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88 Cards in this Set

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Dalton's Law
Total pressure of a gas mixture is equal to the sum of the pressure that each of the gases would exert independently. Total pressure equals the sum of the partial pressures.
(atmospheric pressure at sea level is 760 mmHg)
P dry atmosphere=PO2+PN2+PCO2
O2 is 21% of 760 or 159 mmHg
N2 is 78% of 760 or 593 mmHg
Physical Principles of Gas Exchange
Diffusion in response to concentration gradient
Pressure proportional to concentration
Gas contributes to total pressure in direct proportion to concentration
CO2 20 times as soluble as O2
Diffusion depends on partial pressure of gas
Air is humidified yielding a water vapor pressure of 47 mmHg.
Water vapor
Water vapor – as a gas – adds its own pressure. As water vapor increases in a mixture, it dilutes the concentration of the other gases to the mixture.
P wet atmosphere = PN2+PO2+PCO2+PH2O
So now, at sea level (wet), water vapor pressure at 37o is 47mmHg

the Po2 is 0.21(760-47)=150mmHg
Determinants of Diffusion
Pressure Gradient
Area
Distance
Solubility and MW are fixed

know fick's law
Po2 in the Alveoli
PAlvO2= PIO2- (PCO2/R)

PO2= 149- (40/0.8) = 99

R is respiratory exchange ratio ~0.8

Remember in a normal person alveolar PO2 = arterial PO2, and
alveolar PCO2 = arterial PCO2 .
Pco2 in the Alveoli
PCO2=CO2 production *K
Alveolar Ventilation

K is constant

If ventilation is doubled then Pco2 is _
If ventilation is halved then Pco2 is doubled
Boyle’s Law
the pressure of any given gas is inversely proportional to the volume of its container.
An increase in lung volume during inspiration reduces the pressure on the gas and air goes in
Mechanics of respiration
Inspiration
Passive – diaphragm only
Active – external intercostals, pectoralis minor
Scalenes, sternocleidomastoideaus, serratus anterior, some neck muscles
Expiration
Passive – nothing –the weight of the chest and elastic recoil
Active – internal intercostals, splinting the abdominals
Cell Types in Alveoli
Capillary Endothelial Cells
Alveoli Epithelial Cells
Type 1 cells
Type II cells
Fibroblasts
Macrophages
Mast Cells
Control of Bronchiolar Diameter
Nervous
Sympathetics – both epi and nor-epi
β2 receptors dilate
Parasympathetics
Acetylcholine constrict
And increases mucus production
Humoral
Histamine, acetylcholine » Constrict
Adrenergic (β agonists) » Relax
Intrapleural ‘space’
Visceral and parietal pleura are stuck together like two pieces of glass
In contact by a thin layer of fluid
It is formed as a filtrate from blood – like interstitial fluid – and drained by the lymphatics
It fills a potential space
Movement of Air In and Out of Lungs
Pleural Pressures
Resting -5 cm H20
Inspiration -8 cm H20
Alveolar Pressure
Resting 0 cm H20
Inspiration -1 cm H20
Expiration 1 cm H20
Compliance
ΔV/ΔP 200 ml/cm H20
(1 cm H20 ~ 0.7 mmHg)
Compliance
Lungs are about 100x more stretchable than a toy balloon
Compliance is a change in lung volume relative to the change in transpulmonary pressure
Compliance is reduced by factors that produce a resistance to expansion
If filled with concrete lungs would be unable to respond to transpulmonary pressure and compliance would be 0

