1
Q
What is the purpose of STEP 1 in ECG interpretation?
A
To diagnose the rhythm and identify whether the pacemaker is the SA node.
2
Q
What three basic criteria must be assessed first to suspect sinus rhythm?
A
- Rate
- Regularity
- QRS width
3
Q
What heart rate range is consistent with sinus rhythm?
A
60–100 beats per minute.
4
Q
What rhythm regularity is expected in sinus rhythm?
A
A regular rhythm with constant R–R intervals.
5
Q
What QRS duration supports a sinus rhythm diagnosis?
A
QRS duration less than 120 ms.
6
Q
Why does a narrow QRS support a sinus rhythm?
A
Because ventricular depolarization is occurring via the normal His–Purkinje system
7
Q
What P–QRS relationship must be present to confirm sinus rhythm
A
Every QRS is preceded by a P wave, and every P wave gives rise to a QRS complex
8
Q
What does a 1:1 P-to-QRS relationship confirm?
A
Atrial depolarization is driving ventricular depolarization.
9
Q
In which leads should the P wave be upright and inverted in sinus rhythm?
A
Upright in lead II and inverted in lead aVR.
10
Q
What does this P-wave orientation indicate about the electrical axis?
A
A normal atrial depolarization axis consistent with SA node origin.
11
Q
When can sinus rhythm be confidently diagnosed in STEP 1?
A
When rate is 60–100 bpm, rhythm is regular, QRS is narrow, P waves precede every QRS, and P waves are upright in II and inverted in aVR.
12
Q
Why is STEP 2 still required after diagnosing sinus rhythm in STEP 1?
A
To assess for conduction abnormalities and subtle pathology despite a normal rhythm.
13
Q
In which leads are P waves best assessed?
A
Lead II and lead V1.
14
Q
What is the normal appearance of P waves across the ECG?
A
All P waves look similar and consistent in shape.
15
Q
What is the normal P-wave morphology in lead II?
A
Smooth and round
16
Q
What are the normal size limits of a P wave in lead II?
A
Height < 2.5 mm
* Width < 120 ms
17
Q
What is the normal P-wave appearance in lead V1?
A
Biphasic, with an upright and an inverted component of equal size.
18
Q
What does a normal biphasic P wave in V1 represent?
A
Right atrial depolarization followed by left atrial depolarization.
19
Q
What question should be asked when analyzing P-wave morphology?
A
Are the P waves abnormal in size or shape?
20
Q
What atrial abnormality is suggested by tall, peaked P waves?
A
Right atrial enlargement (RAE).
21
Q
What is the main ECG criterion for RAE in lead II?
A
A peaked P wave taller than 2.5 mm.
22
Q
In which leads is this tall P wave most commonly seen?
A
Lead II and the inferior leads III and aVF.
23
Q
How does RAE affect the P wave in lead V1
A
The initial upright (proximal) component becomes exaggerated compared to the terminal inverted component.
24
Q
Why does right atrial enlargement accentuate the initial P-wave component?
A
Because right atrial depolarization contributes more to the overall atrial signal.
25
What is the classic ECG term for P-wave changes seen in RAE?
P-pulmonale.
26
Why is RAE often called P-pulmonale?
Because it is commonly secondary to pulmonary disease.
27
What cardiac condition is RAE often associated with?
Right ventricular hypertrophy (RVH).
28
What types of diseases commonly lead to RAE?
Chronic lung disease, pulmonary hypertension, and other pulmonary disorders
29
How does identifying RAE help clinically?
It points toward chronic pressure overload on the right heart, often due to lung pathology.
30
What P-wave abnormality is suggested by widening rather than increased height?
Left atrial enlargement (LAE).
31
In which lead is LAE most commonly identified?
Lead V1.
32
What is the key P-wave criterion for LAE in lead V1?
An exaggerated terminal (inverted) portion of the biphasic P wave that is deeper and wider than one small square.
33
Why does LAE exaggerate the terminal negative component in V1?
Left atrial depolarization is prolonged and contributes more to the later part of the P wave.
34
What P-wave change may be seen in lead II with LAE?
A widened, notched P wave.
35
What P-wave duration abnormality suggests LAE in lead II
P-wave width greater than 120 ms.
36
What classic ECG term is used for LAE-associated P-wave changes?
P-mitrale
37
Why is LAE often called P-mitrale?
Because it is commonly associated with mitral valve disease.
38
What cardiac structural abnormality is LAE often associated with?
Left ventricular hypertrophy (LVH).
39
How does LAE differ from RAE in P-wave appearance?
LAE causes P-wave widening and notching, while RAE causes tall, peaked P waves.
40
What does identification of LAE suggest clinically?
Chronic pressure or volume overload of the left atrium, often due to mitral valve or left-sided heart disease
41
Why is lead V1 particularly useful for detecting LAE?
