Respiratory System Study Guide PDF

Study Guide Respiratory System (Week 10) A. Airway Anatomy 1. Briefly compare the distribution of cartilage and smooth muscle between the trachea, bronchi, bronchioles, and respiratory bronchioles i. Cartilage decreases distally in airways...

Study Guide Respiratory System (Week 10) A. Airway Anatomy 1. Briefly compare the distribution of cartilage and smooth muscle between the trachea, bronchi, bronchioles, and respiratory bronchioles i. Cartilage decreases distally in airways (a) Most cartilage is in trachea (b) No cartilage in bronchioles ii. Smooth muscle wherever there isn’t cartilage (a) Bronchioles are almost entirely smooth muscle (a) Exception – respiratory bronchioles 2. State where the greatest resistance to airflow is within the respiratory tract and explain why this is so i. Bronchioles have greatest resistance (a) Have smooth muscle, so they can bronchoconstrict (b) Don’t have cartilage to hold them open B. Airway Function and Dysfunction 1. Describe how ventilation influences airway resistance i. Inspiration – airway resistance decreases (a) As lungs inflate, all tissue gets pulled apart (b) This pulls open the airways ii. Expiration – airway resistance increases (a) As lungs deflate / are compressed, the airways become compressed (b) Since airway size decreases, resistance increases (c) If airway resistance is really high, we get turbulent airflow, which causes a WHEEZE (a) If we can’t get “old” air out of the alveoli, that means there is no room to get “new’ air in (b) That means we can’t effectively carry out normal gas exchange 2. Briefly describe factors which cause bronchoconstriction and bronchodilation i. Sympathetic (neuroepinephrine and epinephrine) (a) Bronchodilation ii. Parasympathetic (Acetylcholine) (a) Bronchoconstriction 3. State three main ways that airway resistance is increased in disease states i. Muscle contraction (bronchoconstriction) (a) Can be acute (e.g., bronchoconstriction during an asthma attack) (b) Can be chronic (e.g., smooth muscle hypertrophy from chronic inflammation) ii. Inflammation (a) Blood in airway walls (b) Edema in airway walls iii. Blockages in airway lumen (a) Mucus  (b) Tumors (c) Foreign objects 4. Briefly describe clinical mechanisms to reduce airway resistance i. Bronchodilators (a) Activate β-adrenergic receptors to cause bronchodilation ii. Inhaled steroids (a) Reduce inflammation 5. Describe the effects of decreased lung compliance (i.e., increased lung stiffness) i. Causes (a) Chronic inflammation (b) Scar tissue ii. If the lung tissue is stiffer, then (a) It takes more effort to inflate the lungs (a) This requires more ATP, and thus increases metabolic rate (b) The lungs may not be inflated all of the way (a) This can ultimately lead to impaired gas exchange (c) The lungs will not recoil as much during expiration (a) Active expiration may become necessary (b) This requires more ATP, and thus increases metabolic rate C. Partial Pressure 1. Describe the concept of partial pressure i. Blood gases are measured in terms of partial pressure, which is why it is important to understand what these numbers mean (a) Note: partial pressure only measures the amount of gas DISSOLVED in the blood (a) For example, oxygen attached to hemoglobin does directly count towards the partial pressure of oxygen in the bloodstream ii. Partial pressure is the product of: (a) Atmospheric pressure (a) 760mmHg at sea level (b) Percent of a given gas in the atmosphere (a) Atmosphere is made of approximately 21% oxygen (c) So, 760mmHg x 21% = 160mmHg O2 2. State the abbreviations associated with respiratory gases i. Abbreviations about the air itself (a) PO2 = Partial pressure of oxygen (a) Generic term, but usually refers to that of the air we are breathing in (b) About 160mmHg at sea level (c) This decreases with higher altitude/elevation (b) FO2 = Fraction of oxygen in the air (a) Atmospheric air is about 21% oxygen, regardless of elevation/altitude (c) FiO2 = Fraction of oxygen in the air we breathe in (a) This is 21% if we just breathe the air from the atmosphere (b) This can be manipulated for clinical  (i) Clinical example: a patient with pulmonary disease may be given supplemental oxygen – if they breathe in 100% oxygen, their FiO2=100 ii. Abbreviations specific to the body (a) PAO2 = Alveolar partial pressure of oxygen (a) About 100-105mmHg at sea level (b) Note, this is an UPPERCASE “A” (b) PaO2 = Systemic arterial partial pressure of oxygen (a) About 100mmHg at sea level (about the same as in the alveoli) (b) Note, this is a lowercase “a” (c) PvO2 = Systemic venous partial pressure of oxygen (a) About 40mmHg at sea level while at rest (b) DECREASES during exercise (as we extra more oxygen out of the blood at the level of the capillaries) iii. We use the same system for other gases (a) For example, PACO2 is the partial pressure of carbon dioxide in the alveoli D. Gas Exchange 1. Describe the process of gas exchange in the alveoli i. Gases follow their concentration gradient, moving from high partial pressure to low partial pressure (a) Oxygen moves from alveolus to blood (a) Partial pressure of oxygen in the alveoli is high (PAO2 is 100-105mmHg) (b) Partial pressure oxygen in pulmonary capillaries is low (40mmHg at rest, lower during exercise) (b) Carbon dioxide moves from blood to