1. Anatomy and Physiology What do we need to consider?
Sam Petty
Clinical Specialist Physiotherapist
John Farman ICU
Addenbrooke’s Hospital
If you put breathing into a search engine you will find hundreds of quotes

2. “I’m breathing......Are you breathing too? It’s nice, isn’t it” Robert Bolt
playwrights

3. “That breath you just took....... that’s a gift” Rob Bell
Pastors.

4. “Breathing is the basic rhythm of life”
Hippocrates
It is automatic, continuous and almost requires no thought. As early as Hippocrates (450 BC) humans were examining what it means to breathe. So.....

5. Respiratory System How? Why? What can go wrong?
When I agreed to step in at the last minute to present this I initially thought Jeepers. Seriously. Read a book!
Then I figured as you all have done that how can we relate it to what we see/do every day

6. Important thing
Inspiration: Active or passive? Expiration: Active or passive?

7. Think lungs? Every day: 300 million alveoli
80 m3 (nearly the size of a tennis court)
Fill to a volume of air and pollutants that could fill an average swimming pool (Hanley and Tyler, 1987)

8. Also involves.... Neural control
Mechanics (chest wall deformity/compliance, muscle strength,length, morphism)
Respiratory pathway (nose to alveoli)
Alveoli and gas exchange
Perfusion
Other

9. Perfusion
Pointless having a well ventilated alveolus if no blood can reach it or conversely a well perfused alveolus that is not ventilated Pulmonary embolus Pulmonary vasoconstriction

10. Other Don’t forget the pleura pleural effusion Pneumothorax
Haemo/hydrothorax

11. Questions?

12. Brain and CNS Respiratory control centres in the medulla and pons
Chemoreceptors on medulla (pH)
Carotid and aortic bodies (PCO2 and PO2)
Phrenic nerve innervation
Intercostal nerves

13. Innervation

14. What can go wrong? SCI (Spinal Cord Injury)
“C3,4,5 keeps the diaphragm alive”
long term-ventilation
inability to cough
poor position of diaphragm
T1-T11 innervates intercostals
fatigue easily with load
reduced cough effectiveness
difficulty changing lung volumes

15. What can go wrong? Guillain-Barre Syndrome (GBS)
hypoventilation due to respiratory muscle weakness or impaired bulbar function or both
20-30% require ventilatory support (Fletcher et al, 2000)
Mortality in the ventilated population 15-30%
Majority require tracheostomy

16. What can go wrong?
Bulbar problems (GBS, MND, polio, Lyme disease, malignancy, MS, myaesthenia gravis)
Impairment of function of the cranial nerves IX, X, XI and XII due to lesion in medulla or of lower cranial nerves outside the brainstem
Symptoms: dysphagia (swallowing difficulty)
Laryngeal weakness, nasal regurgitation, chewing difficulty
Signs: nasal speech, atrophic tongue (with fasciculations), dribbling, absent gag

17. What can go wrong? Myaesthenia Gravis (50-200 per million people)
Autoimmune disease
Antibodies destroy receptors at junction between nerves and muscle
Initial symptom is muscle weakness around the eyes resulting in drooping, double vision
Go on to develop painless weakness which is progressively worse during physical activity

18. Mechanics
Reliant on normal length:tension relationship

19. Mechanics Position of diaphragm (e.g. SCI, pancreatitis)
Shape of the thorax (kyphosis, scoliosis)
Articulations i.e. Ankylosing spondylitis
Multiple rib fractures
Thoracoplasty
Pleural effusions

20. Respiratory Pathway Nose Pharynx – housing epiglottis
Larynx – housing vocal cords
Anatomical dead space
Intrinsic PEEP

21. Coughing
Inspiratory gasp to 90% TLC Closure of glottis and trapping of air in the lungs to raise intrathoracic pressure Rapid opening of glottis resulting in expiratory speed of up to 500 mph

22. Upper airway/cord issues - symptoms
Inability to cough
Hoarse or breathy voice
Inability to raise voice
Choking/coughing while eating
Pneumonia secondary to aspiration
Stridor
wheeze

23. Medical conditions URT tumor Trauma Eppiglottitis
Laryngeal/pharyngeal oedema
Compression from external source
Nerve damage/involvement

24. How do we contribute to problems with URT?
Intubation
Repeated intubation
Tracheostomy (render URT useless)
Dry, high flowing gas
Impairment of mucociliary escalator
Ineffective seal of stoma following decannulation

25. Trachea Normal transverse internal diameter of trachea: Length:
15-25 mm in men
10-21 mm in women
Length:
from inferior end of larynx (C6) to bifurcation at carina (between T5 and T7)
9-15 cm
Houses c-shaped cartilage rings to maintain
rigidity

26. Tracheostomy Why? When? How? Risks? Type?
Important to consider tube diameter in relation to air flow and demands you make on patient
Speaking valves

27. Bronchi/bronchioles Carina – first bifurcation
Right is wider, shorter and more vertical
Lined by respiratory epithelium (holds cilia)
Smooth muscle spiraled under epithelium
Muscle contains mucous secreting glands
Incomplete cartilage rings to provide some structural support

28. Problems Smooth muscle spasm – bronchospasm Inflammation
Mucous plugging
I:E mismatch – prolonged expiratory phase and gas trapping
Structural abnormality/problems e.g. Bronchomalacia, stenosis, bronchiectasis
External compression
fistulas

29. And all of the above before you have even reached...........
The Alveoli

30. Alveoli 300 million 50-100 m2 surface area
90% type I pneumocytes (gas exchange cells)
Type II responsible for surfactant production
Alveolar dead space is minimal in normal lungs
Ventilation gradient = more alveolar ‘dead space’ at the apex

31. Problems at alveolar level
Collapse
Consolidation
Atelectasis
Bullous disease/emphysema
Wasted ventilation (i.e. No perfusion)
Damaged tissue (fibrosis, ARDS)

32. Emphysema Decreased surface area for gas exchange
Shunting (wasted perfusion)
Gas trapping due to change in I:E ratio
Result in type II RF
LTOT

33. ARDS 200,000 pa US 40% estimated mortality 58% mortality if AKI
First described in 1967, Lancet
12 patients suffering from acute onset of tachypnoea, hypoxaemia and loss of compliance
Refractory to supplemental O2, some response to PEEP
PM findings – widespread pulmonary inflammation,oedema and hyaline membrane formation

34. ARDS Pathogenesis Diffuse alveolar damage
Disruption of alveolar capillary membrane
Complex inflammatory infiltrate
Surfacrtant dysfunction
Type II pneumocyte regeneration to replace type Is
Formation of hyaline membranesIncreased alvolar vascular permeability
Epithelial injury secondary to neutrophils, macrophages and RBCs

35. ARDS Shunt Surfactant dysfunction Alveolar instability
Collapse/consolidation
Increased lung water and inflammation
Decreased compliance
High WOB
Pulmonary vasoconstriction