It clearly displays the biphasic P wave, separating right and left atrial depolarization.
42
What is bi-atrial enlargement on ECG?
Enlargement of both the right and left atria, producing combined ECG features of RAE and LAE.
43
How is bi-atrial enlargement recognised on ECG?
By the presence of ECG criteria for both RAE and LAE on the same tracing.
44
What are the P-wave criteria for bi-atrial enlargement in lead II?
A P wave that is tall (>2.5 mm) and wide (>120 ms).
45
What P-wave features are seen in lead V1 with bi-atrial enlargement?
Both the positive (initial) and negative (terminal) components of the biphasic P wave are exaggerated
46
Why are both components of the P wave exaggerated in V1?
Because both right atrial and left atrial depolarization are increased and prolonged.
47
How does bi-atrial enlargement differ from isolated RAE or LAE?
It shows increased height and width of the P wave rather than just one abnormality.
48
What common underlying cardiac process can lead to bi-atrial enlargement?
Progressive worsening of left ventricular hypertrophy (LVH)
49
Why can progressive LVH cause enlargement of both atria?
Chronic pressure overload leads to elevated filling pressures that affect both atria over time.
50
What does bi-atrial enlargement suggest clinically?
Advanced or long-standing cardiac disease.
51
In which ECG leads is bi-atrial enlargement best assessed?
Lead II (for height and width) and lead V1 (for biphasic components).
52
What key question should be asked when a P wave is both tall and wide?
Could this represent bi-atrial enlargement?
53
What is the teaching pearl for recognising bi-atrial enlargement?
Height = right atrium, width = left atrium; both abnormal = both atria enlarged.
54
What does it suggest if P waves are peaked or differ in shape from one another?
An abnormal (non-sinus) pacemaker.
55
Give an example of a rhythm that produces abnormal P-wave shapes.
Atrial tachycardia.
56
Why do abnormal pacemakers produce different P-wave morphologies
Because atrial depolarization originates from a site other than the SA node.
57
How do P waves appear in atrial tachycardia compared to sinus rhythm?
They are often peaked, abnormal in shape, and may vary from beat to beat.
58
Should abnormal P-wave shapes always be analysed further?
Yes, as they suggest a non-sinus atrial rhythm
59
Where is the PR segment best assessed?
On the rhythm strip.
60
What is the PR segment?
The portion between the end of the P wave and the start of the QRS complex.
61
What is the normal position of the PR segment?
On the isoelectric line.
62
Why is the PR segment normally isoelectric?
There is no net electrical activity during AV nodal delay.
63
What key question should be asked when analysing the PR segment?
Is the PR segment displaced?
64
What condition classically causes PR segment displacement?
Acute pericarditis.
65
What PR and ST changes are seen in lead aVR in pericarditis?
PR segment elevation and ST segment depression.
66
What PR and ST changes are seen in lead II in pericarditis?
PR segment depression and ST segment elevation.
67
Why does pericarditis cause PR segment depression in most leads?
Because of atrial involvement and inflammation of the pericardium
68
What is the typical shape of ST elevation in pericarditis?
Saddle-shaped (concave upward).
69
How widespread is ST elevation in pericarditis?
Often diffuse across many leads
70
What rhythm may pericarditis present with?
Sinus tachycardia, with or without other ECG changes.
71
What ECG feature helps distinguish pericarditis from myocardial infarction?
PR segment displacement with widespread, saddle-shaped ST elevation.
72
Which two leads are especially useful for identifying pericarditis-related PR changes?
Lead II and lead aVR.
73
What is the key teaching pearl for PR-segment analysis?
Normal PR = isoelectric; displaced PR = think pericarditis
74
Where is the PR interval best assessed?
On the rhythm strip
75
How is the PR interval measured?
From the start of the P wave to the start of the QRS complex.
76
What is the normal PR interval duration
120–200 ms.
77
What does a constant PR interval from cycle to cycle indicate?
Normal AV nodal conduction.
78
What key question should be asked when analysing the PR interval?
Is the PR interval shortened?
79
What condition is classically associated with a short PR interval?
Wolff–Parkinson–White (WPW) syndrome
80
What is the PR interval criterion for WPW?
PR interval shorter than 120 ms.
81
What distinctive feature follows the shortened PR interval in WPW?
A delta wave.
82
What is a delta wave?
A slurred upstroke at the beginning of the QRS complex.
83
Why does the QRS appear widened in WPW?
Because the delta wave widens only the initial part (base) of the QRS complex.
84
What additional ECG changes may be seen in WPW?
Secondary ST segment and T-wave changes due to abnormal repolarization.
85
What congenital abnormality causes WPW?
An accessory atrioventricular conducting pathway called the Bundle of Kent
86
How does the accessory pathway differ from the AV node?
It conducts impulses faster and bypasses the normal AV nodal delay.
87
Why does WPW produce a short PR interval?
