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1st Year Med > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

what are the functions of the respiratory tract?

A

conduction of air (warms/himidifies)
respiration (gas exchange)
pathogen protection (mucous)

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2
Q

what is the main purpose of breathing?

A

maintains blood-gas homeostasis

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3
Q

what is partial pressure?

A

the sum of the partial pressures of a gas must equal to total pressure

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4
Q

what muscles are involved in breathing?

A

diaphragm (dome shaped skeletal)
other respiratory muscles in strenuous breathing

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5
Q

explain the mechanism of quiet breathing and the activity of inspiration and expiration

A

inspiration (active) - diaphragm contracts downwards pushing abdominal contents outwards
external intercostals pulll ribs outwards and upwards

expiration (passive) - elastic recoil

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6
Q

explain the inspiration mechanism of strenuous breathing

A

active - greater diaphragm and external intercostals contraction (10x more than quiet)
inspiration accessory muscles active

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7
Q

explain the expiration mechanism of strenuous breathing

A

active - abdominal muscles recruited
internal intercostal muscles oppose external intercostals pushing ribs down and inwards

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8
Q

what does the cough reflex do?

A

remove offending material from airway

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9
Q

what is the cough reflex triggered by and how is it activated?

A

rapidly adapting pulmonary stretch receptors (RARs) found in epithelium of respiratory tract

activated by dust, smoke, ammonia, oedema etc.

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10
Q

how does a cough reflex get signalled for?

A

RARs send signal to brain using vagus nerve

brain sends signal to diaphragm/external intercostals via phrenic nerve

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11
Q

explain the stages of a cough reflex

A

air rushes into lungs
abdominal muscles contract to induce expiration
glottis opens to forcefully release air and irritants

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12
Q

what are conducting airways?

A

bronchi containing cartilage and non-respiratory bronchioles
dont partake in gas exchange

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13
Q

what are respiratory airways?

A

bronchioles with alveoli where gas exchange occurs
(from terminal bronchioles to alveoli)

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14
Q

what is the function of bronchial circulation?

A

brongs oxygenated blood to lung parenchyma

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15
Q

what is the partial pressure of O2 inside and outside the body?

A

inside: 150mmHg
outside - 159mmHg

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16
Q

name the structures in alveolar-capillary networks

A

type 1 alveolar epithelial cells
capillary endothelial cells
BM

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17
Q

how is oxygen carried in the blood?

A

dissolved (proportional to PP in an arterial blood sample)
bound to haemoglobin

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18
Q

name the pressure of O2 and CO2 in:
- pulmonary artery
- capillaries
- pulmonary veins
- anatomic dead space

A

PA: O2 = 40, CO2 = 46
PV and capillaries: O2 102, CO2 = 40
anatomic dead space: O2 = 150, CO2 = 0

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19
Q

explain the structure of haemoglobin

A

4 heme groups (2 alpha and 2 beta polypeptide chains)
each group contains Fe++ (site of O2 binding)

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20
Q

describe O2 saturation and what is it measured with

A

amount of O2 bound to Hb relative to maximum (211ml/l) binding capacity

pulse oximeters measure O2 sats
measures ratio of red and infrared absorption by oxyhaemoglobin and deoxyhaemoglobin

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21
Q

what are the general resting tissue requirements/excretions for O2 and CO2?

A

O2: 250ml/min
CO2: 200ml/min

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22
Q

how is CO2 carried in blood?

A

7% dissolved
23% bound to Hb
70% converted into bicarbonate

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23
Q

how do capillaries expel CO2?

A

systemic capillaries expel CO2 produced by tissues into blood
pulmonary capillaries expel CO2 into alveoli

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24
Q

explain the bicarbonate reaction

A

reaction: HCO3 -> H2O + CO2
regulated H+ ions and maintains base balance in body

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25
Q

how are CO2, HCO3 and H+ concentrations linked?

A

stabilise pH through strong buffer reaction (due to HCO3 strength)

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26
Q

what is the V/Q ratio?

A

ventilation:blood flow
defined by single alveolus (alveolar ventilation:capillary flow)
defined by lung (total alveolar ventilation:CO)

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27
Q

what are the general values for alveolar ventilation, pulmonary blood flow and V/Q?

A

alveolar ventilation: 4-6l/min
pulmonary blood flow: 5l/min
V/Q - 0.8-1.2

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28
Q

describe the effects of PO2 on Hb saturation in the O2 dissociation curve

A

drop from 100-60 in PO2 has little effect
60 below has much larger effect (more sensetive to change)

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29
Q

what factors shift the O2 dissociation curve to the right?

A

decreased affinity:
increased temp
increased PCO2
decreased pH

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30
Q

what factors shift the O2 dissociation curve to the left?

A

increased affinity:
decreased temp
decreased PCO2
increased pH

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31
Q

what is the rule of H+ ions on pH?