Determined by elastic forces
Elastic forces
lung tissue
surface tension
Elasticity
Tendency of a structure to return to its original shape after stretching
Since lungs are ‘stuck’ to the chest wall – they are always in a state of elastic tension.
Surface tension
Intra-alveolar fluid coats the type I cells of the alveoli.
Lung cells both secrete and absorb fluid
Fluid absorption is driven by osmosis (based on Na+ active transport).
Fluid secretion is driven by active transport of Cl- out of the cells.
Part of the pathophysiology of cystic fibrosis is a failure of the Cl- carrier, making intra-alveolar fluid less watery and more viscous.
Surfactant
Phospholipids: Dipalmitoylphosphatidylcholine and phosphatidylglycerol – combined with hydrophobic proteins and Ca+2.
Interspersed between water molecules reduces the hydrogen bonding of water. Reduces the surface tension.
Surfactant %age increases as alveolus decreases in diameter.
Even after forceful exhalation, alveoli remain open and don’t collapse.
Preterm babies – less than 28 weeks – mom will be treated with corticosteroids to increase the maturation rate of the baby’s lungs. RDS. Tested for surfactant levels in amniotic fluid
ARDS in adults with septic shock. Cap. permeability increases, lungs fill with protein rich fluid, surfactant levels are normal and compliance is lost. Alveoli collapse
Airway Resistance
Flow = ΔP π r4/(8 μ l)
Resistance = 8 μ l/ (π r4)
Upper airways major resistance because volume-wise they are much smaller than alveoli (under normal conditions)
Decrease in lung volume results in an increase in resistance
Biggest control of lung volume is in the bronchioles – covered with smooth muscle
Pulmonary Capacities
Inspiratory capacity (tv+irv)
Functional residual capacity (er+rv)
Vital Capacity (erv+tv+irv)
Total lung capacity (rv+vc)
Timed Volumes
Minute Respiratory Volume
Tidal volume * respiratory rate
Alveolar Ventilation
(Tidal volume-dead space) * resp rate
Dead Space
ANATOMICAL – nose, pharyx, trachea
about 150 ml
PHYSIOLOGICAL- some alveoli can be non-functional. Scarred or not perfused.
Depends on ventilation-perfusion ratio
Ventilation/perfusion
Ventilation/perfusion

Relationship between adequate flow and adequate ventilation
Defined as V/Q
V/Q = (4 l/min)/ (5 l/min) = 0.8
Va = alveolar ventilation. Q = blood flow
Low V/Q means inadequate ventilation – physiologic shunt – some blood is not being oxygenated, or relieved of its CO2
High V/Q means no blood flow to the lungs
If O2 stays in the alveoli, and is not picked up by the blood, those alveoli are physiologic dead space
If there is no diffusion impairment then the Po2 and Pco2 between an alveolus and end capillary blood are usually the same.
Ventilation/Perfusion
Physiologic shunt
Va/Q < normal
low ventilation
Physiologic dead space
Va/Q > normal
wasted ventilation
Abnormalities
Upper lung Va/Q 3 x normal
Lower lung Va/Q .5 x normal
Abnormal V/Q
Normal upright person: cap perfusion and ventilation are low in the upper regions of the lungs – approaching physiologic dead space
Bottom lung regions have more perfusion than ventilation and approach shunting.
Smokers: bronchiolar obstruction – air trapping – air never gets to alveoli – lowers V/Q
And emphysematous scarred areas hold air but there’s no transfer -shunting blood
COPD
Blood PO2 & PCO2 Measurements
Provide good index of lung function
At normal PO2 arterial blood has about 100 mmHg PO2
PO2 is about 40 mmHg in systemic veins
PC02 is 46 mmHg in systemic veins
Pulmonary Circulation
Rate of blood flow through pulmonary circuit equals flow through systemic circulation
But it is pumped at lower pressure (about 15 mm Hg)
Pulmonary vascular resistance is low
Low pressure produces less net filtration than in systemic capillaries
Avoids pulmonary edema
Pulmonary arterioles constrict where alveolar PO2 is low & dilate where high
This matches ventilation to perfusion
Hemoglobin (Hb) & 02 Transport
Each Hb has 4 globin polypeptide chains & 4 heme groups that bind 02
Each heme has a ferrous ion that can bind 1 02
So each Hb can carry 4 02s

Most 02 in blood is bound to Hb inside RBCs as oxyhemoglobin
Each RBC has about 280 million molecules of Hb
Hb greatly increase

Methemoglobin contains ferric iron (Fe3+) -- the oxidized form
Lacks electron to bind with 02
Blood normally contains a small amount
Carboxyhemoglobin is heme combined with carbon monoxide
Bond with carbon monoxide is 210 times stronger than bond with oxygen
So heme can't bind 02s 02 carrying capacity of blood

