Oxygenation, Pneumonia, Sleep Apnea Notes

Respiratory Anatomy and Gas Exchange

  • Pleura anatomy
    • Parietal pleura lines chest wall; visceral pleura encases the lungs
    • Pleural space is the contact area between the membranes where sliding occurs; normally a potential space with minimal fluid
  • Lower airways structures (reference to figure in Lewis 2014, Fig. 26-3)
  • Gas entry and alveolar gas pressures (pulmonary shorthand)
    • Inspired air contains:
    • A (alveolar) corresponds to alveolar gas partial pressures
    • a (arterial) and v (venous) represent arterial and venous sides
    • Measured pressures in air: PO2, PCO2, PN2, PH2O
    • Inspired gas partial pressures (example values):
    • PO2 ≈ 159 mmHg, PCO2 ≈ 0.3 mmHg, PN2 ≈ 597 mmHg, PH2O ≈ 3.7 mmHg
    • This air mixes with dead space air and is humidified
    • Alveolar gas (in alveolar unit):
    • PAO2 ≈ 104 mmHg, PACO2 ≈ 40 mmHg, CO2 in alveoli is regulated by ventilation
    • O2 transport: O2 moves from alveoli to blood; N2 and H2O remain in gas phase
    • Alveolar capillary blood becomes oxygenated; desaturation and oxygenation changes occur from alveolar gas to systemic circulation
    • Key alveolar/blood partial pressures: PvO2 ≈ 40 mmHg; PaO2 ≈ 97 mmHg; PvCO2 ≈ 45 mmHg; PaCO2 ≈ 40 mmHg
  • Summary concept
    • Gas exchange depends on matching alveolar ventilation to pulmonary perfusion and the partial pressure gradients driving diffusion

Ventilation

  • Inspiration (inhalation)
    • Muscles: respiratory muscles (diaphragm, intercostals, scalene)
    • Action: increases chest dimensions and decreases intrathoracic pressure
    • Result: air flows from higher atmospheric pressure to lower intrathoracic pressure
  • Expiration (exhalation)
    • Normally passive
    • Lungs’ elastic recoil provides restoring force
    • Elasticity is the tendency to resist stretching and to return to the original shape; elasticity is the reciprocal of compliance
    • Overall: ventilation is the process that maintains gas exchange by cycling air in and out of the lungs

Physiologic Dead Space

  • Definition: portions of the airway that do not participate in gas exchange
    • Nose to non-respiratory bronchioles serve as conducting pathways
    • Typical dead space air ~150 mL per breath; total breath ~300 mL in this illustration, leaving ~150 mL for gas exchange (about 50% in this example)
  • Practical implication
    • With each breath, a portion is dedicated to dead space ventilation; only the remaining air participates in gas exchange

Dead Space (DS) Math (illustrative calculations)

  • Example: respiratory rate (RR) 16 breaths/min with tidal volume (VT) 600 mL
    • DS air per minute: 16 × 150 mL = 2400 mL/min
    • Air for gas exchange per minute: 16 × 300 mL = 4800 mL/min; 4800 − 2400 = 2400 mL/min available for gas exchange
  • Alternative example: RR 16 with VT 150 mL DS = 2400 mL/min DS; air for gas exchange 7200 mL/min
    • RR 30 × 150 mL DS = 4500 mL/min DS; air for gas exchange 4500 mL/min
  • Concept: increasing tidal volume or decreasing dead space improves effective gas exchange per minute

Alveoli and Surfactant

  • Surfactant role
    • Lowers alveolar surface tension
    • Decreases the pressure needed to inflate the lungs, increasing pulmonary compliance
    • Decreases tendency for alveolar collapse (prevents atelectasis)
    • Facilitates recruitment of collapsed airways
  • Composition and origin
    • Phospholipoprotein complex
    • Secreted by type II pneumocytes, particularly with deep breaths that stretch alveoli
  • Clinical significance
    • Lack of surfactant leads to alveolar collapse and poor gas exchange (e.g., in premature infants, certain lung injuries)

