12 Lead Mastery; Deeper Cuts
ST elevation in II, III, aVF with reciprocal depression in I and aVL; and ST elevation in V4R
What is inferior STEMI with right ventricular involvement
Irregularly irregular narrow complex tachycardia with no discernible P waves
What is atrial fibrillation with RVR
The PR interval reflects conduction time primarily through this structure
What is the AV node
This coronary artery most commonly supplies the SA node
What is the right coronary artery
Mean arterial pressure is estimated as this formula using systolic and diastolic pressures
What is MAP equals SBP plus two times DBP; divided by three
ST depression maximal in V1 to V3 with tall R waves and upright T waves; no anterior ST elevation; patient has ongoing chest pain
What is posterior MI; a STEMI equivalent
Regular wide complex tachycardia in an adult should be assumed to be this until proven otherwise
What is ventricular tachycardia
Phase 0 of the ventricular action potential is mediated mainly by this ion channel influx
What is fast sodium influx
Inferior MI complicated by bradycardia and hypotension may reflect ischemia to this artery supplying the AV node
What is the right coronary artery
The physiologic principle describing how increasing LV end diastolic volume increases stroke volume up to an optimal point is called this
What is the Frank Starling mechanism
New LBBB with ischemic symptoms and hemodynamic instability should be treated as this; even if classic STE is not obvious
What is a STEMI equivalent requiring emergent reperfusion consideration
Irregular wide complex tachycardia with beat to beat changing QRS morphology; baseline delta wave history; and rates often over 200
What is pre excited atrial fibrillation; AF with WPW
Class IV antiarrhythmics slow conduction and increase refractoriness primarily at this node
What is the AV node
A new harsh holosystolic murmur with shock after MI suggests this complication; most often after anterior MI
What is ventricular septal rupture
A narrow pulse pressure with cool clammy skin most strongly suggests this hemodynamic problem; compared with distributive states which often have wide pulse pressure early
What is low stroke volume; decreased cardiac output
ST elevation in aVR with diffuse ST depression; plus chest pain and diaphoresis; the highest risk culprit pattern suggests this anatomy
What is left main or proximal LAD ischemia; or severe multivessel disease
Polymorphic VT in the setting of prolonged QT; often after a medication change; electrolyte loss; or bradycardia
What is torsades de pointes
Mobitz II localizes to this portion of the conduction system and is high risk for progressing to complete heart block
What is the His Purkinje system; infranodal block
Sudden pulmonary edema with new loud systolic murmur 2 to 7 days after MI suggests this complication; classically inferior MI
What is papillary muscle rupture causing acute severe mitral regurgitation
A positive Kussmaul sign is paradoxical rise in JVP with inspiration; it is most consistent with impaired right sided filling from this physiology
What is right ventricular failure or impaired RV compliance; also acceptable; constrictive pericarditis
In a patient with paced rhythm or LBBB; concordant ST elevation of at least 1 mm in any lead is strongly suggestive of this diagnosis
What is acute occlusion MI; STEMI in LBBB; Sgarbossa criteria positive
Wide complex tachycardia with a twisted axis but normal QT; often triggered by ischemia or catecholamines; and the QRS axis rotates around baseline
What is polymorphic VT due to ischemia; not torsades
Hyperkalemia produces peaked T waves and then QRS widening because increasing extracellular potassium reduces this property of cardiac cells
What is resting membrane potential negativity; it depolarizes cells and inactivates sodium channels reducing conduction velocity
Hypotension; JVD; and clear lung sounds after inferior MI points toward this diagnosis; confirm with this right sided ECG lead
What is right ventricular infarction; confirm with V4R
After initiating positive pressure ventilation in a borderline patient; BP drops and JVD increases; the mechanism is reduced venous return plus increased RV afterload; this pattern most strongly indicates this diagnosis and immediate physiologic countermeasure
What is massive pulmonary embolism with obstructive physiology; counter with fluids and vasopressors while preparing for definitive therapy; also acceptable; consider decreasing intrathoracic pressure strategy and rapid transport for reperfusion