Mechanical properties of chest wall Flashcards

1
Q

Describe the various neural centres that control respiration, their function and their components

A
  • Respiratory Centre
    • Located in the medulla
    • Drives ventilation rate and volume via afferents to respiratory muscles’ motor nerves ^[causes contraction]
  • Neuronal Groups
    • Dorsal Respiratory Group
      • Primarily inspiratory neurons - sending out signals
    • Ventral Respiratory Group
      • Caudal: Mix of inspiratory and expiratory neurons
      • Rostral: Airway dilator functions
      • Pre-Botzinger Complex: Likely central pattern generator site ^[pattern of breathing, start and stop]
    • Botzinger Complex
      • Expiratory neurons
    • Pontine Respiratory Group
      • Fine control of respiration, influences medullary respiratory center
  • Cortex
    • Voluntary breathing interruption, e.g., singing, talking ^[aka influence pattern of breathing]
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2
Q

Describe how neuronal firing is linked to generation of respiratory activity

A

Respiratory Cycle and Neuronal Firing
- No single pacemaker is responsible for generating respiratory activity ^[c.v. cardiac]
- Likely a complex interaction of different groups of neurons (6 - half and half):
- Early inspiratory, inspiratory augmenting, late inspiratory
- Expiratory decrementing, expiratory augmenting, late expiratory
- Firing of neurons results in three respiratory phases: - Inspiratory ^[turn on signals, get muscles involved]
- Expiratory Phase 1 (passive) ^[i.e. recoil of lungs]
- Expiratory Phase 2 (active) ^[turning on signals, get muscles involved]

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3
Q

What is the most important factor that influences respiratory rate and how does it exert influence?

A

CO2 being the most important influence on respiratory rate
- CO2 influences central chemoreceptors

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4
Q

LIST the two main controllers of ventilation

A

Central and peripheral chemoreceptors

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5
Q

Describe central chemoreceptors

A

Central Chemoreceptors
- Neurons that are separate from the respiratory center, in the medulla
- Stimulated by H+ concentration in CSF determined by paCO2 (H+ cannot cross BBB, CO2 diffuses easily) - hence why ‘most important factor in determining ventilation’
- CO2 reacts with H2O to form H2CO3, dissociating into H+ and HCO3
- Increased paCO2 leads to increased afferent firing from chemoreceptors to respiratory center
- Respiratory centre controls efferent output to the respiratory muscles (effector), to increase minute ventilation
- Maintains paCO2 under tight control (+/-3) around 40mmHg: most important determinant of minute ventilation

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6
Q

Describe peripheral chemoreceptors

A

Peripheral Chemoreceptors
- Carotid Bodies
- Respond to paO2, paCO2, and pH
- Afferent signals via glossopharyngeal nerve
- Aortic Arch
- Respond to paO2 and paCO2 ^[potential c/c question within, and compared to centrals]
- Afferent signals via vagal nerve
- Fast acting compared to central chemoreceptors ^[responds to oxygen tension? within vessels] -> drives 20% of response (central 80%), ^[big driver to hypoxia response?]
- Histologically - Glomus or type I cells in contact with synaptic nerve endings
- Activation results from hypoxia, hypercapnia, or acidosis
- Inhibition of K+ channels leads to decreased efflux, and depolarisation, opening VGCCs (and calcium influx)
- Ca2+ triggers neurotransmitter release (dopamine, probably) and afferent signaling via nerves above to respiratory centre (controller), sending efferent signals to respiratory muscles (Effector) to increase minute ventilation

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7
Q

List and briefly describe other controllers of respiration

A
  • lung receptors
    - pulmonary stretch - respond to over distention
    - juxtacapillary receptors - respond to interstitial fluid APO
    - bronchial C - irritants in blood e.g. histamine
    - irritant receptors - irritants in gas e.g. cold and dust
  • baroreceptors - increased mv with hypotension
  • muscle and joint receptors - increased mv ^[minute ventilation] with movement
  • SNS -increased MV with increased SNS activity
  • cortex - can voluntarily override respiratory centre
  • pregnancy and progesterone - directly stimulates respiratory centre
  • exercise increases MV with exercise
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8
Q

Provide an overview of respiration

A
  • Breathing controlled by medullary respiratory centre
  • Efferent signals to respiratory muscles cause volume and pressure changes
    • Contraction leads to volume and pressure changes which draw air into lungs
  • Lungs lie in thorax, separated from chest wall by intrapleural space
  • Lungs tend to collapse; chest wall tends to expand
  • Balance leads to negative intrapleural pressure (approx. -5cmH2O)
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9
Q

