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196 Cards in this Set
- Front
- Back
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What is this term?
normal respiratory rate (12-14 breaths/min) at rest. |
eupnea
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What is this term?
increased respiratory rate greater than 20 breaths/min. |
tachypnea
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What is this term?
increased ventilation that meets metabolic needs. |
hyperpnea
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What is this term?
increased ventilation that exceeds metabolic needs. |
hyperventilate
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What is this term?
decreased respiratory rate less than 10 breaths/min. |
bradypnea
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What is this term?
disorder that involves only slow ventilation |
hypopnea
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What is this term?
decreased ventilation that is below metabolic needs |
hypoventilate
- shallow and/or slow breathing - can have both tachypnea and hypoventilation |
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What is this term?
labored, difficult breathing |
dyspnea
- ex: lung disease |
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What is this term?
cessation of breathing |
apnea
- ex: sleep apnea |
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Thorax is elastic which cause chest to expand and oppose the recoil of lungs. What structure(s) contribute to this elasticity?
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Costal cartilages
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List the inspiratory muscles under normal breathing.
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- diaphram
- external intercostals |
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List the inspiratory muscles during forced inspiration.
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- pectoris minor
- SCM - scalenes |
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List the expiratory muscles during forced expiration.
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- internal intercostals
- obliques - rectus abdominus |
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How much does diaphram flatten when its contracted?
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only 1cm.
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Lungs are elastic. The elastins and collagens in the interstitium causes lungs to ___ when expanded.
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recoil
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Why is the pressure in the pleura always negative under normal condition?
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due to recoil of the lungs and expansion of the thorax.
allow lungs to remain inflated |
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Which part of airway is this?
- greatest resistance - warms and humidifies inhaled air - filters and protects the respiratory tract from pollutants and pathogens: bronchospasm, mucociliary escalator |
conducting zones
- zone 1-17: 1-7 have the greatest resistance - consist of trachea, bronchi, terminal bronchioles |
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What are some reactions of the airway(conducting zone) when polluted air is inhaled?
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- nose hairs and mucus trap larger particles
- bronchospasm (reflex) - mucociliary escalator: mucus produced by goblet cells trap fine particles, ciliated cells propel particles trapped in the mucus to pharynx. |
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How does cold air affect the mucociliary escalator?
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cold air paralyzed ciliated cells
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How does smoking affect mucociliary escalator?
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smoke damages ciliated cells
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Which part of the airway is this?
- site of gas exchange - zone 17-23 |
respiratory zone
- all zones contain alveoli - consists of respiratory bronchioles, alveolar ducts, and alveolar sacs. |
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Which lung volume is this? what is the typical value?
- volume of air inspired or expired during normal, quiet breathing |
Vt: tidal volume, 500ml
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Which lung volume is this? what is the typical value?
- maximum amount of air that can be inspired at the end of a normal inspiration. |
IRV: inspiratory reserve volume
- 3000-3300ml |
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Which lung volume is this? what is the typical value?
- maximum amount of air that can be exspired at the end of a normal exspiration. |
ERV: exspiratory reserve volume
- 1000-1200ml |
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Which lung volume is this? what is the typical value?
- volume of air remaining in the lungs after a forced expiration. |
RV: residual volume
- 1200ml - can not be measured with a spirometer |
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Which lung capacity is this? what is the typical value?
- volume of air in the lungs after a maximal inspiration. |
TLC = Vt + IRV + ERV + RV
- 5700-6200 ml |
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Which lung capacity is this? what is the typical value?
- volume of air forcefully expired from lungs after a maximal inspiration. |
VC = Vt + IRV + ERV
VC = TLC - RV - 4500-5000ml |
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Which lung capacity is this? what is the typical value?
- volume of air remaining in the lungs after a normal expiration. |
FRC = ERV + RV
- 2200-2400ml |
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Which lung capacity is this? what is the typical value?
- volume of air that can be inspired after a normal expiration. |
IC = Vt + IRV\
- 3500-3800ml |
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What are the nornal values for the following?
- FEV1/FVC - FEV3/FVC |
- FEV1/FVC: 70-80%
- FEV3/FVC: 95% |
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Explain the slope between FEF25 tro FEF75 in the respiratory flow-volume loop.
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Effort independent region
- limiting factor: dynamic compression of the airway, limit the excessary expiratoy muscles. |
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How to calculate FRC using helium dilution method?
