Apex-Pulse Deficit

Definition

Formula: Apex-pulse deficit = Apical rate - Radial rate

Mechanism

"When the heart contracts ahead of schedule, the ventricles will not have filled with blood normally, and the stroke volume output during that contraction is depressed or is almost absent. Therefore, the pulse wave passing to the peripheral arteries after a premature contraction may be so weak that it cannot be felt in the radial artery. Thus, a deficit in the number of radial pulses occurs when compared with the actual number of contractions of the heart."

• Guyton and Hall Textbook of Medical Physiology

Causes

Clinical Significance

• An irregular pulse on palpation should prompt auscultation of the apical rate. Roberts & Hedges notes: "An irregular pulse suggests atrial fibrillation or flutter with variable block, and accurate assessment of the pulse should be carried out by auscultation of the apical cardiac sounds."
• The larger the deficit, the more severe the arrhythmia/hemodynamic compromise. A greater pulse deficit in AF generally reflects more severe disease (Roberts & Hedges' Clinical Procedures in Emergency Medicine).
• In AF, the deficit helps guide the urgency of rate control therapy.

How to Measure

1. Two examiners ideally work simultaneously - one auscultates the apex, the other palpates the radial pulse.
2. Both count for exactly 60 seconds (or 30 seconds x 2).
3. Subtract radial rate from apical rate.
4. Even a single examiner can estimate it using a watch, but simultaneous counting is more accurate.

Normal Value

Example Scenario

• Apex-pulse deficit = 130 - 90 = 40 beats/min
• This indicates 40 ventricular contractions per minute are mechanically ineffective at the periphery.

Relation to Monitoring

• Guyton and Hall Textbook of Medical Physiology
• Roberts and Hedges' Clinical Procedures in Emergency Medicine
• Miller's Anesthesia, 10th ed.

Atrial Flutter - ECG Features

12-Lead ECG of Typical Atrial Flutter (Fuster & Hurst's The Heart, 15th ed.)

Core ECG Features

Lead-by-Lead Flutter Wave Morphology

• Leads II, III, aVF: Negative ("inverted") sawtooth flutter waves - the hallmark. The waves show a slow downslope followed by a sharp upstroke.
• Lead V1: Discrete, upright, positive P-like waves (no sawtooth) - because V1 is perpendicular to the frontal plane circuit. This can be mistaken for a different rhythm on telemetry monitoring.
• Lead aVR: Positive flutter waves
• Lead I / aVL: Flutter waves may be small or biphasic

"The negative sawtooth pattern in ECG leads II, III, and aVF represents activation superiorly up the interatrial septum, followed by inferiorly directed activation down the right atrial free wall anterior to the crista terminalis, and then across the tricuspid annulus."

• Fuster and Hurst's The Heart, 15th ed.

• Leads II, III, aVF: Positive flutter waves
• Lead V1: Negative flutter waves
• Same macro-reentrant circuit around the tricuspid annulus, but in the opposite (clockwise) direction

Lead II Rhythm Strip - Classic Sawtooth (Guyton & Hall)

Mechanism Behind the ECG Pattern

Key Distinguishing Points vs. Atrial Fibrillation

Clinical Tip: Unmasking Flutter Waves

• Carotid sinus massage or IV adenosine transiently increases AV block, slowing the ventricular rate and revealing the flutter waves clearly.

"Flutter waves on the ECG may be difficult to see. Atrial flutter waves can be unmasked by vagal maneuvers such as carotid sinus massage or the use of adenosine to block the AV node transiently."

• Fuster and Hurst's The Heart, 15th ed.

• Fuster and Hurst's The Heart, 15th ed.
• Guyton and Hall Textbook of Medical Physiology
• Harrison's Principles of Internal Medicine, 22nd ed. (2025)
• Rosen's Emergency Medicine, 9th ed.

HAS-BLED Score

Purpose

Scoring Table

Note: "A" (renal OR liver) and "D" (drugs OR alcohol) can each score 1 or 2 if both sub-criteria are present, giving the maximum of 9.

Score Interpretation

Score ≥3 = "High risk" - warrants caution and efforts to correct modifiable risk factors.

