Specificity of UPV in patients with Asthma bronchiale/High School (nurse)

Epidemiology

 * 3-6% of the population (1993 - 6.4%) generally a permanent increase !
 * Asthmatic condition – mortality 12% in intubated patients and 1–2% in non-intubated patients.
 * 80% of patients who died with status asthmaticus have bronchial asthma for more than 5 years.
 * The so-called refractory asthma only about 5% of all patients.

Basic characteristics

 * Bronchoconstriction.
 * Airway edema
 * Hyperreactivity of DCs to various stimuli.
 * Airway remodeling.
 * An asthma attack is triggered by SMOKING, dust, pollen, dust mites, drugs (THP, beta blockers, ANP,...), cold, physical exertion.

Pathophysiology from the point of view of UPV

 * Increased resistance in DC.
 * Air trapping.
 * Hyperinflation.
 * An increase in the negativity of pleural pressures.
 * Increase in functional residual capacity, residual volume and total lung capacity.
 * An increase in the ventilation-perfusion ratio.
 * Increase in dead space and alveolar ventilation (until exhaustion, then decrease).‏‏

Treatment of acute exacerbation

 * Higher FiO 2 and high flow oxygen.
 * Inhaled β-mimetic until signs of overdose (aerosol, spacer).
 * Systemic or inhaled steroids (120–180 mg Methylprednisone/24 hours in 3–4 doses after 48 hours → 60–80 mg until the patient's condition improves).
 * Aminophylins in infusion.
 * Mucolytics.
 * ATB only in case of infection.

Non-standard methods of bronchodilation

 * Ketamine 10-40 ucg/kg/min ?
 * Magnesium up to 10 g/24 hours.
 * NO.
 * Helium (the earlier and in more seriously ill patients, the greater the benefit)‏.

UPV in Asthmatics

 * UPV complicated and risky.

Indication

 * Impairment of consciousness.
 * Respiratory rate above 40 D/min.
 * Rising/falling pulsus paradoxus.
 * = Heart rate whose waves are smaller during inhalation than during exhalation systolic pressure decreases during inspiration. As a result of the increase in the volume of blood in the chest during inspiration, this difference is to a certain extent physiological.


 * PDrop in pO 2 below 7.5 kPa.
 * Rise of pCO 2 above 7 kPa → acidosis.
 * Persistent lactic acidosis.
 * Barotrauma.
 * Silent chest despite patient's inspiratory efforts.
 * Inability to communicate, muscle fatigue, exhaustion.

Use of ventilation mode
The goal of UPV is ventilation and oxygenation support and prevention of extreme pH changes and severe hypoxia.
 * The basis is controlled hypoventilation and permissive hypercapnia.
 * Volume-controlled ventilation with constant inspiratory flow is more suitable.
 * Respiratory rate less than 10 D/min. with a 1:3 to 1:4 ratio of inspira to expiria.
 * Low PEEP 2–4 cmH 2 O → distance therapy (keeping the lung open).
 * The patient is semi-sitting.
 * If there are no complications, the time for UPV in a critical condition is 3-5 days.
 * Extubation when bronchospasm resolves, decreased secretion production, good muscle strength.

Complications of UPV

 * Hypotension.
 * PNO.
 * Arrhythmia.
 * ETI dislocation.
 * Pneumonia.
 * Circulation failure.
 * KBleeding into the GIT.
 * Pulmonary embolization.
 * Pneumomediastinum.
 * Subcutaneous emphysema.

Asthma bronchiale in children
A predisposed individual.
 * More heterogeneous character and time course different from adults.
 * 10% of children.
 * Repeatedly in contact with adverse environmental influences (polluted air, smoking, unhealthy lifestyle and nutrition, etc.) → contact with the so-called trigger (allergen, exertion, smoke, viral infection, etc.) → airway obstruction (contraction of the smooth muscles in the bronchi, mucosal swelling and increased mucus secretion) with symptoms of expiratory dyspnea and cough.
 * The most common cause of exacerbation in childhood is viral infections.