02-carrying capacity of blood depends on its Hb levels
In anemia, Hb levels are below normal
In polycythemia, Hb levels are above normal
Hb production controlled by erythropoietin (EPO)
Production stimulated by low P02 in kidneys
Hb levels in men are higher because androgens promote RBC production

High P02 of lungs favors loading; low P02 in tissues favors unloading
Ideally, Hb-02 affinity should allow maximum loading in lungs & unloading in tissues
Oxyhemoglobin Dissociation Curve
Gives % of Hb sites that have bound 02 at different P02s
Reflects loading & unloading of 02
Differences in % saturation in lungs & tissues are shown at right
In steep part of curve, small changes in P02 cause big changes in % saturation

Is affected by changes in Hb-02 affinity caused by pH & temperature
Affinity decreases when pH decreases (Bohr Effect) or temp increases
Occurs in tissues where temp, C02 & acidity are high
Causes Hb-02 curve to shift right & more unloading of 02
Shifts of Dissociation Curve
Right shift at tissue
increased carbon dioxide in blood
decreased affinity for oxygen
maintain partial pressure gradient
Left shift at lungs
loss of carbon dioxide at lungs
increased affinity of oxygen
Transport of Oxygen in Blood
Dissolved oxygen
Solubility 0.003 ml O2/100 ml blood mmHg
Normal blood 0.3 ml O2 / 100 ml blood
Normal oxygen consumption 250 ml O2/min
Would require 83 l/min blood flow
Hemoglobin
97% transported
O2 + HB HBO2
Effect of 2,3 DPG on 02 Transport
RBCs have no mitochondria; can’t perform aerobic respiration
2,3-DPG is a byproduct of glycolysis in RBCs
Its production is increased by low 02 levels
Causes Hb to have lower 02 affinity, shifting curve to right
In anemia, total blood Hb levels fall, causing each RBC to produce more DPG
Fetal hemoglobin (HbF) has 2 γ-chains in place of β-chains of HbA
HbF can’t bind DPG, causing it to have higher 02 affinity
Facilitates 02 transfer from mom to baby
Thalassemia
Thalassemia affects primarily people of Mediterranean descent
Has decreased synthesis of α or β chains; increased synthesis of γ chains
Myoglobin
Is a red pigment found exclusively in striated muscle
Slow-twitch skeletal & cardiac muscle fibers are rich in myoglobin

Has only 1 globin; binds only 1 02
Has higher affinity for 02 than Hb; is shifted to extreme left
Releases 02 only at low P02
Serves in 02 storage, particularly in heart during systole
C02 Transport
C02 transported in blood as dissolved C02 (10%), carbaminohemoglobin (20%), & bicarbonate ion, HC03-, (70%)
In RBCs carbonic anhydrase catalyzes formation of H2CO3 from C02 + H2O

Dissolved
solubility 20X oxygen
venous blood: 2.7 ml/100 ml blood
arterial blood: 2.4 ml/100 ml blood
transported : 0.3 ml/100 ml blood
7% total
Chloride Shift
High C02 levels in tissues causes the reaction C02 + H2O ↔ H2C03 ↔ H+ + HC03- to shift right in RBCs
Results in high H+ & HC03- levels in RBCs
H+ is buffered by proteins
HC03- diffuses down concentration & charge gradient into blood causing RBC to become more +
So Cl- moves into RBC (chloride shift)
Reverse Chloride Shift
In lungs, C02 + H2O ↔ H2C03 ↔ H+ + HC03-, moves to left as C02 is breathed out
Binding of 02 to Hb decreases its affinity for H+
H+ combines with HC03- & more C02 is formed
Cl- diffuses down concentration & charge gradient out of RBC (reverse chloride shift)
Acid-Base Balance in Blood
Blood pH is maintained within narrow pH range by lungs & kidneys (normal = 7.4)
Most important buffer in blood is bicarbonate
H20 + C02 ↔ H2C03 ↔ H+ + HC03-
Excess H+ is buffered by HC03-
Kidney's role is to excrete H+ into urine

