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Physiology Y1 > Cardiorespiratory > Flashcards

Cardiorespiratory Flashcards

1
Q

Define external and internal respiration.

A

External - the exchange of oxygen and carbon dioxide between the external environment and cells of the body.

Internal - intracellular metabolic processes carried out in mitochondria, using oxygen in oxidative phosphorylation to produce ATP and carbon dioxide.

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2
Q

Describe the movement of the diaphragm and external intercostal muscles on inspiration and expiration.

A

Inspiration: Both contract to flatten diaphragm and move ribs upwards and outwards to increase thoracic volume.

Expiration: both relax to dome out diaphragm and let ribs fall inwards and downwards to decrease thoracic volume.

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3
Q

What is the respiratory system’s response to increased exercise?

A

More oxygen demand so rate of inhalations and exhalations increases and amplitude of ventilation increases.

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4
Q

Explain the partial pressures of alveolar gas composition.

A

At lungs: ppO2 = 150 mmHg, ppCO2 = 0.3 mmHg, ppH2O(g) = 47 mmHg

At alveoli: ppO2 = 100 mmHg, ppCO2 = 40 mmHg

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5
Q

What are the properties of the airways?

A

Diameter is inversely proportional to resistance.
Diameter is controlled by contraction and relaxation of smooth muscle via ANS.
Bulk of resistance decreases down bronchial tree despite decreasing diameter due to frequency/net surface area of each airway class increasing.

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6
Q

Define conducting zone and respiratory zone.

A

Conducting zone - permits the movement of air in and out of the lungs.

Respiratory zone - the sit of gas exchange.

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7
Q

What is dead space volume?

A

The volume contained in the conducting zone that does not support gas exchange.

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8
Q

What is tidal volume?

A

The volume of air expired with each breath.

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9
Q

What is the respiratory rate?

A

Number of breaths per minute.

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10
Q

What is the minute ventilation?

A

Minute ventilation = tidal volume x respiration rate

Ve = Vt x RR

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11
Q

What is the alveolar ventilation?

A

Alveolar ventilation = (tidal volume - dead space volume) x respiration rate

Va = (Vt - Vd) x RR

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12
Q

Describe the necessary pressure changes for inspiration and expiration.

A

Inspiration - thoracic pressure is less than atmospheric pressure

Expiration - thoracic pressure is greater than atmospheric pressure

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13
Q

Which muscles are recruited for inspiration and expiration?

A

Inspiration - accessory inspiratory muscles, scalene and sternomastoid muscles.

Expiration - if forced expiration, other abdominal muscles.

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14
Q

Name the 4 pressures to consider in the breathing cycle.

A

Barometric/atmospheric
Intra-alveolar
Intrapleural
Transmural - difference in pressure between intra-alveolar and intrapleural

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15
Q

What is the intrapleural pressure?

A

Outward force = recoil of chest
Inward force = recoil of elastic lungs

Forces are balanced and act on intrapleural fluid, but must be a negative pressure for this to happen.

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16
Q

From a spirometer and vitalograph, what is the expiratory reserve volume, inspiratory reserve volumes, the vital capacity and the functional residual capacity?

A

Expiratory reserve volume - the maximum volume that can be exhaled after a normal, quiet exhalation.

Inspiratory reserve volume - the maximum volume that can be inhaled after a normal, quiet inhalation.

Vital capacity - largest volume that can be in the lungs, where capacity is the sum of 2 or more volumes.

Functional residual capacity - volume remaining at the end of normal expiration.

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17
Q

What are the properties of lung elasticity?

A

Inspiration - lungs must expand when stretched, which is aided by high compliance.

Expiration - lungs must collapse when stretch force is removed, aided by elasticity.

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18
Q

What is elasticity?

A

Comes from elastin fibres. Elasticity reduces resistance and vascular resistance in the pulmonary system.

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19
Q

Name a disease that reduces lung elasticity.

A

Emphysema - loss of elastic tissue. Easier to stretch with increased compliance.

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20
Q

Name 3 diseases that reduce lung compliance.