Describe surface tension, surfactant and its role

A
  • Surface Tension (ST)
    • Force across liquid surface (across imaginary line 1 cm long)
    • Develops at air-water interfaces
    • Greater forces between water molecules than water and gas molecules: liquid surface area becomes as small as possible
    • Result: alveolus has tendency to collapse on itself ^[like a bubble]
  • Law of Laplace
    • Pressure = 2 x ST/radius
      • radius inversely proportional to pressure
      • alveoli would collapse if it weren’t for surfactant, reducing surface tension as radius decreases
  • Surfactant
    • Lipid (90%) fluid from type II alveolar cells
    • Majority phospholipid: mainly dipalmitoyl phosphatidyl choline (DPPC): hydrophilic end faces alveolar fluid lining alveoli, hydrophobic end faces gas filled alveolus
    • Acts as detergent, reducing water molecule attraction, thus reducing surface tension and preventing collapse
    • Decreases ST as lung volume decreases: as lung vol decreases DPPC squeezed together, decreases water-water interaction and thus decreases surface tension
      Note: relevant in compliance
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10
Q

Breakdown the respiratory cycle in terms of the key pressures and volumes

A
  • Starting Point: FRC (Functional Residual Capacity)
    • Intrapleural pressure = -5cmH2O
    • Alveolar pressure = Atmospheric (0cmH2O) - no net movement of air
  • Inspiration
    • Intrapleural pressure falls to -8cmH2O
    • Alveolar pressure falls to -1cmH2O
    • Gas influx into alveoli (~500ml)
  • Expiration
    • Intrapleural pressure rises to -5cmH2O (i.e. more positive)
    • Alveolar pressure rises to +1cmH2O before baseline
    • Gas exits alveoli to atmosphere (~500ml)
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11
Q

Define compliance, factors that contribute to it

A
  • Definition: Ratio of volume change to corresponding pressure change (C = ∆V/∆P) - slope of PV relationship
  • Extent to which lungs expand for each unit increase in transpulmonary pressure (if enough time allowed to reach equilibrium)
  • Two determinants of compliance in respiratory system:
  • Lung Compliance
    • Determined by lung’s elastic recoil (connective tissue, surface tension)
    • Normal value: 200ml/cmH2O
    • Influenced by factors: Surfactant (most important), age (shape and size), posture, size, lung volume, fibrosis (Stiff, more difficult to expand)
  • Chest Wall Compliance
    • Normal value: 200ml/cmH2O
    • Impaired by factors affecting chest wall expansion (e.g., scoliosis, obesity ^[more tissue on chest wall,m ore pressure])
  • Total Lung Compliance: Combination of lung and chest wall compliance (around 100ml/cmH2O)
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12
Q

Describe flow and factors that contribute to it

A

Flow
- Flow Definition: Substance passing point per unit time
- Flow governed by Ohm’s Law
- Two main types of flow:
- Laminar Flow: Straight, unbranched tube; fastest center flow ^[i.e. in middle of tube]
- Turbulent Flow: Irregular or branched tubes; eddies, higher resistance
- n.b. Transitional Flow: Mixture of laminar and turbulent
- in lung: mix of laminar, turbulent and transitional
- Flow Equation: Flow = Pressure difference (pressure coming in - going out) / Resistance
- Resistance Formula: R = 8nl / πr ^4
- n = viscosity ^[usually fixed]
- l = length ^[usually fixed]
- r = radius
- radius most important e.g. half radius = 16 fold change ^[relevance in pathology]
- Laminar Flow
- ‘series of concentric cylinders sliding over each other’
- Faster in center, slower at edge
- ‘even front’
- Turbulent Flow
- higher flow rates/flow through branched or irregular tubes
- causes concentric circles to breakdown
- flow becomes small currents or eddies, higher friction
- Reynolds Number (Re) - describes tendency towards turbulent flow
- Dimensionless number indicating likelihood of turbulent flow
- Re = ρDv / η
- ρ = Gas density
- D = Tube diameter
- v = Flow velocity
- η = Viscosity of gas
- >2000 associated with turbulent flow

