Ventricular Dysrhythmias

Ventricular Dysrhythmias
14 Ventricular Dysrhythmias Fast & Easy ECGs, 2nd E – A Self-Paced Learning Program

Premature ventricular complex (PVC) Ventricular escape complexes or rhythm Ventricular tachycardia Ventricular fibrillation Asystole

Key features: Wide (> 0.12 seconds in duration), bizarre QRS complexes T waves in the opposite direction of the R wave Absence of P waves

Occur when: The atria, AV junction, or both, are unable to initiate an electrical impulse There is enhanced automaticity of the ventricular myocardium

Can be benign or they can be potentially life-threatening (because the ventricles are ultimately responsible for cardiac output) Instructional point: A primary concern when approaching ventricular dysrhythmias is what the impact is on cardiac output. The patient must be carefully assessed for the underlying cause such as myocardial ischemia or infarction. I

Premature Ventricular Complexes (PVCs)
Early ectopic beats that interrupt the normal rhythm Originate from an irritable focus in the ventricular conduction system or muscle tissue Instructional points: PVCs can occur for no apparent reason in individuals who have healthy hearts and are usually of no significance. The incidence of PVCs increases with age and can occur during exercise or at rest. However, PVCs may also be significant for two reasons. First, they can precipitate more serious dysrhythmias such as ventricular tachycardia or fibrillation. The danger is greater in patients experiencing myocardial ischemia and/or infarction. Second, PVCs can result in decreased cardiac output due to reduced diastolic filling time and a loss of atrial kick. PVCs may produce a palpable pulse but they may also produce a diminished or nonpalpable pulse (called a nonperfusing PVC). Patients frequently experience the sensation of “skipped beats.” Note: A PVC is not an entire rhythm—it is a single beat I

Causes of PVCs Enhanced automaticity or reentry, brought about by disruption of the normal electrolyte shifts during cell depolarization and repolarization Causes include:

Appearance of PVCs PVCs are typically followed by a compensatory pause
Question to ask the students: “What is a compensatory pause?” Answer: the pause that follows a premature beat is called a compensatory pause if the normal beat following the premature complex occurs when it was expected. In other words, the period between the complex before and after the premature beat is the same as two normal R-R intervals. Q

Note: “Uni” means single, “multi” means many
Appearance of PVCs PVCs that look the same are called uniform (unifocal) PVCs that look different from each other are called multiform (multifocal) Uniform Instructional point: Multiformed PVCs are more concerning because they suggest that the ventricles are more irritable as the early beats are arising from more than one location. Note: “Uni” means single, “multi” means many I Multiform

Groupings of PVC PVCs that appear after every
other normal beat are called bigeminal PVCs second normal beat are called trigeminal PVCs third normal beat are called qudrigeminal PVCs Bigeminal Trigeminal Quadrigeminal

Couplets of PVCs Two PVCs in a row are called a couplet and indicate extremely irritable ventricles

Interpolated PVCs PVCs that fall between two regular complexes and do not disrupt the normal cardiac cycle are called interpolated PVCs Question to ask the students: “Will interpolated PVCs have a compensatory pause?” Answer: No, they do not. Q

Note: it may also be called a salvo, run, or burst of VT
Run of PVCs Three or more PVCs in a row are called a run of ventricular tachycardia or a run of PVCs Note: it may also be called a salvo, run, or burst of VT

R-on T PVCs PVCs occurring on or near the previous T wave (R-on-T PVCs) may precipitate ventricular tachycardia or fibrillation Instructional point: The reason is that a portion of the T wave is vulnerable to electrical stimulation during what is referred to as the relative refractory period. I

Effects of PVCs PVCs can be significant for two reasons
they can precipitate more serious dysrhythmias such as VT or VF they can result in decreased cardiac output due to reduced diastolic filling time and a loss of atrial kick Instructional point: PVCs may produce a palpable pulse but they may also produce a diminished or nonpalpable pulse (called a nonperfusing PVC). Patients frequently experience the sensation of “skipped beats.” Note: When no pulse is felt during a PVC, it is called a nonperfusing PVC I

