Respiration Quizlet by luca (STUDY THIS ONE FIRST) Flashcards
Ventilation
Movement of gas from the environment to gas exchange space (the lung)
- The product of breathing freq. X tidal volume
Law of partial pressures
he total pressure of a gas is the sum of partial pressures of the gases present
Ptot = P1 + P2 + … + Pn
Dalton’s Law
The partial pressure of a gas can be found by knowing the total pressure and the fractional concentration of the individual gas species
Px = Ptot * Fx
Atmospheric pressure at sea level
760 mmHg = 1 atm
Partial pressure of O2 at sea level
Fractional content inspired O2 gas
Normal arterial O2
100 mmHg
The 3 functions of the nose
- Filters air
- Warms air
- Saturates air with water
Water vapor correction
Air in lung is completely saturated with H2O
- P(H2O) at 37 C = 47 mmHg
So Px = (Pb - 47) * Fx
Pb=barometric pressure
Partial pressure of O2 in the lung
P(O2) = (760-47)*0.209 = 149 mmHg
Henry’s Law
The volume of gas dissolved in liquid is proportional to the partial pressure
Cx = k * Px
k=solubility
Fick’s Law of Diffusion
J = DAalpha(C1-C2)/X
J = rate of diffusion D = permeability constant A = area Alpha = solubility (K in Henry's Law) X = thickness
Sternocleidomastoids
Insert on 1st rib or sternum - stabilize rib 1 when you breathe
Internal intercostals
Primarily expiratory
External intercostals
Primarily inspiratory
Minute ventilation
VdotE = Vt * f
= tidal volume times breathing frequency
Volume of air moving in an out of the lung every minute
Ti
Inspiratory time
Ti > 50% of Ttot is a classic indication of respiratory failure
Te
Expiratory time
Ttot
Total breath time
= Ti + Te
Breathing frequency
=1/Ttot * 60
Vt
Tidal volume
Total amount of air going in and out with each normal breath
Pulse oximeter
Measures percent oxygenation of Hb
Fluid filled pleural space
Lung tissue can slide around easily but it is difficult to separate it from the chest wall (hydrostatic forces)
Ppl
Intrapleural pressure
Inward pulling force of lung is balanced by outward pulling force of chest wall - creates negative pleural pressure
- About -5 cm water at rest
- Can be divided into two parts: compliance and resistance
P(A)
Alveolar pressure
P(TP)
Transpulmonary pressure
= P(A) - Ppl
Palv
Alveolar pressure
= 0 (atmospheric) at rest
Pneumothorax
Air introduced into pleural space through a hole in either the visceral or parietal pleura ~> lung collapse, chest springs outwards
- No lung movement when you breathe
External - pretty easy to fix (usually hit by car, etc.)
Internal - ventilating pneumothorax instead of alveoli (more difficult to fix - debride)
Esophageal pressure
Nearly the same as the pleural pressure
Transdiaphragmatic pressure
A measure of the strength of the diaphragm
Can be measured by putting a probe in the esophagus and a second down in the stomach
P(B)
Barometric pressure
= Patm
Asthma
Resistance problem
Emphysema
Compliance problem
Also decreases surface area because it destroys alveoli and makes them into one big one
- Increased compliance, decreased surface area
- Patients may look barrel chested
- Some treatment available
- FRC increases
Compliance
= deltaV / deltaP
Energy lost overcoming compliance is recovered during expiration
Fibrosis
Compliance problem
- Scar tissue forms, decreased compliance
- No treatment
- FRC decreases
- Ppl goes more negative during inspiration
Lung collapsing forces
Surface tension
Lung elastic recoil
Laplace Law
P = 2tau / r
P = the pressure necessary to keep the air bubble open Tau = surface tension r = radius
So the greater the radius, the lower the pressure required
In lung have lots of small alveoli (necessary for gas exchange) ~> wouldn’t be able to expand lung without surfactant to reduce surface tension
Atelectasis
Alveolar collapse
Surfactant
Phospholipid layer - creates air-oil interface (instead of air-water)
- Produced by alveolar type II cells late in the 3rd trimester
- 2 main functions: reduce surface tension (prevent airway collapse) and prevent transudation of the lung (water will not cross)
- Without surfactant you die
Total lung capacity (TLC)
Maximum volume of air you can fill the respiratory system with
Residual volume
Air still left in lung after you’ve exhaled as much as you can (varies by species)
Work of breathing
How much work the muscles have to do to ventilate the lungs
- Animals try to breathe to the minimum work of breathing
- If increased, you increase energy lost
W = {P dV
Total system compliance
Sum of lung compliance and chest wall compliance
