respi physio Flashcards
pulmonary system pressure
24/10 mmHg
what are the components found in the alveoli + functions? (5)
- 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
what are the function of respi system? (4)
- 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
physiologic RR
12-20breaths/min
what are the physiologic pO2 levels in envt, alveoli & deoxygenated tissues
environment: 150-160mmHg
alveoli: 100mmHg
deoxygenated tissues: 40mmHg
where are cilia found in respiratory tract?
- trachea, bronchi, bronchioles, and some in the respiratory bronchioles
- absent in alveolar ducts and alveolar sacs
where are there smooth muscles in respi tract?
- in trachea, bronchi, bronchioles, some in respiratory bronchioles, some in alveolar ducts
- absent in alveolar sacs
where is there cartilage in respi tract?
- hyaline cartilage in trachea
- patchy in bronchi
- absent in bronchioles (purely smooth muscles), alveolar ducts/sacs
what are the protective mechanisms of the respi tract? (4)
- 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
what is pneumothorax?
air in potential space between visceral & parietal pleura of lung
what is tension pneumothorax?
- 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
what is the pathophysiology of tension pneumothorax?
- 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
what are the effects of tension pneumothorax (air compress on lungs & heart) on HR, arterial BP, pulmonary BP, CVP?
↑↑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
what are the definitions of TV, ERV, IRV, RV
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
what is IC, FRC, VC, TLC
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
what are hyperventilation, hypoventilation, tachypnoea, dyspnea?
Hyperventilation: ↑ ventilation - rapid but deep breathing
Hypoventilation: ↓ ventilation
Tachypnoea: ↑ rate of breathing - rapid but shallow
Dyspnea: difficulty breathing
what is the process of active inspiration?
diaphragm & inspiratory chest wall muscles contract→ chest cavity expands→ intrathoracic volume ↑→ pressure in thorax & pleural cavity ↓→ air flows into lungs
what is the process of active expiration?
diaphragm & inspiratory chest wall muscles relax→ chest cavity recoils→ intrathoracic volume ↓→ pressure in thorax & pleural cavity ↑→ air flows out of lungs
what are the muscles/structures required for expiration/inspiration?
bones: ribs, sternum, clavicles
muscles: diaphragm, intercostal muscles
when ventilation is stimulated eg exercise, extra muscles eg neck, internal intercostal, abdominal muscles are recruited
describe foetal pulmonary circulation
- 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
what happens to foetal circulation after baby’s first breath
- 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
major forms of O2 in blood
- 99% as HbO2
- 1% as dissolved O2 -> exerts pO2
major forms of CO2 in blood
- 70% as HCO3-
- 23% as carbamino Hb
- 7% as dissolved CO2 -> exerts pCO2
what can decrease Hb affinity for O2 (3)
- 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
how does a lung collapse
increase pleural pressures (pneumothorax/ pleural effusion/ haemothorax), causing pleural pressure > 760mmHg
formula for minute ventilation
TV x respiratory rate
**increases with exercise due to increase in TV and RR
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)
what happens to a blocked alveoli over time
collapses as air diffuses out of alveoli into tissues
factors affecting gas exchange (2)
- 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) - blood flow factors:
- perfusion (e.g. embolisms)
- blood flow rate (e.g. severe exercise→ high rate of blood flow → reducing time for gas exchange)
what are the membranes/barriers diffusion occurs across? (3)
- alveolar epithelium
- basement membrane
- capillary endothelium
what factors influence the distribution of blood flow in lungs (2)?
- gravity (upright→ more blood flow at bottom of lungs aka base)
- muscular tone of pulmonary arteries: eg. vasoconstriction→ ↓ blood flow through capillaries
values of normal atm, alveolar, deoxygenated pO2
atm - 160mmHg
alveolar - 100mmHg
deoxygenated - 40mmHg
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
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
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)
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
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
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
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)
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
what factors affect work of breathing? (2)
- lung compliance
- airway resistance
- others (states that affect ventilatory drive) e.g. exercise, drugs
what is lung compliance?
the how easily lungs & chest wall stretch (aka stretchability)
factors affecting compliance of lungs & chest wall (3)
- chest wall: skeletal deformities eg kyphosis
- lungs: alveoli compliance (surface tension in alveoli dependent on surfactant)
- elastic recoil:
- after stretching force is released
- affected by elastic fibres in lung tissue
- eg fibrosis → less stretchable → less compliant
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
what is the pathology of infant respiratory distress syndrome?
- lack of surfactant→ alveoli collapse
- in newborn premature babies
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)
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
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
what are the effects of high altitude? (3)
lower environment pO2 (usually 150-160mmHg)→ lower alveolar pO2 (usually 100mm~Hg)→ decreased tissue pO2
- hypoxia
- increased ventilation
- decreased pCO2, decreased H+ (respiratory alkalosis)
response to high altitude & acclimatization (5)
- acute: increased ventilation
- acute: adaptive change to correct respi alkalosis (caused by hyperventilation) through reduced H+ secretion, reduced HCO3- reabsorption
- low pO2→ global vasoconstriction of pulmonary arterioles→ ↑ pulmonary vascular resistance→ ↑ pulmonary arterial pressure to increase perfusion
- longer term: increased 2,3-DPG in RBC (decrease Hb/O2 affinity→ increase release of O2 into tissues)
- increased erythropoietin in response to hypoxia (produce HIF-1a)
what are the types of V/Q mismatch (2)
- alveolar dead space (yes V, no Q)
- shunt (no V, yes Q)
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
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
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
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
what happens in CO2 gas poisoning
extremely high pCO2 causes CO2 narcosis and further depression of CNS & ventilation
what happens in CO poisoning
CO binds with Hb with higher affinity than O2, forms COHb (cherry pink) and prevents Hb from carrying O2
what happens in N2 narcosis
- severe increase in pN2 cause anaesthetic effect (euphoria, disorientation, loss of coordination, coma)
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
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
what are the effects of cigarette smoke on respi system? (5)
- Cummulative irritation and chronic inflammation of airways & lungs
- Increased mucous secretion
- Depressed ciliary function (ciliary escalator to remove debris)
- Lung diseases (e.g. chronic obstructive pulmonary diseases like emphysema (causes barrel-chestedness) and chronic bronchitis)
- Lung cancer
what are the consequences of smoking? (4)
- ↓ ventilation
- ↓ diffusion
- ↓ amt of functional alveoli
- ↓ overall gas exchange in lungs
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
how does intra-alveolar pressure change before, during and after inpiration?
before inspiration: 760mmHg (0)
during inspiration: 759mmHg (-1)
after inspiration: 760mmHg (+1)
how does intra-pleural pressure change before, during and after inpiration?
before inspiration: 757mmHg (-3)
during inspiration: 754mmHg (-6)
after inspiration: 757mmHg (-3)
what is hypoxic drive response?
↓ arterial PO2 → ↑ ventilation to restore arterial PO2
normal range: 80-100mmHg, (%HbO2 ~97.5%)stimulated when <60mmHg (%HbO2 ~89%)
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
