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66 Cards in this Set

  • Front
  • Back
Fick's Law of Diffusion
volume of gas moved by diffusion =
proportional to area of membrane
inversely proportional to thickness of membrane
transpulmonary pressure (Ptp) =
PA - Ppl
alveoli pressure minus intrapleural pressure
Airway resistance =
(Patm -Palv)/flow rate
resistance in a tube =
R = (8 n l) / (pi r^4)
Boyles Law
PV = nRT

as volume increases, pressure must decrease
as long volume decreases, resistance...
increases, think of smaller endotracheal tubes
Inspiratory Capacity
IC = VT + IRV

tidal volume plus inspiratory reserve volume
(maximum lung inspiration)
FRC (functional residual capacity)
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
Vital Capacity
VC = IRV + VT + ERV

reserve volumes plus tidal volume
amt of air that can be expelled from lungs following forceful inspiration and expiration
Total Lung Capacity
TLC = VC + RV

vital capacity plus residual volume
maximum volume of air that lungs can hold
closing volume
must be less than FRC or lungs will collapse
minute respiratory volume
Vmin = VT + respiratory rate (f)

minute volume = ventilation
anatomic dead space
ventilated (globally) but no gas exchange occurs
a collapsed alveolus is not a part of dead space b/c not being ventilated anymore
alveolar dead space
still ventiated normally but no vasculature perfusion

V/Q > 1
physiologic dead space (Vd)
anatomic plus alveolar dead space
Bohr equation (Vd)/(VT)
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
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)
Vascular resistance =
vascular resistance = (input pressure - output pressure)/blood flow

input pressure = pulmonary artery
output pressure = Left atrium
Zone 3 dynamics
Ppa > Ppv > P subA

distension of capillaries within the alveolar spaces, increased perfusion
ZOne 2 dynamics
Ppa > P subA > Ppv

positive pressure ventilation can push down vasculature, P subA can become greater than MAP, perfusion not as good
Zone 1 dynamics
P subA > Ppa > Ppv

collapse of vasculature, no blood flow
ZONE dynamics at rest in healthy individual
lungs mostly in zone 3, very small amt. near hilus in zone 2
ZONE dynamics during exercise
MAP increases the pressures in the vasculature, so that more of the lung is in zone 3 (instead of 2)

Ppa > P subA
V/Q ratio for alveolar edema
V/Q < 1

fluid accumulation in alveoli themselves, creates physiologic R to L shunt, perfusion occurring at same rate but no ventilation
V/Q > 1
alveolar dead space

ventilation exceeds perfusion
V/Q < 1
physiologic R to L shunt
Henry's Law
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
Alveolar Gas Equation (relates the decrease in alveolar oxygen to the increase in alveolar carbon dioxide during hypoventilation)
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
95-100% saturation of Hemoglobin in mammals
PaO2 is 100 mmHg in arterial blood
75% saturation of hemoglobin in mammals
PaO2 is 40 mmHg in arterial blood
50% saturation of hemoglobin in mammals
PaO2 is 28 mmHg in arterial blood
Lower pH does what to hemoglobin
decreased affinity for O2, less saturation, right shift
lower pH does what to hemoglobin
increased affinity for O2, greater saturation, left shift
Total O2 content of blood (sum of Hb-O2 and dis-O2)
Hb-O2 = (Hb concentration) x 1.34 x %saturation
dis-O2 = PaO2 x 0.003

Total = Hb-O2 plus dis-O2 = (mL O2/ dL)
carbon dioxide to bicarbonate molecular equation
CO2 + H2O <--> H2CO3 <--> H+ + HCO3-
Oxygen Delivery
total O2 content x CO
mL O2/dL dL/min = mL O2/min
average Aleveolar pO2
104 mmHG
average pO2 at arterial end of pulmonary capillary
40 mmHg
Hering Breuer Inflation Reflex
increase lung volume -> stretch receptors fire -> decrease respiratory frequency by increasing the expiratory time
Parts of Central Controller in CNS
1. Cerebrum - voluntary
2. Brainstem- neurons in pons and medulla
3. spinal cord
4. limbic system and hypothalamus
Parts of the Respiratory COntrol System
Sensors (stretch, chemo)
Central Controller
Effectors (muscles of respiration, diaphragm)
medullary respiratory center
basic rythym
has 2 groups-- dorsal (inspiration)
ventral (expiration, extreme exercise makes it active)
apneustic center
sustains inspiration by prolonging inspiratory ramp signal
pneumotaxic center
switches off inspiration so as to stimulate expiration
What molecule diffuses across the blood brain barrier?
CO2
WHat are PCR's?
Peripheral Chemoreceptors located at carotid and aoritc arch
what makes up the conducting airways?
trachea, bronchi, up to terminal bronchioles
what makes up respiratory zone?
respiratory bronchioles, alveolar ducts and alveoli
what areas are most affected by asthma, bronchitis?
areas of large amounts of smooth muscle-- smaller bronchioles have the largest amt of smooth muscle
if CO2 is decreasing in the face of constant metabolism then what is occurring?
hyperventilation -> PCO2 is less than 35 mmHg
large and medium sized particles are removed how?
mucociliary escalator
small sized particles are removed how?
macrophages in alveoli
mucociliary escalator exists all the way to where?
nasal passages to terminal bronchioles
in disease, where is the greatest resistance to flow?
small bronchioles- they are easily occluded and lots of smooth muscle
in health, where is greatest resistance to flow?
medium sized brochioles, b/c the small bronchioles out-number them in cross-sectional area
wheeze
small airway obstruction or collapse, sides are vibrating, continuous sound on expiration
crackles
discontinuous, heard on inspiration and expiration, bubbling through mucous plugged airways
coughing
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
sneeze
irritation to nasal passageways, similar to cough reflex
panting
functions in temperature regulation, respiratory center is responding to core body temp., heat dissipated by increasing anatomical dead space ventilation, evaporation of water
pleonastic
using more words than necessary
quiet breathing
primary function of diaphragmatic movement
during inspiration...
the diaphragm contracts, lungs expand caudally
during expiration...
diaphragm relaxes, elastic recoil of lungs
heavy breathing involves what muscles?
muscles of inspiration: external intercostals, serratus dorsalis cranialis, dorsal scalenus --> need to lift and expand rib cage

muscles of expiration: rectus abdominus, internal intercostals
transpulmonary pressure
Ptp = PA - Ppl

lung inflation is maintained by the transpulmonary pressure