CVS L2: EKG Flashcards
Types of arrhythmias
- Based on heart rate: Bradyarrhythmias & Tachyarrhythmias
- Based on site of origin: Supraventricular & Ventricular
- Based on mechanism:
- Automatic, Triggered, or Re-entrant arrhythmias
Clinical presentation of patients with arrhythmias:
- Palpitation
- Lightheadedness
- Syncope
- Nonspecific presentations: fatigue, dyspnea, or exertional intolerance
Syncope due to cardiac arrhythmias:
- Bradyarrhythmias: Sinus node disease, second- and third-degree heart block and bradycardia associated with pacemaker malfunction
- Tachyarrhythmias: Ventricular tachycardia, torsades de pointes, Ventricular fibrillation and supraventricular tachycardia
- Patients with bradycardia often experience sudden loss of consciousness without warning,
- whereas those with tachyarrhythmias are more likely to describe palpitations
Patient 01: DDx
A 66-year-old man complains sudden onset of
transient loss of consciousness and postural tone since 8 months. The episode lasts for about 10-15 seconds and the patient recovers promptly without any resuscitative measures. Episodes are often associated with palpitations and lightheadedness. PE: BP 95/56 mm Hg
Heart Rate - 44 beats/min, regular
JVP: shows prominent “a” waves
Rest of his physical examination is unremarkable EKG: Number of P waves exceed that of QRS; P-R interval-not measurable; Long R-R intervals
Most likely diagnosis in patient 01 is: Complete Heart Block
- Other differentials are: ]
- Sick sinus syndrome
- Ventricular tachycardia
- Aortic stenosis
- Pulmonary stenosis
- Postural hypotension
- Vasomotor syncope
Presenting symptoms in this patient are: Syncope, palpitations.
Diagnosis of cardiac arrhythmias:
- The 12-lead electrocardiogram
- Vagal maneuvers – carotid massage
- Electrophysiological (EP) studies - The ability to trace specific pathways and map conduction
ECG Frontal Plane
- Normal axis ranges -30° and +110°
- Less than -30° is termed a left axis deviation
- Greater than +110° is termed a right axis deviation
ECG Horizontal plane
- V1 to V6
- Normal Sinus Rhythm
- Rhythm - Regular
- Rate – 60 to100 beats/min
- QRS Duration - Normal
- P Wave - Visible before each QRS complex
- P-R Interval - Normal (<5 small Squares. Anything above this would be 1st degree block)
- Indicates that the electrical signal is generated by the sinus node and travelling in a normal fashion in the heart
Mechanism of Bradyarrhythmias: 1. Reduced automaticity of the sinus node
- Result in slow heart rates or pauses
- If sinus node pacemaker activity ceases, the heart will usually be activated at a slower rate by other cardiac tissues with pacemaker activity (usually AV node)
- Reduced sinus node automaticity can occur during periods of increased vagal tone (sleep, carotid sinus massage), with increasing age and secondary to drugs (beta-blockers, calcium channel blockers)
Effect of stimulation of Vagus (parasympathetic) nerve on heart:
- On SA node: Decreases heart rate
- Known as negative chronotropic effect
- Mechanism: ACh binds with M2 receptors in SAN; Decrease in rate of rise of phase 4 and hyperpolarization of resting membrane potential lead to slow heart rate
Mechanism of Bradyarrhythmias: 2. Conduction block:
- The AV node and His bundle are the most vulnerable sites for blocked conduction between the atria and ventricles
- AV block can occur:
- Increasing age
- Increased vagal input
- Congenital disorders such as muscular dystrophy and tuberous sclerosis
-Acquired disorders such as sarcoidosis, gout, Lyme disease, SLE, ankylosing spondylitis, and coronary artery disease
Patient 02: DDX
A 35-year-old male is referred to a cardiology clinic for evaluation. Patient is asymptomatic. He was incidentally noted to have bradycardia. Physical examination:
Pulse: 40/min, regular BP: 90/46 mm Hg
JVP: Normal
Heart sounds: Normal S1 & S2 without any murmurs, gallops
Lab:
EKG: Markedly prolonged RR intervals with HR of 40 beats/min; PR interval & QRS interval are within limits.
Blood: Normal; Chest X ray: Normal
Most likely diagnosis in this patient: Sinus Bradycardia
Differential diagnosis:
- Hypothyroidism
- Hypothermia
- Digitalis toxicity
- Beta-blocker toxicity
Physiological causes of Bradycardia:
- Increased vagal tone
- Sleeping
Sinus Bradycardia
Sinus Bradycardia
ECG findings:
•Rhythm – Regular (constant RR intervals)
•Rate - less than 60 beats per minute (long RR int)
- QRS Duration - Normal
- P Wave - Visible before each QRS complex
- P-R Interval - Normal
Examples: Athletic person, increased vagal tone, Inferior wall MI, Hypothyroidism, Patient with brain injury with raised intracranial tension, Drug toxicity (Digitalis, Beta-blockers & Ca+2 channel blocker)
1st Degree AV Block
ECG findings:
- Rhythm – Regular
- Rate - Normal
- QRS Duration - Normal
- P Wave - Ratio 1:1
- P Wave rate - Normal
- P-R Interval - Prolonged (>5 small squares)
Mechanism: A conduction delay through the AV node but all electrical signals reach the ventricles. This rarely causes any problems by itself.