Alveolar Atelectasis (Illustration)

  • Electron micrograph of collapsed alveoli due to lack of surfactant or alveolar fluid/exudate
  • Consequence: reduced gas exchange surface area and impaired oxygenation

Compliance and Influencing Factors

  • Compliance: distensibility of lungs and chest wall
    • Increased compliance: lungs/chest wall are easily inflated (e.g., emphysema)
    • Decreased compliance: lungs/chest wall are stiff or difficult to inflate (e.g., pneumonia, pulmonary edema, pulmonary fibrosis)
  • Relationship to work of breathing
    • Higher compliance generally reduces work of breathing for a given volume change; lower compliance increases work of breathing

Asthma: Airway Narrowing Pattern

  • Pathophysiology overview
    • Smaller airway lumen; mucus may fill the airway lumen
    • Smooth muscle layer contracts, further narrowing the airway
    • Muscular effort increases to overcome resistance
  • Clinical cue
    • Accessory muscle use and wheeze may indicate increased work of breathing

Work of Breathing (WOB)

  • Determinants
    • Primarily muscle effort
  • Typical course
    • Normally low; increases dramatically with disease
  • Factors increasing WOB
    • Decreased lung or chest wall compliance; obstructed airways (bronchospasm, mucus plugging)

Regulation of Ventilation

  • Central respiratory control centers
    • Medulla: regulates inspiration and expiration; generates rhythmic breathing
    • Pons: modulates and coordinates ventilation; helps with speaking during breathing
    • Cortex: provides voluntary control over breathing
  • Central chemoreceptors
    • Located near the medulla; respond to H+ concentration in CSF (acid-base status)
    • Chronic hypercapnia can desensitize central chemoreceptors; hypoxic drive may become more important
  • Peripheral chemoreceptors
    • Aortic bodies (aortic arch) and carotid bodies (bifurcation of carotid arteries)
    • Primarily sensitive to PaO2; hypoxic drive activated when PaO2 falls toward ~60 mmHg; less sensitive to pH/minor changes in CO2
  • Lung receptors
    • Irritant receptors: trigger bronchoconstriction and ↑ respiratory rate in response to irritants
    • Stretch receptors: protect by slowing/altering ventilation when lungs are stretched
    • Juxta-pulmonary capillary receptors: respond to pulmonary-capillary pressure; can alter respiratory rate
  • Autonomic nervous system influence
    • Sympathetic: tends to relax airway smooth muscle (β-adrenergic effects)
    • Parasympathetic (vagus): tends to constrict airway smooth muscle

Respiratory Defense Mechanisms

  • Upper airway defenses
    • Nasal hairs filter particles ≥ 5 μm
    • Muco-ciliary clearance traps and moves particles 1–5 μm out of the airways
    • Ciliary beating can be impaired by smoking, dehydration, high oxygen, infection, anesthetics, certain drugs (e.g., atropine), alcohol, cocaine
  • Alveolar defense
    • Alveolar macrophages phagocytose inhaled particles
    • Cough reflex helps clear substances from main airways; works with mucociliary clearance
    • Reflex bronchospasm in response to inhaled irritants
  • Impairment factors
    • Smoking markedly reduces alveolar macrophage function and mucociliary clearance

Alveolar Gas Exchange and Perfusion (Ventilation-Perfusion Concept)

  • Gas exchange and transport define respiration as the delivery of O2 to tissues and removal of CO2
  • Distribution of ventilation and perfusion
    • Ideally matched across lung units
    • Base of the lung typically receives more ventilation and blood flow than the apex due to gravity
  • V/Q relationships
    • Normal V/Q ratio ≈ 0.8 to 1.0 (ventilation to perfusion match)
    • Dead space unit: ventilation without perfusion
    • Shunt unit: perfusion without ventilation
    • Silent unit: both ventilation and perfusion are impaired

