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🔴Right Ventricular (RV) Infarction: A Must-Know ECG Pattern!⤵️
🔹RV infarction often coexists with inferior MI but is frequently overlooked. Missing it can be dangerous, as treatment differs from LV infarcts!
🔹Here’s how to detect it on ECG ⬇️
1️⃣ When to Suspect RV Infarction?
🔹 Any inferior MI (ST ↑ in II, III, aVF)
🔹 Hypotension + JVD + clear lungs
🔹 Bradycardia, AV block
💡 Inferior MI + hypotension? Always check for RV infarct!
2️⃣ Right-Sided ECG
🚑 Standard ECG misses the right ventricle
🩺 Place right-sided chest leads (V3R–V6R) for better detection
🎯 Most sensitive lead? V4R!
🔹 Lead placement for right-sided ECG:
-V1 stays in place
-V2–V6 are mirrored onto the right side of the chest
3️⃣ Key ECG Signs of RV Infarction
✔️ ST elevation in V1 & V4R (Most specific!)
✔️ Failure of reciprocal ST depression in V1–V2
✔️ ST elevation in lead V1 + ST depression in V2
✔️ Hyperacute ST elevation in V4R (82–100% sensitivity)
🚨 But here’s the catch…
4️⃣ The Absence of ST Elevation in V3R/V4R Doesn’t Rule Out RV Infarction!
❌ No ST ↑ in V3R/V4R? RV infarct still possible! Here’s why:
🟢 RV infarction is often patchy → ST changes may be transient
🟢 Right-sided ST elevation peaks early → Can normalize quickly.
5️⃣ Why is This Important?
RV infarcts are preload-dependent!
🚨 What to AVOID?
❌ Nitrates, diuretics, beta-blockers → Can cause severe hypotension!
🩺 How to manage?
✔️ IV fluids (increase preload)
✔️ Inotropes if needed (e.g., dobutamine, milrinone)
🌐 https://www.tg-me.com/cardiology
🔹RV infarction often coexists with inferior MI but is frequently overlooked. Missing it can be dangerous, as treatment differs from LV infarcts!
🔹Here’s how to detect it on ECG ⬇️
1️⃣ When to Suspect RV Infarction?
🔹 Any inferior MI (ST ↑ in II, III, aVF)
🔹 Hypotension + JVD + clear lungs
🔹 Bradycardia, AV block
💡 Inferior MI + hypotension? Always check for RV infarct!
2️⃣ Right-Sided ECG
🚑 Standard ECG misses the right ventricle
🩺 Place right-sided chest leads (V3R–V6R) for better detection
🎯 Most sensitive lead? V4R!
🔹 Lead placement for right-sided ECG:
-V1 stays in place
-V2–V6 are mirrored onto the right side of the chest
3️⃣ Key ECG Signs of RV Infarction
4️⃣ The Absence of ST Elevation in V3R/V4R Doesn’t Rule Out RV Infarction!
5️⃣ Why is This Important?
RV infarcts are preload-dependent!
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🔴Brugada Syndrome: A Silent Threat to the Heart⬇️
🔹What is Brugada Syndrome?
A potentially fatal genetic disorder affecting the heart's electrical system, leading to an increased risk of sudden cardiac death—especially during sleep. It is caused by mutations in the SCN5A gene, affecting sodium channel function and cardiac conduction.
🔹Brugada Pattern vs. Brugada Syndrome
👉 Brugada Pattern:
- An incidental ECG finding without symptoms.
- Can be triggered by fever, medications, or electrolyte imbalances.
- Management: Monitor and avoid triggers.
👉 Brugada Syndrome:
- ECG changes + symptoms (syncope, palpitations, sudden cardiac arrest).
- High risk of sudden death, requiring urgent intervention.
- Management: ICD implantation, quinidine therapy.
🔹Types of Brugada ECG Patterns:
1️⃣ Type 1 (Diagnostic): Coved-type ST elevation in V1-V3.
2️⃣ Type 2: Saddleback ST elevation.
3️⃣ Type 3: Features of Type 1 or 2 but less pronounced.
🔹Differential Diagnosis
Brugada pattern can mimic other conditions:
🔍 Right bundle branch block (RBBB)
🔍 Early repolarization
🔍 Acute pericarditis
🔍 Arrhythmogenic right ventricular cardiomyopathy (ARVC)
🔍 Hyperkalemia or electrolyte imbalances
🔍 Ischemic heart disease
🔍 Pectus excavatum (chest wall abnormalities affecting lead placement)
🔹Key Features of Brugada Syndrome:
🩸 Sodium Channelopathy: Autosomal dominant with familial clustering.
⚠️ Symptoms: Syncope, VT, VF, and sudden death during sleep.
