PS201 Week 4 Cue Cards - Applied Physiology of the Respiratory System

Overview: Structure and Function of the Respiratory System

Objective themes from the video series:
- Outline key elements of structure and function using a model of the respiratory system.
- Cover mechanical properties (pump movement, dynamic compression, secretion clearance, lung compliance), gas transport and analysis, and neural control of respiration.
Visual guide: model icons point to concepts located throughout the respiratory system.
Practical goal: develop clinical reasoning to localize breathing problems in complex systems; relate to physiotherapy assessment, problem solving, and interventions.

Key Mechanical Properties and Movements

Respiratory pump movement: air in and out depends on intact mechanisms
- Motor control: CNS must send signals to muscles of respiration to move air.
- Once air is moving, two types of movement occur in the lung:
- Gas movement: oxygen moves into alveoli → interstitium → bloodstream; carbon dioxide is exhaled (respiratory pump-related).
- Secretion movement: air movement enables mucociliary clearance; concepts include mucociliary clearance, dynamic compression, secretion clearance; these aspects relate to the respiratory load.
“How hard” to inflate and move air (mechanical load): influences ventilatory success and clearance of secretions.
Diagrammatic model (introductory): demonstrates movement and function across components; used to build clinical reasoning.

Mechanical Properties: Specific Concepts

Dynamic compression: during forced expiration, airways collapse due to higher external pressure; creates a point of maximal flow at airway narrowing; exploited clinically for secretion clearance; to be covered in a later video.
Compliance: ease of lung inflation; a measure of lung and chest wall stiffness
- Low compliance: “stiff lungs”; hard to inflate
- High compliance: easy inflation
- Determinants of reduced compliance:
- Thoracic cage restrictions (chest wall, bones, muscles) or postural/structural issues (e.g., kyphosis).
- Airway resistance (bronchospasm, airway narrowing).
- Interstitial tissue resistance (fibrosis, interstitial changes).
- Alveolar surface tension and surfactant layer (surfactant deficiency, e.g., preterm infants; exercise may enhance surfactant protection).
Pulmonary function testing (PFT) / Spirometry:
- Graph of Forced Vital Capacity (FVC): patient inhales deeply, exhales forcefully into a device.
- Y-axis: expired volume (L); X-axis: time to expire
- Normal: ~80% of vital capacity expelled within the first second in healthy lungs.
- Obstructive pattern: slower expulsion; increased airway resistance.
- Restrictive pattern: reduced total lung capacity; overall reduced volumes.
Clinical relevance: spirometry distinguishes obstructive vs restrictive patterns; used to monitor chronic lung conditions in future topics.

