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VETS2011 Structure and Function I > Resp Physiology > Flashcards

Resp Physiology Flashcards

1
Q

Three Features of Respiratory Surfaces

A
  1. Enormous surface area which maximises potential area for gaseous exchange
  2. Highly vascularised to aimise the potential for gaseous exchange
  3. Very thin epithelium to provide a small barrier for gaseous exchange
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2
Q

Mechanism of Inspiration

A
  1. Diaphragm pulls thoracic cavity caudally, intercostal muscles pull ribs upp
  2. pulls on parietal pleura, increasing pleural volume, decreasing intrapleural pressure
  3. This increases the transmural pressure gradient, pullling on visceral pleura
  4. Lungs expand as visceral pressure pulled out
  5. Expansion of lung volume leads to decrease in intrapulmonary pressure, causing ressure gradient between atmospheric pressure and pressure in alveoli
  6. Air rushes in from higher pressure to lower pressure
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3
Q

Mechanism of Expiration

A
  1. Relaxation of diaphragm and external intercostals decreases thoracic volume, increasing intrapleural pressure
  2. Increase in pressure causes visceral pleura to move inwards, decreasing lung volume
  3. Decrease in lung volume increases intrapulmonary pressure, causing pressure gradient between air in alveoli and atmosphere
  4. Results in movement of air up respiratory tract
  5. Intrapleural pressure remains negative throughout because of the elastic recoil of the lungs
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4
Q

Process that Limits Volume of Air

A

Expiration driven by pressure gradient between gas in lungs and gas in atmosphere. As gas is expelled from alveoli, encounters resistance which reduces flow and pressure.

Once pressure of this gas is lower than intrapleural pressure, small airways collapse. This is called dynamic small airway closure.

Volume of air that remains inside lungs after this occurs is termed residual volume and cannot be expired.

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5
Q

Early Dynamic Small Airway Closure

A

Example is cat asthma. Obstructive diseases such as this increase resistance in small airways leading to early dynamic small airway closure and hence increased RV. This means the capacity for expiration is reduced.

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6
Q

Counter-Current Multiplication

A

Much more efficient method of extracting oxygen from air and water in aquatic animals and avian species.

Oxygen flows consistently past oxygen in opposite direction so that an equilibrium in oxygen concentration between the air/water and blood is never met meaning maximum oxygen can be extracted.

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7
Q

Tidal Volume

A

Volume of air moved into or out of the respiratory tract during normal resting conditions

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8
Q

Minute Ventilation

A

VE = tidal volume x respiratory rate

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9
Q

Dead Space

A

Volume of air not exposed to functioning gas exchange surfaces. May be anatomical - volume of air remaining in cinductive pathways or physiological - anatomical dad space plus air in alveolar that is not able to exchange gas.

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10
Q

Respiratory Measurements (IRV, ERV, RV, FRC, VC, TLC)

A

IRV - Inspiratory reserve volume - maximum air which can be inspired additionally to tidal volume.

ERV - Expiratory reserve volume - maximum volume that can be expired additional to tidal volume.

RV - Residual volume - volume of gas remaining in the lungs after maximal expiration, which is determined by limits of rib capacity. Reduces in obstructive diseases.

FRC - Functioning Residual capacity - air reaining after normal exhalation. FRC = ERV + RV

VC - Vital capacity - maximum volume that can be expired following maximal inspiration. VC = IRV + V + ERV

TLC - Total lung capacity - determined when lungs reach elastic limit. TLC = VC + RV

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11
Q

4 Factors Determining Rate of Gas Diffusion

A
  1. membrane thickness
  2. membrane surface area
  3. diffusion coefficient of gas
  4. pressure difference of gas between two sides
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12
Q

3 Factors Preventing Lung Collapse

A
  1. Pulmonary surfactant which reduces surface tension of alveoli, keeping them open and reducing energy required to expand lung
  2. Interdependence of alveoli - walls of adjacent alveoli mutually attached so alveoli all do the same thing
  3. Transmural pressure gradient between gas in lungs ad gas in pleural cavity
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13
Q

Pores of Khon

A

Connect to adjacent alveoli, anastomosing allowing for equalisation of pressure across alveoli and equal expansion of all alveoli. Not present in cow or pig due to heavy CT between lobules. Blockage of alveoli in these species will result in absorption of gas and collapsing of alveoli.