Oxyhemoglobin Association and Dissociation

  • PaO2 normal value: ext{PaO}_2 ext{ in the arterial blood}
    ightarrow [80, 100] ext{ mmHg}
  • Oxygen saturation (SpO2): Normal around 94 ext{–}100 ext{%} when PaO2 is normal
  • Oxygen carried by hemoglobin: Normal Hb capacity yields O2 saturation near 100% under normal conditions

Critical Values for PaO2 and SpO2 (clinical thresholds)

  • PaO2 ≥ 80 mmHg and SpO2 ≥ 94%: Adequate oxygenation unless there are hemodynamic instability or impaired O2 delivery due to hemoglobin issues
  • Mild hypoxemia: PaO2 ≈ 60–79 mmHg with SpO2 ≈ 90–93%
    • Clinical signs: restlessness, tachycardia, dyspnea; supplemental O2 may be required
  • Moderate hypoxemia (chronic or complex cases): PaO2 ≈ 55–60 mmHg with SpO2 ≈ 88% under chronic hypoxemia; may be acceptable if there are no cardiac issues; may require continuous O2 therapy; can include confusion or lethargy
  • Moderate hypoxemia with CO2 retention scenario: PaO2 ≈ 40–50 mmHg with SpO2 ≈ 75–75%; may be acceptable short-term if CO2 retention is present; patient may have respiratory distress and use of accessory muscles; airway support considered
  • Severe hypoxemia: PaO2 < 40 mmHg and SpO2 < 75%; inadequate oxygenation with risk of tissue hypoxia and cardiac dysrhythmias
  • Note: These thresholds apply to rest or exertion; SpO2 values are parallel to SaO2 and share the same critical cutoffs

Decreased Oxygen Saturation & PaO2 Causes

  • Ventilation/Perfusion abnormalities can lower oxygenation
  • Carbon monoxide poisoning competitively inhibits O2 binding to hemoglobin (CO binds ~200× more effectively than O2)
  • CO reduces effective O2 delivery despite normal PaO2 readings

Hypoxemia: Causes and Evaluation

  • Primary causes
    • Hypoventilation
    • Barriers to gas exchange (fluid, infection, exudates)
    • Damage to lung tissue
    • Ventilation/Perfusion (V/Q) mismatch
    • Circulatory issues affecting oxygen delivery
  • Critical step in management: identify the cause to tailor intervention

Assessment and Health History (Pneumonia context)

  • Health history components
    • Co-morbid diseases, allergies, prior surgeries/transplants
    • History of lower respiratory problems
    • Current and past medications (prescription, OTC, antibiotics, cough meds, nebulizers)
    • Home oxygen use and safety practices
  • Health maintenance
    • Vaccines (pneumococcal, COVID-19); nutrition; weight changes; sputum factors; smoking history
    • Mobility/exercise; dyspnea with activity; home barriers; changes in activity
  • Life functioning and sleep
    • Cognitive/perceptual, pain, restlessness, coping, sexuality, beliefs
    • Sleep pattern and apnea indicators (e.g., snoring, apnea episodes, pillows used, ability to lie flat)

Physical Examination for Respiratory Disease

  • Airway assessment: nasal passage deviation, mouth dryness, dentition
  • Pharynx and epiglottis movement; neck/tracheal alignment
  • Chest examination: respiratory pattern, rate, rhythm; skin color (cyanosis, flushing); clubbing of fingers
  • Chest movement: symmetry, accessory muscle use; barrel chest; spine curvature or fractures; diaphragmatic movement
  • Palpation and percussion
  • Cough and sputum assessment: dry vs moist; onset/frequency; tone; postural effects; sputum color/consistency; presence of blood
  • Auscultation: adventitious sounds (crackles/rales, rhonchi, wheezes, stridor), pleural friction rub, absent sounds; bedside tests (bronchophony, whispered pectoriloquy, egophony)
  • Specific crackle descriptions
    • Fine crackles/rales: end-inspiration; sudden alveolar recruitment; sounds like rubbing hair by the ear
    • Diffuse crackles associated with edema, atelectasis, pneumonia, interstitial processes
  • Special signs
    • Rhonchi: low-pitched, continuous rumbling; may clear with coughing

