Respiratory Physiology Flashcards
what are the functions of the respiratory tract?
conduction of air (warms/himidifies)
respiration (gas exchange)
pathogen protection (mucous)
what is the main purpose of breathing?
maintains blood-gas homeostasis
what is partial pressure?
the sum of the partial pressures of a gas must equal to total pressure
what muscles are involved in breathing?
diaphragm (dome shaped skeletal)
other respiratory muscles in strenuous breathing
explain the mechanism of quiet breathing and the activity of inspiration and expiration
inspiration (active) - diaphragm contracts downwards pushing abdominal contents outwards
external intercostals pulll ribs outwards and upwards
expiration (passive) - elastic recoil
explain the inspiration mechanism of strenuous breathing
active - greater diaphragm and external intercostals contraction (10x more than quiet)
inspiration accessory muscles active
explain the expiration mechanism of strenuous breathing
active - abdominal muscles recruited
internal intercostal muscles oppose external intercostals pushing ribs down and inwards
what does the cough reflex do?
remove offending material from airway
what is the cough reflex triggered by and how is it activated?
rapidly adapting pulmonary stretch receptors (RARs) found in epithelium of respiratory tract
activated by dust, smoke, ammonia, oedema etc.
how does a cough reflex get signalled for?
RARs send signal to brain using vagus nerve
brain sends signal to diaphragm/external intercostals via phrenic nerve
explain the stages of a cough reflex
air rushes into lungs
abdominal muscles contract to induce expiration
glottis opens to forcefully release air and irritants
what are conducting airways?
bronchi containing cartilage and non-respiratory bronchioles
dont partake in gas exchange
what are respiratory airways?
bronchioles with alveoli where gas exchange occurs
(from terminal bronchioles to alveoli)
what is the function of bronchial circulation?
brongs oxygenated blood to lung parenchyma
what is the partial pressure of O2 inside and outside the body?
inside: 150mmHg
outside - 159mmHg
name the structures in alveolar-capillary networks
type 1 alveolar epithelial cells
capillary endothelial cells
BM
how is oxygen carried in the blood?
dissolved (proportional to PP in an arterial blood sample)
bound to haemoglobin
name the pressure of O2 and CO2 in:
- pulmonary artery
- capillaries
- pulmonary veins
- anatomic dead space
PA: O2 = 40, CO2 = 46
PV and capillaries: O2 102, CO2 = 40
anatomic dead space: O2 = 150, CO2 = 0
explain the structure of haemoglobin
4 heme groups (2 alpha and 2 beta polypeptide chains)
each group contains Fe++ (site of O2 binding)
describe O2 saturation and what is it measured with
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
what are the general resting tissue requirements/excretions for O2 and CO2?
O2: 250ml/min
CO2: 200ml/min
how is CO2 carried in blood?
7% dissolved
23% bound to Hb
70% converted into bicarbonate
how do capillaries expel CO2?
systemic capillaries expel CO2 produced by tissues into blood
pulmonary capillaries expel CO2 into alveoli
explain the bicarbonate reaction
reaction: HCO3 -> H2O + CO2
regulated H+ ions and maintains base balance in body
how are CO2, HCO3 and H+ concentrations linked?
stabilise pH through strong buffer reaction (due to HCO3 strength)
what is the V/Q ratio?
ventilation:blood flow
defined by single alveolus (alveolar ventilation:capillary flow)
defined by lung (total alveolar ventilation:CO)
what are the general values for alveolar ventilation, pulmonary blood flow and V/Q?
alveolar ventilation: 4-6l/min
pulmonary blood flow: 5l/min
V/Q - 0.8-1.2
describe the effects of PO2 on Hb saturation in the O2 dissociation curve
drop from 100-60 in PO2 has little effect
60 below has much larger effect (more sensetive to change)
what factors shift the O2 dissociation curve to the right?
decreased affinity:
increased temp
increased PCO2
decreased pH
what factors shift the O2 dissociation curve to the left?
increased affinity:
decreased temp
decreased PCO2
increased pH
what is the rule of H+ ions on pH?
changes in H+ of a factor of 2 lead to a pH change of 0.3
name systems affected by acid-base disorders
CVR
metabolic
renal
GI
neurological
what are some of the threats to acid base disorders?
