0.29 CME

Infective Endocarditis: Diagnosis and Management

Speaker: Dr. Naresh Kumar

Alumni- Nizam Institute of Medical Sciences

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Description

Infective endocarditis (IE) carries a high risk of morbidity and mortality. Rapid diagnosis, effective treatment, and prompt recognition of complications are essential to good patient outcomes. Therapy of IE caused by the more commonly encountered organisms, including streptococci, enterococci, staphylococci, and the HACEK organisms (Haemophilus parainfluenzae, Haemophilus aphrophilus, Actinobacillus [Haemophilus] actinomycetemcomitans, Cardiobacterium hominis, Eikenella species, and Kingella species). Echocardiography plays an important role in the diagnosis and management of IE.

Summary Listen

  • Acute Coronary Syndrome (ACS), often associated with chest pain, encompasses a spectrum of conditions including unstable angina and myocardial infarction (MI). This spectrum ranges from situations with minor artery blockage and manageable symptoms to complete artery occlusion requiring immediate intervention. Recognizing the different presentations of ACS is crucial for timely and appropriate treatment.
  • Symptoms of ACS can vary. Classic symptoms include chest discomfort described as tightness, pressure, or heaviness lasting more than 10 minutes. However, atypical presentations are common, especially in the elderly, diabetics, and women. These may manifest as shortness of breath, weakness, sweating, or vomiting, without chest pain, referred to as anginal equivalents.
  • Diagnosing ACS relies on a combination of clinical history, ECG findings, and cardiac enzyme levels. An ECG showing ST-segment elevation (STEMI) indicates complete artery occlusion, while ST-segment depression or T-wave inversion suggests NSTEMI or unstable angina. Elevated cardiac enzymes, like troponin, confirm myocardial damage and help distinguish between unstable angina (normal enzymes) and NSTEMI/STEMI (elevated enzymes).
  • The underlying causes of ACS include plaque rupture leading to thrombus formation, and supply-demand mismatch where the heart's oxygen needs exceed supply. Plaque composition, including factors like a thin fibrous cap and large lipid core, contributes to vulnerability to rupture. Reduced oxygen supply can be caused by stenosis, anemia, or vasospasm, while increased demand occurs with conditions like tachycardia and hypertension.
  • Treatment strategies for ACS depend on the type and severity. STEMI requires immediate reperfusion therapy, either through thrombolysis (clot-dissolving drugs) or percutaneous coronary intervention (PCI, angioplasty with stenting). Unstable angina and NSTEMI may be managed initially with medications like aspirin, clopidogrel, and nitroglycerin, followed by further risk stratification and potentially PCI.
  • Pharmacological interventions in ACS include antiplatelet agents (aspirin, clopidogrel), anticoagulants (heparin, enoxaparin), nitroglycerin, beta-blockers, and statins. Aspirin and clopidogrel reduce clot formation, nitroglycerin dilates blood vessels to improve blood flow, beta-blockers reduce heart rate and blood pressure, and statins stabilize plaque and lower cholesterol.
  • Complications of ACS can include mechanical failures like ventricular septal rupture or papillary muscle rupture, cardiogenic shock, and arrhythmias. Prompt recognition and management of these complications are critical for improving patient outcomes. Adhering to established protocols and guidelines is essential for providing optimal care.
  • Ultimately, early recognition of ACS symptoms, rapid diagnosis, and timely intervention are crucial for minimizing myocardial damage and improving survival. Reperfusion therapies, whether thrombolysis or PCI, aim to restore blood flow to the affected heart muscle as quickly as possible. Balancing the risks and benefits of each treatment option is paramount in managing ACS patients.

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