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13
Q

Describe some clinical implications of respiratory mechanics

A
  • Flow in Large Airways
    • Predominantly turbulent flow
    • frictional forces influences flow (come from lining of airway wall– increases with scarring)
    • note: driving pressures really high, so overall frictional forces do not influence flow
  • Gas Density
    • Different gas densities (e.g., Heliox - gas mixture) to improve flow and oxygen delivery to alveoli
    • more laminar flow due to He low density– get into alveoli more easily
  • Flow in Small Airways
    • Predominantly laminar flow, resistance most important factor
      • Viscosity and length are essentially fixed
      • radius of airway is the most important factor determining resistance
  • Factors Affecting Airway Radius
    • Internal: Fluid, smooth muscle hypertrophy/contraction
    • External: Lung volume, external compression of airway ^[e.g. haemothorax]
  • Compliance
    • Extent of lung expansion per unit increase in transpulmonary pressure
    • Factors influencing decreased compliance
      • Physiological: Age, posture (lying flat is worse), decreased lung volumes
      • Pathological: Fibrosis, alveolar overdistension (COPD over PEEP), chest wall deformities, obesity
  • Time Constants (τ)
    • if initial rate of change continued, at what time would process have been completed
    • alveolar filling and emptying is an exponential process, measured by t
      • one t = 63%
      • 3t = 95%
    • τ = resistance x compliance
    • normally in 0.2s, alveolar filling emptying 95% complete at 0.6s
  • Fast and Slow Alveoli (imp)
    • resistance and compliance not uniform across lung, therefore t varies
    • Fast: Low resistance, compliance, or both (e.g., pulmonary fibrosis): empty and fill quickly
    • Slow: High resistance, compliance, or both (e.g., COPD): empty and fill slowly
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14
Q

Breakdown the work of breathing

A
  • Work = Force x Distance
  • Respiratory Work: Work = Pressure x Volume
    • Normal work small (0.3-0.6J/L), <2% of metabolic rate or 3ml/min O2
    • Note: respiratory muscles are very inefficient and with increased work of breathing this becomes much higher
  • Inspiratory Work
    • Elastic and non-elastic work
    • Compliance work against lung recoil, non-elastic work against airway resistance
  • Expiratory Work
    • Primarily elastic? work
  • Factors Influencing Work
    • Increased work with decreased compliance or increased resistance
  • Elastic work
    • 65% of work
    • Compliance work: to overcome recoil of the lungs
    • Work against elastic forces stored as potential energy which is used during expiration
    • Any factor that decreases compliance will increase elastic work (i.e. inversely related)
  • Non-elastic work
    • 35% of work
    • Work to overcome airway resistance
    • Non-elastic work lost as heat
    • Any factor that increases resistance will increase non-elastic work (directly related)

Pathology and breathing:
- normal: most energy efficient point - more elastic and resistive work: optimal work of breathing
- energy efficient point at higher respiratory rate (greater pressure for ventilation, ventilate at higher respiratory rate)
- air flow resistance: energy efficient point at lower respiratory rate ^[greater gap between breaths, long expiration time; ventilation sets respiratory rate lower]

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15
Q

Review lung volumes and capacities

A
  • Volumes: Directly measured
  • Capacities: Sum of two or more volumes
  • Lung Volumes
    • Tidal volume, inspiratory reserve volume, expiratory reserve volume, residual volume
  • Lung Capacities
    • Total lung capacity, vital capacity, inspiratory capacity, functional residual capacity

Functional Residual Capacity (FRC)
- Amount of gas after tidal expiration
- Balance point between chest wall tendency to expand and lung tendency to collapse
- Functions of FRC
- Minimizes work of breathing, pulmonary vascular resistance, V/Q mismatch, airway resistance
- **Primary oxygen store ^[pre-oxygenation, keeps oxygenated]
- prevents atelectasis (certain volume inside)
- Maintains steady arterial pO2, buffers changes in alveolar pO2 during respiratory cycle

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16
Q

Compare and contrast the role of carotid bodies and aortic arch in regulating respiration

A
  • Carotid Bodies
    • Respond to paO2, paCO2, and pH
    • Afferent signals via glossopharyngeal nerve
  • Aortic Arch
    • Respond to paO2 and paCO2 ^[potential c/c question within, and compared to centrals]
    • Afferent signals via vagal nerve
  • Fast acting compared to central chemoreceptors ^[responds to oxygen tension? within vessels] -> drives 20% of response (central 80%), ^[big driver to hypoxia response?]
  • Histologically - Glomus or type I cells in contact with synaptic nerve endings
    - Activation results from hypoxia, hypercapnia, or acidosis
    • Inhibition of K+ channels leads to decreased efflux, and depolarisation, opening VGCCs (and calcium influx)
      - Ca2+ triggers neurotransmitter release (dopamine, probably) and afferent signaling via nerves above to respiratory centre (controller), sending efferent signals to respiratory muscles (Effector) to increase minute ventilation