Sayeski Review of Pulmonary Physiology
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| 414204730 | What are the properties that affect gas diffusion? | Surface area of the membrane Thickness of the membrane Pressure gradient - delta P Solubility of the gas The molecular weight of the gas (square root of the MW) | |
| 414204731 | How do you calculate gas diffusion of the lung? | DL= V/ΔP The diffusion of a gas through a membrane (V) α (A/T) x (solubility/√MW) x ΔP (V) = DL x ΔP or DL= V/ΔP | |
| 414204732 | Define and explain perfusion limited and diffusion limited. | Perfusion limited: The amount of gas that can be taken up is entirely limited by the blood in the pulmonary capillaries, not by the diffusion of the gas. The gas will come into diffusion equilibrium (ΔP = 0) and the only way change the pressure gradient is to increase perfusion (blood flow). Diffusion limited: The gas is limited by the properties of the blood-gas barrier and the gas itself, not the blood flow. When the blood leaves the pulmonary capillary, the gas has not reached diffusion equilibrium. | |
| 414204733 | Explain perfusion vs. diffusion limited in disease. | Disease and exercise will cause O₂ to change toward diffusion limited. (Rightward shift on the curve). The more severe the disease, the more severe the rightward shift. | |
| 414204734 | What is the role of Hb in O₂ diffusion? | The total amount of O₂ transferred from the alveolar capillary blood is dependant on how much Hb there is to remove O₂ from the dissolved state. Changes in [Hb] in blood can affect the measured value of DL. The amount of O₂ transferred before equilibrium is reached will be less if the [Hb] is decreased. Mathematically, DL = (V)/ ΔP. With less O₂ in the blood, the ΔP will increase, thus lowering DL. | |
| 414204735 | Explain dissolved O₂ qualitative and quantitative properties. | Qualitative: ~ 1% Quantitative: solubility x PaO₂ | |
| 414204736 | Explain oxyhemoglobin qualitative and quantitive properties. | Qualitative: ~ 99% Quantitative: HbO₂ = [Hb] x carrying capacity x % saturation | |
| 414204737 | Calculate total oxygen content. ***This will be a test question*** | Total oxygen content is the sum of dissolved O₂ and HbO2. [Hb] x carrying capacity x % saturation + 0.0031 x PaO₂ mm Hg | |
| 414204738 | Briefly explain the relationship of PaO₂ and Hb saturation as the relate to the HbO₂ curve. | The extent to which we saturate will be driven by our PaO₂. Normally with 98% saturation, we are at ~100 mm Hg. PaO2 = 100 mm Hg, Hb = 98% sat., O2 content = 20 mL O2/dL blood PaO2 = 60 mm Hg, Hb = 90% sat., O2 content = 18 mL O2/dL blood PaO2 = 40 mm Hg, Hb = 75% sat., O2 content = 15 mL O2/dL blood PaO2 = 27 mm Hg, Hb = 50% sat., O2 content = 10 mL O2/dL blood | |
| 414204739 | What is the 60/90 rule? | When Hb saturation = 90%, PaO2 = 60 mm Hg. This is clinical hypoxia. | |
| 414204740 | Explain the significance of a rightward shift on the HbO₂ curve. | Rightward shift means less O2 will bind to Hb at any given PO2. Ex.: exercise, 2,3-DPG, increased temperature, increased PaCO2, and decreased pH. This tells the Hb to give up O2. | |
| 414204741 | Explain the significance of a leftward shift on the HbO₂ curve. | Leftward shift means more O2 will bind to Hb at any given PO2. This tells the Hb to hang onto the O2. CO shifts the curve leftward. | |
| 414204742 | Explain how CO poisoning affects the shape of the HbO₂ curve. | CO shifts the curve leftward. Decreases our saturation 2° competitive binding. | |
| 414204743 | Calculate oxygen delivery. | Cardiac output x (arterial content - venous content) Cardiac Output x ((Arterial) [Hb] x carrying capacity x % saturation + 0.0031 x PaO2 mm Hg) - (Venous) [Hb] x carrying capacity x % saturation + 0.0031 x PaO2 mm Hg) | |
| 414204744 | Explain the changes in O₂ content during polycythemia, anemia, CO poisoning and hyperbaric therapy. | Polycythemia: [Hb] increases Anemia: [Hb] decreases CO poisoning: % saturation Hyperbaric: dissolved O₂ increases | |
| 414204745 | What are the 3 forms by which CO₂ is transported? | Dissolved gas ~5% Carbamino ~5% (CO2 binds to terminal amine groups in blood proteins, Hb) Bicarbonate (HCO3-) ~90% rxn catalyzed via carbonic anhydrase | |
