Physiology Flashcards
tidal volume (VT)
volume of normal breathing
0.5 L
inspiratory reserve volume (IRV)
additional amount of air that can enter during forced inspiration
expiratory reserve volume (ERV)
difference between tidal end volume and forceful expiration end volume
residual volume (RV)
amount of air remaining in the lung at max expiration
inspiratory capacity (IC)
VT + IRV
functional residual capacity (FRC)
ERV + RV
volume of air in the lungs after normal expiration
vital capacity (VC)
IC +ERV
volume that can be expired after max inspiration
total lung capacity (TLC)
VC + RV
includes all lung volumes
6-7 L
most sensitive test for restrictive lung disease
forced vital capacity (FVC)
TV + IRV + ERV
amount of air exhaled during a forceful expiration
forced expiratory volume in 1 second (FEV1)
max inspiration then forced expiration
normal is 80% of FVC
obstructive lung disease
FEV1: FVC ratio reduced: less than 70%
increased: TLC, RV, FRC
reduced: FVC, FEV1
difficult expiration: increased compliance, decreased Patm and Palv pressure: collapses airways on forced exhalation
ex: asthma, emphysema, chronic bronchitis, bronchiectasis
restrictive lung disease
reduced FVC, FEV1, TLC, RV, FRC
normal or increased FEV1: FVC ratio
difficult inspiration: decreased compliance, increased resistance
ex: obesity, weak inspiratory mescles, neuromuscular disorder, interstitial lung disease (fibrosis), ARDS, sarcoidosis, pneumonitis
atelectasis
unstable alveoli that collapse on expiration
Normal arterial PO2 and PCO2.
Normal venous PO2 and PCO2.
Normal alveolar PO2 and PCO2.
systemic arterial/ pulmonary venous: PO2: 100 PCO2: 40 systemic venous/ pulmonary arteries: PO2: 40 PCO2: 46 alveolar: PO2: 105 PCO2: 40
hypoventilation
increase in PACO2
hyperventilation
decrease PACO2
V/Q ratio for base and apex of lung
apex: high V/Q ratio (wasted ventilation)
base: low V/Q ratio (wasted perfusion)
What part of the lung is most perfused and has the most alveolar ventilation? least?
most perfused and alveolar ventilation: base
least perfused and alveolar ventilation: apex
A-a gradient for different causes of hypoxemia:
- hypoventilation
- decreased PIO2
- diffusion limitation
- R to L shunts
- V/Q mismatch
Which cannot be corrected by 100% O2?
- normal
- normal
- increased
- increased, NOT corrected with 100% O2
- increased
Decreased PIO2
- Example?
- A-a gradient increase? Intrinsic lung disease?
- Corrected with 100% O2?
- increased altitude
- A-a does NOT increase; no
- corrected with 100% O2
Hypoventilation
- Example?
- A-a gradient increase? Intrinsic lung disease?
- Corrected with 100% O2?
- drug overdose
- A-a does NOT increase; no
- corrected with 100% O2
Diffusion limitation
- Example?
- A-a gradient increase? Intrinsic lung disease?
- Corrected with 100% O2?
- pulmonary fibrosis, hard exercise, emphysema
- increased; yes
- yes
R to L Shunt
- Example?
- A-a gradient increase? Intrinsic lung disease?
- Corrected with 100% O2?
- ASD/VSD after pulmonary HTN reverses original L to R shunt; ARDS (alveolar flooding and collapse causes shunt)
- increased; yes
- NO
IMPORTANT: 100% oxygen should have a very large increase in PaO2: do the equation for A-a gradient to see if it is corrected
ex: PAO2= (760-47) x 1 - PaCO2/1
FiO2=1 at 100% O2
R= 1 at 100% O2
PaO2 should be in 600s; if not: shunt
V/Q mismatch
- example
- A-a gradient increase? Intrinsic lung disease?
- Corrected with 100% O2?
