Wide complex tachycardia with three or more consecutive ventricular premature beats
Normal Sinus Rhythm
Patient will present as → a 37-year-old woman with a history of hypertension presents to the emergency department with complaints of shortness of breath. She was placed on a telemetry monitor. An EKG is performed and demonstrates a regular rhythm at a rate of 75 bpm, each QRS complex is preceded by a normal P wave, P waves are upright in leads I and II, and inverted in aVR, the PR interval remains constant, and each QRS complex is < 100 ms wide.
Normal sinus rhythm refers to both a normal heart rate and rhythm.
Normal heart rates are from 60 to 100 beats per minute.
Electrical impulse originates in the sinoatrial node (SA).
P waves are upright and appear before each QRS and have the same shape.
Intervals between the P waves are regular although some variations can occur with respiration.
Patient will present as → a previously healthy 34-y/o long-distance runner who sustained a prolonged viral illness followed by persistent fatigue. She was evaluated 6 months later for excessive heart rate increases with minimal exertion (walking across the room) associated with palpitations. She developed near syncope with running and was unable to keep up with her mother for more than a 500-m jog. Her resting heart rate was 95 b.p.m. without orthostatic changes in pulse or blood pressure. Heart rate with minimal exercise was 190 b.p.m., which slowed gradually upon rest; this was reproducible.
Sinus tachycardia is a normal sinus rhythm but with a heart rate over 100 bpm.
It is a normal response to exercise, excitement, and some illnesses
Patient will present as → a 65-year-old woman with a past medical history notable for squamous cell carcinoma of the vallecula. Her vital signs are HR 48 bpm, BP 90/70 mmHg, RR 11 rpm, and T 98.2F. The ECG demonstrates normal sinus rhythm with a rate of 48 beats/min.
Sinus bradycardia is a sinus rhythm with a rate of 40-60 bpm
Patient will present as → a 65-year-old woman with palpitations. Her past medical history is notable for chronic obstructive pulmonary disease (COPD) for which she has been hospitalized once in the last year. On exam her T 98.4F, HR 86, BP 105/70, RR 18, SpO2 94% on room air consistent with her baseline. The ECG demonstrates low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of narrow QRS complexes.
Irritable sites in the atria fire very rapidly, between 400-600 bpm
This very rapid pacemaking caused the atria to quiver
The ventricles beat at a slower rate due to the AV node is blocking of some of the atrial impulses
Elderly, excessive alcohol use
Symptoms range from syncope, dyspnea, palpitations to no symptoms
Irregularly irregular pulse
EKG: Low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of QRS complexes
Rate: Calcium channel blocker (diltiazem, verapamil) or beta-blocker (metoprolol)
Duration <48 hours - cardioversion, amiodarone (obtain echo to determine if a clot is present prior
Duration >48 hours - anticoagulation for 21 days prior to cardioversion
Anticoagulation is determined by CHA2DS2-VASc or CHADS2 scoring to assess the risk of stroke
0 points – no therapy or 81–325 mg/day of aspirin
1 point – either 81–325 mg/day of aspirin or anticoagulation
Patient will present as → a 74-y/o presents for her annual physical examination and notes increasing fatigue over the prior 3 months. Her history is notable for longstanding, but now well-controlled, systolic hypertension. A physical examination demonstrates a blood pressure of 130/70 mm Hg and an irregular pulse of approximately 120 bpm at rest. The ECG shows continuous and regular atrial activation with a sawtooth pattern, most obvious in leads II, III, and aVF.
There are two types of atrial flutter
Type I (also called classical or typical) has a rate of 250-350 bpm
Type II (also called non-typical) are faster, ranging from 350-450 bpm
Patient will present as → a 68-year-old male with complaints of “a fluttering sensation in the chest”, dizziness, and a syncopal episode earlier today. Vital signs are as follows: T 98.8 F, HR 40 (irregular), BP 90/56, RR 28, O2 Sat 95% RA. The physical exam is significant for a weak pulse, widened pulse pressure, crackles auscultated at the bilateral lung bases, and cannon a-waves noted at the internal jugular veins. An electrocardiogram is obtained and is shown here.