A

Fibrosis, pulmonary oedema and surfactant deficiency all cause decreased compliance.

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21
Q

Define surface tension.

A

The molecules in a liquid have an affinity for one another. Forces between fluid molecules cause the surface of the liquid to act like an elastic sheet. Alveoli have fluid surface so have surface tension.

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22
Q

What is the function of surfactant?

A

Is a phospholipid dissolved in alveolar fluid that reduces surface tension.

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23
Q

What cells produce surfactant?

A

Type 2 pneumocytes

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24
Q

What is the physiological significance of lung surfactant?

A

Released in inspiration and as alveoli get smaller, it becomes concentrated in the fluid. It increases pulmonary compliance and reduces work of inflating lungs.

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25
Q

How does surfactant reduce atelectasis?

A

Reduces lung recoil and alveolar collapse (atelectasis) is less likely.

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26
Q

Describe airflow in airways.

A

Airway resistance must be overcome by the action of inspiratory muscles that creates alveolar pressure gradient.

Airflow = pressure gradient / airway resistance

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27
Q

Name 4 diseases where airway resistance is increased.

A

Chronic obstructive pulmonary diseases, such as bronchitis and emphysema - chronic, long lasting airway resistance.

Oedema - fluid restricted airflow.

Asthma - increased constriction of bronchiole smooth muscle, increased mucus secretion and inflammation.

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28
Q

Describe the physical factors affecting airway diameter and resistance.

A

As lung volume increases, resistance decreases because lungs stretch in filling ad forces on small airways help pull them open and reduce resistance via radial tension.

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29
Q

Describe the effect of ANS on airway resistance and resistance.

A

Sympathetic nervous system will increase broncho tone and constrict broncho vessels. Acetylcholine released, activating muscarinic receptors to cause bronchoconstriction. During stress and exercise, sympathetic nervous system releases adrenaline, which acts on beta-2 receptors to cause broncho dilation.

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30
Q

Describe the effect of the Hering-Breuer inflation reflex on bronchial diameter.

A

Stretch receptors stimulated upon inflation, firing vagal afferents to medullary respiratory centre. Sympathetic efferents cause bronchodilation.

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31
Q

Which diseases increase lung compliance?

A

Larger lung volume achieved for same pressure with obstructive diseases, causing impaired expiration. Such as asthma, COPD and bronchieactasis.

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32
Q

What diseases cause decreased lung compliance?

A

Smaller lung volume for same pressure due to impaired inspiration in restrictive diseases. Such as pulmonary fibrosis, interstitial disease and repeated infection.

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33
Q

Link anatomical and physiological dead space.

A

Physiological dead spcae = anatomical dead space + alveolar dead space

In health, physiological dead space = anatomical dead space

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34
Q

Describe measuring lung volume with a spirometer and vitalograph.

A

Detects changes in tidal volume, inspiratory reserve volume and expiratory reserve volume to produce a vitalograph.

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35
Q

Describe measuring lung volume using capnography.

A

Measures end-tidal CO2 volume. Used when a defect in gas exchange is recorded or impaired ventilation, effect of drugs or injury recorded.

36
Q

State the differences between pulmonary and systemic circulations.

A

Pulmonary: MAP = 15 mmHg for dogs, cats, sheep and goats, MAP = 40 mmHg for pigs, cows and horses.

Systemic: MAP = 100 mmHg

37
Q

Explain the alveolar-arterial (A-a) pressure difference.

A

Blood leaving alveoli and lungs both have a partial pressure of oxygen of 100 mmHg. Venous blood from bronchial and coronary veins has a ppO2 of 15 mmHg. Due to left and right anatomical shunt, defects in ventilation and diffusion can increase A-a pressure difference. Causes hypoxia.

38
Q

List 3 causes of increased A-a pressure difference and whether oxygen therapy is useful for each.

A

VQ mismatch - yes
Shunt - limited
Diffusion defect - yes

39
Q

What is the alveolar air equation?

A

To measure A-a gradient, arterial ppO2 and alveolar ppO2 taken. Arterial by blood sampling, alveolar by air equation.