A

changes in H+ of a factor of 2 lead to a pH change of 0.3

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32
Q

name systems affected by acid-base disorders

A

CVR
metabolic
renal
GI
neurological

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33
Q

what are some of the threats to acid base disorders?

A

CO2 generation (aerobic respiration)
food metabolism generating acid or alkali
incomplete respiration (anaerobic)
loss of alkali in stool
loss of acid in vomiting

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34
Q

what are the major components of acid base balance and how do they regulate?

A

buffering
ventilation (CO2 control)
renal regulation (HCO3/H+ secretion and reabsorption)

regulate H+ concentration at the expense of other concentrations (HCO3/CO2)

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35
Q

what are buffers and how do they work?

A

weak acids partially dissociated in solution
react poorly with water
reacts with H+ (base) or OH- (weak acid)

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36
Q

explain how ventilation results in acid-base regulation

A

CO2 remains constant as it is easily diffusable and is exhaled
H+ addition consumes HCO3 generating CO2 (exhaled) and H2O
free H+ leads to HCO3 generation

H+ maintenance = HCO3 maintenance

37
Q

name buffers and describe what they buffer

A

haemoglobin (blood CO2)
proteins (intracellular)
bone (long term)
PO4 (urinary/intracellular)

38
Q

how do buffers and the kidneys work together to regulate acid-base composition

A

dietary acids and anaerobic respiration acids are fixed (cant convert to (CO2)

buffering fixed acids consume HCO3
kidneys generate more HCO3 to remove H+ ions

39
Q

what is the function of the kidneys in acid-base regulation and how do they do it?

A

reabsorb filtered HCO3
secrete fixed acid by titrating PO4 in urine and secreting NH4

done using selective permeability of luminal/basolateral cell membranes to match transport of H+ and HCO3 in opposite directions

40
Q

explain the reabsorption of filtered HCO3

A

active process in mainly proximal tubule
small contributions from DCT and ascending LoH

cant be reabsorbed in state of metabolic acidosis

41
Q

what is respiratory acidosis?

A

levels of CO2 being expelled from the lungs
too much in blood = acidosis
too little in blood = alkalosis

42
Q

what is metabolic acidosis?

A

levels of HCO3 expelled in urine
too much in blood = alkalosis
too little in blood = acidosis

43
Q

what is lactic acidosis and how is it buffered?

A

reduced hepatic clearance of lactic acid produced from glycolytic metabolism of pyruvate

buffered by HCO3 to lactate then metabolised in liver

44
Q

what do chemoreceptors and mechanoreceptors provide feedback on?

A

chemoreceptors - PO2, PCO2, pH levels in blood

mechanoreceptors - mechanical lung status, chest wall, airways

45
Q

what structures receive signals from the brain to maintain breathing?

A

diaphragm/intercostals (rhythmic breathing)
upper airway muscles (laryngeal, pharyngeal, tongue)
reflexes to keep airways pateny (cough, sneeze, gag)

46
Q

what is O2 decrease and CO2 increase medically called?

A

O2 - hypoxia
CO2 - hypercapnia

47
Q

describe peripheral chemoreceptors

A

small, vascularised bodies in carotid sinus and aortic arch
info sent to glossopharyngeal and vagus nerve to brainstem (NTS)
restore blood gases e.g arterial PO2

48
Q

describe central chemoreceptors

A

clusters of neurones in brainstem
activated when PCO2 is increased or pH is decreased

49
Q

explain the result of changes in PCO2

A

small changes have large effects on ventilation
hypercapnic response originating from central chemoreceptora in brainstem

50
Q

describe mechanoreceptors

A

sensory receptors detecting chnges in pressure, movement and touch
(e.g lung inflation and chest movements during inspiration)

51
Q

what is the course of an impulse from mechanoreceptors?

A

stimulus (lung inflation)
neural signal goes through vagus nerve to NTS in brainstem to adjuct ventilation

52
Q

what do mechanoreceptors integrate?

A

respiratory pattern with other movements such as posture or locomotion

53
Q

how do mechanoreceptors terminate inspiration?

A

in airway smooth muscle
detects stimulus of inflation/distension of airways

54
Q

what do mechanoreceptors in the airway epithelium detect?

A

rapid lung inflation/deflation (or oedema)
causes sigh or shortened expiration

55
Q

explain the course of action from the NTS

A

NTS receives signals from mechanoreceptors and peripheral chemoreceptors
info processes in brainstem by neuronal clusters
breathing rhythm generated and sent to respiratory muscles

56
Q

describe the respiratory rhythm generating neurons

A

bilateral clusters of neurons with rhythm generating properties
produce a rhythmic resp output even when isolated

57
Q

where do the rhythmic output signals go after the brainstem?

A

sent down spinal cord which sends signals to resp muscles such as diaphragm (phrenic nerve) or intercostal muscles (thoracic spinal cord nerves)

58
Q

what areas of the brainstem are responsible for resp rhythm generation?

