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Physiology B2 & B3 > Resp > Flashcards

Resp Flashcards

1
Q

Draw the standard spirometry graph, showing all 4 volumes and 5 capacities:

LITER

A
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2
Q

List and explain the static lung volumes

A

IRV: inspiratory reserve volume: is the amount of air in excess of tidal volume that can be inhaled with maximum effort

IC: (TV + IRV) maximum amount of air that can be inspired after a normal tidal expiration

FRC: amount of air remaining in the lungs after a normal tidal expiration

RV: amount of air remaining in the lungs after maximal expiration. Important as it keeps the alveoli inflated between breaths and mixes with fresh air on next inspiration

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3
Q

Why do translung pressure changes (PL=Pa-Ppl) lag behind changes in Ppl?

A

Two major factors:

  • Airway resistance (RAW)
  • Total compliance (CT)

Such that Time = Raw * CL

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4
Q

Which parts of the flow-volume loop are effort dependent and effort independent? What limits the effort independent curve?

A

All of inspiratory curve and vertical part of expiratory curve (effort dependent.

Linear region after PEF (> 2L), effort independent. Limited by lung elasticity and airway resistance

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5
Q

What does a pressure-volume loop represent? Is expiration a passive or active process @ TV?

A

PV loop represents external work during respiration, @ TV expiration is a passive process

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6
Q

What happens to FRC in emphysema?

A

Loss of alveolar tissue -> loss of elastic recoil (barrel chest)

(FRC ↑)

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7
Q

What happens to FRC in fibrosis?

A

Stiff lungs with ↑ elastic recoil

(So FRC occurs at small lung volume)

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8
Q

Draw and label the important pressures in the lungs (barometric, intrapleural etc)

A
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9
Q

Illustrate the phases of the respiratory cycle and what determines them pressure wise

A
  1. FRC: Ppl = -PL (no muscle force). (PA = 0)
  2. Inspiration: muscles contract → Ppl ↓ and -PL ↓ lags (due to RAW & CL): PA < 0 → air flow into alveoli
  3. End of I / start of E: Ppl = -PL, but at a larger magnitude.
  4. Expiration: muscles relax → recoil of system → Ppl ↑ with lagging -PL ↑: PA > 0 → air flow out of alveoli.
  5. 2 parts of Ppl: (Ppl = PA - PL)
    • PA : air flow : lung volume (integrated flow).
    • PL: lung volume (integrated flow)
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10
Q

What is the name for each stepwise components of the respiratory tract?

A
  • Trachea
  • Bronchi, primary -> lobar -> segmental
  • Bronchioles (terminal segments of conducting system) – no glands and cartilage
  • Respiratory bronchioles – first portion of respiratory system
  • Alveolar ducts
  • Alveoli
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11
Q

How does the CSA of the respiratory tract change from trachea to alveoli? How does this relate to velocity of airflow?

A
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12
Q

What structures contribute highest to airway resistance?

A

Lower airways

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13
Q

What is the formula for resistance along a vessel (same as in artery)?

A
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14
Q

What structures are susceptible to transmural pressures?

A

Bronchioles susceptible to transmural pressures due to no cartilage -> dynamic small airway closure due to to collapse

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15
Q

Why is it easier to breathe in that out, particularly in diseased states such as COPD?

A

Lung volumes affect airway diameter dt interconnectedness of alveoli, inspiration, expansion of surrounding alveoli holds alveoli open.

COPD -> increased airway resistance limits ability to expire, but not necessarily inspire -> air trapping

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16
Q

How is static lung compliance related to disease?

A

Emphysema -> ↑↑↑ compliance

Fibrosis -> ↓↓↓ compliance

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17
Q

Explain the V-P loop with respect to dynamic compliance and the hysteresis shape

A

Dynamic compliance can be interpreted as the gradient of the slope in the VP at each point. Ie. Compliance low at start of inspiration, but decreases during inspiration. Low again at start of expiration, but decreases once again.