Functional residual capacity (FRC)
Volume of air in respiratory system at rest position
The point at which the expanding force of the chest wall balances the collapsing force of the lung
- We breathe above FRC (where compliance is high)
- FRC decreases if you decrease lung compliance
- = expiratory reserve volume + residual volume
- Difficult to measure (inhale He)
Volume regulators
Newborns, cats, dogs
Ventilation regulators
Adult humans
Expiratory reserve volume
Volume between FRC and residual volume
Vital capacity
= inspiratory capacity + expiratory reserve
The max. amount of air we can move in and out of the respiratory system
Horses
Breathe around FRC at rest, instead of above it
- Active and passive inhalation, AND active and passive exhalation phases
Lung sounds
Increase because of increased resistance
Total ventilation
= alveolar ventilation + dead space ventilation
Resistance
You LOSE energy as heat to overcome resistance
- If you bronchodilate an animal and they get better then you have a resistance problem
- Resistance is affected by: driving pressure, diameter of tube, length of tube, viscosity of the gas
- Total area increases deeper in the lung, so total resistance goes down
Poiseuille’s Law
Vdot = pi(P1-P2)r^4 / 8nu(l)
R = (P1-P2) / Vdot = 8nu(l) / pi(r^4)
- Area = pi(r^2)
- nu = viscosity
- R = resistance
Stint
A hard tube inserted to hold a tube open
Doesn’t work well in respiratory because the tubes keep expanding and contracting
Conductance
The inverse of resistance
- Linear over varying lung volumes
Resistance over varying lung volumes
Hyperbolic relationship
Inhalation: airways expand, decreasing resistance
Exhalation: airways collapsing back down, increasing resistance
Air flow patterns
Laminar - straight, high velocity in center, lower at edges
Turbulent - increases with higher velocity (decreasing resistance increases velocity)
- Turbulence highest in the largest tubes
- Flow is very laminar in the small airways
- Turbulence can increase resistance
Pleural pressure during breathing
Resistance or compliance issues increase pleural pressure during breathing
- If big dip but comes back to specific point (compliance point) it’s a resistance problem
- If big dip and stays low then it’s a compliance issue
**When there’s no airflow (between inhalation and exhalation) all the pleural pressure is due to compliance (because there is no resistance)
Respiratory assist on venous blood return to the heart
From negative pressure created for inhalation
- Don’t get this on mechanical ventilation
Barotrauma
Some of the smaller airways may pop from high pressures during mechanical ventilation
Peak expiratory flow rate (PEFR)
A measure of total airway resistance
Limited by effort independent region
Effort independent region
For a given lung volume, there is an expiratory flow rate that cannot be exceeded no matter how hard you try due to increasing resistance (airways collapsing as you exhale)
Chronic obstructive pulmonary disease (COPD)
A resistance problem
With a resistance problem you get exercise intolerance because the work of breathing gets too high
Net expiratory pressure
= active pressure + recoil pressure
Equal pressure point (EPP)
In active exhalation, you put positive pressure on the whole respiratory system, not just the alveoli
As you go towards the mouth, pressure reduces to 0 (atmospheric)
So there is a point where pressure inside the tube equals pressure applied to the outside of the tube (squeeze pressure)
- Only happens with active exhalation, no EPP for passive exhalation
- Past EPP collapsing pressure decreases the radius and increases the resistance of the airway
- Why animals have trouble breathing with emphysema or asthma
- Increased expiratory effort ~> increased dynamic airway collapse
- There’s a point where you can’t increase velocity any more because resistance counteracts it
EPP with increased compliance
- With increased compliance, you lose some elastic recoil (have to compensate with active) so the EPP moves closer to the lungs
- Breathing through pursed lips moves EPP further up again by increasing resistance at the end of the system, so pressure backs up
Trapped gas
With high compliance EPP moves closer to the lung, where there’s less cartilage, so you can get small airway collapse
This traps gas and leads to hyperinflation (because you can still get air in, just not out)
- Problem in emphysema, etc. - regional issue
EPP with increased peripheral resistance
Stenosis (narrowing) from asthma, etc.
