CLIX ECG TUTORIAL

Part 3: Ischaemic Heart Disease; Pericarditis;

Embolism; Electrolyte Disturbances; Digoxin
CORONARY ARTERY AREAS OF SUPPLY
 CORONARY ARTERY AREAS OF SUPPLY

Knowledge of the area of myocardium which is perfused by each of the three major
coronary arteries is helpful in determining the site of vascular obstruction when an
individual has sustained a myocardial infarct.
 LEFT ANTERIOR DESCENDING
The LAD supplies the following areas:
 
▫ Anterior wall of LV, apex (V4), lower part of lateral LV (V5, V6) (Diagonal
branch)
▫ Anterior ⅔ ventricular septum (V1 – V4) (Septal perforator)
 LEFT CIRCUMFLEX ARTERY
The LCX generally only supplies:
 
▫ Left atrium
▫ Upper part of the lateral wall of LV (Std I, aVL)
▫ Posterior LV (V7 – V9) and inferior LV (Std II, III, aVF) in 15% of individuals
 RIGHT CORONARY ARTERY
The Right Coronary Artery (RCA) supplies:
 
▫ Right atrium
▫ Virtually entire right ventricle (RV) V1, V3R-V6R
▫ Posterior ⅓ ventricular septum
▫ Postero-inferior LV in 85 % individuals
 BLOOD SUPPLY TO CONDUCTING
SYSTEM:

SA node RCA 75%, dual 25%

 
AV node RCA 80%, left 10%, dual 10%
 
Bundle of hisLCA 75%, RCA 10%, dual 15%
 
Left anterior fascicle LAD
 
Left posterior fascicle Dual
 
Right bundle LCA
 IN SUMMARY
LCA supplies:
 
Most of LV and left atrium
Conducting system below AV node
May contribute to SA and AV nodes
 
RCA supplies:
 
Most of RV and right atrium
Inferior and posterior LV (85% of population)
SA and AV nodes
Contributes to conducting system below AV node
FREQUENCY OF OCCLUSION OF CORONARY ARTERIES
IN ISCHAEMIC HEART DISEASE:

• LAD 40 – 50% (antero-septal/antero-lateral/extensive anterior MI)

• RCA 30 – 40% (inferior MI, often with posterior wall involvement, and in
≤40%, right ventricle)

• LCX 15 – 20% (lateral MI, with postero-inferior involvement in 15%)

Osmosis video: Myocardial Infarction (12 mins):

https://youtu.be/2kLlhlsesRQ
 EXTENT OF AN INFARCT

• Cross section of the left ventricle showing the difference between a

subendocardial infarct, which involves the inner half of the ventricular
wall, and a transmural infarct, which involves the full thickness of the
wall.
 ST SEGMENT CHANGES IN SUB-ENDOCARDIAL AND TRANSMURAL INFARCTION

A With acute subendocardial ischaemia the electrical forces (arrows) responsible for the
ST segment are deviated toward the inner layer of the heart, causing ST depressions in
lead V5, which faces the outer surface of the heart. B With acute transmural ischaemia,
electrical forces (arrows) responsible for the ST segment are deviated toward the outer
layer of the heart, causing ST elevations in the overlying lead. 
Detailed explanation for ST and T wave changes:
http://www.cvphysiology.com/CAD/CAD012
ST SEGMENT ELEVATION ISCHAEMIA AND
MYOCARDIAL INFARCTION
The earliest ECG changes seen with an acute transmural infarction usually
occur in the ST-T complex in two sequential phases.

▫ The acute phase is marked by the appearance of ST segment elevations

and sometimes tall positive (hyperacute) T waves. Reciprocal ST
depressions may occur in leads whose positive poles are directed 180
degrees from those showing ST elevation.

▫ The evolving phase occurs hours or days later and is characterised by

deep T wave inversions in the leads that previously showed ST elevations.
STEMI ECG SEQUENCE
STEMI ECG SEQUENCE
 LOCATION OF A MYOCARDIAL INFARCT

Myocardial infarctions are generally localised to either

(A) the anterior portion of the left ventricle (LV) or
(B) the inferior (diaphragmatic) or infero-posterior portion of the walls of this
chamber. 
Unless otherwise specified, the description of a myocardial infarct applies to
infarction of an area of left ventricular myocardium (isolated right ventricular
infarction is uncommon and generally occurs in conjunction with an inferior MI,
caused by proximal occlusion of the RCA).
Isolated posterior infarction is uncommon.
LOCATION OF A MYOCARDIAL INFARCTION
* The lower part of the lateral left
ventricle is sometimes supplied by
the left circumflex or by the right
coronary artery
 
**Lead aVR shows reciprocal ST
elevation when there is extensive ST
depression in many leads e.g. in a
sub-endocardial MI due to left main
coronary artery/LAD stenosis or
triple vessel disease or ST
depression from another cause e.g.
LVH.
 SUPPLY TO THE LATERAL WALL
OF THE LEFT VENTRICLE
The coronary vascular supply of the lateral wall of the LV varies – the diagonal
branch of LAD supplies a variable amount of the lower part of the lateral wall;
the LCX often supplies the upper part of the lateral wall, but may also supply the
lower part. Occasionally, the RCA may extend right around the back of the heart
and contribute to the blood supply of the lateral wall of LV.
  