• Rosen's Emergency Medicine; Bradley and Daroff's Neurology in Clinical Practice

Annual Bleeding Rate vs. Stroke Risk at Equivalent Scores

Mnemonic: H-A-S-B-L-E-D

Hypertension uncontrolled Abnormal renal/liver function (1 pt each) Stroke history Bleeding history or predisposition Labile INR Elderly (>65) Drugs (antiplatelets/NSAIDs) or alcohol (1 pt each)

Clinical Use - Key Points

1. High HAS-BLED does NOT mean withhold anticoagulation. In most patients with AF, stroke risk (CHA₂DS₂-VASc ≥2) outweighs bleeding risk. The score flags which modifiable factors to address.
2. Modifiable factors to correct: uncontrolled hypertension, labile INR (switch to DOAC), drugs causing bleeding (stop NSAIDs/antiplatelets if possible), excess alcohol.
3. Non-modifiable factors (age, prior stroke, prior bleed) still warrant anticoagulation in most cases but heighten monitoring.
4. DOACs vs. warfarin: Labile INR (L criterion) is eliminated when using DOACs (dabigatran, rivaroxaban, apixaban, edoxaban), which reduces the HAS-BLED score by 1 point and is one reason DOACs are preferred.
5. The score was originally validated in the Euro Heart Survey population and has been externally validated in multiple cohorts. It performs similarly to other bleeding scores (ORBIT, ATRIA) with modest predictive accuracy (c-statistic ~0.60-0.72).

• Rosen's Emergency Medicine, 9th ed. (Box 65.11)
• Harrison's Principles of Internal Medicine, 22nd ed. (2025)
• Bradley and Daroff's Neurology in Clinical Practice (Table 65.3)
• Sabiston Textbook of Surgery, 21st ed.

Supraventricular Tachycardia (SVT) - Emergency Physician's Guide

1. Definition and Classification

"80% or more of cases of paroxysmal SVT are AV nodal reentrant tachycardia, resulting from sustained reentry occurring within the AV node, with an ectopic atrial focus accounting for the remaining 15% to 20%."

• Tintinalli's Emergency Medicine

2. Mechanisms - The Reentry Concept

1. Two pathways with different conduction speeds and refractory periods
2. Unidirectional block in one pathway
3. Slow enough conduction to allow the blocked pathway to recover

P-Wave Location by Mechanism (Rosen's Emergency Medicine):

3. ECG Features of PSVT (Narrow-Complex SVT)

Tintinalli's Table 18-16 - ECG Features:

ECG Example - PSVT converting to sinus (Rosen's/Tintinalli):

4. Clinical Presentation

• Most patients are young, otherwise healthy females (Tintinalli)
• Symptoms: palpitations, lightheadedness, dyspnea, chest tightness, polyuria (from ANP release)
• Onset and termination are abrupt - patients can often describe exactly when it started/stopped
• Hemodynamic instability is uncommon unless underlying cardiac disease
• Syncope can occur at very high rates or with coincident vasomotor abnormalities
• Mild troponin elevation may occur - of uncertain significance unless ischemia suspected (Rosen's)

5. Emergency Management Algorithm

Harrison's 22nd Ed. Treatment Algorithm:

Step-by-Step ED Management

Step 1 - Hemodynamic Assessment

• Immediate synchronized DC cardioversion - 100-200 J biphasic
• Do not delay for vagal maneuvers or drugs

Step 2 - Vagal Maneuvers (First Line, Stable)

"If applied early in the dysrhythmia course, vagal maneuvers are often effective. Attention to technique is important to maximize success rate."

• Tintinalli's Emergency Medicine

Step 3 - Adenosine (First-Line Drug, Stable)

• 6 mg IV rapid bolus (large-bore antecubital vein or central) followed immediately by 20 mL NS flush
• If no effect in 1-2 min: 12 mg IV bolus + flush
• May repeat 12 mg once more
• Via central line or PICC: use 3 mg (shorter transit time to heart)

• Precipitates AF in up to 15% of patients - usually brief but dangerous in WPW
• Contraindicated post-cardiac transplant (hypersensitivity due to denervation)
• Use cautiously in severe asthma (may precipitate bronchospasm)
• Theophylline/caffeine antagonize adenosine - higher dose may be needed
• Dipyridamole potentiates adenosine - use lower dose

"Adenosine may produce transient chest pain, dyspnea, and anxiety. It is contraindicated in patients with prior cardiac transplantation due to potential hypersensitivity."

