Week 7 Flashcards
(34 cards)
Respiratory system basic function and process?
Maintain arterial blood-gas homeostasis, specifically, proper levels of oxygen (O₂) and carbon dioxide (CO₂).
Key Steps:
Pulmonary Ventilation – Movement of air into and out of the lungs
Alveolar Gas Exchange – Exchange of gases between air in the alveoli and blood in pulmonary capillaries
Gas Transport – Transport of O₂ and CO₂ through the bloodstream
Systemic Gas Exchange – Exchange of gases between blood and tissues throughout the body
Structural and functional organisation of respiratory system?
Structural:
Upper (UR) and lower respiratory tracts (LR)
Functional:
Conducting (CZ) and respiratory zone (RZ)
Around 23 airway generations
Nose - UR and CZ start
Nasal Cavity
Pharynx
Larynx - UR ends
Trachea - LR starts
Bronchus
Bronchiole
Terminal bronchiole - CZ ends
Respiratory bronchiole - RZ starts
Alveolar duct
Alveoli - LR and RZ end
Alveolar gas exchange? And cell types?
Alveolar (pulmonary) gas exchange occurs across the pulmonary capillaries in the lungs, where:
O₂ and CO₂ move between alveolar air and blood by simple diffusion, following their partial pressure gradients (high → low).
Two types of alveolar cells (pneumocytes):
Type I cells:
Cover ~95% of the alveolar surface
Thin and flat; critical for efficient gas exchange
Type II cells:
Secrete surfactant, a substance that reduces surface tension, preventing alveolar collapse and aiding in lung expansion
Ficks Law of Diffusion?
Fick’s Law describes the rate of gas transfer across a membrane:
- V̇gas ∝ (A/T) × D × (P₁ – P₂)
Where:
- V̇gas = volume of gas transferred per minute
- A = surface area
- T = membrane thickness
- D = diffusion constant
- P₁ – P₂ = pressure gradient across the membrane
✅ Efficient diffusion requires:
- Large surface area (A)
- Thin membrane (T)
- High pressure difference (P₁ – P₂)
Diffusion path of alveolar gas to erythrocyte?
- Surfactant
- Alveolar epithelium
- Interstitium
- Capillary endothelium
- Plasma
Variables of Mechanics of breathing?
Pressure = Contraction force
Flow = Contraction velocity
Volume = Contraction length
During inspiration = volume of thoracic cavity increases as respiratory muscles contract
Vertical, lateral and anteroposterior diameter all increase
Muscles of respiration?
Inspiration: Sternocleidomastoid, Scalenes, EIM, Parasternal Intercostals, Diaphragm
Expiration: IIM, External abdominal obliques, Internal abdominal obliques
Transverse abdominus and rectus abdominus
Expiration at rest is passive.
During exercise is mainly the diaphragm which is assisted by the rest to increase ventilation and expiration becomes active with muscles above
Airflow and airway resistance ?
Ohm’s law / triangle , VIR
Current (I) = Voltage(V) / resistance (R)
Poiseulles Law
Resistance is dependent upon viscosity length and radius
Exercise induced asmthma?
May have the same sized lungs however instead of dilating when exercising the bronchus constricts limiting airflow.
Pulmonary ventilaton?
Minute ventilaton = Tidal volume x breathing frequency
V(loud of air breathed per min) = VT (Volume of air per breath ) x FB (number of breaths per minute)
Rest -
VT=.5-1L
FB=6-12
V= 6-12L/min
Mild Exercise
VT=1-2L
FB=12-20
V= 15-80L/min
Heavy Exercise
VT=2-4L
FB=40-60
V= 100-200L/min
Alveolar ventilation?
- Alveolar ventilation refers to the amount of air per minute that reaches the alveoli and is available for gas exchange.
- Not all inhaled air reaches the alveoli — dead space (VD) (~150 mL) does not participate in gas exchange.
- Dead space volume does not change during exercise.
Formula:
- VA = (VT – VD) × FB
- VA = Alveolar ventilation (mL/min)
- VT = Tidal volume (air per breath)
- VD = Dead space volume (~150 mL)
- FB = Breathing frequency (breaths/min)
This tells us how much of the breathed-in air actually reaches the alveoli each minute.
Pulmonary volumes and capacities
- Volume = A single measurable amount of air (e.g., Tidal Volume)
- Capacity = A combination of two or more volumes
Key Pulmonary Volumes:
- Tidal Volume (TV): Air moved in/out during normal breathing
- Inspiratory Reserve Volume (IRV): Extra air inhaled after normal inhalation
- Expiratory Reserve Volume (ERV): Extra air exhaled after normal exhalation
- Residual Volume (RV): Air left in lungs after max exhalation
Key Pulmonary Capacities example:
- Total Lung Capacity (TLC): TV + IRV + ERV + RV
What is FVC? Obstructive airway disease? Diagnosis? Characteristics?
- An example is COPD (Chronic Obstructive Pulmonary Disease).
- COPD is a lung condition causing long-term airflow obstruction, making it hard to breathe leading to breathlessness, reduced exercise capacity, and respiratory failure over time.
Diagnosis:
- Spirometry is used to assess lung function and diagnose diseases like COPD.
Forced Vital Capacity (FVC):
- The maximum volume of air that can be forcefully exhaled after a full inspiration.
COPD Characteristics:
- Increased airway resistance.
- Reduced Forced Expiratory Volume in 1 second (FEV₁) relative to FVC.
- FEV₁/FVC ratio ≤ 0.7 indicates airflow obstruction.
What happens to ventilation (VE) during the rest-to-work transition?
