Week 2 Ventricular Rhythms PDF

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Week 2 – 243 Ventricular Rhythms

Objectives -

Describe characteristics, possible causes, S&S, management for: o Premature ventricular complex o Idioventricular o Accelerated idioventricular o Ventricular tachycardia o Torsades de pointes o Ventricular fibrillation o Asystole

Ventricular Rhythms -

Ventricles may assume responsibility for pacing heart if: o SA node fails o Impulse from SA node generated but blocked as it exits SA node o SA node discharge slower than ventricles o Irritable site in either ventricle produces early beat or rapid rhythm

Premature Ventricular Complexes (PVC) -

Not a rhythm, just a single OR multi beat(s)

How Do I Recognize It? -

Arise from irritable focus in either ventricle Occurs earlier than next expected sinus beat QRS typically >0.12 sec T wave usually in opposite direction of QRS Usually and opposite direction of charges (QRS complex) Why is it wide? It goes cell-cell depolarization, slower than normal depolarization

How Do I Recognize It? -

Full compensatory pause usually follows a PVC P wave should be exactly where it is expected to be, stay on rhythm P-P interval will stay the same

PVC Patterns Pairs (couplets) 2 sequential PVCs Runs or bursts >3 sequential PVCs Bigeminal PVCs (ventricular bigeminy) Every other beat is a PVC Trigeminal PVCs (ventricular trigeminy) Every 3rd beat is a PVC Quadrigeminal PVCs (ventricular quadrigeminy) Every 4th beat is a PVC **Important to note: Not all of them conduct pulses

How Do I Recognize It? Uniform PVCs -

Similar morphology in same lead, originate from same ectopic focus

Uniform ventricular bigeminy w/ multiple PVCs

Uniform ventricular trigeminy w/ multiple PVCs

Multiform PVCs -

PVCs have different morphology in same lead Often (but not always) arise from different foci

R-on-T PVCs -

R wave of PVC falls on T wave of preceding beat PVC occurring here (relative refractory period) can cause VT or VF

Pairs and Runs -

2 PVCs in a row called “couplet” or “paired PVCs” >3 PVCs in a row at a rate >100bom called “salvo’, “run”, or “burst” of VT

PVC – How Do I Recognize It? Rate Rhythm P waves PR Interval QRS

Usually normal, but depends on underlying rhythm Depends on underlying rhythm, with premature beats Usually absent or, with retrograde conduction to atria, may appear after QRS (usually upright in ST-segment or T wave) None with PVC because ectopic originates in ventricle >0.12 sec, wide and bizarre T wave usually in opposite direction of QRS complex

What Causes It? -

Normal variant – odd PVC occurring is not concerning unless it falls on the T wave!! Hypoxia Stress, anxiety Digitalis toxicity Acid-base imbalance Myocardial ischemia Electrolyte imbalance Congestive heart failure Exercise Increased sympathetic tone Acute coronary syndromes Stimulants Medications (Sympathomimetics, TCAs, Phenothiazines)

What Do I Do About It? -

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Patients may be asymptomatic or complain of: o Palpitations o “Racing heart” o Skipped beats o Chest or neck discomfort If PVCs are frequent, decreased cardiac output possible o PVCs do not usually generate output Treatment of PVCs is dependent on: o Cause o Signs and symptoms o Clinical situation

Ventricular Escape Beats -

Appear late instead of early, until the SA node kicks in to start depolarization ‘safety’ mechanism

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Look just like a PVC Idioventricular Rhythm

How Do I Recognize It? -

IVR – three or more ventricular escape beats in a row, rate of 20-40 bpm “Agonal rhythm” – usually pre-arrest rhythm o Ventricular rate 0.12 sec, T wave frequently in opposite direction of QRS complex

What Causes It? -

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IVR may occur when: o SA node and AV junction quit o Rate of discharge of SA node or AV junction intrinsic rate slower than ventricular rate o Impulses generated by supraventricular pacemaker site are blocked IVR may also occur because of MI, digitalis toxicity, or metabolic imbalances

What Do I Do About It? -

Slow rate and loss of atrial kick may result in decrease CO If slow, symptomatic: o Consider Atropine (anticholinergic) – block PSNS in the vagus nerve that will affect SA & AV node  therefore increase SA & AV node firing rate

o o

Transcutaneous pacing (TCP) *Tx of choice* Others? Not lidocaine! Accelerated Idioventricular Rhythm

How Do I Recognize It? -

AVIR – three or more ventricular escape beats occur in a row, rate of 41-100 bpm o Some physicians consider ventricular rate range of AIVE to be 41-120 bpm o Vtach tends to be >120 beats/min (in real life)