Ventilation, Diffusion, and Gas Transport

Ventilation (V), Perfusion (Q), and Diffusion (D): core processes of gas exchange
- V: movement of air into and out of the lungs
- Q: blood flow through pulmonary capillaries
- D: diffusion of gases across the alveolar-capillary membrane
Ventilation–Perfusion (V/Q) matching
- Goal: maximize gas exchange by aligning ventilation with perfusion at the alveolar level
- Upright anatomy: apex of lungs tends to be over-expanded (more ventilation potential); bases have greater perfusion due to gravity; ideal V/Q matching occurs at rest or after a deep breath, especially in the bases when upright.
- Lying prone/sideline positions alter matching due to gravity and diaphragmatic movement; dependent lung typically well-ventilated and perfused if diaphragmatic control is intact; poor diaphragmatic control shifts ventilation toward the upper lung with better perfusion in the lower lung, resulting in poorer matching.
- Functional Residual Capacity (FRC): lung volume at end of normal expiration; acts as a buffer reservoir for gas exchange between breaths.
Functional Residual Capacity (FRC)
- Definition: FRC = Expiratory Reserve Volume (ERV) + Residual Volume (RV)
- Significance: buffers changes in arterial gases during ventilation; supports oxygenation if deep breaths aren’t taken.
- Factors reducing FRC:
- Supine positioning (FRC ↓) and anesthesia-related effects
- Impaired diaphragmatic descent
- Obesity (adipose tissue restricting chest wall and diaphragmatic movement)
- Quantitative positioning effects:
- Standing/sitting upright: baseline (100%) FRC
- Supine: ~71% of upright FRC
- Slumped sitting (postoperative): further reductions
- Surgical and anesthetic influences:
- General anesthetics depress respiration and reduce tidal volumes; diaphragm may be paralyzed or displaced; abdominal surgery can mechanically impair diaphragmatic descent.
- Obesity: adipose tissue surrounding the thorax reduces chest wall compliance and FRC, increasing risk of atelectasis.
Distribution of ventilation and manipulation of flow
- Slow inspiratory flow rate → ventilation preferentially to regions with greater compliance (bases in sitting position).
- High inspiratory flow rate → ventilation preferentially to regions of least resistance (apices).
- Practical tip: encourage slow breathing (e.g., ~0.5 L/s) to improve base ventilation; full lung capacity reached in ~6 seconds.
Gas transport overview
- Oxygen transport: most O2 is carried bound to hemoglobin; a small fraction is dissolved in plasma.
- Each hemoglobin molecule can bind up to 4 O2 molecules (conceptual binding capacity).
- Oxygen–hemoglobin dissociation relationship: the relation between oxygen saturation (SpO2) and PaO2 is illustrated by the dissociation curve; small declines in SpO2 can reflect large changes in PaO2.
- Pulse oximetry (SpO2): noninvasive measurement; normal range ~95–98% (may vary with clinical conditions).
- PaO2 reference: commonly around 100 mmHg in healthy adults; SpO2 ~98% corresponds to PaO2 ~100 mmHg (interpreted from the curve).
- Carbon dioxide transport: CO2 is primarily carried as bicarbonate (HCO3−) in plasma after reaction with water, forming H2CO3 which dissociates to H+ and HCO3−; small fractions are dissolved in plasma or bound to hemoglobin.
- CO2 buffering and acid–base balance: excess CO2 lowers pH (more acidic); the body can increase ventilation to blow off CO2 and restore pH; renal buffering also helps via hydrogen ion excretion and bicarbonate retention, but this is slower.
- In exercising or high CO2 production states, rapid CO2 removal via ventilation is the primary short-term mechanism; chronic lung conditions can impair CO2 elimination and drive reliance on the hypoxic drive in some patients.

Neural Control of Ventilation

Central control: the primary drive to breathe is CO2-driven in healthy individuals
- Chemoreceptors in the medulla detect rising CO2 (and H+). This stimulates the respiratory center to increase ventilation.
- Peripheral chemoreceptors located in carotid bodies and aortic arch respond to falls in PaO2 (often described as a hypoxic drive in certain chronic lung conditions).
In chronic CO2 retention (e.g., COPD):
- The CO2 set point shifts upward; breathing is more dependent on hypoxic stimuli rather than CO2 detection.
- High oxygen therapy can suppress the hypoxic drive, potentially reducing the respiratory drive in these patients.
Corollary discharge and higher centers
- Corollary discharge: a copy of motor commands from the brainstem to the lungs is sent to higher brain centers to anticipate the movement and regulate perception and response.
- Perception of breathlessness (dyspnea) involves the cortex and limbic system, integrating sensory input, emotion, prior experience, and expectations.
- This explains why breathlessness can feel more threatening in chronic disease due to emotional and cognitive associations with stairs, walking, or activity.