2 major classes of acids in body:
A volatile acid can be converted to a gas
E.g. C02 in bicarbonate buffer system can be breathed out
H20 + C02 ↔ H2C03 ↔ H+ + HC03-
All other acids are nonvolatile & cannot leave blood
E.g. lactic acid, fatty acids, ketone bodies

Acidosis is when pH < 7.35; alkalosis is pH > 7.45
Respiratory acidosis caused by hypoventilation
Causes rise in blood C02 & thus carbonic acid
Respiratory alkalosis caused by hyperventilation
Results in too little C02

Metabolic acidosis results from excess of nonvolatile acids
E.g. excess ketone bodies in diabetes or loss of HC03- (for buffering) in diarrhea
Metabolic alkalosis caused by too much HC03- or too little nonvolatile acids (e.g. from vomiting out stomach acid)

Normal pH is obtained when ratio of HCO3- to C02 is 20 : 1
Henderson-Hasselbalch equation uses C02 & HCO3- levels to calculate pH:
pH = 6.1 + log = [HCO3-] [0.03PC02]
Respiratory Acid-Base Balance
Ventilation usually adjusted to metabolic rate to maintain normal CO2 levels
With hypoventilation not enough CO2 is breathed out in lungs
Acidity builds, causing respiratory acidosis
With hyperventilation too much CO2 is breathed out in lungs
Acidity drops, causing respiratory alkalosis
Renal Acid-Base Regulation
Kidneys help regulate blood pH by excreting H+ &/or reabsorbing HC03-
Most H+ secretion occurs across walls of PCT in exchange for Na+ (Na+/H+ antiporter)
Normal urine is slightly acidic (pH = 5-7) because kidneys reabsorb almost all HC03- & excrete H+
Na+, K+, & H+ Relationship
Na+ reabsorption in DCT & CD creates electrical gradient for H+ & K+ secretion
When extracellular H+ increases, H+ moves into cells causing K+ to diffuse out & vice versa
Hyperkalemia can cause acidosis
In severe acidosis, H+ is secreted at expense of K+
Reabsorption of HCO3- in PCT
Is indirect because apical membranes of PCT cells are impermeable to HCO3-
Reabsorption of HCO3- in PCT continued
When urine is acidic, HCO3- combines with H+ to form H2C03 (catalyzed by CA on apical membrane of PCT cells)
H2C03 dissociates into C02 + H2O
C02 diffuses into PCT cell & forms H2C03 (catalyzed by CA)
H2C03 splits into HCO3- & H+ ; HCO3- diffuses into blood
Urinary Buffers
Nephron cannot produce urine with pH < 4.5
Excretes more H+ by buffering H+s with HPO4-2 or NH3 before excretion
Phosphate enters tubule during filtration
Ammonia produced in tubule by deaminating amino acids
Buffering reactions
HPO4-2 + H+ → H2PO4-
NH3 + H+ → NH4+ (ammonium ion)
Mechanisms of Hydrogen Ion Regulation
[H+] is precisely regulated at 3 - 5 x 10 -8 moles/L
(pH range 7.2 -7.4)
. Body fluid chemical buffers (rapid but temporary)
bicarbonate - ammonia
proteins - phosphate
Lungs (rapid, eliminates CO2)
[H+] ventilation CO2 loss
Kidneys (slow, powerful); eliminates non-volatile acids
- secretes H+
- reabsorbs HCO3-
- generates new HCO3-
Buffer Systems in the Body
Bicarbonate: most important ECF buffer

Phosphate: important renal tubular buffer
HPO4-- + H+ H2PO 4 -
Ammonia: important renal tubular buffer
NH3 + H+ NH4+
Proteins: important intracellular buffers
H+ + Hb HHb

60-70% of buffering is in the cells)
Importance of Buffer Systems
Normal H+ concentration = 0.00004 mmol/L

Amount of non-volatile acid produced
~ 80 mmol/day

80 mmol /42 L = 1.9 mmol/L

= 47,500 times > normal H+ concentration
Bicarbonate Buffer System
Is the most important buffer in extracellular fluid even though the concentration of the components are low and pK of the system is 6.1, which is not very close to normal extracellular fluid pH (7.4).

