Interpretation of ECG

VU TRAN THIEN QUAN, MD, MSC

Contents
Basic observations
ECG changes in hypertrophy of the heart
ECG changes in Myocardial Ischemia and
Infarction
ECG changes in Electrolytes disorders
ECG in Arrhythmias
Waves

T
P

Q
S
INFORMATION ON THE 12-LEAD
ECG
Basic observations
Heart Rate
Rhythm: regular? sinus?
P wave
PR intervals/segment
QRS complex/ QRS axis
QRS interval
ST segment
T wave
 Rate
1. Regular or irregular (based on DII)
Regular rare = the longest RR - the shortest RR < 4
small box (0.16 sec).
BOX METHOD
 Irregular rate
Count the number of R waves in 6 seconds (30 large
box) then multiply by 10
 Sinus Rhythm

- P waves (at a same lead) are similar.

- Each P wave is accompanied by a QRS complex.
- P (+) DII, aVF, (-) aVR.
- PR interval between 0.12 - 0.2s, constant.
- Frequency: 60-100 beats per min.
< 60 beats per min: sinus bradycardia.
> 100 beats per min: sinus tachycardia.
ECTOPIC BEATS
 P wave

- Atrial depolarization wave.

-Shape: round wave, sometimes with a hook (hook), biphasic.
-Time: 0.08 - 0.1 seconds.
-The amplitude < 2.5 mm.
-P wave (+) in I, II, aVF, V3 - V6;
(-) in aVR;
(+) / (-) / 2 phase at DIII, aVL, V1 – V2
- Wave axis: 0 - 75 degrees (similar to how to calculate QRS
axis)
31
PR interval

◦ Meaning: is the conduction time of the impulse from

the atria to the ventricles.
◦ Time: 0.12 - 0.20 seconds (Vietnamese 0.11 - 0.20
seconds).
◦ Short PR: < 0.12s (in pre-excitation syndrome)
◦ Long PR: >0.2s (in atrioventricular block)
QRS complex

◦ Time of ventricular depolarization.

◦ Time: 0.06 - 0.1 seconds.
◦ Amplitude :
◦ V1 V2 V3 V4 V5 V6
 QRS axis

◦ The axis is how to determine if the heart is depolarized in the normal

direction? (towards down and to the left).
◦ The QRS axis is the sum of the instantaneous ECG vectors during
ventricular depolarization.
To determine the mean electrical axis of the ventricles, we
use Bailey's axis system
QRS axis
 How to quickly determine the
QRS axis
DI = 0O
aVF = 90O
QRS complex

◦ Time of ventricular depolarization.

◦ Time: 0.06 - 0.1 seconds.
◦ Amplitude :
◦ V1 V2 V3 V4 V5 V6
VAT (ventricular activating time)

The beginning of the Q wave (or R wave) to the

projection of the peak of the R wave down the
isoelectric line in the precordial leads.
VAT

Normal value:
< 0.035 seconds (V1 - V2: of the right ventricle).
< 0.045 seconds (V5 - V6: of the left ventricle).
 ST segment

◦ Time: 0.12 seconds

◦ Normal: ST segment is above the isoelectric line, may
be <1mm elevation (limb lead), <2mm (precordial
lead), or <0.5mm depression (any lead)
◦ ST elevation: > 1mm (limb lead)
> 2mm (precordial lead)
◦ ST depression: > 0.5mm (any lead)
 QT interval

◦ Time: 0.35 - 0.41 seconds (Vietnamese people

0.36 - 0.40 seconds), depending on heart rate.
◦ QT changes with heart rate: QT is longer in
bradycardia and shorter in tachycardia, so it is
necessary to calculate QTc (QT adjusted for heart
rate).
◦ QTc = QT√RR
◦ Long QT: QTc > 0.44s (male)
> 0.46s (female)
QT = 15 x 0,04 = 0,6s.
RR = 21 x 0,04 = 0,84s.
QTc = QT/ √RR = 0,65s
→long QT
 T wave

Meaning: Late repolarization phase of the two ventricles.