Oxygenation, Hypoxemia, Hypercapnia, and Respiratory Failure

Hypoxemia: PaO2 < 60 mmHg is a key threshold (low oxygen) with clinical signs such as cyanosis (central then peripheral), tachycardia, hypertension, confusion, restlessness.
Hypercapnia (hypercapnic respiratory failure): PaCO2 > 50 mmHg with signs like flushed appearance, headaches due to increased cerebral blood flow, possible sweating; severe hypercapnia can lead to drowsiness or coma.
Normal reference ranges to remember:
- SpO2: ≈ 95–98% (may vary with conditions)
- PaO2 (normal): around 100 mmHg; SpO2 98% often indicates PaO2 ≈ 100 mmHg
- PaCO2: 35 ext{ to } 45 ext{ mmHg}
- In hypoxemia: PaO_2 < 60 ext{ mmHg}
- In hypercapnia: PaCO_2 > 50 ext{ mmHg}
Respiratory failure types (as described in the lecture):
- Type I respiratory failure: PaO2 < 60 mmHg with normal or low PaCO2 (oxygenation failure only).
- Type II respiratory failure: PaO2 < 60 mmHg with PaCO2 > 50 mmHg (combined hypoxemia and hypercapnia; ventilatory failure).
Assessment tools referenced:
- Arterial blood gases (ABG) for accurate gas tensions (Po2, PCO2) and acid–base status (pH, HCO3−).
- Pulse oximetry (SpO2) as a noninvasive surrogate of oxygenation.
- FiO2 and supplemental oxygen considerations in management of respiratory failure.

Signs and Symptoms in Clinical Assessment

Subjective assessment (dyspnea/breathlessness)
- Dyspnea is a subjective experience with qualitatively distinct sensations and varying intensity and emotional impact.
- Domains of dyspnea:
- Sensory experience: descriptors like hunger for air, chest tightness, work of breathing; intensity scales (0–10).
- Affective domain: emotions such as anxiety, frustration, fear; rated for distress/unpleasantness.
- Functional impact: how dyspnea limits daily activities and performance (e.g., walking distance, exertion level).
- Common scales used:
- Intensity rating scale: 0 (nothing) to 10 (max difficulty).
- Modified Borg Dyspnea Scale: unidimensional scale for breathing difficulty (0–10).
- Numeric Rating Scale (NRS) for unpleasantness of breathlessness (0–10).
- MMRC Dyspnea Scale (Modified Medical Research Council): a 0–4 scale describing daily activity limitation due to breathlessness; a score ≥ 2 suggests significant daily breathlessness.
- Important caveat: dyspnea can be present without functional limitation and vice versa; patients may reduce activity to avoid dyspnea, which must be explored to avoid underestimating impairment.
Objective assessment (observations and measurements)
- Respiratory rate, work of breathing (use of accessory muscles, intercostal indrawing, nasal flaring), chest wall movement, and diaphragmatic excursion.
- Color (cyanosis), level of consciousness, and signs of respiratory distress.
- Auscultation, sounds (gasping, wheezing), and signs of airway obstruction or secretions.
- Cough and sputum production, hemoptysis (to be discussed in a separate lecture).
- Exercise tolerance and mobility status as markers of functional impact.
- Physical exam findings may not always align with patient-reported breathlessness, especially in chronic conditions; interpret in context.
Objective diagnostic tests (ABG, SpO2, FiO2, etc.)
- ABG: direct measurement of PaO2, PaCO2, pH, bicarbonate (HCO3−).
- SpO2: noninvasive reflection of oxygenation; normal range and interpretation can vary with condition.
- FiO2: fraction of inspired oxygen delivered; considerations when increasing oxygen flow in patients with chronic CO2 retention.
- Postural and activity effects on V/Q matching and oxygenation: upright vs supine vs lateral positions; how posture impacts breathlessness and gas exchange.

Pathophysiology of Respiratory System: Where Things Go Wrong (Part 2 overview)

The lung and airways can be affected at multiple levels, leading to ventilatory impairment:
- Central and peripheral nervous system issues that affect motor control and the respiratory pump.
- Musculoskeletal issues: chest wall mechanics, rib integrity, diaphragm function, and pleural integrity.
- Lung tissue and gas exchange mechanics: diffusion across alveolar–capillary membranes, interstitial changes, and perfusion problems.
- Secretion clearance problems: mucociliary transport and airway clearance, to be covered in a separate lecture.
- Overall respiratory load: any factor that increases the work of breathing (e.g., chest wall restriction, airway resistance, secretions, mass-effect on lungs).
Control of ventilation: neural control diagram (simplified)
- A complex integration of automatic receptors feeding the respiratory center (medulla): chemoreceptors for O2/CO2, stretch receptors, intercostal muscle receptors, and vagal afferents from the lungs.
- Higher centers provide context and modulation; impairment (e.g., spinal cord injury at C3–C5) can abolish diaphragmatic drive, critically affecting breathing.
- Pharmacological agents can influence CNS drive: morphine can depress respiratory drive at high doses (but low-dose morphine may help symptom relief in refractory breathlessness).

