Cardiology and EKG Basics - Rhythm, Blocks, STEMI, and Arrhythmias

Cardiology EKG Review Notes

• Key measurement concepts on the EKG grid

  • Small box duration: 0.04\ \,\text{s} per small box.
  • Five small boxes make one big (bold) box.
  • Therefore, every small box equals 0.04\ \text{s}; five small boxes = 0.20\ \text{s} (one big box).
  • PR interval: should be 0.12\text{ s} \le \text{PR} \le 0.20\ \text{s}.
  • Practical mnemonic: roughly 3–5 small boxes (3 × 0.04 = 0.12, 5 × 0.04 = 0.20).
  • If longer, consider AV nodal delay or heart block (AV nodal blockers can widen PR).
  • QRS width: should be < 0.12\ \text{s} (i.e., < 3 small boxes).
  • QT interval: should be no more than 450\ \text{ms} = 0.450\ \text{s} (varies with heart rate; consider QTc).
  • If QRS is wider than normal, think ventricular origin or abnormal conduction (e.g., PVCs, VT).

• Rhythm assessment steps on a rhythm strip

  • Regularity: are the QRS complexes marching regularly?
  • Atrial activity: is there a P wave before every QRS?
  • Consistency: do all P waves look the same? Is there a QRS for every P and a P for every QRS?
  • Pacing considerations: look for pacing spikes if a pacemaker is present (spikes in front of P waves and/or QRS).

• Normal sinus rhythm

  • Regular rhythm, P waves precede each QRS, P waves identical, QRS after each P.
  • Impulse origin: SA node → AV node → His bundle → bundle branches → Purkinje fibers.

• Sinus bradycardia

  • Heart rate < 60 bpm; regular rhythm; normal PR.
  • Common baseline in athletes (marathon runners).
  • Possible underlying issues: hyperkalemia, hypothyroidism, negative chronotropics (beta blockers, calcium channel blockers, digoxin), hypothermia.
  • Treatment: varies; not necessarily harmful unless symptomatic.

• Sinus tachycardia

  • Heart rate > 100 bpm; regular rhythm; P waves normal; PR interval normal.
  • Consider triggers: hyperthyroidism, fever, dehydration, anemia, hypoxia.
  • Management focuses on treating underlying cause.

• Atrial fibrillation with rapid ventricular response (AFib with RVR)

  • Irregular rhythm; no distinct P waves; fibrillatory baseline between QRSs.
  • Requires knowledge from cardiology section two; common board question.

• Atrial flutter

  • Atrial rate faster than ventricular rate with sawtooth flutter waves (P waves that look like teeth).
  • Usually more P waves than QRSs (e.g., 3–4 P waves per QRS).
  • Management similar to AFib: rate control, anticoagulation (calculate CHADS-VASc), consider cardioversion if unstable, ablation as definitive therapy.

• Supraventricular tachycardia (SVT) and AVNRT (AV nodal reentrant tachycardia)

  • Narrow QRS complexes, rapid rhythm, no clear P waves (or P waves hidden in T waves).
  • Trigger example: transient caffeine or energy drinks; sudden palpitations and dizziness can occur.
  • First-line acute management: Valsalva maneuver (bear down and hold as long as possible).
  • Pharmacologic: adenosine is diagnostic and often therapeutic.
  • Dosing: typically start with 6\ \text{mg} IV, may give 12\ \text{mg} if necessary.
  • If recurrent or refractory, consider AVNRT ablation (high success rate).

• Premature beats

  • Premature Atrial Contractions (PACs)
  • Premature beat with a different-looking P wave, QRS usually normal.
  • Compensatory pause after the premature beat.
  • Usually benign; manage electrolytes and caffeine; beta-blockers or calcium channel blockers if symptomatic.
  • Premature Ventricular Contractions (PVCs)
  • Wide, often oppositely deflected QRS complexes; compensatory pause after each PVC.
  • Can be a sign to investigate underlying hypoxia, coronary disease, electrolyte disturbances, or stimulant use (cocaine).
  • Initial treatment focuses on correcting electrolytes and hypoxia; beta blockers often used if symptomatic.

