Respiratory Physilogy Flashcards
Pulmonary ventilation
Convective air move to due to pressure gradients created by respiratory muscle activity
Inspiration–pressure in the intrathoraci airways are less than atmospheric
Expiration–pressure gradient is reversed and higher pressure within the lungs causes air to flow out
Brings the O2 atmospheric air to gas exchange regions (respiration) and alveolar space
Shorten the diffusion distance by ventilating the lungs
Respiration
Diffusion of O2 into pulmonary capillaries for uptake by the blood plasma and RBCs
O2 moves down partial pressure gradient
CO2 moves down its gradient from capillary to alveolar airspace
Pressure gradients for ventilation vs respiration
For ventilation, gases move down airway pressure gradients
For respiration, gases move through regions by partial pressure gradients
Path of diffusion of O2 and CO2 in the lungs
O2 diffuses from alveolar spaces to pulmonary capillaries
CO2 from pulmonary vasculature into acinar space (terminal respiratory unit) then pulmonary ventilation into air
Hypercapnia and Hypoxemia
Hypercapnia–Excess partial pressure of CO2 in the respired air or arterial blood
Hypoxemia–low oxygen availability that can only be sensed on the arterial side of the blood. Results in anaerobic respiration and lactic acid buildup
2 major results from inadequate ventilation
Compromises O2 uptake by the lungs and delivery to the tissue (anaerobic metabolism—>non-volitile acid production (lactic acid)—>acidosis)
Compromises CO2 removal–>buildup of volatile acid–>acidosis
Phonation
Respiratory muscles contracting to create air movement over the vocal cords within the larynx for vocal communication
Lymphatic function of the respiratory system
Largest in body, always taking in air, pathological bacterial,
First line of defense-mucosa lining the airways
Lymphocytes migrate there
Drain into subclavian veins
Changes of air via heat and water exchange
47 mmHG of H2O at 37 degrees Celsius to protect the alveoli
What causes humidification and warming of the inspired ear
Mucous membranes of the nose, turbinates, and pharynx due to their large surface area and rich blood supply
Mucociliary elevators
Small particulates are trapped in bronchial secretions (100 ml/day) which are moved upward toward the pharynx and mouth for removal
Pulmonary artery contents
Out put of the right ventricle (all CO) through the pulmonary artery (contains a minute of all venous blood from all regions of the body) through pulmonary capillary network
Filtration of blood in pulmonary circulation
Ideal for trapping circulating blood clots
Conversion of ATI to ATII
Degredation of Bradykinin
Prostoglandin E series, F2 alpha, completely removed from circulation with one pass
Protoglandin A series adn I2 are unaffected
Circulating epinephrine I not affected,
Norepinephrine is affected
V dot
Gas volume/unit time
V dot O2–O2 consumption per minute
F
Fractional concentration in dry gas phase
D
Diffusing capacity
Va
Volume of alveolar gas
STPD and BTPS
Standard temperature and pressure (0 degrees Celsius, 760 mmHg)
BOdy temperature and pressure saturated with water vapor
Vt
Tidal volume
Either in or out of lungs–not a summation
Pc bar O2
Mean capillary O2 partial pressure
SvO2
Saturation of HB with O2 in mixed venous blood
Arrangement of airways, pulmonary arteries, and pulmonary veins
Airways are associated with deoxygenated pulmonary arteries, mixed venous blood
Pulmonary veins–oxygenated
What generates the motive force to move air from mouth to gas exchange areas
Sub atmospheric pressure within the thorax
Describe the branching pattern of airways
23 generations of irregular dichotomous branching tubes to maximize alveolar surface area for smallest volume
Subsequent branching is narrower in diameter and shorter in length
Conducting airway of bronchi
Branches 1-10 with cartilaginous support–not engaged with gas exchange, the lobar bronchus
Change of cartilage and muscle through bronchi branching
Down the length of the branching airways, cartilage cilia, and mucous secreting cells decline