1st degree AV block: PR interval > .2 seconds
2nd degree AV block (Mobitz) two types:
Mobitz type 1 (Wenckebach) – longer, longer, drop now you’ve got a Wenckebach
Mobitz type 2 – some get dropped some get through now you’ve got Mobitz 2
3rd degree (complete block): P’s and Q’s don’t agree now you’ve got 3rd degree
First degree AV block
Patient will present as → a 45 y/o male presents for a preoperative physical. He feels well, with no significant PMH. A routine EKG is performed demonstrating a PR interval of greater than 0.20 seconds without associated disruption of atrial to ventricular conduction.
PR interval > .2 seconds
First-degree heart block is actually a delay rather than a block. It is caused by a conduction delay at the AV node or bundle of His. This means that the PR Interval will be longer than normal (over 0.20 seconds) without disruption of atrial to ventricular conduction.
(PR interval longer than 1 big box 0.20 seconds)
Second degree AV block Type 1 (Wenckebach) and Type 2 (Mobitz)
Type I: Wenckebach block
Patient will present as → a 44-year-old woman presents to the emergency room with a right radial fracture. Although she denies chest pain, a routine electrocardiogram is performed showing increasing PR intervals followed by a dropped beat.
Wenckebach (longer, longer, longer drop now you've got a Wenckebach)
With second-degree heart block, Type I (Wenckebach) some impulses are blocked but not all. More P waves can be observed vs QRS Complexes on a tracing
Each successive impulse undergoes a longer delay. After 3 or 4 beats the next impulse is blocked
On an EKG tracing, PR Intervals will lengthen progressively with each beat until a QRS Complex is missing. After this blocked beat, the cycle of lengthening PR Intervals resumes
The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4
Type II: Mobitz
Patient will present as → a 72-year-old female with a history of hypertension, hyperlipidemia, and type 2 diabetes presents to the ED for three days of intermittent palpitations and shortness of breath. She states that she has had trouble climbing the stairs at home. She denies any chest pain, syncope or near syncope, cough, or other complaints. Vital signs are normal except for a pulse of 50. An EKG is performed and demonstrates marked sinus bradycardia, nonspecific ST and T wave abnormalities, and P waves which occasionally have no corresponding QRS complex without prior prolongation of the PR interval.
MOBITZ 2 (some get dropped some get through now you've got mobitz 2)
With Mobitz Type II blocks, the impulse is blocked in the bundle of His. Every few beats there will be a missing beat but the PR Interval will not lengthen.
Third-degree AV block (complete heart block)
Patient will present as → a 29 y/o man presents with extreme fatigue and shortness of breath. On physical examination, the patient has bradycardia with a regular heart rate of 32/min and normal blood pressure. EKG demonstrates completely independent atrial and ventricular activity, with no relation between the P wave and the QRS complex.
P’s and Q’s don’t agree now you've got 3rd degree
With this block, no atrial impulses are transmitted to the ventricles.
As a result, the ventricles generate an escape impulse, which is independent of the atrial beat. In most cases, the atria will beat at 60-100 bpm while the ventricles asynchronously beat at 30-45 bpm.
There is no electrical communication between the atria and the ventricles complete AV dissociation. P waves do not match the QRS one for one
Patient will present as → a 32-year-old male presents to your clinic for evaluation of a recent onset of dizziness that occurred while he was upright and was generally associated with exertion. This especially concerned him since he was working as a bricklayer. During one episode at work, he found himself down on the floor but was not sure if he actually passed out. The patient smokes one pack of cigarettes per day and drinks four to six beers daily on the weekend. On physical examination, his blood pressure is 145/88 and his HR is 64 bpm and regular. He is modestly overweight, with a distribution of fat consistent with a beer belly. A 12-lead ECG showed sinus rhythm, rate 60, with an R and R’ (upward bunny ears) in V4-V6. There were no previous ECGs immediately available.
With this conduction block, either the left or right bundle branch is blocked intermittently or fixed.
The QRS complex is wider than normal (> 0.12 sec.).
Using a 12 lead EKG, blocks in either the left or right bundle branch may be diagnosed.
Wolff Parkinson White – Bundle of Kent fibers and delta wave on EKG
Multifocal atrial tachycardia: EKG: Irregular tachycardia, narrow QRS complex, abnormally shaped P waves with different morphology
Valsalva for stable patients
Adenosine for symptomatic patients
Definitive treatment: Radiofrequency ablation
WPW- do not administer adenosine nor calcium channel blockers
A faster than normal heart rate beginning above the heart's two lower chambers in the atria, AV junction, or SA node
Patient will present as → a 25-year-old female patient with complaints of sudden onset of a pounding heartbeat, which is regular and “too rapid to count.” She reports that the episodes begin and terminate abruptly and are associated with shortness of breath and chest discomfort. On exam, the patient appears anxious, her heart rate is 170 bpm. EKG demonstrates a shortened PR interval, widened QRS, and delta waves.