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- known C1, V1
- C2 measured after a normal Vt is expired. C1 x V1 = C2 x (FRC + V1) |
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Why is helium dilution not good for someone who has emphysema?
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It would underestimate FRC since air could not reach damaged lung area.
- artificially elevated C2 results in decreased FRC |
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Which FRC measurement is more accuate for someone who has emphysema?
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body plethysmography
- known P1, V1 - P2 measured after closing mouthpiece - P1 x V1 = P2 x (V1 - v) in the alveoli - P3 before and P4 after closing mouthpiece - P3 x FRC = P4 x (v + FRC) |
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How to obtain FRV using body plethysmography?
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In the plethysmograph:
- known P1, V1 - P2 measured after closing mouthpiece - P1 x V1 = P2 x (V1 - v) In the alveoli - P3 before and P4 after closing mouthpiece - P3 x FRC = P4 x (v + FRC) |
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What is the normal compliance value for the lung?
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0.13 L/cmH2O
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What is the relationship between compliance and elasticity?
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inversely related
- the greater the elasticity, the lower the compliance - the greater the compliance, the easier it is for a change in pressure to change volume |
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What is the underlying cause of hysteresis?
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gas-liquid interface surface tension
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Explain the hysteresis of lung compliance loop.
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- upon inspiration: slope is flatter(low comliance) because of surface tension (deflated alveoli more stiff)
- slope gets steeper - toward the end of inflation, slope flattens due to stiff alveoli (maximally inflated) - upon expiration: flatter slope - slope is steeper and fairly uniform during deflation. |
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Relation between lung recoil and chest expanding force at FRC.
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equal
- no movement |
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Relation between lung recoil and chest expanding force above FRC.
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recoil force greater than chest expanding force.
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Relation between lung recoil and chest expanding force below FRC.
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below FRC (forced expiration)
- recoil force < chest expanding force |
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What does surfactanct do? which value does it change in the LaPlace Law?
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surfactant lower surface tension (T value in LaPlace law)
P = 2T/r - P: collapsing pressure - T: tension - r: alveolar radius |
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What happens to air flow in alveoli if there is no surfactant?
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- high surface tension -> high collapsing pressure -> atelectasis (collapsed alveoli)
- pressure gradient between large and small alveoli: small alveoli collapsing into large alveoli - air flow to large alveli P = 2T / r |
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List some factors that increases airway resistance.
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- bronchial constriction: smaller r
- low lung volume: small r - viscosity of inspired air |
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T/F: P(pleural) is always lower than P(alveolar) under normal condition.
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T.
Even during forced expiration, P(pleural) becomes positive, P(alveolar) is even higher. So alveolar is always kept inflated under normal condition. |
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Decribe the progression of P(pleural) starting from end of expiration.
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- end of expiration: -5 cmH2O
- inspiration: -8 cmH2O - end of inspiration: -8 cmH2O - expiration: -5 cmH2O - forced expiration: +15 cmH2O |
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Decribe the progression of P(alveolar) starting from end of expiration.
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- end of expiration: 0 cmH2O
- inspiration: -1 cmH2O - end of inspiration: 0 cmH2O - expiration: +1 cmH2O - forced expiration: +35 cmH2O |
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Decribe the progression of P(transpulmonary) starting from end of expiration.
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P(alveolar) - P(pleural)
- end of expiration: +5 cmH2O - inspiration: +7 cmH2O - end of inspiration: +8 cmH2O - expiration: +4 cmH2O |
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Give some causes of pneumothorax.
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increased P(pleural) -> collapse alveoli
- spontaneous: lung disease eg emphysema (ruptured bleb on visceral pleura) - trauma: penetrating (bullet) and nonpenetrating (fractured rib) |
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Which is more of an emergnecy, simple or tension pneumothorax?
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tension pneumothorax
- trapped air in pleura - push vital organs eg. heart (decreased CO) |
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What is P(H2O) in the airway?
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always 47mmHg in the body unless temperature drastically changes
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What is the partial pressure of nitrogen and oxygen in atmonspheric air?
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P(nitrogen) = 79%
P(O2) = 21% |
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What is Henry's law?
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dissolved gas = P gas x solubility coeficient
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What is dalton's law?
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partial pressure of one gas = mole fraction of gas x total gas pressure
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What is anatomical dead space?