This change in compliance is dt recruitment of surfactant from micelles, eg. During inspiration, concentrations of surfactant decrease -> recruitment of surfactant from micelles -> ↓↓↓ compliance (vertical part of inspiratory loop)

During expiratory phase, flat at top due to less recoil, but as volume reduces, micceles form and lung volume reduces dramatically

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18
Q

Explain, using laplaces’ law, the role of surfactant in maintaining equal alveoli expansion. What is the other role of surfactant?

A

Surfactant: ↓ surface tension -> ↑ compliance

As an alveolus shrinks, its surface area ↓ and the surface conc. of surfactant rises -> improved stability

Precoil = 2T/r -> smaller radius of alveoli, far harder to inflate, so without surfactant, rapidly expanding alveoli would keep expanding unequally as they will have a far greater compliance (also remember that surface tension is largest determinant of the compliance of lung).

The other role of surfactant is to keep alveoli dry.

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19
Q

Flow conditions in airways:

A
  • Laminar
  • Transitional
  • Turbulent (vocal cords)
  • Turbulance arises at bifurcation points*
  • Flow in airways is transitional*
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20
Q

What are the components of total pulmonary ventilation?

A

Physiological dead space (nil gas exchange), broken down to:

  • Anatomical (conducting airways: nose -> bronchioli)

and

  • Functional dead space ventilated lung parts which are not perfused, very small in non-diseased pt)

+

Alveolar ventilation (ONLY gas exchange)

Va (alveolar) = Vt (total) – Vd (deadspace)

21
Q

Where is ventilation smallest and largest in the lung?

A

Ventilation is smallest at apex, biggest at base (CL)

22
Q

What features of the alveolar respiratory membrane determine diffusion? (imp!)

A
  • Membrane thickness (lung oedema, lung fibrosis)
  • Diffusion coefficient (remember CO2 23x)
  • Total surface area of respiratory membrane
  • Pressure gradients (driving force for diffusion is pressure gradient from capillary to alveolus)
23
Q

Outline factors involved in gas diffusion

A

Alveolar Vascular Sheet

  • Sheet of flowing blood
  • V.close proximity of gas and blood

Alveolar Respiratory Membrane

  • Short diffusion distances (nucleus)
  • Factors affecting gas diffusion
    • Thickness of membrane - Very thin
    • DIffusion coefficient - Depends on gas solubility in membrane
    • Total SA of resp membrane - ↓ with aging
    • Pressure gradients
24
Q

Determine alveolar pressure gradients for CO2 and O2

and

Explain why CO2 diffuses much better than O2

A
  • Driving force for diffusion is difference in partial pressures in capillary and alveolus
    • Pressure gradient:
      • O2 is 2.5 x, and for CO2 is 1.15 x initial value of blood entering alveoli
  • Rate of gas exchange dependent on ventilation, perfusion (CO) and haemoglobin concentration.
25
Q

Identify factors determining perfusion

A
  • Lung perfusion
    • Corresponds to CO
    • Intrathoracic vessels are capacitive elements
    • Pulsatile flow even in capillaries
  • Vascular resistance
    • Low resistance in lung vessels: RL = 10 x smaller than that of systemic circulation.
      • 40% of RL is determined in capillaries
    • Lung volume determines R L (in capillaries) —> dependent on respiration phase
      • RL ↑ at beginning of expiration (because PA ↑) —> **compresses the capillaries **
      • RL ↓ at beginning of inspiration (because PA ↓).
  • Hydrostatic Considerations
    • low-pressure/low-resistance system —> influenced by gravity much more than systemic circulation
26
Q

What are the two main ways pulmonary flow is modulated?

A
  • Vasoconstrictors: Low PAO2
  • Vasodilators: High PAO2

nb. Pulmonary blood flow is not much dependent on PaCO2

27
Q

Explain the V/Q ratio

A

The ratio of ventilation to blood flow

Normal healthy individuals = 0.8

28
Q

What happens to the VQ ratio in hyper and hypoventilation?

A
  • If ventilation > perfusion: (relative hyperventilation)
  • if ventilation < perfusion: (relative hypoventilation)
29
Q

What is the alveolo-vascular effect?