MOST COMMON cause of hypoxemia 1. emphysema, obstructive 2. increased; yes 3. yes normal whole lung V/Q: 0.8
Low V/Q diseases
V/Q less than 1: low ventilation
- obstructive disease (asthma, COPD)
- pulmonary edema
- SHUNT (most extreme of low V/Q)
High V/Q diseases
V/Q more than 1: low perfusion
- pulmonary embolism
- DEAD SPACE like no blood flow (most extreme high V/Q)
DLCO
High: early asthma, pulmonary alveolar hemorrhage, exercise, early CHF, obesity
Low: COPD, fibrosis, emphysema, interstitial lung disease, PAH/PE, anemia
pulmonary shunt
V/Q= 0
unventilated alveoli with preserved perfusion or A-V malformations
How can you use DLCO to differentiate between obstructive diseases (asthma and COPD)?
high: asthma
low: emphysema
How can you use DLCO to differentiate between restrictive diseases (chest wall vs. interstitial lung disease)?
high: chest wall
low: interstitial lung disease
isolated low DLCO indicates what type of disease
pulmonary vascular disease
pulmonary HTN/ pulmonary embolism
ventilation
exchange of gas between atmosphere and alveoli
diffusion
exchange of O2 and CO2 between alveolar air and lung capillaries
DOWN pressure gradient
inspiratory muscles
diaphragm (phrenic nerve)
accessory: scalene, sternocleidomastoid, external intercostal muscles
expiratory muscles
passive at rest
exercise/force: rectus abdominus, internal and external oblique, transverse abdominus, internal intercostal muscles
interdependence
if one alveolus has a tendency to collapse, it will be counteracted by expanding forces of surrounding alveoli
how does surfactant work
phospholipid (dipalmitoyl phosphatidylcholine, lecithin, sphingomyelin) that breaks polar attraction of water molecules and reduces surface tension: prevents atelectasis
deep breath stretches type II cells and stimulates surfactant production
surface tension
attractive forces between liquid molecules pulls surface molecules together at air-liquid interface
Which has more airway resistance: mouth or nose?
nose
How does lateral traction affect airway resistance?
elastic connective tissue fibers attach to airway exterior and pull outward: holding airways open
How does lung volume affect airway resistance?
increase in lung volume increases airway diameter and resistance decreases
How does relaxation/contraction of bronchial smooth muscle affect airway resistance?
relaxation: decreases resistance
contraction: increases reaction
What is the driving stimulus for respiration?
PaCO2
hyperventilation attenuates stimulation of respiration because PaCO2 is decreased
hypoxemia
lower than normal arterial PO2
normal = 100 mmHg
hypoxia
decreased O2 delivery to tissues
due to: decreased blood flow or decreased O2 content
hypercapnia
high arterial PCO2
normal= 40 mmHg
most often due to hypoventilation
where is most of gas exchange completed (even in exercise)?
initial region of pulmonary capillary
PERFUSION limited: all blood leaving capillary has reached equilibrium with alveolar gas
diffusion limited gas exchange diseases
gas does not equilibrate between capillaries and alveolar gas
- CO poisoning
- fibrosis (thick barrier)
- emphysema (decrease SA)
- high altitude
- INTENSE exercise
What determines pulmonary blood flow?
PAO2
How is edema fluid cleared?
repair epithelium
Na from interstitium comes into cell (ENaC) and is then pumped to basolateral side (Na-K ATPase) and water follows (aquaporin)
partial pressure (PO2)
dissolved O2 in plasma
methhemoglobin
Fe3+: O2 can’t bind
caused by nitrites and sulfonamides
HbF
alpha2gamma2
high affinity O2
adult Hb
alpha2beta2
Fe2+
HbS
sickle cell
cyanosis
unsaturated hemoglobin is purple
low Hb saturation causes blue color
CO poisoning
- decreases O2 carrying capacity because it binds more strongly to Hb (decreases O2 content)
- also increases affinity of O2 for Hb and makes unloading in tissues more difficult
Hamburger’s phenomenon
diffusion of HCO3- into plasma causes a decrease in net neg. charge in cell
Cl- moves into cell to compensate dragging water into cell causing it to swell
band three protein
drives Cl- shift into cells HCO3- leaves cell
How are H+ ions buffered in RBC after HCO3- leaves?
buffered by deoxyhemoglobin to prevent acidification
Bohr effect
when CO2 is produced by tissues, HCO3 and H+ are produced in blood.
due to H+ production, pH becomes lower.