Smooth muscles increase, allowing to dilate or constrict through neural and reflex stimulation
Changes in airway diameter are _____ of lung volume
Independent, if caused by neural and reflex stimulation
When does cartilage rings disappear from bronchi
When they enter the parenchyma—surrounded by alveolar tissue
Bronchioles (Branching)
Non cartilaginous conducting from 11-16th generation of branching
Respiratory bronchioles–17-19
Airway dependent on lung volume
Difference between lung volume dependence on airway diameter for bronchi and bronchioles
Bronchi–independent changes to airway diameter
Bronchioles–dependent on air volume
What divisions of the airway are dependent on systemic blood supply
1-16… Depend on bronchial circulation
Pulmonary artery and airways
Associated as they branch and they receive the venous drainage of the alveoli
First bronchioles to be part of gas exchange area
17, smooth muscles isolated areas and elastic fibers
Acinus
Terminal respiratory unit (17th-23rd)
Functional unit of the lung
Involved in gas exchange
Distal to terminal bronchiole, specifically, the respiratory bronchiole, alveolar duct, alveolar sac, and alveolus (23rd branch)
Squamous epithelium
Metabolic requirements are met by diffusion for O2
Metabolic for amino acids, glucose, etc–pulmonary capillary blood supply`
Acinus support
No ciliated epithelium
Relies on surrounding lung tissue (lung parenchyma) via tethering
Parasympathetics to bronchioles
Sympathetic so to bronchioles
Constriction to increase velocity of air movement– want to get debris to bigger airway–think coughing
Dilutions of airways to decrease resistance to airflow
All occurs via smooth muscle in airway walls
Local hypocapnia vs local hypercapnia
Local bronchiole radio construction, directing ventilation away from alveolar regions with poor perfusion
Hypercapnia or hypoxia causes bronchiolar dilation–airflow to alveolar regions with better perfusion
Causes of constriction of bronchi
Parasympathetics Alpha adrenergic antagonists Local irritants Chemoreceptors activation Increased air velocity
Dilation of broncholes
Sympathetic innervation
Beta 2 adrenergic ago it’s
Inhibition of phosphodiesterase (not breaking down CAMP, less Ca2+, relaxation)
Decreased airway resistance
Gas content of perfused vs non-perfused atmospheric air
Perfused–you will have high CO2, low O2
Non-perfused–high O2, low CO2
Alveoli
Small, polyhedral shaped sacs
Walls-type 1
Elastic and I elastic fibers and capillaries within alveolar walls
Thin barrier to diffusion
Largest biological membrane in the human body
Type II can differentiate to become type I
Macrophages
Only thing that can attack Bacteria at level of alveolus because alveoli do not have cilia
Migration to lymphatic system
Clean up phospholipase surfactant that is broken down
Pores of Kohn
Openings between alveoli to allow macrophage and Type II cells to move from one to the other
Gas exchange
Blood-Gas interface
Capillary surface area is nearly equal to alveolar surface area
Thin layer 0.2-0.5 microns thick
Epithelium, interstitial space, capillary endothelium, plasma, and erythrocytes membranes
RBC spends less than a second in alveolar capillary network
Most lung mass is blood in lung
Pulmonary circulation
Pulmonary artery (deoxy) Pulmonary capillaries (oxy) Pulmonary veins (oxy blood mixed with deoxygenated blood from bronchial veins)
Right to left blood shunt
Blood flow drainage into the pulmonary veins from visceral pleura and airways
5% cardiac output
Pulmonary veins have less oxygen in them when they get to the heart than when they started right after the pulmonary capillaries due to venous to arterial right to left shunt
Pleural effusion (abnormal)
The vein (deoxy) from bronchial artery capillary system goes into the pulmonary being from pulmonary capillary
Bronchial circulation
Provide conducting airways with nutrients and oxygen
Pulmonary circulation resistance, pressure, compliance
Low resistance, low pressure, compliant system (15mmHg MAP)
Reduces work of right heart
Helps prevent flooding of alveoli
Decreases diffusion efficiency by increasing distance
Lung parenchyma–alveoli