CO2 generation (aerobic respiration)
food metabolism generating acid or alkali
incomplete respiration (anaerobic)
loss of alkali in stool
loss of acid in vomiting
what are the major components of acid base balance and how do they regulate?
buffering
ventilation (CO2 control)
renal regulation (HCO3/H+ secretion and reabsorption)
regulate H+ concentration at the expense of other concentrations (HCO3/CO2)
what are buffers and how do they work?
weak acids partially dissociated in solution
react poorly with water
reacts with H+ (base) or OH- (weak acid)
explain how ventilation results in acid-base regulation
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
name buffers and describe what they buffer
haemoglobin (blood CO2)
proteins (intracellular)
bone (long term)
PO4 (urinary/intracellular)
how do buffers and the kidneys work together to regulate acid-base composition
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
what is the function of the kidneys in acid-base regulation and how do they do it?
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
explain the reabsorption of filtered HCO3
active process in mainly proximal tubule
small contributions from DCT and ascending LoH
cant be reabsorbed in state of metabolic acidosis
what is respiratory acidosis?
levels of CO2 being expelled from the lungs
too much in blood = acidosis
too little in blood = alkalosis
what is metabolic acidosis?
levels of HCO3 expelled in urine
too much in blood = alkalosis
too little in blood = acidosis
what is lactic acidosis and how is it buffered?
reduced hepatic clearance of lactic acid produced from glycolytic metabolism of pyruvate
buffered by HCO3 to lactate then metabolised in liver
what do chemoreceptors and mechanoreceptors provide feedback on?
chemoreceptors - PO2, PCO2, pH levels in blood
mechanoreceptors - mechanical lung status, chest wall, airways
what structures receive signals from the brain to maintain breathing?
diaphragm/intercostals (rhythmic breathing)
upper airway muscles (laryngeal, pharyngeal, tongue)
reflexes to keep airways pateny (cough, sneeze, gag)
what is O2 decrease and CO2 increase medically called?
O2 - hypoxia
CO2 - hypercapnia
describe peripheral chemoreceptors
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
describe central chemoreceptors
clusters of neurones in brainstem
activated when PCO2 is increased or pH is decreased
explain the result of changes in PCO2
small changes have large effects on ventilation
hypercapnic response originating from central chemoreceptora in brainstem
describe mechanoreceptors
sensory receptors detecting chnges in pressure, movement and touch
(e.g lung inflation and chest movements during inspiration)
what is the course of an impulse from mechanoreceptors?
stimulus (lung inflation)
neural signal goes through vagus nerve to NTS in brainstem to adjuct ventilation
what do mechanoreceptors integrate?
respiratory pattern with other movements such as posture or locomotion
how do mechanoreceptors terminate inspiration?
in airway smooth muscle
detects stimulus of inflation/distension of airways
what do mechanoreceptors in the airway epithelium detect?
rapid lung inflation/deflation (or oedema)
causes sigh or shortened expiration
explain the course of action from the NTS
NTS receives signals from mechanoreceptors and peripheral chemoreceptors
info processes in brainstem by neuronal clusters
breathing rhythm generated and sent to respiratory muscles
describe the respiratory rhythm generating neurons
bilateral clusters of neurons with rhythm generating properties
produce a rhythmic resp output even when isolated
where do the rhythmic output signals go after the brainstem?
sent down spinal cord which sends signals to resp muscles such as diaphragm (phrenic nerve) or intercostal muscles (thoracic spinal cord nerves)
what areas of the brainstem are responsible for resp rhythm generation?