Ventricular depolarization begins early via the accessory pathway.
88
Why does ventricular depolarization eventually become normal in WPW?
The impulse travelling through the AV node arrives shortly afterward and completes ventricular activation.
89
Why is the delta wave only at the start of the QRS complex?
Only the initial part of ventricular depolarization is abnormal.
90
How is WPW commonly discovered?
Incidentally on routine ECGs, such as during medical or insurance screenings.
91
What rhythm disturbance may occur in patients with WPW?
Tachyarrhythmias due to re-entry circuits.
92
How may WPW appear during tachycardia?
The ECG may resemble ventricular tachycardia.
93
Why is WPW clinically important to recognise?
Because certain treatments used for other tachycardias can be dangerous in WPW.
94
What is the classic ECG triad of WPW?
Short PR interval + delta wave + widened/slurred QRS.
95
What PR interval abnormality suggests a 1st degree AV block?
A PR interval that is constant and prolonged >200 ms.
96
What happens to atrial–ventricular conduction in 1st degree AV block?
All impulses are conducted, but conduction is delayed.
97
Where does the conduction delay usually occur in 1st degree AV block?
Most commonly in the AV node; less commonly in the atria.
98
What are common causes of 1st degree AV block?
AV nodal slowing
Drugs (e.g. β-blockers, calcium channel blockers, digoxin)
Increased vagal tone
99
Is 1st degree AV block usually symptomatic?
No—rarely symptomatic unless severe bradycardia or concurrent ischemia is present.
100
How many P waves are conducted in 1st degree AV block?
Every P wave is followed by a QRS complex.
101
What is another name for 2nd degree type I AV block?
Wenckebach phenomenon or Mobitz type I.
102
What is the hallmark ECG pattern of Mobitz type I?
Progressive PR interval prolongation until a non-conducted P wave occurs.
103
What happens after the dropped QRS beat in Mobitz type I?
The PR interval resets to normal, and the cycle repeats.
104
What does a “dropped beat” mean?
A P wave not followed by a QRS complex.
105
Where is the site of block in Mobitz type I?
Usually within the AV node.
106
Is Mobitz type I usually benign?
Yes, unless frequent dropped beats cause symptomatic bradycardia.
107
Why is Mobitz type I important to recognise?
It must be distinguished from Mobitz type II, which is more dangerous.
108
How does Mobitz type II differ from Mobitz type I?
The PR interval remains constant, but QRS complexes are intermittently dropped.
109
Does the PR interval progressively lengthen in Mobitz type II?
No—it stays fixed before and after dropped beats.
110
Where is the block usually located in Mobitz type II?
In the His–Purkinje system (below the AV node).
111
Why is Mobitz type II clinically significant?
It has a high risk of progression to complete heart block
112
How is Mobitz type II typically managed
Often requires urgent pacing, even if asymptomatic
113
How can you quickly distinguish Mobitz I from Mobitz II on ECG?
Mobitz I: PR gets longer → dropped beat
Mobitz II: PR fixed → sudden dropped beat
114
What is a 2nd degree type II AV block also called?
Mobitz type II AV block.
115
What happens to the PR interval in a 2nd degree type II block?
The PR interval is fixed and constant in conducted beats.
116
What defines the dropped beats in Mobitz type II block?
Non-conducted P waves occur suddenly, with no preceding PR prolongation.
117
How are dropped beats patterned in a 2nd degree type II block?
They are unexpected and irregular, with no predictable pattern
118
How does Mobitz type II differ from Mobitz type I (Wenckebach)?
Mobitz II has fixed PR intervals with sudden dropped beats, whereas Mobitz I has progressive PR lengthening before a dropped beat.
119
Where is the conduction problem usually located in Mobitz type II block?
Below the AV node, typically in the bundle of His or His–Purkinje system.
120
Why is a 2nd degree type II block always concerning?
It is always pathological and may progress to 3rd degree (complete) heart block.
121
It is always pathological and may progress to 3rd degree (complete) heart block.
Bundle branch blocks (BBB), often causing a wide QRS
122
Why can Mobitz type II be difficult to interpret on ECG?
Associated BBB and wide QRS complexes can obscure rhythm patterns.
123
What analogy helps recognize Mobitz type II AV block on ECG?
A necklace analogy: normal QRS complexes are beads on a string, but in Mobitz II, some beads are suddenly missing, leaving only the isoelectric baseline.
124
What is the key management implication of Mobitz type II block?
It often requires urgent pacing, even if the patient is asymptomatic.
125
What is a 2nd degree 2:1 AV block?
A conduction abnormality where every second P-wave is non-conducted, resulting in every second QRS complex being dropped.
126
Why can a 2:1 AV block be easily missed on ECG?
Because the rhythm may appear regular and slow/normal, masking the dropped beats.
127
Which ECG checklist step is essential to identify a 2:1 AV block?