🩺 ECG Clues: Coved-type ST elevation + T wave inversion in V1-V3.
🌐 https://www.tg-me.com/cardiology
🔹What is Brugada Syndrome?
A potentially fatal genetic disorder affecting the heart's electrical system, leading to an increased risk of sudden cardiac death—especially during sleep. It is caused by mutations in the SCN5A gene, affecting sodium channel function and cardiac conduction.
🔹Brugada Pattern vs. Brugada Syndrome
👉 Brugada Pattern:
- An incidental ECG finding without symptoms.
- Can be triggered by fever, medications, or electrolyte imbalances.
- Management: Monitor and avoid triggers.
👉 Brugada Syndrome:
- ECG changes + symptoms (syncope, palpitations, sudden cardiac arrest).
- High risk of sudden death, requiring urgent intervention.
- Management: ICD implantation, quinidine therapy.
🔹Types of Brugada ECG Patterns:
1️⃣ Type 1 (Diagnostic): Coved-type ST elevation in V1-V3.
2️⃣ Type 2: Saddleback ST elevation.
3️⃣ Type 3: Features of Type 1 or 2 but less pronounced.
🔹Differential Diagnosis
Brugada pattern can mimic other conditions:
🔍 Right bundle branch block (RBBB)
🔍 Early repolarization
🔍 Acute pericarditis
🔍 Arrhythmogenic right ventricular cardiomyopathy (ARVC)
🔍 Hyperkalemia or electrolyte imbalances
🔍 Ischemic heart disease
🔍 Pectus excavatum (chest wall abnormalities affecting lead placement)
🔹Key Features of Brugada Syndrome:
🩸 Sodium Channelopathy: Autosomal dominant with familial clustering.
⚠️ Symptoms: Syncope, VT, VF, and sudden death during sleep.
🩺 ECG Clues: Coved-type ST elevation + T wave inversion in V1-V3.
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MINOCA: Myocardial Infarction with Non-Obstructive Coronary Arteries
MINOCA is a clinical syndrome where MI occurs without significant coronary artery stenosis (<50% on angiography). It accounts for ~6-10% of all MI cases.
👀 Pathophysiology of MINOCA
The causes are diverse and include both coronary and non-coronary mechanisms:
🟢 Coronary:
•Microvascular dysfunction
•Epicardial spasm
•Spontaneous coronary artery dissection
•Coronary thromboembolism
🟢 Non-coronary:
•Takotsubo cardiomyopathy
•Myocarditis
👀 How is MINOCA diagnosed?
A systematic approach is needed to find the underlying cause. Key tools:
➡️ IVUS/OCT – Detects plaque disruption or dissection
➡️ CMR – Helps identify myocardial inflammation or Takotsubo cardiomyopathy
AHA Guidelines recommend a comprehensive evaluation
👀 Management of MINOCA: A tailored approach :
Since MINOCA has various causes, treatment must be individualized:
✔️ Coronary vasospasm → CCBs, nitrates
✔️ Microvascular dysfunction → β-blockers, ACE inhibitors
✔️ Myocarditis/Takotsubo → Supportive care
🟢 Uncertainty remains due to lack of large RCTs
👀 Why is MINOCA important?
Despite the absence of obstructive CAD, MINOCA is NOT benign.
📌 Associated with significant morbidity & mortality
📌 Requires thorough diagnostic workup to prevent recurrence & guide therapy
A one-size-fits-all approach doesn’t work!
🩺 Research & Future Directions
Ongoing studies are focusing on:
✔️ Better imaging strategies (e.g., OCT, CMR)
✔️ Role of inflammation in MINOCA
✔️ Personalized pharmacotherapy
More data is needed to define optimal treatments!
👥 Take-home message:
✔️ MINOCA is a heterogeneous syndrome requiring careful evaluation
✔️ Advanced imaging (IVUS, OCT, CMR) helps identify the cause
✔️ Treatment depends on the underlying mechanism
✔️ More research is needed for evidence-based management
🌐 https://www.tg-me.com/cardiology
MINOCA is a clinical syndrome where MI occurs without significant coronary artery stenosis (<50% on angiography). It accounts for ~6-10% of all MI cases.
The causes are diverse and include both coronary and non-coronary mechanisms:
•Microvascular dysfunction
•Epicardial spasm
•Spontaneous coronary artery dissection
•Coronary thromboembolism
•Takotsubo cardiomyopathy
•Myocarditis
A systematic approach is needed to find the underlying cause. Key tools:
AHA Guidelines recommend a comprehensive evaluation
Since MINOCA has various causes, treatment must be individualized:
Despite the absence of obstructive CAD, MINOCA is NOT benign.
A one-size-fits-all approach doesn’t work!
Ongoing studies are focusing on:
More data is needed to define optimal treatments!
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