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- conducting zone volume
- average about 150ml |
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What is alveolar dead space?
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- alveoli that do not participate in gas exchange (due to lack of blood supply or damage to alveoli
- normal value is zero for healthy individuals |
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What is physiological dead space?
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- combination of anatomical and alveolar dead space
- should equal to anatomical dead space in healthy individuals |
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How to estimate dead space Vd?
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Vd = Vtx(Pa(CO2) - Pe(CO2))/Pa(CO2)
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According to Fick's law:
volume of gas transferred per unit of time is directly proportional to which 3 factors? |
- diffusion coefficient
- pressure gradient - surface area |
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According to Fick's law:
volume of gas transferred per unit of time is inversely proportional to which factor? |
- distance the gas must diffuse
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How does emphysema affect the gas transfer according to Fick's law?
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decrease gas exchange by decreasing surface area (destruction of alveoli)
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How does pulmonary edema affect the gas transfer according to Fick's law?
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decrease gas exchange by 1) increasing the distance for gas diffusion, 2) decreasing the diffusion coefficient
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What are the partial pressures of O2 and CO2 in the alveoli under normal condition?
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P(O2) = 104 mmHg
P(CO2) = 40 mmHg |
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What are the partial pressures of O2 and CO2 in the conducting zone under normal condition?
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P(O2) = 150 mmHg
P(CO2) = 30 mmHg |
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What are the partial pressures of O2 and CO2 in the arterial end of pulmonary vasculature under normal condition?
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P(O2) = 40 mmHg
P(CO2) = 45 mmHg |
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What are the partial pressures of O2 and CO2 in the venous end of pulmonary vasculature under normal condition?
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P(O2) = 104 mmHg
P(CO2) = 45 mmHg |
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What are the partial pressures of O2 and CO2 in the arterial end of systemic vasculature under normal condition?
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P(O2) = 95 mmHg
P(CO2) = 40 mmHg |
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What are the partial pressures of O2 and CO2 in the venous end of systemic vasculature under normal condition?
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P(O2) = 40 mmHg
P(CO2) = 45 mmHg |
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Why is P(O2) different between alveolar and arterial end of systemic vasculature?
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Physiologic shunt
- 2% of cardiac ouput bypass alveoli (bronchial veins drain directly into pulmonary vein, thebesian veins from coronary circulation drain directly inro LA) |
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How to calculate minute and alveolar ventilation?
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minute ventilation: volume of air moved into or out of the lungs per minute.
Ve = Vt x respiratory rate alveolar rate: amount of air available for gas exchange per minute. Va = (Vt -Vd) x respiratory rate |
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Is it better to increase Vt or respiratory rate in order to increase alveolar ventilation?
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increase Vt: limits the loss of inspired air to Vd.
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All else equal, what happens to Palveolar(CO2) when you increase alveolar ventilation?
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decrease
Valveolar = KxV(CO2)/Palveolar(CO2) |
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All else equal, what happens to Valveolar when you increase V(CO2), CO2 production in the tissue?
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increase
Valveolar = KxV(CO2)/Palveolar(CO2) |
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How do you predict P(O2)alveolar based on P(CO2)alveolar?
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alveolar gas equation
P(O2) alveolar = P(O2)inspired - P(CO2)alveolar/R |
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What is the major local factor that regulates pulmonary blood flow?
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P(O2)alveolar
- blood flow reduces in the area of low P(O2)alveolar: pulmonary vasoconstriction |
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What effect do the following have on pulmonary flow?
- NO - Thromboxane A2 - prostacyclin |
- NO: pulmonary vasodilation to increase blood flow
- Thromboxane A2: pulmonary vasoconstriction to decrease blood flow - prostacyclin: pulmonary vasodilation to increase blood flow |
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What happens to pulmonary blood flow at high altitudes?
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lower P(O2)alveolar -> global vasoconstriction of pulmonary arterioles -> increase pulmonary vascular resistance
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Average V/Q thorughout the lung is around 0.8. But regional variations exist. What are some regional difference in V/Q ratio?
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- V/Q highest in the apex: minimal gravity effect on blood flow -> lowest perfusion rate
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What determines blood flow in zone 1?
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pressure gradient between P(O2)arterial and P(O2)alveolar: P(O2)arterial only slightly higher than P(O2)alveolar
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What determines blood flow in zone ]2?