STEP 2: Confirm that every P-wave is followed by a QRS complex.
128
What key observation reveals a 2:1 AV block?
Non-conducted P-waves that do not produce QRS complexes
129
Why is classification of Mobitz type I vs type II difficult in 2:1 block?
Because PR interval behavior cannot be assessed when every alternate beat is dropped.
130
What is another name for 3rd degree AV block?
Complete heart block.
131
Why is 3rd degree block considered both a rhythm and conduction abnormality?
Because atrial impulses are completely blocked and a new pacemaker takes over ventricular rhythm.
132
How should 3rd degree AV block be diagnosed in STEP 1 of ECG interpretation?
By identifying the ventricular pacemaker, not as “sinus rhythm with block”.
133
What is the correct ECG diagnosis wording for complete heart block?
Ventricular rhythm due to complete heart block.
134
What is the defining ECG feature of 3rd degree AV block?
No relationship between P-waves and QRS complexes (AV dissociation).
135
How do the P-waves and QRS complexes behave in complete heart block?
P-waves occur regularly
QRS complexes occur regularly
They are independent of each other
There are more P-waves than QRS complexes
136
What happens to ventricular rate in complete heart block?
It is slower than normal, depending on the location of the backup pacemaker
137
What causes 3rd degree AV block?
Complete failure of atrioventricular conduction, commonly due to ischemia or infarction
138
What determines the width of the QRS complexes in complete heart block?
The location of the backup pacemaker.
139
What ECG features occur if the block is below the AV node?
Pacemaker arises from bundle branches
Wide/broad QRS complexes
Very slow rate (≈ 15–40 bpm)
140
What ECG features occur if the block is high in the AV node?
Pacemaker arises from the bundle of His
Narrow/normal QRS complexes
Faster rate, sometimes within normal range
141
Why is high-level complete heart block harder to diagnose?
Because the QRS may be narrow and the rate relatively normal, requiring careful assessment of P–QRS relationship.
142
What is the normal duration of the QRS complex?
< 120 ms (less than 3 small squares).
143
What is the normal QRS axis range?
0–90°.
144
What is the normal QRS appearance in V1 and V6?
V1: small R wave with a deep S wave
V6: tall R wave with a small S wave
145
What are the normal size limits for R and S waves?
Tallest R wave < 25 mm
Deepest S wave < 25 mm
146
What are normal Q-wave characteristics?
Duration < 40 ms
Depth < 1 mm
Absent in V1–V3
147
What conditions can cause abnormal QRS complexes?
Ventricular hypertrophy
Bundle branch blocks
Q-wave infarctions
Non-cardiac causes
148
When assessing QRS size, which leads should be checked first?
V1 and V6.
149
What causes the QRS complexes to be large in LVH?
Increased left ventricular muscle mass, generating greater electrical forces.
150
How reliable are ECG criteria for diagnosing LVH?
Highly specific (>90%) when criteria are met
Low sensitivity (misses 40–80% of cases)
151
What is a simple limb-lead criterion for LVH?
R in lead I + S in lead III > 25 mm.
152
What chest-lead R-wave criterion suggests LVH?
R wave in V5 or V6 > 25 mm.
153
What chest-lead S-wave criterion suggests LVH?
S wave in V1–V3 > 25 mm
154
What is the classic Sokolow-Lyon criterion for LVH?
S in V1 + R in V5 or V6 > 35 mm.
155
What global voltage criterion can indicate LVH?
Tallest R wave + deepest S wave > 45 mm
156
What ST-T changes may be seen in LVH?
Left-sided “strain” pattern:
ST segment depression
T-wave inversion in left-sided leads
157
In which leads is LVH strain most commonly seen?
Left-sided leads (I, aVL, V5, V6).
158
Does absence of ECG criteria exclude LVH?
No — many patients with LVH have normal-appearing ECGs.
159
What is right ventricular hypertrophy (RVH)?
An increase in right ventricular muscle mass, usually due to chronic pressure overload.
160
What ECG principle explains RVH changes?
Increased right ventricular muscle produces greater right-directed electrical forces.
161
Which leads are most important when assessing RVH?
V1 and V6.
162
What is the normal QRS pattern in V1?
Small R wave and deep S wave.
163
What is the hallmark QRS change in V1 in RVH?
Dominant R wave in V1 (R > S).
164
What QRS change is seen in V6 in RVH?
Deep S wave with a small R wave.
165
What axis deviation is commonly seen in RVH?
Right axis deviation (> +90°).
166
What chest-lead voltage criteria support RVH?
R in V1 > 7 mm, or
R/S ratio in V1 > 1
167
What limb-lead finding supports RVH?
Right axis deviation with dominant R in aVR.
168
What ST-T changes may be seen in RVH?