Alveolar ppO2 = inspired ppO2 - (alveolar ppCO2 / respiration ratio)

40
Q

What is the PaO2/FiO2 ratio and its normal range?

A

Can also be used to work out A-a gradient. Normal range is 400-500.

41
Q

What is the range of PaO2/FiO2 when an animal has acute respiratory distress?

A

With no ARDs = 400-500
Mild ARDs = 200-300
Moderate ARDs = 100-200
Severe ARDs = less than 100

42
Q

How does lung inflation cause different resistances in different vessels?

A

Blood vessels not in contact with alveoli becomes larger, as they are pulled open by parenchyma. Greater tension causes reduced resistance in extra-alveolar vessels. Alveolar capillaries fill up and compress vessels closer to alveoli, increasing resistance.

43
Q

How does gravity affect perfusion?

A

Perfusion highest at bottom of lungs of larger animals, as capillaries are more open at bottom due to gravity, so have lower resistance.

44
Q

What is ventilation-perfusion ratio?

A

Alveolar ventilation and capillary perfusion is not perfectly matched. ppO2 is determined by this ratio. Ratio id ideally close to 1.

45
Q

Why is ventilation-perfusion ratio less at the bottom of the lung?

A

Greatest ventilation at base of the lungs and ventilation is not uniform, with regional differences.

46
Q

What factors influence diffusion of gas between alveoli and blood?

A

Partial pressure gradient and solubility of gas. Both are directly proportional to diffusion.

47
Q

Give the equation for the diffusion constant.

A

Diffusion constant = solubility / root of molecular weight

Diffusion rate = (surface area x diffusion constant x pressure gradient) / thickness of alveolar membrane

48
Q

What is the difference in solubility between oxygen and carbon dioxide?

A

CO2 is 25 times more soluble than O2.

49
Q

What is the effect of solubility difference when ventilation or diffusion distance is impaired?

A

CO2 will have higher diffusion constant than O2. If thickness of membrane is increased due to disease or partial pressure gradient is decreased, volume of oxygen diffused will be greatly decreased.

50
Q

Distinguish diffusion and perfusion.

A

Diffusion is the difference in gas partial pressure between alveoli and capillaries. A gas is not diffusion limited at equilibrium, pp capillary = pp alveoli.

Perfusion is uptake of gas by cells from capillaries, which can be limited by blood flow.

51
Q

Describe oxygen cascade, starting at 160 mmHg.

A

Humidification with ppH2O = 47 mmHg > mixing with functional residual capacity > VQ mismatch > shunt > loss to tissues > inside cells

52
Q

What is the carrying capacity of haemoglobin when saturated?

A

1g haemoglobin can transport 1.39g oxygen.

53
Q

Describe the oxygen dissociation curves for fetal haemoglobin and myoglobin.

A

For each given ppO2, myoglobin have higher oxygen affinity and saturation than fetal haemoglobin. This helps movement of oxygen across placenta to fetus.

54
Q

Describe the Bohr Effect.

A

For a given ppO2, more oxygen given up at tissues and affinity is lower. Increased CO2 causes increased [H+], increased temperature and increased DPG.

For a given ppO2, less oxygen given up at tissues and affinity is higher. Decreased CO2 causes decreased [H+], decreased temperature and decreased DPG.

55
Q

What is the function and importance of erythrocytes?

A
  • Encapsulates a high concentration of haemoglobin and decreases blood viscosity as a result
  • Provides an environment for DPG to enhance oxygen unloading at tissues
  • Encapsulates and concentrates carbonic anhydrase, essential for Co2 trasnport
  • Prevents haemoglobin loss via kidney filtration
  • Passage through tight spaces due to concave shape
56
Q

What 3 ways is CO2 transported in the blood?

A
  • 5% CO2 dissolved directly
  • 30% CO2 reversibly bound to haemoglobin to form carbaimnohaemoglobin
  • 65% CO2 form bicarbonate: CO2 + H2O > (with carbonic anhydrase) > H+ + HCO3-
57
Q

Describe carbon dioxide dissociation curve and how it differs from oxygen dissociation curve.

