respi physio Flashcards
(67 cards)
1
Q
pulmonary system pressure
A
24/10 mmHg
2
Q
what are the components found in the alveoli + functions? (5)
A
- type 1 alveolar epithelial cells: simple squamous, forms barrier that’s permeable for gas exchange
- type 2 alveolar epithelial cells: simple cuboidal, produce surfactant
- alveolar macrophages: phagocytose foreign particles
- interstitial cells: contain fibroblast to produce collagen for structural support of cells
- capillary endothelial cells: simple squamous, lines capillaries to increase efficacy of gas exchange
3
Q
what are the function of respi system? (4)
A
- Metabolism & Acid-Base Regulation: provides O2 to tissues for metabolism, removes CO2 and regulates pH
- Endocrine functions: produces hormones (e.g. angiotensin converting enzyme to convert angiotension I to angiotensin II for CVS function)
- Immunological functions: clearance of irritants and potential pathogens
- Voice production by larynx
4
Q
physiologic RR
A
12-20breaths/min
5
Q
what are the physiologic pO2 levels in envt, alveoli & deoxygenated tissues
A
environment: 150-160mmHg
alveoli: 100mmHg
deoxygenated tissues: 40mmHg
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
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
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
9
Q
what are the protective mechanisms of the respi tract? (4)
A
- coughing/sneezing reflex
- ciliary escalator (cilia beat to move particles and mucus away from lung to upper respiratory tract)
- humidication & warming of air in upper passages and mucous secretion to protect respiratory epithelium (mucosa) of airways
- alveolar macrophages
10
Q
what is pneumothorax?
A
air in potential space between visceral & parietal pleura of lung
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
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
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
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
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
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
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
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
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
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
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
22
Q
major forms of O2 in blood
A
- 99% as HbO2
- 1% as dissolved O2 -> exerts pO2
23
Q
major forms of CO2 in blood
A
- 70% as HCO3-
- 23% as carbamino Hb
- 7% as dissolved CO2 -> exerts pCO2
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
25
how does a lung collapse
increase pleural pressures (pneumothorax/ pleural effusion/ haemothorax), causing pleural pressure > 760mmHg
26
formula for minute ventilation
TV x respiratory rate
**increases with exercise due to increase in TV and RR
27
formula for alveolar ventilation
(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
what happens to a blocked alveoli over time
collapses as air diffuses out of alveoli into tissues
29
factors affecting gas exchange (2)
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
what are the membranes/barriers diffusion occurs across? (3)
1. alveolar epithelium
2. basement membrane
3. capillary endothelium
31
what factors influence the distribution of blood flow in lungs (2)?
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
values of normal atm, alveolar, deoxygenated pO2
atm - 160mmHg
alveolar - 100mmHg
deoxygenated - 40mmHg
33
what senses changes in arterial pO2 and pCO2? (SENSOR)
- 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
what elicits response to changes in pO2 and pCO2 (CONTROL)
- respiratory centre (pons + medulla)
- pons: modify rate and depth of ventilation
- medulla: regulate automatic ventilation through rhythmic discharge of inspiratory & expiratory neurons
35
factors affecting response of respiratory centre/ventilatory drive (5) (stimulus for sensor)
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
compensatory ventilatory drive in exercise and its results on O2, CO2, H+
exercise→ increased pCO2, increased H+ (due to CO2 & lactic acid production)
increased ventilation→ normal H+, normal pO2, normal/decreased pCO2
37
why does chronic CO2 retention decrease ventilatory drive
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
why we should not give 100% oxygen to patients with chronic CO2 retention?
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
how does ketoacidosis lead to kussmaul breathing (air hunger)
- METABOLIC acidosis
- removal of H+ through CO2 removal (increased ventilation) does not lower ketone acids in blood→ inadequate compensation→ severe ventilation (kussmaul breathing)
40
what is the role of the lungs in metabolism of angiotension?
lungs contain ACE to convert angiotensin 1→ angiotensin 2 as blood flows through the lungs
41
what factors affect work of breathing? (2)
1. lung compliance
2. airway resistance
3. others (states that affect ventilatory drive) e.g. exercise, drugs
42
what is lung compliance?
the how easily lungs & chest wall stretch (aka stretchability)
43
factors affecting compliance of lungs & chest wall (3)
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
how does surfactant affect alveoli/ lung compliance
- 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
what is the pathology of infant respiratory distress syndrome?
- lack of surfactant→ alveoli collapse
- in newborn premature babies
46
what is FEV1, FVC
FEV1: forced expiratory volume of air exhaled in 1 sec after full inspiration
FVC: forced vital capacity (total volume expired after full inspiration)
47
what does FEV1/FVC > 0.7-0.8 mean
- 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
what does FEV1/FVC < 0.7-0.8 mean
- 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
what are the effects of high altitude? (3)
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
response to high altitude & acclimatization (5)
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
what are the types of V/Q mismatch (2)
1. alveolar dead space (yes V, no Q)
2. shunt (no V, yes Q)
52
what is dead space + V/Q value
- 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
what is a shunt + V/Q value
- deoxygentated blood that returns to systemic circulation without passing through ventilated alveoli to get oxygenated
- V absent, Q present→ V/Q=0
54
what is a pulmonary shunt and its effect
- 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
what is a vascular shunt
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
what happens in CO2 gas poisoning
extremely high pCO2 causes CO2 narcosis and further depression of CNS & ventilation
57
what happens in CO poisoning
CO binds with Hb with higher affinity than O2, forms COHb (cherry pink) and prevents Hb from carrying O2
58
what happens in N2 narcosis
- severe increase in pN2 cause anaesthetic effect (euphoria, disorientation, loss of coordination, coma)
59
what happens in N2 decompression sickness + treatment
- 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
what happens in O2 toxicity
- 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
what are the effects of cigarette smoke on respi system? (5)
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
what are the consequences of smoking? (4)
1. ↓ ventilation
2. ↓ diffusion
3. ↓ amt of functional alveoli
4. ↓ overall gas exchange in lungs
63
what is the relationship between intra-alveolar and intra-pleural pressure?
intra-alveolar pressure > intra-pleural pressure so that lungs can expand
if intra-alvelar < intra-pleural pressure, lungs collapse
64
how does intra-alveolar pressure change before, during and after inpiration?
before inspiration: 760mmHg (0)
during inspiration: 759mmHg (-1)
after inspiration: 760mmHg (+1)
65
how does intra-pleural pressure change before, during and after inpiration?
before inspiration: 757mmHg (-3)
during inspiration: 754mmHg (-6)
after inspiration: 757mmHg (-3)
66
what is hypoxic drive response?
↓ arterial PO2 → ↑ ventilation to restore arterial PO2
normal range: 80-100mmHg, (%HbO2 ~97.5%)stimulated when <60mmHg (%HbO2 ~89%)
67
what is hypercapnic drive response?
↑ 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
