Respiratory System Study Guide PDF

Study Guide Respiratory System (Week 9) A. Describe the four main components of respiratory physiology 1. Ventilation i. Movement of air through the airways and the alveoli ii. Dependent on respiratory-associated muscles generating force, whic...

Study Guide Respiratory System (Week 9) A. Describe the four main components of respiratory physiology 1. Ventilation i. Movement of air through the airways and the alveoli ii. Dependent on respiratory-associated muscles generating force, which creates pressure differences between outside air and thoracic cavity 2. Gas Exchange i. Diffusion of oxygen and carbon dioxide between the alveoli and blood stream ii. Depends upon: (a) Gases in the alveoli (b) Blood flow through the alveolar capillaries (c) Capacity of the blood to carry oxygen (and carbon dioxide) (a) Dependent on red blood cells and their hemoglobin 3. Gas Transport i. Transportation of oxygen and carbon dioxide in the blood and body fluids to and from the body’s tissue cells (a) Depends on cardiovascular systems’ ability to move blood through body (b) Depends on hemglobin’s ability to bind to oxygen and carbon dioxide (c) Depends upon tissue’s ability to take up oxygen and give up carbon dioxide 4. Regulation of ventilation i. The CNS controls our depth and rate of respiration, in response to blood gas levels (a) Primarily dependent on CO2 levels (not so much O2 levels) B. Define the terms associated with breathing 1. Tidal Volume i. Volume of air moved with each breath (a) Abbreviated VT 2. Respiratory Frequency i. How many breaths per minute ii. Also known as respiratory rate (a) Abbreviated RR 3. Minute ventilation i. Multiple Tidal Volume by Respiratory Frequency ii. Also known as Ventilatory Equivalent (VE) 4. Eupnea i. Normal ventilatory rate and depth 5. Hyperpnea i. Elevated ventilatory rate AND depth which MEET metabolic demand ii. A NORMAL response to exercise iii. Breathe out “correct” amount of CO2 to maintain acid-base balance 6. Hyperventilation (a) Elevated ventilatory rate and depth which exceeds metabolic demand  (a) Example – a panic attack (b) Breathe out excess amount of CO2 (a) Can lead to acid-base imbalance 7. Tachypnea i. Increased respiratory RATE, but NOT an increase in tidal volume (a) Typically involves a DECREASE in tidal volume (b) Think “shallow” breaths 8. Apnea i. Stoppage of ventilation (a) Can be temporary and self-resolve (a) Example sleep apnea – periods of many seconds of not breathing (b) Can be permanent if no medical intervention (a) Respiratory arrest from stroke, trauma, etc. 9. Dyspnea i. A SYMPTOM of difficult breathing (a) May or may not be pathologic (a) Example of non-pathology – An otherwise healthy person who is “out of shape” feels very out of breath during exercise (b) Example of pathologic – An individual with cardiovascular or pulmonary disease feels difficulty breathing ii. Can also be a SIGN of difficult breathing (a) A clinician can observe signs of distress, gasping for air, accessory muscle breathing, pursed-lip breathing, etc. C. Mechanics of Pulmonary Ventilation 1. State the two basic movements that can expand the lungs/thoracic cavity (and recognize that the opposite movement contracts the lungs/thoracic cage) i. Lengthen thoracic cavity ii. Elevation of ribs (increases anterioposterior diameter of thoracic cavity) 2. State which muscles/forces are responsible for each of these movements during rest and during physical activity (i.e., active breathing) i. Resting (a) Inspiration (a) Contraction of diaphragm lengthens thoracic cavity (b) Expiration (“passive”) (a) Elastic recoil of lungs, chest wall, and abdominal structures ii. Physical activity – All of the above plus these below: (a) Inspiration (a) External intercostals (most important, pull ribs “forward”) (b) Sternocleidomastoid (lift sternum) (c) Anterior serrati (lift many ribs) (d) Scalenes (lift two ribs) (b) Expiration (a) Rectus abdominus (i) Pushes abdominal viscera up to compress thoracic cavity  (b) Internal intercostals (pull ribs “backward”) 3. Describe the mechanics of ventilation, with a focus on how changes in pressure influence inspiration and expiration i. Inspiration (a) Thoracic volume expands (a) See previous points about the muscles involved (i) diaphragm contraction at rest (ii) additional accessory respiratory muscles if needed 1. Exercise 2. Pulmonary-associated diseases (b) Intrapleural pressure decreases (a) This allows the alveoli to expand (b) Molecules in alveoli remain unchanged for the moment, so alveolar pressure decreases (c) Alveolar pressure decreases (see above) (a) Alveolar pressure becomes less than atmospheric pressure (d) Air rushes into alveoli (a) Since air pressure is greater than alveolar pressure, it goes into alveoli (from high pressure to low pressure) (b) Eventually, a sufficient number of gas molecules fill the alveoli (c) Alveolar