Respiratory System

Question 1

Ventilation mechanics

Answer 1

1) Inspiration
Diaphragm and external intercostal muscles contract, causing expansion of thoracic cage
During active inspiration, accessory inspiratory muscles in the neck may contract to further expand thoracic cage
Lungs expand along with thoracic cavity, increasing lung volume
Intra-alveolar pressure drops below atmospheric pressure, causing air to flow into lungs from environment until IA pressure = Atm again

2) Expiration
Diaphragm and external intercostal muscles relax, causing thoracic cavity to recoil to pre-inspiratory size
During active expiration, internal intercostal muscles and abdominal muscles may contract to push diaphragm further up, further decreasing thoracic cavity size
Lungs recoil to pre-inspiratory size along with thoracic cavity, lung volume decreases, intra-alveolar pressure increases above atmospheric pressure. Air flows out of lungs into environment until IA pressure = Atm again

Question 2

Nerve control of respiration

Answer 2

Respiratory Control Centre → sets the basic rhythm

1) Medullary Respiratory Group
DRG (Dorsal Respiratory Group)
Inspiratory neurons
Fires APs to contract muscles for inspiration, otherwise muscles relax for passive expiration
VRG (Ventral Respiratory Group)
Both inspiratory and expiratory neurons
Active expiration

2) Pons Respiratory Centre
Fine tuning, controls Speed and smoothness of breathing
Receives information via afferent fibres
Info on lung volume and environmental factors
Connects main with medullary
Pneumotaxic centre limits inspiration, Apneustic centre assists inspiration

Question 3

Lung compliance, surfactant and surface tension

Answer 3

Surfactant = mixture of phospholipids, neutral lipids and proteins which reduce surface tension at water-air interface and prevent alveolar collapse during expiration

Lung compliance = elasticity, ability to recoil after inspiration during expiration, influenced by amount of elastin in walls

Question 4

Airway resistance diseases (obstructive lung diseases)

Answer 4

Chronic bronchitis

Emphysema
Irreversible condition where alveolar walls break down and smaller airways collapse, leading to formation of larger air spaces in bronchioles

Causes:
Long term exposure to irritants causes excessive macrophage activity (host defence), which release proteases which break down the elastin in alveolar connective tissue
loss of elastin causes decreased elastic recoil (increased compliance), smaller airways collapse under pressure during expiration
Loss of collagen and elastin → septa separating alveoli eventually break down → larger alveoli, less surface area for gas exchange
Anti-trypsin deficiency leaves lungs unprotected from macrophages, even normal levels of macrophage activity.
Symptoms: overinflated lungs, breathlessness

Asthma
Chronic inflammatory disorder
Hypersensitivity to allergens - histamine released from degranulating mast cells
Inflammation of epithelial tissues in respiratory tract leading to airway thickening
Oedema
Hypertrophy of epithelial cells
Excess mucus production from goblet cells
Hyperplasia of goblet cells
Smooth muscle contraction
Bronchospasm - airways constrict
Hypertrophy and hyperplasia of myocytes

Impaired gas exch vs impaired gas transport
Symptoms like wheezing, dyspnea + histological reasoning

Question 5

Other triggers for shortness of breath

Answer 5

Strenuous exercise
Anxiety
High altitude
Extreme temperature change
Poor air quality
Obesity

Question 6

Management during asthma attack

Answer 6

1) Stop dental procedure, remove rubber dams, cotton rolls that may be in mouth/obstructing airway
2) Sit patient up in upright, comfortable position
Upright position helps accessory muscle use
Abdominal pressure lower, diaphragm can contract further down
Chest opens
3) Provide oxygen by full face mask and bronchodilator
4) Continue to observe and activate emergency protocol if symptoms do not improve