Pulmonary Hangman

 
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Minute Ventilation  . V=VT x RR example- 500x12=6000mL  
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)  
Residual Volume  cannot push air out-left in lung, cannot be directly measured, but can be tested for approximates. (1200 ML)  
Vital Capacity  voluntary, max expiratory (4800 ML)  
Capacity  two or more volumes together  
obstructive disease  trouble with flow  
restrictive disease  trouble with volume  
Accessory muscles of ventilation  used when diaphragm is not enough,(help to make more space in chest, increase neg pressure, increase O2) ie: exercise  
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)  
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)  
Apnea-Apneustic Breathing  complete absence of spontaneous ventilation, PAO2 & PaO2 fall rapidly...PACO2 & PaCO2 rise rapidly, death in minutes  
Alveolar Ventilation  VA=VT-VD (Alv Vent= Tid Vol - Dead Space) ie 500-150=350 ML  
Airway Resistance  RAW = change in press (cm H20)/minute vent (L per sec) normal is .5 to 1.5 cm H20/L/sec  
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  
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  
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  
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  
Biot's Respiration  sho0rt periods of rapid , uniform and deep inspiration, followed by 10 to 30 seconds of apnea...can be caused by meningitis  
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  
Carina  Point where R and L main stem bronchi split from trachea.  
PaCO2  Ventilation...represents how well the patient is breathing. normal is 35 to 45, ↑ hypoventilation ↓ Hyperventilation  
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  
Diaphram  MAJOR MUSCLE OF VENTILATION, R & L hemispheres, central tendon, controlled by phrenic nerve, skeletal muscle,Diaph ↓=Vol ↑=press ↓ Diaph ↑= vol ↓ pres ↑  
Dyspnea  difficulty breathing, individual is aware, shortness of breath  
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  
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  
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.  
Eupnea  normal spontaneous breathing  
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  
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  
pressure and flow  bronchial tubes swelling of 16% will cut air flow in half and double the pressure  
Pulmonary surfactant  Type II alveolar cells, 90% phospholipids, 10% proteins-DCCP (phospholipid) is primary surface tension lowering chemical -keeps surface tension from collapsing alveoli  
pulmonary surfactant deficiency Specific  ARDS, IRDS, edema embolism, pneumonia, excessive lavage, hydration, drowning, ECMO (extracorporeal oxygenation-venting outside of patient for gas exchange)  
Pulmonary Surfactant Deficiency General  Acidosis, hypoxia, hyperoxia, atelectasis, pulm vascular congestion  
Passive Constriction  normal expiration causes pressure up (returning to normal resting state)- bronchial airways decrease in length and diameter  
Passive Dilation  normal inspiration causes pressure to decrease- bronchial airways lengthen and increase in diameter  
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.  
Static Compliance  Most often used in respiratory, determined during a time of no gas flow--(no in or ex)  
surface tension  liquid inside the alveolar that keeps tension high, wanting it to collapse/countered with pulm surfactant  
Tachypnea  rapid breathing  
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)  
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)  
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)  
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  
Vertebra  Cervical 7, Thoracic 12, Lumbar 5  
Hyperventilation  increased alveolar ventilation lowers PaCO2 (over ventilating)  
Hypoventilation  decreased alveolar ventilation, increases PaCO2 (under ventilating)  
Hypercarbia  aka hypercapnia above normal PCO2  
Hypercapnia  aka Hypercarbia, above normal PCO2  
Hyperpnea  increased depth and volume breath (deep breath), with or with out increased frequency  
Kussmaul's respiration  increase in depth and rate, metabolic acidosis, seen in diabetics (low sugar causes ketoacidosis)  
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  
Minute Alveolar Ventilation  normal 4200 ·VA=(VT-VD)x breaths per minute (500-150)x12=4200  
Orthopnea  able to breathe most comfortably only in an upright position  
obstructive disease  trouble with flow  
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)  
Physiologic Dead Space  sum of anatomic and alveolar dead space  
paradoxal breathing  ribs and lung do not offer stable pressure...caused by chest damage...broken ribs etc.  
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).  
What nerves control the diaphragm?  Phrenic nerves.  
PAO2  (PB - PH2O) x FIO2 - (PaCO2 x 1.25)