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Repolarization ST wave Abnormalities
The document provides an extensive overview of ST segment abnormalities in ECG readings, detailing causes of ST segment elevation and depression, such as myocardial ischemia, infarction, and various cardiac conditions. It also discusses treatment options including anti-ischemic therapy, antiplatelet and anticoagulation therapy, and surgical interventions like CABG and PCI. Key patterns and their clinical implications are described, with an emphasis on recognizing and differentiating conditions based on ECG morphology.
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Presentation by Mr. Aby Thankachan, M.Sc(N), Ph.D on repolarization ST wave abnormalities.
The ST segment is an isoelectric interval representing ventricular depolarization and repolarization, crucial for diagnosing myocardial ischemia or infarction.
Elevation causes include acute myocardial infarction, coronary vasospasm, and pericarditis among others.
Acute STEMI presents with varied ST elevation morphology: concave, convex or straight.
Introduction to different morphology patterns associated with abnormal ST segments.
Acute STEMI features ST elevation in various leads, such as septal (V1-2) and inferior (II, III, aVF).
Identifies anteroseptal STEMI with associated ECG features.
Prinzmetal's angina shows similar ST elevation to STEMI but is typically transient and reversible.
Acute pericarditis causes widespread ST elevation with specific lead involvement, plus PR segment depression.
BER presents mild ST elevation in young patients, often showing a characteristic fish-hook pattern.
LBBB shows discordance between ST segments/T waves and QRS complexes, affecting ST elevation and depression.
LVH causes similar repolarization abnormality as LBBB, with specific ST elevation/depression patterns.
Ventricular aneurysms post-myocardial infarction can demonstrate ST elevation with deep Q waves.
Brugada syndrome features ST elevation with partial RBBB, often leading to serious arrhythmias.
Includes pulmonary embolism and conditions like hyperkalemia and J-waves leading to ST elevation.
ST depression can indicate various conditions such as myocardial ischemia or specific heart block scenarios.
ST depression is categorized by morphology (upsloping, downsloping, or horizontal) affecting lead interpretations.
ST depression patterns recognizable in leads opposite to the site of myocardial infarction.
Variable ST depression patterns indicative of myocardial ischemia, particularly in left precordial leads.
Reciprocal ST depression occurs simultaneously with ST elevation during STEMI at opposing leads.
Posterior STEMI is characterized by ST depression in anterior leads and ST elevation in posterior leads.
Digoxin use results in characteristic downsloping ST depression impacting the ECG morphology.
Hypokalemia leads to widespread ST depression with additional unique T-wave changes.
Various treatments include fibrinolytic therapy and medications like ACE inhibitors for managing ischemic conditions.
Involves monitoring, nitroglycerin use, and symptomatic treatment for ongoing ischemia.
Administering oxygen to patients with respiratory distress while monitoring arterial oxygen saturation.
Usage of morphine is indicated when NTG fails to relieve severe symptoms accompanying ischemia.
Nondihydropyridine calcium antagonists are recommended for recurrent ischemia in specific patient scenarios.
ACEI administration is indicated for persistent hypertension in patients with specific risk factors.
Used for severe ischemia or hemodynamic instability despite aggressive medical therapy.
Immediate initiation of aspirin and additional thienopyridine therapy for patients intolerant to aspirin.
Parenteral anticoagulation alongside antiplatelet therapy is recommended for managing acute coronary events.
Recommended for certain patient categories lacking acute ST elevation or posterior MI conditions.
CABG and PCI indicated for specific coronary artery diseases with substantial ischemic risk.
PCI is recommended for patients meeting certain criteria, optimizing coronary anatomy interventions.
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Repolarization ST wave Abnormalities
- 1. Mr. Aby Thankachan,M.Sc(N),Ph.D Asst Professor HICON, CBE REPOLARIZATION ST WAVE ABNORMALITIES
- 2. S-T Segment • TheST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave. • The ST Segment represents the interval between ventricular depolarization and repolarization. • The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction.
- 6. Causes of STSegment Elevation • Acute myocardial infarction • Coronary vasospasm (Printzmetal’s angina) • Pericarditis • Benign early repolarization • Left bundle branch block • Left ventricular hypertrophy • Ventricular aneurysm • Brugada syndrome • Ventricular paced rhythm • Raised intracranial pressure
- 7. MYOCARDIAL INFARCTION • AcuteSTEMI may produce ST elevation with either concave, convex or obliquely straight morphology.
- 9. ST Segment Morphology in OtherConditions
- 10. Patterns of STElevation • Acute ST elevation myocardial infarction (STEMI) • ST segment elevation and Q-wave formation in contiguous leads. Follow the links above to find out more about the different STEMI patterns.: • Septal (V1-2) • Anterior (V3-4) • Lateral (I + aVL, V5-6) • Inferior (II, III, aVF) • Right ventricular (V1, V4R) • Posterior (V7-9)
- 11. ST elevation inV2-4
- 12.