Treatment of PVCs Asymptomatic patients seldom require treatment
Patients with myocardial ischemia, treatment of frequent PVCs includes: administration of oxygen and placement of an IV line identifying and correcting the underlying factor causing the PVCs in some settings, administering lidocaine or other antidysrhythmics (e.g., amiodarone) by IV push and a continued maintenance infusion administering potassium chloride intravenously to correct hypokalemia or magnesium sulfate intravenously to correct hypomagnesemia; adjusting drug therapy; or correcting acidosis, hypothermia, and/or hypoxia

Ventricular Escape Beats
Occur when there is temporary cessation of the heartbeat such as with sinus arrest or when the rate of the underlying rhythm falls to less than that the inherent rate of the ventricles

Causes of Ventricular Escape Beats
Are compensatory in nature, occur when a higher pacemaker fails to initiate a heartbeat Meant to preserve cardiac output Can occur in sinoatrial pause/arrest, by a failure of the conductivity from the SA node to the AV node, or by AV (especially 3rd degree AV block)

Effects of Ventricular Escape Beats
Low heart rate associated with the event leading up to the appearance of ventricular escape beats can result in a drop in blood pressure and syncope Ventricular escape beats should be temporary as the heart should resume its normal electrical activity

Treatment of Ventricular Escape Beats
Centers on treating the underlying condition Support circulation, airway, and breathing; deliver oxygen; monitor the ECG, blood pressure and pulse oximetry; and establish an IV infusion Continually reassess the clinical status and correct any reversible conditions A primary goal of treatment is to maintain a ventricular rate sufficient to produce adequate cardiac output Atropine or transcutaneous pacing can be used to treat the symptomatic patient Drugs used to suppress ventricular activity such as lidocaine and amiodarone are contraindicated and may be lethal

Idioventricular Rhythm
Slow dysrhythmia (rate of 20 to 40 BPM) with wide QRS complexes that arise from the ventricles Question to ask the students: “What is the key difference between idioventricular rhythm, accelerated idioventricular rhythm and ventricular tachycardia?” Answer: The heart rate. Instructional points: The decreased cardiac output associated with this dysrhythmia will likely cause the patient to be symptomatic (hypotension, syncope, etc.). Patient assessment is essential because the escape rhythm may be perfusing or nonperfusing. Idioventricular dysrhythmias are also common during cardiac arrest as they represent the final escape rhythm to be generated in an attempt to perfuse the body. Q I

Causes of Idioventricular Rhythm
Massive myocardial ischemia or MI, digoxin toxicity, pacemaker failure, and metabolic imbalances Other causes include:

Effects of Idioventricular Rhythm
Slow ventricular rate and loss of atrial kick can significantly decrease cardiac output resultant decreased cardiac output will likely cause patient to be symptomatic Signs of decreased cardiac output such as disorientation, unconsciousness, hypotension, and/or syncope, and the patient may complain of dizziness, chest pain, and/or shortness of breath In extreme cases, patient is pulseless Instructional point: PVCs may produce a palpable pulse but they may also produce a diminished or nonpalpable pulse (called a nonperfusing PVC). Patients frequently experience the sensation of “skipped beats.” I

Treatment of Idioventricular Rhythm
For symptomatic patients: Support the airway and breathing Deliver oxygen, perform an ECG, monitor the blood pressure and pulse oximetry, and place an IV infusion Continually reassess the clinical status, and correct any reversible conditions Maintain a ventricular rate sufficient to produce adequate cardiac output Administer atropine or deliver transcutaneous pacing In unresolved idioventricular rhythm, the atropine dose may be repeated Lidocaine and amiodarone are contraindicated If there is no pulse, treat the dysrhythmia as if it is pulseless electrical activity (PEA)

Accelerated Idioventricular Rhythm
Idioventricular rhythm that exceeds the inherent rate of the ventricles (60 to 100 BPM)

Causes of Accelerated Idioventricular Rhythm
Same conditions that lead to idioventricular rhythm Also, it is very common following acute MI Further, it is often seen after administering thrombolytic medications For that reason, it is considered a reperfusion dysrhythmia

Effects of Accelerated Idioventricular Rhythm
While accelerated idioventricular rhythm is usually short lived and because the heart rate is close to normal, no ill effect may be seen However, with accelerated idioventricular rhythm there may be decreased cardiac output, particularly when the rate is slower Question to ask the students: “What is a compensatory pause?” Answer: the pause that follows a premature beat is called a compensatory pause if the normal beat following the premature complex occurs when it was expected. In other words, the period between the complex before and after the premature beat is the same as two normal R-R intervals. Instructional point: PVCs may produce a palpable pulse but they may also produce a diminished or nonpalpable pulse (called a nonperfusing PVC). Patients frequently experience the sensation of “skipped beats.” Q I

