| Ventilation Mechanics | Factors Affecting Ventilation | Pulmonary Circulation | Gas Exchange and Transport | Hypoxemia, Acid-base, and Control |
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diameter, length, resistance and velocity all decrease; cross-sectional area increases
What happens to airway length, cross-sectional area, resistance and air flow velocity as you move down the airways?
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Compliance: ease of expanding; Elastance: tendency to collapse "stiffness"; surface tension: liquid being the smallest SA as possible; resistance: opposition to flow by friction; all oppose inspiration except compliance
What are compliance, elastance, surface tension, and airway resistance? How do each affect inflation?
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Pulmonary Arteries: low O2, Pulmonary veins: High O2; Bronchiole arteries: high O2, Veins: low O2; Systemic arteries, High O2, Veins: low O2
Describe the oxygenation or lack thereof of the pulmonary circulation vs Bronchiole circulation vs systemic circulation
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O2: venous side of pulmonary capillary bed (104), arterial blood (95), systemic tissues (40), venous side of systemic capillary bed (40), alveolar air (104), expelled air (120)
CO2: venous side of pulmonary capillary bed (40), arterial blood (40), systemic tissues (45), venous side of systemic capillary bed (45), alveolar air (40), expelled air (27)
What happens to PO2 and PCO@ in each step from ambient air all the way through pulmonary and systemic circulation back to expelled air.
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normal is 0.8, mismatch based on differences in perfusion of blood to different parts of the lung (lower in caudal dorsal, greater in cranial ventral). Bronchitis: decreased ventilation so decreased ratio; Emphysema: decreased perfusion, increased ratio
Describe physiologic V/Q mismatch. What happens if you have chronic bronchitis? What about emphysema?
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Tidal volume, inspiratory reserve volume, expiratory reserve volume, residual volume; inspiratory capacity, functional residual capacity, vital capacity, total lung capacity
Describe the 4 lung volumes and 4 lung capacities
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C = dV/dP decrease compliance at first then great increase in compliance, Pulmonary fibrosis and edema (etc.) decrease; Emphysema increase (problem because decreases SA for gas exchange)
Compliance! relation to volume and pressure, diseases that lower compliance and diseases that increase compliance
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CO is the same as systemic, low pressure so low vascular resistance. Humans: perfusion preference to low because of gravity, Quadrupeds: perfusion preference to caudodorsal region
Inspiration: compress small capillaries to increase pressure in intra-alveolar vessels and decrease pressure in larger extra-alveolar vessels (opposite in expiration).
What are some characteristics of pulmonary circulation? Cardiac output, pressure, resistance, perfusion, effect of inspiration and expiration
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Increase diffusion: solubility, pressure gradient, surface area
Oppose diffusion: molecular weight, thickness of the membrane CO2 is more efficient at diffusion across barriers in fluid/tissue phase (can still move even with a low pressure gradient)
What factors influence the diffusion of gases in the gas phase across membranes and in the fluid compartment of the body
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Respiratory Acidosis: Hypoventilation; Respiratory Alkalosis: hyperventilation.
Metabolic acidosis: increase acid intake or decrease renal excretion (ex. ketoacidosis) Metabolic alkalosis: too much bicarbonate or too little acid (vomiting).
What is responsible for respiratory acidosis and alkalosis? What about metabolic acidosis or alkalosis?
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the volume of air entering the alveoli with each breath or each minute. Alveolar ventilation = breathing rate (tidal vol - dead space) BONUS: Large animals have more dead space
What is alveolar ventilation and how do you calculate minute alveolar ventilation? BONUS do small animals or large animals have a greater dead space to tidal volume ratio?
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P = 2T/r (smaller alveoli will collapse). Alveolar interdependence: elastic recoil of surrounding alveoli pull others open; Surfactants: mostly phospholipids that interfere with hydrogen binding and repel each other. Necessary for first breath! can also bind microorganisms
Surface Tension! relation to compliance and changes in lung volume, 2 factors that prevent surface tension from collapsing the lungs?
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1. Distention - getting fuller
2. Recruitment - increase number of perfused capillaries
What are the 2 mechanisms of accommodation in lungs that allow increases in cardiac output
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oxyHb: oxygen bound to Hb (most is bound, only about 2% dissolved in blood)
carbaminoHb: Carbon bound to Hb but not on same site as oxygen binding Methemoglobin: Fe3+ cannot bind with O2 Carboxyhemoglobin: carbon monoxide, prevents release of O2
What are: oxyhemoglobin, carbaminohemoglobin, methemoglobin, carboxyhemoglobin?