I elastic fibrous network in the most peripheral airways, strong backbone
Elastic fibers–hold open non-cartilaginous supported bronchioles and alveolar ducts–tethering effect
Tethering effect
Elastic fibers holding open the non-cartilaginous supported bronchioles and alveolar ducts… Air diameter in the lung periphery is dependent upon lung volume
Composition of atmospheric Air
- 93% O2
- 04% CO2
- 03% N2
Partial pressure
Barometric pressure times fractional concentration of each gas
So, at the high altitude, total barometric pressure is less and the partial pressure are less
Partial pressure of PO2 at seas level
PB times FiO2 (Pressure barometric times fraction of O2 that is the whole) or 159 mmHg
Dalton’s Law
Each individual gas acts as if it occupies the total volume of the mixture and the pressure it exerts is proportional to its concentration
Dependent on the fraction that the gas of a particular species is in the gas mixture and the total pressure exerted by mixture
Reduction of PO2 by warming and humid flying
Go from 0.2093x 760 to 0.2093 times 713 to make up for the addition of water diluting the other inspired gases
The total pressure exerted by other inspired gases is now lower, lowering all of their partial pressures
Decreases from dry ambient air–160 to tracheal(inspired) at 150
Alveolar air PO2 and CO2
1) water vapor added as diluent
2) metabolism and gas exchange continue through both inspiration and expiration
3) volume of air inspired in a tidal breath is small compared to the volume of gas left in the lung at end-expiration
This is why pO2 decreases to 100 and CO2 increases to 40.
Difference between alveolar air and arterial blood
Normal inequalities of gas exchange and normal right to left shunting of blood
Bronchial and coronary circulation dump deoxygenated blood into oxygenated blood pathways present in right to left shunts (from pleura and airways)
Gravity on us, maldistribution of alveolar ventilation and pulmonary capillary perfusion within lungs
CO2 is essentially the same due to the large diffusivity of CO2 and the small a-v to CO2 gradient
Differences between PO2 and PCO2 between systemic arterial and mixed venous blood
Metabolism
Consumes the O2 to generate ATP and sustain life.
90% of CO2 is produced by metabolism in the venous side of systemic circulation,but this is transported as bicarbonate, not CO2, so that’s only a few mmHg higher
Numbers for changes of PO2 and PCO2 from ambient air, inspired air, alveolar air, arterial blood, and resting venous mixed blood
PO2- 160,150,100,90,40
PCO2–.3,.3,40,40,46
Resting Mixed venous blood
From 90 to 40 mmHg –5ommHG to tissue
From 40-46 mmHg–6 ml from tissue..due to bicarbonate
Two components of Gas exchange
Ventilation (moving air into an out of alveolar regions) External respiration (gas diffusion across the alveolar-capillary membranes)
How do you measure VA (alveolar ventilation
VA=(TWV-DSV) X RR
Minute ventilation (VE)
Volume of gas entering the lungs per minute.
VT-RR
Oxygen delivery by cardiac output
Oxygen Delivery = CO (L/min) X Oxygen content of the blood (mL of O2)
LaPlace’s law
Pressure necessary to keep a sphere open is directly proportional to the surface tension and inversely proportional to the radius of the sphere
Pressure–negative pressure generated by the contraction of the diaphragm
IRV
Additional air that can be forcibly inhaled after the inspiration of normal tidal volume
ERV
The maximum volume of air expired from the resting end-expiratory position (FRC)
RV
The volume of air remaining in the lungs after maximum respiration
Inspiratory capacity
IRV plus TV
Vital capacity
The maximum volume of air expired from the point of maximum inspiration
Inspiratory vital capacity
Maximum volume of air inspired from the point of maximum expiration
FRC
Sum of RV (the plume of air remaining in the lungs after maximum expiration) and ERV (the volume of air expired from FRC)
TLC
The sum of all volume compartments or the volume of air in the lungs after maximum inspiration
What lung capacity and volumes increase with age? Decrease?
Decrease? ERV and VC
Increase? FRV and RV
TLC=?
IRV+ERV+TV+RV
FRC=?