pressure becomes equal to air pressure (i) No more air comes into alveoli (ii) Inspiration ends ii. Expiration (it’s the exact opposite of inspiration – if you can remember one, just remember the opposite happens in the other) (a) Thoracic volume decreases (a) See previous points about muscles involved (i) Diaphragm elastic recoil at rest (ii) Additional accessory respiratory muscles if needed 1. Exercise 2. Pulmonary-associated diseases (b) Intrapleural pressure increases (a) This begins to compress the alveoli (b) Molecules in alveoli remain unchanged for the moment, so alveolar pressure increases (c) Alveolar pressure increases (see above) (a) Alveolar pressure becomes greater than atmospheric pressure (d) Air rushes out of alveoli (a) Since air pressure is lower than alveolar pressure, it goes away alveoli towards the atmosphere (from high pressure to low pressure) (b) Eventually, a sufficient number of gas molecules leave the alveoli (c) Alveolar pressure becomes equal to air pressure (i) No more air goes out of the alveoli (ii) Expiration ends  4. Recognize that ventilation relates to phonation i. Vocal cords are under control of somatic nervous system (a) Skeletal muscle (b) We can control (a) Our voice (b) Our breathing ii. Abnormal vocal cord control can influence our voice and breathing (a) Example – Exercise-induced laryngeal obstruction (formerly known as Vocal Cord Dysfunction) (a) Makes a high pitched inspiratory sound, known as a stridor (b) Since it is a movement that is under voluntary control, neuromuscular coordination training can resolve the issue 5. Briefly describe the energetic demands of ventilation i. Somatic muscles are involved and these require ATP! ii. Around 3-5% of our resting energy expenditure is used for ventilation iii. During exercise, this value increases to 12-15% (a) Greater minute ventilation (VE) requires more muscle involvement! (a) Inspiration (i) Greater frequency of diaphragm contraction (ii) Greater force of diaphragm contraction (iii) Accessory inspiratory muscle activation (b) Active expiration (i) Accessory expiratory muscle activation iv. In populations with pulmonary disease (and obesity), ventilation may be more difficult (a) Greater force production needed to move air (a) Greater force production necessary for inspiration (b) Need for active expiration (b) If greater respiratory muscle activation is needed, then (a) Exercise intolerance (i) Respiratory muscles are already in “exercise” mode, so there is limited ability to further increase ventilation to meet the demands of exercise (b) Resting energy expenditure is increases (i) Can stunt growth in children (i.e., so much energy is being devoted just to ventilation, as opposed to growth) (ii) Can lead to pathologic weight loss in adults (i.e., energy is being devoted to ventilation, instead of other normal functions) (c) Long-term “overuse” of respiratory muscles (i) Reduced respiratory muscle function… (ii) …which makes ventilation even more difficult D. Describe the location of the respiratory center within the brain, including its three subregions and explain their functions 1. Medulla i. Dorsal respiratory group (a) Chiefly controls inspiration with respiratory ramp  (a) Diaphragm (b) External intercostals (b) Generates general rhythm of respiration ii. Ventral respiratory group (a) Essentially inactive during normal quiet breathing (b) Assists inspiration during in heavy ventilation (c) Causes activation of accessory respiratory muscle during high ventilation periods (e.g., exercise) (a) Involved in active expiration 2. Pons i. Pontine respiratory group (a) Apneustic center – gradually starts activating the dorsal respiratory group (gradual, as opposed to sudden) (a) The “respiratory ramp” (b) Pneumotaxic center – controls rate and depth of breathing (a) Essentially says to stop inspiring (i) Shuts off the dorsal respiratory group (b) Gets afferent input from mechanoreceptors in the lungs which detect stretch E. Describe the stages of the Valsalva maneuver, including the relationship between pressure, venous return, coronary artery perfusion, and blood pressure 1. Phase 1 – Initial increase in intrathoracic pressure (beginning of Valsalva maneuver) i. Increased external pressure on vena cava (pressure compresses vena cava) (a) Temporarily increased venous return into right atrium (i.e., whatever blood was in already in the vena cava before we started the Valsalva now gets squeezed into right atrium) (a) Increased right atrial pressure (b) Bainbridge reflex is initiated (i) Increased heart rate (to empty blood out of right atrium) (c) This will then cause an increased ventricular volume, thus end diastolic volume (i) This will ii. Increased external pressure on coronary arteries (a) Decreased blood supply to myocardium (a) This shouldn’t be a problem in a healthy individual (b) If an individual already has limited coronary artery blood