Reason: the components of the system (CO2 and HCO3-) are closely regulated by the lungs and the kidneys
Regulation of H+ secretion
Increased pCO2 increases H+ secretion
i.e. respiratory acidosis

Increased extracellular H+ increases H+
secretion
i.e. metabolic or respiratory acidosis

Increased tubular fluid buffers increases H+
secretion
i.e. metabolic or respiratory acidosis
Acid-Base Disorders
Acidosis:
increased H+ secretion
increased HCO3- reabsorption
production of new HCO3-

Alkalosis:
decreased H+ secretion
decreased HCO3- reabsorption
loss of HCO3- in urine
Ventilation During Exercise
During exercise, arterial PO2, PCO2, & pH remain fairly constant

During exercise, breathing becomes deeper & more rapid, delivering much more air to lungs (hyperpnea)
2 mechanisms have been proposed to underlie this increase:
With neurogenic mechanism, sensory activity from exercising muscles stimulates ventilation; and/or motor activity from cerebral cortex stimulates CNS respiratory centers
With humoral mechanism, either PC02 & pH may be different at chemoreceptors than in arteries
Or there may be cyclic variations in their values that cannot be detected by blood samples
Uptake During Exercise
Increased cardiac output
Decreased transit time
Increased diffusing capacity
Opening up of additional capillaries
Better ventilation/perfusion match
Equilibration even with shorter time (previous graph)
Lactate Threshold
Is maximum rate of oxygen consumption before blood lactic acid levels rise as a result of anaerobic respiration
Occurs when 50-70% maximum 02 uptake has been reached
Endurance-trained athletes have higher lactate threshold, because of higher cardiac output
Have higher rate of oxygen delivery to muscles & greater numbers of mitochondria & aerobic enzymes
Acclimatization to High Altitude
Involves increased ventilation, increased DPG, & increased Hb levels
Hypoxic ventilatory response initiates hyperventilation which decreases PC02 which slows ventilation
Chronic hypoxia increases NO production in lungs which dilates capillaries there
NO binds to Hb & is unloaded in tissues where may also increase dilation & blood flow
NO may also stimulate CNS respiratory centers
Altitude increases DPG, causing Hb-02 curve to shift to right
Hypoxia causes kidneys to secrete EPO which increases RBCs
Regulation of Respiration
Sensors
gather information
Central controller
integrate signals
Effectors
muscles
Respiratory Center
Pneumotaxic center – controls rate and depth
Dorsal resp – inspiratory control
Ventral resp – mainly expiratory control
Pons Respiratory Centers
Activities of medullary rhythmicity center is influenced by centers in pons
Apneustic center promotes inspiration by stimulating inspiratories in medulla
Pneumotaxic center antagonizes apneustic center, inhibiting inspiration
Dorsal Resp Group
Dorsal Respiratory is the rhythm and depth control- rhythmicity center
It’s located in the Solitary Tract
Extends bilaterally most of the length of the medulla
Sensory termination of vagus and glossopharyngeal
Info from chemo, baro and stretch receptors in the lungs
Communicates directly with the reticular formation
Probably ‘self depolarizing’
Inspiratory ramp signal
Not an absolute off and on signal
Begins and increases steadily for ~ 2 sec.s
Then shuts off abruptly for ~ 3 sec.s
Allows for elastic recoil of chest and expiration
Causes a steady volume increase in lungs rather than a gasp
Can control rate of increase of ramp. Fast ramp increase – fast filling
Can control limiting point of ramp. Fast ending – fast resp rate
Pneumotaxic center
Limits ramp signal duration.
Lungs fill only a little, but rate goes up
Ventral Respiratory Group
Inactive during normal quiet breathing
When pulmonary drive (need) is increased, ventral becomes active
Overdrive mechanism for heavy exercise respiration
Both increased inspiration and expiration – rate and depth
Hering- Breuer reflex
Sensory signals from stretch receptors in the bronchi and bronchioles.
Through vagus to dorsal group to switch off ramp duration.
Lungs fill less and rate increases (same as stim from pneumotaxic center
Hering –Breuer activates when lung volume is ~ 3x normal in humans – 1500ml
Lung receptors
Stretch Receptors
inhibit inhalation
Hering-Breuer reflex
Irritant receptors
Bronchoconstriction
Increased ventilation
J receptors
Alveolar wall
Lung disease and edema
Chemoreceptors
Automatic breathing is influenced by activity of chemoreceptors that monitor blood PC02, P02, & pH
Central chemoreceptors are in medulla
Peripheral chemoreceptors are in large arteries near heart (aortic bodies) & in carotids (carotid bodies)
chemoreceptors

