– BHR (BHR) is almost constant but not specific for asthma (it can be seen in bronchitis, COPD, DDB, abortion). It can also be induced by drugs (beta blockers, ACE …).

– Histamine causes bronchoconstriction by direct effect on the smooth muscle. Other bronchoconstrictors products are: leukotriene, thromboxane, prostaglandin D2 PG; acetylcholine; Substance P; α mimetics.

– Consequences -> obstructive ventilatory disorders: decrease in FEV and PEF drop (peak flow), plus VR; increased CRF; CPT increased

– Hypoxaemia originates decrease (effect shunts) or abolition (shunts) ventilation in well-ventilated areas.

– The usual hypocapnia observed in the non-severe asthma attack results from a reflex hyperventilation to hypoxemia.The normo or hypercapnia can occur if the shunt effect is important. hypercapnia (alveolar hypoventilation) may also be associated with the occurrence of fatigue of the inspiratory muscles.

– Severe asthma attacks are associated with right ventricular failure (acute pulmonary heart).

– The paradoxical pulse (decrease in SBP of more than 10mmHg for inspiration). Occurs during severe crises (related to the inspiratory intrathoracic depression).

– In a typical asthma attack -> DEP decline but remains> 200 L / min (> 1/3 of the theoretical)

– Unlike the exercise dyspnea, asthma occurs year after year. It is caused by inhalation of cold, dry air (some sports like swimming its well tolerated).

– Asthma Aspirin: it demonstrates an intolerance to aspirin and NSAIDs; related to inhibition of cyclooxygenase -> increase of arachidonic acid -> increase leukotriene. Between it frequently as part of a Widal’s Syndrome, characterized by a triad of asthma, nasal polyps, aspirin intolerance.

– Allergic Bronchopulmonary Aspergillosis: DDB with bronchial bronchial molds labile infiltrates, no extrarespiratoires sign. reaction type I (eosinophilia, RAST); or type III (immediate skin reaction or semi-delayed).

– Asthma and vasculitis (Churg Strauss syndrome &) -> severe asthma corticosteroid

– Syndrome threat of increasingly frequent crises; more and more intense; intercritical dyspnea; increased consumption in beta-2-agonist; less effective bronchodilators; steady decline in the DEP.

– Asthma Classification

Intermittent asthma -> Symptoms <1 / week. ; brief crises; nocturnal asthma <2 / month; normal intercritical;PEF> 80% predicted; DEP variation <20%.

Mild persistent asthma -> Symptoms> 1 / week. (<1 / d); disturbed sleep and activity; nocturnal asthma> 2 / month;PEF> 80% (variation of PEF between 20 and 30%); use of? 2-mim <3 to 4 times / day

Moderate persistent asthma -> daily symptoms; very troubled sleep and activity; nocturnal asthma> 1 / week. ; ? 2-mim daily use; DEP between 60 and 80%; variation of PEF> 30%

Severe persistent asthma -> permanent symptoms; limitation of physical activity; frequent nocturnal asthma; PEF <60% and variation of PEF> 30%.

– Asthma acute severe:

Severity signs defining a AAG:

* Respiratory signs: difficulty speaking or coughing; EN> 30 / min; orthopnea; sweating; contracture of the SCM;cyanosis; auscultatoire Silence

* Hemodynamic signs: CF> 120 / min; paradoxical pulse> 20 / min

* Neuropsychiatric signs: anxiety, agitation

* PEF <150 L / min or <25% predicted

* PaCO2> 40 mmHg (hypercapnia)

Warning signs:

* Impaired consciousness

* Breaks or respiratory arrest

* Paradoxical breathing

* Hypercapnia> 50 mmHg

– Patients at high risk of death from asthma is the following profile

* Frequent use or recent judgment of oral steroids

* Hospitalization or emergency department visit in the year

* Land psychiatric or psychosocial problems

* Non-compliance with treatment

– Between crises, volumes and flows may be normal spirometry (intermittent asthma); only the flow-volume curve can then objectify a decrease in maximal expiratory flow in the distal portion of the flow-volume curve (small airways).

– Reversibility (by use of a .beta.2-agonist) is defined by an increase of 20% of the measured FEV (over 200 ml).

– Pulmonary embolism +++ reflex bronchoconstriction

– Acute complications: spontaneous pneumothorax; subcutaneous emphysema and mediastinal; bronchial or lung infection.

– Chronic Complications: chest deformity, chronic respiratory failure (corticosteroids can still act); PAH and CPC (rare).

-? 2-mimetic -> active adenylate cyclase with synthesis of cAMP regulates phosphorylation of myosin and the intracellular concentration of Ca2 +; also inhibits mast cell degranulation.

– The side effects of this treatment: fine tremor of the extremities, hypotension, moderate tachycardia, hypokalemia (for intracellular transfer)

– Xanthines (theophylline) -> inhibition of phosphodiesterase: less powerful bronchodilator anti-inflammatory action + + positive inotropic effect on the inspiratory muscles (delays the onset of their fatigue).

– Cromones -> inhibition of mast cell degranulation