Shape: normal T wave in the same direction as the
QRS, asymmetrical (ascending branch longer than
descending), rounded apex.
Time: 0.20 seconds
Amplitude: <5mm (limb lead )
<10mm (precordial lead)
 Rhythm

Sinus Not sinus

Morphology Supraventricular Ventricular

Contents
Basic observations
ECG changes in hypertrophy of the heart
ECG changes in Myocardial Ischemia and
Infarction
ECG changes in Electrolytes disorders
Right atrial enlargement:
DII: amplitude P > 2.5mm
Left atrial enlargement

DII: + time P > 0.11s.

+ P is camel's back with 2 peaks > 0.04s.
V1: biphasic P wave with negative phase >
0.04 mm-second.
Left ventricular enlargement

+ SoKolow - Lyon criteria:

SV1 + RV5 (V6) > 35 mm.
+ Cornell criteria:
SV3 + R aVL > 28 mm (male).
> 20 mm (female).
Right ventricular enlargement:

+ RV1 + SV5 (V6) > 10 mm ( Sokolow–Lyon)

+ R/S ratio < 1 in V5(V6)
R/S > 1 in V1.
+ RV1 > 7 mm.
+ SV5 (V6) > 7 mm.
Contents
Basic observations
ECG changes in hypertrophy of the heart
ECG changes in Myocardial Ischemia and
Infarction
ECG changes in Electrolytes disorders
 ST segment

◦ Time: 0.12 seconds

◦ Normal: ST segment is above the isoelectric line, may
be <1mm elevation (limb lead), <2mm (precordial
lead), or <0.5mm depression (any lead)
◦ ST elevation: > 1mm (limb lead)
> 2mm (precordial lead)
◦ ST depression: > 0.5mm (any lead)
 T wave

Meaning: Late repolarization phase of the two ventricles.

Shape: normal T wave in the same direction as the
QRS, asymmetrical (ascending branch longer than
descending), rounded apex.
Time: 0.20 seconds
Amplitude: <5mm (limb lead )
<10mm (precordial lead)
Coronary artery
The left circumflex coronary artery (LCX) and
its branches usually supply the posterolateral
wall of the left ventricle.
The right coronary artery (RCA) supplies the
right ventricle, the inferior (diaphragmatic) and
true posterior walls of the left ventricle, and the
posterior third of the septum.
The RCA also gives off the AV nodal coronary
artery in 85-90% of individuals; in the
remaining 10-15%, this artery is a branch of
the LCX.
Progression of wave changes
Hyperacute T wave changes - increased T wave
amplitude and width; may also see ST elevation.
Marked ST elevation with hyperacute T wave changes
(transmural injury)
Pathologic Q waves, less ST elevation, terminal T
wave inversion (necrosis) (Pathologic Q waves are
usually defined as duration >0.04 s or >25% of R-wave
amplitude)
Pathologic Q waves, T wave inversion (necrosis and
fibrosis)
Pathologic Q waves, upright T waves (fibrosis)
T wave inversion
T wave inversion may be considered to be
evidence of myocardial ischemia if:
◦ At least 1 mm deep
◦ Present in ≥ 2 continuous leads that have dominant
R waves (R/S ratio > 1)
◦ Dynamic — not present on old ECG or changing
over time
◦ NB. T wave inversion is only significant if seen in
leads with upright QRS complexes (dominant R
waves). T wave inversion is a normal variant in leads
III, aVR and V1.
T wave changes
Ventricular Repolarization (J Point)
➢Point at which the QRS wave meets the
isoelectric baseline
➢Used as a reference point in determining ST
changes
➢Measure the elevation or depression .04 to
.08 seconds after the J poin
Morphology of ST Depression
ST depression can be either upsloping, downsloping, or
horizontal (see diagram below).
Horizontal or downsloping ST depression ≥ 0.5 mm at the J-
point in ≥ 2 contiguous leads indicates myocardial
ischaemia (according to the 2007 Task Force Criteria).
ST depression ≥ 1 mm is more specific and conveys a
worse prognosis.
ST depression ≥ 2 mm in ≥ 3 leads is associated with a high
probability of NSTEMI and predicts significant mortality
(35% mortality at 30 days).
Upsloping ST depression is non-specific for myocardial
ischaemia.
 ST Segment Depression

May or may not

include T wave
inversion
 Flat ST Segment Depression

Results from
subendocardial
infarction
 ST Segment Elevation
Earliest reliable sign that myocardial infarction has
occurred
ST Segment Elevation - Pericarditis
 Pathologic Q Waves

