Case 1: Steven Thomas Flashcards

1
Q

Respiratory Centres in the Medulla Oblongata (1)

A
  1. Dorsal Respiratory Group (DRG)
    - Located in dorsal portion
    - Controls mostly inspiratory movements and their timing.
    - Controls both quiet and forced inspiration.
    - DRG’s inspiratory centre controls:
    - The phrenic nerve which innervates the diaphragm.
    - The intercostal nerves which innervate the external intercostal muscles.
    - Nerves which innervate the accessory respiratory muscles involved in forced inhalation (scalenei muscles, sternocleidomastoid, serratus anterior and pec minor)
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2
Q

Respiratory Centres in the Medulla Oblongata (2)

A
  1. Ventral Respiratory Group (VRG):
    - Located in the ventrolateral part.
    - Mainly causes forced expiration
    - VRG’s expiratory centre controls:
    - The intercostal nerves which innervate the intercostal muscles.
    - Nerves which innervate the accessory respiratory muscles involves in active exhalation (mainly abdominal muscles).
    - VRG’s inspiratory centre aids DRG during forced inspiration. This controls:
    - Nerves which innervate the accessory respiratory muscles involved in maximal inhalation (scalenei muscles, sternocleidomastoid, serratus anterior and pec minor)
    - When the respiratory drive for increased pulmonary ventilation becomes greater than normal, respiratory signals spill over into the VRG from the DRG. This activates the inspiratory centre of the VRG, allowing it to innervate the accessory respiratory muscles of forced expiration.
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3
Q

Inspiratory ‘Ramp’ Signal

A

The signals sent from the respiratory centres to the respiratory muscles occur in bursts of action potentials.
In normal respiration:
1. The signals begin weakly and increase steadily in a ramp manor for approx 2 seconds –> provides stimulation to the inspiratory muscles –> inhalation occurs.
2. Signals then cease abruptly for approx 3 seconds which turns off the excitation of the diaphragm and allows elastic recoil of the lungs and the chest wall to cause expiration (passive exhalation occurs).
3. Then, the inspiratory signal begins again and this cycle repeats again with expiration occurring in between.
ADVANTAGE: causes a steady increase in the volume of the lungs during inspiration, rather than inspiratory gasps.
Deep Breathing: The signals become stronger more quickly. Rate of increase of the ramp signal is faster.
Faster Breathing: The signals start and cease earlier. The ramps are less than 2 seconds.

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4
Q

Respiratory Centres of the Pons

A
  • Apneustic and Pneumotaxic centres of the pons adjust the output of DRG and VRG
  • Their activities regulate the respiratory rate and depth of respiration in response to stimuli or other centres in the brain.
  • STIMULI: impulses from receptors around the body are carried via the vagus or the glossopharyngeal nerves to the respiratory centres.
  • OTHER CENTRES: these include the hypothalamus (deviation in temperature) or the cerebrum.
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5
Q

Apneustic Centres

A
  • Located in the lower pons.
  • Provides continuous stimulation to the DRG, resulting in a long, deep inhalation.
  • The continuous stimulation builds the ramp signal during quiet inspiration.
  • It coordinates transition between inhalation and expiration.
  • Under normal conditions, after the 2 seconds, the apneustic centre is inhibited by the pneumotaxic centre on the same side.
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6
Q

Pneumotaxic Centres

A
  • Located in upper pons
  • Inhibits the apneustic centres. It controls the ‘switch-off’ point of the ramp signal, thus limiting inspiration.
  • Centres in the hypothalamus and cerebrum can alter the activity of the pneumotaxic centres as well as the respiratory rate and depth.
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7
Q

Hypoxia

A

A lack of oxygen

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8
Q

Causes of hypoxia (5)

A
  1. Inadequate oxygenation of the blood in the lungs because of extrinsic reasons
    • deficiency of oxygen in the atmosphere
    • hypoventilation (neuromuscular disorders)
  2. Pulmonary disease
    • hypoventilation caused by increased airway resistance or decreased pulmonary compliance
    • abnormal alveolar ventilation - perfusion ratio
    • diminished respiratory membrane diffusion
  3. Venous-to-arterial shunts (‘right-to-left cardiac shunts’)
  4. Inadequate oxygen transport to the tissues by the blood
    • anaemia or abnormal haemoglobin
    • general circulatory deficiency
    • localised circulatory deficiency (peripheral, cerebral, coronary vessels etc.)
    • tissue oedema
  5. Inadequate tissue capability of using oxygen
    • poisoning of cellular oxidation enzymes (cyanide poisoning)
    • diminished cellular metabolic capacity for using oxygen, because of toxicity, vitamin deficiency, or other factors
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9
Q