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pressure gradient between P(O2)alveolar and P(O2)arterial.
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What determines blood flow in zone 3?
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pressure gradient between P(O2)arterial and P(O2)venous.
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What V/Q defect is this?
- P(O2)alveolar = 0 - P(CO2)alveolar = 0 - P(O2)arterial = P(O2)venous - P(CO2)arterial = P(CO2)venous |
airway obstruction (shunt)
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What V/Q defect is this?
- P(O2)alveolar = 150 mmHg - P(CO2)alveolar = 0 - P(O2)arterial = 0 - P(CO2)arterial = 0 |
pulmonary embolus (dead space)
- no ventilation (gas exchange) |
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What V/Q defect is this?
- high pulmonary P(O2) - low pulmonary P(CO2) |
mild asthma / anxiety
- high V/Q - usually due to slow blood flow -> allow more equalibration time. |
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What V/Q defect is this?
- low pulmonary P(O2) - high pulmonary P(CO2) |
decreased ventilation: low V/Q
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What type of gas exchange is this?
Diffusion continues as long as partial pressure gradient is maintained. |
Diffusion-limited gas exchange
- CO: CO grabbed by hemoglobin right away, partial pressure gradient maintained. - O2 transport during strnous exercise, emphysema, and fibrosis. |
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Give some examples of diffusion limited gas exchange.
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- CO: CO grabbed by hemoglobin right away, partial pressure gradient maintained.
- O2 transport during strenous exercise, emphysema, and fibrosis. |
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What type of gas exchange is this?
- gas partial pressure gradient is not maintained - gas transport is increased by increasing blood flow. |
perfusion-limited gas exhange
- NO2: no partial pressure gradient - O2: |
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How to determine O2 diffusion capacity?
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Use CO method
DL(CO) = Volume of CO diffused/P(CO)alveolar DL(O2) = 1.23 x DL(CO) |
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What does pulse oximeter measure?
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the percent of fully saturated Hb in the blood.
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How much O2/min does body normally need?
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250ml of O2/min
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How to calculate O2 capacity?
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1.36mlO2/gramHb x 15gramHb/100ml blood = 20 vol%
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How to calculate O2 content?
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O2 content = O2 capacity x SaO2
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How to calculate O2 extraction?
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(O2 content in artery - O2 content in vein) / O2 content in artery
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How to calculate O2 delivery?
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O2 delivery = O2 content x cardiac output
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List the factors that shift the O2 saturation curve to the right.
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- high CO2 level
- decreased pH - increase in temperature - increase BPG - hemoglobin S |
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List the factors that shift theO2 saturation curve to the left.
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- low CO2
- high pH - decreased temperature - decreased BPG - hemoglobin F - methemoglobin |
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How does increase in temperature affect O2 binding curve?
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shift to the right
- increase T -> increase in metabolism -> high O2 demand |
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Under what conditions will BPG be high in your body?
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- anemia
- emphysema - high altitude also at the body tissue shift the O2 binding curve to the right |
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Effect of HbF on O2 binding curve (2)
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- shift to the left
- CO2 out of fetal circulation cause further left shift * CO2 to maternal circulation would shift maternal O2 binding curve to the right. |
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What is the effect of BPG on HbF?
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not much
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How does methemoglobin affect O2 binding curve?
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Shift to the left
- Fe3+ that do not bind to O2 - rest Fe2+ hold tighter onto O2 caused by - nitrates, sulfonamides, arsenic, benzene, defieciency of methemoglobin reductase |
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What can cause high level of methemoglobin in yout body?
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- nitrates
- sulfonamides - arsenic - benzene - defieciency of methemoglobin reductase |
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What is the effect of CO on O2 binding curve? (2)
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- displaces O2 from Hb
- increase affinity of O2 to the rest of Hb -> left shift * P(O2) stays the same * pulse O2 is the same * O2 capacity decreases |
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Explain the Haldane effect.
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In the lungs, as more O2 are bound to Hb, more CO2 will be released from Hb. Only 5% carbaminohemoglobin in the arterial blood in the lungs.
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How is CO2 transported in the blood?
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- ~10-30% transported as carbaminohemoglobin
- ~70-90% transported as HCO3-. |
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How is CO2 transported at the body tissues?