alveolus (a) Partial pressure of CO2 in pulmonary capillaries is higher (45mmHg at rest) than that of alveoli (40mmHg) ii. Oxygen must move through (a) Any fluid in lungs (e.g., surfactant) – don’t worry about this (b) Alveolar epithelium (Type I alveolar cells) (c) Epithelial basement membrane (d) Interstitial space (e) Capillary basement membrane (f) Capillary endothelial membrane 2. Describe factors which will limit gas exchange in the alveoli i. Reduced gas concentration gradient (a) May be reduced at high altitude (since PO2 is lower in atmosphere) (b) May be reduced with pulmonary pathology (difficulty removing “old” air and bringing in “new” air) ii. Reduced surface area of membrane (a) Fluid or mucus in alveoli (blocking epithelial surface) (b) Reduce number of active alveoli (e.g., a blocked airway) (c) Reduced total surface area (e.g., alveoli merging together in emphysema) iii. Increased distance between alveoli and capillary (a) Fluid or mucus in alveoli  (b) Fluid in interstitium (c) Scar tissue E. Ventilation-Perfusion Matching 1. Describe the concept of ventilation-perfusion matching i. For gas to be exchanged between the alveoli and the bloodstream, there must be blood flow to the alveoli (a) If the alveoli is not inflating or blocked, there is no gas to exchange, even if blood flow is fine (b) If the capillary is blocked, there is no opportunity for gas exchange, even if the alveolus has air (c) So, we need to match ventilation and perfusion – have enough air in the alveolus and blood flowing through the capillary to perform gas exchange 2. Briefly describe how pulmonary blood flow changes during exercise, including the effects on pulmonary vascular resistance i. Increases >4x during exercise (a) Increased number of open capillaries (decreases vascular resistance) (b) Distending open capillaries to increase rate of blood flow (decreases vascular resistance) 3. Briefly describe the concept of “dead space” and how it relates to expiration i. Air which never reaches the area of gas exchange ii. Air from dead space is removed first, therefore making it more difficult to remove expiratory gases from the alveoli 4. Differentiate between anatomical and physiological dead space i. Anatomic – areas of the respiratory tract where gases cannot be exchanged ii. Physiologic – alveoli where there is incomplete perfusion to allow for gas exchange 5. Briefly describe the danger of a pulmonary embolism i. Blood clots in the pulmonary vessel (a) May be one large blood clot blocking a major pulmonary vessel (b) May be multiple small blood clots blocking many small pulmonary vessesl ii. This causes a lack of perfusion to alveoli, so gas exchange cannot take place (a) “New” oxygen cannot enter blood stream from alveoli (b) “Old” carbon dioxide cannot leave blood stream and go into alveoli iii. The clots also increase resistance in the pulmonary vessels (a) This means that the right side of the heart faces a greater afterload, and has to work harder F. Blood Gas Transport 1. State the normal ways that oxygen is transported in the blood, and the relative contribution of each i. Bound to hemoglobin (97%) ii. Dissolved (3%) 2. Rank the different forms of carbon dioxide transportation in the blood i. Bicarbonate (most, ~70%) ii. Bound to hemoglobin (95%) during even the very most intense exercise in most healthy individuals (some exceptions in elite athletes) 2. Describe some limitations of pulse oximetry i. It only tells you what percentage of the hemoglobin that you have is saturated – it does NOT tell you how much hemoglobin you have! (a) This means it doesn’t tell you your oxygen carrying capacity (a) Example – a person who has lost a substantial amount of blood will still have a normal pulse oximeter reading, since the remaining red blood cells they have likely still have a normal percentage of their hemoglobin bound to oxygen ii. It doesn’t tell you WHAT is bound to hemoglobin (a) Under most conditions, oxygen is what is bound to hemoglobin, BUT carbon monoxide binds to hemoglobin also. So a patient with carbon monoxide poisoning will have a  normal pulse oximeter reading, because their hemoglobin is saturated (but not with oxygen) iii. It is affected by skin pigmentation (a) Greater melanin levels in the skin can interfere with pulse oximeter readings, and make them appear higher than they are (b) This is exacerbated at low hemoglobin saturation levels (a) Hypothetical example – a patient whose actual hemoglobin saturation is 80%, may have a pulse oximeter reading of 90%, and thus appear to have a more mild condition than they really do, and therefore not receive sufficient treatment H. Describe the role of blood gases in regulating ventilation 1. BIG PICTURE = High levels (partial pressures) of carbon dioxide in the blood increase ventilatory stimulus! i. DETAILS (a) Central chemoreceptors in medulla (The major controller) (a) Stimulated by increased hydrogen ions and carbon dioxide (i) There’s nuance to it, but it’s essentially both, CO2 and H+ (b) Stimulation causes increased ventilation (b) Peripheral chemoreceptor role in regulation respiration (Usually a minor role) (a) Located in carotid bodies and aortic (just like the baroreceptors!) (i) Decreased PaO2 causes an increase in stimulation of the chemoreceptors (ii) Generally does not have any effect until PaO2 is