Lethal Rhythms

Ventricular Tachycardia (VT)

A Potentially life-threatening dysrhythmia.
VT exists when 3 or more PVC's occur in immediate succession at a rate of greater than 100 bpm.
VT may occur as a short run lasting less than 30 seconds (nonsustained), but usually persists for more than 30 seconds (sustained).
VT may occur with or after pulses and the patient may be stable or unstable.
VT originates from an ectopic focus in either ventricle.
When the QRS complexes of VT are the same shape and amplitude, the rhythm is termed Monomorphic VT. When the QRS complexes of VT vary in shape and amplitude, the rhythm is termed Polymorphic VT.

Characteristics of Monomorphic VT

Causes and Clinical Significance

VT is often associated with underlying heart ds, especially myocardial ischema.
Most common cause of Monomorphic VT in Americans is CAD with prior MI.
Causes include cardiomyopathy, digoxin toxicity, valvular heart ds, MVP, trauma (myocardial contusion, invasive cardiac procedures), acid-base imbalance, and electrolyte imbalance.
S/s vary.
Syncope may occur due to an abrupt onset. The only warning symptoms may include a brief period of lightheadedness.
S/s of hemodynamic compromise r/t increased heart rate include: shock, CP, hypotension, SOB, pulmonary congestion, CHF, acute MI, and/or decreased LOC.

Interventions

Tx is based on patient's presentation:
- Stable but symptomatic patients are tx with oxygen, IV access, and administration of ventricular antidysrhythmics.
- Unstable patients (usually a sustained heart rate greater than or equal to 150 bpm), whose s/s are a result of the rapid heart rate, are tx with Oxygen, IV access, meds, sedation. CPR should be initiated for the pulseless patient in VT until a defibrillator is available.

Torsades de Pointes (TdP)

A dysrhythmia between VT & VF.
A type of polymorphic VT associated with a prolonged QT Interval.
TdP is french for "twisting of the points," which describes the QRS that changes in shape, amplitude, and width, and appears to "twist."

Characteristics of TdP

Causes and Clinical Significance

TdP may be precipitated by a slow heart rate is associated with meds or electrolyte disturbances that prolong the QT interval, which indicates a lengthened refractory (or vulnerable) period that puts the ventricles at risk for TdP. A prolonged QT interval may be acquired or congenital.
S/s are r/t the decreased C.O. that occurs because of the fast ventricular rate. Patient may c/o palpitations, lightheadedness, or may experience syncopal episodes or seizures.
TdP may be initiated by a PVC and may occasionally terminate spontaneously and recur after several seconds or minutes, or may deteriorate to VF.

Interventions

Obtain a 12 lead ECG, correction of electrolyte abnormalities, and the following may be necessary for termination of sustained episodes and overdrive pacing, mg+, lidocaine, defib.

Ventricular Fibrillation

Chaotic rhythm that originates in the ventricles.
There is no organized depolarization of the ventricles. The ventricular myocardium quivers, and as a result, there is no effective myocardial contraction and no pulse.
Irregularly irregular rhythm with chaotic deflections that vary in shape and amplitude. No normal-looking waveforms are visible.
VF with low amplitude waves (less than 3mm) is called Fine VF.
VF with waves that are more easily visible (greater than 3mm) is called Coarse VF.

Characteristics of VF

Causes and Clinical Significance

85% of ambulatory out-of-hospital cardiac arrests in adults over 30 are r/t VT or VF, most often caused by myocardial ischema.
During progressive myocardial ischema, VT typically deteriorates into VF within an interval of 3 minutes.
The patient in VF is unresponsive, apneic, and pulseless.
Extrinsic factors that enhance the vulnerability of the myocardium to fibrillate include vagal stimulation, metabolic abnormalities, antidysrhythmics, and other meds (digoxin). Intrinsic factors include hypertrophy, ischema, myocardial failure, bradycardia.

Interventions

CPR should be initiated until a defibrillator is available. Defib with unsynchronized shocks, intubate, establish IV access, and administer meds (as per resuscitation guidelines).
A return of spontaneous circulation is more frequently associated with early defib of VF. Defib later in the course of VF is morelikely to result in asystole or PEA.

Asystole

Cardiac standstill.
Total absence of ventricular electrical electricity - thus, there is no ventricular rate or rhythm, no pulse, and no C.O.
Some atrial electrical activity may be evident. If atrial electrical activity is present, the rhythm is called P-wave Asystole.

Characteristics of Asystole

Causes and Clinical Significance

May occur because of extensive myocardial damage (from ischema or infarction), hypoxia, hypo/hyperkalemia, hypothermia, acidosis, drug OD, acute respiratory failure, ventricular aneurysm, traumatic cardiac arrest.

Intervention

Tx includes confirmation of the abuse of a pulse, immediate CPR, confirmation of the rhythm in 2 leads, intubation, IV access, consideration of the possible causes of the rhythm, consideration of early initiation of TCP, and med therapy.

Summary of Characteristics