Questions and Answers
What is the primary cause of Acute Coronary Syndromes (ACS)?
What is the atheroma composed of in atherosclerosis?
What is the outcome if a blood clot occludes the entire coronary artery?
Which of the following is NOT a common symptom of ACS?
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What is anginal equivalence in ACS?
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What is the primary purpose of a 12-lead ECG in diagnosing ACS?
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What increases the pre-test probability of ACS?
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What is the clinical event responsible for triggering ACS?
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What is one of the primary goals of initial management in acute STEMI?
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What is a key aspect of identifying acute inferior STEMI on a 12-lead ECG?
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What is a benefit of aspirin administration in ACS patients?
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What is a characteristic of a patient with right ventricular infarction?
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What is a sign of posterior infarction on a 12-lead ECG?
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What can cause ST elevation mimicking STEMI?
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What is a limitation of the STEMI/Non-STEMI framework?
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What can help identify changes and dynamic myocardial oxygen supply vs. demand?
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What is a reciprocal change seen in lead AVL when identifying acute inferior STEMI?
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What can nitroglycerin administration do in patients with right ventricular infarction?
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Study Notes
Acute Coronary Syndromes (ACS)
Underlying Pathology
- ACS is primarily caused by atherosclerosis, a disease that affects coronary arteries
- Atherosclerosis consists of two main components: atheroma (fatty lipid-rich gruel) and tunica intima (innermost lining of coronary arteries)
- Atheroma grows within the walls of the tunica intima and can cause a pathological thickening of the tunica intima, separating it from circulating blood
- The atheroma's contents are highly thrombogenic, meaning they can trigger a blood clot if exposed to circulating blood
Clinical Event Triggering ACS
- The clinical event responsible for triggering ACS is often plaque rupture, which exposes the atheroma to circulating blood
- Platelets are activated, leading to platelet aggregation and the formation of a blood clot
- If the clot occludes the entire coronary artery, it can cause a myocardial infarction (heart attack)
Signs and Symptoms of ACS
- Chest discomfort or pain (poorly localized, often in the center of the chest, lasting 15 minutes or more)
- Radiation of pain to the arm, neck, back, or jaw
- Shortness of breath, diaphoresis, nausea, vomiting, palpitations, and anxiety or sense of impending doom
- Denial or minimization of symptoms due to fear of hospital bills or previous misdiagnosis
Anginal Equivalence
- ACS can present with anginal equivalence, such as:
- Jaw, neck, ear, or arm pain
- New-onset exertional dyspnea
- Palpitations without chest discomfort
- Syncope (fainting)
- Unexplained fatigue, especially in diabetics
Pre-Test Probability and 12-Lead ECG
- The pre-test probability of ACS is high if the patient presents with typical chest discomfort and signs of acute illness
- A 12-lead ECG is essential in diagnosing ACS, with a focus on:
- ST segment elevation ( STEMI) or depression (NSTEMI)
- Q waves and cardiac biomarkers
- Serial ECGs to monitor changes and dynamic myocardial oxygen supply vs. demand
Goals of Initial Management
- Restore balance between myocardial oxygen supply and demand
- Optimize blood pressure and oxygen supply
- Provide pain control and anxiety relief
- Prepare for reperfusion therapy (PCI or fibrinolytics)
- Defibrillate if necessary
Identifying Acute STEMI on 12-Lead ECG
- Look for ST segment elevation in two or more anatomically contiguous leads
- Consider pre-test probability and rule of proportionality (repolarization proportional to depolarization)
- Normal ECG understanding is essential for recognizing abnormal patterns
- Serial ECGs can help identify changes and dynamic myocardial oxygen supply vs. demand
Secondary Prevention and Reperfusion Therapy
- Aspirin administration has a 25% mortality benefit in ACS patients
- Nitroglycerin is a potent coronary vasodilator that can help restore balance between myocardial oxygen supply and demand
- Reperfusion therapy (PCI or fibrinolytics) is crucial in preventing irreversible heart damage
- Post-PCI outcome data can help improve systems of care and reduce first medical contact to balloon time### Identifying Acute Inferior STEMI
