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Respi > respi physio > Flashcards

respi physio Flashcards

1
Q

pulmonary system pressure

A

24/10 mmHg

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2
Q

what are the components found in the alveoli + functions? (5)

A
  1. type 1 alveolar epithelial cells: simple squamous, forms barrier that’s permeable for gas exchange
  2. type 2 alveolar epithelial cells: simple cuboidal, produce surfactant
  3. alveolar macrophages: phagocytose foreign particles
  4. interstitial cells: contain fibroblast to produce collagen for structural support of cells
  5. capillary endothelial cells: simple squamous, lines capillaries to increase efficacy of gas exchange
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3
Q

what are the function of respi system? (4)

A
  1. Metabolism & Acid-Base Regulation: provides O2 to tissues for metabolism, removes CO2 and regulates pH
  2. Endocrine functions: produces hormones (e.g. angiotensin converting enzyme to convert angiotension I to angiotensin II for CVS function)
  3. Immunological functions: clearance of irritants and potential pathogens
  4. Voice production by larynx
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4
Q

physiologic RR

A

12-20breaths/min

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5
Q

what are the physiologic pO2 levels in envt, alveoli & deoxygenated tissues

A

environment: 150-160mmHg
alveoli: 100mmHg
deoxygenated tissues: 40mmHg

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6
Q

where are cilia found in respiratory tract?

A
  • trachea, bronchi, bronchioles, and some in the respiratory bronchioles
  • absent in alveolar ducts and alveolar sacs
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7
Q

where are there smooth muscles in respi tract?

A
  • in trachea, bronchi, bronchioles, some in respiratory bronchioles, some in alveolar ducts
  • absent in alveolar sacs
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8
Q

where is there cartilage in respi tract?

A
  • hyaline cartilage in trachea
  • patchy in bronchi
  • absent in bronchioles (purely smooth muscles), alveolar ducts/sacs
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9
Q

what are the protective mechanisms of the respi tract? (4)

A
  1. coughing/sneezing reflex
  2. ciliary escalator (cilia beat to move particles and mucus away from lung to upper respiratory tract)
  3. humidication & warming of air in upper passages and mucous secretion to protect respiratory epithelium (mucosa) of airways
  4. alveolar macrophages
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10
Q

what is pneumothorax?

A

air in potential space between visceral & parietal pleura of lung

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11
Q

what is tension pneumothorax?

A
  • air within pleural space is under pressure→ displaces mediastinal structures→ compromise cardiopulmonary function
  • occurs when 1 way-valve is formed when air can flow into pleural space but cannot flow out→ ↑ pressure
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12
Q

what is the pathophysiology of tension pneumothorax?

A
  • pressure ↑ within affected hemithorax→ ipsilateral lung collapses→ hypoxia
  • further buildup of pressure causes mediastinum to shift to contralateral side→ impingement on contralateral lung & vasculature entering right atrium→ worsen hypoxia & compromised venous return
  • IVC kinks first & restricts blood flow back to the heart
  • ↓ oxygen delivery to peripheral tissues → induces anaerobic metabolism, also metabolic acidosis due to ↓ cardiac output
  • ultimately cardiac arrest & death
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13
Q

what are the effects of tension pneumothorax (air compress on lungs & heart) on HR, arterial BP, pulmonary BP, CVP?

A

↑↑HR: compensate for insufficient CO
↓↓arterial BP: insufficient LV CO due to decreased venous return
↑pulmonary BP: due to backup of blood flowing into right atrium
↑↑CVP

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14
Q

what are the definitions of TV, ERV, IRV, RV

A

Tidal volume: volume inspired or expired with each normal breath. Normal value: 0.5L
Inspiratory Reserve Volume: extra vol inspired on max (forced) inspiration. Normal volume: 3.0L
Expiratory Reserve Volume: the extra vol expired on max (forced) expiration. Normal volume: 1.2L
Residual volume: volume left after maximum forced expiration. Normal volume: 1.2L

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15
Q

what is IC, FRC, VC, TLC

A

Inspiratory capacity: TV + IRV
Functional residual capacity: ERV + RV (the equilibrium volume of lungs)
Vital capacity: TV + IRV + ERV
Total lung capacity: RV + TV + IRV + ERV = RV + VC

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16
Q

what are hyperventilation, hypoventilation, tachypnoea, dyspnea?

A

Hyperventilation: ↑ ventilation - rapid but deep breathing
Hypoventilation: ↓ ventilation
Tachypnoea: ↑ rate of breathing - rapid but shallow
Dyspnea: difficulty breathing

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17
Q

what is the process of active inspiration?

