how can a patient with COPD improve their breathing pattern?
-diaphragmatic breathing & pursed lip breathing
what are some of the limitations of bronchodilators
- have limited capacity of what they can accomplish, can cause side effects like increasing HR
- people don’t always bronchodilators/inhalers properly
what are some of the limitations of corticosteriods?
- helps reduce inflm in lungs but have lots of side effects & decrease immune response
- do not want to be managing COPD with corticosteriods longterm
what is the Hypoxic drive theory?
- this theory is outdated
- a small group of pts with COPD do respond this way
- OXYGEN decreases will decrease their drive to breathe, because brain will only tell to breathe if they arent getting enough oxygen
- key to giving pts with COPD oxygen is startl slow 2L/np then asses if makes pt worse
Haldone effect
- true theory
- when given oxygen, oxygen saturates the Hg, body can’t dump CO2 through respiration so dumps it into body or bloodstream causing pt to become acidotic
- acidosis cause a respiratory cascade which will increase resp rate, increase demands on comprimised system, increase restlessness,confusion, change in loc, dizziness, eventual siezures and the potenital for arrest
what are an example of a beta 2- adrenergic agonists?
-Albuterol
how do beta 2 adrenergic agonists (ALBUTEROL) work?
Absorbed by the beta 2 receptors in the lung and other smooth muscles, activate the sympathetic nervous system, minimal absorption when inhaled, PO systemic effects more common
how does the anticholinergic bronchidilator (IPRARTROPIUM) work?
Blocks the parasympathetic nervous system, used in patients where beta2 adrenergic agonists (stim the sympathetic nervous system) are contraindicated or are sensitive to those drugs, has a longer duration of action when used with beta 2 agonists…combivent is a useful combo