This occurs when the impulse travels between the atria and ventricles via an abnormal path, called the bundle of Kent
The impulse, not being delayed by the AV node, can cause the ventricles to contract prematurely
EKG characteristics include a shorter PR Interval, longer QRS complex, and a delta wave (click here)
Multifocal Atrial Tachycardia
Patient will present as → a 72-year-old man is admitted for exacerbation of COPD. On the third day, he reports dizziness associated with occasional chest pain. His telemetry reveals an irregular rhythm with a pulse of 124/min. The EKG demonstrates an irregularly irregular rhythm, rate of 120 bpm, discrete P waves before every QRS complex with 4 different P wave morphologies.
When multifocal atrial tachycardia occurs, multiple (non-SA) sites are firing impulses.
EKG: Rapid irregular rhythm > 100 bpm. At least 3 distinct P-wave morphologies
Patient will present as → a 24-year-old college student complaining of a feeling as though his heart is momentarily stopping followed by a feeling of his heart in his throat. He appears anxious and reports a weight loss of about 7 lbs. over the past 3 months. On auscultation of his heart, you notice an occasional skipped beat, followed by a brief pause and then a regular rhythm. His laboratories reveal a TSH of 0.001 and on his EKG, you notice a wide, bizarre QRS complex, greater than 0.12 sec and no identifiable p wave.
Increased frequency with stimulants (Ie. Caffeine)
EKG: Irregular beats (three types)
PVC – widened QRS
PAC – abnormally shaped P wave
PJC – narrow QRS usually measured at 0.10 sec or less
Every 3rd beat – trigeminy. Every other beat- bigeminy
Treatment: None or beta-blockers if symptomatic
Premature atrial beats
Patient will present as → a 44-year-old man presents with several months of nearly constant palpitations and “skipped beats.” His past medical history is notable for hypertension and obesity, treated with gastric bypass surgery 9 years prior. He denies alcohol and illicit drug use. An EKG performed to assess his current symptoms of palpitations is notable for sinus rhythm with an abnormal (non-sinus) P wave followed by a normal QRS complex. Holter monitoring documented a 19% burden of unifocal PACs.
This occurs when an ectopic site within the atria fires an impulse before the next impulse from the SA node
EKG: An abnormal (non-sinus) P wave is followed by a QRS complex
If the ectopic site is near the SA node, the P wave will likely have a shape similar to a sinus rhythm. But this P wave will occur earlier than expected.
Premature junctional beats
Patient will present as → a 30-year-old woman presented to our outpatient clinic describing a 3-year history of palpitations. An EKG performed in the clinic demonstrates several premature narrow QRS complexes without a preceding p wave.
Premature QRS complexes without a preceding P wave. The QRS morphology is very similar to the sinus complexes
Premature junctional complex (PJC) occurs when an irritable site within the AV node fires an impulse before the SA node. This impulse interrupts the sinus rhythm
EKG: Narrow QRS complex, either (1) without a preceding P wave or (2) preceded by an abnormal P wave with a PR interval of < 120 ms
The QRS complex will be narrow, usually measured at 0.10 sec or less
Premature ventricular contractions
Patient will present as → a 24-year-old woman presents to your clinic with complaints of anxiety along with occasional palpitations. She reports that when they occur she feels a pause in her heart followed by an extra hard beat often times felt in her throat. Laboratory evaluation reveals a TSH of 0.02. EKG demonstrates normal sinus rhythm with occasional broad QRS complexes (≥ 120 ms) with abnormal morphology.
Premature ventricular complexes (PVCs) occur when a ventricular site generates an impulse. This happens before the next regular sinus beat.
EKG: Broad QRS complex (≥ 120 ms) with abnormal morphology.
Look for a wide QRS complex, equal or greater than 0.12 sec
Patient will present as → a 45- year-old male admitted to the hospital because of several months of sudden onset of recurrent weakness accompanied by flushing of the face and dizzy spells. The patient also had recurrent spells of chest pain localized to the sternal area. The symptoms last for 10-15 seconds and sometimes 30 seconds to a minute and go away without treatment. During his stay in the ICU, the patient had similar symptoms several times and the monitor showed long periods of asystole with no ventricular activity. This was associated with blood pressure drops and the patient felt dizzy. The echocardiogram is within normal limits.