• Harrison's, 22nd ed.

Step 4 - Rate-Slowing Agents (Second Line, Stable, Adenosine-Refractory)

Rosen's: "In refractory cases, diltiazem, esmolol, or metoprolol are options. Rarely needed, synchronized cardioversion (at 100 to 200 J, biphasic preferred) can terminate AVNRT refractory to pharmacologic therapy or in a patient with hemodynamic instability."

Step 5 - Electrical Cardioversion (Refractory Stable or Unstable)

• Synchronized DC cardioversion - 100-200 J biphasic (or 50-100 J monophasic)
• Sedate patient first (if time and hemodynamics allow)
• Nearly always successful

6. Special Situation - WPW / Preexcitation Syndromes

1. Short PR interval (<0.12 s)
2. Wide QRS (>0.10 s) with slurred initial upstroke = delta wave
3. Secondary ST/T changes

• Orthodromic AVRT - narrow complex, looks identical to AVNRT - treat with vagal maneuvers + adenosine (safe)
• Antidromic AVRT - wide bizarre QRS at very rapid rates (>200 bpm) - do NOT use AV nodal blockers
• Pre-excited AF - very rapid, irregular wide complex rhythm - medical emergency

The WPW Danger Rule:

NEVER use adenosine, verapamil, diltiazem, digoxin, or beta-blockers in pre-excited AF or antidromic AVRT. These block the AV node but not the accessory pathway, forcing all conduction through the bypass tract → extreme ventricular rates → ventricular fibrillation.

• Hemodynamically unstable: immediate DC cardioversion
• Stable: IV procainamide or ibutilide (work on the accessory pathway directly)

"When the typical QRS antidromic changes are coupled with tachycardia, AV nodal blocking agents may trigger degeneration into ventricular fibrillation."

• Rosen's Emergency Medicine

7. Wide-Complex Tachycardia Differential

"In general, these [wide complex tachycardias] should be managed as ventricular tachycardia until proven otherwise. If the tachycardia is regular and the patient is stable, a trial of intravenous adenosine is reasonable."

• Harrison's, 22nd ed.

8. Disposition from the ED

9. Long-Term / Definitive Management

2019 ESC SVT Guidelines - Key Updates (ACC Summary):

• Amiodarone and digoxin removed from acute management of narrow-complex SVT
• Sotalol and lidocaine removed from wide-complex SVT algorithm
• Ivabradine (with or without beta-blocker) now preferred for inappropriate sinus tachycardia - verapamil/diltiazem no longer recommended for this
• Catheter ablation upgraded as preferred over drug therapy for most symptomatic SVTs
• Amiodarone, sotalol, quinidine, procainamide removed from pregnancy SVT management
• In adult congenital heart disease: sotalol not recommended (proarrhythmic risk); flecainide/propafenone avoided if BBB or structural disease

10. Quick Reference - Drug Summary

• Harrison's Principles of Internal Medicine, 22nd ed. (2025)
• Tintinalli's Emergency Medicine, 9th ed. (Table 18-16, Ch. 18)
• Rosen's Emergency Medicine, 9th ed. (Ch. 65)
• Roberts and Hedges' Clinical Procedures in Emergency Medicine
• 2019 ESC Guidelines for SVT Management (Brugada J et al., Eur Heart J 2020;41:655-720) - ACC 10-point summary
• *Note: No major 2024-2025 SVT-specific guideline update has been published; the 2019 ESC guidelines remain the current reference.*This covers the full emergency physician's theory of SVT drawn from all four requested sources plus the latest guideline updates. Key takeaways worth memorizing:

1. AVNRT is ~60-80% of all PSVT - the most common SVT you'll see in the ED
2. Vagal maneuvers first - the modified Valsalva (supine + leg raise after straining) converts ~43%
3. Adenosine 6→12→12 mg IV rapid push works in 85-90% of cases
4. WPW + AF = do NOT block the AV node - procainamide or immediate cardioversion only
5. Treat all wide-complex tachycardia as VT until proven otherwise
6. The 2019 ESC guidelines removed amiodarone, digoxin, sotalol, and lidocaine from SVT management - these are no longer appropriate acute agents for SVT

VT vs SVT with Aberrancy - Brugada Criteria & Beyond

The Core Rule

Any wide-complex tachycardia must be treated as VT until proven otherwise.

