Introduction Flashcards
Principles of Pulm Med Chapters 1 and 2, and pages 30-34, Chapter 4, and Chapter 22 1. List the components of the chest wall and relate the functions of the muscles of respiration to the movement of air into and out of the alveoli. 2. Describe the exchange of oxygen and carbon dioxide with the atmosphere and relate gas exchange to the metabolism of the tissues of the body. 3. Demonstrate the ability to obtain a health history focusing on the pulmonary process. 4. Discuss physical examinati
Decreased arterial PO2
hypoxemia
increased PCO2
hypercapnia
What is the alveolar gas equation?
PAO2 = FiO2(Pb-PH2O)-(PaCO2/R) which means the alveolar pressure of oxygen is equal to FiO2–fraction of oxygen in inspired air (RA is 0.21) Pb–barometric pressure (760mmHg) PH2O–vapor pressure of water in the alveoli (~47) PaCO2–arterial CO2 tension R–respiratory quotient (CO2 out/O2in = 0.8)
Is there any simpler alveolar gas equation for measurements taken at sea level?
PAO2 = 150-(1.25 x PaCO2)
what is transpulmonary pressure?
the alveolar pressure minus the pleural pressure
If there is air inside the alveoli of the lungs would you expect the pressure to be higher in the alveoli or the pleural space?
pressure would be higher in the alveoli. (or more negative in the pleura)
Your oxyhemoglobin dissociation curve relates the pressure of O2 in the blood to the amount of O2 that is bound to hemoglobin. If this curve has shifted to the _________, oxygen becomes easier to unload (harder to bind). A shift to the ________, makes oxygen harder to unload (easier to bind)
right, left
A right shift means that the body is trying to ______________ oxygen
get rid of
A left shift means that the body is trying to _____________oxygen
hang onto
What are some factors that would cause the body to want to keep oxygen? What direction would this shift be?
increase in pH (alkalosis); decrease in CO2, decrease in temperature are factors causing LEFT shift
Your primary respiratory muscle is the ___________.
Diaphragm
If you needed extra accessory muscles to help you inspire, you’d use what?
SCM, EXternal intercostals and scalenes
If you needed extra accessory muscles to help you expire, you’d use what muscles?
INternal intercostals, external obliques and rectus abdominis
what is the term for dyspnea that occurs in the supine position, typically as a result of a decrease in vital capacity
orthopnea
what is the term for dyspnea that occurs hours after lying down in a supine position resulting from increased venous return to the heart causing interstitial edema? What health problems can cause this?
Paroxysmal Nocturnal Dyspnea. Seen frequently in CFH and occasionally with asthma
what type of pulmonary disease is defined by a low FEV1 and a low FEV1/FVC%? What are some examples of this type of disease?
Obstructive pulm dz, ex: asthma, chronic bronchitis, emphysema, COPD
what type of pulmonary disease is defined by a decrease in the tidal volume of air, but not the rate of its flow?
Restrictive pulm dz
What are the main functions of the lungs?
1) gas exchange 2) protective fxn 3) circulatory fxn (shares vasculature with heart and directly effects cardiac output)
I am an air molecule, I’m entering the lungs in the trachea and destined for the alveolus. What neat sites am I going to see on my way?
mainstem bronchus (oh boy!), lobar bronchus, segmental bronchus, bronchiole, alveolar duct, and destination alveolus!!
In a normal person, during tidal breathing would you expect the active process to be inspiration or expiration?
Work to breath in, expiration is result of elastic recoil
What do the following things stand for: RV, ERV, IRV, TLC, FRC, TV, VC, FEV1?
RV–residual volume ERV–expiratory reserve volume IRV–inspiratory reserve volume TLC–total lung capacity FRC–functional residual capacity TV–tidal volume VC–vital capacity
FEV1–forced expiratory volume per second
In a healthy lung, what is the partial pressure of O2 in the alveoli? what is the partial pressure of O2 in the arteriole?
100mmHg in both
In a healthy lung, what is the partial pressure of CO2 in the Alveoli? what about in the arteriole?
40mmHg in both
If your patient had an airway obstruction and the partial VENOUS pressure of O2 was 40mmHg, what would you expect the partial pressure of O2 to be in the alveoli? The arterioles? AND what would happen as a result of the airway obstruction?
40mmHg in the alveoli, 40mmHg in the arteriole. No gas exchange is occurring due to obstruction, so the lungs will have vasoconstriction which will SHUNT blood away from that part of the lung, to an area where it can receive oxygen.