Treatment of Accelerated Idioventricular Rhythm
Depends on whether the rhythm is sustained and whether or not cardiac output is diminished For the symptomatic patient, transcutaneous pacing or atropine can be used In unresolved idioventricular rhythm, the atropine dose may be repeated A permanent pacemaker may be required in sustained symptomatic accelerated idioventricular rhythm Lidocaine and amiodarone are contraindicated and may be lethal If there is no pulse, treat the dysrhythmia as if it were pulseless electrical activity (PEA)

Ventricular Tachycardia (VT)
Fast dysrhythmia (100 to 250 BPM) that arises from the ventricles Instructional point: Clinically, ventricular tachycardia is always significant. Even if the rhythm results in a pulse, it should be considered as potentially unstable, as patients are likely to develop worse rhythms and cardiac arrest. Usually VT indicates significant underlying cardiovascular disease. I

Ventricular Tachycardia
Present when there are 3 or more PVCs in a row May come in bursts of 6 to 10 complexes or may persist (sustained VT)

Causes of Ventricular Tachycardia
Increased myocardial irritability that may be triggered by: enhanced automaticity, PVCs that occur during the downstroke of the preceding T wave, reentry in the Purkinje system Other causes include:

Effects of Ventricular Tachycardia
Always significant May be perfusing or nonperfusing Even if the rhythm produces a pulse, it should be considered as potentially unstable because patients are likely to develop more life-threatening rhythms which progress into cardiac arrest The rapid rate and concurrent loss of atrial kick associated with VT results in compromised cardiac output and decreased coronary artery and cerebral perfusion Severity of symptoms varies with the rate of the VT and the presence and degree of underlying myocardial dysfunction Instructional point: The gravest concern is that VT may initiate or deteriorate into VF I

Treatment of Ventricular Tachycardia
Maintain a patent airway, administer oxygen, and place an IV line Stable patient can be treated with antidysrhythmics (such as procainamide, amiodarone, or sotalol) Unstable patients are managed with immediate synchronized cardioversion (100 J) Energy level may be increased if the tachycardia does not convert with initial treatments (100, 200, 300, 360 J or the biphasic equivalent) Contributing causes should be considered and treated Patients with pulseless VT should be treated as though they are in VF Instructional Point: The patient experiencing decreased level of consciousness, ongoing chest pain, shortness of breath, low blood pressure, or other signs of shock should be considered clinically unstable. I

Ventricular Tachycardia
Monomorphic - appearance of each QRS complex is similar Polymorphic - appearance varies considerably from complex to complex

Causes of Torsades de Pointes
Associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on the ECG Causes include:

Effects of Torsades de Pointes
Depends on the rate and duration of tachycardia and the degree of cerebral hypoperfusion Findings include rapid pulse, low or normal blood pressure, or syncope or prolonged loss of consciousness Pallor and diaphoresis may be noted, especially with a sustained episode Can degenerate into VF

Treatment of Torsades de Pointes
Cannot be reliably synchronized and should be managed like ventricular fibrillation (VF), with an initial unsynchronized shock Standard antidysrhythmic drugs (such as procainamide) can worsen the condition, leading to cardiac arrest Amiodarone may be effective in stable patients with normal QT interval Magnesium sulfate should be administered in stable patients with prolonged QT interval Offending drug(s) should be discontinued and electrolyte imbalance corrected Patients with pulseless VT should be treated as though they are in VF, with the treatment of choice being prompt defibrillation

Ventricular Fibrillation (VF)
Results from chaotic firing of multiple sites in the ventricles Causes heart muscle to quiver rather than contract efficiently, producing no effective muscular contraction and no cardiac output Instructional point: On the cardiac monitor, ventricular fibrillation appears like a wavy line, totally chaotic, without any logic. I

Ventricular Fibrillation
Most commonly associated with significant cardiovascular system disease Causes include:

Ventricular Fibrillation
Death occurs if patient not promptly treated (defibrillation) Most common cause of prehospital cardiac arrest in adults

