How can I draft a concise case report of a patient aged 65 years or older with chronic obstructive pulmonary disease (GOLD stage II‑III), former smoker, on long‑acting beta‑2 adrenergic agonist/long‑acting muscarinic antagonist therapy, and comorbid coronary artery disease, hypertension and heart failure, who experienced a type 2 myocardial infarction (supply‑demand mismatch) shortly after receiving a short‑acting beta‑2 adrenergic agonist (albuterol) bronchodilator?

Drafting a Case Report: Type 2 MI Following Bronchodilator Therapy in COPD with Cardiovascular Comorbidities

Understanding the Clinical Scenario

Your case represents a well-documented but underrecognized cardiopulmonary complication: type 2 myocardial infarction triggered by short-acting beta-2 agonist therapy in a patient with the dangerous triad of COPD, coronary artery disease, and heart failure. 1, 2

This scenario occurs in approximately 8-10% of patients hospitalized for COPD exacerbations who meet criteria for myocardial infarction, making it a clinically significant phenomenon worthy of case report publication. 2

Key Clinical Elements to Document

Patient Demographics and Baseline Characteristics

• Age ≥65 years with GOLD stage II-III COPD (FEV1 30-80% predicted, moderate to severe airflow limitation) 3
• Former smoker with quantified pack-year history (typically >50 pack-years in this population) 3
• Document all cardiovascular comorbidities: established coronary artery disease, hypertension, and heart failure with specific ejection fraction if available 3, 4
• Baseline medications including LABA/LAMA combination therapy for COPD maintenance 3

The Precipitating Event

• Document the specific indication for albuterol administration (acute dyspnea, wheezing, or COPD exacerbation) 3
• Record the exact dose and frequency: typically 2.5-5 mg nebulized albuterol, with attention to whether multiple doses were given within hours 1
• Note the temporal relationship: chest pain or discomfort developing within 30 minutes to 2 hours after bronchodilator administration 1

Clinical Presentation of Type 2 MI

• Chest tightness, pressure, or discomfort that developed after albuterol, not as the primary presenting complaint (this distinguishes it from type 1 MI) 3, 2
• Document vital signs showing tachycardia (heart rate increase of 10-15 bpm is typical with beta-2 agonists) 3, 5
• Blood pressure response (may show elevation or remain stable) 3

Diagnostic Findings to Present

Electrocardiographic Changes

• Serial ECGs are essential: obtain tracings at 15-30 minute intervals to capture dynamic ST-segment changes 3, 6
• Document transient ST-segment depression ≥0.5 mm in lateral leads (I, aVL, V5-V6) or other territories that resolve with cessation of the trigger 3, 6
• Note any T-wave inversions, which may persist longer than ST changes 3
• Absence of new Q waves (distinguishes type 2 from type 1 MI) 3

Cardiac Biomarkers

• Elevated troponin I or T (the preferred biomarker), with serial measurements at presentation, 1-2 hours, and 6-12 hours 3, 6
• Document the peak troponin level and timing relative to albuterol administration 1, 2
• Note that troponin elevation is present in 10% of COPD exacerbations, but only 8.3% meet full MI criteria with ECG changes 2

Coronary Angiography Findings

• This is the critical diagnostic element: angiography showing smooth coronary arteries without obstructive disease or acute thrombosis 1
• Document any non-obstructive atherosclerosis (<50% stenosis) if present 1
• Left ventriculography or echocardiography showing regional wall motion abnormalities (hypokinesia) corresponding to ECG changes 1

Pathophysiologic Mechanism to Explain

Supply-Demand Mismatch Mechanism

• Beta-2 agonists cause positive chronotropic effects (increased heart rate) and positive inotropic effects (increased contractility), dramatically increasing myocardial oxygen demand 3, 1, 5
• Peripheral vasodilation from beta-2 receptor activation can cause coronary blood flow redistribution away from subendocardial regions 1, 5
• In patients with underlying coronary disease, even non-obstructive, this supply-demand mismatch precipitates ischemia 1, 5

Metabolic and Electrophysiologic Effects

• Albuterol causes hypokalemia (mean decrease 0.52-0.54 mmol/L), which increases arrhythmia risk [3, @17@]
• QT interval prolongation may occur, further increasing cardiac electrical instability 1
• Hypoxia and hypercapnea from COPD exacerbation amplify these cardiac effects 3, 1

Critical Comorbidity Interactions

The High-Risk Triad

• Coronary artery disease increases vulnerability to supply-demand mismatch from any cardiac stressor 3, 4
• Heart failure reduces cardiac reserve and makes the heart more susceptible to tachycardia-induced ischemia 3, 4
• Hypertension contributes to left ventricular hypertrophy and diastolic dysfunction, worsening subendocardial perfusion 3, 4

The Beta-Blocker Paradox

• Despite clear cardiovascular indications (coronary disease, heart failure), only 22% of patients with HF+COPD receive beta-blockers versus 41% with HF alone 7
• Cardioselective beta-blockers (bisoprolol, metoprolol) are safe in COPD and do not affect bronchodilator efficacy, yet remain underutilized 3, 8
• Document whether your patient was on a beta-blocker: absence represents a missed opportunity for cardioprotection that may have prevented the event 3, 8, 7