Lung Volumes and Capacities (Pulmonary Function)

  • Tidal Volume (VT): amount of gas inspired and expired with each breath
  • Vital Capacity (VC): maximum amount of gas that can be expired from the lung
  • FVC: Forced Vital Capacity
  • FEV1: Forced Expiratory Volume in 1 second
  • Note: Spirometry is a core test for pulmonary function including FVC and FEV1; imaging and other tests complement evaluation

Tests of Pulmonary Function and Related Lab Data

  • Tests
    • Spirometry: FVC, FEV1
    • Chest radiographs; ventilation-perfusion scans
    • Bronchoscopy; pulmonary angiography
    • MRI; pleural taps and biopsies
  • Lab data
    • ABGs: arterial blood gas analysis
    • CBC: Hb/RBC indices (MCV, MCH, MCHC) for anemia and O2-carrying capacity
    • WBC differentials (lymphocytes, neutrophils, eosinophils) for infection/allergic processes

Pneumonia

  • Definition and pathology
    • Infection of lung tissue with acute inflammatory response
    • Acquisition routes: aspiration, inhalation, hematogenous spread
  • Causes
    • Bacteria, viruses, fungi, mycoplasma, parasites, chemicals; defense mechanisms may be overwhelmed
    • Impairment of cough/epiglottic reflexes increases aspiration risk
  • Types
    • Community-acquired pneumonia (CAP)
    • Hospital-acquired pneumonia (HAP)
    • Ventilator-associated pneumonia (VAP)
    • Health care–associated pneumonia (HCAP)
    • Aspiration pneumonia (due to aspiration of oropharyngeal contents)
  • Common CAP organisms
    • Influenzae; Streptococcus pneumoniae; MRSA; Pseudomonas aeruginosa; Staphylococcus aureus; Legionella; fungi
  • CAP treatment approach (three-step)
    1) Assess ability to treat at home
    2) Calculate PORT (Pneumonia Outcomes Research Team) risk; factors include demographics, physical findings, labs, comorbidities
    3) Decide inpatient vs outpatient; consider C-reactive protein-guided antibiotics
  • HAP, VAP, HCAP and aspiration definitions and notes
  • SARS-CoV-2 (COVID-19)
    • Viral pneumonia with upper airway involvement; 5% severe pneumonia/ARDS risk; 14% moderate cases
  • Opportunistic infections risk factors (severe malnutrition, immune deficiencies, chemotherapy/radiation, long-term corticosteroids, immune suppression)
  • Pathophysiology course (conceptual figure)
  • Complications
    • Respiratory failure; pleurisy; pleural effusion; atelectasis; persistent infection; bacteremia; lung abscess; empyema; pericarditis
  • Pleural effusion: fluid in the pleural cavity
  • Clinical manifestations of pneumonia
    • Fever, chills; productive cough with purulent sputum; SOB; chest pain; crackles/rhonchi; dull sounds over consolidation; fatigue; confusion; chest X-ray showing consolidation or effusion; ABGs
  • Imaging
    • Chest X-ray findings; COVID-19 radiographs with bilateral ground-glass opacities (example image described)
  • Resolution process
    • Alveolar macrophages remove debris (degenerated neutrophils, fibrin, bacteria)
  • Nursing care and management
    • Monitor vital signs and pulmonary status; report fever >101°F; administer oxygen as ordered; assess oxygen with activity; advise ambulation; position for optimal ventilation; suction and cough/deep-breath exercises; conserve energy; nutrition; hydration; IV antibiotics; pain management; antipyretics; assist with procedures
  • Vaccines and prevention
    • Pneumococcal vaccine indicated for high-risk groups; COVID-19 vaccination guidelines; vaccination timing in acute illness; mild illnesses are not contraindications
  • Patient education and discharge planning
    • Self-care information; complete antibiotic therapy; energy conservation; smoking cessation; coughing and deep-breathing exercises; vaccines
  • Evaluation of care effectiveness
    • Respirations 12–18; clear breath sounds; effective cough; afebrile; adequate nutrition; ability to perform activities of daily living; ABGs within normal limits; pain control satisfactory; patient satisfaction; baseline chest X-ray normalization

