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Pulmonary

Pima Pulmonary Chapter 2, 2/08

QuestionAnswer
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)
Created by: annabannana