Example: Trained athletes
2nd Degree Block – Mobitz Type 1 (Wenckebach)
- Rhythm - Regularly irregular
- Rate - Normal or Slow
- QRS Duration - Normal
- P:QRS ratio - 1:1 for 2,3 or 4 cycles then 1:0.
- P Wave rate - Normal but faster than QRS rate
- P-R Interval - Progressive lengthening of P-R interval until a QRS complex is dropped
- Conduction block of some - not all atrial beats get through to the ventricles at the AV node
2nd Degree Block – Mobitz Type 2
- Rhythm - Regular between the conducted beats
- Rate - Normal or Slow
- QRS Duration – Normal
- P:QRS ratio - 2:1, 3:1
- P Wave rate - Normal but faster than QRS rate
- P-R Interval - Normal or prolonged but constant Cause: Electrical excitation sometimes fails to pass through the A-V node or bundle of His downwards
- Electrical conduction of the conducted beats is the same always (hence have a constant P-R interval)
- Rhythm - Regular
- Rate - Slow
- QRS Duration - Prolonged
- P Wave - Unrelated to QRS (AV dissociation) •P Wave rate - Normal but faster than QRS rate •P-R Interval – Variation
- No atrial impulses pass through the atrioventricular node. Ventricles generate their own impulse through an ‘escape mechanism’ from a focus somewhere within the ventricle at a regular, slow rate.
Tachyarrhythmias: THREE basic mechanisms for Tachyarrhythmias:
- Increased automaticity of pacemaker
- Spontaneous depolarizations
- Reentrant circuit – most common
Mechanism of Tachyarrhythmias:
1.Increased automaticity of the pace maker:
- More rapid phase 4 depolarization of the action potential of SA node leads to faster heart rate
- Examples: Sinus Tachycardia as in hyperthyroidism, Anxiety, Pheochromocytoma and pulm embolism
- Sinus Tachycardia
- Rhythm - Regular
- Rate - More than 100 beats per minute
- QRS Duration - Normal
- P Wave - Visible before each QRS complex
- P-R Interval - Normal
- The impulse generating the heart beats are normal, but they are occurring at a faster pace than normal Occurs in: Exercise, stress, fright, fever
Mechanism of Tachyarrhythmias:
- Spontaneous depolarizations:
- If repolarization is delayed (longer plateau period), spontaneous depolarizations (EAD/DAD) can occur in phase 3 or phase 4 of the ventricular/atrial action potential
- EAD: Early Afterdepolarization
- DAD: Delayed Afterdepol
- These depolarizations can repetitively reach threshold and cause tachycardia
Examples of tachyarrhythmias from spontaneous depolarizations (EAD/DAD) are:
- Long QT syndrome: Due to several specific ion channel defects
- Torsades de pointes: Class III antiarrhythmic drugs block K+ channels and hence their toxicity may produce tachyarrhythmias
Long QT syndrome:
- Reduced function of potassium channels leads to a prolonged plateau period, leading to a prolonged QT interval
- These patients are prone to triggered activity because of reactivation of sodium and calcium channels [early afterdepolarizations (EAD)]
- Triggered activity in the ventricles can lead to life- threatening ventricular arrhythmias
Torsades de pointes:
- A “twisting”, polymorphic ventricular tachyarrhythmia that is observed in situations where the QT interval has been prolonged
- A triggered arrhythmia, which may cause blackouts or even sudden death.
Mechanism of Tachyarrhythmias: 3. Reentrant circuit:
- due to anatomical or electrophysiological abnormalities
- Re-entry requires an area of slow conduction, unidirectional block, and two pathways.
A- Block at slow tract & fast moves down
B- Slow moves retrograde in fast tract and blocks the incoming next fast
C- Retrograde fast reenters in the slow tract
Origin of Re-entrant arrhythmias:
- From atrium: Known as SupraVentricular Tachycardia (SVT) – Examples, atrial tachycardia, atrial flutter and atrial fibrillation
- From Ventricle: known as Ventricular Tachycardia (VT)
- Atrio-Ventricular origin: Example, as in Wolff- Parkinson-White syndrome
Commonly occurring SVTs:
- Atrial Tachycardia (atrial rate: 150-250/min)
- Atrial Flutter (atrial rate: 250-350/min)
- Atrial Fibrillation (atrial rate: 350-600/min & multifoci)
- AV nodal reentrant tachycardia
Patient 03: DDx
A 46-year-old woman arrived in the ER complaining of sudden onset of palpitations, lightheadedness, and shortness of breath. These symptoms began approximately 2 hours previously.