Right-sided strain pattern:
ST depression
T-wave inversion in V1–V3
169
How does RVH affect R-wave progression across the chest leads?
Early R-wave dominance in V1 with reduced progression toward V6.
170
What conditions commonly cause RVH?
Pulmonary hypertension
Chronic lung disease (cor pulmonale)
Pulmonary embolism
Congenital heart disease
171
What ECG feature helps distinguish RVH from RBBB?
RVH: narrow QRS with dominant R in V1
[dominant R in V1] + [R axis deviation] + [deep S in V5-6] +/- RBBB.
RBBB: wide QRS with RSR′ pattern in V1
172
Is ECG sensitive for diagnosing RVH?
No — ECG criteria are specific but not sensitive.
173
What clinical correlation is commonly seen with RVH?
Often associated with right atrial enlargement (P-pulmonale).
174
What is the most useful quick screening sign for RVH?
Dominant R wave in V1 with right axis deviation.
175
Besides RVH, what other conditions can cause a tall R wave in V1?
Right bundle branch block (RBBB)
Posterior myocardial infarction
176
Why does a posterior infarct produce a tall R wave in V1?
Because posterior LV ischemia is seen as a reciprocal (mirror-image) change in anterior chest leads.
177
What does a tall R wave in V1 represent in posterior infarction?
A reciprocal view of a pathological Q wave in the posterior wall.
178
What key feature must NOT accompany a tall R wave in V1 for posterior infarction?
Right axis deviation.
179
What does a wide or deformed QRS complex suggest?
Abnormal ventricular depolarization.
180
What are common causes of wide or deformed QRS complexes?
RBBB
LBBB
Ventricular tachycardia (VT)
Electrolyte or drug abnormalities (e.g. hyperkalaemia, TCA overdose)
181
What is the defining ECG feature of a bundle branch block?
Widened QRS complex with a characteristic notch in specific leads.
182
Are QRS complexes in BBB preceded by P-waves?
Yes — even if the P-wave is hidden within a preceding T-wave.
183
How can BBB be distinguished from ventricular rhythms (VT or complete heart block)?
BBB: P-wave precedes QRS
Ventricular rhythm: P-waves are dissociated from QRS complexes
184
What is an incomplete bundle branch block?
A BBB morphology with normal or near-normal QRS width, indicating partial slowing of conduction.
185
Is a hemiblock the same as an incomplete BBB?
No — a hemiblock involves conduction delay in left bundle fascicles, not incomplete block.
186
What is a key learning tip for recognizing BBB?
Rote-learn the characteristic QRS shapes and always confirm preceding P-waves.
187
What is the classic ECG pattern of RBBB in V1?
rSR′ pattern (“rabbit ears”) in V1.
188
What QRS change is seen in V6 in RBBB?
Wide, slurred S wave.
189
What repolarization changes follow the QRS in RBBB?
Abnormal ST–T changes (secondary repolarization abnormalities).
190
Are P-waves present before QRS complexes in RBBB?
Yes — confirming a supraventricular rhythm.
191
Is RBBB always pathological?
No — it can occur in normal hearts, but may also indicate disease
192
What conditions may cause RBBB?
Ischaemic heart disease
Cardiomyopathy
Structural or degenerative conduction disease
193
What is the most important safety check when seeing a wide QRS with BBB morphology?
Confirm P-waves before the QRS to exclude ventricular rhythms.
194
What is a left bundle branch block (LBBB)?
A conduction abnormality where depolarization of the left ventricle is delayed, causing a wide, abnormal QRS complex.
195
What is the key ECG criterion for diagnosing LBBB?
A wide QRS complex (≥120 ms) with characteristic left-sided morphology.
196
What is the classic QRS pattern seen in V6 in LBBB?
A broad, notched “M-shaped” R wave.
197
What must be present before each QRS complex in LBBB?
A P-wave, confirming a supraventricular origin.
198
What repolarization changes follow the QRS in LBBB?
Abnormal (secondary) ST-segment and T-wave changes.
199
What is the typical QRS appearance in V1 in LBBB?
A deep, broad, and often slurred S wave (the notch may not be obvious)
200
Why does V6 show an “M” pattern in LBBB?
Because the right ventricle depolarizes first, followed by delayed left ventricular activation.
201
Are Q waves usually present in lateral leads in LBBB?
No — normal septal depolarization is reversed, masking Q waves.
202
Is LBBB usually a benign finding?
No — it is almost always pathological.
203
What are common causes of LBBB?
Acute myocardial infarction
Ischaemic heart disease
Cardiomyopathy
Degenerative conduction system disease
204
Why is LBBB clinically important in suspected MI?
Because it can mask ECG signs of ischemia, making MI difficult to diagnose.
205
What is the most important safety check when identifying LBBB?
Confirm a preceding P-wave to exclude ventricular rhythms.
206
What is a left anterior hemiblock (LAHB)?