| 414204746 | Explain the Bohr effect. | Increased CO2 and H+ binding to Hb decreases the affinity of Hb for O2. This occurs in metabolic tissues. This causes a Rightward shift (offloads O2) of the PO2 / Hb saturation curve | |
| 414204747 | Explain the Haldane effect. | Deoxygenation of Hb in the tissues increases the affinity of Hb for CO2. This shifts the CO2 blood equilibrium curve up and to the left. Results in a higher content of CO2 in the venous blood. | |
| 414204748 | What is pulse oximetry measuring, what can we deduce from it and what are it's limitations? | Ratio of R/IR of pulsatile portion of arterial signal. SpO2 is an approximation of the saturation of Hb. Can deduce PaO₂. Can't tell what is bound to Hb. COHb & metHb will give saturation reading, however, this means a false report of high SpO2. The device may give false readings if the battery is low. Acrylic nails wont transmit the signal. | |
| 414204749 | What is capnography measuring, what can we deduce from it and what are it's limitations? | Measures CO2 in a sample of air Approximate the quality of ventilation. Main-stream requires intubation. Side-stream is susceptible to dilution error (under estimates carbon dioxide because of mixing with the room air which contains virtually no carbon dioxide). | |
| 414204750 | Explain the principles of fluid movement | Fluid movement is determined by the balance between hydrostatic (pushes out) and oncotic pressures (pulled back in) of the capillaries and interstitial fluid. | |
| 414204751 | Explain the impact pulmonary edema has on gas diffusion | Diffusion capacity is decreased when fluid in the alveoli increase the thickness of the diffusion path. | |
| 414204752 | Explain the impact pulmonary edema has on shunt. | Shunt: V/Q = 0. Decreased ventilation results in vasoconstriction and diversion of blood. Pulmonary edema results in diffusion limitation and shunting | |
| 414204753 | Explain the impact pulmonary edema has on surfactant. | Washes away surfactant. | |
| 414204754 | Explain the impact pulmonary edema has on compliance. | Decreases compliance. Compliance is ΔV/ΔP | |
| 414204755 | Explain the impact pulmonary edema has on recoil. | Increases recoil. | |
| 414204756 | Explain the impact pulmonary edema has on the work of breathing. | Increases work | |
| 414204757 | Why is pulmonary edema a restrictive lung disorder? | Decreased ability to inflate the lungs, resulting in decreased TLC. "Ceiling comes down." Obstructive, the "floor comes up." | |
| 414204758 | What is the Henderson-Hasselbalch equation? | pH=6.1 + log [HCO3-]/(0.03)[pCO2] | |
| 414204759 | Why is ventilation is α 1/PaCO2 | The respiratory drive (CNS) is controlled by the [PaCO2], NOT [PaO2]. When PaCO2 is high, the respiratory rate increases to remove/decrease [PaCO2]. The definition of ventilation is the removal of CO2. Mathematically: if ventilation increases (the removal of CO2, PaCO2 goes down, thus the inverse relationship. | |
| 414204760 | Explain how CO2 and HCO3- levels change in the four principle acid/base disorders | Respiratory acidosis with renal compensation: PCO2 increases due to hypoventilation & HCO3- increases due to kidney reabsorption. Respiratory alkalosis with renal compensation: PCO2 decreases due to hyperventilation & HCO3- decreases due to kidney elimination. Metabolic acidosis with respiratory compensation: Blood pH decreases 2° to a metabolic issue that the kidneys can't keep up with, so the lungs respond by increasing ventilation, which decreases PCO2. HCO3- is decreased due to the response to pH. Metabolic alkalosis with respiratory compensation: Loss of acids results in an increase in pH - (HCO3- is high), so the lungs compensation by decreasing ventilation, which retains CO2. | |
| 414204761 | What is anion gap? How do you calculate it? What is it used for? | The anion gap is the difference in the measured cations and the measured anions. The normal anion gap is 8-12 mEq per liter. Anion Gap = ([Na+]+[K+])-([Cl-]+[HCO3-])=(137+5)-(108+24)=10 mEq per liter The gap is used for determining metabolic acidosis. | |