Central and Peripheral Nervous System Contributions to Breathing Problems

CNS/Motor control abnormalities can arise from:
- Trauma to brain or brainstem, CVA, spinal cord injuries, infections (polio, meningitis, Guillain–Barré), metabolic encephalopathies, tumors, or pharmacological suppression (e.g., opioids).
Musculoskeletal contributions to dyspnea include:
- Rib fractures, chest wall injuries, diaphragmatic dysfunction, or post-surgical pain limiting deep breaths.
- Diaphragmatic weakness or paresis can impede basal expansion, worsening basilar atelectasis.
- Pleural inflammation (pleuritis) or pleural effusions contribute to pain and restrictive mechanics.
Lung tissue and gas exchange contributions:
- Alveolar issues: alveolar collapse (atelectasis), edema, infection, fibrosis, or edema in the interstitium changing diffusion and perfusion.
- Interstitium thickening (edema or fibrosis) impedes diffusion (D).
- Perfusion issues: capillary bed problems, emboli, or shunting alter Q and V/Q matching.
- Structural changes in chronic disease (emphysema, fibrosis) alter lung mechanics and gas exchange.
Secrets movement and clearance (to be covered separately): mucociliary clearance and dynamic compression affect secretion removal and airway patency.

Ventilation–Perfusion Mismatch: Micro- to Macro-scale View

Micro-level V/Q matching concepts
- Good ventilation and perfusion alignment yields optimal gas exchange.
- In areas with poor ventilation (e.g., mucus plugging) but preserved perfusion, alveoli can collapse (atelectasis) or be underventilated.
- In areas with adequate ventilation but poor perfusion (e.g., pulmonary embolus), ventilation is wasted without gas exchange.
- Intrapulmonary shunting occurs when poorly ventilated regions are still perfused; the pulmonary vasculature may redirect blood flow away from poorly ventilated units to optimize overall gas exchange.
Clinical examples and imaging implications
- Pneumonia: alveolar consolidation increases local tissue density, reducing ventilation in the affected area.
- Pulmonary embolism: reduced regional perfusion causing mismatch.
- X-ray illustration (for teaching) shows areas of airless (white) vs perfused regions and the concept of intrapulmonary shunting.

Functional and Clinical Implications of V/Q and Gas Exchange Concepts

Practical positioning to optimize V/Q matching:
- Upright position generally yields the best overall V/Q matching, especially at the bases due to gravity and diaphragmatic movement.
- Lateral positions: dependent lung tends to have better perfusion and ventilation if diaphragmatic function is intact; poor diaphragmatic control can reverse this pattern.
Medical interventions to modify V/Q:
- Positioning, controlled breathing patterns, and inspiratory flow adjustments to favor ventilation of better-perfused or better-ventilated regions.
- Pulmonary rehabilitation and exercise training to improve overall ventilatory efficiency and endurance.

Oxygen Transport and Acid–Base Homeostasis (Brief recap)

Oxygen carriage:
- Small portion dissolved in plasma; majority bound to hemoglobin (Hb) forming HbO2 complexes (4 O2 per Hb under saturation conditions).
- SpO2 (pulse oximetry) correlates with PaO2; small changes in SpO2 can reflect large changes in PaO2 due to the steep portion of the dissociation curve.
Carbon dioxide carriage and buffering:
- CO2 transported primarily as bicarbonate (HCO3−) in plasma after hydration reaction: CO2 + H2O
  ightleftharpoons H2CO3
  ightleftharpoons H^+ + HCO_3^-
- High CO2 raises H+ (decreases pH); ventilation increases CO2 clearance; kidneys buffer via urinary excretion of H+ and retention of HCO3− (slower).
Clinical relevance of ABGs and gas exchange:
- ABG interpretation informs ventilation strategies and oxygen therapy in acute care.
- Chronic lung disease can shift dependence from CO2-driven drive to hypoxic drive; careful titration of supplemental O2 is essential to avoid suppressing respiratory drive.