A

diaphragm & inspiratory chest wall muscles contract→ chest cavity expands→ intrathoracic volume ↑→ pressure in thorax & pleural cavity ↓→ air flows into lungs

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18
Q

what is the process of active expiration?

A

diaphragm & inspiratory chest wall muscles relax→ chest cavity recoils→ intrathoracic volume ↓→ pressure in thorax & pleural cavity ↑→ air flows out of lungs

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19
Q

what are the muscles/structures required for expiration/inspiration?

A

bones: ribs, sternum, clavicles
muscles: diaphragm, intercostal muscles

when ventilation is stimulated eg exercise, extra muscles eg neck, internal intercostal, abdominal muscles are recruited

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20
Q

describe foetal pulmonary circulation

A
  • HIGH pressure, LOW flow
  • lungs are collapsed
  • foramen ovale present between RA & LA, ductus arteriosus present between pulmonary artery and aorta
  • blood flows: RA→ FO→ LA→ aorta AND RV→ pulm artery→ DA→ aorta
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21
Q

what happens to foetal circulation after baby’s first breath

A
  • LOW pressure, HIGH flow

lungs expand and become functional
→ pulmonary arterioles distend (swell up)→ blood flows through lung & get oxygenated→ placenta lost→ umbilical vein obliterated→ foramen ovale and ductus arteriosus closes

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22
Q

major forms of O2 in blood

A
  • 99% as HbO2
  • 1% as dissolved O2 -> exerts pO2
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23
Q

major forms of CO2 in blood

A
  • 70% as HCO3-
  • 23% as carbamino Hb
  • 7% as dissolved CO2 -> exerts pCO2
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24
Q

what can decrease Hb affinity for O2 (3)

A
  • increase temperature (eg exercising muscles)
  • increase pCO2/ H+ (eg exercising muscles)
  • increase 2,3-DPG (diphosphoglycerate) produced in erythrocytes (eg chronic hypoxia)→ decrease Hb affinity to O2→ O2 release from blood to tissue
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25
Q

how does a lung collapse

A

increase pleural pressures (pneumothorax/ pleural effusion/ haemothorax), causing pleural pressure > 760mmHg

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26
Q

formula for minute ventilation

A

TV x respiratory rate
**increases with exercise due to increase in TV and RR

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27
Q

formula for alveolar ventilation

A

(TV - VD) x respiratory rate
**shallow rapid breaths are less effective for alveolar respiration (TV falls, TV-VD falls) RR increases but by lower proportion (can try calculating)

28
Q

what happens to a blocked alveoli over time

A

collapses as air diffuses out of alveoli into tissues

29
Q

factors affecting gas exchange (2)

A
  1. diffusion across alveolar-capillary barrier:
    - ventilation of alveoli (affected by obstructive diseases)
    - thin barrier for diffusion (affected by fibrosis)
    - presence of partial pressure gradients (e.g. hypoxia)
    - functional surface area for gas exchange (eg alveoli collapse)
  2. blood flow factors:
    - perfusion (e.g. embolisms)
    - blood flow rate (e.g. severe exercise→ high rate of blood flow → reducing time for gas exchange)
30
Q

what are the membranes/barriers diffusion occurs across? (3)

A
  1. alveolar epithelium
  2. basement membrane
  3. capillary endothelium
31
Q

what factors influence the distribution of blood flow in lungs (2)?

A
  1. gravity (upright→ more blood flow at bottom of lungs aka base)
  2. muscular tone of pulmonary arteries: eg. vasoconstriction→ ↓ blood flow through capillaries
32
Q

values of normal atm, alveolar, deoxygenated pO2

A

atm - 160mmHg
alveolar - 100mmHg
deoxygenated - 40mmHg

33
Q

what senses changes in arterial pO2 and pCO2? (SENSOR)

A
  • medullary chemoreceptors (brain)→ sense pCO2 (too much CO2 in blood→ excess diffuse across BBB into ECF→ converted to H2CO3 then H+→ stimulates chemoreceptor→ sends signals to brainstem)
  • carotid & aortic body chemoreceptors (major arteries)→ sense pO2
34
Q

what elicits response to changes in pO2 and pCO2 (CONTROL)

A
  • respiratory centre (pons + medulla)
  • pons: modify rate and depth of ventilation
  • medulla: regulate automatic ventilation through rhythmic discharge of inspiratory & expiratory neurons
35
Q

factors affecting response of respiratory centre/ventilatory drive (5) (stimulus for sensor)

