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

Question-and-answer flashcards covering respiratory structure, function, gas transport, VQ matching, mechanics, and pathophysiology.

What are the two key movement types in the respiratory system model?

Movement of gases (gas exchange: oxygen into the alveoli and carbon dioxide out) and movement of secretions (mucociliary clearance).

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 → interstitial → 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.

Define dynamic compression in the context of respiration.

During forced expiration, airways collapse because external pressure exceeds intraluminal pressure, increasing airflow at the site of narrowing.

What is lung compliance and what factors can affect it?

Compliance is how hard or easy it is to inflate the lungs. It is affected by the thoracic cage, airway resistance, tissue resistance (fibrosis), and alveolar surface tension/surfactant.

• 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).

What do V, Q, and D stand for in gas exchange physiology?

V = ventilation, Q = perfusion, D = diffusion.

What is ventilation-perfusion (VQ) matching and why is it important?

The alignment of ventilation with capillary perfusion to optimize gas exchange and oxygen delivery to tissues.

In an upright person, where is VQ matching best and why?

At the bases of the lungs after a deep breath, because the base has greater potential ventilation and receives more perfusion due to gravity.

How does sideline positioning affect VQ matching when diaphragmatic function is compromised?

There can be better ventilation in the upper lung and better perfusion in the dependent lower lung, leading to poorer overall VQ matching.

What is Functional Residual Capacity (FRC)?

The volume of air remaining in the lungs at the end of a normal expiration; it buffers arterial gas changes.

Name factors that reduce FRC.

Supine positioning, effects of general anesthesia, problems with diaphragmatic descent, and obesity.

How does body position affect FRC values?

Supine position reduces FRC (about 71% of upright); upright sitting is generally better for FRC.

How do surgery and anesthesia impact FRC?

Anesthetics depress respiration and diaphragmatic movement; surgical displacement of the diaphragm can further reduce FRC.

How does inspiratory flow rate influence where ventilation occurs in the lungs?

Slow inspiratory flow favors ventilation to more compliant regions (bases); high inspiratory flow favors the apexes (least resistance).

How is oxygen carried in blood primarily?

Mostly bound to hemoglobin (Four O2 per Hb); a small portion is dissolved; oxygen saturation is measured by SpO2.

How is carbon dioxide transported in the blood?

Primarily as bicarbonate (HCO3-) in plasma; smaller amounts bound to hemoglobin or dissolved; rapid removal via respiration.

Define hypoxemia.

PaO2 less than 60 mmHg.

Define hypercapnia.

PaCO2 greater than 50 mmHg.

Differentiate type I and type II respiratory failure.

Type I: hypoxemia with PaO2 < 60 mmHg and normal/low PaCO2. Type II: PaO2 < 60 mmHg with PaCO2 > 50 mmHg; requires ventilation support.

What primarily triggers the ventilatory drive in healthy individuals?

Rise in CO2 (and hydrogen ions) sensed by central chemoreceptors in the medulla, increasing ventilation.

What is the “hypoxic drive” and when is it clinically relevant?

In chronic CO2 retainers, breathing is driven by low O2 via carotid bodies; high O2 can suppress this drive.

What are the three domains of dyspnea assessment?

1) Sensory experience (descriptors of breathing)

2) Affective response (anxiety, frustration)

3) Impact on daily life/functional status

Name two scales used to quantify dyspnea intensity and unpleasantness.

Modified Borg Dyspnea Scale (intensity) and Numeric Rating Scale (unpleasantness).

What is MMRC and what score indicates significant daily breathlessness?

Modified Medical Research Council dyspnea scale; a score of 2 or higher indicates significant daily breathlessness.

Where is breathlessness generated and what neural factors influence it?

Generated in the brain; influenced by brainstem centers, corollary discharge, limbic/emotional systems, and higher association cortex, reflecting a mismatch between ventilatory demand and actual ventilation.

What are the primary inputs to the respiratory center for automatic control?

Lung stretch receptors and vagal feedback, carotid and aortic chemoreceptors (O2), CSF receptors (CO2), chest wall/muscle receptors, and joint receptors.