- 13. Coronary Vasospasm (Prinzmetal’s angina) •This causes a pattern of ST elevation that is very similar to acute STEMI — i.e. localised ST elevation with reciprocal ST depression occurring during episodes of chest pain. • However, unlike acute STEMI the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis. • It may be impossible to differentiate these two conditions based on the ECG alone.
- 14. Pericarditis • Acute Pericarditiscauses widespread concave (“saddleback”) ST segment elevation with PR segment depression in multiple leads, typically involving I, II, III, aVF, aVL, and V2-6. • Concave “saddleback” ST elevation in leads I, II, III, aVF, V5-6 with depressed PR segments. • There is reciprocal ST depression and PR elevation in leads aVR and V1.
- 16. Benign Early Repolarization •Benign Early Repolarization (BER) causes mild ST elevation with tall T-waves mainly in the precordial leads. BER is a normal variant commonly seen in young, healthy patients. There is often notching of the J-point — the “fish-hook” pattern. • The ST changes may be more prominent at slower heart rates and disappear in the presence of tachycardia.
- 18. Left Bundle BranchBlock (LBBB) • In Left bundle branch block (LBBB), the ST segments and T waves show “appropriate discordance” — i.e. they are directed opposite to the main vector of the QRS complex. • This produces ST elevation and upright T waves in leads with a negative QRS complex (dominant S wave), while producing ST depression and T wave inversion in leads with a positive QRS complex (dominant R wave).
- 19. • ST elevationin leads with deep S waves — most apparent in V1-3. • ST depression in leads with tall R waves — most apparent in I and aVL.
- 21. Left Ventricular Hypertrophy(LVH) • Left Ventricular Hypertrophy (LVH) causes a similar pattern of repolarization abnormalities as LBBB, with ST elevation in the leads with deep S-waves (usually V1-3) and ST depression/T-wave inversion in the leads with tall R waves (I, aVL, V5-6).
- 22. Deep S waveswith ST elevation in V1-3 ST depression and T-wave inversion in the lateral leads V5-6
- 23. Ventricular Aneurysm • Ventricularaneurysms are one of the many complications that may occur after a heart attack. The word aneurysm refers to a bulge or 'pocketing' of the wall or lining of a vessel commonly occurring in the blood vessels at the base of the septum, or within the aorta. • In the heart, they usually arise from a patch of weakened tissue in a ventricular wall, which swells into a bubble filled with blood.This, in turn, may block the passageways leading out of the heart, leading to severely constricted blood flow to the body. • A left ventricular aneurysm can be associated with ST elevation . ST elevation and deep Q waves will be observed in patients with previous myocardial infarction.
- 24. ST elevation withdeep Q waves and inverted T waves in V1-3.
- 25. Brugada Syndrome • BrugadaSyndrome is an inherited channelopathy (a disease of myocardial sodium channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in young patients. • The tell-tale sign on the resting ECG is the “Brugada sign” — ST elevation and partial RBBB in V1-2 with a “coved” morphology.
- 26. ST elevation andpartial RBBB in V1-2 with a coved morphology — the “Brugada sign”.
- 27. Less Common Causesof ST segment Elevation • Pulmonary embolism and acute cor pulmonale (usually in lead III) • Acute aortic dissection (classically causes inferior STEMI due to RCA dissection) • Hyperkalaemia • Sodium-channel blocking drugs (secondary to QRS widening) • J-waves (hypothermia, hypercalcaemia) • Following electrical cardioversion • Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease
- 28. Causes of STDepression • Myocardial ischaemia / NSTEMI • Reciprocal change in STEMI Posterior MI • Digoxin effect • Hypokalaemia • Supraventricular tachycardia • Right bundle branch block • Right ventricular hypertrophy • Left bundle branch block • Left ventricular hypertrophy • Ventricular paced rhythm
- 29. Morphology of STDepression • ST depression can be either upsloping, downsloping, or horizontal. • Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 leads indicates myocardial ischaemia. • Upsloping ST depression in the precordial leads with prominent De Winter T waves is highly specific for occlusion of the LAD. • Reciprocal change has a morphology that resembles “upside down” ST elevation and is seen in leads electrically opposite to the site of infarction. • Posterior MI manifests as horizontal ST depression in V1-3 and is associated with upright T waves and tall R waves.
- 30.
