ECG Diagnosis of MI

ECG Diagnosis of MI - ELECTROCARDIOGRAPHIC DIAGNOSIS OF...

Info iconThis preview shows page 1. Sign up to view the full content.

View Full Document Right Arrow Icon
This is the end of the preview. Sign up to access the rest of the document.

Unformatted text preview: ELECTROCARDIOGRAPHIC DIAGNOSIS OF ACUTE CORONARY SYNDROMES By Robin Mraz, M.D. Advocate Christ Hospital BASIC CARDIAC ANATOMY AND PHYSIOLOGY PHYSIOLOGY q The Conducting System q Basic Cardiac Electrophysiology q The Coronary Circulation THE CONDUCTING SYSTEM THE The conducting system consists of the SA node, AV node, Bundle of His, bundle branches and Purkinje system. In a healthy heart, the AV node is the only connection between the atria and ventricles. BASIC CARDIAC ELECTROPHYSIOLOGY ELECTROPHYSIOLOGY The SA node initiates the sinus beat. Depolarization spreads out over the atria forming the P wave. Excitation slows at the AV node forming the PR segment. The stimulus travels down the His Bundle to the bundle branches and Purkinje system. The QRS represents the depolarization of the ventricles, while the T wave represents the repolarization of the ventricles. THE CORONARY CIRCULATION THE The RCA supplies the SA node, most AV nodes, the right atria, the right ventricle, the right bundle branch and occasionally the left posterior fascicle. The RCA divides to form the posterior descending artery and a posteriorlateral branch. In some people the RCA supplies part of the apex and may anastomose with the LCA The LCA consists of a short left main coronary artery which divides into the LAD and Cx. The left supplies a minority of AV nodes, the left anterior fascicle and most left posterior fascicles. Branches of the LAD are called septal perforators. Branches of the Cx are called obtuse marginals. EKG SUMMARY EKG q q q Read the name, date and time on the EKG Get an old EKG for comparison Systematic Evaluation: q Rate q Rhythm q Intervals q PQRST RATE RATE EKG paper moves at 25 mm/sec q Each little box = 0.04 sec q Each big box = 0.2 sec q Quick and easy: 300, 150, 100, 75, 60 q qUse the rhythm strip and one of the QRS Use complexes, start counting with the first big box until you hit another QRS complex until RHYTHM RHYTHM q q q q What is the rate of the QRS? Tachy/bradycardia Is the QRS regular or irregular? Is the QRS narrow or wide? Are there P waves? Check leads II, V1 and V2 INTERVALS INTERVALS q PR Interval- measured from the beginning of the P to the beginning of PR the QRS. Nl is between 0.12-0.21 sec the q Short PR interval is <0.12s = WPW q Long PR interval is >0.21s = AV Block q QRS Interval- measured from the start of the Q or R wave to the end QRS of the S wave. Nl is <0.12 sec of q Lengthened QRS may result from a ectopic ventricular beat, impairment Lengthened of the conduction system (BBB, aberrant beats, WPW) or if the ventricle is being paced is q QT Interval- measured from the start of the QRS complex to the end QT of the T wave. Varies w/ HR so the QTc = QT/ √RR interval. Nl is RR <.42 sec. At normal sinus rates the QT should equal less than one half the length of the preceding RR interval. the ETIOLOGY OF PROLONGED QT ETIOLOGY q q q q q Antiarrhythmics, especially quinidine and Antiarrhythmics, procainamide, amoidarone, CCB procainamide, Other meds: phenothiazines and TCAs Idiopathic- Long QT Syndrome Hypothermia Electrolyte abnormalities- hypocalcemia PQRST PQRST q q q q q P waves: look in II and V1. Abnormal conduction would be waves: demonstrated in leads II, III and aVL as inverted P waves ‘retrograde’ demonstrated Q waves: Hallmark of infraction R wave progression: normally the R waves are small in V1-V2 and wave grow larger as you move laterally. The R wave should be the dominant deflection in the QRS by V3-V4. Early R waves in V1-V2 as large as those in the next leads can reflect posterior infarction. Poor R wave progression is when the R waves do not dominate until V5wave V6. This may also represent infarction. ST Segments- between the end of the