Case 1: T Petty - Central Ventilation Control

Triage Information

TPR + pulse oximetry

Triage: T

Temp

Normal: 37ºC (36.5-37.5)

Regulated by hypothalamus

Triage: P

Pulse rate and BP

Normal: 60-100 bpm

• Higher: Tachycardia

• Lower: Bradycardia

BP varies

• When measuring:

  • No caffeine and nicotine

  • Empty bladder

  • Sitting, uncrossed legs

Triage: R

Respiratory rate

Normal Adult: 12-20 breaths per min

• Child: 30-60 breaths per min

  • Decrease with age

• High: Tachypnea

• Lower: Bradypnea

Breathing depth

• Increased Depth: Hyperpnea

Hyperventilation: Increase breathing rate and depth

Triage: Pulse Oximetry

Normal: 95-100%

Smoking status for clarification

Ventilation Muscles

Diaphragm

Intercostal Muscles

Abdominal Muscles

Diaphragm

Inspiratory muscle

Dome-shaped

• Connected to sternum, 6 lower ribs, vertebral column, pericardium

Innervated by phrenic nerves from spinal cord (C3-5)

Intercostal Muscles

External

Internal

External Intercostal Muscles

Inspiratory muscles

Outer muscles under ribs

Anterior and inferior fibres

Internal Intercostal Muscles

Expiratory muscles

Inner muscles under external intercostals

Anterior and superior fibres

Accessory Muscles

Scalene

Abdominals

Accessory Muscles: Scalene

Inspiratory

Accessory Muscles: Abdominal Muscles

Expiratory muscles

3 layers

Anatomy: CNS Breathing Control

Brainstem

• Delicate location

• Pressure/obstruction stops breathing

Brainstem

Midbrain

Medulla oblongata

Pons

Brainstem: Medulla Oblongata

Contain:

• Dorsal Respiratory Group (DRG)

  • Sensory termination of:

    1. Vagus Nerve (Lungs): Central Chemoreceptors

    2. Glossopharyngeal Nerves (Carotid, Aortic): Peripheral Chemoreceptors

• Ventral Respiratory Group (VRG)

  • Pre-Botzinger complex

Brainstem: Pons

Contain:

• Pontine respiratory group

Physiology: Central Respiration Control

Respiratory Centre: Neurons in medulla oblongata and pons

• DRG: Inspiration

• VRG: Inspiration + Expiration

• Pontine Respiratory Group: Breathing rate/depth

Respiratory Centre: DRG

Integrate signals from chemoreceptors + baroreceptors

Respiration:

1. Transmit ramping signal to muscles for 2 secs = Contraction = Inspiration

2. Signal stops for 3 secs = Muscles relax = Expiration

3. Cycle repeats

Heavy Respiration: Increase ramp signal speed = Rapid lung filing

Frequent Respiration: Decrease ramp signal limit = Shorter inspiration length

Respiratory Centre: VRG

For forced inspiration and expiration

• Inspiration: Increase respiratory drive

• Expiration: Stimulate accessory muscle contraction

Pre-Botzinger Complex: Pacemaker neurons controlling respiration rate/pattern

Respiratory Centre: Pontine Respiratory Group

Control “off” point of inspiratory ramp

• Strong Signal: Decrease inspiration time (30-40 breaths per min)

• Weak Signal: Increase inspiration time (3-5 breaths per min)

Contains:

• Apneustic Centre: Inspiration depth

• Pneumotaxic Centre: Inspiration duration

Physiology: Chemical Respiration Control

CO2, H+, O2

Detected by chemoreceptors

• Central: Brain + brainstem

• Peripheral: Carotid arteries + aortic arch

Chemical Respiration Control: Blood CO2 and H+

Direct control

Increase CO2 (Hypercapnia)

• Cross BBB = Increase H+ = Decrease pH

• Stimulate central chemoreceptors in chemosensitive areas (ventrolateral medulla + retrotrapezoid nucleus) to contract respiratory muscles

• Increase respiratory rate + depth

Decrease CO2

• Decrease H+ = Increase pH

• Decrease respiratory rate + depth

Chemical Respiration Control: Blood O2

Indirect control

Decrease O2 (Hypoxia)

• MUST be dissolved in blood, unbound to hemoglobin

• Stimulate peripheral chemoreceptors to signal respiratory centre to contract muscles

• Increase respiration

Physiology: Mechanical Respiration Control

Stretch receptors

Ventilation Pathophysiology: Hyperventilation

Increased breathing rate + depth

Insufficient gas exchange

• Decrease blood CO2

• Increase pH

• Consistent O2

Ventilation Pathophysiology: Hypoxemia

Decreased blood O2

Stimulate peripheral chemoreceptors to increase respiration rate + depth

Opioids

Analgesic compounds working on opioid receptors

CNS depressant

Includes:

• Morphine

• Codeine

• Endogenous opioid peptides

  • Endorphins

  • Enkephalins

  • Dynorphins

Opioid Receptors

Agonists of:

• μ-opioid receptor

  • Major analgesic receptor

  • Morphine > codeine

• δ and κ opioid receptor-like subtype 1 receptors

Opioid Treatment

Naloxone

• Opioid receptor antagonist

• Half-Life: 30-80 mins

Opioid Pharmacokinetics: A

Well absorbed subcutaneously, intramuscularly, orally

• Oral: First-pass effect = Higher dose (variable outcome)

  • Less in codeine and oxycodone

Other Methods: Oral mucosa (lozenges), transdermal patches

Opioid Pharmacokinetics: D

To high perfusion tissues

• Skeletal Muscle: Main reservoir

• Adipose tissue

Opioid Pharmacokinetics: M

Into polar metabolites

Adverse effects for renal failure patients

Prolonged doses = Excess CNS excitation

Opioid Pharmacokinetics: E

By kidneys in urine

• Renal impairment = Sedation + respiratory depression risk

Opioid Pharmacodynamics (MOA)

1. Bind opioid receptors (G protein-coupled receptors) in brain and spinal cord

   • Mostly μ receptors in spinal cord dorsal horn

2. Decrease NT release to cause

   • Sedation

   • Respiratory depression (difficult to overcome)

   • Mioisis

   • Analgesia

   • Euphoria

   • Cough suppression

3. Tolerance and dependence from repeated use

Opioids: Effect on Respiratory Drive

Dose-dependent effects

1. Opioids bind μ receptors in brainstem respiratory centre

   • Inhibit excitatory signals

2. Decreased response to increased CO2 levels

   • No increase in respiratory drive (rate + tidal volume) when CO2 increases

3. Decreased respiratory drive = Respiratory depression

   • Dangerous/fatal for patient