Sleep Apnea

  • Sleep Apnea syndrome criteria
    • ≥ 10 seconds of apnea episodes, more than 5 times per hour
    • Common in males aged 30–60 years (example demographics)
  • Obstructive sleep apnea (OSA) characteristics
    • Upper airway collapse/obstruction during sleep; chest wall and respiratory muscles may be normal; snoring indicates partial obstruction
    • Hypoxia triggers awakening to breathe; repeated episodes disrupt sleep
  • Risk factors
    • Enlarged soft tissue structures in the airway; enlarged jaw; obesity (BMI > 30); large neck circumference (> 17 inches); family history
  • Mechanism
    • Relaxation and displacement of tongue and airway structures cause obstruction; apnea episodes lead to ↑ PaCO2 and ↓ pH; arousal restores airway patency; cycle repeats; resulting fatigue and sleep disruption
  • Management strategies
    • Weight reduction; sleep position optimization (avoid supine), avoid alcohol and sedatives, avoid tobacco use
    • Humidifier for dryness; positive airway pressure therapy (CPAP/BiPAP) is a common treatment
  • Hospitalized patient considerations
    • Nursing interventions: maintain headgear, inform surgical team, place patient in room near nursing station, monitor carefully with sedation/pain meds, high-alert for airway management

Quick Connections and Practical Relevance

  • Gas exchange relies on ventilation-perfusion matching (V/Q) and adequate diffusion across the alveolar-capillary membrane; hypoxemia severity guides treatment urgency and methods
  • Surfactant is essential for preventing alveolar collapse, especially in injury or prematurity; poor surfactant increases work of breathing and lowers oxygenation
  • Pneumonia disrupts gas exchange via consolidation, edema, and effusions; understanding V/Q mismatch guides oxygen therapy and antibiotics strategies
  • Sleep apnea has systemic consequences beyond sleep disruption, including cardiovascular and metabolic risks; management improves daytime function and reduces complications

Formulas and Key Values (LaTeX)

  • Normal V/Q ratio: ext{V/Q} \in [0.8, 1.0]
  • Normal arterial oxygen tension: ext{PaO}_2 \in [80, 100] \text{mmHg}
  • Oxygen saturation (SpO2) target range: approximately 94\% \leq \text{SpO}_2 \leq 100\%
  • Alveolar gas pressure examples:
    • ext{PAO}2 \approx 104 \text{ mmHg}, \quad \text{PACO}2 \approx 40 \text{ mmHg}
  • Capillary-to-tissue oxygen pressure: ext{PaO}2 \approx 97 \text{ mmHg}, \quad \text{PvO}2 \approx 40 \text{ mmHg}
  • Critical PaO2 thresholds (approximate from table):
    • Adequate: ext{PaO}2 \ge 80 \text{ mmHg}, \quad \text{SpO}2 \ge 94\%
    • Mild hypoxemia: 60 \le \text{PaO}2 \ 80 \text{ mmHg}, \quad 90\% \le \text{SpO}2 < 94\%
    • Moderate hypoxemia (caution when chronic): \text{PaO}2 \approx 55-60 \text{ mmHg}, \quad \text{SpO}2 \approx 88-88\%
    • Severe hypoxemia: \text{PaO}2 < 40 \text{ mmHg}, \quad \text{SpO}2 < 75\%