What makes up the bony skeleton of the thorax?
-12 ribs, 12 vertebrae, sternum
Which muscles are involved in quiet inspiration and expiration?
Inspiration: diaphragm, external intercostals Expiration: largely passive recoil of the lungs
Which muscles are involved in forced inspiration and expiration?
Forced inspiration: diaphragm, external intercostals, accessory muscles (scalenes, sternocleidomastoid)
Forced expiration: abdominal, internal intercostals, neck and back muscles
How are pressures in the lung measured?
in mmH20, relative to atmospheric pressure
What is the normal tidal volume?
What is the normal dead air space?
What is the normal functional residual capacity?
Anatomic (in conducting airways): 150 mL (~ 1mL per pound of body weight)
Alveolar (in respiratory airways): 25 mL
Physiologic= anatomic + alveolar
Conduction airways vs. gas-exchange airways?:
-which structures are part of wach category?
-how many divisions in the lungs and names of the divisions, starting with trachea
Conducting airways are: nasal cavities, nasopharynx/oropharynx, larynx, trachea, bronchi, bronchioles.
Gas exchange (respiratory) airways are: respiratory bronchioles, pulmonary alveoli
- Conducting zone is from trachea (0) to 16 trachea-->bronchi-->bronchioles-->terminal bronchioles
- Gas exchange zone (17-23) respiratory bronchioles-->alveolar ducts--> alveolar sacs .
2 general ways to get a pneumothorax
- air can penetrate directly from the atmosphere into the pleural space, or can go through a rupture pulmonary bullae
The static lung volumes and what they are
Resting tidal volume: what you normally breathe in and out.
Inspiratory reserve volume: how much you can breathe in on top of the resting tidal volume
Expiratory reserve: how much you can breathe out past your normal tidal volume
Residual volume: dead air. The volume of air always in the lungs
The lung capacities and what they are
Inspiratory capacity (IC): tidal volume+ inspiratory reserve volume
Vital capacity (VC): tidal volume + inspiratory reserve volume + expiratory reserve volume
Functional residual capacity (FRC): expiratory reserve volume + residual volume
Total lung capacity (TLC): everything!
Which volume cannot be directly measured by spirometry?
The residual volume and therefore the functional residual capacity (FRC) and the total lung capacity (TLC) cannot be measured by spirometry.
Volumes are determined by... Capacities are determined by..
Volumes are determined mostly by respiratory effort (except RV). Capacities are determined mostly by the size of the chest/lungs
What are the mechanical properties of the chest wall and lungs at rest?
The chest wall wants to EXPAND due to:
- the tendency of the ribs to spring outwards
- the resting tension of the muscles of respiration
The lungs want to RECOIL due to:
- the elasticity of the lungs
- surface tension in alveoli
What is intrapleural pressure at rest and what is it determined by?
Pressure in the intrapleural space (Ppl). The inward recoil of the lungs and the outward recoil of the chest wall create a partial vacuum that is -5 mmH20
**it will fluctuate with breathing, but is always less than atmospheric**
What is transpulmonary pressure and what is it determined by?
The transpulmonary pressure is the alveolar pressure minus the intrapleural pressure. It is a distending force that determines the volume of alveoli
Ptp= Palv - Ppl
How to increase the Ptp ?
You can force air into the alvoeli (increase Palv ) or make the intrapleural space more negative by sucking air out of it (Ppl)
What is Boyle's law?
pressure is inversely proportional to volume
How and why does air flow into the alveoli during respiration
1) expand the chest --> makes intrapleural pressure even more negative
2) therefore the transplural pressure increases and the alveoli expand
3) an expanded alveoli with the same volume has a lower pressure
4) air flows from high to low pressure until pressures are equal
How and why does air flow out of alveoli during expiration?
1) inspiratory muscles relax--> intrapleural pressure becomes less negative
2) transpulmonary pressure decreases-->alveoli decrease in size
3) Pressure increases in alveoli (via Boyle's law)
4) air flows out of alveoli until the pressure in the alveoli is the same as atmospheric
What forces must respiratory muscles overcome to initiate inspiration?
1) the recoil of the lung from elastin and surface tension
2) frictional resistance to air flow (and to a much lesser extent the friction from the deformation of the lungs --> tissue resistance)
What happens to the elastic recoil of the lung in emphysema and pulmonary fibrosis? How do the static volumes and capacities change.
Emphysema: loss of elastin makes the lung easier to inflate (loss of elastic recoil), but more likely to collapse during expiration. Airways are then narrower and resist flow more. The residual volume (RV) increases, so FRC and TLC also increase.
Fibrosis: deposition of collagen makes the lung more difficult to inflate (increased elastic recoil). RV decreases, so FRC and TLC decrease too.
What are two big actions of surface tension in alveoli?