Effects of Hypoxia

A
  • Acute Effects:
    - drowsiness
    - lassitude (lack of energy)
    - mental and muscle fatigue
    - headache and nausea
  • one of the most important effects of hypoxia is decreased mental proficiency, which decreases judgement, memory. and the performance of discrete motor movements
  • cyanosis: blueness of the skin:
    - caused as a result of excessive amounts of deoxygenated haemoglobin in the skin blood vessels
    - this deoxygenated blood has an intense dark blue-purple colour that is transmitted through the skin
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10
Q

Work of Breathing depends on … (4)

A
  1. Tidal Volume:
    • increased tidal volume = more work done by lungs
  2. Respiratory Frequency:
    • increased frequency = more work done by lungs
  3. Lung Compliance:
    • increased compliance = less work done by lungs
  4. Airways Resistance:
    • increased resistance = more work done by lungs
      • Increased work of breathing, leading to fatigue, is one cause of respiratory failure.
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11
Q

Airways Resistance

A

Airflow = Change in pressure/Airways resistance
Change in pressure = alveolar pressure - atmospheric pressure
Airways resistance is proportional to length/radius^4
The longer the airway, the greater the airways resistance.
The narrower the airway, the greater the airways resistance.

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12
Q

Compliance

A

-Compliance is the indication of a lung’s expandability, or how easily the lungs expand and contract.
-Lower the compliance = greater the force required to fill and empty the lungs.
-Greater the compliance = easier it is to fill and empty the lungs.
Factors effecting compliance:
-Elastic forces of the lung tissue
-Elastic forces caused by surface tension of the fluid that lines the inside walls of the alveoli and other lung air spaces

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13
Q

Surfactant

A

-A surface active agent in water - greatly reduces the surface tension of water.
-Secreted by special surfactant-secreting epithelial cells called type II alveolar epithelial cells, which constitute about 10% of the surface area of the alveoli.
Surfactant is a complex mixture of several phospholipids, proteins and ions.

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14
Q

Dead space

A
  • The amount of ‘fresh air’ reaching the alveoli/gas exchange areas of the lung (alveolar ventilation) is less than the amount of fresh air entering the airways at the mouth and nose (pulmonary ventilation).
  • Alveolar ventilation will vary with breathing pattern:
    - For the same amount of pulmonary ventilation, slow deep breathing gives more alveolar ventilation than fast rapid breathing.
  • Alveolar ventilation is important for gas exchange, and so the composition of arterial blood.
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15
Q

Pneumothorax

A
  • A collection of air between the visceral and parietal pleura causing a real rather than potential pleural space.
  • Normal conditions: pressure within the intrapleural space is negative with respect to the atmosphere and with respect to alveolar gas.
  • If connection is made with atmospheric pressure and the pleural cavity, gas will flow into the intrapleural space, increasing its pressure to atmospheric pressure.
  • Lung partially collapses due to the elastic recoil pressure.
  • CLINICAL PRESENTATION: if pneumothorax enlarger, the patient becomes more breathless and may develop pallor and tachycardia
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16
Q

Types of pneumothorax (4)

A
  1. Primary spontaneous pneumothorax
  2. Secondary spontaneous pneumothorax
  3. Traumatic pneumothorax
  4. Tension pneumothorax
17
Q

Primary spontaneous pneumothorax

A
  • Most common type of pneumothorax
  • Caused by rupture of a small subpleural emphysematous bulla or pulmonary bleb (usually apical) - thought to be dye to congenital defects in connective tissue. This is a weakness and out - pouching of the lung tissue, which can rupture. This introduces air into the pleural space, causing the lung to start collapsing.
  • As the lung collapses, the hole formed by the ruptured bleb seals, preventing more air from entering the intrapleural cavity.
  • Tall, thin, young men (20-40years old) with no underlying disease usually affected.
  • In patients over 40 years, the usual cause is underlying COPD.
  • Male/female ratio = 5:1
  • Both lungs are affected with equal frequency.
  • Rarely causes significant physiological disturbance.
  • People who have had one spontaneous pneumothorax are at higher risk of recurrence.
  • RISK FACTORS: smoking, tall stature and presence of apical subpleural blebs.
  • TREATMENT: pleurodesis (needle aspiration and chest drain) to fuse visceral and parietal pleura by medical (bleomycin/talc) or surgical (abrasion of pleural lining).
18
Q

Secondary spontaneous pneumothorax

A

-Much more deadly
-Caused by respiratory diseases that damage lung structure: most commonly COPD and asthma, fibrotic or infective diseases (pneumonia), rarely inherited diseases (eg. Marfan’s and cystic fibrosis)
-Incidence increases with age (peaks in males aged 15-30 years) and severity of underlying disease
-Usually occurs in males > 55 years
-ICU patients with lung disease are at particular risk for SSP due to high presses (barotrauma) and alveolar distention (volutrauma) associated with mechanical ventilation.
Protective ventilation strategies using low pressure, limited volume ventilation reduce this risk.

