Respiratory Physiology

·         Salt water increases COMPLIANCE by decreasing ST. so lung floats. Whereas fresh clean water, lungs sink.

·         SURFACTANT:

1.       Lowers ST

2.       Promotes stability among different sized alveoli

3.       Reduces capillary filtration forces

·         FUNDA: Hyperventilation: Respi Alkalosis

        HyperRespiration: Respi Acidosis (as Rapid & Shallow breathing, only conducting zone exchanged)

·         The Gas least expected to be in CONDUCTING ZONE at the END OF INSPIRATION is CO2.

·         Rate is to CO2 as the DEPTH is to O2.

·         Emphysema has more COMPLIANCE but less ELASTICITY.

·         Compliance is inverse to Elasticity.

Compliance is inverse to Recoil. Recoil is determined by ST & Laplace law.

·         During inspiration, the greatest airflow to alveoli is at: MID-INSPIRATION

·         In pneumothorax, interpleural pressure becomes more positive.

·         Alveolar pressure at the beginning of Insp: 0

Alveolar pressure at the end of Insp: 0

·         During EXERCISE, PACO2 remains normal, what increases is the PVCO2.

·         PACO2 = metabolism / alveolar ventilation

·         PAO2 depends on Patm & FiO2.

·         PiO2 = (Patm-47) x FiO2

So PAO2 = PiO2 – PACO2

·         Solubility in Blood: CO > CO2 > O2

Affinity to Hb: CO > O2 > CO2

·         P50 is when Hb is 50% saturated 50% with O2. At that point PO2 is around 26 mmHg.

·         Chloride Shift: occurs at TISSUES. to maintain electrical neutrality as HCO3 moves out of RBCs, Cl moves in. its imp for CO2 transport. Cl influx into RBCs.

·         Reverse Chloride Shift: at LUNGs. Cl efflux into RBCs.

·         Even after ACCLIMATIZATION at high altitude, remember that you still Hyperventilate and your Peripheral Receptor remains stimulated because PO2 is not changed yet. Even your Hb saturation remains decreased. Your Hb conc will increase.

·         Normal (A-a) difference: 0-10 (age x 0.4)

·          

·         ­AVO₂ Difference

Tissue will extract more O₂ d/t lack of RBC and Hb available → Therefore, patient will not appear SOB

• Heart has highest AVO₂ difference at rest onlyà will extract the most O₂
• Muscle will have the highest AVO₂ after exercise
• GI will have the highest AVO₂ after a meal
• Kidney has the lowest AVO₂ all the time.

·         Tidal Volume = 10 – 15 cc/kg

·         The physiological dead space can be calculated using the Bohr equation:

VD = VT · [PaCo2 – PeCo2] ÷ PaCo2

·         Compliance = ΔV/ΔP

·         Flow is matched at the middle of the lung.

·         V/Q is greater at the top overall because flow is less at the top.

·         V/Q is greater at the bottom ONLY with inspiration.

·         Every V/Q mismatch presents with restrictive pattern.

·         A:a gradient (Alveoli:arteriole)

If ↑ = A > a = restrictive

If ↓ = A < a = Hb picking up too much O₂

·         Afferent (CN IX) and Efferent (CN X) for carotid body

Afferent and Efferent are both CN X for Aortic body.

·         A diffusion-limited (CO & O2) transport process is one in which the alveolar gas does not reach equilibrium with the end-pulmonary capillary blood. Carbon monoxide (CO) is transported by a diffusion-limited process because it is avidly bound to hemoglobin. So much CO binds to hemoglobin that the partial pressure of CO in the capillary blood remains near zero. As a result, the concentration gradient from alveolar gas to capillary blood remains constant and the amount of CO diffusing across the alveolar capillary interface depends only on the permeability of the gas.

In contrast, all of the other gases reach equilibrium with the capillary blood, and, therefore, the amount of those gases that diffuses across the alveolar capillary membrane is dependent on the amount of blood passing through the pulmonary capillaries. This type of transport process is described as perfusion-limited (O2, CO2, N2O).

·         Diffusing Capacity is the volume of gas transported across the lung per minute per mmHg partial pressure difference.

 It is determined by the surface area and the thickness of the alveolar-capillary interface.

Increases in the diffusing capacity can be produced by opening pulmonary capillaries, expanding the surface area of the pulmonary capillaries, optimizing the V/Q ratio within the lung, or by increasing the concentration of hemoglobin within the blood (polycythemia).

It can be decreased by mismatching of ventilation and perfusion, pulmonary edema, or pulmonary emboli, all of which interfere with gas diffusion.