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- CO2 diffuse into RBC
- CO2+H2O -> HCO3- + H+ (carbonic anhydrase) - HCO3- diffuse out to plasma in exchange for Cl- into the RBC. - Cl shift into the RBC |
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How is CO2 transported at the lungs?
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- CO2 diffuse out of RBC to alveoli
- HCO3- diffuse into RBC in exchange for Cl- out into plasma - Cl shift |
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What is this disease?
- FEV1 reduced - FEV1/FVC reduced - increased TLC, FRC, RV - greatest difficulty getting air out of lungs (barrel chest) |
COPD
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What does the flow-volume loop look like for someone with COPD?
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- loop shift to the left
- increased RV, TLC, FRC - concave shaped expiration curve |
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List some COPDs.
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- emphysema
- chronic bronchitis |
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Pathogenesis of emphysema.
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- loose elastic fiber (proteases, elastase released by neutrophils and macrophages) -> increased compliance
- alveoli loose elastic recoil - overinflation of alveoli -> larger inefficient alveoli, collapsed alveoli - impair gas exchange: lower P(O2)arterial, higher P(CO2)arterial - later stage: damage pulmonary capillary bed -> impairs gas exchange |
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Which is the most common type of emphysema, centriacinar/centrilobular or panacinar/panlobular?
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centriacinar/centrilobular
- mainly affect respiratory bronchioles of acinus |
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Which part of lung is damaged?
- centriacinar/centrilobular |
respiratory bronchioles of acinus
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Which part of lung is damaged?
- panacinar/panlobular |
entire acinus of lung
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Causes of emphysema.
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1) smoking
- increases release of proteases by neutrophils and macrophages - paralyzes mucociliary escalator -> pathogens remain in the lungs -> more neutrophils and macrophages - centriacinar most common 2) AAT deficiency - AAT normaly inhibits proteases from breaking down elastic fibers - panacinar most common |
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Explain the underlying cause of increased FRC in emphysema.
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- decreased elastic fiber -> increased compliance -> less recoil at normal FRC -> lungs need larger volume to balance opposing force of chest wall expansion
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Why do persons with emphysema expire through pursed lips?
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increased compliance -> Palveolar and airway pressure less positive -> Ptp may become negative in large airways -> airway collapse
purse lips to raise airway pressure, prevents airway collapse. |
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What is this COPD?
- increased daily mucus production for at least 3 months in 2 or more consecutive years |
chronic bronchitis
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Pathogenesis of chronic bronchitis.
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- hyperplasia and hypertrophy of goblet cells of the submucosa and thickening of mucosa
- airway obstruction, cough and sputum production - no damage to pulmonary capillary bed (fine perfusion) - narrowed airway -> hypoventilation of alveoli (hypoxemia, hypercapnia) |
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Causes of chronic bronchitis.
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smoking
- release of inflammatory mediators - paralyzes mucociliary escalator -> excess mucus |
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What is this disease?
- recurrent episodes of airway obstruction - completely or partialy reversible with/without treatment - airway inflammation - bronchoconstriction - airway hypersensitiveness |
asthma
three basic characteristics - airway inflammation - bronchoconstriction - airway hypersensitiveness |
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What is the acute response of asthma?
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- inflammation via mast cells
- edema - relieved with beta-2 agonist |
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What is the late phase response of asthma?
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- last days to weeks
- more inflammatory mediators - chronic inflammation leads to airway remodeling |
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Asthma: mild, moderate, or severe?
- normal FEV1/FVC - normal - slightly elevated Pa(O2) - normal - slightly decreased Pa(CO2) |
mild
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Asthma: mild, moderate, or severe?
- 60-80 FEV1/FVC - normal - slightly decreased Pa(O2) - normal - slightly increased Pa(CO2) |
moderate
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Asthma: mild, moderate, or severe?
- FEV1/FVC < 60% - decreased Pa(O2) - increased Pa(CO2) |
severe
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How does asthma cause hypoxemia and respiratory alkalosis?
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hyperventilation
- low P(CO2) -> left shift of O2 saturation -> less O2 release to tissue -> hypoxemia - low P(CO2) -> less HCO3- -> alkalosis |
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Methods used to diagnose asthma.
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- spirometry
- inhalation challenge using cholinergic agonist (methacholine) |
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Rescue drugs for asthma.
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- inhaled albuterol (beta2 agonist)
- inhaled Ipatropium (anti-cholinergic): used more in COPD - short course of corticosteroids |
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Long term control drugs for asthma.