A conduction abnormality caused by disruption of the left anterior fascicle, affecting activation of the anterior wall of the left ventricle
207
Why does LAHB not usually widen or notch the QRS complex?
Because conduction via the left posterior fascicle remains intact, allowing ventricular activation to continue.
208
What is the key ECG hallmark of LAHB?
Left axis deviation (LAD) with an otherwise normal-looking QRS
209
What axis range is typical for left anterior hemiblock?
Approximately −45° to −90°
210
Why does left axis deviation occur in LAHB?
Ventricular activation proceeds inferiorly and posteriorly first, then spreads upward and leftward.
211
Why can LAHB be easily missed by beginners?
Because the QRS duration and shape may appear normal, with axis deviation being the only clue.
212
What ECG finding should raise strong suspicion of LAHB?
A seemingly normal ECG with marked left axis deviation.
213
Is LAHB the same as an incomplete LBBB?
No — LAHB is a fascicular block, not a partial bundle branch block.
214
In which clinical contexts is LAHB commonly seen?
Ischaemic heart disease
Degenerative conduction disease
Structural heart disease
215
What is the most important checklist step when suspecting LAHB?
Careful assessment of the QRS axis, even when QRS width is normal.
216
What is a Q-wave on an ECG?
The first negative deflection of the QRS complex before the R-wave.
217
In which leads are Q-waves normally absent?
V1–V3.
218
In which leads may normal Q-waves be seen?
Left-sided leads: I, II, aVL, V5–V6.
219
What are the normal size limits for a Q-wave?
< 40 ms wide
< 1 mm deep
220
When is a Q-wave considered pathological?
If any of the following are present:
Depth > 2 mm
Width > 40 ms
Depth > 25% of the height of the following R-wave
221
What do pathological Q-waves represent physiologically?
Non-conducting (dead) myocardium, usually from a previous myocardial infarction.
222
Why do Q-waves form in myocardial infarction?
Electrical forces move away from infarcted tissue, creating a negative deflection
223
In which ECG leads would an old inferior MI produce pathological Q-waves?
Contiguous inferior leads: II, III, and aVF.
224
Why is lead contiguity important when assessing Q-waves?
Pathological Q-waves appear in adjacent leads supplying the same myocardial territory.
225
Can pathological-appearing Q-waves occur outside MI?
Yes, e.g. in pulmonary embolism
226
What is the most important checklist question when seeing a Q-wave?
Is it too deep, too wide, or too large relative to the R-wave?
227
Does the presence of pathological Q-waves indicate acute or old infarction?
Usually old or established infarction.
228
What does it mean if there are additional QRS complexes on an ECG?
The presence of premature (ectopic) beats occurring outside the normal sinus rhythm.
229
What types of premature beats can be seen on ECG?
Premature atrial complexes (PAC)
Premature junctional complexes (PJC)
Premature ventricular complexes (PVC)
230
What causes a premature (ectopic) beat?
An irritable focus fires early, initiating a depolarization wave that spreads in all directions.
231
How does a premature atrial or junctional beat appear on ECG?
An abnormal or early P-wave, followed by a normal-looking, narrow QRS complex.
232
Why is the QRS complex narrow in supraventricular ectopic beats?
Because depolarization still travels down the normal His–Purkinje pathway.
233
What feature helps identify a PAC on ECG?
A premature P-wave with an abnormal shape, followed by a normal QRS.
234
What is a premature ventricular complex (PVC)?
A premature beat originating from the ventricular myocardium.
235
How does a PVC appear on ECG?
A wide, bizarre QRS complex not preceded by a P-wave.
236
Why are PVC QRS complexes wide and bizarre?
Depolarization spreads slowly cell-to-cell rather than via the His–Purkinje system.
237
How can the origin of a PVC affect its QRS shape?
RV-origin PVCs may mimic LBBB morphology
LV-origin PVCs may mimic RBBB morphology
238
What is characteristic about the T-wave in a PVC?
The T-wave is always opposite in polarity to the QRS complex.
239
When are PVCs considered frequent?
More than 6 PVCs per minute.
240
What is a multifocal PVC pattern?
PVCs with different QRS shapes, indicating multiple ventricular foci.
241
What is ventricular bigeminy?
A rhythm where every second QRS complex is a PVC.
242
Which drug toxicity is classically associated with bigeminy?
Digoxin toxicity.
243
What are PVC couplets?
Two PVCs occurring consecutively.
244
What defines a run of ventricular tachycardia (VT)?
Three or more PVCs in rapid sequence.
245
What is the R-on-T phenomenon?
A PVC that falls on the terminal portion of the preceding T-wave.
246
Why is the R-on-T phenomenon dangerous?
It can precipitate ventricular fibrillation (VF).
247
Are PVCs always pathological?
No — occasional PVCs can be normal, especially in older adults, but certain patterns require urgent attention.
