Nurses Revision

Respiratory Medicines: Bronchodilators, Steroids, Oxygen and Emergency Care

Respiratory Medicines: Bronchodilators, Steroids, Oxygen and Emergency Care

Why this topic matters in emergency medical care

Respiratory medicines can rapidly open narrowed airways, reduce inflammation, reverse anaphylaxis, treat infection, relieve pulmonary oedema or support ventilation. They can also cause tachyarrhythmia, hypokalaemia, hypercapnia, adrenal suppression or delayed recognition of a failing airway. EMT students therefore need more than a list of inhalers: they must understand the mechanism, delivery device, dose safety, oxygen target and reassessment plan.

This detailed lesson is for supervised learning and revision. Apply current Uganda Ministry of Health guidance, facility protocols, prescriber instructions, product information and age-specific emergency algorithms.

Learning outcomes

  • Describe airway, bronchial smooth-muscle, alveolar and pulmonary vascular targets of respiratory medicines.
  • Classify bronchodilators, inhaled/systemic corticosteroids, leukotriene modifiers, mucolytics, antibiotics, diuretics, pulmonary vasodilators and oxygen therapies.
  • Recognise and initially treat acute asthma, COPD exacerbation, anaphylaxis, pulmonary oedema, respiratory infection and opioid-related hypoventilation.
  • Choose an appropriate route and delivery system: inhaler, spacer, nebuliser, oral, intramuscular, intravenous or oxygen device.
  • Monitor response using work of breathing, respiratory rate, wheeze or silent chest, peak flow when appropriate, SpO2, mental status and blood gases.
  • Identify adverse effects, contraindications, interactions, special-population considerations and escalation triggers.

1. Respiratory physiology and medicine targets

Ventilation moves air to the alveoli; perfusion brings blood for gas exchange; diffusion transfers oxygen and carbon dioxide across the alveolar–capillary membrane. Airway resistance, lung compliance, respiratory muscle effort, haemoglobin and cardiac output all influence oxygen delivery. Respiratory medicines may relax bronchial smooth muscle, reduce airway inflammation, thin secretions, remove fluid, treat infection, reverse bronchospasm or support oxygenation.

TargetPhysiological problemMedicine examplesEmergency relevance
β2-adrenergic receptorsBronchial smooth-muscle constrictionSalbutamol, terbutaline, formoterolRapid bronchodilation; high doses may cause tremor, tachycardia and hypokalaemia.
Muscarinic receptorsVagal bronchoconstriction and mucus secretionIpratropium, tiotropium, glycopyrroniumUseful in COPD and severe asthma; dry mouth, urinary retention and glaucoma risk.
Airway inflammationEosinophilic or neutrophilic inflammation and mucosal oedemaInhaled corticosteroids, prednisolone, hydrocortisoneReduces exacerbation severity but onset is slower than a rescue bronchodilator.
Leukotriene pathwayBronchoconstriction, oedema and mucusMontelukastPreventive role; not a substitute for immediate rescue treatment.
Alveolar fluidPulmonary oedema and impaired diffusionFurosemide, nitrates, vasodilatorsRelieves congestion when cardiac or fluid overload is responsible; monitor BP and renal function.
Blood oxygenationHypoxaemiaControlled oxygen, high-flow oxygen, CPAP/BiPAPTarget saturation depends on condition; excessive oxygen can worsen hypercapnia in susceptible COPD patients.

