Ectopic atrial rhyghms seen in

Ectopic atrial rhythms arise from foci outside the sinoatrial node firing spontaneously. They are seen in:

Digitalis toxicity
Chronic obstructive pulmonary disease (COPD) / cor pulmonale
Electrolyte disturbances (hypokalemia, hypomagnesemia)
Structural heart disease (mitral valve disease, cardiomyopathy)
Hypoxia / hypercapnia
Alcohol use ("holiday heart")
Caffeine or stimulant excess
Post-cardiac surgery
Rheumatic heart disease

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Now let me also check for the etiology/causes section in the Family Medicine textbook, which had a very relevant mention of digitalis and lung/heart disease:

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Here is a complete, textbook-sourced answer on ectopic atrial rhythms:

Ectopic Atrial Rhythms

Definition

An ectopic atrial rhythm is a nonsinus atrial rhythm arising from a single focus outside the sinoatrial (SA) node, producing a single, consistent P wave morphology that differs from normal sinus P waves (i.e., P waves are not upright in leads I, II, and III). Rate is typically <100 bpm but faster than sinus rhythm. When the rate exceeds 100 bpm, it is called ectopic atrial tachycardia.

A wandering atrial pacemaker is a related condition with at least three distinct P wave morphologies at rates between 50-100 bpm, indicating multiple shifting ectopic foci.

Goldman-Cecil Medicine, p. 566; Textbook of Family Medicine 9e, p. 720

Seen In (Clinical Associations)

Category	Specific Causes
Drug toxicity	Digitalis (digoxin) toxicity - a classic cause
Pulmonary/Lung disease	COPD, cor pulmonale, hypoxia, hypercapnia
Heart disease	Rheumatic heart disease, cardiomyopathy, mitral valve disease, hypertrophic cardiomyopathy
Electrolyte disturbance	Hypokalemia, hypomagnesemia
Exogenous stimulants	Caffeine, tobacco, alcohol excess, sympathomimetic drugs
Structural/extrinsic	Extrinsic compression of the atrium by adjacent abnormal structures
Normal variant	Can be seen in otherwise healthy individuals - often asymptomatic
Sick sinus syndrome	SA node abnormally susceptible to suppression by ectopic atrial activity; ectopic rhythms emerge as escape

Textbook of Family Medicine 9e, p. 719-720; Bradley and Daroff's Neurology in Clinical Practice

ECG Findings

The P wave morphology is abnormal (not upright in limb leads I, II, III); P-P intervals are approximately equal; QRS is typically narrow unless aberrant conduction is present.

ECG showing ectopic atrial rhythm at 85 bpm with negative P waves in lead II, replaced transiently by sinus rhythm

ECG: Ectopic atrial rhythm at 85 beats/min with negative P waves in lead II, replaced by slower sinus rhythm (upright P waves) mid-strip, then returning at the end. - Textbook of Family Medicine 9e, Fig. 27-39

Clinical Features

Usually asymptomatic - often incidentally found on routine ECG or Holter monitoring
Rarely, a very slow ectopic rhythm causes fatigue
Incessant rapid ectopic atrial tachycardia can lead to tachycardia-induced (rate-related) cardiomyopathy
In Wolff-Parkinson-White (WPW) syndrome or severe structural heart disease (e.g., HCM), a supraventricular arrhythmia can rarely precipitate cardiac arrest

Key Distinction from PACs

Multiple sequential PACs can mimic ectopic atrial rhythm. A consistent P wave morphology and regular P-P intervals distinguish a sustained ectopic atrial rhythm from sequential PACs. - Goldman-Cecil Medicine, p. 566

Treatment

Asymptomatic: No specific treatment required
Symptomatic/rapid: Beta-blockers or calcium channel blockers to reduce ectopy and slow ventricular response
Incessant tachycardia with cardiomyopathy: Class Ia, Ic, or III antiarrhythmics; catheter ablation may be needed
Very slow ectopic rhythm causing fatigue: Atrial pacing at a rate faster than the ectopic rhythm

Rsr pattern in v1 v2

An RSR' pattern in V1-V2 (a small r, deep S, then a second r' "rabbit ear" pattern) is classically associated with right bundle branch block (RBBB), but has several important causes.