LEADS SHOWING ECG CHANGES ACCORDING TO THE SITE OF INFARCTION

Standard leads II, III, and aVF (↑ST) inferior

V1, V3R – V5R (↑ST) right ventricle
V1 – V4 (Prominent R waves and ↓ST) posterior

V7 – V9 (Q waves and ↑ST) posterior

V1 – V4 (loss of r waves → QS waves, ↑ST) antero-septal (V1–
V2=septum; . V3–
V4=anterior)
V5 – V6 lower part lateral wall
Std I, aVL upper part lateral wall
 SHAPE OF ST ELEVATION

The ST segment elevation seen with acute MI may have different shapes, including:
 
∙ plateau shaped
∙ dome shaped
∙ oblique elevation
∙ resemblance to a tombstone
 ANTERIOR STEMI
Anterior STEMI results from occlusion of the left anterior descending artery
(LAD). Anterior myocardial infarction carries the worst prognosis of all
infarct locations, mostly due to larger infarct size.
ST segment elevation with Q wave formation in the precordial leads (V1-6)
± the high lateral leads (I and aVL).
Reciprocal ST depression in the inferior leads (mainly III and aVF).
NB. The magnitude of the reciprocal change in the inferior leads is
determined by the magnitude of the ST elevation in I and aVL (as these
leads are electrically opposite to III and aVF), hence may be minimal or
absent in anterior STEMIs that do not involve the high lateral leads. 
 ANTERIOR STEMI
The different infarct patterns are named according to the leads with
maximal ST elevation:

Septal = V1-2
Anterior = V2-5
Anteroseptal = V1-4
Anterolateral = V3-6, I + aVL
Extensive anterior  / anterolateral = V1-6, I + aVL

NB. While these definitions are intuitive, there is often a poor correlation
between ECG features and precise infarct location as determined by imaging
or autopsy.
 ANTERIOR STEMI

ST elevation is maximal in the anteroseptal leads (V1-4). Q waves are present in the septal leads (V1-2).
There is also some subtle STE in I, aVL and V5, with reciprocal ST depression in lead III. There are
hyperacute (peaked ) T waves in V2-4. These features indicate a hyperacute anteroseptal STEMI
 INFERIOR STEMI
Inferior MIs account for 40-50% of all myocardial infarctions.

Generally have a more favourable prognosis than anterior myocardial

infarction (in-hospital mortality only 2-9%), however certain factors indicate
a worse outcome.
Up to 40% of patients with an inferior STEMI will have a concomitant right
ventricular infarction. These patients may develop severe hypotension in
response to nitrates and generally have a worse prognosis.
Up to 20% of patients with inferior STEMI will develop significant
bradycardia due to second- or third-degree AV block. These patients have
an increased in-hospital mortality (>20%).
Inferior STEMI may also be associated with posterior infarction, which
confers a worse prognosis due to increased area of myocardium at risk.
 INFERIOR STEMI
How to recognise an inferior STEMI
-ST elevation in leads II, III and aVF
-Progressive development of Q waves in II, III and aVF
-Reciprocal ST depression and T wave inversion in aVL (± lead I, V1, V2)

• The vast majority (~80%) of inferior STEMIs are due to occlusion of the
dominant right coronary artery (RCA). Less commonly (around 18% of the
time), the culprit vessel is a dominant left circumflex artery (LCx).
 INFERIOR STEMI

Hyperacute (peaked) T waves in II, III and aVF with relative loss of R wave height. Early ST elevation and Q-
wave formation in lead III. Reciprocal ST depression and T wave inversion in aVL. ST elevation in lead III >
lead II suggests an RCA occlusion; the subtle ST elevation in V4R would be consistent with this.
 POSTERIOR STEMI
Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the
context of an inferior or lateral infarction.
Isolated posterior MI is less common (3-11% of infarcts).
Posterior extension of an inferior or lateral infarct implies a much larger area of
myocardial damage, with an increased risk of left ventricular dysfunction and
death.
Isolated posterior infarction is an indication for emergency coronary reperfusion.
However, the lack of obvious ST elevation in this condition means that the
diagnosis is often missed.

Be vigilant for evidence of posterior MI in any patient with an inferior or lateral

STEMI.
https://youtu.be/A6VZNVc4SdI
https://youtu.be/_XnxAvXVJgs
 POSTERIOR STEMI
Posterior infarction is confirmed by the presence of ST elevation and
Q waves in the posterior leads (V7-9).

