What is demand ischemia (reduced blood flow due to increased oxygen demand)?

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From the Guidelines

Demand ischemia should be managed by reducing myocardial oxygen demand and/or increasing blood flow to the ischemic area, using drugs such as beta-blockers, calcium antagonists, and organic nitrates, as recommended by the European Society of Cardiology 1. Demand ischemia occurs when the heart's oxygen demand exceeds its supply, leading to myocardial ischemia without coronary artery obstruction. This condition typically presents in patients with severe anemia, hypotension, tachycardia, or left ventricular hypertrophy. Some key factors to consider in managing demand ischemia include:

  • Reducing myocardial oxygen demand by controlling heart rate and blood pressure
  • Increasing blood flow to the ischemic area using vasodilators
  • Optimizing oxygen supply through oxygen therapy and treating underlying conditions such as anemia
  • Using anti-anginal drugs, as outlined in the European Society of Cardiology guidelines 1, to reduce symptoms of angina pectoris and signs of ischemia. The pathophysiology of demand ischemia involves an imbalance in the oxygen supply-demand ratio, where increased demand or decreased supply leads to myocardial injury despite patent coronary arteries. Key management strategies include:
  • Beta-blockers to reduce heart rate and myocardial oxygen consumption
  • Calcium antagonists to reduce blood pressure and increase blood flow
  • Organic nitrates to reduce cardiac workload and increase blood flow
  • Oxygen therapy to maintain saturation above 94%
  • Blood transfusions to maintain hemoglobin above 7-8 g/dL in cases of anemia.

From the Research

Demand Ischemia

Demand ischemia occurs when the heart's oxygen demand exceeds its oxygen supply. This can happen due to various factors, including:

  • Increased heart rate
  • Increased contractility
  • Increased left ventricular wall stress 2 Myocardial oxygen requirements rise with increases in these factors, leading to an imbalance between myocardial oxygen supply and demand.

Treatment Options

Treatment options for demand ischemia include:

  • Anti-anginal medications, such as:
    • Nitrates, which act principally by venous vasodilation, but also probably by coronary dilation 2
    • Beta-blockers, which act mainly by reducing heart rate and cardiac contractility 3, 2
    • Calcium channel blockers, which act principally by arterial and coronary vasodilation 3, 2
  • Invasive techniques, such as coronary artery bypass and coronary angioplasty, which improve myocardial oxygen supply by relieving or circumventing the atherosclerotic obstruction responsible for ischemia 2

Pathophysiology

The pathophysiology of demand ischemia involves an imbalance between myocardial oxygen supply and demand, causing cardiac dysfunction, arrhythmias, myocardial infarction, and sudden death 4. The coronary circulation matches blood flow with oxygen requirements by coordinating the resistances within microvasculature, where the endothelium plays an important role by liberating several vasodilator substances 4.

Current Concepts

Current concepts of myocardial ischemia suggest that it is not just an oxygen supply-demand imbalance, but rather a lack of coronary blood flow to below 8-10 µl/g per beat, with consequences for myocardial electrical, metabolic, contractile, and morphological features 5, 6. All therapeutic interventions must aim to improve blood flow to ischemic myocardium as much and as quickly as possible 6.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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