2. Practical classification of respiratory medicines

GroupExamplesMain roleCritical caution
Short-acting β2 agonistsSalbutamol/albuterol, terbutalineRapid relief of bronchospasmTachycardia, tremor, hypokalaemia and lactic acidosis in high-dose therapy
Long-acting β2 agonistsFormoterol, salmeterol, indacaterolMaintenance bronchodilationNot all LABAs are suitable as sole asthma therapy; follow prescribed combinations.
AntimuscarinicsIpratropium, tiotropium, glycopyrroniumBronchodilation, especially COPDDry mouth, blurred vision, urinary retention and narrow-angle glaucoma caution
Inhaled corticosteroidsBudesonide, beclometasone, fluticasoneControl airway inflammation and prevent exacerbationsOral candidiasis, dysphonia and systemic effects at high dose; rinse mouth.
Systemic corticosteroidsPrednisolone, hydrocortisone, methylprednisoloneModerate/severe exacerbations and inflammatory emergenciesHyperglycaemia, infection risk, mood effects and adrenal suppression
MethylxanthinesTheophylline, aminophyllineLimited specialist roleNarrow therapeutic window, arrhythmias, vomiting and seizures
MucolyticsAcetylcysteine, carbocisteineReduce mucus viscosity in selected chronic diseaseBronchospasm or nausea; not a substitute for airway clearance.
AntibioticsAmoxicillin, doxycycline, macrolidesBacterial respiratory infection or selected COPD exacerbationsDo not use routinely for viral illness; allergy, QT, resistance and renal dosing matter.
Oxygen/ventilatory supportControlled oxygen, high-flow oxygen, CPAP/BiPAPCorrect hypoxaemia or reduce work of breathingOxygen is a drug: prescribe target, device, flow and reassessment.

3. Inhaler devices and administration technique

DeviceTechnique essentialsCommon error
Pressurised metered-dose inhalerShake, exhale away, seal lips, press once while inhaling slowly and deeply, hold breath and repeat after the interval.Pressing before inhaling, inhaling too fast or failing to shake
Spacer chamberAttach inhaler, release one puff at a time, inhale slowly or take several tidal breaths; use a mask if needed.Multiple puffs into the chamber or poor mask seal
Dry-powder inhalerLoad dose, exhale away, inhale rapidly and deeply, hold breath; keep device dry.Using a slow inhalation or exhaling into the device
NebuliserUse prescribed drug/diluent, suitable mask or mouthpiece, upright position and specified oxygen/air flow.Delivering nebulisation to a tiring patient without preparing escalation.
“BREATHE” inhaler check

Breathe out first · Right device and dose · Exhale away from powder · Actuate once · Take the correct inhalation · Hold breath · Evaluate response and rinse after steroid.

4. β2-agonist bronchodilators

β2 agonists activate airway smooth-muscle receptors, increase cyclic AMP and produce bronchodilation. Salbutamol is the common short-acting rescue medicine; formoterol has a rapid onset and is used in specific maintenance-and-reliever regimens. A patient who needs repeated rescue doses may be deteriorating even if wheeze temporarily improves.

MedicineOnset/roleAdverse effectsMonitoring and teaching
SalbutamolRapid relief of bronchospasm by inhaler, spacer or nebuliserTremor, tachycardia, palpitations, hypokalaemia and headacheCount doses, reassess work of breathing and pulse; frequent nebulisation requires senior review.
TerbutalineShort-acting bronchodilator; inhaled or systemic protocols varySimilar β2 effects; systemic route increases adverse effectsUse the authorised route and concentration; consider ECG and potassium in severe attacks.
FormoterolRapid-onset long-acting bronchodilator in selected combination inhalersTremor, tachycardia, crampsDo not assume every LABA is a rescue drug; check the actual inhaler regimen.
Indacaterol/salmeterolLong-acting maintenance bronchodilationPalpitations, tremor and paradoxical bronchospasmNot for rapid rescue unless the product specifically indicates it.

4.1 β2-agonist toxicity

  • High-dose nebulised salbutamol may cause a metabolic lactic acidosis that increases tachypnoea; do not interpret every rapid breath as worsening bronchospasm.
  • β2 stimulation drives potassium into cells, so severe attacks or repeated treatments can produce hypokalaemia and arrhythmia.
  • Chest pain, marked tachycardia, syncope or new arrhythmia requires ECG and escalation rather than automatic repeat dosing.
  • Paradoxical bronchospasm after an inhaled product is rare but serious; stop the suspected product and call for help.

5. Antimuscarinic bronchodilators

Ipratropium and related medicines block muscarinic receptors in airway smooth muscle, reducing vagal bronchoconstriction and mucus secretion. They are especially valuable in COPD exacerbations and are often combined with a β2 agonist in severe asthma.

MedicineRoleSafety points
IpratropiumShort-acting inhaled bronchodilator for COPD and severe asthmaDry mouth, blurred vision, urinary retention; avoid spray into eyes and use caution in narrow-angle glaucoma.
TiotropiumOnce-daily maintenance bronchodilatorNot an acute rescue medicine; monitor anticholinergic effects.
Glycopyrronium/aclidiniumLong-acting COPD bronchodilationDevice technique and regular use matter; do not duplicate long-acting antimuscarinics.