248
What is the most important checklist question when ectopic beats are seen?
Are they supraventricular (narrow QRS) or ventricular (wide, bizarre QRS)?
249
What is the normal position of the ST segment on an ECG?
The ST segment lies on the isoelectric baseline.
250
The ST segment lies on the isoelectric baseline.
It reflects myocardial injury or ischemia, especially in acute coronary syndromes.
251
What are the ECG criteria for ST segment elevation?
≥1 mm elevation in 2 or more contiguous limb leads, OR
≥2 mm elevation in 2 or more contiguous chest leads
252
What does “contiguous leads” mean?
Adjacent leads that view the same coronary artery territory.
253
What does ST segment elevation indicate?
Acute myocardial injury, classically a ST-elevation myocardial infarction (STEMI).
254
Which coronary territory is assessed by leads II, III, and aVF?
The inferior wall of the heart
255
What are the ECG criteria for ST segment depression?
≥0.5 mm ST depression in 2 or more contiguous leads.
256
What does ST segment depression usually represent?
Myocardial ischemia, often seen in NSTEMI or unstable angina
257
Can ST depression ever be reciprocal?
Yes — it may represent reciprocal changes opposite a STEMI.
258
What is the earliest ECG change in acute MI?
Hyperacute T waves (tall, broad T waves).
259
What ECG change follows hyperacute T waves?
ST segment elevation begins to appear.
260
What is the “tombstone” pattern?
Marked ST elevation with hyperacute T-wave, merging into a dome shape.
261
When do pathological Q-waves appear in MI?
With myocardial necrosis, indicating non-conducting tissue.
262
What ECG changes define a “fully evolved” MI?
Pathological Q-waves
ST elevation resolves
T-wave inversion
263
What do inverted T waves represent post-MI?
Myocardial ischemia or injury during recovery.
264
What ECG findings are seen during fibrosis after MI?
Persistent pathological Q-waves
T waves may normalize (upright)
265
Can pathological Q-waves disappear over time?
Yes, they may become smaller or disappear as fibrosis stabilizes.
266
Are all stages of MI evolution always seen on ECG?
No, not all six patterns are necessarily present in every patient.
267
What is the single most important question when assessing the ST segment?
Is it elevated or depressed in contiguous leads?
268
What should ST elevation always prompt clinically?
Urgent evaluation for acute MI and reperfusion therapy.
269
What is a mandatory step when interpreting ST changes on ECG?
Always localize the MI (STEMI or NSTEMI) using the affected leads.
270
Why is MI localization important?
It identifies the affected myocardial territory and the culprit coronary artery, guiding urgency and management.
271
Which ECG leads indicate a septal MI?
V1 – V2
272
Which coronary artery is usually involved in septal MI?
Which coronary artery is usually involved in septal MI?
273
Which ECG leads indicate an anterior MI?
V3 – V4
274
Which coronary artery supplies the anterior wall?
LAD
275
Which ECG leads indicate an apical MI?
V5 – V6
276
Which artery is usually the culprit in apical MI?
Distal LAD
277
Which ECG leads indicate a lateral MI?
I and aVL
278
Which coronary artery supplies the lateral wall?
Left circumflex artery (LCx)
279
Which ECG leads indicate an inferior MI?
II, III, and aVF
280
Which coronary artery most commonly causes inferior MI?
RCA (~90%)
LCx (~10%)
281
Why is posterior MI difficult to detect on standard ECG?
No posterior chest leads are routinely placed.
282
How does posterior MI appear on standard anterior leads?
As reciprocal ST depression in V1 – V3.
283
Which posterior leads can be added to confirm posterior MI?
V7, V8, and V9 (ST elevation confirms posterior MI)
284
Which coronary arteries may cause posterior MI?
RCA or LCx
285
What ECG pattern suggests infero-posterior MI?
ST elevation in II, III, aVF
ST depression in V1 – V3
286
Does localization apply to NSTEMI as well as STEMI?
Yes — NSTEMIs localize by ST depression and/or T-wave inversion in the same territories.
287
Which artery involvement is most dangerous due to large territory?
Proximal LAD (“widow maker”)
288
What should always be correlated with ECG localization?
Patient symptoms
Hemodynamics
Troponin levels
Echo findings
289
Which ECG finding should always raise suspicion of acute pericarditis?
PR segment displacement with widespread ST elevation
290
Which leads show characteristic PR segment changes in pericarditis?
Lead II and aVR
291
What PR segment change is seen in lead II in pericarditis?
PR segment depression
292
What PR segment change is seen in aVR in pericarditis?
PR segment elevation
293
What ST segment change is seen in lead II in pericarditis?
ST segment elevation
294
What ST segment change is seen in aVR in pericarditis?
ST segment depression
295
How is ST elevation distributed in acute pericarditis?