A

I EDITED THIS!!
1. chemoreceptors in major arteries → more sensitive to O2, hypoxic drive via glossopharyngeal & vagal nerves
2. chemoreceptors in medulla → more sensitive to PCO2, hypercapnic drive
3. lung stretch fibres (vagus nerve discharge that inhibits inspiration when lungs are stretched)
4. joint/ muscle propioceptors (stimulate ventilation during movement of joints)
5. sedatives & opioids causing depression of respiratory control centre -> reduced ventilation & ventilatory responses (severe increase in pCO2 that follows - CO2 narcosis - will decrease ventilation further)

36
Q

compensatory ventilatory drive in exercise and its results on O2, CO2, H+

A

exercise→ increased pCO2, increased H+ (due to CO2 & lactic acid production)

increased ventilation→ normal H+, normal pO2, normal/decreased pCO2

37
Q

why does chronic CO2 retention decrease ventilatory drive

A

body adapts by buffering H+: H+ increase in buffered by HCO3-→ extracellular fluid in brain is less acidic (compared to acute CO2 retention)→ less stimulation of medullary chemoreceptors→ ventilation drive is less sensitive to increases in pCO2

38
Q

why we should not give 100% oxygen to patients with chronic CO2 retention?

A

patients main drive to increase ventilation is the hypoxic drive (low O2) instead of the hypercapnic drive

giving 100% oxygen decreases hypoxic drive→ decrease ventilation→ ↓ excretion of CO2→ ↑ PCO2

39
Q

how does ketoacidosis lead to kussmaul breathing (air hunger)

A
  • METABOLIC acidosis
  • removal of H+ through CO2 removal (increased ventilation) does not lower ketone acids in blood→ inadequate compensation→ severe ventilation (kussmaul breathing)
40
Q

what is the role of the lungs in metabolism of angiotension?

A

lungs contain ACE to convert angiotensin 1→ angiotensin 2 as blood flows through the lungs

41
Q

what factors affect work of breathing? (2)

A
  1. lung compliance
  2. airway resistance
  3. others (states that affect ventilatory drive) e.g. exercise, drugs
42
Q

what is lung compliance?

A

the how easily lungs & chest wall stretch (aka stretchability)

43
Q

factors affecting compliance of lungs & chest wall (3)

A
  1. chest wall: skeletal deformities eg kyphosis
  2. lungs: alveoli compliance (surface tension in alveoli dependent on surfactant)
  3. elastic recoil:
    - after stretching force is released
    - affected by elastic fibres in lung tissue
    - eg fibrosis → less stretchable → less compliant
44
Q

how does surfactant affect alveoli/ lung compliance

A
  • surface tension (T) generates pressure in alveoli (by inducing contraction), too much causes collapse of smaller alveoli as pressure is inversely proportional to radius of alveoli (P ∝ T/R)
  • surfactant decreases surface tension and increase stretchability/ compliance of lung
  • surfactant lines inner surface of alveolar epithelium
45
Q

what is the pathology of infant respiratory distress syndrome?

A
  • lack of surfactant→ alveoli collapse
  • in newborn premature babies
46
Q

what is FEV1, FVC

A

FEV1: forced expiratory volume of air exhaled in 1 sec after full inspiration

FVC: forced vital capacity (total volume expired after full inspiration)

47
Q

what does FEV1/FVC > 0.7-0.8 mean

A
  • restrictive pulmonary disease
  • reduced lung compliance (lung has high recoil)
    **both values of FEV1 and FVC will be lower than a normal person as total lung volumes are reduced
48
Q

what does FEV1/FVC < 0.7-0.8 mean

A
  • obstructive pulmonary disease, obstruction cause low exhalation
    **both values of FEV1 and FVC will be lower than a normal person as total lung volumes are reduced
49
Q

what are the effects of high altitude? (3)

A

lower environment pO2 (usually 150-160mmHg)→ lower alveolar pO2 (usually 100mm~Hg)→ decreased tissue pO2

  1. hypoxia
  2. increased ventilation
  3. decreased pCO2, decreased H+ (respiratory alkalosis)
50
Q

response to high altitude & acclimatization (5)

A
  1. acute: increased ventilation
  2. acute: adaptive change to correct respi alkalosis (caused by hyperventilation) through reduced H+ secretion, reduced HCO3- reabsorption
  3. low pO2→ global vasoconstriction of pulmonary arterioles→ ↑ pulmonary vascular resistance→ ↑ pulmonary arterial pressure to increase perfusion
  4. longer term: increased 2,3-DPG in RBC (decrease Hb/O2 affinity→ increase release of O2 into tissues)
  5. increased erythropoietin in response to hypoxia (produce HIF-1a)
51
Q

what are the types of V/Q mismatch (2)