Causes of asthma problems in children

 * The etiology varies in different periods.
 * Respiratory viruses:
 * Infants/toddlers - temperatures are often present → very good prognosis even with recurrences; usually disappear by school age.
 * the exception is especially human rhinoviruses, which damage the mucous membrane of the bronchi and thus can contribute to the later development of persistent asthma.


 * Allergies.
 * Atopic predisposition → worse prognosis, often progression to persistent asthma.
 * The later obstructive bronchitis manifests itself in childhood, the more likely the allergic etiology and progression to persistent asthma.


 * Other.
 * Physical stress, stress, cigarette smoke, etc. → less often in children, schoolchildren/adolescents.


 * Around the age of 3, 3 basic groups of children are symptomatically intertwined:
 * The so-called transient wheezers → children who "grow out" of the problem on their own.
 * Non-atopic wheezers → děti s poškozenými dýchacími cestami v důsNon-atopic wheezers → children with damaged airways due to infection, this defect is reversible in case of non-allergenic terrain.
 * Real asthmatics.

Investigation

 * Medical history - family history, especially atopy, smoking, pets,...
 * Laboratory height – inflammatory markers, …
 * Immunological examination including total IgE and ECP, possibly. specific IgE.
 * Spirometry (approx. from 3-4 years).
 * Whole-body body plethysmography → an airtight chamber allowing pressure and volume changes that take place inside to be measured (also possible in non-cooperative children).

Asthma predictive index

 * Major criteria – asthma in the parents, atopic eczema in the child, sensitivity to airborne allergens.
 * Small criteria – wheezing outside the cold season, eosinophils in the blood count >4%, food sensitivity
 * → presence of one major or 2 minor criteria → probability of asthma.

Acute bronchial obstruction

 * The 1st choice is short-acting inhaled bronchodilators → β 2 -mimetic (salbutamol), anticholinergic (ipratropium bromide) newly questionable meaning.
 * In the case of insufficient effect or severe p.os course; and corticosteroids.
 * Hospitalization if the clinical condition does not improve after 3 repeated inhalations of bronchodilators.

Long-term treatment

 * Indicated if the frequency or severity of exacerbations significantly impairs quality of life and asthma is not under control (control criteria same as for adults).
 * 1st choice of inhaled corticosteroids (treatment effectiveness is evaluated after at least 3 months),
 * → after control is achieved, the dose is reduced to the lowest level,
 * → if there is insufficient control,
 * → → necessary control of correct use, compliance with measures → if in order,
 * → increase the dose of inhaled corticosteroids (ICS) or add a leukotriene receptor antagonist (montelukast = Singulair).


 * Long-acting β 2 mimetics (=LABA) – they are not recommended in monotherapy, in combination only if ICS alone are not enough.
 * Measures to eliminate causative agents.

Inhaler attachments

 * Significant simplification of inhalation, coordination of inhalation and squeezing is eliminated.
 * Wash the spacer and let it dry, do not wipe!!!! → formation of static electricity trapping particles.
 * 1 injection from the dispenser = 5-10x calm inhalation and exhalation without removing the dispenser and spacer.

Determining the fullness of the aerosol dispenser

 * Immerse the dispenser in the water and determine the fullness of the dispenser according to the drop towards the bottom (see picture).



Adverse effects of ICS

 * LOCAL:
 * Common: oropharyngeal candidiasis, throat, tongue, pharynx, esophagus irritation, cough.
 * More rarely: early and delayed hypersensitivity reactions in the face, lips, eyes, pharynx, redness, rash, urticaria, eczema, swelling, angioedema, bronchospasm.


 * SYSTEMS:
 * To varying extents with all ICS, they are dose-dependent, but long-term negative effects on children's development have not been proven.
 * Adrenal effects - cortisol synthesis.
 * Induction of osteoporosis, slowing of growth rate.
 * Psychological changes.
 * At high doses, deterioration of healing, atrophy of the skin.
 * Disorders of glucose tolerance.
 * Increased incidence of glaucoma and cataracts.

Links

 * Asthma