Widespread ST elevation in most leads
296
Which lead typically does not show ST elevation in pericarditis?
aVR (and sometimes V1)
297
What is the typical shape of ST elevation in pericarditis?
Concave (“saddle-shaped”) ST elevation
298
How does ST elevation in pericarditis differ from STEMI?
Pericarditis: diffuse, concave, no reciprocal ST depression (except aVR)
STEMI: localized, convex, reciprocal ST depression present
299
Can pericarditis present with sinus tachycardia?
Yes, with or without other ECG changes
300
What is the key “ECG exception rule” in pericarditis?
ST elevation everywhere EXCEPT aVR, which shows ST depression + PR elevation
301
What is the normal appearance of a T-wave?
Upright in most leads, smooth and asymmetrical, following the QRS complex.
302
What does an abnormal T-wave generally indicate?
Disordered ventricular repolarization
303
What is the earliest T-wave abnormality in acute myocardial infarction?
Hyperacute T-waves (tall, broad, and symmetric)
304
How do T-waves evolve during STEMI?
1. Hyperacute (tall, broad)
2. ST elevation
3. T-wave inversion (ischemia/necrosis)
4. Possible normalization or persistent inversion
305
What T-wave abnormality is typical of NSTEMI or ischemia?
T-wave inversion in contiguous leads.
306
What is the classic T-wave abnormality in hyperkalaemia?
Tall, peaked (“tented”) T-waves
307
How do hyperkalaemic T-waves differ from hyperacute MI T-waves?
Hyperkalaemia: narrow-based, sharp, symmetric
MI: broad-based, bulky, symmetric
308
What happens to the P-waves in worsening hyperkalaemia?
Flattening and eventual disappearance of P-waves
309
What QRS change is seen as potassium levels rise further?
Progressive widening of the QRS complex
310
What dangerous rhythms can severe hyperkalaemia lead to?
Ventricular fibrillation, sine-wave pattern, asystole
311
A patient has tall T-waves, absent P-waves, and a wide QRS. What is the most likely diagnosis
Severe hyperkalaemia
312
Why are T-wave abnormalities clinically important?
They may be the earliest sign of life-threatening conditions such as MI or electrolyte imbalance.
313
What does the QT interval represent on an ECG?
The total time for ventricular depolarization and repolarization.
314
From where to where is the QT interval measured?
From the start of the QRS complex to the end of the T-wave.
315
How can you quickly screen for QT prolongation on a rhythm strip?
If the QT interval is longer than half of the preceding R-R interval, it is prolonged
316
What formula is used to correct QT for heart rate?
Bazett’s formula:
QTc = QT / √RR
317
What QTc values are considered prolonged using Bazett’s formula?
Men: QTc > 0.44 s (440 ms)
Women: QTc > 0.46 s (460 ms)
318
What are the three main categories of causes of QT prolongation?
What are the three main categories of causes of QT prolongation?
319
What congenital condition is classically associated with prolonged QT?
Congenital Long QT Syndrome
320
Which electrolyte abnormalities commonly prolong the QT interval?
Hypokalaemia
Hypocalcaemia
Hypomagnesaemia
321
Name common drug classes that prolong the QT interval.
Antiarrhythmics (e.g. Class Ia, Class III)
Antipsychotics
Tricyclic antidepressants
Some antibiotics (e.g. macrolides)
322
Why is QT prolongation dangerous?
It predisposes to torsades de pointes, a potentially fatal polymorphic VT.
323
What rhythm is torsades de pointes associated with on ECG?
Polymorphic ventricular tachycardia occurring in the setting of a prolonged QT.
324
What clinical symptoms may suggest QT-related arrhythmias?
Syncope, seizures, palpitations, or sudden cardiac death.
General Medicine
flashcards
Decks in class (37)
# Cards
-
EOB Exams659
-
ECG Module 196
-
ECG Module 2153
-
ECG Module 3: normal sinus rhythm284
-
ECG Module 4: Wave abnormalities324
-
ECG Module 5: Rhythm abnormalities243
-
Chest X- ray165
-
Hypertension52
-
Advanced Airway Management341
-
CPR48
-
Post Cardiac Arrest Care35
-
CardioPulmonary Resuscitation532
-
Basic Airway Management122
-
Capnography41
-
Ventilator Settings27
-
Ventilation15
-
Anaphylaxis130
-
Cardiac Infections75
-
Benzodiazepine Overdose112
-
Iron Overdose92
-
Opioid Overdose122
-
Paracetamol Overdose107
-
TCA Overdose80
-
Bradycardia198
-
Tachycardia251
-
Hyponatremia121
-
Hyperthermia27
-
Hypothermia71
-
Hypertensive Emergency146
-
Delirium127
-
Sepsis105
-
Status Epilepticus108
-
Snack bites155
-
Acute Kidney Injury101
-
Pneumonia22
-
Bronchiectasis23
-
COPD40