What is atelectasis and how does it affect ventilation?

Collapse of alveoli leading to reduced or absent ventilation in affected regions.

What is the role of the interstitium and its thickening in gas exchange?

Thickening or edema of the interstitium increases the diffusion barrier, hindering O2 and CO2 exchange.

Explain intrapulmonary shunting.

Perfusion of poorly ventilated areas or non-ventilated alveoli; the pulmonary vasculature may vasoconstrict to redirect flow, temporarily optimizing overall gas exchange but causing mismatch.

Why must oxygen therapy be used cautiously in patients with chronic CO2 retention (COPD)?

High O2 can suppress the hypoxic drive and worsen hypercapnia; use low oxygen flow to preserve the patient’s drive to breathe.

What signs indicate respiratory distress to observe clinically?

Tachypnea, use of accessory muscles, tracheal/intercostal indrawing, nasal flaring, cyanosis, pallor, altered mental status, diaphoresis.

What noninvasive and invasive tests assess oxygenation and ventilation?

Noninvasive: pulse oximetry (SpO2). Invasive: arterial blood gas (ABG) analysis providing PaO2, PaCO2, pH, and bicarbonate.

What are common structural lung changes that impair ventilation (e.g., COPD, fibrosis)?

Emphysema with alveolar destruction, fibrosis with stiffened lung tissue, and general chest wall or diaphragmatic dysfunction affecting ventilation.

What is the spectrum of inadequate ventilation in the lung?

From localized atelectasis to segmental or whole-lung collapse, due to alveolar collapse, airway obstruction, or external compression.

What are the main categories of issues that can lead to ventilatory impairment in the respiratory system?

- Central and peripheral nervous system issues affecting motor control and the respiratory pump.

- Musculoskeletal issues, including chest wall mechanics, rib integrity, diaphragm function, and pleural integrity.

- Lung tissue and gas exchange mechanics, involving diffusion, interstitial changes, and perfusion problems.

- Secretion clearance problems.

- Increased overall respiratory load, which increases the work of breathing.

How is automatic ventilation controlled and what factors can influence this control?

Automatic ventilation is controlled by a complex integration of receptors (chemoreceptors for O2/CO2O2/CO2, stretch receptors, intercostal muscle receptors, vagal afferents) feeding the respiratory center in the medulla. Higher brain centers modulate this control, and impairments (e.g., spinal cord injury at C3–C5C3–C5) or pharmacological agents (e.g., high-dose morphine) can depress respiratory drive.

What are some causes of CNS/Motor control abnormalities that can lead to breathing problems?

Trauma to the brain or brainstem, CVA, spinal cord injuries, infections (e.g., polio, meningitis, Guillain–Barré), metabolic encephalopathies, tumors, and pharmacological suppression (e.g., opioids).

How do musculoskeletal issues contribute to dyspnea and ventilatory impairment?

Musculoskeletal issues such as rib fractures, chest wall injuries, diaphragmatic dysfunction (weakness/paresis), and post-surgical pain can limit deep breaths and basal expansion, leading to worsened basilar atelectasis. Pleural inflammation (pleuritis) or effusions also cause pain and restrictive mechanics.

Describe how lung tissue and gas exchange issues contribute to respiratory problems.

Lung tissue issues include alveolar collapse (atelectasis), oedema, infection, or fibrosis. Interstitial thickening (oedema or fibrosis) impedes diffusion. Perfusion issues like capillary bed problems, emboli, or shunting alter perfusion (Q) and V/Q matching. Structural changes from chronic diseases (e.g., emphysema, fibrosis) also impact lung mechanics and gas exchange.

How do problems with secretion movement and clearance impact the respiratory system?

Inadequate mucociliary clearance and issues with dynamic compression can impede the removal of secretions, leading to airway obstruction and compromised airway patency.

Explain V/Q mismatch at the micro-level, including conditions of poor ventilation and poor perfusion.

