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CP Phys Chap 2

Ventilation

QuestionAnswer
What is ventilation? The process that moves gases between the external environment and the alveoli. It is the mechanism by which oxygen is delivered to the alveoli and carbon dioxide is carried from the aveoli to the atmosphere.
What is pressure gradient? The difference between two pressures.
Pressure gradient is responsible for what? Moving air in and out of the lungs and for maintaining the lungs in an inflated state.
Driving Pressure means what? The pressure difference between two points in a tube or vessel; it is the force moving gas or fluid through the tube or vessel.
Transairway pressure, Pta, (aka transrespiratory pressure) is what? The barometric pressure difference between the mouth pressure (Pm) and the alveolar pressure (Palv). Pta = Pm - Palv
+Pta happens when? Inspiration
-Pta happens when? Expiration
Transmural pressure, Ptm, is what? The pressure difference across the airway wall. Intra-airway pressure minus outside airway pressure. Ptm = Piam - Poaw
Transpulmonary pressure, Ptp, is what? The difference between the alveolar pressure and the pleural pressure. Ptp = Palv - Ppl
In the normal lung, Palv is always greater/less than the Ppl? Greater, this is what maintains the lungs in an inflated state.
Transthoracic pressre, Ptt, is what? The difference between the alveolar pressure and the body surface pressure. Ptt = Palv - Pbs
Transthoracic pressure is another way to view what other pressure? Transairway pressure
The flow of gas in and out of the lungs is caused by what? The Ptp & Pta chages that occur in response to the action of the diaphragm.
When stimulated to contract by the phrenic nerve, the diaphragm does what? Contracts, causing inspirations, and moves downward, causing the thoracic volume to increase and the intrapleural and intra-alveolar pressures to decrease (less than barometeric pressure).
End-inspiration (pre-expiration), end-expiration (pre-inspiration) equilibrium is what? When the intra-alveolar pressure nd the barometric pressure are equal.
The diaphragm during expiration does what? Relaxes and moves upward, causing thoracic volume to decrease and the intrapleural and intra-alveolar pressure to increase.
Intrapleural pressure during normal inspiration and expiration is always more/less than the barometric pressure? Less.
At rest, normal excursion of the diaphragm is what? 1.5cm
At rest, normal intrapleural pressure change is what? 3cm - 6cm H2O
Deep inspiration can result in what? Diaphragm movement as much as 6 - 10cm, which causes intrapleural pressure to drop as low as 50cm H2O.
Forced expiration can result in what? Intrapleural pressure between 70 - 100cm H2O.
Pressure Force per unit area; mmHg or cmH2O
Flow Volume transfer per unit time; L/min, L/sec or mL/sec
Resistance Impedance to gas flow. When ther's resistance we increase pressure to breath. cmH2O/L/min or cmH2O/L/sec
Elastance Ability of a substance to return to resting shape after being distorted by an external force; recoiling force of the lungs. The higher the elastance the stiffer the lungs. Opposite of compliance.
Compliance - Cl = V/P The measure of ease of inflation of the lungs. Decreased compliance means stiffer lungs. Opposite of elastance.
Decreased Cl Stiff lungs, ie CF, scarring, etc.
Increased Cl Elastic lungs, ie emphysema, air trapping, etc.
Normal Cl 100 mL/cmH2O or 0.1 L/cmH2O
How is negative pressure, or tension, maintained between the parietal pleura and the visceral pleura? The lungs are fibrous and want to contract, while the thorax wants to expand. This causes the intra-pleural pressure to remain negative.
Intra-pleural pressure 1. Always negative, but, 2. Drops 1-2 mmHg during normal inspiration. 3. Increases 1-2 mmHg on normal expiration.
Diaphragm Primairy muscle of ventilation
Functional Residual Compacity - FRC The resting volume of our lungs.
Ventilation is opposed by: 1. Elastic resistance, ie lung tissue, lung compliance, surface tension. 2. Nonelastic resistance, ie airway resistance, mucous, bronchospasms, tube size.
Hooke's Law Once the elastic limits of the lung unit are reached, little or no volume change occurs in response to pressure change. If the pressure increases and the elastic limits are exceeded the lung will rupture.
Normal volume-pressure curve 1. A shift to the right = decreased lung compliance. 2. A shift to the left = increased
Resistance How much pressure is needed to allow gas to flow. Determined by physical properties of the airway. Accounts for about 85% of nonelastic resistance to ventilation.
Raw (Airway resistance) = Raw = P/v, where v = flow measured in time
Normal Raw = 0.5 - 1.5 cmH2O/L/sec
Causes of increased resistance are, 1. Increased gas viscosity/density, 2. Increased tube length, 3. Decreased tube radius (MOST importang & has GREATEST effect on resistance!)
Decreased tube radius A decrease by 1/2 increases resistance 16 times!
Other causes of increased resistance are, Secretions, inflammation, bronchospasm, tumors
Effects of airway resistance Uneven alveolar ventilation, V/Q abnormality, hypoxemia, increased WOB, increased O2 consumption, fatigue, hypoventilation
Treatment for airway resistance Bronchodilator, suctioning, remove obstruction, bronchial hygene to mobilize secretions, low density gas treatment
Types of gas flow through bronchial airway 1. Laminar 2. Turbulent 3. Tracheobronchial or Transitional Flow
Laminar Flow Streamlined, parallel gas flow that occurs at low flow rates & pressure gradients.
Turbulent Flow Random movement that occurs at high flow rates & pressure gradients, ie nose, pharynx, larynx, cirina.
Tracheobronchial or Transitional Flow Both laminar and turbulent, occurs where the airways branch.
Upper airways contribution to airway resistance 60%
Reynolds Number Used to determine type of flow. It has no label, it is dimensionless. It is based on gas density, viscosity, velocity and tube radius. If > 2000 = turbulent, < 2000 = laminar.
Poiseuille's Law Shows what tube size does to flow and pressure. That flow is directly proportional to pressure and inversly proportional to r to the 4th power (r = radius).
Surface Tension Molecular cohesive force of molecules in a liquid-gas interface.
Surfactant Liquid film that lines the interior surface of the alveoli and creates surface tension.
Pulmonary Surfactant Molecules Hydrophobic end faces the gas, while the hydrophilic end faces the alveolar fluid.
Pulmonary Surfactant Produced and stored in the alveolar type II cells. Composed of phospholipids (about 90%) and protein. Phospholipid DPPC is main tension-lowering chemical that has a hydrophobic & hydrophilic end.
Critical Opening(Closing) Pressure The high pressure (with little volume change) that is initially required to overcome the liquid molecular force during the formation of a new bubble - similar to the high pressure first required to blow up a new ballon.
Laplace's Law - P = 2ST/r The distending pressure of a liquid bubble (not the alveolus) is influenced by (1) the surface tension of the bubble and (2) the size of the bubble itself.
Distending Pressure of liquid sphere Directly proportional to surface tension and inversely proportional to the radius. Otherwise, as surface tension increases the distending pressures increases. As the size increases the distending pressure decreases.
Alveolus Surface Tension Low tension when uninflated because of ratio of surfactant to alveolar area. Higher tension as inflated because same surfactant has to cover more alveolar area!
Pulmonary Surfactant Deficiency - General Causes Acidosis, hypoxia, hyperoxia, atelectasis, pulmonary vascular congestion.
Pulmonary Surfactant Deficiency - Specific Causes ARDS, IRDS, pulmonary edema, pulmonary embolism, pnuemonia, excessive pulmonary hydration or lavage, drowning, extracorporeal oxygenation.
Created by: mfredenburg