Indicate presence of
irreversible
myocardial damage
or myocardial
infarction
Inferior MI
Pathologic Q waves and evolving ST-T
changes in leads II, III, aVF.
Q waves usually largest in lead III, next largest
in lead aVF, and smallest in lead II
Inferior MI
Inferoposterior MI
ECG changes are seen in anterior precordial leads V1-3,
but are the mirror image of an anteroseptal MI,
Increased R wave amplitude and duration (i.e., a
"pathologic R wave" is a mirror image of a pathologic Q).
R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces).
Hyperacute ST-T wave changes: i.e., ST depression and
large, inverted T waves in V1-3.
Late normalization of ST-T with symmetrical upright T
waves in V1-3.
Often seen with inferior MI (i.e., "inferoposterior MI")
Inferoposterior MI
Inferoposterior MI
Right Ventricular MI
Right Ventricular MI (only seen with proximal
right coronary occlusion; i.e., with inferior
family MI's)
ECG findings usually require additional leads
on right chest (V1R to V6R, analogous to the
left chest leads)
ST elevation, >1mm, in right chest leads,
especially V4R.
Right Ventricular MI
Anterior MI
High Lateral MI
What is the diagnosis?
MI plus LBBB
Q waves of any size in two or more of leads I, aVL, V5, or V6 (See
below: one of the most reliable signs and probably indicates
septal infarction, because the septum is activated early from the
right ventricular side in LBBB).
Reversal of the usual R wave progression in precordial leads.
Notching of the downstroke of the S wave in precordial leads to
the right of the transition zone (i.e., before QRS changes from a
predominate S wave complex to a predominate R wave complex);
this may be a Q-wave equivalent.
MI plus LBBB
Notching of the upstroke of the S wave in precordial leads to the
right of the transition zone (another Q-wave equivalent).
rSR' complex in leads I, V5 or V6 (the S is a Q-wave equivalent
occurring in the middle of the QRS complex)
RS complex in V5-6 rather than the usual monophasic R waves
seen in uncomplicated LBBB; (the S is a Q-wave equivalent).
"Primary" ST-T wave changes (i.e., ST-T changes in the same
direction as the QRS complex rather than the usual "secondary"
ST-T changes seen in uncomplicated LBBB); these changes may
reflect an acute, evolving MI.
Old MI plus LBB
Non-Q wave MI
Recognized by evolving ST-T changes over time without the formation of
pathologic Q waves (in a patient with typical chest pain symptoms and/or
elevation in myocardial-specific enzymes)
Although it is tempting to localize the non-Q MI by the particular leads
showing ST-T changes, this is probably only valid for the ST segment
elevation pattern.
Evolving ST-T changes may include any of the following patterns:
Convex downward ST segment depression only (common)
Convex upwards or straight ST segment elevation only.
Symmetrical T wave inversion only (common)
Non-Q wave MI
Differential MI pattern
WPW preexcitation (negative delta wave may
mimic pathologic Q waves)
IHSS (septal hypertrophy may make normal
septal Q waves "fatter" thereby mimicking
pathologic Q waves)
LVH (may have QS pattern or poor R wave
progression in leads V1-3)
RVH (tall R waves in V1 or V2 may mimic true
posterior MI)
Complete or incomplete LBBB (QS waves or
poor R wave progression in leads V1-3)
Differential MI pattern
Pneumothorax (loss of right precordial R waves)
Pulmonary emphysema and cor pulmonale (loss of R
waves V1-3 and/or inferior Q waves with right axis
deviation)
Left anterior fascicular block (may see small q-waves
in anterior chest leads)
Acute pericarditis (the ST segment elevation may
mimic acute transmural injury)
Central nervous system disease (may mimic non-Q
wave MI by causing diffuse ST-T wave changes
ST-elevation myocardial infarction (STEMI) – Symptoms & diagnosis

Typical symptoms of acute myocardial

infarction (AMI)
• Onset may be sudden or gradual
• Symptoms vary depending on the location of the infarct

Often described as a tightness, heaviness or constriction in the chest

Chest pain or
Usually in the centre of the chest, but radiate to neck, jaw, stomach, shoulder, back
discomfort
and arms (typically left arm)

Breathing difficulty /
Due to left ventricular dysfunction or dynamic mitral regurgitation
shortness of breath

Profuse sweating

Nausea and/or vomiting

Dizziness

Syncope Usually due to an arrhythmia or severe hypotension

Tachycardia Due to sympathetic nerve activation

Bradycardia Patients with inferior STEMI may have bradycardia due to vagus nerve activation

Cardiogenic shock Due to impaired myocardial function

Dörr. Heart 2010;96(18):1434-1435.