• VT is the most common cause of wide-complex tachycardia (~80%)
• Misdiagnosing VT as SVT and giving AV-nodal blockers (verapamil, diltiazem) can cause hemodynamic collapse
• Treating SVT as VT (with amiodarone or cardioversion) is almost never fatal

Brugada Algorithm (1991) - The Classic 4-Step Stepwise Approach

Algorithm Flowchart (Rosen's Emergency Medicine):

The Four Criteria in Detail

"Only when the response to all four questions is negative is a supraventricular rhythm with abnormal conduction diagnosed. As soon as a single 'yes' answer is noted, VT is diagnosed."

• Rosen's Emergency Medicine, 9th ed.

Step 4 - Lead Morphology Criteria Explained

RBBB-like (positive in V1 - tall right precordial leads):

LBBB-like (negative in V1 - left precordial leads dominant):

Griffith Algorithm (1994) - The Alternative Approach

Harrison's Algorithm - AV Dissociation + aVR Focus

"A monophasic R wave or Rs complex in aVR, or concordance from V1 to V6 of monophasic R or S waves, is also relatively specific for VT."

• Harrison's, 22nd ed.

Vereckei Algorithm (2008) - Lead aVR Only

Pava Criterion (2010) - Simplest Single Rule

R-wave peak time in lead II >50 ms = VT

All 5 Algorithms Compared (Tintinalli Table 18-22)

"Neither has proven consistently superior. Simplicity favors the Vereckei or Pava approaches."

• Tintinalli's Emergency Medicine, 9th ed.

Classic Clinical Features Favoring VT vs SVT (Rosen's Table 65.5)

Pitfalls and Limitations

1. AV dissociation is pathognomonic for VT but present in only ~20-30% of VT cases - its absence does NOT exclude VT
2. 1:1 retrograde VA conduction can occur in VT - a P wave after every QRS does not mean SVT
3. Sodium channel toxicity (tricyclic poisoning, flecainide overdose) and hyperkalemia can produce wide bizarre QRS mimicking VT - look for clinical context
4. Antidromic WPW produces very wide QRS that satisfies Brugada VT criteria yet is not VT - adenosine/cardioversion are appropriate; avoid AV-nodal blockers
5. Bundle branch reentry VT can look identical to native LBBB in sinus rhythm
6. Brugada pattern (sodium channelopathy) is NOT the same as Brugada VT/SVT algorithm
7. All algorithms have lower accuracy in patients with severe structural heart disease

ED Management of Undifferentiated WCT

Wide-complex tachycardia (QRS >120 ms, rate >100 bpm)
         |
         ↓
  Hemodynamically UNSTABLE?
   → Immediate synchronized DC cardioversion (200 J biphasic)
         |
         ↓ (stable)
  Apply Brugada algorithm (or Vereckei/Pava if faster)
         |
    → VT diagnosed or uncertain: treat as VT
    → Adenosine trial reasonable if regular, stable, possibly SVT
         |
  VT treatment:
  - Amiodarone 150 mg IV over 10 min (preferred if structural heart disease)
  - Procainamide 15-17 mg/kg IV over 30-60 min (if no structural disease)
  - Lidocaine 1-1.5 mg/kg IV (third line)
  - Synchronized cardioversion if refractory

• Rosen's Emergency Medicine, 9th ed. (Table 65.5, Fig. 65.32)
• Tintinalli's Emergency Medicine, 9th ed. (Table 18-22)
• Harrison's Principles of Internal Medicine, 22nd ed. (Fig. 261-1)
• Braunwald's Heart Disease, 12th ed.
• Original: Brugada P et al. Circulation 1991;83:1649-1659
• Vereckei A et al. Heart Rhythm 2008;5:89-98
• Pava LF et al. J Am Coll Cardiol 2010;55:2017-2023

VT vs SVT - Brugada Criteria with ECG Explanation

The Overriding Rule

All wide-complex tachycardias (QRS >120 ms, rate >100 bpm) are VT until proven otherwise.

