Lungs 2 Flashcards
gas exchange
-simple diffusion
-driven by partial pressure of difference of gas (not concentration)
-driving force = difference in pressure
-also depends of diffusion coefficient
-CO2 has a much higher diffusion coefficient -> diffuses faster than O2
diffusion capacity- ficks law
-1. diffusion coefficient of the gas
-2. surface area of the membrane
-3. thickness of the membrane
-CO (carbon monoxide) measures this bc diffusion of CO is limited only by diffusion -> rate of disappearance of CO is proportional to diffusion capacity
-diffusion limited during exercise
emphysema
-reduced surface area
-decreases diffusion capacity
fibrosis or pulmonary edema
-membrane is thicker
-diffusing lung capacity decreases
exercise
-increase amount of blood flow to lungs -> increase SA for gas exchange
-increase diffusing lung capacity
Henry’s law- dissolved gas
-henrys law- concentration dissolved gas in a solution is proportional to PP of O2
-at a given partial pressure -> higher solubility of gas -> higher concentration of gas in solution
-total gas concentration = dissolved gas + bound gas + chemically modified gas
-only dissolved gas contributes to PP
-dissolved gas- nitrogen is only dissolved molecule
-bound gas- gas is bound to protein (ex. O2 bound to hemoglobin)
-chemically modified gas- CO2 -> bicarbonate in the blood
gas exchange in lungs
-O2 leaves alveolar air -> into pulmonary capillary blood
-CO2 leaves pulmonary capillary blood -> into alveolar air
-O2 and CO2 transfer = consumption and production
-pulmonary mixed venous blood- PP of O2 is low (40) bc its been used; CO2 PP is high (46) bc tissues produce CO2 and add it into venous blood
-diffusion of O2 into pulmonary capillary is driven by low O2 pp in venous blood -> equilibrates to alveolar O2 pp
systemic arterial blood
-same pressure as alveolar air
-PP O2 is 100 and PP CO2 is 40
-goes to left heart
pressure in dry, humidified, tracheal, alveolar, and pulmonary capillary blood
-dry inspired air- O2 (160), CO2 (0)
-humidified tracheal air- O2 (150), CO2 (0)
-alveolar air- O2 (100), CO2 (40)
-mixed venous blood- O2 (40), CO2 (46)
-systemic arterial blood- O2 (100), CO2 (40)
high altitude
-barometric pressure reduced
-PP of O2 in alveolar gas will also be reduced
-decreases the gradient -> less drive for diffusion
-slower equilibration / diffusion -> pulmonary capillary does not equilibrate by the end of the capillary
-can impair tissue perfusion
-this is exaggerated in pts with fibrosis
forms O2 is carried and hemoglobin
-dissolved and bound to hemoglobin
-% saturation- precent of heme groups (4) that are bound
-iron must be in ferrous state to bind
-methomoglobin- when iron is in ferric state -> does not bind O2
-fetal hemoglobin (HbF) - higher affinity for O2 (2 beta chains and 2 gamma) -> O2 goes from mom to fetus -> replaced by HbA during life
-hemoglobin S- sickle cell shape (alpha subunits are normal and beta are abnormal) -> affinity for O2 decreases; also causes occlusion, pain
O2 hemoglobin dissociation curve
-% saturation increases steeply as O2 pressure increases from 0 to 40
-levels off between 50-100
-affinity increases as more O2 binds to the 4 heme groups -> positive cooperativity
-P50- O2 pressure where hmg is 50% saturated
-if P50 is increased- decrease affinity
-P50 is decreased- increase affinity
-hmg saturation is maintained from 60-100 -> we can tolerate these changes in alveolar O2 pressure without compromising tissue perfusion
pulse oximetry
-measure % saturation of arterial blood
-does NOT directly measure pressure of O2 in arterial blood
-% saturation can help you estimate O2 pressure from O2 hemoglobin dissociation curve though
decreased affinity of O2 on hmg
-right shift
-P50 increase- 50% saturation is achieved at higher than normal O2 pressure
-increase CO2 pressure
-decrease pH
-increase temperature
-increase 2,3 DPG
-unloading of O2 is good
increased affinity for O2 on hmg
-left shift
-decrease P50- 50% saturation occurs at lower than normal O2 pressure
-unloading of O2 is more difficult
-decrease CO2 PP
-increase pH
-decrease temp
-decrease 2,3 DPG
-hemoglobin F