.
100
ST-elevation myocardial infarction (STEMI) – Symptoms & diagnosis

Diagnostic criteria for AMI

Any one of the following criteria meets the diagnosis for AMI
according to the Joint ESC/ACCF/AHA/WHF Task Force:

• Symptoms of ischaemia
A rise and/or fall of cardiac • New or presumed-new significant ST-segment-T wave
biomarkers (preferably troponin (ST-T) changes or new left bundle branch block (LBBB)
(cTn)) with at least one value
above the 99th percentile upper
reference limit (URL) together with
+ • Development of pathological Q waves in the ECG
• Imaging evidence of new loss of viable myocardium or
new regional wall motion abnormality
at least one of the following: • Identification of an intracoronary thrombus by angiography
or autopsy

Cardiac death with prior new ischaemic ECG changes and symptoms suggestive of myocardial
ischaemia, without definitive biomarker evidence

PCI-related MI*

Stent thrombosis associated with MI*

Coronary artery bypass grafting (CABG)-related MI*

*See notes

Thygesen et al. J Am Coll Cardiol 2012;60(16):1581-1598.

101
 1
ST-elevation myocardial infarction (STEMI) – Symptoms & diagnosis 0
2

Diagnosis of STEMI: ECG changes

• ST-segment elevation with pathological Q-wave formation

• Sometimes T-wave inversion may be found but it is a non-specific feature
• ST-segment elevation indicates full thickness cardiac muscle injury, pathological Q-
wave indicates muscle necrosis and T-wave inversion indicates muscle ischaemia

QRS QRS QRS QRS

Segment Segment Segment Segment

R R R R
T-wave
ST Elevation ST depression inversion
ST ST
PR Segment PR PR PR Segment
Segment Segment Segment Segment

P T P P T P

Q Q Q Q
PR Interval
S S S
QT Interval

Normal ECG STEMI NSTEMI NSTEMI

ST-elevation myocardial infarction (STEMI) – Symptoms & diagnosis

Diagnosis of STEMI

• Troponin is the preferred biomarker for

Cardiac markers diagnosis

• Elevation of white blood cell count is usual

Full blood count • Erythrocyte sedimentation rate (ESR) and
C-reactive protein (CRP) may be elevated

Chest X-ray • For assessing pulmonary oedema

• Not essential, but helpful if ECG is

Echocardiography inconclusive

O’Gara et al. J Am Coll Cardiol 2013;61(4):e78-e140.

.
103
ST-elevation myocardial infarction (STEMI) – Symptoms & diagnosis

STEMI types defined by ECG changes

STEMI Occluded Prognosi
Area affected ECG findings
type vessel s
Reciprocal ST-
ST segment
segment
elevation
depression
Inferior leads II, III and
Anterior Anterior wall of LV LAD branch of LCA Leads V1 – V6 Poor
aVF

Area between LV and Inferior leads II, III and

Antero-septal LAD septal branches Leads V1 – V4 --
RV aVF)

1st diagonal branch of

Leads I, aVL, V5 and Inferior leads II, III and
Lateral Lateral wall of LV LAD and obtuse --
V6 aVF
marginal branch of LCX

Superior portion of 1st diagonal branch of Inferior leads II, III and
High lateral Leads I and aVL --
the lateral wall of LV LAD aVF

Anterior and lateral Proximal LAD or LAD + Leads I, aVL, V4 – Inferior leads II, III and
Antero-lateral --
wall of LV LCX V6 aVF

Inferior Inferior wall of LV RCA Leads II, III and aVF Leads I and aVL Gooda

Posterior descending Leads V7 – V9

Posterior Posterior part of LV --
artery (posterior leads)b

Right sided chest

RV infarctionc --
leads (V3 R– V6 R).

LV, left ventricle; RV, right ventricle; LAD, left anterior descending artery; LCX, left circumflex artery; LCA, left coronary artery; RCA, right
coronary artery. a ~40% of these patients have a concomitant RV infarction and a poor prognosis; b Not directly visualised by the
standard 12-lead ECG – must be confirmed by 15-lead ECG; C RV infarction is uncommon.