ERV plus RV
Muscle movements during inspiration
Diaphragm contracts, increasing longitudinal area of chest wall, expands until lower ribs elevated=limit of abdominal wall compliance
External intercostals fix anterior posterior area of thorax (oriented obliquely downward and anteriorly), raising ribs
Scalene–elevation of first 2 ribs, enlarging upper rib cage
SCM–anterior posterior thorax and increase thoracic volume
Passive description of expiration
Recoil of elastic and I elastic structures of the lungs and surface forces
Elastic and inelastic fibers of lung parenchyma—lung volume back to FRC
Expansion of lungs alters attractive forces between fluid molecules, reduce alveolar volume.
Muscles of expiratoin
Internal intercostals–obliquely downward and posteriorly, ribs downward and inward, decreasing anterior-posterior dominions
Abdominal muscles–pull down ribs and inward, compression of abdominal cavity, diaphragm upward into thoracic cavity, decreasing longitudinal distance
Pathological decrease in lung recoil
Emphysema
Rl decreases, less opposition to Rcw–less Ppl (less negative, closer to atmosphere), chest wall move to a larger thoracic volume (unopposed)
New equilibrium is at a larger thoracic volume and a less negative intraplueral pressure
Pathological increase in lung recoil
Pulmonary fibrosis
More Rl to oppose normal Rcw, more resistance, more negative Ppl, smaller volume in chest
Inspiration and recoil
Increasing thoracic volume via muscle contraction leads to lung expansion through coupling with chest wall, Ppl more negative since elastic recoil of the lungs increases with lung expansion
Increase in thoracic volume results in a Decrease in pressure within the thorax–.>alveolar pressure, air moves down gradient
Ppl and elastic recoil with lung expansion
Ppl more negative since elastic recoil of lung increase with lung expansion
Ppl, elastic recoil, lung volume on expiratoin
Lung volume back to normal (FRC), decrease in thoracic and lung volume results in an increase of alveolar pressure, air from lungs into atmosphere
Relaxed breathing–Ppl still remains negative
Active expiration–Ppl can be positive with respect to atmosphere, compression of lung due to elastic and surface forces and chest wall movement.
Alveolar pressure is zero?
End-inspiration and end-expiration
Alveolar pressure on inspiration and expiration
Inspiration– negative
Positive–expiration
Cl measurement, normal value
Distensibility of the lung (how easy or difficult to expand the lungs)
Volume of change produced by a unit of transpulmonary pressure change
200 ml/cm H20
What what volume is the lung most compliant?
FRC
Airway structure/geometric arrangement/inelastic/elastic at FRC
At FRC, collagen/fibrin and elastin are stretched to twice their resting length due to their geometry
Account for less than half of elasticity
Hysteresis
More difficult to open previously closed airways on inflation from low volume (high surface tension) and likewise, airways that are open at high volumes (low surface tension) tend to stay open as pressure is reduced.
They are influenced by the history of the previous volume.
Due to the surface forces acting at the air-fluid interface
Hysteresis is due to:
Surface forces within the lungs
Non-perfect elasticity of the lungs
Inertia of the lungs
Addition of saline (hysteresis curve)
Elimination of surface forces…which means that surface forces act to make the lung stiffer or harder to inflate
Surfactant in small alveoli vs large alveoli
Small alveoli, surfactant is packed to keep surface tension low and prevent collapse
Large alveoli, unpacking of surfactant so the surface tension is proportional to alveolar size.
Small surface tension is small alveoli, increase surface tension is larger alveoli
A-a gradient is normal in situations of hypoxia:
Hypo ventilation
High altitude.. Low Fi inspired O2
Hyperventilation effect on CO2
Decreases lower than normal (
What causes airway obstruction in asthma? What produces relaxation (drug)?