6. Inhaled and systemic corticosteroids

Corticosteroids reduce airway inflammation, mucosal oedema and cytokine activity. Inhaled corticosteroids prevent exacerbations and improve asthma control, but they are not a substitute for rapid bronchodilation during a severe attack. Systemic corticosteroids are used early in moderate or severe exacerbations according to protocol.

ClassExamplesClinical roleAdverse effects
Inhaled corticosteroidsBudesonide, beclometasone, fluticasoneAsthma controller therapy; selected COPD combinationsOral thrush, dysphonia, bruising and systemic effects at high dose; rinse mouth.
Oral corticosteroidsPrednisoloneAcute asthma or COPD exacerbation when prescribedHyperglycaemia, mood change, insomnia, infection risk and gastric irritation.
IV/IM corticosteroidsHydrocortisone, methylprednisoloneUnable to take oral therapy, severe exacerbation or adrenal supportHyperglycaemia, fluid retention and delayed infection recognition.

7. Acute asthma exacerbation

Asthma involves variable airway narrowing, inflammation and mucus. Severe or life-threatening attacks may present with inability to speak, exhaustion, cyanosis, altered consciousness, silent chest, poor respiratory effort or a normalising/falling carbon dioxide despite severe distress. Wheeze disappearing is not always improvement: very little air movement may produce no sound.

Severity clueWhat to look forMedicine/support implication
Moderate exacerbationIncreased symptoms, wheeze, increased work of breathing but preserved speech and alertnessRepeated inhaled SABA through spacer or nebuliser, early steroid and reassessment.
Severe exacerbationMarked tachypnoea, tachycardia, difficulty speaking, accessory-muscle use, low peak flowContinuous monitoring, repeated SABA plus ipratropium and systemic steroid; urgent transport.
Life-threateningSilent chest, exhaustion, confusion, cyanosis, poor respiratory effort or impending arrestCall advanced airway/critical-care help, high-concentration oxygen for hypoxaemia and prepare escalation including IV magnesium or ventilation under protocol.

7.1 EMT sequence

  1. Perform ABCDE, sit the patient upright, minimise exertion and obtain a focused trigger/medicine history.
  2. Measure SpO2, respiratory rate, pulse, blood pressure, mental state and peak flow when the patient can perform it safely.
  3. Give rapid inhaled bronchodilator via the best available device; severe attacks often need nebulised SABA plus ipratropium.
  4. Give systemic corticosteroid early according to age, route and local protocol; do not delay transfer while waiting for full response.
  5. Reassess speech, work of breathing, air entry, pulse, SpO2, fatigue and mental status after each treatment.
  6. Arrange urgent transport; worsening fatigue, silent chest, altered consciousness, rising CO2 or poor response requires advanced airway planning.

8. COPD exacerbation

COPD exacerbation is an acute worsening of dyspnoea, cough and/or sputum over days. Bronchodilators are central; systemic corticosteroids improve recovery in severe exacerbations, and antibiotics are reserved for likely bacterial infection or selected high-risk presentations. Oxygen should be controlled rather than automatically maximised because some patients retain carbon dioxide.

Medicine/interventionPurposeSafety considerations
SABA or SAMARelieve acute airflow limitationMonitor tachycardia, tremor, dry mouth and response; combine classes when protocol indicates.
Systemic corticosteroidShortens recovery and improves lung function in significant exacerbationCheck diabetes, infection and mental-health effects; use prescribed duration.
AntibioticSelected bacterial exacerbation, especially increased sputum purulence/volume and dyspnoeaAssess allergy, renal function, QT interactions and local antimicrobial guidance.
Controlled oxygenCorrect hypoxaemia while avoiding unnecessary hyperoxiaUse prescribed target range and repeat observations; do not withhold oxygen from a severely hypoxaemic patient.
NIV (CPAP/BiPAP)Reduces work of breathing and improves ventilation in selected hypercapnic patientsRequires cooperative patient, intact airway and trained monitoring; vomiting or reduced consciousness may contraindicate.