• Ventricular arrhythmias

  • Ventricular tachycardia (VT)
  • Wide QRS, monomorphic (same shape across beats), regular rhythm; no P waves.
  • QRS width > 0.12 s ( > 3 small boxes).
  • Evaluate for electrolytes, ischemia, hypoxia.
  • If stable: IV antiarrhythmics; if unstable or pulseless: defibrillate and perform CPR.
  • Ventricular fibrillation (VF)
  • Chaotic, no organized rhythm, no pulse.
  • Immediate CPR and defibrillation; ACLS protocols apply.

• Heart blocks (AV conduction disorders)

  • First-degree AV block
  • Regular rhythm; P waves present with QRS; PR interval prolonged (> 0.20 s, i.e., >5 small boxes).
  • Often asymptomatic; may be due to AV nodal blockers (e.g., calcium channel blockers like diltiazem).
  • Second-degree AV block, Type I (Wenckebach)
  • Progressive PR interval lengthening with intermittent dropped QRS (a P wave without a subsequent QRS).
  • Often asymptomatic; monitor and correct electrolytes; conservative management typical.
  • Second-degree AV block, Type II (Mobitz II)
  • Intermittent dropped QRS with a constant PR interval for conducted beats; more P waves than QRS
  • More likely to progress to complete heart block; often requires pacemaker.
  • Third-degree AV block (complete heart block)
  • No fixed relationship between P waves and QRS; AV node fails to conduct, ventricles may rely on Purkinje system.
  • Requires pacemaker.

• Sick sinus syndrome and sinus node dysfunction

  • Sick sinus syndrome: alternating bursts of atrial tachycardia, sinus bradycardia, and pauses on Holter monitoring.
  • Treatment: pacemaker is the mainstay.
  • Sinus arrhythmia: beat-to-beat variation with respiration; normal variant in young, healthy people; more evident at rest or sleep.

• Long QT interval and torsades de pointes

  • Long QT defined as QT interval excessively prolonged; specifics vary with rate (target often < 450 ms in many adults).
  • Causes include drugs (e.g., antiarrhythmics like amiodarone, antibiotics like levofloxacin, antipsychotics like quetiapine), electrolyte abnormalities, hypothermia, ischemia, and other non-medication issues.
  • Prolonged QT can predispose to torsades de pointes (polymorphic VT with a sine-wave appearance).
  • Management: IV magnesium is first-line for torsades; defibrillation if pulseless; treat underlying causes (electrolyte correction, drug review).

• Bundle branch blocks (BBB) and ECG clues

  • Right bundle branch block (RBBB)
  • V1 often shows an RSR' pattern (one tall upright R with a small initial r, then a second R’).
  • V2–V3 may show terminal S waves; overall QRS widened but distinctly RSR' in V1.
  • New RBBB with chest pain may suggest pulmonary embolism; urgent evaluation.
  • Left bundle branch block (LBBB)
  • Wide QRS with broad, often notched terminal forces in V5–V6; characteristic rabbit ears pattern in lateral leads (V5–V6, sometimes V4).
  • Often associated with T-wave inversions in lateral leads; broader PR interval changes across the chest leads.
  • New LBBB with chest pain can mimic STEMI and warrants urgent evaluation for MI.
  • Practical approach: check V1–V3 for RBBB; check V4–V6 for LBBB; use presence of “rabbit ears” and broader QRS to distinguish BBB type.

• STEMI patterns and coronary artery localization

  • Key concept: ST elevation in specific leads points to the affected territory and thus the culprit artery.
  • Inferior STEMI
  • ST elevation in leads II, III, and aVF.
  • Most likely culprit: Right coronary artery (RCA).
  • Reciprocal changes commonly seen in leads I and aVL, sometimes V2–V3.
  • Lateral STEMI
  • ST elevation in leads I, aVL, V5, V6.
  • Most likely culprit: Circumflex artery (CX).
  • Reciprocal changes often seen in leads II, III, and aVF.
  • Anterior STEMI
  • ST elevation in leads V3 and V4 (classic anterior wall).
  • Most likely culprit: Proximal left anterior descending artery (LAD).
  • May involve septal branches off the LAD.
  • Posterior STEMI
  • Subtle ST changes in V1–V3 (often ST depression), and reciprocal ST elevation in posterior leads or when using posterior leads V7–V9.
  • Posterior infarct artery: often the posterior descending artery (PDA), a branch of the RCA in many people.
  • Practical management for STEMI
  • Activate cath lab, administer aspirin, heparin, and antiplatelet agent (clopidogrel or ticagrelor), and prepare for urgent reperfusion within about 90 minutes.