| 414204762 | Explain the role of DRG. | Dorsal Respiratory Group (DRG), located in the medulla and is responsible for inspiration. | |
| 414204763 | Explain the role of VRG. | Ventral Respiratory Group (VRG) are also located in the medulla and mediate expiration under non-rest conditions, such as exercise. Otherwise, they are quiet. | |
| 414204764 | Describe the central chemoreceptors. | Located in the medulla and are connected to the inspiratory neurons of the DRG. They are directly activated by H+. They do not respond to PaO2 or PaCO2. However, CO2 crosses the BBB and is converted into H+. So, Central Chemoreceptors respond indirectly to PCO2. | |
| 414204765 | Describe the peripheral chemoreceptors. | Respond to H+, PaCO2 and PaO2. There are two different peripheral receptors, Aortic Bodies and Carotid Bodies. The Aortic Bodies are located in the aortic arch and extend nerves into the inspiratory control neurons of the medulla (DRG). Carotid bodies are located in the bifurcation of the common carotid artery and extend nerves into the inspiratory control neurons of the medulla (DRG). | |
| 414204766 | What happens when a patient becomes desensitized to chronically increased levels of CO2 as in the case of COPD? | In COPD PaCO2 levels are chronically evelated. Over time, the central chemoreceptors become desensitized to the high PaCO2. Eventually, patients will rely in the low PaO2 acting via the peripheral chemoreceptors for their "drive to breathe" Supplemental O2 will increase PaO2, which the peripheral chemoreceptor responds to by decreasing the ventilation/breathing rate. | |
| 414204767 | When do we ventilate the best? | We ventilate the greatest when PCO2 is high and PO2 is low | |
| 414204768 | Reduction in PaO₂ does what to the sensitivity of PaCO₂? | Increases. | |
| 414204769 | Reduction in PaCO₂ does what to the sensitivity of PaO₂? | Decreases. | |
| 414204770 | What is the role of the Apneustic center? | The Apneustic center alters the respiratory rhythm by electrical stimulation that excites the medullary inspiratory center (DRG) to produce a sustained contraction of the diaphragm. | |
| 414204771 | What is the role of the Pneumotaxic center? | Electrical stimulation late in inspiration facilitates termination of inspiration. The Pneumotaxic center can inhibit the Apneustic center. | |
| 414204772 | What is the role or PSRs? | located in the smooth muscle of airways. Neural discharge is dependent on lung inflation. Discharge increases with inflation and decreases with deflation. | |
| 414204773 | What is the role of J-receptors? | accessible through pulmonary circulation. They respond strongly to histamine, prostaglandins, pulmonary congestion and pulmonary embolism. They promote rapid shallow breathing (tachypnea) or sometimes apnea. | |
| 414204774 | What is the role of RARs? | are located in airway epithelium and smooth muscle and are activated by mechanical and chemical irritants. They can discharge during both inflation and deflation. The consequence of discharge is cough and/or sneeze | |
| 414204775 | How does compliance change in exercise? | Overall we see a decrease in lung compliance with exercise because it is harder to inflate any more air to a full lung. | |
| 414204776 | What is the main factor that regulates breathing during exercise? | Increased CO2 acting on the central chemoreceptors is the main driving force to increase respiratory rates during exercise and after exercise. | |
| 414204777 | What factor contributes to hypoxemia at high altitude? | High altitude hypoxemia is due to decreased barometric pressure and not decreased FIO2. | |
| 414204778 | Describe high altitude induced pulmonary edema. | Decreased barometric pressure results in low PAO2 in ALL alveoli. The resulting hypoxic vasoconstriction increases pulmonary vascular resistance throughout both lungs and results in a marked increase in hydrostatic pressure within the pulmonary vasculature, which pushes fluid out of the blood and into the alveoli. This pulmonary edema is a rapid onset (within hours) and results in a painful death. |