Constricted bronchioles
Relaxation beta 2 adrenergic
Volume of lungs during inspiration
FRC+TV
ERV equation
ERV=VC-(TV+IRV)
Intrapleural pressure and transpulmonary pressure at base vs apex
Intraplueral pressure is more negative and transpulmonary pressure is more positive at the top of the thorax because the lung is pulling away from the surrounding thoracic cage
Pressure gradients for the 3 lung zones
Zone 1 PA>Pa>Pv (no perfusion)
Zone 2 Pa>PA>PV
Zone 3 Pa>PV>PA (high perfusion)
Highest resistance airways
Medium sized bronchi
Early changes in resistance in alveoli are often unnoticed
When Patm=PA, what is happening with airflow and where are the lungs at (Capacity)?
When Patm=PA there’s no airflow. No pressure gradient.
Lungs are in functional residual capacity
Compliance of lung+chest wall vs lung OR chest wall
Compliance of lung or chest wall alone is greater than that of the combined system (slopes of curve steeper than individual slopes
V/Q at base vs apex and PCO2 vs PO2 in capillaries
V/Q is higher in apex than at the base because the differences in ventilation aren’t as great as for perfusion, so more ventilation at apex
More ventilation at apex means higher PO2 in capillaries, lower PCO2 in capillaries
Base–less PO2, higher PCO2
Stimulation of peripheral chemoreceptors
Carotid and aortic bodies, hypoexemia=hyperventilation
Stimulation of central (medullary) chemoreceptors
CO2 or H+
ventilation rate and O2 consumption during exercise
Ventilation rate increases ot match the increased O2 consumption and increased CO2 production
No change in mean PO2 or PCO2
Venous PCO2 increases
No increase in PCO2 of arteries because we have an increased ventilation to combat
What occurs in the blood during transport of CO2 from tissues
- -H2O joins CO2 to form H+ and bicarbonate
- -H+ is buffered by deoxy heme
- -acidification of RBCs
- -bicarbonate out, Cl in.
- -bicarbonate is carried into the lungs via plasma***
- -CO2 binds directly to Hb, carbaminoHb
Causes of decreased O2 in the blood
- -decreased Hb concentration (anemia)
- -decreased O2 binding capacity of Hb (CO poisoning)
- -decreases arterial PO2 (Hypoxemia)
Only form of hypoxia associated with an increased A-a gradient
Right to left shunt
Lack of O2 equilibration between alveolar gas and systemic arterial blood
Right heart output is not oxygenated in lungs and is thereby dilutes the PO2 of normal oxygenated blood.
Hypoxia with a normal A-a gradient
High altitude, hypoventilation. Both alveolar and arterial PO2 are decreased
Decreased PaCO2 and breathing
Result of Hyperventilation which increases pH, inhibition of breathing.
Hyperventilation
Respiratory alkalosis
FEV1, FEV1/FVC, and FEF25-75 for fibrosis and emphysema
FEV1– lower for both
FEV1/FVC–lower for emphysema, normal or increased for pulmonary fibrosis
FEF25-75–decreased in emphysema, increased or near normal in fibrosis
Emphysema and Fibrosis comparisons for capacity and volumes
E- decrease Recoil, increase compliance, increase RV, increase FRC, increase TLC
F–increase recoil, decrease compliance, decrease RV, FRC, TLC
Location of central chemosensitive regions
Ventral lateral medulla
Ventilators response to hypercapnia (increase PaCO2)
Minute to minute control of ventilation
Unaltered after denervatio now peripheral chemoreceptors
Law of Laplace
P=2T/r pressure inside the alveolus
Without surfactant, this law states that the pressure inside small alveoli would be greater than that in large alveoli.
So small alveoli would empty into large alveoli and collapse
Two forces that prevent alveolar flooding
Negative intrapleural pressure and surfactant
Compliant work vs resistive work
Compliant–surface forces and elastic and inelastic forces
Resistive–flow-resistive and inertialyes forces of lung and chest wall
Resistance to airflow in the respiratory system
R= 8nl/pi r^4
If airway is reduced by 1/2, the resistance increases 16 fold. If driving pressure doesn’t increase, airflow will be reduced by 16-fold
R=driving pressure/flow ratE
Total airway resistance in inspiration vs expiration
Higher during expiration because during inspiration, tethering occurs
Airway resistance decreases, diameter increases on inspiration
Major structures for airway resistance
Mouth/nasal cavity (20%)
Medium sized bronchi
Effort and lung volumes/airflow rate
During expiration after lung volume is less than FRC heading toward RV, effort only compresses the airways more, increasing resistance to airflow. This is the effort-independent region.