• Pacemakers and device-related ECG patterns

  • Dual-chamber (AV sequential) pacemaker
  • Spikes in front of P waves and spikes in front of QRS complexes reflect atrial and ventricular pacing, respectively.

• Quick word associations and clues (clinical pearls from the lecture)

  • Hyperkalemia: peaked T waves, especially in V2–V3.
  • Hypokalemia: U waves after the T wave.
  • Delta wave: WPW pattern; pre-excitation leading to possible rapid SVT; treat with ablation if symptomatic.
  • Digoxin toxicity: diffuse sagging ST segments (“digitalis effect”); can present with atrial fibrillation or other rhythm disturbances; watch digoxin levels.
  • Post-acute kidney disease / digoxin toxicity example: aging patient with decreased urine output and sagging ST segments.

• Special case review prompts and associations

  • Inferior STEMI suspicion: ST elevation in II, III, aVF; consider RCA occlusion; look for reciprocal changes.
  • Lateral STEMI suspicion: ST elevations in I, aVL, V5, V6; consider CX occlusion.
  • Anterior STEMI suspicion: ST elevations in V3–V4; consider proximal LAD occlusion.
  • Posterior STEMI suspicion: subtle changes in V1–V3 with possible ST depression; confirm with posterior leads V7–V9 if available.

• Practical clinical exam notes

  • For board-style questions, be able to quickly identify major patterns (AFib with RVR, VT, VF, AV blocks, BBBs, STEMIs) and know the typical artery involved for STEMIs.
  • Remember the 90-minute goal for reperfusion in STEMI and the basic pharmacologic steps (antiplatelets, anticoagulation, analgesia, anti-ischemic therapy).
  • Recognize the importance of addressing reversible contributors (electrolytes, hypoxia, caffeine/cocaine intake) in premature beats and tachyarrhythmias.

• Study tips referenced in the video

  • Memorize the small-box timing and translate to interval measurements (PR, QRS).
  • Use lead placement rules (V1–V3 for right bundle, V4–V6 for left bundle) to quickly identify bundle branch blocks.
  • Practice correlating ECG patterns with likely coronary artery involvement for STEMI questions.
  • Use delta wave, hyperkalemia, and digoxin clues as quick associations in unclear rhythm strips.

• Quick reference calculations (for board-style checks)

  • PR interval from small boxes: ext{PR} = 3-5 ext{ small boxes} \Rightarrow \text{PR} \approx 0.12-0.20\ \text{s}
  • QRS width: < 3 ext{ small boxes} \Rightarrow < 0.12\ \text{s}
  • QT interval: \text{QT} \le 0.450\ \text{s} (may require correction for heart rate)

• Common exam question takeaways

  • Distinguish first-degree vs second-degree type II block:
  • First-degree: PR interval > 0.20 s with 1:1 P:QRS.
  • Second-degree type II: P waves with QRS sometimes missing; PR interval remains constant across conducted beats.
  • Recognize when a rhythm warrants a pacemaker (sick sinus syndrome, Mobitz II, high-grade AV block, third-degree block).
  • Be able to identify and differentiate PVCs, VT, and VF and know the initial management sequence (stabilize, assess, defibrillate if needed).

• Real-world relevance and ethical/practical implications

  • Rapid STEMI recognition saves myocardium; timely cath lab activation is critical.
  • Correct identification of arrhythmias informs immediate patient management and disposition (e.g., pacemaker consideration, urgent cardiology involvement).
  • Awareness of medication-induced rhythm changes (e.g., AV nodal blockers, QT-prolonging drugs) guides safer prescribing and monitoring.