Stable or Unstable?

     Assessment and management of ventricular tachycardia with pulses At 0934 on a Sunday morning you are dispatched to a 64-year-old male simply reported as "pale." Upon your arrival, the first responder reports that the patient's wife noticed "he did not look right" after breakfast. Your patient is seated in his easy chair, alert and oriented, with no chief complaint other than his wife's observation of paleness. The first responder also reports that he cannot feel a radial pulse or auscultate a blood pressure, which you confirm. The patient is already on oxygen, 12 liters per minute via non-rebreather mask. The heart monitor shows ventricular tachycardia at 190 beats per minute.

     How do you treat this patient? He has no complaint, yet has no blood pressure. Hypotension—low blood pressure—is a sign of hemodynamic instability, so you must prepare for the worst. Clearly, this patient needs immediate care. His hypotension means cardioversion is indicated; however, he is not in obvious distress, so should you medicate? Sedation is preferred before cardioversion, so why not try a round of antiarrhythmics first? This article will help clarify hemodynamic instability regarding ventricular tachycardia management when pulses are present.

WHAT IS VT?

     Ventricular tachycardia is a serious and often fatal dysrhythmia that can occur with or without pulses. Each year over 300,000 patients die from sudden cardiac death, which includes ventricular tachycardia and ventricular fibrillation. This represents nearly one-half of all cardiac-related deaths. Estimating the actual number of patients is difficult because not all patients who experience ventricular tachycardia seek medicial aid before going into cardiac arrest. Untreated, pulsed v-tach can quickly deteriorate into ventricular fibrillation.

     Too often, paramedics are trained to look for ventricular tachycardia on the cardiac monitor and then determine if the patient is stable or unstable. Instead, a well-trained provider at any level of care should look at the patient, not the cardiac monitor, to determine the patient's stability. For example, there are patients with stable and unstable chest pain. Patients experiencing shortness of breath can be stable. Nonetheless, a stable patient may still require field management, advanced life support and an ambulance. Thus, determining whether a patient is stable or unstable cannot be the deciding factor for whether an EMT-Basic requests ALS or a paramedic initiates ALS care. Stable patients can still be in distress and have serious medical problems. Thorough medical providers must anticipate what may go wrong and have interventions in place to either prevent or be ready for those potential problems. Use your experience, good judgment and consultation with online medical control to determine the best patient care and transport priority.

CAUSES OF VT

     Ventricular tachycardia is one of the more commonly treated life-threatening dysrhythmias in the United States. Myocardial ischemia and infarction are the leading causes of ventricular tachycardia with pulses.1 When myocardial tissue is deprived of adequate oxygenation, it becomes irritable and experiences an increase in its automaticity. Irritated and oxygen-deprived myocardial cells can stimulate a heart to contract. An increase in irritability and automaticity allow multiple foci to stimulate cardiac contractions. Cardiomyopathy, the dilation and hypertrophy of the left ventricle, is directly correlated to an increased risk of sudden cardiac death and ventricular fibrillation. Many forms of heart disease can cause VT, including aortic stenosis heart failure, structural deterioration, congenital disorders, myocarditis and cardiomyopathy.

     Electrolytes in the body, such as potassium and calcium, must remain in a narrow therapeutic, or beneficial, range. When electrolyte concentrations become too high or too low, a variety of cardiac dysrhythmias can develop. The most common electrolyte-based causes of ventricular tachycardia include hypokalemia, hypocalcemia and hypomagnesemia.² It is critical for paramedics to recognize these conditions; if they are left untreated, rhythm correction is nearly impossible. Of the three imbalances, hypokalemia poses the greatest risk for dysrhythmia development, followed by hypomagnesemia, which can trigger torsade de pointes. Of interest, patients with preexisting heart disease may also develop VT from hyperkalemia.¹

     Any sympathomimetic agent (a chemical that stimulates the sympathetic nervous system, or stimulates a sympathetic response) can trigger ventricular tachycardia. An excellent example of this is cocaine. Treatment of drug-induced ventricular tachycardias often requires special treatments and is beyond the scope of this article.

