COPD Flashcards
COPD Definition
COPD is a group of respiratory diseases characterised by airflow limitation that is progressive, not fully reversible and is associated with an abnormal response to noxious gas or particles. COPD is a combination small airway disease and destruction of lung parenchyma including chronic bronchitis, emphysema, bronchiectasis and asthma.
Chronic bronchitis pathophysiology
- Continual exposure of the airway tissue over a period of time to irritants causes chronic inflammation with swelling and excess mucus production, altereing the cells, causing narrowinf of the bronchus and bronchioles resulting in VQ mismatch.
- Chrmical meditors are releeased, causing initally vasoconstriction followed by vasodilation, prompting inflammatory response. This increases hydrostatic pressure and therefore increased capillary permeability.
- antibodies bind to mast cells, stimulating degrannulation = histamine release, leading to more vasodilation = leady capillaries.
- Constant expsure to irrtant causes damage to cilliated cells, eventually destroying function which are replaced by goblet cells (good evonrimonet for infections).
- Chronic cough developped because of increased muvous and inability to clear.
= Over a period of time, causes scarring and remodelling, narrowing the airways and limiting airflow. Also decrease ACE.
Emphysema pathophysiology
- Characterised by abnormal enlargement of the airways due to destruction of the alveoli surface tension, resulting in poor recoil, decreased gas echange and gas trapping.
- With the loss of alveoli integrity, alveoli collpase on exhalation, and reduced SA for gas exchange.
- The decrease elasticity of the tissue decreases the ability of the air to flow passively out through the airways, causes inglation of the alveoli and gas trappping = “barrel chest” appearance.
- Exposure to irrtants also famages the surrounding vasculature, further decreasing gas exchange.
Patient presentation (Bronchitis)
- Productive cough
- Systemic odema due to R) HF
- Cynosis due to hypoventilation and HF
Patient presentation (emphysema)
- Rapid breathing and increased WOB
- Pursed lips due to increased work of expiration algainst collapsed airways
- Thin and barrelled chest
Bohr effect
The affinity of O2 to Hb decreases as pH decreases (more acidic)
The Haldane effect
The Haldane effect describes the shift in the CO2 dissociation curve caused by oxygenation of Hb. Oxygenation of blood in the lungs displaces CO2 from Hb which increases the removal of CO2.
- As deoxygenated Hb binds to CO2 with greater affinity than oxygenated Hb, there is a R) shift of the Oxy-Hb curve in an attempt to transport and exhale more CO2 for the blood to carry more CO2
- In patients with severe COPD who cannot increase monute ventilation, the haldane effect accounts for 25% of the total PaCO2 increase due to O2 administration.
Oxy-Hb dissociation curve
- Sigmoid shaped curve which represents the relationship between partial pessure of O2 and O2 saturation
- The amount of O2 bound to Hb is determined by PO2.
- Left shift: increases affinity for O2 affected by increased pH decreased temp
- Right shift: decreased affinity for O2 affected by decreased pH and increased temp - more CO2 is able to bind to Hb for exhalation and to stabilise pH.
Cor Pulmonale - Definition & causes
Decreased function of the right ventricle due to an increase in pulmonary hypertension as a result of increased resistence.
Causes:
- Chornic hypoxia leads to pulmonary arterior constriction through over increased invonlvment of physiological mechanism to maintain the baalnce of ventilation and perfusion in the lungs.
- Chornic hypercapnia and respiratory acsidosis also cause pulmonary vasoconstriction
Generalised patient presentation for COPD
Febrile
Wheeze
dyspnoea
fatigue
peripheral oedmea
chest tightness not relieved by GTN
haemoptysis due to pulmonary arteriole rapture
hepatic congestion
Resp infections
prolonged expiratory phase
Pathophysiology of hypercapnic respiratory failure secondary to excessive O2 administration
- Chemoreceptors within the CSF of the brain stem adjust to normally having excess CO2.
- When O2 is administered, increased SpO2, this decreases resporatory drive, leading to dangerous hypercapnia.
- COPD pts optimise gas exchange by hypocia vasoconstriction, excessive O2 overcomes this, leading to increased blood flow to poorly ventilated alveoli, therefore, increased VQ mismatched and increase physioogical dead space.This normal physiologic compensation, when overcome with excessive O2 administration, results in worsening V/Q ratios, that is to say, more areas in the lung where V/Q ratios are low and more areas of high V/Q. The extreme high V/Q areas that have no flow (no Q) represent dead space. In a situation where total minute ventilation remains constant, an increase in dead space diminishes CO2 excretion and results in higher PaCO2 values.
Why in COPD patients dose hypoxia vasoconstriction occur
serves to redirect blood flow away from under-ventilated lung in order to optimize the V/Q ratio.
COPD management
All exacerbations of COPD:
- Salbutamol MDI: 8puffs every 10mins (or 10ml neb)
- Ipratropium 4 puffs every 10mins (or 500mcg neb)
- Dexamethasone 8mg
- Titrate SpO2 88-92%
Altered conscious state:
- Ventilate 5-8/min (7-12 secs)
- Gentle lateral chest compression