Ventilation increases in three phases during steady-state exercise:
Phase 1:
- Immediate rise in VE at exercise onset
- Due to neural input (central command and proprioceptors)
Phase 2:
- Exponential increase in VE
- Begins to match metabolic demand
- Regulated by chemoreceptors (aortic arch & carotid bodies)
Phase 3:
- Plateau phase
- VE stabilizes to maintain steady-state gas exchange
Ventilation During Incremental Exercise?
Ventilation (VE) increases linearly with workload until the ventilatory threshold (VT).
VT typically occurs at ~50–75% of VO₂max, where ventilation begins to increase disproportionately.
After VT, hyperventilation occurs, resulting in a decrease in PaCO₂.
Highly trained endurance athletes may experience:
→ Exercise-induced arterial hypoxaemia (EIAH): a reduction in PaO₂ of ≥10 mmHg from resting levels.
What is Exercise-induced arterial hypoxaemia (EIAH)? Possible causes? Theory??
A drop in arterial oxygen pressure (PaO₂) during intense exercise
— Common in highly trained males and most females
Possible Causes:
- Diffusion Limitation
— Impaired oxygen transfer across alveolar-capillary membrane
- Relative Hypoventilation
— Inadequate breathing rate/volume despite high oxygen demand
- Ventilation–Perfusion (V/Q) Mismatch
— Uneven distribution of air and blood flow in the lungs
Underlying Theory:
- Occurs when oxygen demand exceeds respiratory system capacity, even though that capacity is generally high enough/sufficient
Changes in Breathing Patterns During Exercise
At exercise onset:
- VE increases primarily through ↑ tidal volume (VT)
During heavy exercise:
- VT plateaus (~60% of vital capacity)
- Further increases in VE come from ↑ breathing frequency (fb)
Blood gases & pH:
- Arterial PO₂ (~90 mmHg), PCO₂ (~40 mmHg), and pH (~7.4) stay stable
- Until very intense exercise, when homeostasis may be disrupted
Neural Control of Respiration? Groups? Models?
Brainstem (pons & medulla) contains respiratory central pattern generators that regulate breathing automatically.
Three main neural groups:
- Ventral respiratory group (VRG): controls both inspiration and expiration
- Dorsal respiratory group (DRG): controls inspiration only
- Pontine respiratory group (PRG): modulates breathing rhythm and smooths transitions
3-compartment model:
- Central controller (CC): brainstem areas (pons, medulla) generate rhythm
- Effectors: respiratory muscles (diaphragm, intercostals) execute breathing
- Sensors: chemoreceptors and lung receptors provide feedback to CC
This system ensures breathing is automatic, adaptable, and responsive to the body’s needs (like CO₂ levels), maintaining effective gas exchange.
Chemoreceptors and Ventilatory control?
Peripheral Chemoreceptors (Carotid & Aortic Bodies):
- Detect ↓PO₂, ↑PCO₂, and ↓pH in blood.
- Signal the medulla via vagus (CN X) and glossopharyngeal (CN IX) nerves.
- ↓PaO₂ → ↑ Ventilation (VE).
Central Chemoreceptors (Ventral Medulla, RTN):
- Detect ↑PaCO₂ and ↑H⁺ in cerebrospinal fluid (CSF).
- ↑PaCO₂ → ↑ VE.
Feedback Process:
- Chemoreceptors detect blood-gas imbalance (e.g., ↑CO₂).
- Afferent signals sent to brainstem.
- Activation of DRG & VRG respiratory neurons.
- ↑ Ventilation (faster, deeper breathing) to restore balance.
Ventilatory Responses to O₂ and CO₂?
Why doesn’t hypoxaemia increase VE substantially?
The ventilatory response to O₂ is curvilinear – small drops in PaO₂ cause only minor increases in VE.
In contrast, the response to CO₂ is linear – small rises in PaCO₂ trigger large increases in VE.
Peripheral chemoreceptors (mainly carotid bodies) only respond strongly when PaO₂ falls below ~65 mmHg.
This is due to the shape of the oxyhaemoglobin dissociation curve, which flattens at higher PaO₂ levels, reducing stimulus strength
Ventilatory Control Mechanisms During exercise?
Mild-to-Moderate Exercise (Below Ventilatory Threshold)
- Primary drive must be Feedforward with respect to PaCO2 (and pH)
- Central and peripheral nerve stimuli from Higher brain centres and skeletal muscles anticipateincreased ventilation needs.
- Fine-tuned by peripheral chemoreceptors.
- May involve learned responses.
Heavy-Severe Exercise (Above Ventilatory Threshold)
- Metabolite accumulation (H⁺)→ Causesacidosis, stimulatingchemoreceptors.
Other factors affecting ventilation:
- Increasedbody temperature.
- ElevatedK⁺ and adrenaline.
- Neurogenic inputfrom brain & skeletal muscle.
Effects of Endurance Training on Ventilation?
VE is 20–30% lower in trained individuals during submaximal exercise.
Training enhances aerobic capacity, leading to:
- Reduced metabolite accumulation (e.g., H⁺, lactate).
- Decreased afferent feedback from working muscles.
- A lower ventilatory drive for a given workload.
Does the pulmonary system adapt significantly to endurance training?
Major adaptations occur in the cardiovascular, haematological, and muscular systems:
- ↑ RBC mass, plasma volume, LV size/thickness, mitochondrial density, capillarisation, type I fibres.
- Improves O₂ delivery, uptake, and ATP turnover.
Pulmonary system (lungs & airways):
- Lung size and airways do not change significantly.
- Diffusing capacity remains largely unchanged.
- Respiratory muscles (diaphragm, intercostals) may improve in strength and fatigue resistance.
- Some maladaptations may occur, e.g., airway hyperresponsiveness in swimmers/skiers.