higher H+ concentration increases H+ binding to Hb and decrease in O2 affinity: O2 unloads in tissues (right shift)
Haldane effect
oxygenation of Hb displaces CO2 from carboxyhemoglobin to form oxyhemoglobin
shifts equilibrium toward CO2 formation: CO2 is released from RBC’s into plasma
increases PCO2
respiratory acidosis
low pH PCO2 greater than 40 cause: hypoventilation ex: obstruction, acute or chronic lung disease, sedatives/opioids, weak respiratory muscles compensation: increase HCO3 (slow)
respiratory alkalosis
high pH PCO2 less than 40 cause: hyperventilation ex: hysteria, hypoxemia, high altitude, salicylate, tumor, PE compensation: decrease HCO3 (slow)
metabolic acidosis
low pH
PCO2 less than 40
low HCO3
compensate: hyperventilation (immediate)
metabolic alkalosis
high pH
PCO2 greater than 40
high HCO3
compensate: hypoventilation (immediate)
central chemoreceptors
MOST IMPORTANT
respond to change in brain extracellular fluid
MEDULLA
stimulus: decrease in pH (increased PCO2)
MINUTE to MINUTE breathing
peripheral chemoreceptors
respond to changes in arterial blood 1. PO2 less than 60 mmHg: increase ventilation 2. changes in pH increase (exercise): hyperventilation decrease (vomit): hypoventilation 1. carotid bodies 2. aortic bodies anemia does not stimulate
carotid bodies
stimulus: decreased PO2 greater than PCO2 greater than decreased pH
RAPID: PO2 less than 60 mmHg
high blood flow is key: EXERCISE
aortic bodies
RAPID
stimulus: decreased P02 greater than PCO2
lung receptors
- pulmonary stretch receptors
- irritant receptors
- J receptors
pulmonary stretch receptors
stimulated by lung distention
Bering-Breuer reflex: slows down frequency
irritant receptors
stimulated by noxious gas, smoke, dust, cold air, low PCO2
causes hyperpnea and bronchoconstriction
hypersensitive: asthma
juxtapulmonary capillary receptors (J receptors)
stimulated by increase in pulmonary interstitial fluid
causes shallow, rapid breathing, apnea, hypotension
nose and upper airway receptors
role in sneezing, coughing, bronchoconstriction
joint and limb muscle receptors
role in early adjustment to exercise
muscle spindles within respiratory muscles
sense muscle elongation
arterial baroreceptors
increase BP can cause reflexive hypoventilation
pain and temperature receptors
trigger period of apnea followed by hyperventilation
What happens when a patient has a chronic elevation of PCO2?
adaptation of central chemoreceptors: brain extracellular pH reset by increased HCO3 transport (normal brain fluid pH at high arterial PCO2)
ex: COPD
oxygen becomes chief stimulus of ventilation through peripheral chemoreceptors
IMPORTANT: raising PO2 by placing patient on O2 may remove any stimulus to breathe and cause sudden death (MONITOR)
response to exercise
- arterial PO2 constant: ventilation and O2 consumption increase in proportion
- moderate: alveolar ventilation increases in proportion to CO2 production; venous PCO2 increases but arterial PCO2 remains constant
- strenuous: lactic acid is released increasing arterial pH; arterial PCO2 decreases due to hyperventilation
response to high altitude
decreased inspired PO2
- immediate: hyperventilation: respiratory alkalosis
- several days: renal HCO3 excretion increases, HCO3 leaves CSF, pH of CSF decreases to normal; hyperventilation resumes
- hypoxia stimulates EPO synthesis
- increased 2,3- DPG causes right shift (decreased affinity)
- increase pulmonary resistance: hypertrophy of right ventricle
causes for worsening hypercapnia with supplemental O2
- Haldane effect
2. increased O2 abolishes hypoxic induced vasoconstriction: increased blood flow to low ventilation (low V/Q) areas
spirometry
expiration for at least 6 sec
measures vital
predictors: age, sex, Ht
What can a plethysmograph measure that a spirometer cannot?
residual volume
What part of the flow volume loop is effort independent?
end of expiration
Scoop on flow volume loop
COPD
hamburger on flow volume loop
upper airway obstruction (inspiratory stridor): vocal cord paralysis, tracheal stenosis, goiter
How is DLCO measured?
single breath need inhaled VC greater than 1 L hold breath for 10s CO due to high affinity for Hb normal 81-140%
What decreases FRC?
obesity, pregnancy, ascites
restrictive disease
Is peak flow effort dependent or effort independent?
dependent