As the posterior myocardium is not directly visualised by the standard 12-lead

ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3. 
Posterior MI is suggested by the following reciprocal changes in V1-
3:
Horizontal ST depression
Tall, broad R waves (>30ms)
Upright T waves
Dominant R wave (R/S ratio > 1) in V2

In patients presenting with ischaemic symptoms, horizontal ST depression in

the anteroseptal leads (V1-3) should raise the suspicion of posterior MI.
 INFEROLATERAL STEMI.

Posterior extension is suggested by: Horizontal ST depression in V1-3; Tall, broad R waves (>
30ms) in V2-3; Dominant R wave (R/S ratio > 1) in V2; Upright T waves in V2-3
 THE SAME PATIENT, WITH POSTERIOR LEADS RECORDED:

Marked ST elevation in V7-9 with Q-wave formation confirms involvement of the posterior
wall, making this an inferior-lateral-posterior STEMI (= big territory infarct!).
 RIGHT VENTRICULAR
INFARCTION
Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated
RV infarction is extremely uncommon.
Patients with RV infarction are very preload sensitive (due to poor RV
contractility) and can develop severe hypotension in response to nitrates
or other preload-reducing agents.
Hypotension in right ventricular infarction is treated with fluid loading, and
nitrates are contraindicated.

The ECG changes of RV infarction are subtle and easily missed!

https://youtu.be/4p-Tc-tnQoo
 RIGHT VENTRICULAR
INFARCTION
Right ventricular infarction is confirmed by the presence of ST elevation in
the right-sided leads (V3R-V6R).

In the standard 12 lead ECG The first step to spotting RV infarction is to suspect
it… in all patients with inferior STEMI! In patients presenting with inferior STEMI,
right ventricular infarction is suggested by the presence of:
ST elevation in V1 – the only standard ECG lead that looks directly at the right
ventricle.
ST elevation in lead III > lead II  – because lead III is more “rightward facing”
than lead II and hence more sensitive to the injury current produced by the right
ventricle.
Other useful tips for spotting right ventricular MI:
ST elevation in V1 > V2.
ST elevation in V1 + ST depression in V2 (= highly specific for RV MI).
Isoelectric ST segment in V1 with marked ST depression in V2.
 RIGHT VENTRICULAR INFARCTION

Inferior STEMI. Right ventricular infarction is suggested by:

-ST elevation in V1
-ST elevation in lead III > lead II
 RIGHT VENTRICULAR INFARCTION

Repeat ECG of the same patient with V4R electrode position:

There is ST elevation in V4R consistent with RV infarction
NON-ST-ELEVATION ACUTE CORONARY SYNDROME
Non-ST-elevation acute coronary syndrome (NSTEACS) encompasses two main entities:
-Non-ST-elevation myocardial infarction (NSTEMI).
-Unstable angina pectoris (UAP).

The differentiation between these two conditions is usually retrospective, based on the
presence/absence of raised cardiac enzymes at 8-12 hours after the onset of chest pain.
Both produce the same spectrum of ECG changes and symptoms and are managed
identically in the Emergency Department.
 NSTEACS: PATTERNS OF MYOCARDIAL ISCHAEMIA
Two main ECG patterns associated with NSTEACS:
ST segment depression
T wave flattening or inversion

While there are numerous conditions that may simulate myocardial

ischaemia (e.g. left ventricular hypertrophy, digoxin effect), dynamic ST
segment and T wave changes (i.e. different from baseline ECG or
changing over time) are strongly suggestive of myocardial ischaemia.

Other ECG patterns of ischaemia

Pseudonormalisation of previously inverted T waves (i.e. becoming
upright).
Another, less well-known ECG feature of myocardial ischaemia (NSTEACS,
STEMI or Prinzmetal’s) is U-wave inversion.
 NSTEACS PATTERNS

U-wave inversion V5 and V6

 NSTEACS

ST depression due to subendocardial ischaemia is usually widespread — typically present in leads I, II,
V4-6 and a variable number of additional leads. A pattern of widespread ST depression plus ST elevation
in aVR > 1 mm is suggestive of left main coronary artery occlusion. ST depression localised to a
particular territory (esp. inferior or high lateral leads only) is more likely to represent reciprocal change
due to STEMI. The corresponding ST elevation may be subtle and difficult to see, but should be sought.
 NSTEACS: T WAVE INVERSION

T wave inversion may be considered to be evidence of myocardial

ischaemia 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.
 NSTEACS: T WAVE INVERSION