A
  • No air -> no blood
  • Increasing resistance in vessels perfusing lung areas that are poorly ventilated.
  • Ie. ↑CO2alveolar ↓O2alveolar -> ↑ resistance in vessels
30
Q

What is the alveolo-bronchiolar effect?

A
  • No blood -> no air
  • ↑O2 alveolar ↓CO2alveolar -> ↑Air way resistance
31
Q

How does ventilation and perfusion change over lung from apex -> base?

A

Both increase, but perfusion increases to a greater extent .

Therefore, V/Q ratio decreases from apex -> base

32
Q

How does this change in perfusion affect resistance in pulmonary vessels and airway resistance from apex -> base of the lung.

A

Relative hyperventilation at apex:

  • Alveolo-vascular effect decreases resistance in vessels dt ↑alv o2.
  • Alvelo-bronchiolar effect ↑alv o2 -> ↑ airway resistance

Relative hypoventilation at apex:

  • Alveolar vascular effect (no air -> no blood) -> ↑vascular resistance
  • Alveolo-bronchiolar effect (no blood, no air) -> ↓airway resistance
33
Q

Describe anatomical and physiological shunts

A

Alveoli are perfused as normal but ventilation fails to supply perfused area

Anatomical shunt:

  • Small degree is normal
  • Occurs when too much of the blood supplying the lung tissues via the bronchial arteries is being returned via the pulmonary veins without undergoing gas exchange
  • also some of the coronary veins drain directly into the left ventricle of the human heart
  • This is why the arterial PO2 is slightly lower than the alveolar PO2.
  • Blood never “sees” O2 so O2 therapy does not help

Physiological shunt:

  • (also known as venous admixture) can develop when **ventilation to lung units is **absent in the presence of continuing perfusion
  • blood perfusing this unit is mixed venous blood; because there is no ventilation, no gas is exchanged in the unit
  • effect is similar to anatomical: deoxygenated blood bypasses gas-exchanging unit, mixes with arterial blood
  • e.g. mucus plugs, airway oedema, tumour, foreign bodies
34
Q

What are the three basic elements of control for breathing?

A

Gas exchange regulated via control of ventilation:

  • I.  Sensors: central and peripheral (chemoreceptors, airway, lung, etc.)
    • Negative feedback via sensors.
  • II.  Central controller (CPG): brain (pons, medulla, SC, higher centres)
  • III.  Effectors: respiratory muscles
35
Q

What are the sensors involved in respiration?

A
  • Chemoreceptors
    • Central (most important for control)
    • Peripheral (less important, but take over if CO2 is chronically high)
  • Tracheo-bronchial receptors
    • Stretch receptors (mechanoreceptors; Hering-Breuer reflexes)
    • Irritant receptors
    • J receptors (“juxta-capillary”)
  • Other receptors (e.g. nose & upper airway etc)
  • – Nose and upper airway receptors: similar to irritant receptor
36
Q

Where are the central chemoreceptors located and what do they respond to?

A
  • Specialised cells in ventrolateral surface of medulla
  • respond to changes in pH
  • Only CO2 can cross BBB
  • Response to changes in Co2 rapid, adaptation to HCO3- is slow
37
Q

Where are the peripheral chemoreceptors located and what do they respond to?

A
  • Peripheral chemoreceptors located in carotid bodies
  • Primarily respond to changes in PO2, but also changes in pH (but difficult to separate from PaCO2) but sensitivity modulated by changes in PCO2.
  • They are responsible for
  • **These sensors are responsible for all ventilation↑ due to ↓ in PaO2 **
  • Therefore if a patient has COPD and chronic hypoximia and provide rapid oxygen therapy this may inhibit the patients respiratory drive and bring about respiratory suppression
38
Q

How do the central and peripheral receptors repsond to a rise in CO2, O2, and or pH?

A
  • **Arterial PCO2 is the most important of these regulators. **
  • At normal PaCO2, response ↑ only at low PaO2.
    • Normally small; significant at high altitude.
  • pH↓ stimulates ventilation (ketoacidosis)
39
Q

How does the central pattern generator of respiration work?