A

No saturation, as CO2 is very soluble in plasma and is linear over physiological CO2 range.

Haldane Effect - differences between venous and arterial blood enhances CO2 upload from tissues to the blood. At lower ppO2, haemoglobin have greater CO2 affinities. Venous blood curve lies above arterial blood curve, as venous blood contains more CO2 at any ppCO2 than arterial blood.

58
Q

What is chloride shift?

A

Exchange of chloride ions and bicarbonate ions over red blood cells, affecting plasma pH and CO2 transport.

59
Q

What is chemical control of respiration?

A

Increased CO2 = respiratory acidosis

Decreased CO2 = respiratory alkalosis

60
Q

What is the relationship between alveolar partial pressure of carbon dioxide and alveolar ventilation?

A

Inversely proportional

61
Q

What is the location , stimulus and response of peripheral chemoreceptors?

A

Near major blood vessels. Stimulated by decreased partial pressure of oxygen.

Aortic body sends afferents to aortic nerve, which joins to vagus nerve.
Carotid bodies send afferent signal to sinus nerve, a branch of the glossopharyngeal nerve.

Both terminate at NTS, nucleus tractis solitarii in medulla. Fast response to increase ppO2.

62
Q

What is the location, stimulus and response of central chemoreceptors?

A

Medulla oblongata. Not stimulated by blood pH changes due to blood brain barrier.
Protons cannot cross but CO2 can. CO2 in cerebrospinal fluid acted upon by carbonic anhydrase to produce protons and bicarbonate. Slow response.

63
Q

What stimulates peripheral chemoreceptors?

A 
Hypoxia
Hypercapnia 
Combination of hypoxia and hypercapnia
Haemorrhage
Acidosis
Increased sympathetic activity
64
Q

Compare and contrast ventilatory response to hypoxia and hypercapnia.

A

Hypoxia - ventilation increases sharply then decreases more slowly.

Hypercapnia - ventilation has hockey stick relationship, starts slow and then increases sharply.

Both involve increased sympathetic activity and increased release of adrenaline from adrenal medulla.

65
Q

What is hypocapnic breaking effect?

A

Partial pressure of CO2 is permitted to fall in response to hypoxia.

66
Q

What is the problem with pH when hypoxia drives ventilation?

A

Haemoglobin enable oxygen content in the blood to be relatively independent of the oxygen content of inspired air due to flat section of oxygen dissociation curve. Implies that close regulation of this is unnecessary.

Close regulation of CO2 content is necessary to regulate blood pH. Regulation of both O2 and CO2 is not possible. Increased ventilation due to hypoxia will blow off some CO2 and cause respiratory alkalosis.

67
Q

Name 8 functions of ventilatory muscles.

A 
Eating/drinking 
Breath-holding 
Thermoregulatory panting for some species
Vocalisaton
Coughing 
Sneezing - only in small animals
Sniffing 
Intrathoracic pressures - positive pressures in Valsalva (such as defecation) and negative pressures in vomiting.
68
Q

What are the pontine and medullary areas of the brainstem responsible for?

A 
Pontine = rhythm generation 
medullary = pattern formation

They drive output to respiratory muscles to generate a breathing pattern. Sensory inputs from peripheral chemoreceptors, lung stretch receptors, joint position and muscle metabolism.

69
Q

How are respiratory outflows regulated in exercise?

A

Depth of ventilation and frequency of ventilation increase.

70
Q

Why is increasing ventilation frequency not as effective as increasing depth of ventilation (tidal volume) in increasing alveolar ventilation?

A

For example, at respiration rate 60, tidal volume is 100ml but air is only moved inside the dead space, as alveolar ventilation is 0, which cannot support life.
At respiration rate 2, tidal volume is 3 litres and alveolar ventilation is 5.7 litres.

71
Q

How could heart failure be confused with defects in gas exchange?

A

In heart disease, volume of blood, amount of haemoglobin, amount of oxygen in arterial blood may be unchanged but cardiac output is decreased, so oxygen to tissues is impaired.
Defects in gas exchange is not known. Only known that both are unwilling to exercise, be breathless and may present very similarly.