104
Contents
Basic observations
ECG changes in hypertrophy of the heart
ECG changes in Myocardial Ischemia and
Infarction
ECG changes in Electrolytes disorders
ECG Changes in Hypercalcaemia
The main ECG abnormality seen with
hypercalcaemia is shortening of the QT interval
In severe hypercalcaemia, Osborn waves (J
waves) may be seen
Ventricular irritability and VF arrest has been
reported with extreme hypercalcaemia
ECG changes in Hypocalcaemia
Hypocalcaemia causes QTc prolongation
primarily by prolonging the ST segment
The T wave is typically left unchanged
Dysrhythmias are uncommon, although atrial
fibrillation has been reported
Torsades de pointes may occur, but is much
less common than with hypokalaemia or
hypomagnesaemia
Torsades de pointes
ECG features of hyperkalaemia
Hyperkalaemia is defined as a serum
potassium level of > 5.2 mmol/L.
ECG changes generally do not manifest until
there is a moderate degree of hyperkalaemia
(≥ 6.0 mmol/L).
The earliest manifestation of hyperkalaemia is
an increase in T wave amplitude.
ECG features of hyperkalaemia
Peaked T waves
P wave widening/flattening, PR prolongation
Bradyarrhythmias: sinus bradycardia, high-
grade AV block with slow junctional and
ventricular escape rhythms, slow AF
Conduction blocks (bundle branch block,
fascicular blocks)
QRS widening with bizarre QRS morphology
ECG features of hyperkalaemia
With worsening hyperkalaemia… (> 9.0
mmol/L):
◦ Development of sine wave appearance (pre-terminal
rhythm)
◦ Ventricular fibrillation
◦ PEA with bizarre, wide complex rhythm
◦ Asystole
ECG features of hyperkalaemia
The push-pull effect
ECG features of hypokalaemia
Hypokalaemia is defined as a serum
potassium level of < 3.5 mmol/L.
ECG changes generally do not manifest until
there is a moderate degree of hypokalaemia
(2.5-2.9 mmol/L).
The earliest ECG manifestation of
hypokalaemia is a decrease in T wave
amplitude.
ECG features of hypokalaemia
Increased P wave amplitude
Prolongation of PR interval
Widespread ST depression and T wave
flattening/inversion
Prominent U waves (best seen in the
precordial leads V2-V3)
Apparent long QT interval due to fusion of T
and U waves (= long QU interval)
ECG features of hypokalaemia
With worsening hypokalaemia…
◦ Frequent supraventricular and ventricular
ectopics
◦ Supraventricular tachyarrhythmias: AF, atrial
flutter, atrial tachycardia
◦ Potential to develop life-threatening
ventricular arrhythmias, e.g. VT, VF and
Torsades de Pointes
Arrhythmia
 Objectives
 Define bradyarrhythmia and tachyarrythmia

 Know the most common brady- & tachyarrythmias

 Recognise them on an ECG.

 Know the main signs and symptoms, aetiology and

treatments of each.
THE IDENTIFICATION OF RHYTHM
ABNORMALITIES
1. Is the abnormality occasional or sustained?
2. Are there any P waves?
3. Are there as many QRS complexes as P
waves?
4. Are the ventricles contracting regularly or
irregularly?
5. Is the QRS complex of normal shape?
6. What is the ventricular rate?
Recognizing ECG abnormalities
Types of bradyarrhythmia
Sinus Bradycardia
 HR < 60bpm
 Causes
◦ Physiological (normal in athletic people)
◦ Iatrogenic (Beta blockers, Ca channel blockers, digoxin, anticholinergics)
◦ Hypothyroidism
◦ Metabolic e.g. hyperkalemia
◦ Hypoxia
◦ Hypothermia
◦ Acute MI/ischemia

 Treatment
◦ Remove cause (ie drugs)
◦ Treat cause (ie hypothyroidism)
 1st degree AV node block
 PR interval >0.2secs (more than 5 small squares)
 Delayed conduction through/near the AVN
 Usually asymptomatic
 Narrow QRS complex indicates block within AVN
 Wide QRS complex indicates His-Purkinje block.
 Causes
◦ MI
◦ Myocarditis/endocarditis
◦ SLE