- Criteria for sinus rhythm: p waves, QRS complexes in a one-to-one relationship, constant PR interval between 120-200 milliseconds
- In lead 2, PR interval measures 132 milliseconds, indicating sinus rhythm borderline sinus bradycardia at a rate of 60
- Presence of ST segment elevation in leads 2, 3, and AVF, indicating acute inferior STEMI
- Reciprocal change in lead AVL (down-sloping ST segment) supports the diagnosis of acute inferior STEMI
Reciprocal Changes
- Inferior leads (2, 3, and AVF) are reciprocal to high lateral leads (1 and AVL)
- Right precordial leads (V1, V2, and V3) are reciprocal to the posterior wall of the left ventricle
- Look for reciprocal changes in the right precordial leads when identifying acute inferior STEMI to potentially spot acute isolated posterior STEMI
Right Ventricular Infarction
- Can be a complication of acute inferior STEMI, especially with proximal occlusion of the right coronary artery
- Patients with right ventricular infarction are preload dependent, relying on central venous pressure to maintain cardiac output
- Nitroglycerin can drop central venous pressure, exacerbating the condition
- Suspect right ventricular infarction in patients with acute inferior STEMI, especially if the culprit artery is the right coronary artery
Case Study
-
79-year-old female with chest discomfort, history of previous heart attack
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Initial 12-lead ECG shows sinus rhythm, ST elevation in leads 2, 3, and AVF, and reciprocal change in lead AVL, indicating acute inferior STEMI
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No reciprocal changes in the right precordial leads; however, a modified lead V4R (placed on the right side of the chest) shows ST elevation, indicating right ventricular infarction
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Initial blood pressure was 100/55, which dropped to 90/40 after a trial dose of nitroglycerin, highlighting the importance of caution when administering nitroglycerin in such cases### Recognizing Myocardial Infarction Patterns on the ECG
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Worsening ST elevation in lead V1 indicates right ventricular infarction
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Extensive anterior ST elevation in leads V1-V6 suggests left anterior descending (LAD) artery occlusion
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Reciprocal ST changes in inferior leads with anterior ST elevation help confirm diagnosis
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High lateral ST elevation may be subtle, look for reciprocal changes in lead III to identify
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Inferior lead ST elevation with reciprocal changes in aVL indicates lateral wall infarction
Isolated Posterior Infarction
- Posterior infarction can present without obvious ST elevation on a 12-lead ECG
- Look for isolated ST depression in right precordial leads (V1-V3) as a sign of posterior infarction
- The "carousel pony" sign - tall R waves and down-upsloping ST depression in V2 - can indicate posterior involvement
- Flipping the ECG over to view a "mirror image" can reveal posterior ST elevation
Mimics of Acute MI
- Left bundle branch block, pacemaker rhythms, and left ventricular hypertrophy can all cause ST elevation mimicking STEMI
- These represent secondary ST-T wave changes from abnormal ventricular depolarization, not acute ischemia
- Differentiating these from true STEMI requires assessing concordance of ST changes with QRS, clinical presentation, and serial ECG changes
Limitations of the STEMI/Non-STEMI Framework
- The current STEMI/Non-STEMI paradigm misses some patients with occluded arteries who do not meet strict ST elevation criteria
- Examples include hyperacute T-waves, de Winter T-waves, and isolated posterior infarction
- A shift to an "occlusion MI/non-occlusion MI" framework may better identify all patients who would benefit from emergent reperfusion therapy
Acute Coronary Syndromes (ACS)
- ACS is primarily caused by atherosclerosis, which affects coronary arteries
- Atherosclerosis consists of atheroma (fatty lipid-rich gruel) and tunica intima (innermost lining of coronary arteries)
Underlying Pathology
- Atheroma grows within the walls of the tunica intima, causing a pathological thickening that separates it from circulating blood
- Atheroma's contents are highly thrombogenic, triggering blood clots when exposed to circulating blood
Clinical Event Triggering ACS
- Plaque rupture exposes atheroma to circulating blood, leading to platelet activation, aggregation, and blood clot formation
- If the clot occludes the entire coronary artery, it can cause a myocardial infarction (heart attack)
Signs and Symptoms of ACS
- Chest discomfort or pain, often poorly localized and lasting 15 minutes or more
- Radiation of pain to the arm, neck, back, or jaw
