Study.pdf - Respiratory Mechanics

CLO 2: Differentiate factors that contribute to mechanics of breathing, gas exchange, and regulation of breathing 2.1 Evaluate the mechanics of breathing including the pressure gradients and forces that oppose ventilation 2.2 Evaluate the mechanical and metabolic work of breathing 2.3 Characterize t...

CLO 2: Differentiate factors that contribute to mechanics of breathing, gas exchange, and regulation of breathing 2.1 Evaluate the mechanics of breathing including the pressure gradients and forces that oppose ventilation 2.2 Evaluate the mechanical and metabolic work of breathing 2.3 Characterize the efficiency and effectiveness of ventilation including tidal volume dead space, and minute ventilation 2.4 Discuss regional and local factors that contribute to the distribution of ventilation 2.5 Define diffusion gradient and its determinants 2.6 Define the alveolar air equation 2.7 Describe normal and variations from ideal gas exchange including shunt and V/Q mismatching 2.8 Describe the process of gas transport including oxygen cascade and oxygen content 2.9 Identify the oxygen dissociation curve and factors that contribute to shifting of the P50 2.10 Define the major physical and chemical controls of breathing 2.11 Identify reflex controls of breathing 2.12 Discuss the role of the central and peripheral chemoreceptors 2.1 Evaluate the mechanics of breathing including the pressure gradients and forces that oppose ventilation Ventilation: Process of moving gas(air) in and out of the lungs. Supply’s body with O2 and removes the co2. Tidal Volume (Vt) air moved over phase, facilitates the removal of co2, replenishes O2. To ventilate pressure gradient is required. Pressure Gradient – High to Low pressure difference Gasses Move due to pressure gradients PAO- Airway opening pressure (mouth, nose, larynx, carina) Ppl- Pleural Pressure pressure changes in esophagus pressure. Always negative PA- Alveolar pressure, negative during inspiration, positive during expiration. Pressure in the alveolar region PBS- Body surface pressure Shunt- Perfusion without ventilation e.g. Emphasyma, COPD, atelectasis, pulmonary edema. Transrespiratory pressure (Ptr)- Everything that exists between pressure measured at airway opening (P ) and pressure measured at body surface (P ) AO BS This pressure gradient causes gas flow in and out of the lungs P =P –P TR AO BS Transpulmonary Pressure (Ptp)- maintains alveolar inflation P =P –P TP AO pl Static Breathing (no flow) Dynamic ( air flow) Transthoracic pressure difference (P )- Causes gas to flow into and out of alveoli during breathing TT P =P –P TT A BS On exhalation P is higher than P A AO Thoracic recoil causes Ppl to decrease, Transpulmonary pressure positive change Forces Opposing Ventilation The lungs have a tendency to recoil inward, whereas the chest wall tends to move outward; these opposing forces keep the lung at its resting end-expiratory volume (i.e., FRC). Elastic Forces- Tissue of the lung, thorax, and abdomen, surface tension in Alveoli Frictional Forces- Caused by gas flow(Natural and artificial) through the airways, occurs only when the system is in motion; there is no friction when there is no motion. Tissue viscous resistance and airway resistance Hysteresis ( referring to the lungs) – the difference between inspiratory and expiratory pressure-volume curves by the lung. Partly caused by surface tension Alveoli at bases expand more than alveoli at the apex Base of lungs receive 4 times as much ventilation 2.2 2.2 Evaluate the mechanical and metabolic work of breathing Inhalation is active Exhalation is passive Pulmonary disease can dramatically increase WOB, can be greater due to increased airway resistance Stiff lungs will breathe faster, due to ^ elastic WOB Metabolic Impact Respiratory muscles consume O2 to perform work In shock, intubation and mechanical ventilation may be indicated to decrease excess oxygen consumption of respiratory muscles Preserves O2 for vital organs Tidal Volume(Vt) decreases, Respiratory Rate(RR) increases, muscle fatigue, gas exchange does not function well Ventilation and Perfusion V/Q (Normal Value is 0.8) Upright lung V/Q are best matched at bases (The Dependent Area) Ventilation; Air movement in and out of the lungs Perfusion – Circulation of blood through tissues Increased lung compliance require more time to inflate while a decreased lung compliance require less time to inflate 2.3 Characterize the efficiency and effectiveness of ventilation including tidal volume dead space, and minute ventilation Effective: Ventilation of the body must meet the need for O2 uptake and CO2 removal Efficient: Ventilation should consume little O2 and produce maximum CO2 Tidal Volume (Vt) air moved over phase, facilitates the removal of co2, replenishes O2. To ventilate pressure