EKGs Flashcards
EKGs
Seizures
Seizures- ischemia, arrhythmia, brugada, HCM, QT, WPW, arrhythmogenic, RV dysplasia
EKGs
Causes of Long QT-
Long QT- hypokalemia, hypomagnesemia, hypocalcemia, type Ia meds, increase ICP, hypothermia, hereditary
EKGs
Pericardial Effusion-
Pericardial Effusion: electrical alternans, tachycardia, low voltage (QRS in I+II+III < 15 or V1+V2+V3 < 30)
EKGs
PE-
PE- sinus tachycardia, S1Q3T3, rightward axis, new RBBB or incomplete RBBB, SVT, ventricular dysrhythmia, STE/D, T wave inversions (anteroseptal +/- inferior leads)
If old findings T waves→ COPD, Pulm HTN New→ PE
EKGs
Wide QRS-
Wide QRS- ventricular ectopy, paced beats, BBB, WPW, LVH, Na blocking, metabolic (hyperK, severe acidosis)
Junctional (narrow), Ventricular (wide)
EKGs
Short PR-
Short PR- junction rhythm, pre-excitation [WPW (delta, wide QRS) vs Lown-Gaunog-Levine Syndrome (no delta, normal QRS, no
clinical relevance)], normal variant
EKGs
Poor R wave progression-
Poor R wave progression- R in V3 should be 3 mm- anterior STEMI, LVH
EKGs
STE in aVr-
STE in aVr- can be predictive of acute L main , triple vessel or proximal LAD- should have STD in other leads
EKGs
Arrythmogenic RV dysplasia-
Arrythmogenic RV dysplasia- northern Italy, Newfoundland, syncope
Progressive replacement of RV myocardium by fibrofatty tissue → interference
Epsilon waves (Specific not sensitive) TWI V1-2 (sensitive), slight prolonged QRS, LBBB type VT or PVCs
Will need Echo and maybe cardiac MRI
Tx: high risk→ ICD, Low risk → B blocker (sotalol)
EKGs
Wide complex tachycardia:
Wide complex tachycardia: SVT w/ RBBB vs VT- multiple tools to determine, not very good
Likely VT in aVR: Initial R, width of initial r or q > 40, notching on initial down stroke of negative QRS
EKGs
Athletic heart-
Athletic heart- high voltage, TWI, early repolarization
Type I: suggestive of athletic athletic training
High ventricular voltages, TWI (can be biphasic in V1)- V1-4 in african or caribbean, male, </= 15, early repol,
Increase vagal tone (sinus brady, AVB, RBBB, notched QRS in V1)
Type II: suggestive of cardiac disease
Deep > 2mm TWI (inferior and lateral leads), STD, pathologic q waves
EKGs
Atrial septal defect:
Atrial septal defect: crohetage pattern- notching in inferior leads (II, III, aVF)
EKGs
AV block- 1st degree
PR interval >200ms
Causes: increased vagal tone, athletic training, inferior MI, mitral valve surgery, myocarditis, electrolyte disturbances, AV nodal
blocking drugs (beta-blockers, ca channel blockers, digoxin, amiodarone)
No specific treatment needed
EKGs
AV block- 2nd degree, Mobitz I (Wenckebach)
Progressive prolongation of PR interval culminating in a non-conducted P wave
PR interval is longest immediately before the dropped beat
PR interval is shortest immediately after dropped beat
Mechanism: reversible conduction block at AV node, AV node cells progressively fatigue until fail to conduct an impulse
Causes: beta-blockers, ca blockers, digoxin, amiodarone, increased vagal tone, inferior MI, myocarditis, following cardiac
surgery
Significance: usually benign, if symptomatic usually respond to atropine
EKGs
AV block-2nd degree, Mobitz II
Intermittent non-conducted P waves without progressive prolongation of PR interval
PR interval in the conducted beats remains constant
P waves march through at a constant rate
Mechanism: failure of conduction at the level of the His-Purkinje system (below AV node, due to structural damage to
conduction system, typically have pre-existing LBBB or bifascicular block, if distal to bundle of His will cause broad QRS,
His-Purkinje cells suddenly and unexpectedly fail to conduct impulse
Causes: Anterior MI, idiopathic fibrosis, cardiac surgery, inflammatory conditions, autoimmune, infiltrative, hyperkalemia,
beta-blockers, ca channel blockers, digoxin, amiodarone
Significance: more likely to be associated with hemodynamic compromise and progression to 3rd degree heart block, risk of