carbon monoxide
-decreases O2 bound to hmg
-left shift
-binds to hmg with MUCH higher affinity compared to O2
-forms carboxyhemoglobin
-reduces O2 binding sites -> decrease O2 binding capacity
-sites that are open bind O2 more tightly than usually -> hard to drop it off to tissue
erythropoietin (EPO)
-glycoprotein
-stimulus for erythropoiesis -> RBC
-induced by kidneys in response to hypoxia
-chronic renal failure -> decrease EPO -> decrease production of RBC -> decrease in hmg concentration -> anemia :(
-treat with recombinant human EPO
CO2 carried in blood
-3 forms:
-1. dissolved CO2
-2. carbaminohemoglobin (CO2 bound to hemoglobin)
-3. bicarbonate (HCO3-) - MOST important
-almost all CO2 carried is in chemically modified form HCO3- (90%)
-aerobic metabolism -> systemic capillary blood -> converted to HCO3- -> lungs -> converts back to CO2 -> expired
henrys law in regards to CO2
-concentration of CO2 in blood is PP multiplied by solubility of CO2
CO2 binding to hemoglobin
-binds at a different site than O2
-Bohr effect- CO2 binding reduces the affinity for O2 binding bc it causes a right shift of O2 hemoglobin dissociation curve
-haldane effect- when less O2 is bound to hemoglobin affinity for CO2 increases
-this makes sense bc as you are binding CO2, O2 is being dropped off to tissue and when you drop of CO2, O2 is being picked up
pulmonary circulation
-pulmonary blood flow = CO of right heart = CO of left heart
-pulmonary circulation is MUCH lower pressure and resistance
-flow is regulated by resistance of arterioles via arteriolar smooth muscle
-regulated by local vasoactive substance -> mostly O2
-decrease Pa O2 -> vasoconstriction (hypoxic vasoconstriction)
-this seems wrong but vasoconstriction directs blood away from poorly ventilated areas and towards well ventilated areas -> better gas exchange
-this doesnt happen during exercise bc arterial O2 is not changed during exercise!!!
fetal circulation
-global hypoxic vasoconstriction
-Pa O2 is low in fetus bc it does not breathe
-vasoconstriction in fetal lungs -> increases pulmonary vascular resistance -> reduce to 15% of CO
-first breath increase Pa O2 to 100 -> vasoconstriction reduced -> resistance reduces -> eventually equals CO
pulmonary blood flow and gravity
-uneven distribution of blood flow in lungs
-sitting- blood flow highest at base and lowest at apex
-supine- nearly uniform distribution
shunt
-portion of CO or blood flow that is diverted or rerouted
-physiological shunt- some blood (2%) bypasses alveoli to go to bronchial blood flow
-right to left shunt- ventral wall defect causes bypassing of lungs -> HYPOXEMIA ALWAYS bc large portion of CO (up to 50%) is not delivered for oxygenation
-left to right shunts- MC- patent ductus arteriosus or/and trauma -> oxygenated blood from left heart goes to right and causes pulmonary blood flow > systemic
-leaves lungs and goes to right heart -> P O2 on right side will be elevated
-left to right shunts- DOES NOT cause hypoxemia
ventilation/perfusion ratio
-ratio of alveolar ventilation to pulmonary blood flow -> matching -> ideal gas exchange
-similar to blood distribution, V/Q is uneven due to gravity too
-Zone 1- apex- lowest perfusion and ventilation -> Zone 3- base- highest perfusion and ventilation
-perfusion varies MORE compared to ventilation due to gravity
-V/Q ratio is highest at zone 1 and lowest at zone 3
4 components to control breathing system
-1. chemoreceptors for O2, CO2, and H+
-2. mechanoreceptors in lungs and joints
-3. control centers in brain stem (medulla and pons)
-4. respiratory muscles controlled by brain stem
-voluntary control can also be done by cerebral cortex (breath holding, voluntary hyperventilation)
involuntary breathing
-controlled by 3 groups of neurons or brain stem centers:
-medullary respiratory center
-apneustic center
-pneumotaxic center- turns off inspiration by limiting tidal volume
inspiratory center
-located in dorsal respiratory group (DRG)
-controls basic rhythm by setting frequency for inspiration
-sensory input from chemoreceptors in glossopharyngeal and vagus and from mechanoreceptors in lungs via vagus