A collective term used to describe dysfunction in the sinus node automaticity and impulse generation
Sinus bradycardia: Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age in children
Sinus pause: pause < 3 seconds
Sinus arrest: pause > 3 seconds
Tachy-Brady Syndrome: Episodes of alternating sinus tachycardia and bradycardia
Patient will present as → an 18-year-old student radiographer presents with a five-month history of blackouts which had latterly been occurring three or four times a day. They invariably occurred when she was standing, and from her description, there was no reason to think that the blackouts were other than vasovagal attacks, but their frequent occurrence was inconvenient. There were no other symptoms and no previous medical complaints. The pulse rate was 60 beats per minute and irregular; blood pressure was 100/60 mmHg with no postural drop. A three-minute electrocardiogram recorded during spontaneous respiration showed marked variation in the P-P intervals induced by respiration with an amplitude of 20-1%, well outside the normal range.
Sinus arrhythmia represents normal, minimal variations in the SA Node pacing rate in association with the phases of respiration.
Heart rate frequently increases with inspiration and decreases with expiration
Patient will present as →a 46-year-old female with a history of alcohol abuse is brought to the emergency room for altered mental status. Physical examination reveals a cachectic appearing female, normal breath sounds, and normal heart sounds without murmurs. In the emergency room, she becomes completely unresponsive for 1 minute and her blood pressure decreases to 50/30.
Torsade de Pointes is a special form of ventricular tachycardia
EKG: Polymorphic ventricular tachycardia that appears to be twisting around a baseline
Patient will present as → a 72-year-old male who develops coarse ventricular fibrillation while being monitored following an uneventful colonoscopy. He is immediately defibrillated using a biphasic defibrillator at 120 joules. The countershock is successful and he is converted to a sinus tachycardia. He has resumed spontaneous breathing.
Chaotic irregular deflections of varying amplitude and no useful contractions
No identifiable P waves, QRS complexes, or T waves
Rate 150 to 500 per minute
Amplitude decreases with duration (coarse VF -> fine VF)
Treat with unsynchronized cardioversion
Unsynchronized cardioversion - start CPR
Give 3 sequential shocks (120, 150, 180); assess rhythm
If VF persists --> do CPR and intubate
Administer two doses amiodarone 2-4 min. Administer 1 mg IV bolus epi every 3-5 minutes (will ↑ myocardial blood flow and ↓ cerebral blood flow and ↓ defib threshold)
An implantable cardioverter-defibrillator may be necessary
Patient will present as → a 68-year-old female who arrives at the emergency department after a syncopal episode at work. Physical exam reveals an obese, unresponsive female with bilateral nonpalpable radial, carotid, and distal pedal pulses. Vital signs are as follows: T 99.4 F and BP 88/47. An emergent EKG is obtained (seen here).
A sequence of three PVCs in a row is ventricular tachycardia.
The rate will be 120-200 bpm.
There are several different varieties of VT — the most being Monomorphic VT
Ventricular Tachycardia Monomorphic
Monomorphic ventricular tachycardia occurs when the electrical impulse originates in one of the ventricles. The QRS complex is wide. Rate is above 100 bpm.
EKG: Wide complex tachycardia
Stable- amiodarone, lidocaine
Unstable- CPR and defibrillation
Ventricular Tachycardia Polymorphic
Polymorphic ventricular tachycardia has QRS complexes that vary in shape and size. If a polymorphic ventricular tachycardia has a long QT Interval, it could be Torsade de Pointes.
Patient will present as → a 78-year-old man who was admitted with 3 days history of fluttering in the chest, shortness of breath, and epigastric pain radiating to the back. His medical history includes exertional angina, unobstructed coronaries in 2015, hypercholesterolemia, and a single-chamber permanent pacemaker for complete heart block in 1995. The patient is conscious and tachycardiac with a blood pressure of 105/70 mm Hg. His chest is clear with signs of congestive heart failure. Blood chemistry results showed normal serum sodium, potassium, calcium, and magnesium. His cardiac troponin is >1000. ECG demonstrates ventricular tachycardia with a pacing spike followed by a P wave or QRS complex.
Atrial and ventricular pacing can be seen on the ECG as a pacing stimulus (spike) followed by a P wave or QRS complex, respectively.
EKG: 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
EKG Pacing Spikes: Vertical spikes of short duration, usually 2 ms.