Exam 1 physio Flashcards
Compliance and emphysema
compliance increases
Compliance and pulmonary fibrosis/edema/ARDS
compliance decreases
Elastance forces on the lungs
lungs tend to collapse inward
chest wall tends to expand outward
Pressure at functional reserve capacity
airway P=atmospheric P
lung collapse=chest wall expasion
in equilibrium
Pressure at volume less than FRC
airway pressure (-)
forced expiration
tendancy to expand (decrease lung elastance, increase chest wall expansion forces)
Pressure at volume more than FRC
airway pressure (+)
inspiration
tendancy to collapse (increase lung elastance, decrease chest wall expansion forces)
Muscles for inspiration
diaphragm
external intercostals
Intrapleural pressure and phase of respiration
rest: (-) intrapleural pressure
inspiration: more (-) intrapleural pressure
forced expiration: (+) intrapleural pressure
Impact of surfactant on lungs
decrease collapse of small alveoli
increase lung compliance (easier inspiration)
Pulmonary vascular resistance factors
inspiration increases P by expanding alveoli
forced expiration compresses vessels
Normal Hemoglobin levels in blood and oxygen binding capacity
15g/dL
20.1mL oxygen/dL
Fetal Hb and oxygen affinity
has increased oxygen affinity due to 2 gamma (instead of beta) subunits that decrease DPG affinity (which stabilizes T state)
Reason for sigmoid shape of Hb dissociation curve
positive cooperativity of Hb
Pressure of oxygen in pulmonary and systemic capillaries
pulmonary: 100mmHg (97.5% Hb sat)
systemic: 40mmHg (75% Hb sat)
The Bohr effect
increased H+/temp/Pco2/BPG causes decreased Hb affinity for oxygen
allows increased release of oxygen to metabolically active tissues
Causes of hypoxemia in pulmonary circulation
high altitude (decreased available oxygen)
hypoventilation
V/Q mismatch
diffusion limitation (pulmonary fibrosis/edema)
What is hypoxemia?
decreased A-a gradient
Haldane effect
decreased oxygen binding to Hb causes increased CO2 binding to Hb
seen in systemic capillaries
Bicarb formation in RBC’s
CO2 diffuses in, converted via carbonic anhydrase
bicarb exchanged for Cl- to exit cell in systemic capillaries
reactions reversed in pulmonary capillaries (to form gaseous CO2)
Impacts on gas diffusion across pulmonary capillaries
increased MW/thickness cause decreased diffusion
decreased solubility/surface area/P gradient decreases diffusion
Pathologies and diffusion
emphysema decreases surface area/diffusion
fibrosis increases thickness/decreases diffusion
Perfusion limited oxygen transport
oxygen saturates Hb and blood sat 1/3 way through pulmonary capillary during rest
only way to increase transport is increase perfusion rate
Diffusion limited oxygen transport
during strenuous exercise/fibrosis/emphysema speed of diffusion impacts Hb sat and oxygen in blood
Lung zones and pressures while standing
Zone 1: PA>Pa>Pv (compressed vessels from PA)
Zone 2: Pa>PA.Pv (blood flow dictated by Pa and PA)
Zone 3: Pa>Pv>PA (blood flow dictated by Pa and Pv, most capillaries open/high flow)
V/Q ratios and locations in lung
apex: highest V/Q
base: lowest V/Q
both V and Q increase at base, but Q increases more
Normal and ideal V/Q
Normal: 0.8
Ideal: 1, seen in exercise with apex vasodilation
Meaning of V/Q ratio
High means wasted ventilation
Low means wasted perfusion
V/Q and pulmonary embolism
Q=0 V/Q goes to infinity physiologic dead space with no perfusion PA of oxygen=atmospheric=150mmHg PA of CO2=0mmHg
V/Q and airway obstruction
shunt, V=0
V/Q goes to 0
PA of oxygen=40mmHg
PA of CO2=46mmHg
Respiratory response to high altitudes (5)
hyperventilation (to increase oxygen)
respiratory alkalosis (breathing off CO2)
hypoxic pulmonary vasoconstriction (from low oxygen)
increased erythropoietin/RBC production
increased BPG (more oxygen release in tissues)
Medulla and dorsal respiratory group
nucleus tractus solitarius
input from CN X and IX
only inspiratory neurons
synpase onto spinal cord (alpha motor neurons)
Medulla and ventral respiratory group
inspiratory and expiratory neurons
Pre-Botzinger complex (generates rhythm)
Pons and respiration
apneustic center (prevents inspiratory shutdown) pneomotaxic center (inhibits inspiration)
Slowly adapting pulmonary stretch receptors
myelinated
inhibits TV/overdistention of alveoli (Hering-Breur reflex)
over 1L TV, causes prolonged expiration
Rapidly adapting irritant receptors
myelinated
b/t epithelial cells
irritant chemicals causes vagus stimulation
results in cough/bronchoconstriction/mucous secretion
Pulmonary C fiber receptors
juxtacapillary receptors
unmyelinated
stimulated by mechano/chemo insult
causes slow shallow breathing with mucous and bronchoconstriction
Respiratory control of Po2
below 60mmHg, increase ventilation
monitored by CN IX and X (bodies)
Respiratory control of Pco2
arterial Pco2 increase causes increase in ventilation
very sensitive
Metabolic acidosis impact of respirations
increased ventilation
blows off/removes CO2 (which is H+)
Central control of respiration by Pco2
monitor H+ generated by CO2 and H2O
increased Pco2, increases ECF H+ in brain, causes increased ventilation and removal of H+
High altitude and respiration
pressure decreases at higher altitude
which decreases PI02/PA02
response is increased ventilation via Po2 receptors
Acclimatization to high altitudes
hyperventilation causes respiratory alkalosis
increased bicarb renally excreted
decreased pH of CSF by active transport out of CSF
Equation for Pressure of inhaled oxygen
PIo2=Fi02 * (Pb-Ph20)
Fio2=0.21
Pb=760mmHg at sea level
Ph20=47mmHg
Equation for respiratory minute ventilation
Ve=Vt * frequency
Equation for alveolar minute ventilation
VA= f * (Vt-Vd)
Vt=tidal volume
Vd=dead space
Reason for hysteresis in lung compliance
overcoming surface tension of alveoli to expand in inspiration