-motor output to diaphragm via phrenic
expiratory center
-located in ventral respiratory neuron
-passive process
-inactive during quiet breathing
-during exercise -> expiration becomes active -> activated
apneusis
-abnormal breathing pattern
-prolonged inspiratory gasps followed by brief expiratory movement
chemoreceptors
-sensory information sensed by chemoreceptors -> brain stem -> output to motor -> diaphragm via phrenic
-senses Pa O2, Pa CO2, and arterial pH in carotid bodies -> DRG
-decrease CSF pH -> hyperventilation
-increase CSF pH -> hypoventilation
mechanoreceptors
-lung stretch receptors
-in smooth muscle of airways
-stimulated by distention
-Hering Breuer reflex- stretch -> reflex -> decrease in breathing rate by prolonging expiratory time
-joint and muscle receptors- early response to exercise detects movement and instructs inspiratory center to increase breathing rate
irritant receptors
-noxious chemicals and particles
-located between epithelial cells lining airways
-travel to medulla by vagus -> reflex constriction of bronchial smooth muscle -> increase breathing rate
J receptors
-juxtacapillary receptors
-in the alveolar walls near capillaries
-when pulmonary capillaries fill with blood and increases interstitial fluid volume -> active receptors -> increase breathing rate
-ex. left sided heart failure- blood backs up in pulmonary circulation -> J receptors mediate breathing change -> rapid shallow breathing and dyspnea (difficulty breathing)
exercise O2 and CO2 levels
-demand for O2 increase -> ventilation rate increases
-arterial P O2 and P CO2 DONT change -> excellent matching
-P co2 of mixed venous blood MUST increase bc skeletal muscle is adding more CO2 to venous blood -> increase ventilation to rid of the excess CO2 in venous blood -> expire CO2 -> excess CO2 never reaches the systemic blood
exercise CO
-CO increases to meet demand for O2
-bc pulmonary flow = CO of left heart = CO of right heart -> increase in CO will increase pulmonary blood flow
-decrease in pulmonary resistance
-perfusion of more capillary beds -> improved gas exchange
-blood flow becomes more evenly distributed -> V/Q ratio becomes more even -> decrease in physiologic dead space
exercise hemoglobin dissociation curve
-shifts to right
-increased tissue P co2, decreased tissue pH, increased temperature
-increase in P50 and decreased affinity of hemoglobin for O2
-allows for easy unloading of O2 in the exercising skeletal muscle
high altitude
-hypoxemia
-decreased P O2 inspired and alveolar air
-headache, fatigue, dizzy, nausea, palpitations, insomnia -> due to initial hypoxia and respiratory alkalosis
-response:
-1. hyperventilation
-2. increase in RBC concentration (polycythemia) -> increase Hmg concentration -> increases O2 content of blood even though P O2 is less
-polycythemia is good for O2 transport but bad for blood viscosity
-3. increased synthesis of 2,3DPG by RBC -> O2 hemoglobin dissociation curve shifts to right
-4. vasoconstriction of pulmonary vasculature (hypoxic vasoconstriction) -> increased resistance -> increase pulmonary arterial pressure -> right ventricle has to work harder -> hypertrophy of right ventricle
-5. respiratory alkalosis
hypoxia
-decreased O2 delivery or utilization of O2 by tissues
-caused by decreased CO or decreased O2 content of blood (O2-hemoglobin)
-hypoxemia causes hypoxia (not the only cause)- decrease Pa O2 reduces % saturation of hmg -> decrease O2 content of blood
-anemia- decreases hmg concentration -> decrease O2 in blood
-CO poisoning- CO binds hmg and decreases O2 content of blood
-cyanide poisoning- EXCEPTION- does not involve decreased CO or decreased O2 content -> interferes with O2 utilization of tissue
hypoxemia
-decrease in arterial P O2
-high altitude
-hypoventilation- decreasing alveolar P O2 (less fresh inspired air into alveoli)
-diffusion defects (fibrosis, pulmonary edema) - increases diffusion distance or decreasing SA for diffusion
-V/Q defect- can be associated with dead space, high V/Q, low V/Q, shunt
-right to left shunt- bypasses lungs
A-a gradient
-difference between P O2 of alveolar gas and P O2 of systemic arterial blood