Treatment of Ventricular Fibrillation
Prompt delivery of CPR and defibrillation Organize ACLS actions around uninterrupted periods of CPR Initiate securing the airway and placing an IV line in the course of treatment After one shock and a 2-minute period of CPR, administer epinephrine or vasopressin Amiodarone may be considered when VF/VT is unresponsive to CPR, defibrillation, and vasopressor therapy If amiodarone is unavailable, lidocaine may be considered if allowed by local protocol Continue CPR, stopping only to defibrillate and reassess rhythm. Minimize interruptions in chest compressions before and after shock; resume CPR beginning with compressions immediately after each shock Instructional Point: It is critical to provide high-quality CPR (with chest compressions of adequate rate and depth, allowing complete chest recoil after each compression, minimizing interruptions in chest compressions, and avoiding excessive ventilation). Rotate the person delivering chest compressions every 2 minutes. When an out-of-hospital cardiac arrest is not witnessed by healthcare or EMS personnel, you may initiate CPR while checking the rhythm with the AED or on the ECG and preparing for defibrillation. In such instances, 1½ to 3 minutes of CPR may be considered before attempting defibrillation. I

Treatment of Ventricular Fibrillation
If the rhythm is successfully converted to an effective electromechanical rhythm (with a pulse and good perfusion): assess vital signs, support airway and breathing, provide medications to support blood pressure, heart rate, and rhythm and to prevent reoccurrence

Asystole Absence of any cardiac activity
Appears as a flat (or nearly flat) line Complete cessation of cardiac output Instructional point: The presence of asystole should always be verified in two leads prior to initiating treatment. I

Ventricular Standstill
Called ventricular standstill when the atria continue to beat but the ventricles have stopped Seen as the presence of only P waves

Asystole Terminal rhythm Chances of recovery extremely low
Instructional point: Asystole may be the primary event in cardiac arrest or it may occur in complete heart block when there is no functional escape pacemaker. I

Treatment of Asystole Promptly initiate CPR, deliver high-concentration oxygen, place an IV line, and secure the airway Administer epinephrine, repeating its administration every 3 to 5 minutes One dose of vasopressin may replace either the first or second dose of epinephrine Continue CPR throughout the resuscitation effort, stopping periodically to reassess for a change in rhythm and to check for presence of a pulse Follow local protocols for terminating resuscitation efforts Always verify the presence of asystole in two leads prior to initiating treatment Misplacement of an ECG lead or a loose wire can mimic asystole (or VF) on the monitor

Pulseless Electrical Activity (PEA)
Condition that has an organized electrical rhythm on the ECG monitor (which should produce a pulse) but patient is pulseless and apneic Instructional point: Sinus rhythm, sinus tachycardia, idioventricular rhythm, or other rhythms may be the electrical activity seen with PEA. I

Treatment of PEA Includes prompt initiation of CPR, high-concentration oxygen, placing an IV line, securing the airway and confirming placement Administer epinephrine, repeating its administration every 3 to 5 minutes One dose of vasopressin may replace either the first or second dose of epinephrine Continue CPR throughout the resuscitation effort, stopping periodically to reassess for a change in rhythm and to check for a pulse

Practice Makes Perfect
Determine the type of dysrhythmia Answer: Atrial rate absent, Ventricular rate 40 BPM, regular rhythm, absent P waves, QRS complexes are wide and bizarre-looking at 0.20 seconds, PRI is immeasurable, QT 1.12 seconds. Idioventricular rhythm. I

Determine the type of dysrhythmia Answer: Atrial rate absent, Ventricular rate 188 BPM, regular rhythm, absent P waves, QRS complexes are wide and bizarre-looking at 0.16 seconds, PRI is immeasurable, QT 0.32 seconds. Ventricular tachycardia. I

Determine the type of dysrhythmia Answer: Immeasurable heart rate, totally irregular, absent atrial waveforms, no QRS complexes, PRI is immeasurable, QT is immeasurable. Ventricular fibrillation. I

Determine the type of dysrhythmia Answer: Atrial rate absent, Ventricular rate 56 BPM, regular rhythm, absent P waves, QRS complexes are wide and bizarre-looking at 0.16 seconds, PRI is immeasurable, QT seconds. Accelerated idioventricular rhythm. I

Determine the type of dysrhythmia Answer: Atrial rate absent, Ventricular rate 188 BPM, regular rhythm, absent P waves, QRS complexes are wide and bizarre looking at 0.24 seconds, PRI is immeasurable, QT is immeasurable. Ventricular tachycardia. I