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14
Q

Pulmonary Vascular Resistance

A

In contrast to the systemic circulation, the pulmonary circulation is a low pressure, low resistance, high compliance system. Both have same blood flow but pulmonary vessels are wider and do not show thick muscular coats as systemic vessels do.

PVR = mean pulmonary arterial pressure - left atrial pressure / cardiac output

Left atrial pressure can be measured by balloon tipped catheter inserted into pulmonary artery

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15
Q

Changes in PVR during Breathing

A

Changes in PVR during inflation and deflation gives opposing effects on alveolar and extra-alveolar vessels.

High PVR during deflation as extra-alveolar vessels narrow, ressitance decreases during inflation due to vessel dilation. Inflation above functional residual capacity increases PVR as the capillaries are flattened by high tension in septa leading to increased resistance flow.

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16
Q

Changes in PVR during Exercise and Hypoxia

A

During exercise, extra blood flow is accommodated by increasing the number of open capillaries, which decreases PVR, distending capillaries and increasing the rate of flow which decreases PVR and increasing pulmonary arterial pressure. Overall PVR is decreased.

Local hypoxia causes vasconstriction or pulmonary arteries to prevent blood flow to poorly ventilated regions and divert blood flow to better ventilated regions. This increases PVR.

Although in these circumstances there is opposite effects on PVR, in both situations blood flow to oxygenated areas is increased.

17
Q

Factors Affecting the Movement of Fluid in/out of Capillaries

A

Move in:

  • plasma osmotic pressure

Move out:

  • capillary pressure
  • osmotic pressure
  • negative interstitial pressure

There is a net movement of fluid out of the capillaries. But most of the fluid returns to capillaries at other end of bed and the rest is drained by the lymphatics.

18
Q

Pulmonary Oedema

A

Rapid leakage of proteins and fluid from capillaries into spaces and alveoli. This causes interstitial spaces and alveoli to become filled with free fluid.

Two causes may be left sided heart failure or mitral valvular disease and capillary membrane damage.

19
Q

Pleural Effusion

A

Free fluid collects in pleural space, due to blockage of lymphatic drainage, cardiac failure, reduced plasma osmotic pressure, infection and inflammation of pleural surfaces. This makes breathing difficult as it is harder to expand lungs.

20
Q

Factors for O2 and CO2 Concentration in Alveolus

A

O2 concentration:

  • rate of removal from alveoli by blood
  • rate of entry into alveoli be ventilation

CO2 concentration:

  • rate of entry into alveoli from blood
  • rate of removal from alveoli by ventilation
21
Q

Transport Methods of O2

A

Dissolved in blood, proporitonal to partial pressure and bound to haemoglobin which also depends on partial pressure of O2

22
Q

Bohr Shift

A

Is the shifting of the oxygen dissociation curve to the right. Shifting to the right means decrease in haemoglobin saturation at the same partial pressure of O2 in the blood. This means more O2 is given up to the surrorunding tissues which is beneficial in exercise. Factors that cause this include

  • increase in partial pressure of CO2
  • increase in H+ ions, decrease in pH
  • increase in temperature
  • increase in 2,3-bisphosphoglycerate
    *
23
Q

Transport Methods of CO2

A
  • Dissolved CO2
  • Bicarbonate which is formed in red blood cells from CO2 and H2O
  • Carbamino compounds where CO2 combines with some proteins
24
Q

Haldane Effect

A

Promotes CO2 transport. Movement of CO2 is facilitated by deoxygenated haemoglobin in tissues. There is more deoxygenated haemoglobin during exercise due to the bohr effect, facilitating pick up of CO2 in the tissues. The bondong of O2 with Hb in the lungs makes it a stronger acid, displacing CO2 from the blood and aiding unloading of CO2 in alveoli.

25
Q

Ventilation-Perfusion Ratio

A

V = alveolar ventilation and Q = blood flow. Ideally you want V/Q = 1 as this means ventilation of lungs matches airflow allowing for maximum gas exchange to occur.

A V/Q towards 0 means there is obstruction of alveolus although normal blood flow.

A V/Q towards infinity means there is an obstruction of pulmonary vessels meaning there is good ventilation but blood isnot reaching the alveolus to exchange gas.

