Test 3: Wk12: 1 V/Q Balance Special Breathing Patterns - Puri Flashcards
FRC is the
point of equilibrium
At FRC Chest wall recoil — Lung recoil
=
Volume above FRC Chest Wall Recoil — Lung Recoil
less than
Volume Below FRC Chest Wall Recoil — Lung Recoild
> greater than
At FRC atmospheric pressure= Intrapleural pressure = Alveolar pressure = Transpulmonary pressure =
atmospheric pressure= 0
Intrapleural pressure = neg
Alveolar pressure = 0
Transpulmonary pressure = pos
the slope of the PV compliance curve =
compliance
PTP (Transpulmonary Pressure) =
PTP = PA - PIP
PA Alveolar Pressure
PIP Intrapleural Pressure
As diaphragm contracts PIP (intrapleural pressure) becomes
more negative
PIP is equal and opposite to
PTP (transpulmonary pressure)
— is the only pressure that fluctuates above and below 0 during regular quiet breathing
alveolar pressure
emphysema shifts curve
left, increase in compliance
Restrictive lung Dz shifts curve
right, decrease in compliance
higher the compliance higher the
resting lung volume
Airflow =
Palveolar - PBarometric / r
— contribute most to resistance
central, segmental airways
Bronchodilation Nerves
sympathetic
Bronchodilation receptors
B2 adrenergic
nonadrenergic, noncholinergic bronchodilators nerves VIP
Bronchodilation
Bronchoconstriction Nerves
Parasympathetic (Vagal)
Bronchoconstriction Receptors
Muscarinic Cholinergic Receptors M3
Alpha-adrenergic Receptors
Bronchoconstriction
airway resistance — and lung volume decreases
increases
At high lung volume
conduction airways are filled with air and expanded
radial traction applied by adjacent alveoli expands airways
intrapleural pressure only becomes positve during
forceful exhalation
Frictional resistance causes a fall in this driving pressure along the length of the conducting airways. At some point, the driving pressure will equal the surrounding pleural pressure; in this event, the net transmural pressure is zero
equal pressure point
in emphysema and bronchitis, the qeual pressure point is shifted
down towards lower airways
barrel chest is due to
lung hyperinflation from increased compliance
Pursed lips do what
increase air resistance at mouth increasing airways preventing collapse during expiration
In restrictive lung dz the equal pressure point is
shifted towards upper airways
airflow increased
airway resistance — in restrictive dz due to dynamic compression of upper airways
increases
— is the only volume that us decreased in obstructive lung dz
Expiratory Reserve Volume
why is residual volume increased so much in obstructive lung dz
air is trapped from dynamic compression
steady state
Vol CO2 produced = Vol O2 taken up
300mL/min = 300 mL/min
Hyperventilation
disproportionate increase in alveolar ventilation as
compared to metabolic state
Hypoventilation
a disproportionate decrease in alveolar ventilation as
compared to metabolic state
Total Ventilation Equation
VE = VT x F
Alveolar ventilation =
VA = VT-D x f
Total Ventilation in L/min
~ 6 L/min
Alveolar Ventilation in L/min
~4.2 L/min
Alveolar Gas Equation
PAO2 = [(Patm - 47) x .21] - (PACO2 / 0.8)
only 2 ways to change PACO2
change alveolar ventilation
change metabolism
Change in alveolar ventilation effect on PAO2
no effect bc O2 is coming from environment
PAO2 =
PiO2 - PACO2
Extraalveolar and alveolar vessels are arranged in
series
Total PVR is lowest
at FRC
↑ lung volume above FRC → ↑
Alveolar PVR by compression of alveolar vessels →
↑ Total PVR
↓ lung volume below FRC → ↑
Extraalveolar PVR by compression and less traction on extraalveolar vessels →
↑ Total PVR
Hypoxic Pulmonary Vasoconstriction
response to Alveolar O2
Decrease in PAO2 leads to precapillary pulmonary vasoconstriction which increases PVR
Hypoxic Pulmonary Vasoconstriction Occurs in
High Altitude
Hypoxemia caused by hypoventilation , shunting, V/Q mismatch
Fetal Circulation
Opioids suppress respiration by acting on the
central pattern generator
in chronic hypoventilation
PaCO2 is increased and PaO2 is decreased
Oxygen inducted hypoventialtion
administration of high concentrations of oxygen to a person with chronic hypercapnia will increase PaO2 and knock out hypoxic drive
Hypoxic Drive
central chemoreceptors are no longer stimulated by CSF acidosis, the main stimulus to breathe becomes the ↓ PaO2, which is mediated by the carotid body chemoreceptors (
Hypoxic (↓PaO2) ventilatory drive–primarily mediated by — accentuated by
peripheral chemoreceptors
hypercapnia (respiratory acidosis
Hypercapnic (↑PaCO2) ventilatory drive—primarily mediated by — accentuated by
central chemoreceptors
Hypoxia and metabolic acidosis
Opiates and BZDs reduce or abolish
ventilatory drive
to hypoxia and hypercapnia
Apneusis
prolonged inspirations separated by brief expirations, typically seen in
animals with lesions of the rostral pons—rare
Cheyne-Stokes Respiration
cycles of a gradual increase in tidal volume, followed by a
gradual decrease in tidal volume, and then a period of apnea
Cheyne-Stokes Respiration Seen with
bilateral
cortical disease or congestive heart failure, or in healthy people during sleep at high
altitude
Ataxic Breathing (Biot’s)
highly irregular inspirations, often separated by long
periods of apnea—medullary lesions
Cluster Breathing
similar to ataxic breathing, with groups of breaths, often of
differing amplitude, separated by long periods of apnea—medullary or pontine lesions
Kussmaul breathing
hyperventilation seen with metabolic acidosis, especially diabetic ketoacidosis (DKA)
Thus, V/Q ratio is greater at the
apex
V/Q ratio is lowest at the
base