Determine the type of dysrhythmia Answer: Atrial rate 86 BPM, Ventricular rate 86 BPM, frequent irregularity, upright and normal P waves in the underlying rhythm there are no P waves associated with premature beats, normal QRS complexes at 0.08 seconds in underlying rhythm wide, bizarre looking QRS complexes at 0.16 seconds in early beats, PRI seconds in underlying rhythm and absent in the premature beats, QT in the underlying rhythm and 0.40 seconds in the premature beats. Normal sinus rhythm with frequent premature ventricular complexes (PVCs) (2nd, 5th complexes). I

Determine the type of dysrhythmia Answer: Atrial rate 136 BPM, Ventricular rate 136 BPM, patterned irregularity (every fourth beat is a premature beat quadrigeminy), P waves are upright and tall in the underlying rhythm but absent with the premature beats, QRS (more accurately described as QS) complexes are 0.06 seconds in duration in the underlying rhythm but wide and bizarre in the early beats at 0.20 seconds, PRI seconds in duration for the normal beats but absent with the premature beats, QT 0.28 seconds in the underlying rhythm and 0.36 seconds in the early beats. Sinus rhythm with quadrigeminal premature ventricular complexes (PVCs). I

Determine the type of dysrhythmia Answer: Atrial rate 98 BPM, Ventricular rate 98 BPM, frequent irregularity, upright and notched P waves in the underlying rhythm but P waves are absent with the premature beats, QRS complexes are normal at 0.12 seconds in duration in the underlying rhythm but wide and bizarre in the early beats at 0.14 seconds, PRI seconds in duration for the normal beats but absent with the premature beats, QT seconds in the underlying rhythm and 0.40 seconds in the premature beats. Normal sinus rhythm with frequent multiformed premature ventricular complexes (PVCs) (2nd, 4th, 7th and 9th complexes). I

Determine the type of dysrhythmia Answer: Atrial rate 82 BPM, Ventricular rate 82 BPM, occasional irregularity, upright and normal P waves in the underlying rhythm but P waves are absent with the premature beats, QRS complexes are normal at 0.08 seconds in duration in the underlying rhythm but wide and bizarre in the early beats at 0.14 seconds (in the 1st PVC) and 0.20 seconds (in the 1st PVC), PRI 0.12 seconds in duration for the normal beats but absent with the premature beats, QT 0.30 seconds in the underlying rhythm and 0.36 to 0.40 seconds in the premature beats. Normal sinus rhythm with multiformed premature ventricular complexes (PVCs) (2nd and 7th complexes). I

Summary Ventricular dysrhythmias occur when the atria, AV junction, or both, are unable to initiate an electrical impulse or when there is enhanced excitability of the ventricular myocardium A key feature of ventricular dysrhythmias are wide (greater than 0.12 seconds in duration), bizarre QRS complexes that have T waves in the opposite direction of the R wave and an absence of P waves Ventricular dysrhythmias include: premature ventricular contraction (PVC), ventricular escape complexes or rhythm, ventricular tachycardia, ventricular fibrillation, and asystole

Summary Premature ventricular complexes are early ectopic beats that interrupt the normal rhythm and originate from an irritable focus in the ventricular conduction system or muscle tissue Idioventricular rhythm is a slow dysrhythmia with wide QRS complexes that arise from the ventricles at a rate of 20 to 40 beats per minute

Summary Ventricular tachycardia is a fast dysrhythmia, between 100 to 250 beats per minute that arises from the ventricles. It is said to be present when there are three or more PVCs in a row. It can occur with or without pulses, and the patient may be stable or unstable with this rhythm.

Summary VT may be monomorphic, where the appearance of each QRS complex is similar, or polymorphic, where the appearance varies considerably from complex to complex Ventricular fibrillation (VF) results from chaotic firing of multiple sites in the ventricles causing the heart muscle to quiver rather than contracting efficiently, producing an absence of effective muscular contraction and cardiac output Asystole is the absence of any cardiac activity Appears as a flat (or nearly flat) line on the monitor screen and produces a complete cessation of cardiac output

Summary Pulseless electrical activity (PEA) is a condition in which there is an organized electrical rhythm on the ECG monitor (which should produce a pulse) but the patient is pulseless and apneic Sinus rhythm, sinus tachycardia, idioventricular rhythm, or other rhythms may be the electrical activity seen with PEA

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