ECG Flashcards
Palpitations
Light headed
SOB
ECG……
Atrial Flutter 2:1
Narrow complex tachycardia (usually 130 - 170)
Fairly Predictable atrial rate ~ 300BPM
Flutter waves in II, III, AVF
Ventricular rate determined by conduction ration.
Usually VR is 150 (2:1). Higher blocks are usually due to disease or medication. can have variable rate. If Ar and VR both 300 BPM emergency TFR to ED department.
Faint
SOB
slow pulse
Complete Heart Block
Bradycardia ~ 30BPM
Regular atrial rate
complete dissociation between P and QRS complexes.
Routine ECG,
Patient asymptomatic
Right Bundle Branch Block
Features rSR in Lead V1-V3 (M)
Lateral leads I, AVL, V5-V6 have a slight slur to the S wave (W) qRs
QRS if < 120 incomplete (esp young children, usually inocent),
QRS > 120 complete
Causes of Complete RBB include: PE, Right ventricular hypertorphy, IHD, Rheumatic HD, Myocarditis, Degenerative disease, Congenital Heart defect eg ASD.
Collapse
ECG……
Ventricular Fibrillation
Chaotic, Irregular
No discernable P wave, QRS or T wave
Rate > 150
Progressively changing amplitude, (Not as organised as Torsades which is a type of polymorphic VT)
Immediate Defibrillation
Palpitations
SOB
Tachycardia
Ventricular Tachycardia (Monophasic)
Broad complex QRS
Regular rate
signs of AV dissociation (may have to look hard for this)
Causes: Cardiomyopathy, IHD, HOCM, Brugada Syndrome.
Urgent transfer to ED
Progressively short of breath
Fatigue
Right Ventricular Hypertrophy
Features:
Right axis deviation of +110° or more.
Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
QRS duration < 120ms (i.e. changes not due to RBBB).
Supported by:
RV STrain Pattern: ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads.
Causes: Pulmonary hypertension, Mitral stenosis, Pulmonary embolism, Chronic lung disease (cor pulmonale), Congenital heart disease (e.g. Tetralogy of Fallot, pulmonary stenosis), Arrhythmogenic right ventricular cardiomyopathy
Nausea, vomiting, diarrhoea
Blurred vision, yellow/green discolouration, haloes
Palpitations, syncope, dyspnoea
Confusion, dizziness, delirium, fatigue
Digoxin Toxicity
ECG changes:
From typical Digoxin effect
Downsloping ST depression with a characteristic “sagging” appearance (Dalis Moustache).
Flattened, inverted, or biphasic T waves inc TU wave.
Shortened QT interval.
To:
Assorted Blocks, Bigeminy and Bidirectional VT
Palpitations
SOB
Muscle paralysis
Nausea and Vomiting
Parasthesiaes
Hyperkalemia
ECG changes:
Mild: peaked T waves
Moderate: P wave flattening, PR lengthening
Severe: Prolonged QRS, Bizarre QRS morphology, Heart blocks, Sinus Brady or Slow AF, Sine wave appearance
Arrest: Asystole, VF, PEA
Numbness and tingling of hands, feet, mouth and lips
Muscle cramps
Muscle Spasms (Tetany)
Convulsions
Diagnosis + Causes
Hypocalcemia
Prolonged QTc interval >450 Male, >470 Female
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)
Trouseaus sign - brachial artery occlusion for 3 mins causes wrist and MCP flexion, finger adduction and DIP + PIP extension (obstetricians hand)
Short of breath
Left ventricular hypertrophy
Large voltage on V1-V3 leads
LV strain pattern on lateral leads esp V6 = ST depression + T wave inversion. without coresponding ST elevation in inferior leads
ST elevation in V1-3.
Left axis deviation
Asymptomatic
1st degree AV HB
Constant prolonged PR interval > 200ms (5 small squares)
No dropped beats
Causes:
Inferior MI, Hyperkalemia, Beta Blockers, Ca Ch Blockers, Amiodarone, Myocarditis, Increased vagal tone, training, normal variant.
Management: No specific treatment required.
35 YO
Chest Pain
Syncope
Father died at 40
Brugada Syndrome
Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave
And one of:
Documented VF or polymorphic VT
Family history of sudden cardiac death at <45 years old .
Coved-type ECGs in family members.
Inducibility of VT with programmed electrical stimulation .
Syncope.
Nocturnal agonal respiration.
Management: Implantable Cardioverter - Defibrillator
Palpitations
Poor sleep
Agitation
Weight loss
ECG…….
Thyrotoxicosis
Associated with Sinus tachycardia or AF +/- High Left ventricular voltage (as in this example)
Patients with unexplained sinus tachycardia or atrial fibrillation should have their TSH and T4 checked to look for evidence of thyrotoxicosis.
Fatigue
Weakness
Low Mood
Constipation
Hoarse Voice
ECG ……
Hypothyroidism (myxoedema)
ECG:
Bradycardia
Low QRS voltage
Widespread T-wave inversions (usually without ST deviation)
May also have QT prolongation.
Corrects with T4 replacement.