- 31. Reciprocal change inSTEMI Posterior MI
- 32. Patterns of STdepression • Myocardial Ischaemia • ST depression due to subendocardial ischaemia may be present in a variable number of leads and with variable morphology. It is often most prominent in the left precordial leads V4-6 plus leads I, II and aVL. • Widespread ST depression with ST elevation in aVR is seen in left main coronary artery occlusion and severe triple vessel disease.
- 34. Reciprocal Change • STelevation during acute STEMI is associated with simultaneous ST depression in the electrically opposite leads: • Inferior STEMI produces reciprocal ST depression in aVL (± lead I). • Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF (± lead II). • Reciprocal ST depression in V1-3 occurs with posterior infarction
- 35. Reciprocal ST depressionin aVL with inferior STEMI
- 36. Posterior Myocardial Infarction •Acute posterior STEMI causes ST depression in the anterior leads V1-3, along with dominant R waves (“Q-wave equivalent”) and upright T waves. There is ST elevation in the posterior leads V7-9.
- 38. Digoxin Effect • causesdownsloping ST depression with a “sagging” morphology,
- 39. • Hypokalaemia causeswidespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval. • Right ventricular hypertrophy (RVH) causes ST depression and T-wave inversion in the right precordial leads V1-3. • Right Bundle Branch Block (RBBB) produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3. • Supraventricular tachycardia causes horizontal ST depression, most prominent in the left precordial leads (V4-6).
- 40. Treatment • Fibrinolytic therapy •ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists and HMG CoA reductase inhibitors. • Nitrates • Morphine • Primary percutaneous coronary intervention (PCI)
- 41. Anti-Ischemic Therapy • Bedrest with continuous ECG monitoring for ischemia and arrhythmia detection in patients with ongoing rest pain. • Nitroglycerin (NTG), sublingual tablet or spray, followed by intravenous administration, for immediate relief of ischemia and associated symptoms.
- 42. • Supplemental oxygenfor patients with cyanosis or respiratory distress; finger pulse oximetry or arterial blood gas determination to confirm adequate arterial oxygen saturation (Sao2>90%) and continued need for supplemental oxygen in the presence of hypoxemia.
- 43. • Morphine sulfateintravenously when symptoms are not immediately relieved with NTG or when acute pulmonary congestion and/or severe agitation is present. • A β-blocker, with the first dose administered intravenously if there is ongoing chest pain, followed by oral administration, in the absence of contraindications.
- 44. • In patientswith continuing or frequently recurring ischemia when β-blockers are contraindicated, a nondihydropyridine calcium antagonist (eg, verapamil or diltiazem), followed by oral therapy, as initial therapy in the absence of severe LV dysfunction or other contraindications.
- 45. • An ACEIwhen hypertension persists despite treatment with NTG and a β- blocker in patients with LV systolic dysfunction or CHF and in ACS patients with diabetes. • Oral long-acting calcium antagonists for recurrent ischemia in the absence of contraindications and when β-blockers and nitrates are fully used.
- 46. • Intra-aortic balloonpump counterpulsation for severe ischemia that is continuing or recurs frequently despite intensive medical therapy or for hemodynamic instability in patients before or after coronary angiography.
- 47. Antiplatelet and AnticoagulationTherapy • Antiplatelet therapy should be initiated promptly. Aspirin (ASA - acetylsalicylic acid) is the first choice and is administered as soon as possible after presentation and continued indefinitely. • A thienopyridine (clopidogrel or ticlopidine) should be administered to patients who are unable to take ASA because of hypersensitivity or major gastrointestinal intolerance.
- 48. • Parenteral anticoagulationwith intravenous unfractionated heparin (UFH) or with subcutaneous LMWH should be added to antiplatelet therapy with ASA, or a thienopyridine. • A platelet GP IIb/IIIa receptor antagonist should be administered, in addition to ASA and UFH, to patients with continuing ischemia or with other high-risk features (see Table 2) and to patients in whom a percutaneous coronary intervention (PCI) is planned. Eptifibatide and tirofiban are approved for this use. (Level of Evidence: A) Abciximab can also be used for 12 to 24 hours in patients with UA/NSTEMI in whom a PCI is planned within the next 24 hours.
- 49. • Intravenous thrombolytictherapy in patients without acute ST-segment elevation, a true posterior MI, or a presumed new left bundle-branch block.
- 50. Coronary Revascularization (CABG/ PCI) • CABG – for left main CAD, 3-vessel disease, 2-vessel disease with significant proximal left anterior descending CAD and either abnormal LV function (EF <0.50) or demonstrable ischemia on noninvasive testing. • PCI or CABG for patients with 1- or 2-vessel CAD without significant proximal left anterior descending CAD but with a large area of viable myocardium and high-risk criteria on noninvasive testing.
- 51. • PCI forpatients with multivessel coronary disease with suitable coronary anatomy, with normal LV function, and without diabetes.