Widespread T wave inversion due to myocardial ischaemia (most prominent in the lateral leads)
 PRINZMETAL’S ANGINA
Prinzmetal's angina, often referred to as "variant" angina, is a temporary
increase in coronary vascular tone (vasospasm) causing a marked, but
transient reduction in luminal diameter. This coronary vasospastic state is
usually focal at a single site and can occur in either a normal or diseased
vessel. Patients are predominantly younger women who may not have the
classical cardiovascular risk factors (except for cigarette use).
PVA has been associated with vasospastic disorders such as Raynaud's
phenomenon and migraine headaches. Arrhythmias are common and may
be life threatening especially when the effects of vasospasm are seen in
those ECG leads that reflect the potential variations of the epicardial
surface of the left ventricle. Pain often occurs in clusters, at rest and at
night, rather than on exertion.
ECG shows ST segment elevation which returns to normal when pain
resolves. There may be a small troponin rise, especially with long attacks.
Treatment is with nitrates and calcium channel blockers, pending
angiography.
 PRINZMETAL’S ANGINA
• Angina attacks are usually short in duration (2-5 minutes, but sometimes
only 30 sec) and may recur in clusters of more episodes within 20-30
minutes. Angina usually responds promptly to sublingual nitrates and may
show a circadian pattern with a prevalence in the early morning or nocturnal
hours. Effort tolerance is typically well preserved, but exercise may induce
spasm in about one fourth of patients. Variant angina may present “hot
phases”, with frequent recurrence of angina, alternated to “cold phases”,
with remission of symptoms for weeks or months.
•
The diagnosis can be confirmed by recording transient ST-segment elevation
(>1 mm) on the ECG during angina. When it is difficult to obtain 12-lead
ECG during pain, the diagnosis can often be achieved by ambulatory ECG
recording of 24 or more hours, which frequently reveals the presence of
silent ischemic episodes, representing 75-80% of all ischemic attacks.
PRINZMETAL’S ANGINA
TAKOTSUBO CARDIOMYOPATHY*
 TAKOTSUBO CARDIOMYOPATHY
A STEMI mimic producing ischaemic chest pain, ECG changes +/- elevated
cardiac enzymes with characteristic regional wall motion abnormalities on
echocardiography.
Typically occurs in post-menopausal women in the context of severe
emotional distress (“broken heart syndrome”).
Patients have normal coronary arteries on angiography.
Originally described in Japan within the last 20 years, Takotsubo has
become increasingly recognised, possibly in no small part due to the
increased use of angiography in cardiology.
Mayo Clinic Criteria for takotsubo cardiomyopathy (widely but not universally accepted):
-New ECG changes (ST elevation or T wave inversion) or moderate troponin rise.
-Transient akinesis / dyskinesis of left ventricle (apical and mid-ventricular segments) with
regional wall abnormalities extending beyond a single vascular territory.
-Absence of coronary artery stenosis >50% or culprit lesion.
 ACUTE PERICARDITIS
Pericarditis overview
• Inflammation of the pericardium (e.g. following viral infection) produces characteristic chest pain
(retrosternal, pleuritic, worse on lying flat, relieved by sitting forward), tachycardia and dyspnoea.
• There may be an associated pericardial friction rub or evidence of a pericardial effusion.
• Widespread ST segment changes occur due to involvement of the underlying epicardium (i.e.
myopericarditis).

Causes of Pericarditis
• Infectious – mainly viral (e.g. coxsackie virus); occasionally bacterial, fungal, TB.
• Immunological – SLE, rheumatic fever
• Uraemia
• Post-myocardial infarction / Dressler’s syndrome
• Trauma
• Following cardiac surgery (post pericardiotomy syndrome)
• Paraneoplastic syndromes
• Drug-induced (e.g. isoniazid, cyclosporin)
• Post-radiotherapy

Osmosis video (7 mins): https://youtu.be/jqClJsqnFFA

 ACUTE PERICARDITIS
How To Recognise Pericarditis
• Widespread concave ST elevation and PR depression throughout most of the limb leads
(I, II, III, aVL, aVF) and precordial leads (V2-6).
• Reciprocal ST depression and PR elevation in lead aVR (± V1).
• Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial
effusion.
• NB. ST- and PR-segment changes are relative to the baseline formed by the T-P
segment. The degree of ST elevation is typically modest (0.5 – 1mm).

PR depression and ST elevation in V5 Reciprocal PR elevation and ST

depression in aVR
 ACUTE PERICARDITIS
Stages of Pericarditis
• Pericarditis is classically associated with ECG changes that evolve through
four stages.
• Stage 1 – widespread STE and PR depression with reciprocal changes in aVR
(occurs during the first two weeks)
• Stage 2 – normalization of ST changes; generalized T wave flattening (1 to 3
weeks)
• Stage 3 – flattened T waves become inverted (3 to several weeks)
• Stage 4 – ECG returns to normal (several weeks onwards)
• NB. Less than 50% of patients progress through all four classical stages and
evolution of changes may not follow this typical pattern.
 ACUTE PERICARDITIS

Sinus tachycardia. Widespread concave STE and PR depression (I, II, III, aVF, V4-6). Reciprocal ST depression and
PR elevation in V1 and aVR.
 ACUTE PULMONARY EMBOLISM

The ECG changes associated with acute pulmonary embolism may be seen in any condition that
causes acute pulmonary hypertension/ cor pulmonale:

• Non-specific ST segment and T wave changes, including ST elevation and depression.