26
Q

Dorsal Respiratory Group

A

Dorsal medulla, respopnsible for inspiration. Basic rhythm of respiration is generated in the dorsal group which emits a burst of inspiratory action potentials. Initiates ramp and cyclic signals.

27
Q

Ramp and Cyclic Signals

A

Ramp signal is when a nervous signal is transmitted to primary inspiration muscles increasing volume of breaths. Not instantaneous but begins weakly and increases steadily, then allows for elastic recoil of lungs and expiration. Then starts again.

Cyclic signal causes steady increase in lung volume during inspiration rather than a gasp and is controlled by the rate of increase in ramp signal and limiting point at which ramp ceases leading. An earlier stop point leads to a shorter inspiration duration.

28
Q

Ventral Respiratory Group

A

Inactive during normal respiration and doesn’t participate in basic rhythmical oscillations that control respiration. Contributes when respiratory drive for increased pulmonary ventilation is greater than normal. Contributes to both inspiration and expiration, providing powerful expiration signals to muscles during heavy breathing.

29
Q

Apneustic Centre

A

Lower pons. Sends signal to dorsal group to prevent or retard the off switch for inspiration ramp signal resulting in short expiration gasps.

30
Q

Pneumotaxic Centre

A

Nucleus parabrachialis of upper pons transmits signals to inspiratory centre. Controls the switch off point for inspiratory ramp signal therefore controls the duration of lung filling. A strong signal gives a short duration and a weak signal gives a long duration. Therefore limits duration but increases breathing rate as shortens expiration and therefore respiration period.

31
Q

Hering-Breuer Reflex

A

Signals from stretch receptors in muscular portion of bronchi and bronchioles transmitted through vagi to dorsal neurons to prevent the overstretching of lungs. This causes a feedback response to switch off ramp and increases the rate of respiration.

32
Q

Changes in CO2 (Chemosensitive Area)

A

ocated bilaterally beneath the ventral surface of the medulla. Sensitive to changes in blood PCO2 or H+ ion concentrations and excites other portions of the respiratory centre. H+ ions direct stimulus for neurons however cannot pass blood brain barriers so CO2 has more of an effect.

  1. CO2 passes through blood-brain barrier when PCO2 in blood increases
  2. Also increases in interstitial fluid of medulla and CS fluid
  3. Reacts with water of tissues to form carbonic acid
  4. Dissociates to H+ and bicarbonate ions
  5. Centre activity increases
  6. Causes increases in ventilation
33
Q

Changes in O2 (Periphereal Chemoreceptor System)

A

PO2 no direct effec on respiratory centre but indirect through periphereal chemoreceptor system. CO2 major controller of respiration, not O2.

  1. Periphereal chemoreceptor detects O2 change in blood but responds to CO2 and H+
  2. Transmits signal to respiratory centre to regulate activity
  3. Mostly in carotid bodies, some in aortic bodies. In carotid bodies these pass through Herning’s nerves to glossopharyngeal nerves and then to dorsal respiratory area
  4. Afferents of aortic bodies pass through vagi to dorsal centre
  5. Hence is exposed to arterial blood with no O2 removal due to extreme blood flow
34
Q

Local Control of Alveolus due to O2 and CO2

A

Increase in CO2 causes local bronchodilation to decrease air way resistance and increase ventilation.

Changes in O2 can lead to changes in pulmonary vascular smooth muscles. Local vasoconstriction leads to increased arteriole resistance which decreases the blood flow to the area and balances out the increased oxygen levels.

35
Q

Nervous Control of Breathing

A

Parasympathetic supply by:

  • Vagus nerve - release of ACh, binds to muscuranci receptors, muscle contraction and bronchoconstriction
  • Adrenal medulla may release catecholamines that activate beta adreergic receptors causing dilation of airways and relaxation
  • Irritant receptors activated in response to irritants
  • Inflammatory mediators histamine and leukotrienes cause contraction

Sympathetic supply by:

  • Noradrenaline on beta adrenergic receptors causin airway dilation
  • Noradrenergic noncholinergic inhibitory nervous system consists of efferent fibres from vagus nerve and nitric oxide neurotransmission are a bronchodilator

VETS2011 Structure and Function I (8 decks)

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