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66 Cards in this Set

  • Front
  • Back

Central controllers of respiration?

Pons, medulla etc.

Initiation of ventilation:


Role of Pneumotaxic center in pons

first


sends signals to apneustic center

Initiation of ventilation:


Role of apneustic center in pons

second


controls dorsal and ventral respiratory groups in medulla

Initiation of ventilation:


Dorsal respiratory group is ?

inspiratory

Initiation of ventilation:


Ventral respiratory group is ?

inspiratory + expiratory

Central chemoreceptors location where?

Ventral medullae

Central chemoreceptors respond to what?

Hypercapnic drive

Peripheral chemoreceptors locationS where?

- Aortic arch


and


- carotid bodies of carotid arteries

Peripheral chemoreceptors respond to what?

Hypoxic drive

What drives ventilation - hypoxia or hypercapnia?

hypercapnic drive usually


 


hypoxic drive only if high altitude or chronic lung disease

What is hypoxic drive?

- incr ventilation rate response to falling PO2


- peripheral chemoreceptor mediated


- non linear response due to O2 affinity of haemoglobin

What is hypercapnic drive?

- incr ventilation rate response to rising PCO2


- largely central chemoreceptor mediated


- linear, immediate & significant response

Explain the synergistic effect of hypoxia & hypercapnia

elevated PCO2 - incr hypoxic effect on ventilation


 


reduced PO2 - incr hypercapnic effect on ventilation

Functions of respiratory system (just the unobvious ones)

"A-BAPI-FAPI"


- Arachdonate metabolites get synthesised


- Blood reservoir


- Acid base balance via CO2 removal


- Phonation


- Inactivation of neurotransmitters


- Filters particles


- Angiotensin 1 ---> Angiotensin 2 conversion


- Produces surfactant


- IgA secretion into bronchial mucus

main muscles of resp.

diaphragm


external intercostals

accessory muscles of resp.

scalene


pectorals


latissimus dorsi


Trapezius


abdominals (forced exhalation)


internal intercostals (forced exhalation)

normal resp rate = ?

15 breaths / min (10 - 18)

How many further branching levels does the tracheobronchial tree undergo between bifurcation to the level of alveolar sacs?

23!!!

name the levels of tracheobronchial tree

" Mainly loving small brothers with terminal respiratory dsa "


main bronchi


lobar bronchi


small bronchi


bronchioles


terminal bronchioles


respiratory bronchioles


alveolar ducts, sacs and alveoli

As you go down levels of the tracheobronchial tree...


with increased branching comes:

- Smooth muscle reduction


- Goblet and cillia cells reduction


- Seromucous glands reduction


- Cartilage reduction


- pseudostratified to squamification


- bulk flow to diffusion


- no more bronchial blood flow

Atmospheric pressure eqn

PB = PH2O + PO2 + PCO2 + PN2

dry air atm pressure eqn

PB = PCO2 / FCO2

wet air atm presure eqn

PB = (PCO2 / FCO2) + 47

ideal gas eqn

pV = nRT

Deadspace

lung area that is ventilated but not perfused

Anatomical deadspace

Air in conducting zones that don't oxygenate blood

Physiological deadspace

Additional volumes of lung that can't oxygenate blood 


on top of anatomical deadspace

Anatomical deadspace should equal physiological deadspace but can change due to factors:

Obesity


pulmonary embolism


emphysema

VA - Alveolar ventilation -

flow of air that oxygenates blood


70% of tidal volume usually

Minute ventilation - 

Airflow into lungs per minute

Vital capacity

Volume of air moved by max inspiration and expiration

Tidal Volume (VT)

Volume of air moved by regular inspiration and expiration

Inspiratory reserve volume

Max vol. inspirable on top of tidal volume

Expiratory reserve volume

Max vol. expirable on top of resting expiratory level

total lung capacity

vol. in lungs after max inspiration

Residual volume

Air remaining even after maximal expiration

Inspiratory capacity

Max vol inspirable from resting expiratory level

Functional residual capacity

Max vol expirable from resting expiratory level

resting expiratory level

normal breathing, after air has been expired regularly

Effects on PaCO2?


Hyperventilation -


Hypoventilation - 

Hyperventilation - reduces PaCO2


Hypoventilation - increased PaCO2

How to measure airway resistance

Measure:


1) PEFR


2) FEV1 / FVC

% of airway resistance from upper airways?

50%

Factors affecting airway resistance:

- Lung volume (collapsed/narrowed airways)


- Bronchial smooth muscle contraction

What drugs can relax bronchial muscle and dilate airways?

β-2 agonists and anticholinergics

Diaphragm's innervation?

Phrenic nerve from C3 - C5

External intercostals innervation?

Intercostal nerves

Whats Transpulmonary / transmural pressure 

Difference between Alveolar pressure (PA) and Intrapleural pressure (Ppl)



PA - Ppl

Why is transpulmonary pressure always +ive?

cause intrapleural pressure always is -ive

What happens when transpulmonary pressure = 0 such as in a pneumothorax?

elastic recoil causes lungs to collapse

Effect of asthma on lungs

1) Bronchial tube muscles tighten


2) airways inflame and mucus builds up


3) narrowed airways ---> dynamic hyperinflation


4) work done to move air larger

Effect of COPD or emphysema on lungs

loss of elasticity in airways ---> dynamic hyper inflation

Dynamic hyperinflation is...

tendency for airways to collapse during expiration thus trapping air in alveoli

Compliance is...

how compliant it is to change in volume with given pressure change

compliance eqn, C = ?

C = change in V / Change in transpulmonary p

How to obtain compliance curve?

Plot transpulmonary pressure against lung volume

Gradient of compliance curve means...?

compliance

Disease states:


Fibrosis

Fibrosis - reduced compliance


because lung parenchyma replaced with collagen

Disease states:


Emphysema

Emphysema - increased compliance


because elastin destroyed and alveolar septae destroyed


 


may cause dynamic hyperinflation


also loss of surface area for gas exchange

What is Respiratory distress syndrome

Premature babies:


- Insufficient surfactant


- lungs unable to expand

Surfactants are secreted by:

Type 2 alveolar cells

Surfactants help to ...

reduce surface tension so alveoli don't recoil inwards and collapse

Law of Laplace eqn :

P = 2T / r


 


Pressure needed to balance out collapsing force from surface tension over a certain alveolar radius

Laminar flow


Turbulent flow

smooth


rough

W - Work done in breathing eqn:

W = P * change in V


P - pressure


V - volume

Resistive load?

e.g. in COPD


stuff resisting/blocking

Elastic load?

e.g. pulmonary fibrosis


more force to breathe