A
  1. alveolar dead space (yes V, no Q)
  2. shunt (no V, yes Q)
52
Q

what is dead space + V/Q value

A
  • air inhaled that does not reach perfused areas in alveoli
  • anatomical dead space: volume of conducting airways where no gas exchange takes place
  • physiological dead space: volume of lungs not participating in gas exchange (anatomical dead space + alveolar dead space)
  • V (ventilation) present, no Q (perfusion)→ V/Q=infinity
  • eg pulmonary embolism/ poor cardiac output causing lower blood flow
53
Q

what is a shunt + V/Q value

A
  • deoxygentated blood that returns to systemic circulation without passing through ventilated alveoli to get oxygenated
  • V absent, Q present→ V/Q=0
54
Q

what is a pulmonary shunt and its effect

A
  • lack of alveolar ventilation due to collapsed alveoli (atelectasis) or fluid filled alveoli (eg edema, inflammation, pneumonia)
  • cause hypoxic vasoconstriction→ reduces effect of shunt by constricting and redirecting blood to better ventilated regions
55
Q

what is a vascular shunt

A

blood flow bypasses alveoli and drains directly into systemic circulation

*normal shunts -> eg bronchial capillaries supply airways with oxygenated blood and immediately returns to LA without pass through alveoli, cause mixing of some de-O2 blood with O2 blood in LA (physiological)
*abnormal shunt -> not normal, eg L to R shunt in heart

56
Q

what happens in CO2 gas poisoning

A

extremely high pCO2 causes CO2 narcosis and further depression of CNS & ventilation

57
Q

what happens in CO poisoning

A

CO binds with Hb with higher affinity than O2, forms COHb (cherry pink) and prevents Hb from carrying O2

58
Q

what happens in N2 narcosis

A
  • severe increase in pN2 cause anaesthetic effect (euphoria, disorientation, loss of coordination, coma)
59
Q

what happens in N2 decompression sickness + treatment

A
  • rapid ascent from deep diving cause dissolved N2 (at high P) to bubble out in tissues→ cause pain in joints and obstruct blood flow
  • recompression in hyperbaric chamber (100% O2 at high atm), slow release of pressure
60
Q

what happens in O2 toxicity

A
  • too high→ form of free radicals (eg H2O2)
  • prolonged 80-100% O2 cause irritation of respiratory passages
  • 100% O2 administered at high atm cause CNS toxicity (muscle twitching, convolusions)→ hyperbaric O2 therapy suitable for limited periods only
61
Q

what are the effects of cigarette smoke on respi system? (5)

A
  1. Cummulative irritation and chronic inflammation of airways & lungs
  2. Increased mucous secretion
  3. Depressed ciliary function (ciliary escalator to remove debris)
  4. Lung diseases (e.g. chronic obstructive pulmonary diseases like emphysema (causes barrel-chestedness) and chronic bronchitis)
  5. Lung cancer
62
Q

what are the consequences of smoking? (4)

A
  1. ↓ ventilation
  2. ↓ diffusion
  3. ↓ amt of functional alveoli
  4. ↓ overall gas exchange in lungs
63
Q

what is the relationship between intra-alveolar and intra-pleural pressure?

A

intra-alveolar pressure > intra-pleural pressure so that lungs can expand

if intra-alvelar < intra-pleural pressure, lungs collapse

64
Q

how does intra-alveolar pressure change before, during and after inpiration?

A

before inspiration: 760mmHg (0)
during inspiration: 759mmHg (-1)
after inspiration: 760mmHg (+1)

65
Q

how does intra-pleural pressure change before, during and after inpiration?

A

before inspiration: 757mmHg (-3)
during inspiration: 754mmHg (-6)
after inspiration: 757mmHg (-3)

66
Q

what is hypoxic drive response?

A

↓ arterial PO2 → ↑ ventilation to restore arterial PO2

normal range: 80-100mmHg, (%HbO2 ~97.5%)stimulated when <60mmHg (%HbO2 ~89%)

67
Q

what is hypercapnic drive response?

A

↑ arterial PCO2/H+ → ↑ ventilation to excrete CO2 & restore arterial PCO2/H+

normal range: 35-45mmHg, stimulated when 45-70mmHg

Body is more sensitive to ↑ PCO2 than ↓ PO2

Respi (2 decks)

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