Pulmonary Word Scramble

 
 

 
 

 
 

 
 
 
 
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Chat about Respiratory Therapy
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Minute Ventilation. V=VT x RR example- 500x12=6000mL
Tidal VolumeNormal 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 Volumecannot push air out-left in lung, cannot be directly measured, but can be tested for approximates. (1200 ML)
Vital Capacityvoluntary, max expiratory (4800 ML)
Capacitytwo or more volumes together
obstructive diseasetrouble with flow
restrictive diseasetrouble with volume
Accessory muscles of ventilationused 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 Expirationdecrease chest size, increase pressure. Internal TIRE Internal intercostals Traverse Abdominus Internal abdominus Rectus abdominus (pushes diaphragm) External abdominus (push diaphragm)
Apnea-Apneustic Breathingcomplete absence of spontaneous ventilation, PAO2 & PaO2 fall rapidly...PACO2 & PaCO2 rise rapidly, death in minutes
Alveolar VentilationVA=VT-VD (Alv Vent= Tid Vol - Dead Space) ie 500-150=350 ML
Airway ResistanceRAW = change in press (cm H20)/minute vent (L per sec) normal is .5 to 1.5 cm H20/L/sec
RAWAirway 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 SpaceAlveolar 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 SystemHeart 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 Respirationsho0rt periods of rapid , uniform and deep inspiration, followed by 10 to 30 seconds of apnea...can be caused by meningitis
Blood flow in the lungsBlood 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
CarinaPoint where R and L main stem bronchi split from trachea.
PaCO2Ventilation...represents how well the patient is breathing. normal is 35 to 45, ↑ hypoventilation ↓ Hyperventilation
Cheyne-Stokes Respiration10-30 seconds of apnea-gradual increase in volume &frequency-gradual decrease in vol and freq- apnea again- caused by cerebral disorders
DiaphramMAJOR MUSCLE OF VENTILATION, R & L hemispheres, central tendon, controlled by phrenic nerve, skeletal muscle,Diaph ↓=Vol ↑=press ↓ Diaph ↑= vol ↓ pres ↑
Dyspneadifficulty breathing, individual is aware, shortness of breath
Dead SpaceAnatomic=conducting airways (1 ML per LB) average is 150 ML, Alveolar -no gas exchange, no blood flow (unpredictable volume), Physiologic- anatomic plus alveolar
Dynamic Compliancemeasured 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
DCCPPhospholipid 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.
Eupneanormal spontaneous breathing
ElastanceOpposite 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 flowbronchial tubes swelling of 16% will cut air flow in half and double the pressure
Pulmonary surfactantType II alveolar cells, 90% phospholipids, 10% proteins-DCCP (phospholipid) is primary surface tension lowering chemical -keeps surface tension from collapsing alveoli
pulmonary surfactant deficiency SpecificARDS, IRDS, edema embolism, pneumonia, excessive lavage, hydration, drowning, ECMO (extracorporeal oxygenation-venting outside of patient for gas exchange)
Pulmonary Surfactant Deficiency GeneralAcidosis, hypoxia, hyperoxia, atelectasis, pulm vascular congestion
Passive Constrictionnormal expiration causes pressure up (returning to normal resting state)- bronchial airways decrease in length and diameter
Passive Dilationnormal inspiration causes pressure to decrease- bronchial airways lengthen and increase in diameter
Lobe lung functionsupper 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 ComplianceMost often used in respiratory, determined during a time of no gas flow--(no in or ex)
surface tensionliquid inside the alveolar that keeps tension high, wanting it to collapse/countered with pulm surfactant
Tachypnearapid breathing
transairway pressuredifference 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 Pressuredifference 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 Pressuredifference in pressure between alveolar and body surface press (ambient air)-Ptt=Palv-Pbs (transthoracic press=press of alv-press of body surface)
Tripoddingusing 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
VertebraCervical 7, Thoracic 12, Lumbar 5
Hyperventilationincreased alveolar ventilation lowers PaCO2 (over ventilating)
Hypoventilationdecreased alveolar ventilation, increases PaCO2 (under ventilating)
Hypercarbiaaka hypercapnia above normal PCO2
Hypercapniaaka Hypercarbia, above normal PCO2
Hyperpneaincreased depth and volume breath (deep breath), with or with out increased frequency
Kussmaul's respirationincrease in depth and rate, metabolic acidosis, seen in diabetics (low sugar causes ketoacidosis)
Lung ComplianceHow 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 Ventilationnormal 4200 ·VA=(VT-VD)x breaths per minute (500-150)x12=4200
Orthopneaable to breathe most comfortably only in an upright position
obstructive diseasetrouble with flow
Plural MembraneVisceral 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 Spacesum of anatomic and alveolar dead space
paradoxal breathingribs and lung do not offer stable pressure...caused by chest damage...broken ribs etc.
Intrapleural PressureThe 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)