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Pima Pulmonary Chapter 2, 2/08

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Question
Answer
Minute Ventilation   . V=VT x RR example- 500x12=6000mL  
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Tidal Volume   Normal quiet breathing (450-500 ML normal) VT= Minute V/RR (6000/12=500mL) Calc for vent set up, 3-4 mL x body weight (3x150=450mL)  
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Residual Volume   cannot push air out-left in lung, cannot be directly measured, but can be tested for approximates. (1200 ML)  
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Vital Capacity   voluntary, max expiratory (4800 ML)  
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Capacity   two or more volumes together  
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obstructive disease   trouble with flow  
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restrictive disease   trouble with volume  
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Accessory muscles of ventilation   used when diaphragm is not enough,(help to make more space in chest, increase neg pressure, increase O2) ie: exercise  
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Accessory muscles of Inspiration   (make more space in chest, increase neg press, raise O2) STEPS= Scalene (ribs up) Trapezius (cage up) External intercostals (keep ribs out)Pectoralis major (larger chest) Sternocleidomastoid (raise sternum, copd'ers use it)  
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Accessory muscles of Expiration   decrease chest size, increase pressure. Internal TIRE Internal intercostals Traverse Abdominus Internal abdominus Rectus abdominus (pushes diaphragm) External abdominus (push diaphragm)  
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Apnea-Apneustic Breathing   complete absence of spontaneous ventilation, PAO2 & PaO2 fall rapidly...PACO2 & PaCO2 rise rapidly, death in minutes  
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Alveolar Ventilation   VA=VT-VD (Alv Vent= Tid Vol - Dead Space) ie 500-150=350 ML  
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Airway Resistance   RAW = change in press (cm H20)/minute vent (L per sec) normal is .5 to 1.5 cm H20/L/sec  
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RAW   Airway Resistance...Pressure difference between ambient air & alveoli divided by the flow rate. RAW=ΔP/·V normal RAW is .5 - 1.5 cm H20/L/sec  
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Alveolar Dead Space   Alveolar is ventilated but not perfused with blood-air is flowing , but no gas exchange, blood is stopped in capillary, amount of space is unpredictable  
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Anatomical Dead Space   -volume of gas in conducting airways-equal to 1 ML/lbs of body weight-located in nose mouth pharynx, larynx, lower airway to terminal bronchiole  
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Autonomic Nervous System   Heart rate= Symp up-Para down, Bronchial muscles=sympa relax-para contract, Bronchial Glands= Symp decrease-Para increase, Salivary glands=symp decrease-para increase, pulmonary vessels= symp constrict-para relax  
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Biot's Respiration   sho0rt periods of rapid , uniform and deep inspiration, followed by 10 to 30 seconds of apnea...can be caused by meningitis  
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Blood flow in the lungs   Blood is heavy and gravity dependent, causing blood to have higher flow in lower lobes. fewest RBC's in upper lobe, gas exchange best in lower lobes  
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Carina   Point where R and L main stem bronchi split from trachea.  
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PaCO2   Ventilation...represents how well the patient is breathing. normal is 35 to 45, ↑ hypoventilation ↓ Hyperventilation  
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Cheyne-Stokes Respiration   10-30 seconds of apnea-gradual increase in volume &frequency-gradual decrease in vol and freq- apnea again- caused by cerebral disorders  
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Diaphram   MAJOR MUSCLE OF VENTILATION, R & L hemispheres, central tendon, controlled by phrenic nerve, skeletal muscle,Diaph ↓=Vol ↑=press ↓ Diaph ↑= vol ↓ pres ↑  
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Dyspnea   difficulty breathing, individual is aware, shortness of breath  
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Dead Space   Anatomic=conducting airways (1 ML per LB) average is 150 ML, Alveolar -no gas exchange, no blood flow (unpredictable volume), Physiologic- anatomic plus alveolar  
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Dynamic Compliance   measured during a time of flow-static and dynamic are equal in healthy lungs-obtained using partially swallowed esophageal pressure balloon----rarely used except in neonates  
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DCCP   Phospholipid molecule of pulmonary surfactant- surface tension lowering chemical of alveoli- hydrophobic and hydrophilic molecule-alveolus size ↓-DCCP ↑, tension ↓-alveolus size↑, DCCP ↓, tension ↑**smaller the alveoli-the more it wants to collapse.  