Reported in up to 50% of patients with PE.
• Sinus tachycardia – seen in 44% of patients.
• Right ventricular strain pattern –  ST depression and T wave inversions in the right precordial
leads (V1-4) ± the inferior leads (II, III, aVF). This pattern is seen in up to 34% of patients and is
associated with high pulmonary artery pressures.
• SI QIII TIII  pattern – deep S wave in lead I, Q wave in III, inverted T wave in III. This “classic”
finding is neither sensitive nor specific for pulmonary embolism; found in only 20% of patients with
PE.
• Complete or incomplete RBBB – associated with increased mortality; seen in 18% of patients.
• Right axis deviation – seen in 16% of patients. Extreme right axis deviation may occur, with axis
between zero and -90 degrees, giving the appearance of left axis deviation (“pseudo left axis”).
• Dominant R wave in V1 – a manifestation of acute right ventricular dilatation.
• Clockwise rotation – shift of the R/S transition point towards V6 with a persistent S wave in V6
(“pulmonary disease pattern”), implying rotation of the heart due to right ventricular dilatation.
• Right atrial enlargement (P pulmonale) – peaked P wave in lead II > 2.5 mm in height. Seen in
9% of patients.
 DIFFERENTIAL DIAGNOSIS
The ECG changes described above are not unique to PE. A similar spectrum of ECG changes may be
seen with any cause of acute or chronic cor pulmonale (i.e. any disease that causes right
ventricular strain / hypertrophy due to hypoxic pulmonary vasoconstriction).

Acute cor pulmonale

• Severe pneumonia
• Exacerbation of COPD / asthma
• Pneumothorax
• Recent pneumonectomy
• Upper airway obstruction

Chronic cor pulmonale

• Chronic obstructive pulmonary disease
• Recurrent small PEs
• Cystic fibrosis
• Interstitial lung disease
• Severe kyphoscoliosis
• Obstructive sleep apnoea
 PULMONARY EMBOLISM

RBBB; Extreme right axis deviation (+180 degrees); SI QIII TIII; T-wave inversions in V1-4 and
lead III; Clockwise rotation with persistent S wave in V6
ELECTROLYTE DISTURBANCES AND THE
ECG
• Hyperkalaemia

• Hypokalaemia

• Hypercalcaemia

• Hypocalcaemia

EKG Guy Video (13 mins): https://youtu.be/5l2Bq7SOqks

 HYPERKALAEMIA
Background
• Potassium is vital for regulating the normal electrical activity of the heart.
• Increased extracellular potassium reduces myocardial excitability, with
depression of both pacemaking and conducting tissues.
• Progressively worsening hyperkalaemia leads to suppression of impulse
generation by the SA node and reduced conduction by the AV node and His-
Purkinje system, resulting in bradycardia and conduction blocks and ultimately
cardiac arrest.
• Suspect hyperkalaemia in any patient with a new bradyarrhythmia or AV block,
especially patients with renal failure, on haemodialysis or taking any combination
of ACE inhibitors, potassium-sparing diuretics and potassium supplements.

Definitions
• Hyperkalaemia is defined as a potassium level > 5.5 mEq/L
• Moderate hyperkalaemia is a serum potassium > 6.0 mEq/L
• Severe hyperkalaemia is a serum potassium > 7.0 mE/L
 EFFECTS OF HYPERKALAEMIA ON THE ECG

(Warning! In individual patients, the serum potassium level may not correlate
closely with the ECG changes. Patients with relatively normal ECGs may still
experience sudden hyperkalaemic cardiac arrest.)

Serum potassium > 5.5 mEq/L is associated with repolarization

abnormalities:
• Peaked T waves (usually the earliest sign of hyperkalaemia)
 EFFECTS OF HYPERKALAEMIA ON
THE ECG
Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the
atria:
• P wave widens and flattens
• PR segment lengthens
• P waves eventually disappear

Prolonged PR segment Loss of P waves

 EFFECTS OF HYPERKALAEMIA ON THE ECG
Serum potassium > 7.0  mEq/L is associated with conduction abnormalities and bradycardia:
• Sinus bradycardia or slow AF
• High-grade AV block with slow junctional and ventricular escape rhythms
• Any kind of conduction block (bundle branch blocks, fascicular blocks)
• Prolonged QRS interval with bizarre QRS morphology
• Development of a sine wave appearance (a pre-terminal rhythm)
Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:
• Asystole
• Ventricular fibrillation
• EMD with bizarre, wide complex rhythm

Bradycardia Sine wave

 EFFECTS OF HYPERKALAEMIA ON THE ECG

Prolonged PR interval. Broad, bizarre QRS complexes — these merge with both the preceding P wave and subsequent T
wave. Peaked T waves.
This patient had a serum K+ of 9.2. 
 HYPOKALAEMIA
Decreased extracellular potassium causes myocardial hyperexcitability with the
potential to develop re-entrant arrhythmias

Hypokalaemia Definitions
• Hypokalaemia is defined as a potassium level < 3.5 mmol/L
• Moderate hypokalaemia is a serum level of < 3.0 mmol/L
• Severe hypokalaemia is defined as a level < 2.5 mmol/L