QRS and the beginning of the T ST wave. They are evaluated from elevation/depression against the TP segment not the PR interval. ST elevation = infarction ST depression/flattening = ischemia depression/flattening T Waves are monitored for ischemia or electrolyte imbalances. Nl Waves inverted in aVR and upright in I, II, V3-V6. Hyperacute/tall T waves are the earliest sign if MI. are PQRST PQRST q q q q q P waves: look in II and V1. Abnormal conduction would be waves: demonstrated in leads II, III and aVL as inverted P waves ‘retrograde’ demonstrated Q waves: Hallmark of infraction R wave progression: normally the R waves are small in V1-V2 and wave grow larger as you move laterally. The R wave should be the dominant deflection in the QRS by V3-V4. Early R waves in V1-V2 as large as those in the next leads can reflect posterior infarction. Poor R wave progression is when the R waves do not dominate until V5wave V6. This may also represent infarction. ST Segments- between the end of the QRS and the beginning of the T ST wave. They are evaluated from elevation/depression against the TP segment not the PR interval. ST elevation = infarction ST depression/flattening = ischemia depression/flattening T Waves are monitored for ischemia or electrolyte imbalances. Nl Waves inverted in aVR and upright in I, II, V3-V6. Hyperacute/tall T waves are the earliest sign if MI. are PQRST PQRST q q q q q P waves: look in II and V1. Abnormal conduction would be waves: demonstrated in leads II, III and aVL as inverted P waves ‘retrograde’ demonstrated Q waves: Hallmark of infraction R wave progression: normally the R waves are small in V1-V2 and wave grow larger as you move laterally. The R wave should be the dominant deflection in the QRS by V3-V4. Early R waves in V1-V2 as large as those in the next leads can reflect posterior infarction. Poor R wave progression is when the R waves do not dominate until V5wave V6. This may also represent infarction. ST Segments- between the end of the QRS and the beginning of the T ST wave. They are evaluated from elevation/depression against the TP segment not the PR interval. ST elevation = infarction ST depression/flattening = ischemia depression/flattening T Waves are monitored for ischemia or electrolyte imbalances. Nl Waves inverted in aVR and upright in I, II, V3-V6. Hyperacute/tall T waves are the earliest sign if MI. are PQRST PQRST q q q q q P waves: look in II and V1. Abnormal conduction would be waves: demonstrated in leads II, III and aVL as inverted P waves ‘retrograde’ demonstrated Q waves: Hallmark of infraction R wave progression: normally the R waves are small in V1-V2 and wave grow larger as you move laterally. The R wave should be the dominant deflection in the QRS by V3-V4. Early R waves in V1-V2 as large as those in the next leads can reflect posterior infarction. Poor R wave progression is when the R waves do not dominate until V5wave V6. This may also represent infarction. ST Segments- between the end of the QRS and the beginning of the T ST wave. They are evaluated from elevation/depression against the TP segment not the PR interval. ST elevation = infarction ST depression/flattening = ischemia depression/flattening T Waves are monitored for ischemia or electrolyte imbalances. Nl Waves inverted in aVR and upright in I, II, V3-V6. Hyperacute/tall T waves are the earliest sign if MI. are Morphology of the ST Segment Morphology (a): In the AMI patient, the initial upsloping portion of the ST segment is usually either flat or convex (b): Patients w/ ST elevation due to non-AMI syndromes may demonstrate concavity of this portion of the waveform *pericarditis and benign early repolarization Electrocardiographic Differential Diagnosis of ST Segment Elevation ST A: Acute Pericarditis E: AMI B: Benign Early Repolarization F: LVH C: AMI G: LBBB D: AMI H: Paced Rhythm ST Segment Depression of ACS ST A: Horizontal B: Horizontal C: Downsloping D: Upsloping Electrocardiographic Differential Diagnosis of ST Segment Depression ST A: Digoxin Effect E: ACS B: LBBB F: ACS C: LVH G: ACS D: AMI Posterior Wall H: ACS PQRST PQRST q q q q q P waves: look in II and V1. Abnormal conduction would be waves: demonstrated in leads II, III and aVL as inverted P waves ‘retrograde’ demonstrated Q waves: Hallmark of infraction R wave progression: normally the R waves are small in V1-V2 and wave grow larger as you move laterally. The R wave should be the dominant deflection in the QRS by V3-V4. Early R waves in V1-V2 as large as those in the next leads can reflect posterior infarction. Poor R wave progression is when the R waves do not dominate until V5wave V6. This may also represent infarction. ST Segments- between the end of the QRS and the beginning of the T ST wave. They are evaluated from elevation/depression against the TP segment not the PR interval. ST elevation = infarction ST depression/flattening = ischemia depression/flattening T Waves are monitored for ischemia or electrolyte imbalances. Nl Waves inverted in aVR and upright in I, II, V3-V6. Hyperacute/tall T waves are the earliest sign if MI. are HYPERACUTE T WAVE Electrocardiographic Differential Diagnosis of the Hyperacute T Wave the A: AMI B: AMI C: Hyperkalemia D: Benign Early Repolarization E: Acute Pericarditis F: LBBB G: LVH T Wave Inversion in ACS Wave ORDER OF EKG CHANGES IN AMI ORDER q Earliest: Increased R and T wave amplitudes; giant R wave and Earliest: Hyperacute T waves Hyperacute q Progressive ST elevation q Q waves at approximately 9 hours q Loss of R waves at approximately 12 hours INFARCTION DISTRIBUTION INFARCTION TERRITORY EKG LEADS ARTERY Anterior V2-V6 LAD Inferior II, III, aVF RCA Lateral I, aVL, V5-V6 Circumflex Posterior Tall R in V1-V2 Variable ANTERIOR AMI ANTERIOR STE in V1-V4 ANTEROLATERAL AMI ANTEROLATERAL STE in V2-V4 Anterior STE in I, aVL, V5-V6 Lateral LATERAL AMI LATERAL STE in I, aVL *Note the ST depression in II, III, aVF consistent with reciprocal changes, as well as in V2-V3 which may represent a posterior MI INFERIOR AMI INFERIOR STE in II, III, aVF *Note the ST depression in I, aVL consistent with reciprocal change, as well as in V1-V4 representing a posterior MI POSTERIOR WALL AMI POSTERIOR ST Segment Depression in V1-V3 and posterior thoracic leads with STE RIGHT VENTRICULAR AMI RIGHT Right-sided anterior thoracic leads LEFT VENTRICULAR HYPERTROPHY LEFT Progression of ST changes with serial EKGs Progression Chest Pain in the Low Risk Patient Chest CPEP Program q q q q q q 4 baby ASA Xanax Oxygen Cardiac Enzymes Q6h x2 EKGs Q3h x3 Stress Test in 7h if above remain wnl Treatment Protocol of Unstable Angina Treatment q q q q q q q q q q 4 Baby ASA Plavix Nitroglycerin- IV if continued CP, NTP if h/o chest pain Lopressor Lovenox/Heparin Integrilin : +TnI, ST depression, recurrent chest pain in ED MSO4 Oxygen Xanax Admit to TELE CODE 60 CODE Treatment of STE AMI q q q q q q q q q q q CALL: PMD, Interventionalist, Fellow and Cath Lab Team 2 Large bore IV s 4 baby ASA Plavix Nitroglycerin IV (careful w/ RCA lesion- will drop BP) Lopressor 5mg IV q15m x3 Heparin MSO4 MSO4 Xanax Oxygen To Cath Lab- If not Thrombolytics INDICATIONS FOR THROMBOLYTIC THERAPY THERAPY q q q q STE >1 mm in 2 or more contiguous leads New LBBB Less than 12h from the onset of symptoms Age <75y CONTRAINDICATIONS TO THROMBOLYTIC THERAPY THROMBOLYTIC q ABSOLUTE CONTRAINDICATIONS: q q q q q q Active Internal Bleeding OR recent internal bleeding <10d CNS Tumor, AVM or CNS Surgery last 2 months Hx of CVA <2-6m or any hemorrhagic CVA Major surgery/trauma at a non-compressible site <10d Suspected aortic dissection RELATIVE CONTRAINDICATIONS: q q q q q q q q q Known bleeding diathesis Severe uncontrolled HTN (SBP>200 or DBP>120) Active PUD CPR >10 min Use of anticoagulation CVA >6 months Pregnancy Puncture of non-compressible blood vessel Trauma/major surgery >2 weeks but <2 months ...
View Full Document

This note was uploaded on 01/11/2012 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

Ask a homework question - tutors are online