 Treatment
◦ Usually benign
◦ Can progress to other forms of AV block
◦ If symptomatic, consider pacemaker
Mobitz type 1 (Wenkebach)
 PR interval progressively lengthens until a P wave is not
followed by a QRS complex.
 Continues as a cycle.
 Due to a conduction defect within the AVN
 Causes:
◦ Inferior MI
◦ Drugs
◦ Myocarditis

 Treatment
◦ None required (unless reversible cause)
Mobitz type 2
 Intermittent non-conducting P waves.
 May occur in regular pattern e.g. every 3rd p
wave is not followed by a QRS complex (3:1
block)
 Causes
◦ Anterior MI
◦ Inflammatory (rheumatic fever, myocarditis)
◦ Autoimmune (SLE, systemic sclerosis)
◦ Hyperkalaemia
◦ Infiltration (sarcoid, haemochromatosis, amyloid)

 Treatment
◦ Internal pacing eventually as likely to progress to 3rd degree heart block
Complete AV block
 Complete dissociation between atrial &
ventricular depolarisations
 All impulses from atria blocked by the AVN
 Very symptomatic & very syncopal.
 Causes
◦ Inferior MI
◦ Drugs (ca channel blockers, beta blockers, digoxin)
◦ Progression of Mobitz 1 & II
◦ Congenital (if mother has SLE)
◦ Lev's disease: idiopathic fibrosis & calcification of conducting system

 Treatment
◦ Internal pacing
Adult Bradycardia Algorithm
 Sinus tachycardia
 HR > 100bpm
 Causes:
Intra-cardiac causes Extra-cardiac causes
Ishcaemic heart disease •Drugs
Valvular heart disease •Alcohol
Heart failure •Stimulants e.g. caffeine
Cardiomyopathy •Stress
Congenital heart disease •Hyperthyroidism
•Infection/Sepsis
 Treatment
 Treat the cause.
Broad and Narrow Complex tachycardias
 Broad Complex Tachyarrhythmias
Ventricular Tachycardia
Torsades de Pointes
Ventricular Fibrillation

 Narrow Complex Tachyarrhythmias

(Supraventricular Tachycardias)
Sinus Tachycardia
Atrial Tachycardia
Reentrant Tachycardias (AVNRT and AVRT)
Atrial Fibrillation
Atrial Flutter
 Atrial Flutter
 SVT, regular
 Saw-tooth flutter waves.
 Flutter waves rate = 300 bpm
 Ventricular rate = 150 bpm or 100 bpm, due to AVN block ratio of 2:1
or 3:1
 Ectopic atrial beat causes a re-entrant circuit within the atria.
 Causes
 As for AF
 Hyperkalaemia
 Digoxin toxicity.
 Treatment
 As for AF (discussed later)
 Can be differentiated from Fast AF with vagal manouvres/adenosine.
 Ventricular tachycardia
Broad complex tachycardia
Causes
◦ Electrolyte derangement (hypokalaemia, hypomagnesaemia,
hypocalcaemia)
◦ Myocardial ischaemia/infarct
◦ Cardiomyopathy
◦ Congenital (HOCM, long QT)

Treatment
◦ Amiodarone
◦ ICDs
 Atrial Fibrillation
Atria chaotically fibrillate.
Fibrillation rate between 350 & 600bpm.
Variable impulse conduction through the AVN
Irregularly irregular rhythm
Most common arrhythmia.
10% of population >80 years old.
Significant morbidity due to thromboembolic disease
Unmanaged = 5% yearly stroke risk.
 Atrial Fibrillation
 Types
Paroxysmal (acute onset, spontaneous termination within 1 week)
Persistent (>7 days, can be cardioverted)
Permanent (> 1 year not terminated by cardioversion)

 Causes
Cardio (HTN, valvular disease, CAD, myositis)
Pulmonary (PE, pneumonia, COPD, lung Ca)
Metabolic (hyperthyroidism)
Infection
Drugs (alcohol, illicit drugs)
 AF
 Investigations
 Bedside – ECG/24 hour tape
 Bloods – FBC, U&Es, LFTs, TFTs, coag screen
 Imaging – CXR, echo

 Management (Rate vs Rhythm)

 Rate –
 Beta blockers
 Digoxin

 Rhythm
 Cardioversion
 Sotalol
 Amiodarone (HF)
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