO2 leaving blood into alveoli
3 factors that determine amount of O2 bound to Hgb
- amount of Hgb in system
- capacity of O2 to be bound to Hgb (determined by existence of methemoglobin - iron in ferric form, 3+)
- degree to which Hgb is saturated (can bind 1-4 molecules) - determined by PO2
difference in amount of O2 Hgb can bind v. capacity of O2 to bind Hgb
Hgb binds 1.39 ml O2 / gram Hgb
1.34 grams O2 will combine with 1 gram Hgb
Note: 0.05 ml difference is due to presence of ferric iron (oxidized iron) and methemoglobin - exists to a small degree under normal conditions
Note: ferrous iron (Fe2+) is required for heme to reversible associate with oxygen
4 factors that effect Hgb’s affinity for oxygen
i.e. what make Hgb an effective transport molecule for oxygen / factors that decrease its affinity for oxygen
Partial pressure of CO2: increasing CO2
Proton concentration (H+): increasing proton conc. (decreasing pH – more acidic)
Temperature: increase in temperature
2,3-BPG (same as 2,3-BPG): increase in metabolic activity→inc. in 2,3 BPG (BPG is a reflection of overall glycolytic activity in RBCs)
PulseOx
provides degree of saturation of hemoglobin (percentage reading)
Clinically: indirect window to PaO2
Recall: tells us nothing about amount of Hgb in system (can have very anemic person with normal PulseOx)
extraction ratio
difference in oxygen conc. (vol./dL blood) between venous and arterial blood; how much oxygen is extracted by certain tissues
- Kidneys - 10% (small percentage since the blood flow is so massive to kidneys)
- Heart - 60-65% (peak extractor of O2 on continuous basis)
- Exercising muscle - 90% (huge ER) ; muscle at rest is about 30%
oxygen saturation of Hgb effects CO2 concentration for any given PCO2 (since Hgb is also a CO2 carrier)
Deoxy-hgb: reacts to a greater degree with CO2 (binds more CO2)
- periphery: PO2 40mmHg - deoxygenated Hgb is carrying more CO2 (picking it up – more effective “sink” for CO2)
- capillary-alveolar interface: PO2 is 100mmHg (more oxygenated / more fully saturated Hgb, Hgb does not carry as much CO2)