Pulmonary Functions

Question 1

Association & Dissociation Definition

Answer 1

• Association: how much O2 can stay on hemoglobin
• Dissociation: how likely O2 is going to leave hemoglobin

Question 2

LEFT shift definition

Answer 2

• Hemoglobin holds onto O2
• O2 stays on hemoglobin

Question 3

RIGHT Shift Definition

Answer 3

• Hemoglobin releases O2
• O2 leaves hemoglobin
• Rest of body needs more O2

Question 4

Causes of LEFT & RIGHT shifts

Answer 4

• Hypocapnia/Hypercapnia (Haldane effect)
  
  • HYPOcapnic pts ⇒ oxyhemoglobin less likely to release O2 ⇒ left shift
  • HYPERcapnic pts ⇒ oxyhemoglobin wants to give O2 to other cells of body ⇒ right shift
• Alkalosis/Acidosis (Bohr effect)
  
  • ALKAlotic pts ⇒ oxyhemoglobin less likely to release O2 ⇒ left shift
  • ACIDotic pts ⇒ oxyhemoglobin wants to give out O2 bc they can’t fully excrete CO2 ⇒ CO2 builds up and means body needs more O2 to make energy to get rid of it and other wastes ⇒ so hemoglobin gives up O2 to rest of body ⇒ right shift
• Heat/Cold (Temperature)
  
  • COLD ⇒ rest of body needs less oxygen and wants to shunt blood to main organs ⇒ hemoglobin holds onto O2 ⇒ left shift
  • HEAT/FEVER ⇒ rest of body needs more O2 for energy ⇒ hemoglobin releases O2 ⇒ right shift
• 2,3-Diphosphoglycerate (2,3-DPG) (seen in High Altitudes)
  
  • NORM/LOW Altitude ⇒ O2 abundant in air so rest of body doesn’t need it ⇒ hemoglobin keeps O2 ⇒ left shift
  • HIGH Altitude ⇒ other cells of body need O2 bc of reduced O2 in atmosphere ⇒ hemoglobin gives up O2 ⇒ right shift

Question 5

Kussmaul respirations and why does this occur?

Answer 5

• Kussmaul respirations:
  
  • Tachypneic breathing: rapid but shallow breathing
  • “Weird sugary breathing”
• Occurs when:
  
  • Pt is metabolically acidotic (↓ pH lvls / ↑ CO2 lvls)
    
    • When pt is acidotic ⇒ CO2 building up bc it isn’t being excreted fully ⇒ ↑ acidity/↓ pH
    • ↑ CO2 and ↓ pH reduces hemoglobin’s affinity for oxygen ⇒ hemoglobin tends to release O2 more to tissues that need it most (right shift)
      
      • pH Bohr effect: describes how ↑ CO2 and ↓ pH reduces hemoglobin’s affinity for oxygen ⇒ hemoglobin releases oxygen more readily to tissues that need it ⇒ right shift indicates at any given partial pressure of oxygen (pO₂), hemoglobin releases more oxygen than it would under normal pH conditions

Question 6

Ventilation definition + factors influencing ventilation

Answer 6

• Ventilation: how much air you can breathe in and out
• Main Factors:
  
  • Chemoreceptors…
    
    • Central chemoreceptors in medulla senses ↑ CO2 lvls
    • Peripheral chemoreceptors in carotid and aortic bodies senses ↓ O2
  • Signals respiratory center in brainstem
  • Stimulates ventilation
• Other Factors:
  
  • Emotions: (↑ ventilation)
  • Pain: (↑ ventilation)
  • Medication side-effect of respiratory depression (↓ ventilation)

Question 7

Spirometry measures what?

Answer 7

• How much volume of air person can take with deep breath in and out + speed of that airflow during action
• Deep breath in ⇒ expand ⇒ ↑ perfusion

Question 8

Clinical significance of HYPOventilation (specifically CO2 and pH lvls)

Answer 8

• Means pt can’t push out CO2 adequately ⇒ ↑ CO2/↓ pH (acidotic)
• Hypercapnic: ↑ blood CO2 lvls bc CO2 isn’t adequately coming out
• ↓ capnography (measure of how much CO2 is coming out of pt)

Question 9

Clinical significance of HYPERventilation (specifically CO2 and pH lvls)

Answer 9

• Means pt is pushing out lots of CO2 ⇒ ↓ CO2/↑ pH (alkalotic)
• Hypocapnic: ↓ blood CO2 lvls bc CO2 is coming out too fast
• ↑ capnography

Question 10

Mechanism of Acute Respiratory Distress Syndrome (ARDS) as it relates to pulmonary edema