flow (e.g. atherosclerosis), this could become problematic (i.e. insufficient blood for muscle contraction) iii. Increased external pressure on aorta (a) Increases left ventricular afterload iv. When the increase in stroke volume AND increased afterload, the left ventricle is working harder (a) Not an issue in a healthy individual (b) Can be problematic in individuals with (a) Coronary artery blockages (i) May not be able to get sufficient blood supply to left ventricle (b) Cardiac damage or failure (i) Inability to sufficiently increase left ventricular contraction to overcome afterload 2. Phase 2 – Maintained increase in intrathoracic pressure (i.e., if Valsalva maneuver continues to be held more than just 2-3 seconds, such as during a long isometric contraction) i. Maintained increased external pressure on vena cava (a) Decreased filling of the vena cava (REMEMBER, pressure is now higher inside the thorax, and after squeezing a bunch of blood out of the vena cava in Phase 1, that extra compression now makes it hard to get new blood into the vena cava) (a) Decreased venous return (b) Decreased cardiac output (i) IN RESPONSE TO THIS, Aortic arch and carotid body baroreceptors sense a decrease in blood pressure 1. Sympathetic nervous system activity increases in attempt to compensate for this (i.e. heart rate and contractility increase) ii. Maintained increased external pressure on the coronary arteries (a) Supply to the myocardium remains low, just like in phase I… (b) ADDITIONALLY, the cardiac output is now lower (a) Even less blood can go to myocardium (b) This is really problematic if: (i) Coronary arteries are already limited in blood flow (e.g., atherosclerosis) (ii) Ventricles are already weakened (e.g., previous heart disease, heart failure, etc.) (c) Drastic reduction in cardiac output can cause fainting (syncope) or further cardiac ischemia 3. Phase 3 – The Valsalva maneuver is released (i.e., back to normal breathing) [This phases is just 1-2 seconds] i. Intrathoracic pressure on the vena cava decreases (back towards normal) (a) The previously compressed vena cava can now fill with blood (a) It doesn’t enter into the right atrium just yet (i) As such, venous return remains low during Phase 3 (same as Phase 2) (ii) As such, cardiac output remains low during Phase 3 (same as Phase 2) (iii) As such, systolic blood pressure remains low during Phase 3 (same as Phase 2) (iv) As such, the baroreceptors are still firing at a high rate during Phase 3 (same as Phase 2) ii. Intrathoracic pressure on the coronary arteries decrease (back towards normal) (a) The coronary arteries can fill with more blood (a) This sudden surge of blood (following a limited flow) could potentially destabilize a plaque or clot to cause a myocardial infarction 4. Phase 4 – The cardiovascular system fully recovers from the Valsalva maneuver i. Intrathoracic pressure on the vena cava is back to normal (a) All of the blood that filled the vena cava in Phase 3 now gets into the right atrium (a) Right atrial pressure increases (just like in Phase 1) (i) Bainbridge reflex is initiated (just like in Phase 1) (b) A surge of blood gets then will go into the right ventricle (i) Ventricular contractility (and thus myocardial O2 demand) increases (just like in Phase 1) 1. Cardiac output QUICKLY increases 2. Systolic blood pressure QUICKLY increases (ii) These quick increases in cardiac output abruptly raise blood pressure (albeit temporarily) 1. This can potentially dislodge clots or rupture aneurysms  ii. Intrathoracic pressure on the coronary arteries is back to normal (a) There is greater blood supply available to meet the increased myocardial O2 demand F. Describe the cough reflex 1. Larynx and carina of trachea sensitive to mechanical and chemical stimuli 2. Afferent nerve impulses travel from vagus nerve to medulla 3. Rapid inspiration 4. Epiglottis closes and vocal cords shut tightly 5. Forceful abdominal muscle and intercostal muscle contraction i. In patients with recent thoracic or abdominal surgery, this could disrupt surgical repairs ii. In patients with thoracic or abdominal trauma, can disrupt healing or exacerbate trauma 6. Increased pressure in lungs (and thoracic cavity) i. This causes a sudden increase in blood pressure (a) In patients with recent thoracic or abdominal surgery, this could disrupt surgical repairs (b) In patients with recent brain surgery or brain vascular disease, this could increase intracranial pressure and cause damage (e.g. rupture aneurysm) 7. Sudden opening of epiglottis and vocal cords 8. Air explodes out G. Describe the sneeze reflex 1. Similar to cough reflex, with following exceptions i. Initiated by irritation in nasal pathways (not trachea/carina) ii. Afferent impulses pass through fifth cranial nerve (not vagus) iii. Uvula depressed to allow airflow through nose 2. Same risks in certain patient populations, as described above