increased co2
medullary, aortic and carotid
chemoreceptors

decreased ph
aortic and carotid bodies
chemoreceptors

decreased po2
carotid bodies
Chemical Control of Respiration
Carbon Dioxide
central
Hydrogen Ions
central
Oxygen
peripheral
Effects of Blood PC02 & pH on Ventilation
Chemoreceptors modify ventilation to maintain normal CO2, O2, & pH levels
PCO2 is most crucial because of its effects on blood pH
H20 + C02 ↔ H2C03 ↔ H+ + HC03-

Hyperventilation causes low C02 (hypocapnia)
Hypoventilation causes high C02 (hypercapnia)

Brain chemoreceptors are responsible for greatest effects on ventilation
H+ can't cross BBB but C02 can, which is why it is monitored & has greatest effects
Rate and depth of ventilation adjusted to maintain arterial PC02 of 40 mm Hg
Peripheral chemoreceptors do not respond to PC02, only to H+ levels
Effects of Blood P02 on Ventilation
Low blood P02 (hypoxemia) has little affect on ventilation
Does influence chemoreceptor sensitivity to PC02
P02 has to fall to about half normal before ventilation is significantly affected
Emphysema blunts chemoreceptor response to PC02
Oftentimes ventilation is stimulated by hypoxic drive rather than PC02
Effects of Pulmonary Receptors on Ventilation
Lungs have receptors that influence brain respiratory control centers via sensory fibers in vagus
Unmyelinated C fibers are stimulated by noxious substances such as capsaicin
Causes apnea followed by rapid, shallow breathing
Irritant receptors are rapidly adapting; respond to smoke, smog, & particulates
Causes cough
Hering-Breuer reflex is mediated by stretch receptors activated during inspiration
Inhibits respiratory centers to prevent overinflation of lungs
Restrictive Disorders
Are characterized by reduced vital capacity but with normal forced vital capacity
E.g. pulmonary fibrosis
Obstructive Disorders
Have normal vital capacity but expiration is retarded
E.g. asthma
Diagnosed by tests, such as forced expiratory volume, that measure rate of expiration
Pulmonary Disorders
Are frequently accompanied by dyspnea, a feeling of shortness of breath
Asthma results from episodes of obstruction of air flow thru bronchioles
Caused by inflammation, mucus secretion, & broncho constriction
Inflammation contributes to increased airway responsiveness to agents that promote bronchial constriction
Provoked by allergic reactions that release IgE, by exercise, by breathing cold, dry air, or by aspirin

Emphysema is a chronic, progressive condition that destroys alveolar tissue, resulting in fewer, larger alveoli
Reduces surface area for gas exchange & ability of bronchioles to remain open during expiration
Collapse of bronchiole during expiration causes air trapping, decreasing gas exchange
Commonly occurs in long-term smokers
Cigarette smoking stimulates macrophages & leukocytes to secrete protein-digesting enzymes that destroy tissue