Answer 10

• ARDS: widespread inflammation and damage to alveoli
• Pathophysiology:
  
  • Direct insult to alveoli and capillary ⇒ activates inflammatory response
  • IS response damages alveoli and capillary ⇒ makes them leaky
  • Capillary fluid leaks into alveoli ⇒ impairs gas exchange
  • More fluid leaking into alveoli ⇒ gunk builds up in alveoli
  • Fluid accumulation ⇒ pulmonary edema

Question 11

Key inflammatory mediators of asthma

Answer 11

• IgE in asthma…
  
  • Marks irritants and alerts phages to it eat
  • Releases histamines ⇒ bronchoconstriction ⇒ wheezing
  • Releases leukotrienes ⇒ stimulates mucus production ⇒ coughing

Question 12

1 causative factor of COPD

Answer 12

• COPD #1 Cause: smoking
• COPD: irritant (smoking) ⇒ chronic alveolar destruction ⇒ breaks down surfactants that usually ↑ alveoli elasticity ⇒ ↓ alveoli expansion ⇒ ↓ gas exchange
  
  • Leads to emphysema & chronic bronchitis
    
    • Emphysema: destruction of alveolar septa, airway instability
    • Chronic bronchitis: bronchial edema, hypersecretion of mucus, chronic cough, bronchospasms
• Patient education: smoking cessation

Question 13

Clinical significance of tapering steroid therapy for treatment of COPD

Answer 13

Glucocorticoid therapy (prednisone) suppresses adrenal glands bc steroids are naturally built in body sent by adrenal glands during fight/flight response → so if body is getting it from med instead → suppresses body’s adrenal glands ⇒ taper off meds bc if you suddenly stop meds adrenal glands are still going to be suppressed

Question 14

Uses for glucocorticoid and beta2-adrenergic agonist therapy for COPD

Answer 14

• Anti-inflammatory agents: Glucocorticoids (prednisone) MOA: ↓ synthesis and release of inflammatory mediators/cells ⇒ ↓ edema of airway mucosa
  
  • Blunts IS bc it’s a steroid
  • Suppresses adrenal glands bc steroids are naturally built in body sent by adrenal glands during fight/flight response → so if body is getting it from med instead → suppresses body’s adrenal glands ⇒ taper off meds bc if you suddenly stop meds adrenal glands are still going to be suppressed
  • It’s a glucose ⇒ monitor for hyperglycemia
• Bronchodilators: Beta2-adrenergic agonists (albuterol): a short-acting-beta-agonist (SABA) that stimulates beta2 receptors in lungs that cause bronchodilation
• USE BOTH for synergistic effects of…
  
  • Glucocorticoids: ↓ airway mucosal inflammation
  • Beta2-adrenergic agonists: bronchodilation

Question 15

Drug classes for treating ACUTE SEVERE asthma exacerbations (AIM)

Answer 15

• Albuterol: short-acting-beta2-adrenergic agonist that stimulates beta2 receptors in lungs to cause bronchodilation to relieve bronchospasm that causes inadequate air in and out lungs
  
  • Adverse effects: systemic effects of tachycardia, angina, tremor
• Ipratropium: anticholinergic that blocks the acetylcholine that normally causes bronchoconstriction ⇒ vasodilation
  
  • Adverse effects: everything dries up and blindness
• Methylprednisolone: long-term glucocorticoid Tx that ↓ mucosal inflammatory-caused airway blockage
  
  • Adverse effects: adrenal suppression, hyperglycemia, oropharyngeal candidiasis, dysphonia

Question 16

Geriatric considerations for pulmonary disease

Answer 16

• Loss of elastic recoil bc of ↓ surfactant that gives elasticity for lung expansion ⇒ ↓ gas exchange
• Stiffening of chest wall bc of degradation of intercostals and muscles can lead to…
  
  • Degrades vasculature ⇒ ↓ gas exchange
  • ↑ in flow resistance: harder for air to flow freely through airway
• Alveoli tend to lose alveolar wall tissue and capillaries ⇒ ↓ surface area for gas exchange ⇒ harder for O2 to enter bloodstream and to exhale CO2
• Monitor for hypoxemia bc they have less gas change, elasticity, muscles ⇒ means gunk stays in lungs longer bc they can’t breathe them out properly
• ↓ in PaO2 and diminished ventilatory reserve ⇒ ↓ exercise tolerance
• ↓ resp muscle strength and endurance

Question 17

Identification of respiratory distress

Answer 17

• Tripod position
• Accessory and/or Secondary muscle use
• ↑ RR
• Nasal flaring
• Pursed lips