Breathlessness (Dyspnea): Mechanisms, Assessment, and Psychophysiology

Nature of dyspnea
- Dyspnea is a subjective, multifactorial experience with sensory descriptors, emotional responses, and functional impact.
- It arises from a mismatch between ventilatory demand and the central processing of feedback about ventilation and gas exchange.
Neurophysiological model of breathlessness
- Brainstem generators (medulla) modulated by sensory input from lungs (stretch receptors, vagal afferents), chemoreceptors (O2/CO2), and chest wall receptors.
- Corollary discharge: copies of motor commands feed back to higher brain centers to predict and regulate responses.
- Limbic system and association cortex contribute emotional responses (anxiety, fear) and expectations based on prior experiences.
- Result: breathlessness is not purely a local lung issue; it is a brain-mediated perception influenced by emotion and past experience.
Assessment of dyspnea
- Sensory domain: descriptors of breathing sensation; intensity scales (0–10).
- Affective domain: anxiety, frustration, fear; rated for distress/unpleasantness.
- Functional impact: daily activities, walking distance, exercise tolerance.
- MMRC dyspnea scale: 0–4 scale; MMRC ≥ 2 indicates significant daily breathlessness.
- Descriptive tools include intensity scales (0–10), Borg scale, and NRS for unpleasantness.
Clinical implications for management
- Breathlessness involves central processing and autonomic responses; pulmonary rehabilitation and exercise can be beneficial long-term.
- Morphine in low doses may reduce the perception of breathlessness by altering sensory processing, while high doses risk respiratory depression.
- Acute distress is often managed with calming strategies and pacing, with consideration for the neurophysiological drivers of dyspnea.

Practical Considerations: Pathophysiology in Acute and Chronic Respiratory Conditions

Involvement of different systems in respiratory failure
- CNS and peripheral nervous system impairments can compromise motor control of ventilation (e.g., spinal injuries, brainstem lesions, neuromuscular diseases).
- MSK issues compromising rib movement, diaphragmatic descent, and pleural integrity can produce hypoventilation and reduced lung expansion.
- Lung tissue pathology (emphysema, fibrosis, edema) affects gas exchange and mechanical properties.
- Secretion clearance problems lead to airway obstruction and increased work of breathing; a separate lecture topic.
Spectrum of inadequate ventilation
- Atelectasis: alveolar collapse due to insufficient ventilation.
- Widespread alveolar collapse or lobar collapse.
- Interstitial thickening (edema or fibrosis) reduces diffusion efficiency.
- Pulmonary edema and fibrosis widen the interstitial space, thickening alveolar membranes and hindering diffusion.
- Diffusion limitations at alveolar-capillary membranes and capillary perfusion problems (pulmonary emboli) cause poor oxygen delivery.
Clinical decision-making implications
- Distinguish whether ventilatory impairment is mechanical (pump/muscle), airway resistance, gas exchange (diffusion), or secretion-related.
- Recognize when physical therapy interventions can help (e.g., improving diaphragmatic movement, chest wall mechanics, airway clearance strategies) versus cases requiring medical management (e.g., anticoagulation for embolus, infection control, or surgical interventions).