Everywhere else, size of loop depends on effort
Airflow rates for emphysema vs fibrosis
Emphysema– diminished peak expired airflow rates despite high lung volumes because of reduced lung recoil
Fibrosis–increased lung recoil but diminished peak expired airflow rates because of low lung volume
Increasing effort at mid-low lung volumes
Increases intrapleural pressure, pressure gradient from alveolus to mouth increases–airflow
Alveolar ventilation vs minute ventilation
Alveolar is always less than minute ventilation
The degree depends on the dead space fraction of the tidal volume and frequency of breathing
Increasing VT is a better increaser
If you increase dead space without increasing minute ventilation, you have a decreased alveolar ventilation
Physiological dead space
Sum of anatomical dead space and volume of gas in non functioning alveoli
Ventilated but not perfused
Anatomical DS + 25% of Vt at rest
Perfused but not ventilated
Right to left shunt
Mixed expired CO2 and dead space
As you increase dead space, you decreases the amount of mixed expired CO2
Hyperventilation and hypoventilation on O2 and CO2
hyper–Increases alveolar O2 while decreasing alveolar CO2
Ventilation of basal vs apical alveoli based on gravity
Basal will be more ventilated than apical due to less transpulmonary pressure
Base is more compliant, so a lot of ventilation for a small pressure (less transpulmonary pressure allows this)
More transpulmonary pressure, larger alveoli==less compliant
FRC, alveoli, compliance, transpulmonary pressure, apex
Greater transpulmonary pressure, greater dinstending pressure, alveoli are larger. Slide up the pressure-volume curve, region is less compliant and less ventilated
Increase pulmonary vascular pressure
Decrease pulmonary vascular resistance due to recruitment of the capillaries opened by pressure increase and increase in individual capillary diameter
Global hypoxia
Global vasoconstriction, pulmonary hypertension, increase workload on the right ventricle, pulmonary edema
Alveolar blood vessels vs extra-alveolar blood vessels during inspiration
Alveolar–compressed during inspiration
Extra-alveolar–tethered open by lung parenchyma`
Perfusion and ventilation at apex and base compared to each other
Perfusion is greater than ventilation at the base
Ventilation is greater than perfusion at the apex
Think 3 lung regions that are based on perfusion (not ventilation)
Basal alveoli will be better ventilated than apex
PRG vs DRG
PRG is fine tuning, upper pons
DRG inspiratory to phrenic motor neurons and VRG (external and accessory respiratory muscles
PRG
- -bilateral upper pons
- -fine tuning respiratory rate, switching from inspiration to expiration
- -NPM and K-F
- -modulates medullary centers responses to other stimuli
Apneustic Area
Inspiratory gasps
Not part of PRG, but does have effect on inspiration
Cut between PRG and apnuestic area
Increases Vt and decreases respiratory rate
Vagus nerve
DRG
Ventral lateral NTS
Inspiratory neurons to phrenic motoneurons
Afferents from 9th and 10th cranial nerves
Integrate visceral sensory information to determine respiratory motor response or drive
To I neurons of the VRG
Interneurons from DRG to VRG
Elicit increased activity in non-phrenic inspiratory muscles
VRG
Inspiratory and expiratory neurons
Expiratory–internal intercostals and abdominal
Inspiratory–external intercostals, accessory, and phrenic
Inhibitory expiratory neurons prevent inspiratory discharge during expiration
Mechanism for carotid chemoreceptors
Hypoxia, hypercapnia, and acidosis inhibit K+ channels, depolarizing cells, increasing glom us Ca, inducing transmitter release, and stimulating afferent fiber
What stimulates peripheral chemoreceptors
Decreased Ocygen (hypoxia or Hypoxemia) Hypercapnea Acidosis
Increase firing rate to increase ventilation
Accute response to hypoxia, metabolic acidosis or alkalosis,
Location of CCR
Ventrolateral medulla
CCR detect?