What Is a Wide-Complex Tachycardia (WCT)?

1. VT - impulse originates in ventricle, spreads slowly cell-to-cell without the fast conduction system
2. SVT with aberrancy - supraventricular impulse with pre-existing or rate-related bundle branch block
3. Pre-excited tachycardia (WPW antidromic / pre-excited AF) - accessory pathway bypass

ECG of Ventricular Tachycardia (Monomorphic):

Brugada 4-Step Algorithm (1991) - The Stepwise Flowchart

Flowchart (Washington Manual / Rosen's):

Criterion 1 - Absence of RS Complex in ALL Precordial Leads

Criterion 2 - R-to-S Nadir Interval >100 ms in Any Precordial Lead

Normal RS (SVT): R peak → S nadir occurs in ≤100 ms  (fast, conducted)
VT RS pattern:   R peak → S nadir takes >100 ms       (slow, cell-to-cell)

Criterion 3 - AV Dissociation

• Independent P waves "marching through" QRS complexes at a slower rate
• Capture beats - a rare narrow QRS amid the wide-complex beats when a sinus impulse successfully conducts through to the ventricles (pathognomonic for VT)
• Fusion beats - intermediate-width QRS when a sinus beat partially conducts and fuses with the ventricular beat (also pathognomonic for VT)

Three VT ECGs Showing Brugada Criteria Applied (Rosen's Emergency Medicine):

Criterion 4 - QRS Morphology Criteria for VT in V1-2 AND V6

Morphology Images (Rosen's - Criterion 4A = RBBB-like; 4B = LBBB-like):

RBBB-like WCT (V1 mainly positive)

• V1: "Wrong rabbit ear" - the FIRST hump (R) is taller than the second (R'), or no second hump at all (monophasic R)
• V6: Deep S or Q wave - ventricle depolarizing away from V6 (opposite to normal)

LBBB-like WCT (V1 mainly negative)

• V1/V2: The descent to S nadir is slow and dirty (notched, wide initial r, delayed nadir) - slow cell-to-cell spread
• V6: Any Q wave = VT. True LBBB never has a Q in V6.

Washington Manual Summary Table (LBBB vs RBBB criteria):

Additional High-Yield ECG Signs (Non-Brugada)

Concordance

Positive Concordance ECG (Symptom to Diagnosis, 4th ed.):

Extreme ("Northwest") Axis

• QRS axis between -90° and ±180° (negative in both lead I and aVF)
• "No man's land" axis - never produced by normal or BBB conduction
• Strongly favors VT

QRS Duration

• 160 ms in RBBB-like = strongly VT (LR+ 22.9 for QRS >160 ms per Symptom to Diagnosis)

• 140 ms in LBBB-like = favors VT

aVR Criterion (Vereckei 2008)

• Initial R wave in aVR alone = VT
• Initial r or q >40 ms in aVR = VT
• Used as a quick bedside single-lead check

Complete Visual Summary

WIDE COMPLEX TACHYCARDIA (QRS >120 ms, rate >100 bpm)
         ↓
STEP 1: Any RS complex in V1-V6?
    NO (all monophasic) → VT ✓
    YES → STEP 2
         ↓
STEP 2: R-to-S nadir > 100 ms in any lead?
    YES → VT ✓
    NO → STEP 3
         ↓
STEP 3: AV dissociation? (independent P waves / fusion / capture beats)
    YES → VT ✓
    NO → STEP 4
         ↓
STEP 4: VT morphology in BOTH V1-2 AND V6?
  RBBB-like: V1 = mono-R, QR, or RS(R>S) AND V6 = S dominant / QS / QR
  LBBB-like: V1/V2 = wide r ≥30ms / notched S / nadir >70ms AND V6 = any Q wave
    YES → VT ✓
    NO → SVT with aberrancy

Real-World Tips

• Rosen's Emergency Medicine, 9th ed. (Table 65.5, Fig. 65.32, 65.33, 65.36)
• Washington Manual of Medical Therapeutics (Fig. 7-2)
• Tintinalli's Emergency Medicine, 9th ed. (Table 18-22)
• Symptom to Diagnosis, 4th ed. (Fig. 31-6, 31-7)
• Original: Brugada P et al. Circulation 1991;83:1649-1659