A
  • Central pattern generator can be overridden by voluntary control (“higher centres”)
  • If early inspiratory neurones inhibit late inspiratory cells, switching results: one cell population drives another…
  • Therefore, inspiration and expiration are distinct functions and one does not induce the other, as is the common belief, but one of two dominates the behavior by generating a faster rhythm.

Pool A: NTS -> tonic inspiratory output to motorneurons and pool B

Pool B : NPA (pneumotaxic centre, triggered by ramp signals), NA -> stimulates pool C, additional stimulation of inspiratory neurons; modulated by vagal afferents

Pool C: (botz complex (NRF) and NRA -> inhibits pool A -> inspiratory cut-off switch

40
Q

What happens to PCO2 and PO2 during exercise? What drives the increase in ventilation with exercise?

A

Exercise:

  • PO2 ~
  • PCO2 ~ or ↓
  • Limb movement and ↑body temps thought to be main drivers for increased resp. during exercise
  • ventilation ↑ immediately when exercise begins, and this ↑ in minute ventilation closely matches ↑ in O2 consumption and CO2 production that accompanies exercise
  • ↓ arterial pH stimulates ventilation that is out of proportion to the level of exercise
41
Q

What is the role of the respiratory system in acid-base balance?

A
  • CO2 combines with water to form carbonic acid
  • Carbonic accid dissociates immediately to H+ and HCO3-
  • Changes in ventilation affect PCO2, and therefore the body’s acid-base status
  • Respiratory acidosis and alkalosis are the two types of disturbance caused by changes in ventilation
  • The lungs can also compensate for metabolic disturbances by altering ventilation, unlike the renal system they can react quickly
42
Q

What happens in respiratory acidosis?

A
  • CO2 is increased
  • Respiratory acidosis resutls from hypoventilation or ventilation:perfusion mismatch
  • Can occur in many respiratory diseases including asthma, a blocked airway or collapsed lung
  • Drugs that reduce resp drive (e.g. morphine or barbituates) may cause respiratory acidosis
  • The renal system may act to compensate, but this takes time
43
Q

What happens in respiratory alkalosis?

A
  • CO2 is reduced
  • Respiratory alkalosis generally results from hyperventilation or blowing off too much CO2
  • It can be stimulated by hpoxic drive in diseases such as COPD
  • Damange to the brainstem, some drugs (e.g. aspirin) and hysterical overbreathing can also cause respiratory alkalosis
  • The renal system may act to compensate, but this takes time
44
Q

What are the largest chemical buffer pools in our body?

A
  • ECF: inorganic H2PO4-, plasma proteins
  • ICF: Cellular proteins and organic HPO4-
  • Bone: Mineral H2PO4-

These minimise pH change but do not remove acid or base.

45
Q

How does Hb work as a buffer and how does this relate to the Bohr effect?

A
  • Hb can bind and release H+ ions, therefore acts as buffer.
  • The Bohr effect is due to ↑ [H+] (and therefore ↓pH) resulting in a right shift of the Hb-O2 dissociation curve. At a given PO2, Hb will have a lower O2 saturaiton -> more unloading.
46
Q

Why is bicarbonate such a good buffer?

A
  • Components HCO3 + CO2 are abundant
  • System is open
  • Controlled by both lungs and kidneys
47
Q

What are the bicarbonate buffer & Henderson hasselbalch equations?

A

Bicarbonate buffer equation:

H20 + CO2 H2CO3 HCO3- + H+

Henderson hasselbalch equation:

pH = 6.1 + log [HCO3-] / [CO2]

  • Normal pH requires HCO3-:CO2 = 20:1
  • In above equation PCO2 expressed as mmol/L
  • To convert to PCO2 * 0.03
  • pH = 6.1 log [HCO3-]/ (0.03 * PCo2)
48
Q

What does it mean that the bicarbonate buffer system is open?

A

Means that the components of the system can be added or removed from the body at controlled rates

Achieved by three mechanisms:

  1. Metabolism provides large stores of CO2
  2. Respiration can change the amount of CO2 in the ECF
  3. Kidneys can change the amount of HCO3- in the ECF

Physiology B2 & B3 (5 decks)

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