Rate Rhythm P waves PR Interval QRS

41-100 bpm Essentially regular Usually absent or, with retrograde conduction to atria, may appear after QRS (usually upright in ST-segment or T wave) None >0.12 sec, T wave frequently in opposite direction of the QRS complex

What Causes It? -

Usually considered benign, transient escape rhythm o Appears when sinus rate slows, disappears when sinus rate speeds up Often seen during first 12 hours of MI Common after successful reperfusion therapy, usually paroxysmal Digitalis toxicity Cocaine toxicity Subarachnoid hemorrhage Acute myocarditis Hypertensive heart disease Dilated cardiomyopathy – chamber of ventricle gets enlarged and then you lose contractility

What Do I Do About It? -

Treatment usually unnecessary Danger of deterioration If patient is symptomatic because of loss of atrial kick: o Atropine may be indicated

Atrial pacing may be attempted (attempt to overdrive) No ventricular antiarrhythmics? Don’t chock it unless absolutely necessary!  Not Vtach, pt. still has a pulse, rhythm can resolve itself

o o

Ventricular Tachycardia (VT)

How Do I Recognize It? -

VT – three or more PVCs occur in a row, rate of >100 bpm* (in the field >120 bpm) o Non-sustained VT – A short run lasting 30 sec

Non-sustained VT 

Sustained VT 

Monomorphic VT Rate Rhythm P waves PR Interval QRS

101-250 bpm (some will argue 121-250) Essentially regular Usually absent (if present, dissociated) None 0.12 sec – often difficult to tell QRS from T wave

Polymorphic VT – middle ground between monomorphic and VF* Rate Rhythm P waves PR Interval QRS

150-300 bpm Typically 200-250 bpm May be regular or irregular, d/t multiple sites in the ventricle firing off None None >0.12 sec Gradual alteration in amplitude and direction of QRS complexes Typical cycle consists of 5-20 QRS complexes

 Monomorphic VT

Polymorphic VT  Polymorphic VT – TDP -

Twisting of the points Hard to get rid of Can go into VF Treatment of choice is magnesium sulfate

VT – What Causes It? Anything that can make the ventricles irritable Long QT interval can cause someone to have an arrhythmia -

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Acute coronary syndromes Cardiomyopathy TCA overdose Digitalis toxicity Valvular heart disease Cocaine abuse Mitral valve prolapse Acid-base imbalance Trauma o Myocardial contusion o Invasive cardiac procedures Electrolyte imbalance o Low K+, high K+, low Mg+ Abnormal QT interval Brugada – congenital disease that is hard to detect, usually only in an electrophysiology lab

VT – What Do I Do About It? -

Signs and symptoms vary Syncope/near-syncope may occur because of abrupt onset of VT o Only warning symptom may be transient light headedness Treatment based on patient’s signs and symptoms and type of VT o PMVT usually symptomatic Severity of symptoms depends on: o How rapid ventricular rate is o Duration of tachycardia o Presence and extent of underlying heart disease

Important Note -

SVT with aberrant conduction can be difficult++ to distinguish from VT o Treat rhythm as VT until proven otherwise Vtach is more common than SVT with aberancy (blockage in bundle branches)

Pulseless Electrical Activity (PEA) -

PEA – a clinical situation, nor a specific dysrhythmia PEA: organized electrical activity (not VT/VF) present on monitor, but patient VSA

PEA – Causes -

Pulmonary embolism Acidosis Tension pneumothorax Cardia tamponade Hypovolemia (most common cause of PEA) Hypoxia Heat/cold (hypothermia/hyperthermia) Hypokalemia/hyperkalemia (and other electrolytes) Myocardial infarction Drug overdose/accidents (cyclic antidepressants, calcium channel blockers, beta-blockers, digoxin)

Ventricular Fibrillation (VF)

How Do I Recognize It? -

Chaotic rhythm originating in ventricles Ventricles quivering – low amplitude Always pulseless

VF – What Causes It? -

Increase SNS activity Vagal stimulation Electrolyte imbalances Antiarrhythmic & other meds Environment (eg. Electrocution) Hypertrophy ACS Heart failure Other arrhythmias

What Do I Do About It? -

CPR & defibrillation Drugs??

Asystole -

Absence of any (ventricular) rhythm Tx: resuscitate

Questions and Answers Why is a PVC always wide? A. B. C. D.

One of the bundle branches is blocked Depolarization happens cell to cell They originate from the AV junction Depolarization is more rapid than usual

What do you call a rhythm in which every other beat is a PVC? A. B. C. D.

Sustained V-tach Ventricular trigeminy A salvo Ventricular bigeminy...