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66 Cards in this Set
- Front
- Back
Fick's Law of Diffusion
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volume of gas moved by diffusion =
proportional to area of membrane inversely proportional to thickness of membrane |
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transpulmonary pressure (Ptp) =
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PA - Ppl
alveoli pressure minus intrapleural pressure |
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Airway resistance =
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(Patm -Palv)/flow rate
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resistance in a tube =
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R = (8 n l) / (pi r^4)
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Boyles Law
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PV = nRT
as volume increases, pressure must decrease |
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as long volume decreases, resistance...
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increases, think of smaller endotracheal tubes
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Inspiratory Capacity
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IC = VT + IRV
tidal volume plus inspiratory reserve volume (maximum lung inspiration) |
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FRC (functional residual capacity)
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FRC = RV + ERV
residual volume (volume that always stays) plus expiratory reserve volume ( air that can still be pushed out with force) FRC is air remaining in lungs after normal passive expiration |
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Vital Capacity
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VC = IRV + VT + ERV
reserve volumes plus tidal volume amt of air that can be expelled from lungs following forceful inspiration and expiration |
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Total Lung Capacity
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TLC = VC + RV
vital capacity plus residual volume maximum volume of air that lungs can hold |
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closing volume
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must be less than FRC or lungs will collapse
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minute respiratory volume
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Vmin = VT + respiratory rate (f)
minute volume = ventilation |
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anatomic dead space
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ventilated (globally) but no gas exchange occurs
a collapsed alveolus is not a part of dead space b/c not being ventilated anymore |
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alveolar dead space
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still ventiated normally but no vasculature perfusion
V/Q > 1 |
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physiologic dead space (Vd)
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anatomic plus alveolar dead space
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Bohr equation (Vd)/(VT)
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physiological dead space / tidal volume
how much tidal volume is going to fill up dead space Vd/VT = (PaCO2 - PeCO2)/PaCO2 have to determine CO2 elimination by capnometer and PaCo2 by blood gas analysis *value can never be zero, will always have dead space |
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Rate of alveolar ventilation (VsubA)
what amt of minute volume is actually getting to alveoli |
V subA = frequency (f) x (VT - Vd)
have to subtract physiological dead space to increase V subA you either have to breath deeper (VT) or breath faster (f) |
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Vascular resistance =
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vascular resistance = (input pressure - output pressure)/blood flow
input pressure = pulmonary artery output pressure = Left atrium |
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Zone 3 dynamics
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Ppa > Ppv > P subA
distension of capillaries within the alveolar spaces, increased perfusion |
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ZOne 2 dynamics
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Ppa > P subA > Ppv
positive pressure ventilation can push down vasculature, P subA can become greater than MAP, perfusion not as good |
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Zone 1 dynamics
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P subA > Ppa > Ppv
collapse of vasculature, no blood flow |
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ZONE dynamics at rest in healthy individual
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lungs mostly in zone 3, very small amt. near hilus in zone 2
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ZONE dynamics during exercise
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MAP increases the pressures in the vasculature, so that more of the lung is in zone 3 (instead of 2)
Ppa > P subA |
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V/Q ratio for alveolar edema
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V/Q < 1
fluid accumulation in alveoli themselves, creates physiologic R to L shunt, perfusion occurring at same rate but no ventilation |
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V/Q > 1
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alveolar dead space
ventilation exceeds perfusion |
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V/Q < 1
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physiologic R to L shunt
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Henry's Law
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concentration of a gas in solution is proportional to its partial pressure
gas pressures are essentially due to the number of molcules present P=nC derived from Boyle's Law |
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Alveolar Gas Equation (relates the decrease in alveolar oxygen to the increase in alveolar carbon dioxide during hypoventilation)
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PalvO2 = PiO2 - (PalvCO2/R)
PalvCO2 should be equal with PaCO2 in arterial blood PiO2 is partial pressure of inspired oxygen ( 21% x barometric pressure - water vapor pressure (47 mmHg)) R is respiratory quotient = 0.8 hypoventilation, inadequate removal of CO2 lowers alveolar partial pressure of oxygen |
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95-100% saturation of Hemoglobin in mammals
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PaO2 is 100 mmHg in arterial blood
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75% saturation of hemoglobin in mammals
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PaO2 is 40 mmHg in arterial blood
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50% saturation of hemoglobin in mammals
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PaO2 is 28 mmHg in arterial blood
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Lower pH does what to hemoglobin