- Shortness of breath, diaphoresis, nausea, vomiting, palpitations, and anxiety or sense of impending doom
Anginal Equivalence
- ACS can present with anginal equivalence, such as:
- Jaw, neck, ear, or arm pain
- New-onset exertional dyspnea
- Palpitations without chest discomfort
- Syncope (fainting)
- Unexplained fatigue, especially in diabetics
Pre-Test Probability and 12-Lead ECG
- High pre-test probability of ACS requires typical chest discomfort and signs of acute illness
- 12-lead ECG is essential in diagnosing ACS, focusing on:
- ST segment elevation (STEMI) or depression (NSTEMI)
- Q waves and cardiac biomarkers
- Serial ECGs to monitor changes and dynamic myocardial oxygen supply vs. demand
Goals of Initial Management
- Restore balance between myocardial oxygen supply and demand
- Optimize blood pressure and oxygen supply
- Provide pain control and anxiety relief
- Prepare for reperfusion therapy (PCI or fibrinolytics)
- Defibrillate if necessary
Identifying Acute STEMI on 12-Lead ECG
- Look for ST segment elevation in two or more anatomically contiguous leads
- Consider pre-test probability and rule of proportionality (repolarization proportional to depolarization)
- Normal ECG understanding is essential for recognizing abnormal patterns
- Serial ECGs can help identify changes and dynamic myocardial oxygen supply vs. demand
Secondary Prevention and Reperfusion Therapy
- Aspirin administration has a 25% mortality benefit in ACS patients
- Nitroglycerin is a potent coronary vasodilator that can help restore balance between myocardial oxygen supply and demand
- Reperfusion therapy (PCI or fibrinolytics) is crucial in preventing irreversible heart damage
- Post-PCI outcome data can help improve systems of care and reduce first medical contact to balloon time
Identifying Acute Inferior STEMI
- Criteria for sinus rhythm: p waves, QRS complexes in a one-to-one relationship, constant PR interval between 120-200 milliseconds
- Presence of ST segment elevation in leads 2, 3, and AVF, indicating acute inferior STEMI
- Reciprocal change in lead AVL (down-sloping ST segment) supports the diagnosis of acute inferior STEMI
Reciprocal Changes
- Inferior leads (2, 3, and AVF) are reciprocal to high lateral leads (1 and AVL)
- Right precordial leads (V1, V2, and V3) are reciprocal to the posterior wall of the left ventricle
- Look for reciprocal changes in the right precordial leads when identifying acute inferior STEMI to potentially spot acute isolated posterior STEMI
Right Ventricular Infarction
- Can be a complication of acute inferior STEMI, especially with proximal occlusion of the right coronary artery
- Patients with right ventricular infarction are preload dependent, relying on central venous pressure to maintain cardiac output
- Nitroglycerin can drop central venous pressure, exacerbating the condition
- Suspect right ventricular infarction in patients with acute inferior STEMI, especially if the culprit artery is the right coronary artery
Recognizing Myocardial Infarction Patterns on the ECG
- Worsening ST elevation in lead V1 indicates right ventricular infarction
- Extensive anterior ST elevation in leads V1-V6 suggests left anterior descending (LAD) artery occlusion
- Reciprocal ST changes in inferior leads with anterior ST elevation help confirm diagnosis
- High lateral ST elevation may be subtle, look for reciprocal changes in lead III to identify
- Inferior lead ST elevation with reciprocal changes in aVL indicates lateral wall infarction
Isolated Posterior Infarction
- Posterior infarction can present without obvious ST elevation on a 12-lead ECG
- Look for isolated ST depression in right precordial leads (V1-V3) as a sign of posterior infarction
- The "carousel pony" sign - tall R waves and down-upsloping ST depression in V2 - can indicate posterior involvement
- Flipping the ECG over to view a "mirror image" can reveal posterior ST elevation
Mimics of Acute MI
- Left bundle branch block, pacemaker rhythms, and left ventricular hypertrophy can cause ST elevation mimicking STEMI
- These represent secondary ST-T wave changes from abnormal ventricular depolarization, not acute ischemia
- Differentiating these from true STEMI requires assessing concordance of ST changes with QRS, clinical presentation, and serial ECG changes
Limitations of the STEMI/Non-STEMI Framework
- The current STEMI/Non-STEMI paradigm misses some patients with occluded arteries who do not meet strict ST elevation criteria
- Examples include hyperacute T-waves, de Winter T-waves, and isolated posterior infarction
- A shift to an "occlusion MI/non-occlusion MI" framework may better identify all patients who would benefit from emergent reperfusion therapy
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Description
This quiz covers the underlying pathology of Acute Coronary Syndromes (ACS), including atherosclerosis, atheroma, and tunica intima. Learn about the causes and effects of ACS on coronary arteries.
