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88 Cards in this Set
- Front
- Back
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Dalton's Law
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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 |
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Physical Principles of Gas Exchange
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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. |
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Water vapor
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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 |
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Determinants of Diffusion
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Pressure Gradient
Area Distance Solubility and MW are fixed know fick's law |
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Po2 in the Alveoli
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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 . |
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Pco2 in the Alveoli
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PCO2=CO2 production *K
Alveolar Ventilation K is constant If ventilation is doubled then Pco2 is _ If ventilation is halved then Pco2 is doubled |
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Boyle’s Law
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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 |
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Mechanics of respiration
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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 |
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Cell Types in Alveoli
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Capillary Endothelial Cells
Alveoli Epithelial Cells Type 1 cells Type II cells Fibroblasts Macrophages Mast Cells |
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Control of Bronchiolar Diameter
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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 |
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Intrapleural ‘space’
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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 |
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Movement of Air In and Out of Lungs
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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) |
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Compliance
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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 |
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Elasticity
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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. |
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Surface tension
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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. |
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Surfactant
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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 |
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Airway Resistance
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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 |
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Pulmonary Capacities
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Inspiratory capacity (tv+irv)
Functional residual capacity (er+rv) Vital Capacity (erv+tv+irv) Total lung capacity (rv+vc) |
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Timed Volumes
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Minute Respiratory Volume
Tidal volume * respiratory rate Alveolar Ventilation (Tidal volume-dead space) * resp rate |
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Dead Space
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ANATOMICAL – nose, pharyx, trachea
about 150 ml PHYSIOLOGICAL- some alveoli can be non-functional. Scarred or not perfused. Depends on ventilation-perfusion ratio |
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Ventilation/perfusion
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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. |
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Ventilation/Perfusion
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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 |
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Abnormal V/Q
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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 |
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Blood PO2 & PCO2 Measurements
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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 |
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Pulmonary Circulation
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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 |
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Hemoglobin (Hb) & 02 Transport
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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 |
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Oxyhemoglobin Dissociation Curve
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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 |
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Shifts of Dissociation Curve
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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 |
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Transport of Oxygen in Blood
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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 |
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Effect of 2,3 DPG on 02 Transport
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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 |
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Thalassemia
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Thalassemia affects primarily people of Mediterranean descent
Has decreased synthesis of α or β chains; increased synthesis of γ chains |
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Myoglobin
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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 |
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C02 Transport
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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 |
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Chloride Shift
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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) |
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Reverse Chloride Shift
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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) |
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Acid-Base Balance in Blood
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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] |
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Respiratory Acid-Base Balance
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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 |
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Renal Acid-Base Regulation
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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+ |
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Na+, K+, & H+ Relationship
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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+ |
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Reabsorption of HCO3- in PCT
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Is indirect because apical membranes of PCT cells are impermeable to HCO3-
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Reabsorption of HCO3- in PCT continued
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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 |
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Urinary Buffers
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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) |
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Mechanisms of Hydrogen Ion Regulation
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[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- |
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Buffer Systems in the Body
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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) |
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Importance of Buffer Systems
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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 |
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Bicarbonate Buffer System
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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 |
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Regulation of H+ secretion
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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 |
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Acid-Base Disorders
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Acidosis:
increased H+ secretion increased HCO3- reabsorption production of new HCO3- Alkalosis: decreased H+ secretion decreased HCO3- reabsorption loss of HCO3- in urine |
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Ventilation During Exercise
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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 |
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Uptake During Exercise
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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) |
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Lactate Threshold
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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 |
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Acclimatization to High Altitude
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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 |
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Regulation of Respiration
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Sensors
gather information Central controller integrate signals Effectors muscles |
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Respiratory Center
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Pneumotaxic center – controls rate and depth
Dorsal resp – inspiratory control Ventral resp – mainly expiratory control |
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Pons Respiratory Centers
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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 |
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Dorsal Resp Group
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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’ |
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Inspiratory ramp signal
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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 |
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Pneumotaxic center
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Limits ramp signal duration.
Lungs fill only a little, but rate goes up |
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Ventral Respiratory Group
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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 |
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Hering- Breuer reflex
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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 |
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Lung receptors
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Stretch Receptors
inhibit inhalation Hering-Breuer reflex Irritant receptors Bronchoconstriction Increased ventilation J receptors Alveolar wall Lung disease and edema |
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Chemoreceptors
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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) |
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chemoreceptors
increased co2 |
medullary, aortic and carotid
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chemoreceptors
decreased ph |
aortic and carotid bodies
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chemoreceptors
decreased po2 |
carotid bodies
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Chemical Control of Respiration
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Carbon Dioxide
central Hydrogen Ions central Oxygen peripheral |
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Effects of Blood PC02 & pH on Ventilation
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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 |
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Effects of Blood P02 on Ventilation
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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 |
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Effects of Pulmonary Receptors on Ventilation
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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 |
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Restrictive Disorders
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Are characterized by reduced vital capacity but with normal forced vital capacity
E.g. pulmonary fibrosis |
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Obstructive Disorders
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Have normal vital capacity but expiration is retarded
E.g. asthma Diagnosed by tests, such as forced expiratory volume, that measure rate of expiration |
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Pulmonary Disorders
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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 |
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Ventilation During Exercise
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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 |
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Lactate Threshold
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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 |
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Acclimatization to High Altitude
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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 |
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Peripheral Chemoreceptors
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Carotid body-bifurcation of the carotids
responds to oxygen (greatest Po2<100 mmHg) responds to carbon dioxide and hydrogen ion |
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Control of Respiration
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Changes in arterial PCO2 have greater effect than changes in arterial pH
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CO2 Retention
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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 |
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Respiration During Exercise
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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 |
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Other Factors to Influence Respiration
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Voluntary control
Activity from vasomotor center Body temperature increased production of carbon dioxide direct effect on respiratory center Irritants Anesthesia |
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Resistance Pathology
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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 |
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FEV and Forced Exp Vital capacity
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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 |
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Chronic Obstructive Pulmonary Disease
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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 |
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Emphysema
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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 |
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Pneumonia
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Alveoli infected and filled with fluid – interstitial, inflammatory, blood cells, microorganisms
‘Consolidated’ areas Can form fibrin and scar tissue |
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Restrictive Diseases
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Decreased expansion of the lungs
Lung volumes reduced VC, normal resistance Diffuse Interstitial Pulmonary Fibrosis thick collagen deposits Pneumothorax |
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Atelectasis
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collapse of alveoli
airway obstruction lack of surfactant pneumothorax |
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Hypoxia
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inadequate oxygenation of lungs
pulmonary disease inadequate transport anemia, abnormal hemoglobin blood flow inadequate usage Cyanide, CO |