Hypokalaemia is often associated with hypomagnesaemia, which increases the risk

of malignant ventricular arrhythmias
Check potassium and magnesium in any patient with an arrhythmia
Top up the potassium to 4.2-4.5 mmol/l and the magnesium to > 1.0 mmol/l to
 stabilise the myocardium and protect against arrhythmias – this is standard
practice in most CCUs and ICUs
 HYPOKALAEMIA
ECG changes when K+ < 2.7 mmol/l
• Increased amplitude and width of the P wave
• Prolongation of the PR interval
• ST depression
• T wave flattening and inversion
• Prominent U waves (best seen in the precordial leads)
• Apparent long QT interval due to fusion of the T and U waves (= long QU interval)

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
 HYPOKALAEMIA

T wave inversion and prominent U Long QU interval in hypokalaemia

waves in hypokalaemia
 HYPOKALAEMIA

ST depression. T wave inversion. Prominent U waves. Long QU interval.

This patient had a serum K+ of 1.7
 HYPERCALCAEMIA
Hypercalcaemia Overview
• Normal serum corrected calcium = 2.2 – 2.6 mmol/L
• Mild hypercalcaemia =  2.7 – 2.9 mmol/L
• Moderate hypercalcaemia = 3.0 – 3.4 mmol/L
• Severe hypercalcaemia =  greater than 3.4 mmol/L
Causes of Hypercalcaemia
• Hyperparathyroidism (primary and tertiary)
• Myeloma
• Bony metastases
• Paraneoplastic syndromes
• Milk-alkali syndrome (OD Ca supplements or antacids)
Osborn (J waves): a positive deflection at the J
• Sarcoidosis point ( also seen in hypothermia)
• Excess vitamin D (e.g. iatrogenic)
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
 HYPERCALCAEMIA

This is the ECG of a 41-year old man with a parathyroid adenoma who presented to ED critically unwell with
a serum calcium of 6.1 mmol/L. He suffered a VF arrest not long after this ECG was taken. The ECG shows:
• Bizarre-looking QRS complexes
• Very short QT interval
• J waves = notching of the terminal QRS, best seen in lead V1
 HYPERCALCAEMIA

Hypercalcaemia causing marked shortening of the QT interval (260ms).

 HYPOCALCAEMIA
• Hypocalcaemia Overview
• Normal serum corrected calcium = 2.2 – 2.6 mmol/L.
• Mild-moderate hypocalcaemia =  1.9 – 2.2 mmol/L.
• Severe hypocalcaemia = < 1.9 mmol/L.

• Causes of Hypocalcaemia
• Hypoparathyroidism
• Vitamin D deficiency
• Acute pancreatitis
• Hyperphosphataemia
• Hypomagnesaemia
• Diuretics (frusemide)
• Pseudohypoparathyroidism
• Congenital disorders (e.g. DiGeorge syndrome)
• Critical illness (e.g. sepsis)
• Factitious (e.g. EDTA blood tube contamination)
 HYPOCALCAEMIA

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.
 HYPOCALCAEMIA

QTc 500ms in a patient with hypoparathyroidism (post thyroidectomy) and serum corrected calcium of 1.40 mmol/L
 HYPOMAGNESAEMIA*
Hypomagnesaemia Overview
• Normal serum magnesium = 0.8 – 1.0 mmol/L.
• Hypomagnesaemia = <0.8 mmol/L

ECG changes in Hypomagnesaemia

• The primary ECG abnormality seen with hypomagnesaemia is a prolonged QTc.
• Atrial and ventricular ectopy, atrial tachyarrhythmias and torsades de pointes
are seen in the context of hypomagnesaemia, although whether this is a specific
effect of low serum magnesium or due to concurrent hypokalaemia is uncertain.
• Nevertheless, correction of serum magnesium to >1.0 mmol/L (with concurrent
correction of serum potassium to >4.0 mmol/L) is often effective in suppressing
ectopy and supraventricular tachyarrhythmias, while a rapid IV bolus of
magnesium 2g is a standard emergency treatment for torsades de pointes.
 HYPOMAGNESAEMIA

Hypomagnesaemia causing long QTc (510ms)

 DIGOXIN
Digoxin Effect and Toxicity Video EKG Guy (12 mins): https://youtu.be/Uupvly1ZlmM
 
Digoxin Mechanism of Action
 
• Slows heart rate (─ve chronotropic effect)
In sinus rhythm, slows rate of discharge of SA node. → sinus bradycardia
 
• Slows AV conduction
The reason for the use of digoxin in atrial fibrillation is that it slows AV conduction by increasing vagal activity
via an action on the CNS; this → slowing of the ventricular rate. Even though the atrial dysrhythmia is still present,
the slowing of the conduction allows for increased efficiency of the heart due to increased ventricular filling time.
 