72
Q

Name the mechanoreceptors that regulate ventilation.

A

Pulmonary stretch (Hering-Breuer), respiratory muscle, skeletal muscle and proprioceptors in joints.

73
Q

Name the chemical receptors that regulate ventilation.

A

Peripheral (carotid and aortic), central and intrapulmonary chemoreceptors (birds and reptiles only).

74
Q

Describe the Hering-Breuer reflex.

A

Slowly adapting stretch receptors stimulated by lung stretch in inspiration and bronchoconstriction. Increased activity terminates inspiration, prolongs expiration, slowing breathing in haemoglobin reflex, causing bronchodilation.

75
Q

Describe the cough reflex.

A

Rapidly adapting stretch receptors embedded in lung parenchyma. Activated by smoke, noxious gases and histamine. Causes increased ventilation rate, reduces tidal volume, increases bronchoconstriction to increase air resistance.

76
Q

What is the impact of disease on VQ mismatch?

A

Increased VQ mismatch. Chemoreceptors respond and there is increased drive and ventilation until CO2 normalises. CO2 normalised before oxygen so pH is normalised before hypoxia.

77
Q

Demonstrate the integration of receptors in metabolic acidosis.

A

Stimulates peripheral chemoreceptors. Central chemoreceptors not stimaulted, as protons cannot cross the blood brain barrier. Ventilation increased, reducing ppCO2 and increases brain pH, reducing the activity of central and peripheral chemoreceptors.

78
Q

Demonstrate the integration of receptors in exercise.

A

Increased ppCO2. Stimulates peripheral and central chemoreceptors. Peripheral chemoreceptors afferents stimulate respiratory centre via nucleus of tractus solitarius. Central chemoreceptors cell bodies in medulla. Increased output of pre-motor neurones.

79
Q

Define pulmonary air conditioning.

A

The warming and wetting of air to protect alveoli from drying out.

80
Q

How can sniffing protect the pulmonary system?

A

Sniffing allows air to make contact with olfactory receptors without air entering the lungs.

81
Q

How can particles of different sizes be removed and filtered from inspired air?

A
  • Larger particles have larger inertias, so impact on respiratory surfaces when airflow changes direction at nasopharynx. Mucous allows particles to be swallowed and sent down the oesophagus.
  • Small particles sediment on bronchi surfaces due to gravity and mucociliary escalator removes these and transports particles to the top of the oesophagus to be swallowed.
  • Tiny particles can be pushed to the edges of alveoli due to Brownian motion and removed by macrophages in alveoli via phagocytosis.
82
Q

What is mucociliary escalator?

A

Bronchi are lined with ciliated epithelia that beat in coordination. Goblet cells and mucous glands produce mucus.

83
Q

Give examples of restrictive diseases and their effect.

A

Pulmonary fibrosis
Interstitial lung disease
Repeated infection

Low lung volume, impaired inspiration, leading to increased inelastic tissue and reduced compliance.

84
Q

Give examples of obstructive diseases and their effect.

A

COPD
Asthma
Bronchiectasis

High lung volume, impaired expiration, leading to hypertrophic muscle and mucus plug.

85
Q

Define blood reservoir as a non-respiratory function of the lungs.

A

Pulmonary vessels have capacitance. In dogs, 0.5 litres.

86
Q

Describe blood filtration as a non-respiratory function of the lungs.

A

Natural - fibrin and fat cells
Pathologic - detected cancer cells, platelets, expired erythrocytes

These become trapped in pulmonary capillary beds, where they are filtered using lytic enzymes, macrophages and lymphatic drainage.

87
Q

Describe the metabolic function of the lungs.

A

ACE, angiotensin converting enzyme - activated angiotensin I to angiotensin II and breaks down bradykinin to inactive peptides.

Phosphatase - ATP + ADP > AMP

5-Nucleotidase - AMP > adenosine

Adenosine kinase > adenosine > ATP

Monoamine oxidase - noradrenaline and serotonin > inactive metabolites

Physiology Y1 (12 decks)

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