1) Contributes to elastic recoil of lung because it acts to make the alveoli as small as possible
2) Promotes alveolar instability
Laplace's Law for alveoli
-what does this mean for alveolar stability?
-what reduces the pressure in an alveoli?
P=(2*surface tension/ radius)
Small alveoli are higher pressure and will collapse into larger alveoli.
Surfactant helps reduce the pressure generated from the surface tense and opposes alveolar instability
What is compliance? What does it assess?
A measure of the distensibility of an elastic structure (e.g. the lung): change in volume/change in pressure. It is a way of assessing the elastic recoil against which the muscles of the chest have to work to expand the thorax.
What do the static compliance curves for a normal lung, a fibrosed lung and an emphysemic lung look like?
What are the determinants of airway resistance?
1. pattern of airflow: turbulent flow requires a higher driving pressure to produce the same flow rate as laminar flow
2. airway dimension: larger radius, less resistance
How much do small radius airways contribute to airway resistance? Why?
Not much because they have such a high total cross-sectional area- it's like pouring water through a honeycomb (many small airways for the same volume) instead of through a funnel (few bronchi for the same volume)
How does elastic recoil of lungs and outward recoil of the chest wall determine the functional residual capacity?
If the lungs have greater recoil, they will pull the chest wall in more than usual and there will be a smaller residual volume.
If the lungs have less elastic recoil than usual, they will be pulled out by the chest wall more than usual and there will be a greater residual volume
FRC (the end of a quiet expiration) is the point at which these are balanced
What are 4 main functions of the respiratory system?
-movement of air (inspiration and expiration)
What are two main kinds of assisted ventilation and which is more common and which has fewer complications?
Negative pressure: iron lung, or cuirass. Less common, but fewer complications
Positive pressure: more common, but more complications
What is an important function of the FRC?
The FRC is the amount of air left in the lungs after a normal expiration. This volume continues to participate in gas exchange and maintains continuity of oxygenation of the blood.
Restrictive lung disease vs. obstructive lung disease
Restrictive lung disease is anything that reduces the compliance of the lungs (e.g fibrosis, chest wall deformities) and therefore makes it harder to breathe
Obstructive lung disease is anything that prevents air from entering the lungs and therefore makes it hard to breath (e.g. epmphysema where the airway resistance is really high, asthma, epiglotitis)
What is FEV1 and FVC? What are these values used for?
FEV1: the forced expired volume in 1 second, from maximal inhalation
FVC: forced vital capacity: the total volume of air expired from max inspiration to max expiration
They are used as a surrogate measure for airway resistance (they assess the flow instead of the resistance directly)-->the more airway resistance, the more the work the muscles of the chest have to do to breathe
What does FEV1:FVC look like in restrictive and obstructive lung disease?
In patients with obstructive lung disease it tells you if there is more resistance than a normal person (normal is 80%). Both values will be reduced, but the FEV1 will fall proportionally more than the FVC
In patients with restrictive lung disease FEV1 and FVC will both be reduced, but by the same proportion.
What is FEF25-75%? What does it depend on? What does a reduction indicate?
Forced expiratory rate between 25% and 75% points of a forced expiration
Dependent on age and sex
Reductions indicate obtructive lung disease
Restrictive lung disease usually has a normal value
What are the layers of the intercostal muscles? Where do the intercostal nerves and vessels run?
What are the important vessels in the thorax?
Spatial location of the phrenic nerve and vagus nerve in the thorax?
Location of the right and left recurrent laryngeal nerves?
The right recurrent loops around the right subclavian artery and the left recurrent loops around the aortic arch.
Lung fissure locations in the lateral view
Lung fissures in the posterior view
Lung fissures in the anterior view
Basic anatomy of the diaphragm
What 3 variables is successful gas exchange in a unit of lung dependent on?
1) alveolar ventilation
Define minute ventilation and alveolar ventilation
Minute ventilation: the amount of air that enters the lung per minute (tidal volume x RR)
Alveolar ventilation: the volume of air that enters the alveoli per minute ( [tidal volume-dead space] x RR
What are the normal PaO2, PaCO2, PAO2, PACO2, PvO2, PvCO2?
Mixed venous blood
- PvO2= 40 mmHg
- PvCO2= 46 mmHg
- PaO2= 95 mmHg
- PaCO2= 40
- PAO2= 100 mmHg
- PACO2= 25 mmHg
What is the alveolar ventilation equation? What does it signify?
PaCO2= (volume of CO2 produced per minute/ alveolar minute ventilation)=VCO2/VA
PaCO2 is kept within a narrow range in the body, so if there is an increase int he production of CO2, then there must be an accompanying increase in the alveolar ventilation.