PATIENT ASSESSMENT

     Last year, my uncle experienced a sudden onset of crushing chest pain. Before he could reach the phone, he collapsed on the floor, gasping for air. Fortunately, he was wearing a cardiac monitor that alerted his physician's office and paramedics were automatically dispatched. When the paramedics arrived, they made a forced entry and found my uncle, pale, diaphoretic and only able to speak in fragmented sentences. Every provider would agree he was an unstable patient. If you are a BLS provider, what would you have done in this situation if you had arrived on scene before paramedics?

     Remember the patient introduced in the beginning of this article? The chief complaint was his wife's observation of paleness. Was he stable or unstable? Although he had no blood pressure, he had no complaints and was perfusing adequately. He did not change over time. He was stable.

     Begin assessing all patients by determining the chief complaint. If there are no initial-assessment life threats, obtain a history of present illness using the O-P-Q-R-S-T mnemonic. Ask if the patient has attempted any interventions like taking a prescribed nitroglycerin tablet.

     Use the information gained from O-P-Q-R-S-T to help make your decision on whether the patient is stable or unstable, knowing an EKG rhythm is not needed to make the decision. Obtaining a SAMPLE history and a focused physical exam will help further your decision- making. During the physical exam inspect for: jugular vein distention, peripheral cyanosis, rales, diaphoresis, hypoxemia and mental status changes. Check pulse oximetry and the patient's blood sugar. Quite often, patients have a decreased pulse oximetry. Provide supplemental oxygen to all symptomatic patients.

     There are many signs and symptoms associated with pulsed VT. The most common include:

• Jugular vein distention
• Peripheral cyanosis
• Rales
• Diaphoresis
• Hypoxemia
• Mental status changes
• Chest pain
• Palpitations
• Shortness of breath
• Dizziness
• Weakness
• Nausea
• Anxiety.

     Remember to determine patient stability without using the cardiac monitor. One symptom alone generally doesn't make a patient unstable. Unstable patients will have many of these symptoms, while a stable patient may present with only one or two subtle symptoms.

     According to the American Heart Association, a patient is unstable when he presents with v-tach and a pulse, and v-tach is the cause of one or more of the following:

• Altered mental status
• Loss of consciousness
• Shock
• Hypotension with symptoms of hemodyamic instability
• Pulmonary edema
• Poor perfusion.³

     Simply put, a patient is unstable whenever ventricular tachycardia causes hemodynamic instability, which is recognizable with good BLS patient assessment skills. It does not require cardiac monitoring or rhythm identification. In most cases, patients who are awake, oriented and able to speak in full sentences are stable. Patients who present with a rapidly declining mental status are unstable. Patients who are clearly not perfusing adequately and are visibly declining in front of you or over a short period of time are unstable.

     Begin cardiac monitoring after you have made your decision, then print a rhythm strip for analysis. Most cardiac monitors have the option of monitoring and printing three leads at one time. Take advantage of this feature, because proper rhythm analysis requires multiple lead views. If time and training allow, obtain a 12-lead EKG on all stable patients.

     There are no absolute criteria for diagnosing ventricular tachycardia. When determining VT, consider heart rate and width and shape of the QRS complexes.¹ Ventricular tachycardia is partially identified by a rate greater than 120 beats per minute (bpm) and usually less than 220 bpm. Remember that tachycardia is any rate over 100 bpm. It is uncommon for VT to develop at a rate less than 120 bpm, and it is even less common to see VT with serious symptoms below 150 bpm.

     The QRS complex represents ventricular contraction. A normal ventricular contraction takes less than 120 milliseconds. In ventricular tachycardia, this contraction takes longer because of the distance the electric signal causing the contraction must travel. By definition, the QRS complex must be at least 120 milliseconds wide during ventricular tachycardia. On a rhythm strip, this is represented with a widened QRS complex (120 milliseconds equals three small boxes on EKG paper).