·         The pulmonary transfer of O2 and CO2  is perfusion-limited over a wide range of activity levels.

·         The tissue transfer of O2 and CO2  is diffusion-limited over a wide range of activity levels.

·         The standard affinity of the haemoglobin-CO reaction is 250 times greater than that of haemoglobin-O2 .

·         The single-breath CO diffusing capacity (transfer factor) is normally 3 ml STPD s-1 kPa-1 at rest and 7.5 during maximal exercise.

·         There are four mechanisms of hypoxemia: anatomical shunt, physiological shunt, [Vdot]/[Qdot] mismatching, and hypoventilation.

There are two mechanisms of hypercarbia: increase in dead space and hypoventilation.

A change in cardiac output is the only nonrespiratory factor that affects gas exchange.

·         Three cell types produce mucus: surface secretory cells, tracheobronchial glands and Clara cells.

·         At high altitudes, the atmospheric pressure is decreased; however, the percentage of O2 in the atmosphere remains the same. Hypoxemia stimulates peripheral chemoreceptors causing respiratory alkalosis, which shifts the OBC to the left. However, alkalosis activates phosphofructokinase in glycolysis causing increased production of 1,3-BPG, which is converted to 2,3-BPG. This brings the OBC back to normal or slightly to the right, leading to increased release of O2 to tissue.

·         PaCO2 is inversely proportional to alveolar ventilation: PaCO2 ∝ 1/VA

If the patient in the question doubles his tidal volume, his alveolar ventilation (VT − VD) will increase from 3 L/min (see question 209) to [(800 mL − 100 mL) и 10 breaths/min] = 7 L/min

Therefore, his PaCO2 will decrease from 50 mmHg to 21 mmHg:

PaCO2 и VA = constant

50 mmHg и 3 L/min = PaCO2 и 7 L/min

PaCO2 = 21 mmHg

·         V/Q mismatches will cause arterial oxygen levels (PaO2) to decrease. Decreased PaO2 will stimulate the peripheral chemoreceptors, which, in turn, will increase alveolar ventilation and decrease PaCO2. The decreased PaCO2 will cause a respiratory alkalosis (increasing pH). Hypoxemia will also cause lactate levels to rise, increasing the anion gap (and blunting the rise in pH). The fall in PaO2 causes the A-a gradient to rise.

·         The physiological dead space can be calculated using the Bohr equation: VD = VT и [PaCO2 − PeCO2] ÷ PaCO2

·         The modified alveolar gas equation is: PaO2 = PiO2 − (PaCO2 /R)

·         In the tissues, the diffusing capacity is the volume of gas transported across the lung per minute per mmHg partial pressure difference. It is determined by the surface area and the thickness of the alveolar-capillary interface. Increases in the diffusing capacity can be produced by opening pulmonary capillaries, expanding the surface area of the pulmonary capillaries, optimizing the V/Q ratio within the lung, or by increasing the concentration of hemoglobin within the blood (polycythemia). It can be decreased by mismatching of ventilation and perfusion, pulmonary edema, or pulmonary emboli, all of which interfere with gas diffusion.

·         The forces tending to remove fluid from the alveoli are the negative interstitial fluid pressure and the osmotic pressure exerted at the alveolar membrane by ions and crystalloid molecules in the interstitial fluid. Fluid movement into pulmonary capillaries, however, is a function of plasma oncotic pressure.

·         The central chemoreceptors are located at or near the ventral surface of the medulla. They are stimulated to increase ventilation by a decrease in the pH of their extracellular fluid (ECF).

·         The pulmonary capillaries are more permeable to proteins than the skeletal muscle capillaries, and, therefore, the interstitial concentration of protein is greater in the pulmonary circulation.

·         Hyperventilation occurs when the rate of alveolar ventilation reduces the arterial PCO2 below 40 mmHg. Pregnancy produces hyperventilation because progesterone stimulates the brain stem respiratory centers to increase alveolar ventilation above that required to maintain arterial PCO2 at 40 mmHg.

·         During exercise, ventilation increases in parallel with carbon dioxide production so that the arterial PCO2 remains at 40 mmHg. Metabolic alkalosis causes a small decrease in alveolar ventilation, producing a compensatory respiratory acidosis.

·         The respiratory alkalosis will cause Ca2+ to bind to plasma proteins, lowering the concentration of ionized Ca2+.

·         Most of the airway is within the thoracic cavity, and, therefore, the intrathoracic pressure affects airway diameter and resistance. The intrathoracic pressure is most negative at the total lung capacity. The negative thoracic pressure increases airway diameter and decreases airway resistance.