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- inhaled corticosteroids: Budesonide (preferred because of minimal disruption of HPA axis
- anti-inflammatory drugs: inhaled cromolyn, anti-leukotrienes (singulair) - inhaled long-acting beta2 agonist: salmeterol |
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What is this disease?
- limitation of air getting into lungs - decreased FEV1 - increased FEV1/FVC - decreased Pa(O2) - increased Pa(CO2) - right shift of flow-volume loop |
restrictive pulmonary disease
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What are the two causes of restrictive pulmonary disease?
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1. parenchymal: damage to bronchioles, alveoli, pulmonary capillaries
2. extraparenchymal: problem with chest wall that restrict expansion of lungs |
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Pathogenesis of parenchymal cause of restrictive pulmonary disease.
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damage to bronchioles, alveoli, pulmonary capillaries
- inflammation -> fibrosis, damaged parenchyma -> thickened alveolar or capillary walls -> impaired diffusion -> decreased Pa(O2) and increased Pa(CO2) |
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Pathogenesis of extraparenchymal cause of restrictive pulmonary disease.
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problem with chest wall that restrict expansion of lungs
- decreased volume of air for gas exchange -> decreases Pa(O2), increases Pa(CO2) |
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What is this disease?
flow-volume loop - decreased RV - decreased TLC, FVC - no change in slope |
restrictive lung disease
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What does flow-volume loop look like for restrictive lung disease?
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flow-volume loop
- decreased RV - decreased TLC, FVC - no change in slope |
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List some restrictive pulmonary diseases.
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- interstitial lung disease
- diseases affecting respiratory muscles - infant respiratory distress syndrome - acute respiratory distress syndrome |
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Which restrictive pulmonary disease is this?
- parechymal scarring and fibrosis - decrease in compliance (stiff lungs): lower FRC (sollapsing force greater than expansion force) - hypoxemia and hypercapnea - O2 becomes diffusion limited gas exchange |
interstitial pulmonary disease
- occupational exposure: asbestos, pollutants - infections: pneumonia, histoplasmosis - radiation therapy |
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What are some causes of interstitial pulmonary diseases?
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- occupational exposure: asbestos, pollutants
- infections: pneumonia, histoplasmosis - radiation therapy |
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Why does O2 exchange become diffusion limited in people with interstitial lung disease?
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Fibrosis leads to thicker alveolar wall which makes gas diffusion difficult. Thus O2 which usually equilibrates in the lung capillary no longer happens, there is a need to increase diffusion to get further addition of O2.
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Which restrictive pulmonary disease is this?
- extraparenchymal damage - decreased air flow and ventilation - hypoxemia and hypercapnea |
diseases affecting muscles of respiration
- ALS (Lou Gehrig's disease): degeneration of lower motor neurons - Guillian Barre: acute inflammatory demyelinating polyneuropathy(ascending) - myasthenia gravis - muscular dystrophy |
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What are some causes of diseases affecting muscles of respiration?
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- ALS (Lou Gehrig's disease): degeneration of lower motor neurons
- Guillian Barre: acute inflammatory demyelinating polyneuropathy(ascending) - myasthenia gravis - muscular dystrophy |
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Pathogenesis of diseases affecting muscles of respiration.
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decreased change in lung volume -> decrease pressure gradient -> decreased air flow -> decreased ventilation -> low Pa(O2), high Pa(CO2)
(P=nRT/V, air flow = pressure gradient/R) |
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What is this restrictive pulmonary disease?
- parenchymal damage - immature respiratory system fails to produce surfactant - usually in premature infants born <30 wks gestation |
IRDS (infant respiratory distress syndrome)
- no surfactant -> high surface tension -> high collapsing pressure in small alveoli -> atelectasia of smaller alveoli -> pressure gradient from smaller to larger alveoli -> decrease in ventilation |
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Pathophysiology of IRDS.
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- no surfactant -> high surface tension -> high collapsing pressure in small alveoli -> atelectasia of smaller alveoli -> pressure gradient from smaller to larger alveoli -> decrease in ventilation
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How to treat IRDS?
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- surfactant therapy with artificial and animal derived surfactant.
- child put on continuous positive airway pressure |
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What is this restrictive pulmonary disease?
- diffuse alveolar and capillary damage caused leakiness - stiff lung (pulmonary edema) |
ARDS (acute respiratory distress syndrome)
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Pathophysiology of ARDS.