A

pontine group (pons)
ventral group (pattern/rhythm generating neurons)
dorsal resp group (NTS)

59
Q

what types of higher centre modulation control breathing?

A

volitional and emotional

60
Q

what is the neural basis for voluntary control attributed to?

A

motor cortex

61
Q

explain the role of the corticospinal tract in breathing regulation

A

cortical breathing control occurs here
volitional breath control has upper motor neurones in primary motor cortex
they descent the corticospinal tract and synapse with lower motor neurones in anterior horn of C3-5 (phrenic nerve)

62
Q

what are the physiological effects of asthma?

A

loss of airway epithelium
thickening of BM
hypertrophy of smooth muscle layer (including mast cells)

63
Q

what is asthma?

A

inflammatory disease of medium sized airways
hyper-responsiveness to normal triggers of contraction
abnormal contraction in response to benign triggers

64
Q

what can asthma cause in the airway?

A

increased force contraction
twitchy smooth muscle
variable airway calibre
loss of relaxation after contraction

65
Q

what are the symptoms of asthma?

A

triggered breathlessness
wheezing
diurnal variation (night/morning)
coughing

66
Q

how is asthma measured?

A

bronchial hyper-reactivity is induced
exaggerated response to usually constricting stimuli (often histamine used) is seen

67
Q

what does spirometry measure and how does it do it?

A

measures airflow velocity
a narrowed/constricted airwa yrelaxes and dilates in response to salbutamol (adrenaline beta agonist)

68
Q

what are the common triggers of asthma?

A

allergy
infection
exercise
drugs (beta blockers/NSAIDs)
cold air
scents

69
Q

describe the smooth muscle only stage of asthma

A

triggered by direct mediator (histamine)
causes rare wheezing

70
Q

describe the chronic inflammation stage of asthma

A

irritates smooth muscle and causes regular wheezing

71
Q

describe the acute inflammation stage of asthma

A

caused by viral infection and results in clinical exacerbations

72
Q

what are the inflammatory factors often associated with asthma?

A

cells (lymphocytes, eosinophils, mast cells)

cytokines (Il-4, IL-5)

prostanoids (PGE2, leukotriene D4)

immunoglobulins (IgE)

73
Q

explain the role of mast cell mediators

A

e.g histamine at H1 receptor, prostoglandin at PC2 receptor
causes smooth muscle contraction, blood vessel formation and airway wall oedema

74
Q

explain the role of beta 2 agonists in asthma

A

e.g salbutamol
active adrenaline receptor
activated G-protein on GPCR which activates cAMP resulting in smooth muscle relaxation

75
Q

what do corticosteriods do in asthma?

A

block transcription factors causing an inflammatory response
reduce muscle twitchiness
reduce exhaled NO

76
Q

what do anti-leukotrine receptor drugs do in asthma?

A

trats resistant inflammation
targets onlt leukotrine D4 in airway effecting mast cells and smooth muscle

77
Q

what is the 4D approach to prescribing inhalers?

A

diagnosis
drug and device
disease control
device disposal

78
Q

what is a preventer inhaler?

A

anti-inflammatory inhaler using inhaled corticosteroids (ICS)

79
Q

what is a combination inhaler?

A

uses inhaled corticosteroids (ICS) and long acting beta agonist (LABA)

80
Q

what is a reliever inhaler?

A

bronchodilating inhaler containing a short acting beta agonist (SABA) or a long acting beta agonist (LABA)

81
Q

how can asthma and COPD be distinguished?

A

asthma patients will respond more to a bronchodilator and oral prednisolone
peak flow will vary ~20% daily

COPD isnt present if the FEV1/FVC ratio returns to normal with drugs

82
Q

describe NO exhalation measurement

A

only valid in non-smokers
normal results: <25ppb
abnormal results: >50ppb

indicates eosinophilic inflammation in airways

83
Q

how does COPD develop?

A

inflammatory cells produce excess protease enzymes (neutrophil elastase) and insufficient antiprotease enzymes (a1 antitrypsin)
imbalance causes lung tissue damage and COPD development

84
Q

what are the effects of emphysema?

A

elastic support loss causing airway compression
this causes airway obstruction (peripheral airway disease)
ventilation maldistribution (poor gas exchange)

85
Q

what are some common diseases associated with COPD?

A

asthma
bacterial colonisations
hypoxia
reflux
underlying bronchiectasis

86
Q

explain the symptoms of bronchiectasis

A

purulent daily sputum
50% idiopathic
recurrent infections
lungs crackle on exam

87
Q

what is bronchodilation and bronchoconstriction generally caused by?

A

bronchodilation - inhibitory nerves, circulating epinephrine

bronchoconstriction - excitory nerves, vagus nerve

88
Q

briefly explain what COPD is

A

largely irreversible airflow obstruction often including emphysema

1st Year Med (52 decks)

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