• ↑Force of Contraction (+ve inotropic effect)
Digoxin inhibits the Na+/K+ pump. The increased Na+ concentration inside the cardiac myocyte slows extrusion of
Ca++ via the Na+/Ca++ exchange transporter
Increased Ca++ stored in the sarcoplasmic reticulum increases the amount of Ca++ released in each action
potential  more powerful contraction

 Clinical use of Digoxin

 ▫ To slow rate in AF
▫ Treatment of heart failure in patients who remain symptomatic despite optimal use of diuretics and ACE-inhibitors
 DIGOXIN EFFECT
The ECG features of digoxin effect are seen with therapeutic doses of
digoxin and are due to:
Shortening of the atrial and ventricular refractory periods — producing a
short QT interval with secondary repolarisation abnormalities affecting the
ST segments, T waves and U waves.
Increased vagal effects at the AV node — causing a prolonged PR interval.
NB. The presence of digoxin effect on the ECG is not a marker of digoxin
toxicity. It merely indicates that the patient is taking digoxin.

Digoxin effect refers to the presence on the ECG of:

• Down-sloping ST depression with a characteristic “Salvador Dali sagging”
(or “reverse tick”) appearance
• Flattened, inverted, or biphasic T waves.
• Shortened QT interval.
 DIGOXIN EFFECT
Additional ECG Features
• Mild PR interval prolongation of up to 240 ms (due to increased vagal tone).
• Prominent U waves.
• Peaking of the terminal portion of the T waves.
• J point depression (usually in leads with tall R waves).
 DIGOXIN EFFECT

The morphology of the QRS complex / ST segment is variously described as either “slurred”, “sagging” or “scooped” and
resembling either a “reverse tick”, “hockey stick” or (my personal favourite) “Salvador Dali’s moustache”!
 DIGOXIN EFFECT

Sagging ST segments are most evident in the lateral leads V4-6, I and aVL .
Clinical features of Digoxin Toxicity DIGOXIN TOXICITY
• GIT: Nausea, vomiting, anorexia, diarrhoea
• Visual: Blurred vision, yellow/green discolouration, haloes
• CVS: Palpitations, syncope, dyspnoea
• CNS: Confusion, dizziness, delirium, fatigue

ECG Features of Digoxin Toxicity

Digoxin can cause a multitude of dysrhythmias
Dysrhythmias are usually due to:
• increased automaticity (increased intracellular calcium)
• decreased AV conduction (increased vagal effects at the AV node)
The classic dysrhythmia associated with digoxin toxicity is the combination of
• supraventricular tachycardia (due to increased automaticity)
• slow ventricular response (due to decreased AV conduction)

Other common dysrhythmias associated with digoxin toxicity include:

• Frequent PVCs (the most common abnormality), including ventricular bigeminy and trigeminy
• Sinus bradycardia
• Slow Atrial Fibrillation
• Any type of AV block (1st degree, 2nd degree & 3rd degree)
• Regularised AF = AF with complete heart block and a junctional or ventricular escape rhythm
• Ventricular tachycardia, including polymorphic and bidirectional VT
 DIGOXIN TOXICITY

Sinus rhythm with frequent PVCs in a pattern of ventricular bigeminy

Paroxysmal atrial tachycardia with high-grade AV block and PVCs

 DIGOXIN TOXICITY: REGULARISED AF

Coarse atrial fibrillation with 3rd degree AV block and a junctional escape rhythm.
 DIGOXIN TOXICITY:ATRIAL FLUTTER WITH AV BLOCK

Atrial flutter with a slow ventricular rate due to digoxin toxicity.

 DIGOXIN TOXICITY: BIDIRECTIONAL VT

This is a great example of Bidirectional VT. There is a broad complex tachycardia with a frontal-plane
axis that alternates by 180 degrees with each successive beat.
 TRICYCLIC OVERDOSE (SODIUM-CHANNEL BLOCKER
Sodium Channel Blocking Medications
TOXICITY)*
• Tricyclic antidepressants (= most common)
• Type Ia antiarrhythmics (quinidine, procainamide)
• Type Ic antiarrhythmics (flecainide, encainide)
• Local anaesthetics (bupivacaine, ropivacaine)
• Antimalarials (chloroquine, hydroxychloroquine)
• Dextropropoxyphene
• Propranolol
• Carbamazepine
• Quinine
Sodium Channel Blocking Effects
The two main adverse effects of sodium-channel blocker poisoning include:
• Seizures
• Ventricular dysrhythmias (due to blockade of sodium channels in the CNS and myocardium)
Handy tip: An ECG should be taken in all patients who present with a deliberate self-poisoning (or
altered GCS of unknown aetiology) to screen for TCA overdose.
 ELECTROCARDIOGRAPHIC FEATURES OF SODIUM-CHANNEL BLOCKADE

Features consistent with sodium-channel blockade

are:
• Interventricular conduction delay — QRS > 100 ms in
lead II
• Right axis deviation of the terminal QRS:
• Terminal R wave > 3 mm in aVR
• R/S ratio > 0.7 in aVR
• Patients with tricyclic overdose will also usually
demonstrate sinus tachycardia secondary to
muscarinic (M1) receptor blockade.

