Asthma Flashcards
Describe the respiratory system and explain it’s function
Air enters through mouth and nasal passages - moves through pharynx (throat) past epligottis (covers larynx) - through larynx (contains vocal chords) - down trachea (main airway with cartilage rings) - through L & R bronchi - through bronchioles into terminal bronchioles and into alveoli for gas exchange.
Function: to get oxygen into the blood and expel carbon dioxide out of the body.
Explain the mechanics of breathing
Air always flows from an area of high pressure to area of low pressure
Inspiration: is an active process. Diaphragm contracts downwards and intercostal muscle contract causing the ribcage to expand - this expands the thorax and causes an increase in volume causing a decrease in alveolar pressure -> air flows in due to pressure decrease below the atmospheric pressure.
Expiration: is a passive process. Respiratory muscles relax, the elastic recoil of lungs causes tissue to move back into original shape - decreased thoracic volume = increased alveolar pressure above atmospheric pressure, causing air to flow out. The abdominal and internal intercostal muscles can be used to force out air beyond a normal breath.
Explain the O2/Hb dissociation curve
The 02/Hb curve describes the changing affinity of 02 for Hb. On X axis is 02pp and on Y axis is oxyhaemaglobin saturations. The amount of 02 that binds to Hb is related to 02PP. Each time 02 binds to Hb, the Hb changes shape slightly and it is easier for the next 02 to bind. Eventuallty reaches a plateau where increasing p02 doesnt = increasing saturation.
Right shift = reduced affinity caused by increased C02 (decreased pH), increased temp and DPG - useful in tissues such as muscle for 02 unloading.
Left shift = increased affinity caused by decreased C02 (increased pH), decreased temp and DPG - useful in lungs for 02 binding.
(DPG = organic phosphate in rbc’s that control 02 movement between rbc’s and tissue).
Brief definition of asthma
A chronic inflammatory disease of the small airways.
Explain the pathophysiology of asthma
-Atopic = extrinisic caused by environment (most common)
-Non-atopic = internal caused by local IgE prod.
-Bronchioles of asthmatics = increased goblet cells, increased eosinophils, increased basophils/mast cells, increased neutrophils and SMC hypertrophy.
-Allergen is inhaled - crosslinks with IgE/mastcell complex = release of inflam mediators
-Histamine = H1-3 receptors, leukotrienes, prostaglandins - bronchoconstriction, mucus prod, permeability + swelling.
-Allergen stimulates Ach release = cholinergic muscarinic bronchoconstriction
-Neutrophils (highly inflammatory), eosinphils (remodelling) and basophils (mast cells) are recruited to the area = damage and remodelling of airways = further release of inflam mediators
-damage = exposed bronchial nerves = hypersensitivity = increased mucus production and swelling as protective measures.
UNTREATED:
-develop respiratory acidosis due to mucus plugging and inability to expire C02
-gas trapping = pneumothoracies and hyperinflation = impeded venous return = obstructive shock.
Outline the management of mild - moderate asthma patients
MILD: MDI + spacer: salbultamol 1200mcg repeat once if required, consider GP referral
MODERATE:
-MDI and spacer: 1200mcg salb (can repeat 3x 20minutely), ipratropium 160mcg do not repeat
-Neb: Salbutamol 5mg (repeated 3x 20minutely), ipratropium 500mcg do not repeat
If patient fails to improve escalate to next severity.
Outline the management of severe - life-threatening asthma patients
Severe: High flow 02, early clinical support, salbutamol 15mg (repeat as needed), ipratropium 500mcg (repeated 3x 20minutely), transport and notify
Life-threatening: high flow 02, continuous salbutamol, ipratropium 500mcg (3x 20minutely), IV fluid bolus 500mL, consider IM adrenaline 10mcg/kg to max 500mcg if no response after 5m repeat dose, transport and notify.
Describe the complications of an asthmatic arrest
Continuous nebs of salbutamol and ipratropium (repeated 3x 20minutely) via in-line neb
IPPV with slow ventilation rates and small tidal volumes to allow for adequate chest deflation
Ventilation should be gentle to avoid barotrauma in hyper-inflated lungs with high airway pressures
Consider adrenaline
How does salbutamol work?
Type of drug: selective B2 adrenergic receptor agonist
Onset: 2-5m. Duration: 15-60m. Half life: 1.5hrs
Metabolism: Hepatic. Excretion: Renal.
Indication: bronchospasm
Contraindications: allergy patients <1 years
MOA: binds to B2 adrenergic receptor - activation of adenyl cyclase - increase in cAMP - lowers intracellular calcium - smc relaxation.
Side effects: tachycardias - some b1 effects, tremors, anxiety
How does ipratropium work?
Drug type: anticholinergic
Onset: 1-3m. Duration: 4-6hours. Half life: 3 hours.
Metabolism: Hepatic. Excretion: Renal
Indications: bronchospasm
Contraindications: allergy, patients <1 year
MOA: acts as an antagonist of muscarinic acetylcholine receptor. This causes inhibition of the parasympathetic nervous system. In airways, the PNS causes bronchial secretions and constriction, therefore ipratropium reverses this effect.
How does adrenaline work for asthmatics?
Drug type: naturally occuring catecholamine.
Onset: 1m. Duration: 5-10m. Half life: 2m.
Metabolism: broken down in sympathetic nerve endings
Indications: life-threatening bronchospam
Contraindications: nil
MOA: Acts on alpha and beta adrenergic receptors. A1 = vasoconstriction (in asthma helps overcome obstructive shock), A2 = various effects, B1 = increases HR and FOC,
B2 = bronchodilation.
Side effects: anxiety, hypertension, tachycardia, tremors.
Increases HR in an already hypoxic patient = increased stress on heart - only use as a life-threatening option.
What can an ICP offer?
Hydrocortisone
Magnesium
Adrenaline infusion
IV fluids in paeds.