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1. Hypoventilation: does not cause an A-a gradient, yes would respond to O2
2. Diffusion Limitation: due to diffusion barrier, increase in A-a gradient, yes would respond to O2 3. Shunts: wold cause an A-a gradient from capillaries to arteries, would NOT respond to O2 therapy 4. V/Q mismatch: A-a gradient increased often, will often respond to O2
What are the 4 types of hypoxemia? What are the changes in A-a gradient for each? Which would be responsive to O2 supplementation or not?
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Normal: increase in lung volume relates to decreased pressure relative to the atmosphere which pulls air in down the pressure gradient. Pneumothorax: Lungs collapse, Pleural effusion: fluid prevents expansion (decreased pulmonary volume)
How does Boyle's Law relate to the changes in pleural effusion normally during inspiration and expiration? What about when there is pneumothorax and pleural effusion?
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Velocity decreases, Resistance as a whole decreases because of great increase in cross sectional area despite decrease in radius (parallel system), and decrease in length.
What happens to air flow rate/velocity and resistance as air moves down into the alveoli?
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If alveolar oxygen decreases, the arteriole to that region will constrict to shunt blood to a region that has normal O2 to maximize gas exchange. Chronic low areolar O2 leads to pulmonary hypertension. Right side heart failure: jugular vein distention, hepatomegaly, brisket disease
What is the purpose of hypoxic vasoconstriction and how does it influence pulmonary blood pressure? What are the signs?
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70% is bicarbonate, Carbonic anhydrase is a necessary enzyme to convert CO2 to H2CO3 (carbonic acid). The chloride shift allows CO2 that became bicarbonate in the cells to be released into the blood, and vice versa.
CO2! what form is mostly transported in blood? What is the role of carbonic anhydrase? What is the chloride shift and reverse chloride shift?
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Medulla oblongata and pons. DRG = initiates and maintains inspiration; VRG = expiration during exercise. Apneustic center (long inspiration) Pneumoaxic center (inhibits inspiration)
What part of the brain is responsible for involuntary breathing? What are the actions of the dorsal respiratory group and ventral respiratory group? What important features are in the Pons?
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oronasal zone, conducting zone, respiratory zone; type 1 = respiratory, type 2 = surfactant; diaphragm, external intercostal, internal intercostal, abdomen; anatomic dead space is conducting zone, physiologic is disease
Describe all of the anatomy that relates to ventilation mechanics: Different zones, type 1 and 2 pneumocytes, muscles involved, dead space (anatomic and physiologic)
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Obstructive: decreased FEV1, decreased FEV1/FVC ratio, normal lung capacity and forced vital capacity (emphysema, asthma, chronic bronchitis, heaves; forced expiration); Restrictive: reduced total lung capacity and forced vital capacity, normal FEV1 and ratio (interstitial lung disease, fibrosis; forced inspiration)
Describe obstructive vs restrictive diseases: FEV1/FVC, affect on inspiration, expiration, and vital capacity, some examples of each
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high interstitial colloid osmotic pressure (some hydrostatic pressure) moved fluid into alveoli, opposed by capillary osmotic pressure, fluid is drained through lymphatics, Pulmonary edema caused by left side heart failure (cardiogenic) or anything that increases vascular permeability
Fluid Movement! forces that move and oppose movement of water from capillaries to interstitial space, where does fluid in alveoli come from and go, what causes pulmonary edema?
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Right shift: decreased affinity (decrease pH, increase PCO2, increased temp)
Left shift: increased affinity (increased pH, decreased PCO2, decreased temp) Haldane: oxygen causes decreased binding of CO2 to Hb (right shift of CO2 dissociation curve) Bohr: H+ in tissues causes a decreased binding of O2 to Hb (right shift in O2-Hb dissociation curve)
What are factors that cause a right shift in the oxyhemoglobin association curve? a Left Shift?
Describe the Haldane affect and Bohr effect. |
Central: in medulliary chemosensitive area, only sense CO2 status indirectly through H+. Peripheral: in carotid and aortic bodies, sense CO2, O2, and pH. CO2 and H+ have the greatest influence unless O2 gets REALLY low. (Review detection of physical changes)
Describe the detection of Chemical Changes: Peripheral vs central receptors, location, affect on ventilation. BONUS: what chemical has the greatest influence on ventilation?
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