- Optimal Gas Exchange: Occurs with good ventilation (V) and perfusion (Q) alignment.

- Poor Ventilation with Preserved Perfusion: Leads to alveolar collapse (atelectasis) or underventilation (e.g., due to mucus plugging).

- Adequate Ventilation with Poor Perfusion: Results in wasted ventilation without gas exchange (e.g., due to pulmonary embolus).

- Intrapulmonary Shunting: Perfusion of poorly ventilated regions, often compensated by pulmonary vasoconstriction to optimise overall gas exchange.

Provide clinical examples of V/Q mismatch due to specific lung conditions.

- Pneumonia: Leads to reduced ventilation in affected areas due to alveolar consolidation and increased tissue density.

- Pulmonary Embolism: Causes reduced regional perfusion, leading to V/Q mismatch where ventilation is adequate but perfusion is compromised.

How can body positioning and medical interventions optimize V/Q matching?

- Body Positioning: Upright position generally optimises V/Q matching, particularly at the bases. In lateral positions, the dependent lung typically has better perfusion and ventilation, assuming intact diaphragmatic function.

- Medical Interventions: Includes strategic positioning, controlled breathing patterns, and adjustments to inspiratory flow to direct ventilation to better-perfused or better-ventilated regions. Pulmonary rehabilitation and exercise training also enhance overall ventilatory efficiency.

Summarize oxygen and carbon dioxide transport in the blood and their roles in acid-base homeostasis.

- Oxygen Transport: Mostly bound to hemoglobin (4 O2O2 per Hb); a small amount is dissolved in plasma. SpO2SpO2 reflects PaO2PaO2.

- Carbon Dioxide Transport: Primarily as bicarbonate (HCO3−HCO3−) in plasma, formed by the reaction: CO2+H2O⇌H2CO3⇌H++HCO3−CO2+H2O⇌H2CO3⇌H++HCO3−.

- Acid-Base Homeostasis: High CO2CO2 increases H+H+ (lowers pH); ventilation clears CO2CO2. Kidneys excrete H+H+ and retain HCO3−HCO3− (slower). ABG analysis guides ventilation and oxygen therapy. In chronic lung disease, the ventilatory drive may shift to hypoxic drive, requiring careful oxygen titration.

Describe the nature and neurophysiological mechanisms of dyspnea (breathlessness).

Dyspnea is a subjective, multifactorial experience characterized by sensory descriptors, emotional responses, and functional impact. It results from a mismatch between ventilatory demand and the central processing of feedback. Neurophysiologically, it involves brainstem generators modulated by sensory inputs (lungs, chemoreceptors, chest wall), corollary discharge, and emotional influences from the limbic system and association cortex, making it a brain-mediated perception.

What are the clinical management strategies for dyspnea, considering its neurophysiological basis?

Management involves pulmonary rehabilitation and exercise for long-term benefits. Low-dose morphine can reduce the perception of breathlessness by altering sensory processing (high doses risk respiratory depression). Acute distress is managed with calming strategies, pacing, and addressing the neurophysiological drivers of dyspnea.

Outline the systemic involvement in respiratory failure, covering CNS/PNS, MSK, lung tissue, and secretion issues.

- CNS/PNS Impairments: Affect motor control of ventilation (e.g., spinal injuries, brainstem lesions, neuromuscular diseases).

- MSK Issues: Compromise rib movement, diaphragmatic descent, and pleural integrity, leading to hypoventilation and reduced lung expansion.

- Lung Tissue Pathology: Conditions like emphysema, fibrosis, or oedema affect gas exchange and mechanical properties.

- Secretion Clearance Problems: Result in airway obstruction and increased work of breathing.

What are the clinical decision-making implications for ventilatory impairment?

It is crucial to distinguish whether ventilatory impairment is mechanical (pump/muscle), due to airway resistance, gas exchange (diffusion), or secretion-related. This helps determine if physical therapy interventions (e.g., improving diaphragmatic movement, chest wall mechanics, airway clearance) are appropriate, or if medical management (e.g., anticoagulation, infection control, surgery) is required.