The degree of QRS broadening on the ECG is

correlated with adverse events:
• QRS > 100 ms is predictive of seizures
• QRS > 160 ms is predictive of ventricular arrhythmias
(e.g. VT)
 TCA OVERDOSE

Typical ECG of TCA toxicity demonstrating: Sinus tachycardia with first-degree AV block (P waves hidden
in the T waves, best seen in V1-2). Broad QRS complexes. Positive R’ wave in aVR.
 TCA OVERDOSE: WORSENING TOXICITY

A second ECG of the same patient showing worsening TCA cardiotoxicity with marked QRS broadening
producing a sine wave appearance reminiscent of hyperkalaemia.
 FLECAINIDE OVERDOSE

Similar ECG changes are seen with other sodium-channel blocking agents.
This ECG demonstrates QRS widening and positive R’ wave in aVR consistent with sodium-channel
blockade in a patient with flecainide poisoning.
 PACED ECG – ELECTROCARDIOGRAPHIC FEATURES

The appearance of the ECG in a paced patient is

dependent on the pacing mode used, placement
of pacing leads, device pacing thresholds, and the
presence of native electrical activity. Features of
the paced ECG are:

Pacing spikes
• Vertical spikes of short duration, usually 2 ms.
• May be difficult to see in all leads.
• Amplitude depends on position and type of lead.
• Bipolar leads result in a much smaller pacing
spike than unipolar leads.
• Epicardially placed leads result in smaller pacing
spikes than endocardially placed leads.
PACED ECG – ELECTROCARDIOGRAPHIC FEATURES
Atrial Pacing
• Pacing spike precedes the p wave.
• Morphology of p wave dependent of lead placement but may appear normal.
Ventricular Pacing
• Pacing spike precedes the QRS complex.
• Right ventricle pacing lead placement results in a QRS morphology similar to LBBB.
• Left epicardial pacing lead placement results in a QRS morphology similar to RBBB.
• ST segments and T waves should be discordant with the QRS complex i.e. the major
terminal portion of the QRS complex is located on the opposite side of the baseline from
the ST segment and T wave.
Dual Chamber Pacing
• Dependent on areas begin paced.
• May exhibit features of atrial pacing, ventricular pacing or both.
• Pacing spikes may precede only p wave, only QRS complex, or both.
The absence of paced complexes does not always mean pacemaker failure as it may reflect
satisfactory native conduction.
PACED ECG – ELECTROCARDIOGRAPHIC FEATURES

• Atrial and ventricular pacing spikes

Appropriate discordance in a ventricular paced rhythm

 ATRIAL PACING

Atrial paced rhythm with 1st degree AV block: There are regular pacing spikes at 90 bpm. Each pacing spike is
followed by a P wave, indicating 100% atrial capture. P waves are conducted to the ventricles with a prolonged PR
interval (280 ms).
 VENTRICULAR PACING

Ventricular pacing spikes precede each QRS complex (except perhaps complex #2 — although the QRS
morphology in this complex is identical to the rest of the ECG, suggesting that this beat is also paced) No atrial
pacing spikes are seen. The underlying native rhythm is probably coarse atrial fibrillation — there are several
possible P waves visible in V1 but otherwise the atrial activity is chaotic.
 DUAL CHAMBER PACING

A-V sequential pacing: Atrial and ventricular pacing spikes are visible before each QRS complex. There is 100%
atrial capture — small P waves are seen following each atrial pacing spike. There is 100% ventricular capture —
a QRS complex follows each ventricular pacing spike. QRS complexes are broad with a LBBB morphology,
indicating the presence of a ventricular pacing electrode in the right ventricle.
 LIMB LEAD REVERSAL: LEFT ARM/ RIGHT ARM*

With reversal of the LA and RA electrodes, Einthoven’s triangle flips 180

degrees horizontally around an axis formed by lead aVF.
 LIMB LEAD REVERSAL: LEFT ARM/ RIGHT
ARM
This has the following effects on the ECG: -Lead I becomes inverted.
-Leads II and III switch places. -Leads aVL and aVR switch places.
-Lead aVF remains unchanged.

Baseline LA/RA reversal

 LIMB LEAD REVERSAL: LEFT ARM/ RIGHT
ARM
?Abnormal p
wave axis
?Extreme RAD
?Inferior TWI

This reversal is the most common limb lead reversal.  The tell-tale sign is an inverted p wave, QRS complex, and T
wave in lead I.  In the absence of dextrocardia, this is pathognomonic of arm electrode reversal.  Remember, as
general rule I and V6 point the same direction and should look the same on the EKG.  aVR and aVL have switched
places, so they both look grossly abnormal as well.
REPEAT ECG WITH LEADS
CORRECTED
OTHER LIMB LEAD REVERSALS