Hypoventilation: a rate of ventilation that is insufficient to meet the body's metabolic gas exchange needs. A rise in PaCO2 (hypercapnia)
Hyperventilation: a rate of ventilation that is higher than required to meet the body's metabolic gas exchange needs. A fall in PaCO2 (hypocapnia)
What is the alveolar (air) gas equation?
PAO2= FiO2 (Patm-PH20)- PaCO2/R
- Patm= 760 mmHg
- PH20= 47 mmHg
- R= 0.8 for typical north american diet
- PaCO2 ~ PACO2
What is the A-a gradient? What is it's normal range? What does a derangement signify?
Normally 10-20 mmHg due to imperfect diffusion +/- V/Q matching, and deoxy blood from the lung tissue goes back to the heart in the same vessels.
The A-a gradient helps differentiate between causes of hypoxemia
Hypoxia: when the whole body is oxygen deprived
Hypoexmia: when arterial blood is oxygen deprived
What are the 5 causes of hypoxemia?
1) lower PiO2 (normal A-aDO2)
2) hypoventilation (normal A-aDO2)
3) diffusion impairment (high A-aDO2)
4) V/Q mismatch (high A-a DO2)
5) Shunt (high A-a DO2)
What is Fick's Law and what are the key factors that affect gas exchange across the alveolar-capillary membrane?
Rate of gas transfer is proportional to
- tissue area
- the partial pressure difference between the two sides
- the diffusion coefficient of the gas
And inversely proportional to
- the thickness
What are the 3 distinct components of the neural control of breathing?
Factors that generate the alternating inspiration/expiration rhythm
Factors that regulate the magnitude of ventilation (rate and depth)
Factors that modify respiratory activity for other purposes (speech, coughing, sneezing...)
What kind of neurons control the muscles of respiration and what nerves do they come from?
Motor neurons from the phrenic nerves control diaphragmatic contraction.
Motor neurons from the external intercostal nerve controls the external intercostal muscles.
Motor neurons from the internal intercostal nerve controls the internal intercostal muscles.
What is the firing pattern of the phrenic nerve, external intercostal nerve and internal intercostal nerve during quiet and active respiration?
Phrenic nerve: bursts of firing during inspiration that intensify during active respiration
External intercostal nerves: bursts of firing during inspiration that intensify during active respiration
Internal intercostal nerves: no firing during quiet respiration, bursts of firing during active expiration.
What are the respiratory centres that establish rhythm and what are the respiratory centres that regulate rhythm?
dorsal respiratory group (DRG): primarily inspiratory neurons
ventral respiratory group (VRG): 2 areas expiratory, one area inspiratory
- pontine respiratory group (PRG): inspiratory and expiratory. regulates smoothness of breathing
The central pattern generator (CPG) is probably in the VRG and establishes the rhythm, and the rest regulate the rhythm.
What do slow-acting stretch receptors do?
They are stimulated by lung inflation, and the more they are stimulated the longer we exhale (so that we breathe out the same amount we breathe in)
What do rapidly adapting stretch receptors do?
These are irritant receptors, stimulated by chemical and mechanical stimuli. They cause cough, bronchospasm and increased mucus production
What do flow receptors do?
when high air flow hits your nose you decrease your ventilation
Where are peripheral and central chemoreceptors and what do they each respond to?
- carotid bodies and the aortic arch (have afferents to the medulla)
- respond to PaO2 and pH (which reflects changes in PaCO2)
Central chemoreceptors are located in the medulla
- Responds to H+ in the CSF which is produced by the coversion of CO2 (H+ can't diffuse across the BBB, but CO2 can)
- Does not response to PaO2
When does a drop in PaO2 trigger increased ventilation? Why is it not an immediate reflex?
When you get to ~60 mmHg. According the the oxy-Hb dissociation curve, Hb is still well saturated until about 60 mmHg
When does a drop in PaCO2 trigger an increase in ventilation?
-Triggered with any small rise. Note that none of the chemoreceptors measure PaCO2 directly
What are the chronic effects of emphysema on blood gases and how is the drive to breathe in an emphysemic patient altered? What would happen if you gave supplemental O2 to a patient with COPD?
- chronic hypercapnia
- chronic hypoxia
Central chemoreceptors adapt to the chronic hypercapnia, and so most of the drive to breathe comes from peripheral chemoreceptors sensing hypoxemia, therefore: giving supplemental O2 can decrease the drive to breathe.
What is the instigating factor in sleep apnea?
- a narrow upper airway that required neuromuscular compensation to keep open
- during sleep the neuromuscular compensation stops and the airway collapses
What are some things that can contribute to alveolar hypoventilation (hint: think of the PBL case with Frank Daly)?
shallow breathing due to pain
Principles of acute pain management (2)
-provide enough medication so that the pain is tolerable to the patient
Do you need permission to perform a blood alcohol level in the emergency department?
No, it is part of a diagnostic work-up