Increased resistance causes dissipation of energy
So EPP moves deeper into the lung ~> small airway collapse ~> gas trapping
Treat with bronchodilator
Dead space ventilation
The last gas in and the first gas back out
At the end of exhalation, the dead space is filled with gas that was in the alveoli
Terminal bronchioles
Just before alveoli start budding off
Respiratory bronchioles
Have alveoli coming off the sides
Division between conducting zone (dead space) and respiratory zone (alveoli)
Transition point between terminal and respiratory bronchioles
VdotO2
Rate of oxygen absorption into the blood
- Depends on blood flow and alveolar ventilation
VdotCO2
Rate of carbon dioxide release into the alveoli
Alveolar ventilation
VdotA = (VT - VD) * f
Can only be changed in 2 ways: volume and frequency changes
- Increasing tidal volume - greater effect on VA
- Increasing frequency - less work
Alveolar CO2
PACO2 = (VdotCO2 / VdotA) * k
PACO2 ~= PaCO2
PACO2 = rate you get rid of it over rate you’re bringing it to the alveoli, times the concentration
Alveolar O2
PAO2 = PIO2 - [(VdotO2 / VdotA) * k]
- Max is 149
- More complex than PACO2 because you have to account for atmospheric conc.
- Changing PIO2, VdotO2, or VdotA can change alveolar O2
- Can also express this using respiratory quotient and exhaled CO2
Hyperventilation
PCO2 is low
Hypoventilation
PCO2 is high
Breathing strategies
- Horse at rest breathes around FRC (stiff chested)
- Exercising quadruped gait limited, uses 1:1 gait-to-f
- Neonate active FRC
Lung diffusion constant
D(L) = DAalpha / X
D(L) = VdotO2 / deltaP(O2)
CO lung diffusion constant (DLCO)
D(L)CO = J(CO) / P(ACO)
Decreased in any condition that affects effective alveolar surface area and/or thickness
Gravity dependent alveolar ventilation
Easier to ventilate lower lung (in biped)
During diastole, poor perfusion to apical lung
So apical lung tends to be underperfused and underventilated - regional diffusion in the human
- Not as big a deal in quadrupeds (except in large, laterally recumbent animals - can shut off airflow to bottom lung)
Capillary transit time
Time the RBC is in contact with the alveolus
Normal is about 3/4 of a second
Can get problems with gas exchange if transit time is too short or if time required for gas exchange is increased (e.g. edema)
Pulmonary embolism
Clot in lung vasculature ~> shunt
Anatomical dead space
Incapable of gas exchange, doesn’t change
Physiologic dead space
lveolar regions that aren’t perfused + anatomical dead space
O2 transport methods
- Dissolved in plasma
2. Bound to Hb
C(O2)
Oxygen content
Oxygen solubility
= 0.003 ml O2/dL/mmHgO2
C(aO2)
= solubility * P(O2)
Hb-bound O2 content
= 1.39 [Hb] %saturation
P50
Partial pressure at which 50% of Hb is bound - a measure of O2 affinity of Hb
Factors affecting Hb affinity for O2
- pH (direct)
- CO2 (inverse)
- Temperature (inverse)
Total blood oxygen content
Sum of Hb bound and dissolved contents
= (1.39 X [Hb] X %saturation) + (0.003 X PO2)
Oxygen toxicity
FiO2 too high ~> production of radicals and oxidative damage to the airways
Volume of O2 extracted by the tissues
= CaO2 - CvO2
CO2 transport methods
- Dissolved
- Protein bound - carbamino compounds
- Bicarbonate
Carbonic anhydrase reaction
CO2 + H20 H2CO3 HCO3- + H+
Haldane effect
Affinity of Hb for CO2 changes depending on how much O2 is in the blood (and vice versa)
Ventilation-perfusion relationship
VdotA / Qdot
= 1 in normal ventilation
Hypoxemia
Below normal PaO2
5 causes of hypoxemia
- Hypoxic hypoxemia
- Alveolar hypoventilation
- Diffusion limitation
- Shunt
- VA/Q mismatch
- Hypoxic hypoxemia
causes of hypoxemia
Low PaO2, low PaCO2, low PIO2
- Low PaCO2 b/c low PIO2 makes you want to breathe more
- High altitude or O2 tank runs out
Tx: increase PIO2
- Alveolar hypoventilation
causes of hypoxemia
Low PaO2, high PaCO2
- Strong analgesics (barbituates - shut off CO2 response)
Tx: increase alveolar ventilation (just increasing PIO2 will shut off the last signal to keep breathing!!!)