8.1 Oxygen targets and hypercapnia

  • Oxygen is indicated for hypoxaemia, not simply breathlessness.
  • Use the locally authorised target range; patients at risk of hypercapnic respiratory failure are often managed with a lower controlled target than other acutely ill adults.
  • Obtain blood gases when available if drowsiness, confusion, severe COPD, rising oxygen requirement or suspected CO2 retention is present.
  • Do not remove oxygen abruptly from a hypoxaemic patient; titrate and escalate with monitoring.

9. Magnesium and second-line bronchodilation

IV magnesium sulfate may be considered in severe or life-threatening asthma that is not responding adequately to inhaled therapy and systemic corticosteroid. It relaxes smooth muscle and may reduce bronchospasm. It is not routine for every wheeze.

  • Check blood pressure, reflexes, renal function and local maximum dose; rapid administration can cause flushing, hypotension or weakness.
  • Prepare airway support because a failing patient may deteriorate while the medicine is being given.
  • Do not delay transfer or definitive ventilation planning while waiting for magnesium response.

10. Aminophylline and theophylline

Theophylline inhibits phosphodiesterase and antagonises adenosine receptors, but it has a narrow therapeutic window and many interactions. Nausea, vomiting, tremor, tachycardia, hypokalaemia, arrhythmia and seizures may indicate toxicity. It is not a casual rescue drug and should be used only under a specialist protocol with level monitoring.

11. Anaphylaxis and airway-threatening allergy

Anaphylaxis can cause airway swelling, bronchospasm, hypoxaemia, vasodilation and shock. IM adrenaline is the first-line medicine; antihistamines and corticosteroids must never delay adrenaline or replace ABCDE support. Severe bronchospasm without wheeze may indicate minimal air movement and impending respiratory failure.

  1. Call for help, remove the trigger if possible and assess airway, breathing, circulation, skin and gastrointestinal symptoms.
  2. Give IM adrenaline using the authorised concentration, site and age/weight dose; repeat according to the local algorithm if airway, breathing or circulation problems persist.
  3. Lay the patient appropriately: supine with legs elevated for shock, or semi-recumbent if breathing is worse lying flat; do not allow a shocked patient to stand.
  4. Give high-concentration oxygen for hypoxaemia or shock and establish IV/IO access for trained responders.
  5. Use nebulised salbutamol for persistent bronchospasm as an adjunct, not as a replacement for adrenaline.
  6. Antihistamines may help skin symptoms after stabilisation; corticosteroids are not first-line rescue for airway or circulatory collapse.
  7. Prepare advanced airway and refractory-anaphylaxis support; observe for biphasic reactions.
MedicineWhat it treatsWhat it cannot replace
IM adrenalineAirway oedema, bronchospasm, vasodilation and shockNothing—this is the first-line emergency medicine.
Salbutamol nebuliserResidual bronchospasmAdrenaline and circulatory resuscitation
AntihistamineItch, urticaria and flushing after stabilisationAdrenaline for ABC problems
CorticosteroidSelected adjunctive inflammatory treatmentImmediate reversal of airway or circulatory collapse

12. Pulmonary oedema and cardiac breathlessness

Acute pulmonary oedema produces severe dyspnoea, crackles, hypoxaemia, orthopnoea and sometimes pink frothy sputum. The cause may be left-ventricular failure, myocardial infarction, hypertensive crisis, valvular disease, renal failure or fluid overload. Furosemide removes sodium and water over time; nitrates reduce preload and afterload when blood pressure permits. Neither should delay ventilation support.

Medicine/supportMechanismSafety check
NitratesVenodilation and, at higher doses, arterial dilation reduce cardiac filling pressuresCheck blood pressure, right-ventricular infarction, severe aortic stenosis and recent PDE-5 inhibitor use.
FurosemideLoop diuretic increases renal sodium and water excretionMonitor BP, renal function, potassium and urine output; onset is not immediate in all cases.
CPAP/NIVRaises airway pressure, recruits alveoli and reduces work of breathingRequires alert patient with protected airway; monitor BP, mask fit, vomiting and fatigue.
OxygenCorrects hypoxaemiaTitrate to target; avoid unnecessary hyperoxia.

13. Respiratory infection medicines

Antibiotics treat susceptible bacterial infection; they do not treat uncomplicated viral coughs. EMT learners must recognise sepsis, pneumonia, tuberculosis risk and antimicrobial-resistance concerns. The medicine choice depends on local guidelines, site of infection, allergy, pregnancy, renal function and culture results.