Differential Diagnosis to Address

Excluding Type 1 MI

• Absence of acute plaque rupture or coronary thrombosis on angiography 1
• Temporal relationship to bronchodilator administration rather than spontaneous onset 1
• Chest pain was not the primary presenting complaint (patient presented for respiratory symptoms) 2

Excluding Takotsubo Cardiomyopathy

• While one case report describes takotsubo from repetitive albuterol use, this typically shows apical ballooning on ventriculography 3
• Your case should show regional wall motion abnormalities corresponding to a coronary distribution 1

Management Approach Documented

Immediate Interventions

• Discontinuation of albuterol and transition to alternative bronchodilators (ipratropium bromide, a short-acting muscarinic antagonist without cardiac effects) 3
• Aspirin 162-325 mg (chewed) unless contraindicated 3, 6
• Sublingual nitroglycerin if blood pressure permits (systolic >90 mmHg) 3, 6
• Oxygen supplementation targeting SpO2 88-92% in COPD patients 3

Antiplatelet and Anticoagulation Therapy

• Dual antiplatelet therapy: aspirin plus ticagrelor 180 mg loading dose (preferred over clopidogrel for high-risk features like dynamic ST changes) 6
• Anticoagulation with fondaparinux, enoxaparin, or unfractionated heparin 6

Beta-Blocker Initiation

• This is a Class I indication for beta-blocker therapy if not already prescribed 3, 8
• Start bisoprolol 1.25 mg daily (first choice due to highest beta-1 selectivity) or metoprolol succinate 12.5-25 mg daily 8
• Titrate every 1-2 weeks as tolerated, monitoring for bronchospasm (wheezing, increased dyspnea) 8
• If bronchospasm develops, increase inhaled bronchodilator therapy first before reducing beta-blocker dose 8

Statin Therapy

• High-intensity statin: atorvastatin 80 mg or rosuvastatin 40 mg daily 6

Long-Term COPD Management Modifications

Bronchodilator Strategy

• Continue LABA/LAMA combination therapy for maintenance (safe cardiovascular profile with long-acting agents) 3, 9
• Avoid or minimize short-acting beta-2 agonists (albuterol): use ipratropium bromide (short-acting muscarinic antagonist) as rescue therapy instead 3
• Document that LABA and LAMA monotherapy or combination have similar cardiovascular safety profiles 9

Monitoring Protocol

• Serial troponin measurements until downtrending 6
• Continuous telemetry monitoring for 24-48 hours 6
• Repeat ECG every 8 hours for first 24 hours, then daily 6
• Echocardiography to assess for new wall motion abnormalities and ejection fraction 1

Discussion Points for Case Report

Clinical Significance

• Type 2 MI occurs in 8.3% of COPD exacerbations but is frequently unrecognized because chest pain is attributed to respiratory disease 2
• Beta-2 agonists are associated with increased risk of myocardial infarction, heart failure, and sudden cardiac death, particularly in patients with underlying cardiac disease 5
• The combination of COPD with cardiovascular comorbidities creates a "cardiopulmonary dilemma" where treating one condition may exacerbate the other 3, 4

Preventive Strategies

• Cardioselective beta-blockers should be prescribed to all eligible patients with COPD and cardiovascular disease, as they reduce mortality without worsening pulmonary function 3, 8, 7
• High-dose or frequent short-acting beta-2 agonists should be avoided in patients with known cardiac disease 3, 1, 5
• Close ECG and metabolic monitoring (potassium levels) is recommended before administering repeated high doses of albuterol 1

Literature Context

• Only 6 prior case reports of albuterol-associated MI existed as of 2004, making additional case reports valuable 1
• The 2023 International Consensus on Resuscitation documented tachycardia, arrhythmias, and decreased potassium as known adverse effects of short-acting beta-2 agonists 3
• One case report described takotsubo cardiomyopathy from repetitive albuterol use, demonstrating the spectrum of cardiac complications 3

Common Pitfalls to Highlight

Diagnostic Pitfalls

• Attributing chest pain solely to COPD exacerbation or musculoskeletal causes: 51% of COPD exacerbation patients have chest pain, but only 8.3% have true MI 2
• Relying on a single ECG: dynamic ST changes may be missed without serial tracings at 15-30 minute intervals 3, 6
• Dismissing troponin elevation as "demand ischemia": this IS demand ischemia (type 2 MI) and requires full acute coronary syndrome management 3, 2

Management Pitfalls

• Continuing albuterol despite cardiac symptoms: switch to ipratropium immediately 3
• Withholding beta-blockers due to COPD: cardioselective agents are safe and reduce mortality in this population 3, 8, 7
• Using non-selective beta-blockers: propranolol, nadolol, labetalol, and carvedilol are absolutely contraindicated in COPD 8
• Starting beta-blockers at standard doses: always begin with lowest available dose (bisoprolol 1.25 mg or metoprolol 12.5 mg) and titrate gradually 8

Conclusion Framework

Your case report should emphasize that type 2 MI from short-acting beta-2 agonists represents a preventable complication through:

• Judicious use of albuterol in patients with cardiovascular comorbidities 1, 5
• Preferential use of anticholinergic bronchodilators (ipratropium) as rescue therapy in high-risk patients 3
• Aggressive implementation of cardioselective beta-blocker therapy in all eligible COPD patients with cardiovascular disease 3, 8, 7
• Heightened clinical suspicion and serial ECG/troponin monitoring when cardiac symptoms develop during COPD exacerbations 3, 6, 2