- Diffusion limitation
causes of hypoxemia
Low PaO2, normal PaCO2
- Diffusion problem, insufficient capillary transit time
- PaCO2 normal to slightly low because it diffuses much faster and breathing will be stimulated
- Shunt
causes of hypoxemia
Low PaO2, slightly high PaCO2
- A/a gradient is a measure of shunt
- Thebecian veins - natural shunt
- Lateral recumbent horse
Tx: increasing PIO2 has no effect
- VA/Q mismatch
causes of hypoxemia
Low PaO2, high PaCO2
- VA/Q does not equal 1
- Partial airway or bloodflow restriction (much more common than complete)
- Smaller changes in CO2 because more soluble
Tx: increase PIO2
VdotA/Qdot extremes
Shunt extreme: perfusion, no ventilation
- VA/Q very low
- PAO2 approaches venous (40)
- PACO2 approaches venous (45)
Physiologic dead space extreme: ventilation, no perfusion
- VA/Q very high
- PAO2 approaches atmospheric (150)
- PACO2 approaches atmospheric (0)
When mixing blood
O2 content equilibrates (average)
Find PO2 from saturation curve
Pulmonary vessel constriction
Constricted region: - Lower blood volume going through - PAO2/CO2 approach atmospheric - So blood is doing lots of gas exchange, but low volume Normal region: 2 complications 1. Decreased transit time 2. Increased volume of Hb passing exchange surface 3. Increased oxygen extraction 4. Decreased CaO2/dL 5. Decreased PaO2 6. Hypoxemia
Respiratory quotient
R = VdotCO2 / VdotO2
Rate at which CO2 is released over rate at which oxygen is extracted
Alveolar gas equation prediction of PAO2
PAO2 = PIO2 - PACO2/R
PAO2 ~ PaO2
- PAO2 = 100 mmHg
- PaO2 = 95 mmHg
Normal shunt
Extracellular pH
7.35 - 7.45
Mechanisms for H+ regulation
- Extracellular buffering
- Adjustments to blood PCO2 by altering the ventilatory capacity of the lungs
- Adjustments to renal acid excretion or base resorption
Alkalemia
pH > 7.45
Acidemia
pH < 7.35
Acid
Proton donor
Base
Proton acceptor
Buffer
Reduces changes in pH resulting from addition of strong acids or bases
Dissociation constant (Henderson-Hasselbach equation)
HA H+ + A-
K = [H+][A-] / [HA]
pH = pKa + log ([A-]/[HA])
Strong acid: large K
Weak acid: small K
Buffers in the body
Bicarbonate
Phosphates
Proteins (Hb, etc.)