Changes in CO2 and H+
Hypercapnia
Minute to minute control of ventilation
H+ in intersitial fluid–hypoxia (anaerobic metabolism)
Moderate brain Hypoxemia vs severe brain Hypoxemia
Moderate–switch to anaerobic metabolism, lactic acid and H+ formation, stimulation of breathing
Severe–depressed breathing.
Affects of arterial hypercapnia and arterial blood pH on CSF
Not a lot of buffer proteins (only buffer is bicarbonate), arterial hypercapnia leads to a greater change in CSF pH than arterial blood pH because H+ cannot diffuse through the membrane like CO2 which becomes hydrated
How does CSF restore pH
Active transport of bicarbonate from blood to CSF
Low CO2, bicarbonate goes from CSF to blood
Pulmonary stretch receptors
Mechanoreceptors
Stimulated by distension of the lungs
Activation causes inhibition of inspiratory activity to prevent hyperventilation
Hering-Breuer inflation reflex
To PSR increased Vt,decreased breathing rate
RARs
Irritant receptors
Between airway epithelial cells, vagus nerve
Noxious gases, dust, smoke, cold air, and rapid volume changes
Hyperventilation, bronchostriction, coughing
C-fibers
Alveolar-capillary interstitial space, bronchi
Non-myelinated vagus
Distension or congestion
Bronchoconstriction, rapid, shallow breathing, and increased mucous secretion into airways (turbulant airflow)
Hypoxic Hypoxemia
Less than normal PO2 in inspired air, decreased O2 in plasma, stimulation of breathing
Anemic Hypoxemia
Carotid bodies uneffected, normal PO2
CO poisoning
If severe enough, anaerobic metabolism, metabolic acidosis, increased ventilation
Stagnant hypoxia
Low blood flow, anaerobic metabolism, CB stimulated due to metabolic acidosis increasing firing rate, increasing ventilation
Histotoxic hypoxia
Low ATP production, blocking ETC of ATP (CN)
Anaerobic metabolism, acidosis, stimulation of breathing,
CBs respond as if there’s not O2
Ventilation PO2 and PCO2
You must decrease PO2 by 50% to produce a doubling in ventilation
Increase PCO2, you increase ventilation at a much higher PO2 than you would with a normal PCO2(40)
You only have to increase PCO2 by 5mmHg (10%) to get a doubling of ventilation
At any PCO2, what is the relationship between CO2 and ventilation if pH is changed
If the pH is decreased, ventilation will increase. Addind acidosis increases ventilation, but does not change the sensitivity of CO2.
Changing arterial pH does change ventilators threshold. If you are acidotic, you begin to breath at a lower CO2 than under normal conditions
Ventilatory sensitivity to CO2 in response to CO2 and O2
Change CO2, sensitivity doesn’t change
Change O2, sensitivity is altered (increasing PO2 decreases the carotid bodies sensitivity to elevated CO2)
Threshold is unchanged by CO2 but changed by PO2
High Altitude
Reduced PaO2, normal A-a, normal PaCO2 unless O2 drops below 60mmHG
Alveolar hypoventilation
Reduced PAO2 and PaO2
Normal A-a
Increased PaCO2
Diffusion impairment
Normal PaO2 but increased diffusion barrier leads to reduced PaO2
Widened A-a
Nml (CO2 isn’t diffusion limited)or reduced PaCO2 (reduced if the hypoxia stimulates breathing)
Causes- thickening of alveolar-capillary gas barrier, decreased in ST, and pulmonary capillary transit time (ncreased flow)
Right to left shunt
Perfused but not ventilated Bronchial and coronary circulation Dependent on shunt fraction of cardiac output, mixed venous O2 content, and O2-Hb dissociation curve Increased PaCO2 Widened A-a Normal PA, abnormal PaO2