pontine group (pons)
ventral group (pattern/rhythm generating neurons)
dorsal resp group (NTS)
what types of higher centre modulation control breathing?
volitional and emotional
what is the neural basis for voluntary control attributed to?
motor cortex
explain the role of the corticospinal tract in breathing regulation
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)
what are the physiological effects of asthma?
loss of airway epithelium
thickening of BM
hypertrophy of smooth muscle layer (including mast cells)
what is asthma?
inflammatory disease of medium sized airways
hyper-responsiveness to normal triggers of contraction
abnormal contraction in response to benign triggers
what can asthma cause in the airway?
increased force contraction
twitchy smooth muscle
variable airway calibre
loss of relaxation after contraction
what are the symptoms of asthma?
triggered breathlessness
wheezing
diurnal variation (night/morning)
coughing
how is asthma measured?
bronchial hyper-reactivity is induced
exaggerated response to usually constricting stimuli (often histamine used) is seen
what does spirometry measure and how does it do it?
measures airflow velocity
a narrowed/constricted airwa yrelaxes and dilates in response to salbutamol (adrenaline beta agonist)
what are the common triggers of asthma?
allergy
infection
exercise
drugs (beta blockers/NSAIDs)
cold air
scents
describe the smooth muscle only stage of asthma
triggered by direct mediator (histamine)
causes rare wheezing
describe the chronic inflammation stage of asthma
irritates smooth muscle and causes regular wheezing
describe the acute inflammation stage of asthma
caused by viral infection and results in clinical exacerbations
what are the inflammatory factors often associated with asthma?
cells (lymphocytes, eosinophils, mast cells)
cytokines (Il-4, IL-5)
prostanoids (PGE2, leukotriene D4)
immunoglobulins (IgE)
explain the role of mast cell mediators
e.g histamine at H1 receptor, prostoglandin at PC2 receptor
causes smooth muscle contraction, blood vessel formation and airway wall oedema
explain the role of beta 2 agonists in asthma
e.g salbutamol
active adrenaline receptor
activated G-protein on GPCR which activates cAMP resulting in smooth muscle relaxation
what do corticosteriods do in asthma?
block transcription factors causing an inflammatory response
reduce muscle twitchiness
reduce exhaled NO
what do anti-leukotrine receptor drugs do in asthma?
trats resistant inflammation
targets onlt leukotrine D4 in airway effecting mast cells and smooth muscle
what is the 4D approach to prescribing inhalers?
diagnosis
drug and device
disease control
device disposal
what is a preventer inhaler?
anti-inflammatory inhaler using inhaled corticosteroids (ICS)
what is a combination inhaler?
uses inhaled corticosteroids (ICS) and long acting beta agonist (LABA)
what is a reliever inhaler?
bronchodilating inhaler containing a short acting beta agonist (SABA) or a long acting beta agonist (LABA)
how can asthma and COPD be distinguished?
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
describe NO exhalation measurement
only valid in non-smokers
normal results: <25ppb
abnormal results: >50ppb
indicates eosinophilic inflammation in airways
how does COPD develop?
inflammatory cells produce excess protease enzymes (neutrophil elastase) and insufficient antiprotease enzymes (a1 antitrypsin)
imbalance causes lung tissue damage and COPD development
what are the effects of emphysema?
elastic support loss causing airway compression
this causes airway obstruction (peripheral airway disease)
ventilation maldistribution (poor gas exchange)
what are some common diseases associated with COPD?
asthma
bacterial colonisations
hypoxia
reflux
underlying bronchiectasis
explain the symptoms of bronchiectasis
purulent daily sputum
50% idiopathic
recurrent infections
lungs crackle on exam
what is bronchodilation and bronchoconstriction generally caused by?
bronchodilation - inhibitory nerves, circulating epinephrine
bronchoconstriction - excitory nerves, vagus nerve
briefly explain what COPD is
largely irreversible airflow obstruction often including emphysema
