Week 7 Flashcards
(35 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?
Volume of gas transfer across membrane per minute
Is proportional to
Surface area / thickness x diffusion constant x pressure difference of two surfaces
V gas per minute & A/T x D x (P1 - P2)
Therefore ideal diffusion is a thin membrane with large SA
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?
Not all air breathed in reaches alveoli, air not participating in gas exchange is called dead space. (VD)
150 ml does not change during exercise
Alvelar volume equation?
VA = VT - VD x FB= how much air reaches alveoli, tidal volume - dead space
Pulmonary volumes and capacities
Volume is one section
Capacity is two or more
Total capacity is residual volume, expiratory reserve volume, tidal volume and inspiration reserve volume.
Obstructive airway disease?
Spirometers can be used to diagnose pulmonary disease such as as COPD
Forced vital capacity is the max air plume air can forcefully expired after ax inspiration
COPD is characterised by increased airway resistance and reduced FVC
0.7 or less
Rest to work transition?
Ventilation (VE) during steady-state exercise occurs inthree phases:
- Phase 1:Immediate increasein ventilation at the onset of exercise.
- Phase 2:Exponential increasein VE, matching metabolic demand.
- Located at theaortic archandcarotid body.
- Phase 3:Plateau phase, where VE stabilizes.
Ventilation During Incremental Exercise?
- VE increaseslinearlywith workloaduntil the ventilatory threshold (VT).
- VT occurs at~50-75% of VO₂max, where ventilationincreases disproportionately.
- After VT,hyperventilation occurs, leading tolower PaCO₂.
Highly trained endurance athletesmay experience:
- Exercise-induced arterial hypoxaemia (EIAH)→ Reduction inPaO₂of ≥10 mmHg from rest.
Possible causes of Exercise-induced arterial hypoxaemia (EIAH)?
Defined as reduction in PP of O2 mmHG from rest, occurring in highly trained males and majority of females.
Theorised to be when demand > capacity, despite capacity usually being more than enough for demand
- Diffusion limitation– Impaired oxygen transfer in the lungs.
- Relative hypoventilation– Inadequate ventilation.
- Ventilation-perfusion (V/Q) mismatch– Uneven airflow and blood flow distribution.
Changes in Breathing Patterns During Exercise
- Duringheavy exercise, VTplateausand further VE increases are due toincreased breathing frequency (fb).
- Atexercise onset, increases in VE are due toincreased tidal volume (VT).
- VT does not exceed 60% of vital capacity.
- Arterial PO₂ (90) , PCO₂ (40mmHG), and pH (7.4) remain stableuntilintense exercise.
Neural Control of Respiration?
- Thebrainstem (pons & medulla)regulates breathing viarespiratory central pattern generators.
- Three main neural groups:
- Ventral respiratory group (VRG)→ Controlsinspiration & expiration.
- Dorsal respiratory group (DRG)→ Controlsinspiration.
- Pontine respiratory group (PRG)→ Modulates breathing rhythm
3 Compartment model:
- Central controller (CC) - Pons, medulla and other parts of brain
Output to >
Effectors - Respiratory muscles
Then to >
Sensors - Chemoreceptors, lung and other receptors
Inputs back to CC >.
Chemoreceptors and Ventilatory control?
Peripheral Chemoreceptors(Carotid & Aortic Bodies)
- Detectchanges in PO₂, PCO₂, and pHin the blood.
- Send sensory input to themedulla (NTS)via thevagus (CN X)andglossopharyngeal (CN IX)nerves.
- ↓PaO₂ = ↑ Ventilation (VE).
Central Chemoreceptors(Brainstem)
- Located in theventral medulla(Retrotrapezoid Nucleus, RTN).
- Sensitive toPaCO₂ and H⁺ levelsin cerebrospinal fluid (CSF).
- ↑PaCO₂ = ↑ VE.
Chemoreceptor Feedback Process:
- Detects changesin blood-gas homeostasis (e.g., increased PaCO₂).
- Sendsafferent signalsto the brainstem.
- Activatesrespiratory premotor neurons(DRG & VRG).
- Increases VE(faster & deeper breathing).
- Restoresblood-gas balance.
Ventilatory Responses to O₂ and CO₂?
Why doesn’t hypoxaemia increase VE substantially?
- O₂ responseiscurvilinear– Small drops in PaO₂do notsignificantly increase VE.
- CO₂ responseislinear– Small increases in PaCO₂ causelarge increases in VE.
-The shape of the oxyheamoglobin curve. Oxygen sensorsdo notrespond strongly unlessPaO₂ < 65 mmHg.
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 individualsduring submaximal exercise.
- Training improvesaerobic capacityby:
- Reducing metabolite accumulation.
- Decreasing afferent feedbackfrom muscles.
- Lowering ventilatory drive.
