Case 10: Sarah Rosenthal

Central Ventilation Control

In T Petty

1. Sensors: Chemoreceptors

2. Central Controller: Brainstem and cortex

3. Effectors: Resp muscles

Central Control 1: Chemoreceptors

Central: Respond to changes in blood PCO2 and CSF pH

• In brain

• Main control (CO2)

Peripheral: Respond to changes in blood PO2 (decreased), PCO2 (increased) and pH (decreased)

• In carotid arteries and aortic bodies

Central Control 2: Brainstem and Cortex

Brainstem: Medulla and pons

• Phrenic nerve

• Medulla:

  • DRG controls inspiratory ramp (resp pattern)

  • VRG controls expiration (pre-Botzinger complex, during forced expiration)

• Pons:

  • Pontine resp group controls “off” point of inspiratory ramp (inspiration rate and depth)

Cortex: Voluntary resp control

Central Control: Resp Muscles

Passive: Diaphragm, external intercostals, accessory muscles (scalenes, sternocleidomastoids)

Active: Abdominal, internal intercostals

Central Control During Hypoxia

1. Low PO2 in blood stimulate peripheral chemoreceptors

2. Signal DRG to increase resp drive = Increase resp ramp (resp rate and depth)

3. DRG signals inspiratory muscles to contract and match resp drive

COPD Effects on Central Control

1. Chronic air trapping → Hypercapnia

• Decrease air entering/leaving lungs = Decrease gas exchange

2. Central chemoreceptors sense increased PCO2 = Signal DRG to increase resp drive

3. Lung hyperinflation causes inspiratory muscle restriction/weakness = Cannot increase inspiration rate and depth

4. High resp drive is compensated with rapid and shallow breathing

Opioid Effects on Central Control

In T Petty

1. Bind opioid receptors in brain and spinal cord

2. Decrease NT release to cause:

• Sedation

• Resp depression

• Mioisis

O2 Therapy Indication with COPD

Severe with hypoxemia

Not for mild or moderate

O2 Therapy in Mild and Moderate COPD

Decrease physiological shunting (vasoconstriction) away from damaged alveoli (poor V)

• Increase perfusion to damaged alveoli = Dead space ventilation

• Increase V/Q

  • Same ventilation (alveoli blocked)

  • Decrease perfusion (perfusing non-ventilated alveoli, low perfusion of functioning alveoli)

Increase PaCO2 → Hypercapnia

Pulmonary Hypertension (PH): Description

High mean pulmonary arterial pressure > 20mmHg

Normal: 10-14 mmHg

PH: Epidemiology

Risk Factor: >65 years

PH: Etiology

Complication from other pathologies (cardiac and pulmonary causes)

• Group 1: Pulmonary arterial hypertension

• Group 2: Left heart disease

• Group 3: Lung disease/hypoxia (COPD)

• Group 4: Pulmonary artery obstruction (thromboembolism)

• Group 5: Unclear/Multifactorial

PH: Pathogenesis

1. Chronic hypoxia from COPD = Pulmonary arteriole constriction

2. Chronic constriction = Vascular remodelling

• Endothelial cell dysfunction decrease vasodilator (NO) and increase vasoconstrictor (endothelin 1) production

• Smooth muscle hypertrophy

• Inflammatory cell infiltration

3. Decrease artery diameter = Increase resistance = Increase pressure

4. Progress to cor pulmonale (right ventricle disease)

PH Pathogenesis in Emphysema

Alveolar destruction = Decrease pulmonary capillaries (in parallel) = Increase resistance = Increase pressure

PH: Investigation

Transthoracic Echocardiology (TTE): Heart ultrasound

• Determine mPAP

• Hypertrophy = High right ventricular pressure

• Dilation = Right ventricular failure

Right Heart Catheterization:

• Confirm diagnosis

• mPAP > 20 mmHg

PH: Clinical Presentation

From right ventricle dysfunction

Common during exercise

• Dyspnea

• Fatigue

• Palpitations and chest pain

PH: Treatment/Management

Treat underlying disease

Calcium channel blockers and other pulmonary vasodilators

COPD Exacerbation Management/Treatment

Antibiotics

O2 therapy

Mucolytics

Mechanical ventilation

Surgery

COPD Exacerbation: Antibiotics

Indications:

• Resp tract infection or unknown

• Changes in sputum quantity, colour, thickness

COPD Exacerbation: O2 Therapy

Indications: Severe hypoxemia and PH

Administration: Nasal prongs, aim for 88-92%

COPD Exacerbation: Mucolytics

Reduce disulfide bonds in mucus = Liquify mucus = Increase mucociliary clearance

COPD Exacerbation: Mechanical Ventilation

Indication: Acute resp failure

COPD Exacerbation: Surgery

Indication: COPD unresponsive to therapy

Administer:

• Lung volume reduction surgery

  • Remove portion of lungs

  • Increase elasticity + decrease hyperinflation

  • Restore diaphragm position

• Lung transplant

  • For AATD