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Here is a complete, textbook-sourced breakdown of the RSR' pattern in V1-V2:

RSR' Pattern in V1-V2

The RSR' (also written rSR', rsR', or "M-shaped" / "rabbit ears") pattern in leads V1-V2 reflects delayed right ventricular activation - the terminal QRS vector is oriented to the right and anteriorly, producing the characteristic double-peak in V1.

Causes (Most to Least Common)

1. Normal Variant / Incomplete RBBB

An RSR' with QRS < 120 ms and R' amplitude NOT greater than the initial R wave = incomplete RBBB, which is a normal finding in young individuals and athletes
Right ventricular conduction delay (RVCD) is more frequent in people under 21 years and in athletes
Does not necessarily progress to complete RBBB
Pfenninger and Fowler's Procedures for Primary Care, p. 4340

2. Complete Right Bundle Branch Block (RBBB)

QRS ≥ 120 ms, rSR' in V1, wide terminal S wave in V5-V6
The terminal QRS vector shifts right and anteriorly due to delayed right ventricular depolarization
Occurs in:
- No structural disease (most common for RBBB vs LBBB)
- Congenital heart disease - especially atrial septal defect (ASD)
- Acquired heart disease - valvular, ischemic, cor pulmonale, myocarditis
- Trauma to the right bundle
Harrison's Principles of Internal Medicine 22E, p. 1915; Pfenninger and Fowler, p. 4340

3. Atrial Septal Defect (ASD)

A classic association - both incomplete and complete RBBB patterns with RSR' in V1 are seen
Due to right ventricular volume overload from left-to-right shunting
Fixed splitting of S2 is the clinical clue
Harrison's 22E; Pfenninger and Fowler

4. Brugada Pattern / Brugada Syndrome

Type 1 (diagnostic): Coved ST elevation ≥ 2 mm in V1-V2, downsloping, followed by T-wave inversion - the rSR'/Rsr' is part of this pattern
Type 2: Saddle-back ST elevation with RSR' - not diagnostic alone
Associated with risk of polymorphic VT/VF and sudden cardiac death in structurally normal heart
Harrison's 22E - "a Brugada pattern of Rsr' with ST elevation in leads V1 or V2"

5. Right Ventricular Hypertrophy (RVH)

RSR' in V1 with R' > 15 mm in infants or > 10 mm in children (after 1st year of life)
Seen in: pulmonary hypertension, COPD, pulmonary valve stenosis, Eisenmenger syndrome
Tintinalli's Emergency Medicine

6. Pulmonary Embolism (Acute)

Acute right heart strain can produce transient RSR' or incomplete RBBB in V1
Part of the S1Q3T3 pattern constellation (though RSR' may appear alone)
Pfenninger and Fowler: "Any pulmonary disease process can be associated with RVCD, and RVCD can occur acutely with exacerbation of lung disease or pulmonary embolus"

7. Posterior Wall MI

Posterior MI produces increased R wave in V1-V2 (reciprocal change), which can mimic RSR' morphology
The R/S ratio in V1 becomes ≥ 1 with ST depression

8. Wolff-Parkinson-White (WPW) - Left-sided Accessory Pathway

Left-sided pathways produce a dominant R in V1 that can superficially resemble RSR'
Delta wave and short PR distinguish this

9. Hyperkalemia / Drug Toxicity

Class Ia antiarrhythmics, tricyclic antidepressants, phenothiazines can slow right ventricular conduction and produce intraventricular conduction delay resembling RBBB pattern
Harrison's 22E, p. 1916

Quick Memory Summary

QRS Duration	Pattern	Think of
< 120 ms, small R'	Incomplete RBBB / RVCD	Normal variant, athlete, ASD, pulmonary disease
≥ 120 ms	Complete RBBB	Organic heart disease, congenital, ischemia
RSR' + ST elevation (coved) V1-V2	Brugada Type 1	Sudden death risk - refer urgently
RSR' + right axis + fixed S2 split	ASD	Echo + bubble study
RSR' + acute dyspnea/hypoxia	Acute cor pulmonale / PE	CT-PA / V-Q scan

Key point from Harrison's 22E: "A distinctive abnormality simulating right bundle branch block with ST-segment elevations in the right chest leads is seen with the Brugada pattern" - this must always be distinguished from benign RBBB.

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