  • Assess fever, respiratory rate, oxygen saturation, mental status, perfusion, pleuritic pain and sputum.
  • Give oxygen for hypoxaemia and arrange urgent transfer for cyanosis, hypotension, confusion, severe work of breathing or inability to maintain oral intake.
  • Do not delay antibiotics in suspected sepsis when authorised, but obtain cultures first only if this does not delay treatment.
  • Check for tuberculosis symptoms or exposure and apply infection-prevention measures.
  • Document the last antibiotic, allergy history and recent admissions to support antimicrobial stewardship.

14. Cough, mucus and upper-airway medicines

GroupExamples/roleImportant cautions
MucolyticAcetylcysteine reduces mucus viscosity in selected chronic diseaseMay cause bronchospasm or nausea; combine with airway clearance and hydration advice.
AntitussiveDextromethorphan or codeine suppress cough reflex in selected situationsCan sedate, interact with serotonergic medicines or worsen respiratory depression; cough may be protective.
DecongestantPseudoephedrine or topical sympathomimeticMay raise BP, cause palpitations, urinary retention or rebound congestion.
AntihistamineReduces allergic rhinorrhoea and itchingFirst-generation agents cause sedation and anticholinergic effects; not an anaphylaxis rescue.
Saline/steam supportMoistens secretions and relieves irritationAvoid burns from hot steam; do not delay assessment of respiratory distress.

15. Oxygen and ventilatory support as medicines

DeviceTypical useKey safety point
Nasal cannulaLow-to-moderate oxygen requirement; comfortable and allows communicationCheck actual flow and patient response; mouth breathing and congestion reduce delivery.
Simple face maskModerate oxygen deliveryDo not use at very low flow because exhaled CO2 can accumulate.
Non-rebreather maskHigh oxygen concentration for severe hypoxaemia or shockInflate reservoir before placing and reassess; prepare definitive airway if the patient tires.
Venturi maskControlled oxygen concentration, particularly in COPD riskUse the correct colour/flow combination and do not cover entrainment ports.
High-flow nasal oxygenHigh flow with warmed humidification and controlled FiO2Requires monitoring and escalation plan; not a substitute for a protected airway.
CPAP/BiPAPPositive pressure for pulmonary oedema or selected hypercapnic failureContraindicated or unsafe with vomiting, severe agitation, shock or inability to protect airway.

16. Monitoring respiratory medicines

  • Before treatment: respiratory rate, pattern, work of breathing, speech, accessory muscles, air entry, wheeze/crackles, SpO2, pulse, BP, temperature, mental status and peak flow when appropriate.
  • During treatment: check device delivery, patient position, pulse, rhythm, SpO2, fatigue, tremor, chest pain and response to each dose.
  • After treatment: repeat observations, document oxygen device/flow, record response and watch for recurrence or delayed deterioration.
  • Blood gases: consider when severe COPD, drowsiness, altered consciousness, escalating oxygen, fatigue or suspected CO2 retention is present.

17. Interactions and special populations

SituationRiskAction
β2 agonist + diuretic or steroidAdditive hypokalaemiaMonitor ECG and potassium in severe or repeated therapy.
Theophylline + macrolide/ciprofloxacinRaised theophylline level and toxicityCheck the full medicine list and avoid unmonitored combinations.
Non-selective beta-blocker + asthmaBronchospasm and reduced β2 rescue responseAsk about eye drops and cardiac medicines; seek prescriber review.
Opioid/benzodiazepine + respiratory diseaseRespiratory depression and CO2 retentionTitrate cautiously and monitor ventilation, not only SpO2.
PregnancyUntreated maternal hypoxaemia threatens mother and fetusUse authorised medicines and treat significant hypoxaemia promptly; involve obstetric care.
ChildrenSmall airways deteriorate quickly and dosing is weight-basedUse paediatric spacer/nebuliser technique and age-specific algorithms.
Older adults/heart diseaseβ2 agonists and decongestants may trigger tachyarrhythmiaCheck pulse, ECG and chest pain; use the minimum effective protocol dose.