Summary of Core Concepts to Remember

The respiratory system functions as a pump (ventilation), a transport system (gas exchange), and a clearance system (secretion management), with the diaphragm as a central driver and accessory muscles supporting effort.
Mechanical properties (compliance, dynamic compression, and mucociliary clearance) determine the ease of ventilation and secretion clearance.
V/Q matching is the cornerstone of efficient gas exchange; body position, diaphragmatic function, and inspiratory flow rate influence matching.
FRC acts as a gas exchange reservoir; factors that reduce FRC (supine position, anesthesia, obesity) increase risk of hypoxemia due to airway closure and atelectasis.
Oxygen transport combines Hb-bound oxygen and dissolved oxygen; CO2 is primarily transported as bicarbonate and is buffered by renal and respiratory systems; pH balance is closely linked to these processes.
The drive to breathe is CO2-driven in healthy individuals but becomes more dependent on hypoxic drive in some chronic lung diseases; high O2 can suppress this drive and must be titrated.
Breathlessness is a brain-driven perceptual experience with sensory, affective, and functional dimensions; assessment uses scales like the Borg, NRS, and MMRC.
Pathophysiology of respiratory distress spans CNS/pns motor control, MSK mechanics, and lung tissue gas exchange; secretion movement has its own dedicated focus.
Type I and Type II respiratory failures describe hypoxemic and combined hypoxemic-hypercapnic states, guiding clinical management and physiotherapy priorities.

Key Formulas and Numerical References (LaTeX)

Oxygen transport and Hb binding concepts (qualitative):
- Each Hb molecule binds up to 4 O2 molecules: ext{Hb} + 4O2 ightarrow ext{Hb}(O2)_4
Oxygen saturation and PaO2 relationship (conceptual):
- SpO2 roughly corresponds to PaO2 via the oxyhemoglobin dissociation curve (qualitative relationship, not a single equation here)
Normal reference ranges (as stated in the video):
- SpO2: 95 ext{–}98 ext{ extpercent}
- PaO2: about 100 ext{ mmHg} (typical healthy value; lower in disease)
- PaCO2: 35 ext{ to } 45 ext{ mmHg}
Hypoxemia and hypercapnia thresholds (as stated):
- Hypoxemia: PaO_2 < 60 ext{ mmHg}
- Hypercapnia: PaCO_2 > 50 ext{ mmHg}
Functional Residual Capacity (FRC)
- FRC relation: FRC = ERV + RV
- Normal upright vs supine:
- FRC_{ ext{sitting}} ext{ as } 100 ext{ extpercent}
- FRC{ ext{supine}} oughly 71 ext{ extpercent of } FRC{ ext{sitting}}
Lung volumes example (tidal volume):
- V_T
  oughly 500 ext{ mL}
Inspiratory flow rate example:
- Slow: v_{ ext{in}}
  oughly 0.5 ext{ L/s}}, ext{time to full capacity }
  ightarrow ext{ about } 6 ext{ s}
Gas exchange compartments abbreviations (for reference):
- V = ext{Ventilation}, ag{airflow into alveoli}
- Q = ext{Perfusion}, ag{pulmonary capillary blood flow}
- D = ext{Diffusion}, ag{gas exchange across alveolar–capillary membrane}
Diffusion equation (conceptual):
- While not given as a single equation in the lecture, diffusion depends on surface area, membrane thickness, and gradient; expressed broadly in Fick’s principle conceptually, e.g., gas exchange rate ∝ surface area × gradient / thickness (not explicitly written in the transcript).
Carbon dioxide transport equilibrium (chemical equation):
- CO2 + H2O
  ightleftharpoons H2CO3
  ightleftharpoons H^+ + HCO_3^-

Connections to Practice and Real-World Relevance

Clinically, the framework supports: locating the origin of breathing difficulty (central, MSK, or lung/tissue), selecting appropriate physiotherapy interventions, and understanding when medical management is required (e.g., embolism, edema, infection).
The dyspnea model informs subjective assessment and helps tailor interventions to sensory, affective, and functional domains, promoting patient-centered care.
Understanding V/Q matching and FRC helps in choosing patient positioning, breathing strategies, and targeted rehabilitation to optimize gas exchange.
Awareness of hypoxic vs. hypercapnic drives informs oxygen therapy strategies in patients with chronic lung disease to avoid respiratory drive suppression while ensuring adequate oxygenation.
The material underscores the interdependence of neural control, muscular function, chest wall mechanics, alveolar gas exchange, and perfusion in maintaining healthy respiration and in guiding rehabilitation after injury or illness.