History of known CAD
Presents with central chest pain
Left Bundle Branch Block
Broadened QRS complex >120s (3 small squares) if complete
Dominant S waves V1-V3 (right precordial leads)
Broad Dominant R wave (often notched) in I V5,V6 (lateral leads) producing a prolonged time to peak of >60ms in V5-V6
Discordant ST depression and T wave inversion (opposite direction to QRS dominance)
Often left axis deviation
Causes: Aortic stenosis, IHD, Hypertension, Dilated cardiomyopathy, Anterior MI, Hyperkalemia, Digoxin toxicity.
Chest pain + New LBB = urgent review.
Shortness of breath
Nonspecific chest pain
+/- calf pain and swelling
PE
Features:
Tachycardia (44%)
Non specific ST and T wave changes (50%)
Right Ventricular Strain (34%) T wave inversions precordial Vi,V2,V3 +/- inferior ii, III, AVF.
SiQiiiTiii (deep S in I; prominent Q in III; inverted T wave in IIi (20%)
RBBB (18%)
Right Axis Deviation (16%)
Nausea, Abdominal pain
Bone pain
Depression or Impaired cognition
ECG….
Hypercalcemia:
Shortening of the QT interval
J waves (Notched R wave esp in V1) (Severe)
Ventricular irritability and VF arrest with extreme hypercalcaemia
Irregular heart beat
Otherwise well
2nd Degree AV Block, Mobitz 1 (Wenckeback)
Progressive increase in PR interval with an eventual dropped beat
Note that an unconducted p wave is not required (though usually present)
Chest pain
Worse on lying flat
Relieved by lying forward
Acute 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.
Medications Causing QT prolongation
QTc > 460 Females
QTc > 440 Males
Antipsychotics: Olanzapine, Quetiapine
Antiarrhythmics: Amiodarone, sotalol
Antidepressants: TCA (eg. Amitriptyline ) SSRI (eg. escitalopram, venlafaxine, bupropion (zyban))
Antihistamines: eg loratadine
Antibiotics: Macrolides eg erythromycin, clarithromycin
QT interval should be measured in either lead II or V5-6
QTc > 500 is associated with increased risk of torsades de pointes
QTc is abnormally short if < 350ms
short of breath
Previous MI
Bifasicular Heart Block
Typically RBBB + LAFB
RBBB = Notched dominant R wave V1-V3, Dominant S wave V6
LAFB = Left axis deviation, tall R wave in AVL, small R in II, III and AVF
Same causes as LBBB: IHD, MI, Aortic Stenosis, Hyperkalemia, Digoxin, Hypertension
Female
Sudden Onset of Palpitations and dizziness
Chest tightness
Diagnosis and Management
AV Nodal Rentry Tachycardia (SVT)
The commonest cause of Supraventricular tachycardias in normal hearts esp: Female
Features: QRS < 120ms (If no other underlying condition,
Sometime alternating amplitude of QRS (QRS alterans)
Tachycardia 140 - 280,
P waves absent/burried or sometimes inverted in II, III, AVF
Often Have wide spread ST depression (non usually ischemic)
Management:
- Reassurance
- Attempt vasovagal maneuvers (iced water, Blow out syringe plunger, etc) Carotid massage,
- Adenosine
- CCB, BB, amiodarone sometimes used.
- DC cardiversion (Rare)
Irregular heart beat
Otherwise well
Variable 2nd Degree, Mobitz 2, AV Block (3:2 and 2:1)
Dropped QRS complex
Regular atrial rate
PR distance is constant for conducted beats (not progressively lengthening)
Often a pre existing LBBB or bifasicular block
Conduction pattern may be fixed or variable
Most likely due to structural damage eg: MI, Fibrosis, Autoimmune (SLE), Inflammatory (Rheumatic HD), Hyperkalemia, Meds: BB, CCB, Amiodarone
Weakness, Fatigue
Muscle cramps
Palpitations
Depression or psychosis
Hypokalemia
ECG Features: Increased amplitude and width of the P wave
increased PR interval, T wave flattening and inversion
ST depression, Prominent U waves
Apparent long QT interval due to fusion of the T and U waves (= long QU interval)
Late stages: AF, atrial flutter, atrial tachycardia, then Torsades, VT, VF
What is this ECG?
How would you manage this?
- Bradycardia - Tachicardia or Sick Sinus Syndrome
- a) Cease any Betablockers, CCBs or Digoxin
b) Correct Hypothyroidism or electrolyte disturbance (eg hyperkalemia)
c) Investigate for idiopathic fibrosis, Ischemic heart Disease, Cardiomyopathies, sarcoidosis, haemachromatosis, congenital cardiac abnormalities.
d) Urgent Cardiac review for monitoring and pacing.
45 YO
Dizziness
Palpitations
SOB
Wolff Parkinson White Syndrome
Features:
PR interval <120ms
Delta wave – slurring slow rise of initial portion of the QRS
QRS prolongation >110ms
ST Segment and T wave discordant changes – i.e. in the opposite direction to the major component of the QRS complex
Pseudo-infarction pattern can be seen in up to 70% of patients: eg. prominent R wave in V1-3 (mimicking posterior infarction).