Buffer value
= delta[HCO3-] / deltapH
Respiratory acid
CO2
Metabolic acid
Any acid other than CO2
Respiratory acidemia
pH: low
PaCO2: high
HCO3-: normal
Compensation: kidney retains HCO3-
e.g. hypoventilation
Respiratory alkalemia
pH: high
PaCO2: low
HCO3-: normal
Compensation: kidney loses HCO3-
e.g. hyperventilation
Metabolic acidemia
pH: low
PaCO2: normal
HCO3-: low
Compensation: decrease CO2 (hyperventilation)
Lots of disease states (e.g. diabetes, heart failure, renal failure, diarrhea)
Metabolic alkalemia
pH: high
PaCO2: normal
HCO3-: high
Compensation: increase CO2 (hypoventilation)
e.g. loss of H+ through vomiting
3 components of the respiratory control system
- Central neural activity
- Peripheral sensory neural feedback
- Chemical status of blood and CSF
Medulla
Both essential and sufficient for generating the pumping actions of the respiratory system
- Irregular with no other higher centers
Apneustic center
In caudal pons
Without higher centers this generates long sustained inspiration with short expiration
Produces the on signal
Pneumotaxic center
In rostral pons
Without higher centers, this provides a regular rhythm to the respiratory cycle
Produces the off signal
Phrenic nerve
Innervates diaphragm (inspiratory)
Rat/human: 3,4,5, to stay alive
Dog/cat: 5,6,7 to keep you from heaven
Medullary oscillator
= brainstem oscillator = respiratory control neural network
Interneurons and inspiratory and expiratory neurons in the medulla
The central control - everything else is modifying this system
Slowly adapting pulmonary stretch receptors (PSRs)
Endings in epithelium of the airway
Myelinated (fast conducting)
When lung expands, you get APs
Gives information about how much you are inflating the lung
Rapidly adapting pulmonary stretch receptors (PSRs)
Inspiratory inhibitory/protectory - prevents animal from breathing on top of hyperinflation
Burst of APs during inflation that falls off quickly (rapidly adapting)
- Also respond to certain chemicals (e.g. smoke)
Gives information about the rate of inflation
Vagus nerve
Primary sensory pathway from the lung to the brain
- PSRs travel in it
Pulmonary C-fibers
Unmyelinated (slow conducting)
Alveoli surface - sit between alveolus and capillary
Chemoreceptors
Give information on the status of the respiratory surface/diffusion barrier (e.g. edema)
Bronchiole C-fibers
Unmyelinated
Bronchiole surfaces
Chemoreceptors
Give information on irritants, chemicals, particles, etc. in the epithelium of the conducting airways
Respiratory muscle afferents
- Muscle spindles
- Tendon organs
- Joint receptors
Also need to know if the pump is providing the right force (monitor work of breathing)
Tell us whether the pump is pumping or not
Muscle spindles
Monitor muscle length
Tendon organs
Monitor muscle tension (a function of muscle length)
Joint receptors
Measure the rotation of the ribs at the costovertebral joints
Aortic bodies
Measure PO2 in aorta (NOT content)
- Low oxygen ~> higher AP frequency
- Low O2 sensed by PNS only
Also monitors H+ (~CO2)
- High H+ ~> higher AP freq.
Carotid bodies
Measure PO2 in carotid (NOT content)
- Low oxygen ~> higher AP frequency
- Low O2 sensed by PNS only
Also monitors H+ (~CO2)
- High H+ ~> higher AP freq.
Low O2 response
Increase breathing frequency
High CO2 response
Increase tidal volume
Hypoxic response index
deltaV(E40) = isocapnic increase in V(E) when P(ACO2) is reduced to 40 mmHg
CO2 sensing
Sensed in both peripheral blood (carotid and aortic bodies) and CSF
About 60% are central - sensitive to H+ and to a lesser extent
Dysphagia
Disordered swallow
- Some therapy available
Dystussia
Disordered cough
- No therapy exists
Reflex pathway for cough
Larynx (?) + lungs/airways (RARs, SARs, C-fibers) ~> superior laryngeal n. (larynx) + vagus n. (lung) ~> brainstem cough generator ~> respiratory muscles
Diving response
Nasal/facial receptors ~> trigeminal n.
~> sympathetic nerves ~> vasoconstriction
~> vagus n. ~> bradycardia
~> apnea
Laryngeal chemoreflex
Larynx ~> superior laryngeal n. ~> swallowing + laryngospasm + apnea + (~> vagus n. ~>) bradycardia
Primarily a neonatal response - prevents aspiration of fluids
Bronchomotor tone
Baseline contractile activity
Epiphase
Viscous mucus
Hypophase
Layer of serous fluid that the mucus floats on
Hering-Breuer reflex
Mediated by slowly adapting PSRs
Hyperinflation of the lungs leads to apnea