Sometimes lung damage leads to pulmonary fibrosis instead of emphysema
Characterized by accumulation of fibrous connective tissue
Occurs from inhalation of particles <6μm in size, such as in black lung disease (anthracosis) from coal dust
Ventilation During Exercise
During exercise, breathing becomes deeper & more rapid, delivering much more air to lungs (hyperpnea)
2 mechanisms have been proposed to underlie this increase:
With neurogenic mechanism, sensory activity from exercising muscles stimulates ventilation; and/or motor activity from cerebral cortex stimulates CNS respiratory centers
With humoral mechanism, either PC02 & pH may be different at chemoreceptors than in arteries
Or there may be cyclic variations in their values that cannot be detected by blood samples
Lactate Threshold
Is maximum rate of oxygen consumption before blood lactic acid levels rise as a result of anaerobic respiration
Occurs when 50-70% maximum 02 uptake has been reached
Endurance-trained athletes have higher lactate threshold, because of higher cardiac output
Have higher rate of oxygen delivery to muscles & greater numbers of mitochondria & aerobic enzymes
Acclimatization to High Altitude
Involves increased ventilation, increased DPG, & increased Hb levels
Hypoxic ventilatory response initiates hyperventilation which decreases PC02 which slows ventilation
Chronic hypoxia increases NO production in lungs which dilates capillaries there
NO binds to Hb & is unloaded in tissues where may also increase dilation & blood flow
NO may also stimulate CNS respiratory centers
Altitude increases DPG, causing Hb-02 curve to shift to right
Hypoxia causes kidneys to secrete EPO which increases RBCs
Peripheral Chemoreceptors
Carotid body-bifurcation of the carotids
responds to oxygen (greatest Po2<100 mmHg)
responds to carbon dioxide and hydrogen ion
Control of Respiration
Changes in arterial PCO2 have greater effect than changes in arterial pH
CO2 Retention
Severe lung disease, COPD
Develop hypoxemia and hypercapnia
Respiratory drive due to oxygen
Renal control of acid-base balance
Treat with oxygen inhibits respiratory drive
High levels of PCO2
Minimal levels of oxygen, monitor blood gases
Respiration During Exercise
Linear increase in ventilation with increasing oxygen consumption
arterial PO2, PCO2 and pH do not change in response to increased ventilation
PCO2 may decrease slightly

Overflow of signals from cortex
Body movements
Increased body temperature
Designed to control PCO2
Learned response
Other Factors to Influence Respiration
Voluntary control
Activity from vasomotor center
Body temperature
increased production of carbon dioxide
direct effect on respiratory center
Irritants
Anesthesia
Resistance Pathology
Increased resistance to airflow
Lumen
excessive secretions
obstruction due to aspiration
Airway
contraction of smooth muscle
hypertrophy of bronchial wall
Outside of airway
destruction of lung parenchyma
FEV and Forced Exp Vital capacity
Patient takes a maximum inspiration then blows out as fast and hard as they can.
Volume differences aren’t that marked, but slope is very different.
In obstructive dz, slope (within the first second of expiration is reduced.
Indicates obstruction – usually asthma
Chronic Obstructive Pulmonary Disease
Chronic pulmonary emphysema
infection (secretions)
obstruction
loss of parenchyma
Consequences
high airway resistance
decreased diffusing capacity
pulmonary hypertension

Chronic bronchitis
excessive mucus production
Asthma
bronchiole constriction
Emphysema
Means ‘excess air’
Obstructive and destructive condition
1. chronic infection
2. mucus and edema (obstructive)
3. difficult to expire – air trapping in alveoli
4. airway obstruction – scarring and mucus
5. loss of alveolar walls limits diffusion
6. decreased # of cap.s increases pressure – pulmonary hyopertension
7. right sided heart failure
8. different lung areas dead, scarred or obstructed – some areas poorly ventilated, low V/Q and physiologic shunt, high V/Q and phys. dead space, in the same lung
Pneumonia
Alveoli infected and filled with fluid – interstitial, inflammatory, blood cells, microorganisms
‘Consolidated’ areas
Can form fibrin and scar tissue
Restrictive Diseases
Decreased expansion of the lungs
Lung volumes
reduced VC, normal resistance
Diffuse Interstitial Pulmonary Fibrosis
thick collagen deposits
Pneumothorax
Atelectasis
collapse of alveoli
airway obstruction
lack of surfactant
pneumothorax
Hypoxia
inadequate oxygenation of lungs
pulmonary disease
inadequate transport
anemia, abnormal hemoglobin
blood flow
inadequate usage
Cyanide, CO