PE: BP 95/70 mm Hg
Heart Rate - averages 170 beats/min, regular Rest of her physical examination is unremarkable
EKG: rapid P waves; P-R intervals are short but measurable; normal QRS complexes
- Most likely diagnosis in patient is:
- Supraventricular Tachycardia (most likely due to atrial tachycardia)
- Other differentials are:
- Ventricular tachycardia
- Acute MI
- Pulmonary embolism
How do you differentiate Supraventricular Tachycardia (SVT) from Ventricular Tachycardia (VT)
Look at the QRS complex:
- If the QRS complex is narrow/normal (within normal limits) - SVT
- If the QRS complex is wide – VT
- Atrial tachycardia - an example of SVT
- Rhythm - Regular
- Heart Rate - 140-220 beats per minute
- QRS Duration - Normal (narrow)
- P Wave - Often buried in preceding T wave
- P-R Interval - Depends on site of supraventricular pacemaker
- Impulses stimulating the heart are not being generated by the sinus node, but instead are coming from a collection of tissue around and involving the atrioventricular (AV) node
- Atrial Flutter – example of SVT
- Rhythm - Regular
- Heart Rate - Around 110 beats per minute
- QRS Duration - Normal
- P Wave - Replaced with multiple F (flutter) waves, usually at a ratio of 2:1 (2F - 1QRS) but sometimes 3:1
- P Wave rate - 300 beats per minute
- P-R Interval - Not measurable
- As with SVT the abnormal tissue generating the rapid heart rate is in the atria; the AV node is not involved in this case.
Patient 05: DDx
A 44-year-old male complains of occasional palpitations, shortness of breath, dizziness and chest discomfort.
Physical examination:
- Pulse: Irregularly irregular
- JVP: absent “a” waves
- Heart sounds: variable intensity S1
- Lab:
- EKG: Variable ventricular rate (80-180); Indistinguishable P waves; PR interval not measurable & Irregular RR intervals.
- Blood: CK-MB normal
- Chest X ray: Normal
Most likely diagnosis in this patient: Atrial Fibrillation (AF)
Differential diagnosis:
- Atrial tachycardia
- Atrial flutter
- Ventricular tachycardia
- Wolff-Parkinson-White syndrome
Most common complication of AF: systemic thromboembolism
Atrial Fibrillation
- Rhythm - Irregularly irregular
- Heart Rate - usually 80-180 beats per minute
- QRS Duration - Usually normal
- P Wave - Not distinguishable as the atria are firing off all over (absent or fibrilatory waves)
- P-R Interval - Not measurable
- Many sites within the atria are generating their own electrical impulses, leading to irregular conduction of impulses to the ventricles that generate the irregular pulse
Patient 04:
A 17-year-old boy is referred to a cardiologist by a primary care physician for evaluation of recurrent spells of dizziness. During the episodes, he feels intense anxiety with palpitations and breathlessness. He is asymptomatic in between episodes; There is no h/o chest pain or syncope.
Physical examination:
No abnormalities detected
Lab:
EKG: Short PR interval; wide QRS with a slurred upstroke.
Blood: Normal; Chest X ray: Normal
Most likely diagnosis in this patient: Wolff-Parkinson-White Syndrome
Differential diagnosis:
- Atrial fibrillation
- Atrial flutter
- Syncope
- Nodal re-entry tachycardia
- Ebstein anomaly
Electrophysiological studies confirm presence of a bypass tract (Bundle of Kent)
- Short PR interval
- Wide QRS
- Delta wave (at arrow)
Ventricular Tachycardia (VT)
- Rhythm - Regular
- Rate - 180-190 Beats per minute
- QRS Duration – Prolonged (“wide QRS”)
- P Wave - Not seen
- Mechanism: Abnormal tissues in the ventricle generate a rapid heart rate and tachyarrhythmia
- Associated with a poor cardiac output
Ventricular Fibrillation (VF)
- Rhythm - Irregular
- Rate - 300+, disorganized
- QRS Duration - Not recognizable
- P Wave - Not seen
- This patient needs to be defibrillated!!
- Disorganized electrical signals cause the ventricles to quiver instead to contract in a rhythmic fashion
- Patient becomes unconscious as there in NO cardiac output
-This condition may occur during or after a myocardial infarct.
A Quick approach to Arrhythmias:
- First look at the heart rate:
- >100 bpm = tachycardia
- <60 bpm = bradycardia
- Are there extra beats? → Ectopic Beats Secondly assess the origin of the arrhythmia:
- If the QRS < 120ms (a narrow complex), then it is either a sinus arrhythmia, supraventricular rhythm or a junctional tachycardia
- If the QRS > 120ms it is either a ventricular tachycardia or a supraventricular rhythm with additional bundle branch block, additional accessory AV pathway