If your patient has a blood clot in the capillaries just before reaching the alveoli, what will likely happen?
The alveoli will constrict, creating a dead space by diverting its air supply to other well perfused alveoli
What is the expected Alveolar-arterial gradient for O2 in a healthy person?
Patient’s age/10 + 10. (on room air. if patient is on O2, the A-a increases 5-7mmHg for every 10% increase in FiO2) the larger the gradient, the more serious the respiratory compromise
what are some problems that could cause a large A-a gradient?
alveolar membrane dz, shunt, interstitial dz, VQ mismatch
So, your patient is 70 and in the office for dyspnea on room air. You’d like to determine her optimal A-a gradient to see if you can tell if there is a problem when you plug her actual values into the alveolar gas equation. What is her target A-a gradient?
17
1) Low inspired oxygen (high altitude)
2) Hypoventilation (drugs, neurologic injury, anesthesia, severe lung disease)
3) R>L shunt (intrapulmonary or intracardiac)
4) Ventilation/perfusion inequality
5) Decreased diffusion (diseases which reduce effective area for gas transfer or thicken the alveolar wall)……could all cause ______________
hypoxemia
what effect on the lungs is the end result of smoking?
INCREASED RESISTANCE TO FLOW. (resulting ffrom chronic irritation causing overproduction of thick mucus, hypertrophy of mucus glands, bronchial wall thickening, and bronchoconstriction)
what effect on the alveoli is the end result of smoking?
REDUCED ELASTIC RECOIL (old slinky phenomenon)
What happens when the air pressure inside the alveoli becomes less than the pressure in the pleural space?
The increased pressure in the pleural space will collapse the bronchioles and patients will have to work to force air out.
what happens to your COPD patient when they try to breath faster to compensate for their dyspnea?
Breathing faster does not help because the flow of air out of your lung is so slow that you do not have enough time to fully expire. The amount of air left in your lung at the end of an expiration (FRC) increases with each breath (dynamic hyperinflation)
As your COPD patient experiences dynamic hyperinflation, how would they feel subjectively?
Like they are suffocating, because their lungs are already full of air, and they need to keep inhaling to get enough oxygen, but there isn’t room
If there is an increase in the partial pressure of CO2, it will trigger a(n) ____________ in minute ventilation, which maintains PaCO2 and pH levels withing the normal range.
increase! This is allows matching of ventilation with perfusion
If PaCO2 levels rise, respiration rate increases to try to get rid of it. What do we call this?
Ventilation
If the capillary blood in an alveoli does not experience a gas exchange, what defense mechanism will occur?
Shunting
How does the bronchiole tree itself contribute to the defense of the lung against infection?
The many branching points interrupt the laminar flow of air that potentially contains particles. This particles will hit an air current (eddy) and particles will likely stick to the mucosal lining in the lungs before reaching distal lung
What’s one of the main ways the lungs rid themselves of foreign bodies?
mucociliary transport/clearance
What layer of the lungs contains the antimicrobial peptides that are important to immunity? What are some of these peptides?
the SOL layer. Peptides include the lysozymes, lactoferrins, and defensins, collectins (surfactant proteins A and D)
What cells are responsible for scavenging the particles and bacteria in the airways and alveoli?
the pulmonary alveolar macrophages
The primary function of ______- cells is to sample the airway microenvironment, ingest and process antigens and then migrate to regional lymph nodes to prepare an immune response
dendritic cells (Langerhans cells are dendritic cells)
These cells respond to a bacterial infection by promoting an inflammatory response and then directly attacking and killing bacteria
Polymorphonuclear leukocytes
______________ cells are part of the rapid initial response and are capable of killing microorganisms without prior sensitization
Natural born killer cells
which response involves recognizing and responding to specific antigenic materials after prior sensitization?
Adaptive immune responses
What is the defense mechanism that secretes IgA and IgG in order to bind to viruses and bacteria, preventing their attachment to epithelial cells?
Humoral immune mechanisms
T lymphocytes are capable of interacting with the humoral immune system to modify antibody production. They are known to produce cytokines which attract macrophages. What part of the immune response do T cells belong to?
Cellular Immune Mechanisms
Coughing is a routine and necessary defense mechanism of the lungs. What patients may have trouble coughing?
weak/paralyzed diaphragm, quadriplegic will not be able to have a full inspiration, tracheostomy, paralyzed vocal cord
what types of surfaces allow for optimal diffusion?
thin with a large surface area
This difference in inflation and deflation volumes at a given pressure is called ______________
hysteresis