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- diffuse alveolar and capillary damage -> pulmonary edema (leakiness) -> impaired gas diffusion -> decreased ventilation
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How to treat ARDS?
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Difficult to treat
- give high levels of O2 - but prolonged O2 would also cause ARDS (free oxygen radicals and defective enzymes) - 50% mortality rate |
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Diffusion or perfusion limited gas exchange?
- O2 exchange at high altitude |
perfusion limited
- although it takes longer for O2 to equilibrate due to decreased pressure gradient across alveoli, it still achieves equilibration at the venous end of the pulmonary capillary. |
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Diffusion or perfusion limited gas exchange?
- O2 exchange in people with restrictive pulmonary disease. |
diffusion limited
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Diffusion or perfusion limited gas exchange?
- N2O exchange |
perfusion limited
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Diffusion or perfusion limited gas exchange?
- CO exchange at high altitude |
diffusion limited
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What are some adaptations to high altitude/hypoxemia?
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- hyperventilation: occurs when Pa(O2) is less than 60mmHg
- polycythemia: kidney release EPO to increase RBC production to increase O2 capacity. But it increases viscosity (increase BP and blood clots) - increase in BPG: cause right shift of O2 binding curve (good at tissue, not so at lungs) - pulmonary vasoconstriction: respond to low PA(O2) leads to increased pulmonary vascular resistance. thus cause increased pulmonary pressure to maintain blood flow, but will lead to RVH. |
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What are some manifestations of altitude sickness?
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- acute mountain sickness: occurs at altitude beyond 8000 feet. Headache, fatique, dizziness, nausea, palpitations, insomnia, peripheral edema.
- pulmonary edema: occurs at altitude above 10000 feet. vasoconstriction favors filtration of plasma from blood vessels. Dyspnea, marked fatigue, confusion, potentially fatal. - cerebral edema: occurs at altitude above 10000 feet. Cerebral vasodilation increases intracranial pressure. Severe headache, loss of coordination, hallucinations, memory loss. Can lead to coma or death. |
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Do age, gender and physical fitness have influences on whether a person develops acute mountain sickness?
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No.
only varies with rapidity of ascend and time spent at a given altitude. |
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These are symptoms of someone who has been to a high altitude area (above 8000 feet). What is the name of the manifestation?
- headache - fatigue - dizziness - palpitations - insomnia - peripheral edema |
Acute mountain sickness
- symptoms of hypoxemia and alkalosis - starts from a few hrs to 24 hrs after arrival to elevated altitude - should acclimate in 1 to 3 days |
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These are symptoms of someone who has been to a high altitude area (above 10000 feet). What is the name of the manifestation?
- dyspnea - marked fatigue - confusion |
HAPE (high altitude pulmonary edema)
- pulmonary vasoconstriction increase pressure -> favors filtration of plasma from blood vessels -> accumulation of fluid in lungs -> poor gas exchange - symptoms manifest 12-96 hours - predisposing factors (level of altitude, rapidity of ascend, individual predisposition) - potentially fatal |
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These are symptoms of someone who has been to a high altitude area (above 10000 feet). What is the name of the manifestation?
- severe headache - loss of coordination - hallucinations - memory loss |
HACE (high altitude cerebral edema)
- manifest within 12-96 hours - cerebral vasodilation -> increase fluid level -> increase hydrostatic pressure -> favor filtration -> increase fluid in the brain -> increase intracranial pressure - predisposing factors (level of altitude, rapidity of ascend, individual predisposition) - can lead to coma and death |
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How to treat acute mountain sickness (AMS)?
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mild case:
- stop ascend and descend - acetazolamide moderate case - immediate descend - supplement O2 - increased dose of acetazolamide |
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How to prevent AMS (acute mountain sickness)?
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- acetazolamide: increase HCO3- excretion by kidneys, counteract alkalosis. diuretic counteract edema.
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How to treat HAPE (high altitude pulmonary edema)?
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- supplemental O2
- hyperbaria (Gamow bag) - immediate descent - nifedipine: decrease increased pressure of pulmonary vasculature |
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How to prevent HAPE(high altitude pulmonary edema)?
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slow ascend of 1000 feet per day
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How to treat HACE (high altitude cerebral edema)?