     When ventricular tachycardia is slow, between 100 and 130 beats per minute, P waves may occasionally be visible, at which time there will be no correlation between the P waves and QRS complexes. Total AV disassociation is another indicator that the rhythm is ventricular tachycardia. Monomorphic ventricular tachycardia originates from a single ectopic foci and is recognized by all QRS complexes, appearing uniform in shape and size. You can recognize polymorphic ventricular tachycardia by the presence of multiple differently shaped QRS complexes. Polymorphic ventricular tachycardia originates from two or more ectopic foci.

     One of the most notorious forms of polymorphic VT is torsade de pointes, translated literally as a "twisting of the points." This represents a shifting of the axis of QRS complexes and is usually caused by drug exposures or physiologic conditions that cause a prolonged Q-T interval.¹ Torsade is usually recognized by its twisting appearance. It is imperative to recognize torsade de pointes because rhythm conversion can only be obtained by correcting the underlying cause. Do not attempt to defibrillate torsade.

     Once recognized, ventricular tachycardia with a pulse requires rapid management and correction. Although a patient may appear to be compensating well for the dysrhythmia, ventricular tachycardia can rapidly deteriorate into pulseless ventricular tachycardia or ventricular fibrillation.

STABLE OR UNSTABLE?

     Ventricular tachycardia is unstable any time a patient is in dysrhythmia and hemodynamic compromise. This is most often associated with mental status changes or a loss of consciousness.

     Ventricular tachycardia may also be considered unstable when the patient presents with at least two of the following:

• Respiratory distress
• Ongoing or worsening chest pain
• Hypotension
• Signs of shock
• Pulmonary edema
• Inadequate perfusion.

     It is uncommon to see these symptoms when the heart rate is less than 150 beats per minute, and the symptoms typically are not seen alone, but present grouped together. If your patient presents with only one symptom, use caution in selecting immediate synchronized cardioversion. If you are considering sedation to decrease the level of consciousness prior to cardioversion, be sure you have already tried an IV antiarrhythmic.

     Once you have determined whether the patient with VT is stable or unstable, develop a treatment plan. As you begin care, consider whether the patient's heart rhythm is causing the symptoms you see, or if some other condition is causing the patient to be in ventricular tachycardia. If you can identify the underlying problem, correct it while treating the rhythm. Failing to correct the underlying cause will often result in inability to correct the rhythm.

     Stable or unstable, all patients with ventricular tachycardia should receive reassurance and be placed in a position of comfort. Always provide VT patients with supplemental oxygen via nasal cannula or non-rebreather mask. Monitor pulse oximetry to ensure adequate oxygenation; attempt to keep SpO₂ above 90%.

     Monitor blood pressure and check vital signs at a minimum of every 5 minutes. ALS providers should initiate large-bore IV access because the patient's blood pressure could drop at any point. IV access will also facilitate administration of antiarrhythmic medications.

     If the patient presents in stable ventricular tachycardia, confirm the rhythm with a 12-lead EKG, keeping in mind that the following rhythms can mimic ventricular tachycardia:

• SVT and atrial fibrillation with aberrancy
• Accelerated idioventricular rhythms
• Pre-excited tachycardias with accessory pathways
• Torsade de pointes.⁴

     Remember, if there is no AV disassociation, the rhythm is not ventricular tachycardia. AV disassociation is signaled by the presence of P waves not correlated to any QRS complexes.

MEDICATIONS

     After confirming ventricular tachycardia, and the patient is stable, ALS providers may administer antiarrhythmic medications. Antiarrhythmics work to decrease irritability of the heart, which may allow the heart's inherent pacemaker to take over contraction stimulation. The ideal antiarrhythmic treatment includes a drug bolus followed by a maintenance infusion.