18. Clinical scenarios

Scenario 1: Severe asthma

A 19-year-old cannot complete sentences, is using accessory muscles and has a very quiet chest. Sit upright, give rapid inhaled bronchodilator plus ipratropium and systemic steroid under protocol, provide oxygen for hypoxaemia, call advanced help and prepare ventilation. A silent chest is a danger sign, not reassurance.

Scenario 2: COPD with drowsiness

A patient with COPD is drowsy and receiving increasing oxygen. Use controlled oxygen to the prescribed target, assess ventilation and obtain blood gases urgently. Do not assume that a normal SpO2 means adequate ventilation.

Scenario 3: Anaphylaxis

Minutes after an injection, a patient develops wheeze, lip swelling and hypotension. Give IM adrenaline immediately, call for help, position safely, give oxygen and use nebulised salbutamol only as an adjunct.

Scenario 4: Pulmonary oedema

An older adult has orthopnoea, crackles and severe hypertension. Sit upright, give oxygen for hypoxaemia, consider CPAP and nitrates if authorised and BP permits, and arrange cardiac monitoring and urgent transport.

Scenario 5: Theophylline toxicity

A patient taking theophylline has repeated vomiting, tremor and palpitations. Stop further doses, obtain ECG and urgent drug-level/renal assessment, and watch for seizures and ventricular arrhythmia.

Scenario 6: Pneumonia with sepsis

A febrile patient is confused, tachypnoeic and hypotensive with low SpO2. Treat ABCDE and sepsis priorities, give oxygen to target, establish access, obtain cultures when feasible and do not delay authorised antibiotics or transfer.

19. Documentation and handover

Record the indication, baseline respiratory findings, inhaler/nebuliser technique, oxygen device and flow, medicine name/concentration, route, time, response, adverse effects, repeat doses, peak flow or blood gases and escalation calls. Handover should include trigger, last rescue dose, current oxygen requirement, fatigue, mental state and concern for recurrence.

20. Revision questions

  1. Compare SABA, LABA, SAMA and LAMA bronchodilators.
  2. Why can high-dose salbutamol cause tremor, hypokalaemia and lactic acidosis?
  3. Why should a nebuliser not delay airway preparation in severe asthma?
  4. List signs of life-threatening asthma.
  5. Explain why oxygen is a prescribed drug in COPD.
  6. When are systemic corticosteroids used in asthma or COPD exacerbation?
  7. What is the role of ipratropium in severe bronchospasm?
  8. Why is theophylline a high-risk medicine?
  9. What is first-line treatment for anaphylaxis?
  10. Why are antihistamines not a substitute for adrenaline in anaphylaxis?
  11. List the major contraindications or hazards of CPAP/BiPAP.
  12. How do nitrates and furosemide help pulmonary oedema?
  13. What are the clues to opioid-related hypoventilation in a respiratory patient?
  14. Why must antibiotics not be prescribed for every cough?
  15. How can inhaler technique change treatment effectiveness?
  16. What monitoring is required during repeated nebulised β2 agonist therapy?
  17. Why can silent chest indicate worsening airflow obstruction?
  18. Which medicines can interact with theophylline?
  19. How should a respiratory medicine response be documented?
  20. Write a safe plan for a deteriorating COPD patient who becomes confused.

21. Key takeaways

  • Open the airway, support breathing and assess severity before choosing a respiratory medicine.
  • Salbutamol is rapid rescue bronchodilation, but repeated doses demand reassessment for arrhythmia, hypokalaemia and fatigue.
  • Inhaled corticosteroids prevent exacerbations; systemic corticosteroids are used early in significant attacks under protocol.
  • Controlled oxygen and ventilation targets matter, especially in COPD or hypercapnic respiratory failure.
  • IM adrenaline is first-line for anaphylaxis; bronchodilators, antihistamines and steroids are adjuncts.
  • Pulmonary oedema often needs upright positioning, oxygen/positive pressure, BP-appropriate vasodilation and urgent cardiac care.
  • Every treatment requires device verification, monitoring, documentation and a clear escalation plan.

22. Recommended references for further study

Clinical note: This page supports EMT learning and revision. It does not replace an authorised prescription, local emergency protocol, senior supervision or patient-specific advice. In a deteriorating patient, stabilise ABCDE, call for advanced help and transfer urgently.

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