19
Q

Traumatic Pneumothorax

A
  • Blunt (road traffic accident) or penetrating (stab wounds, fractured ribs) chest trauma
  • Gas may enter the intrapleural space either from the atmosphere through a hole in the chest wall or from alveoli through a hole in the lung
  • The flow of air two way
  • Therapeutic procedures such as line insertion or thoracic surgery are common causes.
  • Traumatic pneumothorax can usually be associated with heamothorax (accumulation of blood within the pleural cavity)
20
Q

Tension pneumothorax

A
  • Most common during mechanical ventilation/following traumatic pneumothorax.
  • The flow of air is one way (from lung into pleural cavity) upon inspiration. Upon inspiration, the air from the atmosphere enters the pleural cavity (from the stab wound) down the pressure gradient.
  • Upon expiration, the air cannot escape from the pleural cavity and remains trapped there because the pleural pressure doesn’t increase above the atmospheric pressure.
  • Every inspiration results in a build up of air and pressure (tension).
  • Specific symptoms: cyanosis, severe breathlessness
  • Treatment: needle aspiration and chest drain.
21
Q

Clinical features of pneumothorax

A
  • A spontaneous pneumothorax will present the chest pain and breathlessness.
  • The pain is usually of sudden onset, localised to the affected side and made worse on inspiration.
  • Dyspnoea (laboured breathing) is partly produced by the difficulty in taking a deep breath, but is also dependent on the size of the pneumothorax and the presence of underlying lung disease.
  • The most consistent finding is a reduction in breath sounds on the affected side.
  • Movement on the chest wall may be reduced.
  • The percussion note will be resonant.
22
Q

Diagnosis of pneumothorax

A
  • Examination of the chest with a stethoscope reveals decreased or absent breath sounds over the affected lung.
  • The diagnosis is confirmed by chest x-ray
  • An x-ray can illustrate the collapse of the lung as extra black space, indicating the presence of air, will be seen in the x - ray around the lung.
  • In tension pneumothorax, the lung shrivels up away from the affected side and the mediastinum will shift towards the unaffected side - trachea displacement.
  • The combination of absent breath sounds and resonant percussion is diagnostic of pneumothorax.
23
Q

Physical examinations of pneumothorax

A
  1. Inspection
    • patient looks distressed and is sweating
    • dyspnoea (SOB) may be apparent
    • cyanosis, depending on degree of respiratory inadequacy
  2. Palpation
    • palpation may show affected side moves less than normal side (air in intrapleural space allows ribcage to expand outwards)
  3. Percussion
    • affected side sounds hyperresonant (sound similar to percussion of puffed cheeks)
  4. Auscultation
    • breath sounds on the affected side are diminished
    • this is because less gas enters the collapsed lung during inspiration, air in intrapleural space acts as a barrier to the transmission of sounds from lung to the chest wall
  5. Trachea displaced away from side of collapsed lung in tension pneumothorax
  6. Pulse examination
    • tachycardia common, pulse rate>135 bpm suggests tension pneumothorax
    • pulsus paradoxicus (slow pulse on inspiration) suggests severe pneumothorax
  7. Monitoring reveals hypotension and desaturation (less oxygen being carried in the blood)
24
Q

Investigations of Pneumothorax

A
  1. Chest x-ray confirms the diagnosis:
    • clear line of visceral pleura with absence of peripheral lung markings beyond it
    • trachea and mediastinum may also be deviated away from affected side
    • standard erect posterior anterior films are usually adequate
    • A: airways, B: breathing and bones, C: cardiac, D: diaphragm, E: everything else
  2. Arterial blood gases will show hypoxia (insufficient oxygen supply to the body). More disturbed in SP - less reserve in the presence of pre - existing lung disease
  3. CT scan not used in routine, but may be helpful to differentiate a large bulla from a pneumothorax, may detect localised pneumothaces.
25
Q

Treatment of primary pneumothorax (dependent on degree of collapse)

A

Complete - aspirate/chest drain
Moderate - aspirate
Small - observe

26
Q

Treatment of secondary pneumothorax (dependent on degree of collapse)

A

Complete - chest drain
Moderate - chest drain
Small - chest drain

27
Q

Treatment of traumatic pneumothorax (dependent on degree of collapse)

A

Complete - chest drain
Moderate - chest drain
Small - chest drain

28
Q

Immediate management of pneumothorax

A
  • tension pneumothorax must be drained immediately
  • small Primary spontaneous pneumothorax can be managed by observation using clinical assessment and chest x - ray
  • primary spontaneous pneumothorax > 30% aspirated in the second intercostal space in the midclavicular line, using a 15mL syringe, connected to a 3-way tap and underwater seal. Used to such out as much air as possible, if patient coughs, this is acheived
  • spontaneous and traumatic pneumothoraces always require hospital admission and intercostal chest drainage. multiple may be needed