Week 2 Flashcards
Describe the steps of normal respiration.
- respiratory controller (voluntary or involuntary)
- respiratory muscles (rib cage and abdomen) create a pressure gradient to draw air in
- movement of air
- alveolar ventilation
What drives involuntary respiratory control?
increased carbon dioxide in the blood
What reduces respiratory drive from the respiratory centre or cortical control?
medications i.e. anesthetic, head injuries, tumours, CVA’s
Which muscles are involved in respiration?
diaphragm, intercostals, SCM, scalenes
What can reduce muscle activation during respiration?
reduced nerve conduction (i.e. GBS, spinal cord injury, poliomyelitis)
myopathies, muscle dystophy, fatigue, surgical incisions (reduced muscle function as well as pain inhibition)
What can reduce rib movement during respiration?
rib fractures (pain inhibition), kyphoscoliosis, pneumothorax/haemothorax/pleural effusion, abnormal chest wall compliance
What can reduce alveolar ventilation?
secretions or tumour/s within bronchi, bronchitis, asthma
decreased surfactant, pulmonary oedema, inflammation (i.e. in pneumonia), or emphysema in the alveolus
What is the functional residual capacity (FRC)?
the volume of gas in the lungs after a normal inspiration- this participates in gas exchange during inspiration and expiration
we always want to increase FRC to maintain fresh air in the lungs
supine position= reduced FRC
sitting and standing upright= increased FRC
the abdominal contents move down with gravity, allowing the diaphragm to expand more which increases the FRC
What is the closing capacity (CC)?
the volume of air in the lungs when small airways start to collapse during expiration, trapping air inside
in a healthy individual, this is at the residual volume i.e. CC=RV, and does not encroach on FRV i.e. CC<FRC
in abnormal respiration, CC>FRC resulting in early collapse of airways resulting reduced ventilation
How does the relationship between CC and FRC change with age?
by 45 years the CC encroaches on the FRC in supine and by 65 years the CC encroaches on the FRC upright
the weaker the respiratory muscles and the more obese, the more difficult the respiration (adipose tissue presses on lungs)
What is hypoxaemic pulmonary vasoconstriction?
a protective response that will constrict the pulmonary vessels if there is a reduction of oxygen in a particular area of the lungs
this diverts blood to areas with greater ventilation therefore increasing oxygen in the blood
What is atelectasis?
‘imperfect expansion’ or collapsed alveoli due to inadequate ventilation
What are the different types and causes of atelectasis?
micro atelectasis (patchy areas seen in post-op patients due to anaesthesia affecting surfactant)
plate atelectasis (small areas of collapse due to pulmonary oedema or pneumonia)
compression atelectasis (structural reason for collapse i.e. tumour or cardiomegaly)
absorption atelectasis (physical blockage of a bronchiole by mucous plug)
What are the effects of atelactasis?
there is a ventilation-perfusion mismatch resulting in hypoxemia and in some cases hypercapnia (high levels of CO2)
this results in reduced FRC and lung compliance and therefore work of breathing increases and more oxygen will be consumed
What are the clinical signs of atelectasis?
Palpation:
decreased chest wall movement
+/- increased temperature
Auscultation:
decreased or absent breath sounds
+/- fine end-inspiratory crackles (as the alveoli reinflate at the end of inspiration)
Special tests:
decreased SPO2, Pa)2 and chest xray
What are some risk factors for atelectasis?
surgical incision
previous respiratory condition
smoking history
obestiy
age
impaired cognitive function
monotonous pattern of mechanical ventilation (absence of normal sigh/changes in breathing pattern)
body position (supine, slouched)
How can we reverse ateletasis?
maintain air in the lungs at all times to overcome the critical opening pressure
encourage ‘slow laminar flow’ inspiration acknowledging the Newtonian Law of Viscosity
use inspiratory holds to:
-overcome different time constants
-encourage collateral ventilation
-use alveolar interdependence to open up alveoli
-stimulate surfactant release
What is critical opening pressure?
the pressure needed to overcome surface tension and achieve initial reinflation of collapsed regions
What is the Newtonian Law of Viscosity?
sticky surfaces peel apart more easily when the action is done slowly
What is collateral ventilation?
relying on neighboring alveoli to inflate blocked-off alveoli via collateral channels
different names of channels:
inter bronchiolar channels of Martin
bronchiolar-alveolar channels of Lambert
alveolar pores of Kohn
What is alveolar interdependence?
if one alveolus starts to collapse, it will exert a stretching force on a neighbouring alveoli and force the reopening of the collapsed alveoli
this is increased at vital capacity vs tidal volume hence why we use deep breaths to make use of this concept
What are time constants?
refers to the timing of ventilation of the alveolar (time constant= compliance x resistance)
in a healthy lung, alveoli are relatively uniform so it takes the same rate and pressure to inflate them
in an unhealthy lung, there may be increased resistance and increased or decreased compliance resulting in varying time to fill
inspiratory holds can overcome this by allowing for different time constants
What occurs during increased work of breathing (WOB)?
increase accessory muscle use, increased respiratory rate and decreased energy available for other organs
How do we manage increased work of breathing (WOB)?
through positioning and breathing control
position:
-recovery/supported positions i.e. forward lean sitting/standing (reverse origin/insertion of pectorial muscles to assist with expanding the thorax)
-breathe control encourages gentle tidal breathing through nose and focusing on the lower chest expanding