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- supplemental O2
- hyperbaria (Gamow bag) - immediate descent - dexamethasone: powerful glucocorticoids to decrease inflammation |
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How to prevent HACE(high altitude cerebral edema)?
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slow ascend of 1000 feet per day
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What is the absolute pressure 33 feet under seawater?
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2 atm
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What is the absolute pressure in a hyperbaric chamber of 100% O2?
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2 atm
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Benefits of HBO (hyperbaric oxygen) therapy?
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- increase O2 concentration in all body tissue
- stimulate angiogenesis to locations with reduced circulation - stimulate increase in superoxide dismutase - aid in the treatment of infection by enhancing neutrophil action |
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Indications for HBO (hyperbaric oxygen) therapy?
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- HAPE, HACE
- CO poisoning - cyanide poisoning - burns - necrotizing soft tissue infections (eg MRCA) - chronic wounds |
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What are some problems with hyperbaria?
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- inert gas narcosis
- decompression sickness - pulmonary overinflation syndrome |
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Why do deep sea divers use helium instead of nitrogen gas in their gas tank?
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Inert gas narcosis
- at high pressure, N2 dissolvable in lipids (membranes of neurons and glia) - feeling of euphoria - loss of coordination and possibly coma |
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What do you get when you ascend rapidly after a dive?
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1) decompression sickness (the bends/ gas embolism)
- N2 bubbles out of blood, lodged in small vessels and joints - activates powerful inflammatory response: platelet aggregation -> thrombus -> stroke, heart attack, pulmonary embolism 2) pulmonary overinflation syndrome - pressure decrease -> volume increase -> inflate alveoli (P=nRT/V) |
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How to prevent decompression sickness?
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- slow ascend: < 30 feet per min
- don't race the bubbles |
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How to treat decompression sickness?
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- recompression therapy using hyperbaric chamber
- followed by slow depressurization |
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How to prevent pulmonary overinflation syndrome?
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- divers should exhale during ascend
- control ascend rate |
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How to treat pulmonary overinflation syndrome?
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recompression therapy
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What happens when people are exposed to PO2 greater than 760mmHg?
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- convulsions
- tonic-clonic/ grand mal seizures |
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DRG or VRG?
- most active during inspiration - primarily drive the diaphram |
DRG
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DRG or VRG?
- most active during inspiration and expiration - primarily drive the intercostals - contains pacemaker neurons (pre-Botzinger complex) |
VRG
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When does cerebrum loose voluntary control of breathing?
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CO2 build up causes override of cerebrum
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What is the role of hypothalamus on breathing?
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emotional aspect
- increase respiratory rate during stress, excitement and pain. |
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What makes your respiratory rate increase during stress, excitement and pain?
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hypothalamus
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Which breathing control center is this?
- not vital - regulate duration of inspiration - cause short, fast, shallow inspiration |
pontine respiratory group/pneumotaxic center
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Which breathing control center is this?
- not vital - regulate duration of inspiration - cause long, slow, deep inspiration |
apneustic center (pontine)
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Where are the central chemoreceptors located?
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medulla and pons
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Where are the peripheral chemoreceptors located?
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carotid arteries (glomus cells)
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Which regulator (center) plays the biggest role in the regulation of breathing?
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central chemoreceptor
- monitor levels of CO2/pH of arterial blood - increased CO2 /decreased pH is the main stimulus of breathing |
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What is the role of central chemoreceptor on the regulation of breathing?
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- monitor levels of CO2/pH of arterial blood
- increased CO2 /decreased pH is the main stimulus of breathing |
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What is the role of central chemoreceptor on the regulation of breathing?
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- regulate levels of O2 in the arterial blood
- O2 stimulates breathing in extreme instances (PaO2 < 60mmHg) |
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What is Ondine syndrome?
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central chemoreceptor not respond to CO2 -> hypoventilate
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What is the cause of central apnea?
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central chemoreceptor not respond to CO2 -> hypoventilate
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Name two diseases that are associated with unresponsive central chemoreceptors.
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- Ondine syndrome
- central apnea |
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Which regulator of breathing send inhibitory impulses to brainstem via vagus nerve when lungs are inflated?
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pulmonary stretch receptors -> inflation reflex/Hering-Breuer reflex
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How does proprioceptors and exteroreceptors regulate breathing?
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stimulate breathing when stimulated (during exercise or pain)
located throughout limbs and body |