asystole is 35% per year, immediate admission for monitoring and pacemaker
EKGs
AV block-3rd degree, complete
Complete absence of AV conduction, perfusing rhythm is maintained by a junctional or ventricular escape rhythm, may suffer
ventricular standstill → syncope or sudden cardiac death, severe bradycardia
Atrial rate ~ 100, ventricular rate ~ 40
Mechanism- end point of Mobitz I or II
Causes: same as Mobitz I and II- most common are inferior MI, AV-nodal blocking drugs, idiopathic degeneration
Significance: high risk of ventricular standstill and sudden cardiac death, need pacemaker
Ischemia/injury/infarction
Radiation, diaphoresis, worse with exertion, chest pain, vomiting
T waves concerning for ischemia- straight intial part, RT phenomenon (check), disproportionate T waves to QRS
STD in any leads other than aVR + V1 concern for ischemia
Straight STE early sign of cardiac ischemia
Anterior infarction
Anterior infarction
Occlusion of LAD
Worse prognosis due to larger infarct size
STE and Q waves in precordial leads (V1-6) +/- high lateral leads (I and aVL)
Reciprocal STD in inferior leads (III and aVF)
Anterior-inferior STEMI
Anterior-inferior STEMI due to occlusion of wraparound LAD
STE in precordial and inferior leads
L main coronary artery occlusion
L main coronary artery occlusion
Widespread STD with STE in aVR > V1
Wellens’ syndrome
Deep precordial T wave inversion or biphasic T waves in V2-3, indicating critical
Proximal LAD occlusion (warning sign for imminent anterior infarct)
Type A- biphasic 25%, Type B- deeply inverted 75%
Sudden occlusion of LAD → transient anterior STEMI (symptomatic) → reperfusion of LAD (CP resolves)
and have T wave changes (A or B) → if artery remains open biphasic will become deeply inverted → if
perfusion is unstable have pseudonormalization of T waves -hyperacute STEMI→ if remains occluded
develops anterior STEMI or stuttering pattern
De Winter’s T waves
Upsloping STD with symmetrically peaked T waves in precordial leads-STEMI
Equivalent- acute LAD occlusion
Proximal LAD/LMCA occlusion worse prognosis- first septal branch(aVR and V1) and first diagonal branch (I and aVL)
Inferior infarction
Inferior infarction
Up to 40% will have concomitant right ventricular infarction- hypotension (get right sided leads)
Risk of bradycardia due to second or third degree AV block
Ischemia of AV node, Bezold-Jarisch reflex (increase vagal tone)
STE in II, III, aVF
Reciprocal STD and T wave inversion in aVL (+/- I)- may occur before STE (should get serial EKGs)
Occlusion of dominant RCA (STE III> II, reciprocal STD I, signs of RV infarct- STE in V1 and V4R), less common dominant
LCx (STE I and V5-6, STE II=III, absence of reciprocal STD in I), or wraparound LAD
Lateral infarction
Lateral infarction
STE I, aVL, V5-6
Reciprocal STD in inferior leads (III and aVF)
Anterolateral- LAD occlusion
Inferior-posterior-lateral- LCx occlusion
Isolated lateral- smaller branch arteries- D1, OM or ramus intermedius
Posterior infarction
Posterior infarction
Accompanies 15-20% of STEMIs, usually inferior and lateral- increased risk of death (RCA or circ)
V1-3: horizontal STD, Tall-broad R waves (>30 ms), upright T waves, dominant R wave (R/S > 1) in V2
Anteroseptal leads directed from anterior towards internal surface. Posterior activity is recorded from anterior and the
typical STE and Q waves are inverted
STE→ STD, Q waves → R waves, Terminal T wave inversion → upright T wave
Confirmed by presence of STE and Q waves in posterior leads (V7-9-below L scapula)
Right ventricular infarction
Right ventricular infarction
Very preload sensitive and can develop severe hypotension in response to nitrates- fluid responsive
Common with inferior STEMI
In patient with inferior STEMI- STE in V1 (only lead that looks directly at RV), STE III>II, STE V1>V2, STE in
V1 + STD in V2, isoelectric ST segment in V1 with marked STD in V2
Confirmed by STE in right sided leads (V3R-V6R)