gradient is required. Va and PaO2 are proportional while Va and PACO2 have an inverse relationship - Healthy lungs waste some gas due to dead space Deadspace- Ventilation without Perfusion e.g. pulmonary embolism Anatomic Dead Space- Airways leading to alveoli Alveolar Dead Space- Volume of gas ventilating unperfused alveoli. -High V/Q ratios -Apical alveoli have minimum or no perfusion in normal upright subject at rest Mechanical Dead Space- Artificial airways including ventilator Circuits Total Deadspace = Anatomic + Alveolar + Mechanical Minute Ventilation(Ve) – Total volume moved in and out per minute - Normal Ve = 5-10L/min - Ve = RR (Respiratory Rate) x Vt (Tidal Volume) o Move decimal over 3 times to the left. 2.4 Discuss regional and local factors that contribute to the distribution of ventilation Alveoli at bases expand more than alveoli at the apex Base of lungs receive 4 times as much ventilation 2.2 2.5 Define diffusion gradient and its determinants Diffusion occurs along pressure gradients - Barriers to diffusion - A/C membrane has three main barriers - Alveolar epithelium - Interstitial space and its structures - Capillary endothelium - RBC membrane - Fick’s law: The greater the surface area, diffusion constant, and pressure gradient, the more diffusion will occur Given that the area of and distance across the alveolar-capillary membrane are relatively constant in healthy people, diffusion in the normal lung mainly depends on gas pressure gradients. Pulmonary diffusion gradients - Diffusion occurs along pressure gradients - Time limits to diffusion: - Pulmonary blood is normally exposed to alveolar gas for 0.75 second, during exercise may fall 0.25 second - Normally equilibration occurs in 0.25 second - With diffusion limitation or blood exposure time of less than 0.25 seconds, there may be inadequate time for equilibration PACO2 varies directly with the body’s production of carbon dioxide (CO2) and inversely with alveolar ventilation (VA). - Under normal conditions it is maintained at approximately 35 to 45 mm Hg. - The PACO2 will increase above normal if carbon dioxide production increases while alveolar ventilation remains constant. - An increase in dead space (gas not participating in gas exchange), can also lead to an increased PACO2 PACO2 decreases if CO2 production decreases or alveolar ventilation increases 2.6 Define the alveolar air equation PaO2 = (PB – 47) FiO2 –(PaCO2 x1.25) ( Round Up) Healthy PCO2 is 40 mmHg (range 35-45mmHg) PaO2 =(760 -47 ).23 –(40 x 1.25) (713) (.23) 164 – 50 =114 mmHg PaO2 = (680 – 47).38 –(50 x1.25) (633) (.38) 241 – 63 =178 mmHg PaO2 = (500 -47).97 – (55 x 1.25) (453) (.97) 440 – 69 = 371 mmHg 2.7 Describe normal and variations from ideal gas exchange including shunt and V/Q mismatching Alveolar fibrosis- thickening of alveolar wall Pneumonia- Alveolar consolidation (filled with products of disease) Pulmonary Edema- Frothy Secretions Inertial edema- excess fluids in the interstitial space Emphysema – alveolar capillary destruction Atelectasis- collapsed alveolar Alveolar ventilation and PaO2 share a proportional relationship while PaCo2 has a inverse relationship 2.8 Describe the process of gas transport including oxygen cascade and oxygen content O2 Shows a downwards cascade as goes from the atmospheric level to the cellular level Co2 has an inverse relationship, as O2 decreases, CO2 will rise as it goes down to the cellular level 2.9 Identify the oxygen dissociation curve and factors that contribute to shifting of the P50 2.10 Define the major physical and chemical controls of breathing 2.11 Identify reflex controls of breathing Hering-Breuer inflation reflex: Prevents further inspiration (ex. cruise control) - Found in smooth muscle of both large and small airways - Vt greater than 800mL Deflation reflex: Sudden Lung collapse stimulates a strong inspiratory effort which results in hyperpnea as seen with pneumothorax. Heads paradoxical reflex: Maintains tidal volume prevents alveolar deflation Irritant receptors: Stimulated by irritants and or mechanical factors -causes bronchospasm, cough, sneeze, tachypnea J- receptors: found in lung parenchyma stipulated by pneumonia, CHF, and pulmonary edema Cause rapid shallow breathing Peripheral Prioceptors: found in muscles, tendons and joints/pian receptors Movement stimulates hyperpnea H+ proportional to PaCo2 2.12 Discuss the role of the central and peripheral chemoreceptors Central Chemoreceptors – Located bilaterally in the medulla, -CO2 sensitive cells (CO2 35-45 mmHg) -will trigger Ve response (45+) hypercapnia Peripheral Chemoreceptors- Located in the aortic arch and bifurcations of common carotid arteries -PaO2 less than 60 mmHg -O2 sensitive cells, react to reductions of O2 levels in the arterial blood -Only affected by PaO2 not CaO2 -PaO2 less than 60 Ve will rise