Respi physio pt 3/3 ("Other" knowledge) Flashcards
note: for this deck of cards, answers are in Onennote's notes
Name and explain 3 protective mechanisms of the respiratory system. (RMM)
R: airway Reflexes (cough, sneezing, swallowing reflex)
- note: swallowing reflex incl. epiglottis closing glottis/trachea during swallowing)
M: Mucociliary action
- mucus trap foreign particles and dust
- cilia sweep it up and out of respi airways
- mucus also moisten/ filter/ warm air
M: alveolar Macrophages
- phagocytoses pathogens (esp in lungs where there’s no more goblet cells)
What are the normal ABGA results?
pH (is respi physio vs renal physio)
PaCO2
PaO2
HCO3
O2 sats (SpO2/ SaO2)
What is the significance of doing a spirometry test?
Explain
(i) what is FEV1 and FVC, how they are obtained
(ii) normal FEV1/FVC ratio?
(iii) different FEV1/FVC ratios expected in different classes of respi conditions?
Hint for (iii):
Thin of values in terms of:
‘Restrictive’ = prob going in
‘Obstructive’ = prob for air gg Out
What is narcosis? (for context about gas toxicities)
Narcosis is a state of unconsciousness/ stupor.
Explain the gas toxicity: CO2 narcosis: (fill blank)
- due to severe increase in ___
- causes depression in ____ –> decrease in ____
- due to severe increase in PCO2
- causes depression in respi centre in medulla –> decrease in ventilation
Explain the gas toxicity: CO narcosis: (fill blank)
- CO is an air pollutant from ___
- inhalation of CO that competes with __ for binding sites on ___ –> forming _____ - that gives blood a cherry-pink colour.
- CO-Hb carried by rbcs decrease the ____ of blood –> lead to _____
Treatment:
- _____________
- CO is an air pollutant from combustion engines
- inhalation of CO that competes with O2 for binding sites on Hb –> forming CO-Hb (carboxy-Hb) - that gives blood a cherry-pink colour.
- CO-Hb carried by rbcs decrease the O2-carrying capacity of blood –> lead to tissue hypoxia
Treatment:
- hyperbaric chamber using v high Partial p.a. of O2 in atmosphere to displace CO from Hb
Explain the gas toxicity: O2 narcosis: (fill blank)
- at high p.a 100% O2 administration (at 4-6x atm p.a.) (eg. in mechanical ventilation/ hyperbaric O2 therapy),
- __________ can occur (symptoms: muscle twitching, convulsions) –> cuz of ________ (eg. H2O2, O2- forms)
- at high p.a 100% O2 administration (at 4-6x atm p.a.) (eg. in mechanical ventilation/ hyperbaric O2 therapy),
- CNS toxicity can occur (symptoms: muscle twitching, convulsions) –> cuz of free radicals derived from O2 (eg. H2O2, O2- forms)
Explain what is hyperbaric O2 therapy + uses?
- 100% O2 admin at moderately high atm p.a. for treatment for limited period
- in hyperbaric (high p.a.) chamber
- for healing of bad wounds, ischaemic injuries –> cuz highh atm of O2 increase PO2 in blood (increased conc grad –> increase Gex) –> improves tissue oxygenation and promotes healing (probs cuz regeneration or repair needs O2 for oxidative phosphorylation to generate ATP –> energy for cellular and repair processes)
Explain the gas toxicity: N2 narcosis (on descent): (fill blank)
- happens when divers _______
- N2 ____in blood
Symptoms (mimic anaesthetic CNS effects)
- _____
- loss of _________
- coma
- happens when divers breathe in more N2 in air tanks when diving (increased air and N2 p.a. in air tanks –> increased conc grad –> increase Gex)
- N2 dissolves in blood
Symptoms (mimic anaesthetic CNS + neuromuscular effects)
- euphoria
- loss of coordination
- coma
Explain the gas toxicity: N2 narcosis (on ascent) (aka. Decompression sickness):
(fill blank)
- alot of N2 dissolved in blood from diving (increased p.a. of N2 in air tanks when diving)
- _____ causes _____ out of N2 -> N2 gas emboli
–> cause pain in ____
–> obstruct _____
Symptoms:
- ______
- ______
Treatment + principle of therapy:
__________
- alot of N2 dissolved in blood from diving (increased p.a. of N2 in air tanks when diving)
- rapid ascent causes bubbling out of N2 -> N2 gas emboli
–> cause pain in joints
–> obstruct blood flow
Symptoms:
- dizziness
- joints aches/ pain
Treatment:
Hyperbaric chamber
- recompress then decompress slowly to atm p.a. to prevent bubbling
What does stimulating the cephalic end of a cut vagus nerve cause respiration to?
Ans:
causes a cessation of breathing,
Reason:
cephalic = ‘head’ end
“This is because the cephalic end of the cut vagus nerve carries VISCERAL SENSORY FIBRES (visceral afferent) to the brainstem, and their (cephalic end of - viscerosensory fibres- in vagus nerve) stimulation is interpreted as excessive lung inflation by the brain. Consequently, the brain sends inhibitory signals to the respiratory muscles to stop further inhalation, leading to apnea (stop breathing).
Note: This mechanism is part of the Hering-Breuer reflex, which normally helps regulate the rhythm and depth of breathing.
Explain the Hering-Breuer reflex (aka. Lung stretch receptor reflex) (in preventing lung over-expansion.)
Hint: start w
1. location of stretch receptors
2. stimulation of stretch recptors by? and actions that follow
3. visceromotor
- Lung stretch receptors are located in the walls of the bronchi and bronchioles detect lung inflation.
- When these receptors are stimulated by lung inflation, they send signals via the afferent fibers of the vagus nerve (cranial nerve X) to the brainstem (medulla oblongata mainly > pons) respi centre.
- Medulla/ respi centre in brainstem processes these signals and sends inhibitory signals to the respiratory muscles, via (parasympathetic = visceromotor nerve fibres in) the vagus nerve, to prevent further inhalation, thereby initiating exhalation.
This feedback loop helps maintain normal breathing patterns and prevents lung over-expansion.
Functional Residual Capacity is?
FRC = ERV + Residual Volume