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decreased affinity for O2, less saturation, right shift
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lower pH does what to hemoglobin
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increased affinity for O2, greater saturation, left shift
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Total O2 content of blood (sum of Hb-O2 and dis-O2)
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Hb-O2 = (Hb concentration) x 1.34 x %saturation
dis-O2 = PaO2 x 0.003 Total = Hb-O2 plus dis-O2 = (mL O2/ dL) |
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carbon dioxide to bicarbonate molecular equation
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CO2 + H2O <--> H2CO3 <--> H+ + HCO3-
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Oxygen Delivery
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total O2 content x CO
mL O2/dL dL/min = mL O2/min |
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average Aleveolar pO2
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104 mmHG
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average pO2 at arterial end of pulmonary capillary
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40 mmHg
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Hering Breuer Inflation Reflex
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increase lung volume -> stretch receptors fire -> decrease respiratory frequency by increasing the expiratory time
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Parts of Central Controller in CNS
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1. Cerebrum - voluntary
2. Brainstem- neurons in pons and medulla 3. spinal cord 4. limbic system and hypothalamus |
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Parts of the Respiratory COntrol System
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Sensors (stretch, chemo)
Central Controller Effectors (muscles of respiration, diaphragm) |
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medullary respiratory center
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basic rythym
has 2 groups-- dorsal (inspiration) ventral (expiration, extreme exercise makes it active) |
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apneustic center
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sustains inspiration by prolonging inspiratory ramp signal
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pneumotaxic center
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switches off inspiration so as to stimulate expiration
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What molecule diffuses across the blood brain barrier?
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CO2
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WHat are PCR's?
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Peripheral Chemoreceptors located at carotid and aoritc arch
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what makes up the conducting airways?
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trachea, bronchi, up to terminal bronchioles
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what makes up respiratory zone?
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respiratory bronchioles, alveolar ducts and alveoli
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what areas are most affected by asthma, bronchitis?
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areas of large amounts of smooth muscle-- smaller bronchioles have the largest amt of smooth muscle
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if CO2 is decreasing in the face of constant metabolism then what is occurring?
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hyperventilation -> PCO2 is less than 35 mmHg
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large and medium sized particles are removed how?
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mucociliary escalator
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small sized particles are removed how?
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macrophages in alveoli
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mucociliary escalator exists all the way to where?
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nasal passages to terminal bronchioles
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in disease, where is the greatest resistance to flow?
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small bronchioles- they are easily occluded and lots of smooth muscle
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in health, where is greatest resistance to flow?
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medium sized brochioles, b/c the small bronchioles out-number them in cross-sectional area
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wheeze
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small airway obstruction or collapse, sides are vibrating, continuous sound on expiration
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crackles
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discontinuous, heard on inspiration and expiration, bubbling through mucous plugged airways
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coughing
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stimulated by subepithelial irritant receptors, close epiglottis momentarily and then forcefully exhale air causing extreme pressure, air explodes through non-cartilaginous parts of trachea b/c of partial collapse there
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sneeze
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irritation to nasal passageways, similar to cough reflex
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panting
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functions in temperature regulation, respiratory center is responding to core body temp., heat dissipated by increasing anatomical dead space ventilation, evaporation of water
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pleonastic
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using more words than necessary
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quiet breathing
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primary function of diaphragmatic movement
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during inspiration...
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the diaphragm contracts, lungs expand caudally
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during expiration...
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diaphragm relaxes, elastic recoil of lungs
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heavy breathing involves what muscles?
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muscles of inspiration: external intercostals, serratus dorsalis cranialis, dorsal scalenus --> need to lift and expand rib cage
muscles of expiration: rectus abdominus, internal intercostals |
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transpulmonary pressure
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Ptp = PA - Ppl
lung inflation is maintained by the transpulmonary pressure |