Pathogenesis of severe asthma
Bronchoconstriction: In severe or acute exacerbations of asthma, bronchial smooth muscle contraction occurs rapidly to narrow the airways in reaction to exposure to a variety of stimuli including allergens or irritants. Allergen-induced acute bronchoconstriction results from IgE –dependent release of mediators from mast cells that includes tryptase, histamine, leukotrienes, and prostaglandins that directly contract airway smooth muscle.
Non-steroidal anti-inflammatory drugs and aspirin can also cause acute airflow obstruction in some of the patients, and also indicators show that non-IgE –dependent response also involves mediator release from airway cells. Some other stimuli which include cold air, exercise and irritants can also cause acute airflow obstruction.
Airway edema: As the time goes by and the disease also becomes more persistent and inflammation more progressive, some factors affect the airflow which includes inflammation, edema, mucus hypersecretion and formation of inspissated mucus plugs.
Airway hyperresponsiveness: This is an exaggerated bronchoconstriction response to a wide variety of stimuli. Many factors influence hyperresponsiveness which includes structural changes, dysfunctional neuro-regulation, and inflammation. Furthermore, the major factor that affects hyperresponsiveness is inflammation, so treating this factor improves asthma control.
Airway modeling involves an activation of many of the structural cells, with consequences permanent change in the airway that increases airflow obstruction and airway responsiveness and renders the patient less responsive to therapy. Also, it associates with a progressive loss of lung function that is not prevented by or wholly reversible by current treatment. The structural changes include subepithelial fibrosis, airway smooth muscle hypertrophy, thickening of the sub-basement membrane, mucous gland hyperplasia and hypersecretion, and blood vessel proliferation and dilation.
Retractions and wheezing
Retraction is the inward movement of the breastbone (sternum) during inspiration and is an abnormal breathing pattern. The trouble a patient goes through getting air into the lungs is due to either to obstruction of the airways or stiffness of the lungs. In a situation that the patient finds, it difficult to breathe, it means the retractions are at its worst. Mild to moderate difficulty in breathing is mostly associated with substernal reactions, intercostal responses, and subcostal reactions.
Substernal retractions are inward movements of the abdomen just below the breastbone.
Intercostal retractions: are inner changes of the skin between the ribs
Severe difficulty in breathing associated with supraclavicular retraction, suprasternal responses, and sternal responses. The difficulty in breathing that causes withdrawal mostly caused by lower airway obstruction, upper airway obstruction, and lung tissue diseases e.g. pulmonary edema, and acute respiratory distress syndrome.
Supraclavicular retractions are inward movements of the skin of the neck just above the collarbone.
Wheezing: is a piercing whistling sound made while a patient breathes; this sound is heard most clearly when the patient exhales, but in acute cases, it can happen when the patient inhale. Inflammation or narrowed airways cause wheezing.
Expiratory wheeze: Happens due to narrowing of a person’s trachea and mainstream bronchi. As the air rushes out through the narrowed trachea or mainstream bronchi, the wheezing sound produced. One of the causes of this is tracheomalacia which causes the patient’s trachea is flaccid and fails to remain open at its normal diameter.
Inspiratory wheeze: is a musical sound that indicates hindrance of the airway in the trachea outside the chest. It results as a collapsed airway lumen progressively opens during inspiration.
Reasons why an asthmatic patient can’t speak except one word
Well, patients with asthmatic problems have a difficulty with speaking in complete sentences and a severe case a single word. The reason is that the patients need air in their lungs to talk, and lack of air that asthma can cause and make it difficult to do so. Also, every word a patient speaks hinders his or her body’s ability to breathe in more air, hence not easy to talk. Normally, an individual who is not suffering from asthma isn’t an issue speaking, but an individual suffering from asthma can make him or her incredibly difficult to speak a word since every breath is precious to this person.
Patient not responding well to medication
Well, this is caused by abnormalities in glucocorticoid receptor number, glucocorticoid receptor binding or abnormalities in the glucocorticoid-glucocorticoid receptor complex binding the DNA. Also, it is because of the severe bronchospasm and mucus plugging prevents the distal drug delivery by the aerosol route.
Mode of action of intravenous salbutamol
Intravenous salbutamol stimulates
β2 adrenergic receptors which are predominant receptors in the bronchial smooth muscle of the lung. Stimulation of β2 receptors prompts the activation of enzyme adenyl cyclase that forms cyclic adenosine-mono-phosphate (AMP) from adenosine-tri-phosphate (ATP). This high level of cyclic adenosine-mono-phosphate relaxes bronchial smooth muscle and decreases airway opposition by lowering intracellular ionic calcium concentrations. Salbutamol loosens the smooth muscles of airways, from the trachea to terminal bronchioles.
Intravenous salbutamol is usually a tolerated drug. However, it has some effects which include fine tremor of skeletal muscle especially in the hands and nervousness, palpitation, chest discomfort, muscle cramps, tachycardia, hypokalemia, and difficulty in paradoxical bronchospasm and micturition.
Monitoring for and respond to any adverse effects
The effects of salbutamol and its severity usually depend on the route of administration and dosage used during the dispensation. In the case of the effects discontinue the administration of salbutamol and also administer cardio-selective beta receptor blocking drug (Metoprolol, Atenolol).