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Eupnea   normal spontaneous breathing  
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Elastance   Opposite of compliance-natural ability of matter to respond to force and return to original position, CL ↑ elastance ↓=lung stiff-COPD, CL ↓ Elastance ↑ =lung floppy-emphysema  
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Flow & Pressure ↓ ↑   Flow is proportional to press and Radius to the 4th power and Pressure is a function radius to the 4th-↓ R by 1/2 will ↓ flow 1/16, but increase press 16 times(16 ML/sec to 1ML/sec and 1cmh2o to 16cmh2o) ↑ bronchial tube by 16% ↑ press 2 times normal  
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pressure and flow   bronchial tubes swelling of 16% will cut air flow in half and double the pressure  
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Pulmonary surfactant   Type II alveolar cells, 90% phospholipids, 10% proteins-DCCP (phospholipid) is primary surface tension lowering chemical -keeps surface tension from collapsing alveoli  
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pulmonary surfactant deficiency Specific   ARDS, IRDS, edema embolism, pneumonia, excessive lavage, hydration, drowning, ECMO (extracorporeal oxygenation-venting outside of patient for gas exchange)  
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Pulmonary Surfactant Deficiency General   Acidosis, hypoxia, hyperoxia, atelectasis, pulm vascular congestion  
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Passive Constriction   normal expiration causes pressure up (returning to normal resting state)- bronchial airways decrease in length and diameter  
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Passive Dilation   normal inspiration causes pressure to decrease- bronchial airways lengthen and increase in diameter  
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Lobe lung functions   upper lobe-greatest neg press, alveoli expanded the most, least gas exchange(fewest RBC's). Lower lobe has lowest neg pressure, is the most efficient and has the best gas exchange and ventilation.  
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Static Compliance   Most often used in respiratory, determined during a time of no gas flow--(no in or ex)  
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surface tension   liquid inside the alveolar that keeps tension high, wanting it to collapse/countered with pulm surfactant  
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Tachypnea   rapid breathing  
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transairway pressure   difference in barometric pressure between mouth and alveolar-represents the driving pressure that forces gas into and out of lungs- Pta=PM-PAlv(press trans airway = press at mouth -press at alveoli)  
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Trans pulmonary Pressure   difference in pressure between alveolar and plural space -plural space is always slightly negative- Ptp=Palv-Ppl (trans pulmonary press = press of alv- press of plural space)  
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Transthoracic Pressure   difference in pressure between alveolar and body surface press (ambient air)-Ptt=Palv-Pbs (transthoracic press=press of alv-press of body surface)  
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Tripodding   using the pectoralis major to expand the chest cavity to get more air- COPD patients lean on desk or table to brace arms, increases neg pressure  
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Vertebra   Cervical 7, Thoracic 12, Lumbar 5  
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Hyperventilation   increased alveolar ventilation lowers PaCO2 (over ventilating)  
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Hypoventilation   decreased alveolar ventilation, increases PaCO2 (under ventilating)  
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Hypercarbia   aka hypercapnia above normal PCO2  
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Hypercapnia   aka Hypercarbia, above normal PCO2  
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Hyperpnea   increased depth and volume breath (deep breath), with or with out increased frequency  
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Kussmaul's respiration   increase in depth and rate, metabolic acidosis, seen in diabetics (low sugar causes ketoacidosis)  
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Lung Compliance   How readily the elastic force of the lungs accepts inspired air, change in lung volume (ΔV) per unit pressure (ΔP) change. compliance determines how much air the lungs will accommodate (.1 L/cm H2O normal) CL=ΔV/ΔP- cl↓vol↓elast↑resp↑stiff CL↑ vol↑floppy  
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Minute Alveolar Ventilation   normal 4200 ·VA=(VT-VD)x breaths per minute (500-150)x12=4200  
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Orthopnea   able to breathe most comfortably only in an upright position  
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obstructive disease   trouble with flow  
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Plural Membrane   Visceral Pleura (on top of lung surface)-Pleural Space (tiny fluid fill space with slight neg pressure)- Parietal Pleura (lines inside of thoracic cavity)  
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Physiologic Dead Space   sum of anatomic and alveolar dead space  
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paradoxal breathing   ribs and lung do not offer stable pressure...caused by chest damage...broken ribs etc.  
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Intrapleural Pressure   The negative intrapleural pressure at the top/apex of the lung is normally greater (-7 to -10 cmH2O) compared to the bottom of the lung (-2 to -3 cmH2O).  
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What nerves control the diaphragm?   Phrenic nerves.  
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PAO2   (PB - PH2O) x FIO2 - (PaCO2 x 1.25)  
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