AMIODARONE

     Amiodarone is the American Heart Association's antiarrhythmic of choice for VT;⁴ however, this was not based on evidence but rather on expert opinion. Several recent drug reviews found amiodarone less effective at rhythm conversion than procainamide and just as effective as lidocaine.^5,6 After confirming ventricular tachycardia, administer 150 milligrams of amiodarone IV over 10 minutes. This generally can be repeated once in the prehospital setting, although a maintenance IV is often established in the ED at a rate of 1 mg/min. If allowed, establish an amiodarone drip following rhythm conversion.³

PROCAINAMIDE

     Ventricular tachycardia can be managed with procainamide, which eliminates the dysrhythmia more effectively than amiodarone.⁵ Procainamide decreases ventricular automaticity and slows conduction through the myocardium. Since only two studies have ever demonstrated its effectiveness, it remains a second-line medication. Administer procainamide 20–30 mg/min through an IV drip. Procainamide has been shown to cause hypotension, especially in situations when left ventricle function has been impaired. This drug has also been known to induce atrioventricular conduction disturbances, including heart block, and must be used with extreme caution in patients who have previously received amiodarone.¹

     Discontinue procainamide administration as soon as one of the following conditions is met:

• The dysrhythmia is converted
• The patient becomes hypotensive—a systolic blood pressure less than 90
• The QRS complex widens by 50%
• The patient is given a total of 17 mg/kg.

LIDOCAINE

     Lidocaine, formerly the drug of choice for v-tach termination, has been linked to an increase in asystole following defibrillation; however, there are few other side effects, and it is considered safer than some antiarrhythmics. Lidocaine suppresses premature ventricular contractions by raising the irritability threshold of ventricular tissues.7 The recommended dose is 1–1.5 mg/kg given as an IV bolus. This dose can be repeated at 5- to 10-minute intervals to a maximum dose of 3 mg/kg. If necessary, lidocaine can be administered through an endotracheal tube; amiodarone cannot.⁴ Following rhythm conversion, begin a lidocaine drip between 1–4 mg/min.³

MAGNESIUM SULFATE

     When a patient presents in torsade de pointes with pulse, administer 1–2 grams of magnesium sulfate over 5 to 60 minutes as an IV drip diluted in 50–100 ml of D₅W.⁴

UNSTABLE VT

     Unstable ventricular tachycardia is treated by ALS providers with immediate synchronized cardioversion. Begin preparation for cardioversion by placing the cardiac monitor pads on the patient. The American Heart Association recommends the use of hands-free pads over hand-held paddles.⁴ Hands-free pads provide better skin contact, are safer and provide more consistent electricity delivery.

     When considering sedatives and analgesics for cardioversion, remember that synchronized cardioversion is a very invasive emergency procedure performed on unstable patients. If your patient is stable enough to delay cardioversion for sedatives, he or she is likely also stable enough to have antiarrhythmics administered before cardioversion. Sedation is generally administered to patients to help prevent the memory of cardioversion. Midazolam is more frequently used, but may worsen or cause hypotension. Amidate does not have as profound an effect on blood pressure and may be more appropriate for patients who are already hypotensive.

     Also consider administering an analgesic either with sedation or shortly following cardioversion. Sedatives have no pain control properties, thus using a sedative alone may sedate patients, but they will still experience the pain associated with cardioversion. Since analgesics are not routinely administered with cardioversion, consult your medical director before initiating this practice.

SYNCHRONIZED CARDIOVERSION

     Synchronized cardioversion is an advanced cardiac life support skill that cannot be performed by basic EMTs or with an automated external defibrillator. Before each cardioversion attempt, be sure to press the cardiac monitor's synchronization button to synchronize energy delivery at the appropriate point during QRS complex. Failure to synchronize cardioversion can result in energy delivery during the heart's relative refractory stage, which is likely to result in ventricular fibrillation. You will know the heart monitor is synchronized by the presence of a dot on the top of each QRS complex. Press the synchronization button before each attempted cardioversion.

UNSYNCHRONIZED CARDIOVERSION

     Patients with polymorphic ventricular tachycardia can also present with instability; however, it is often impossible to perform synchronized cardioversion in these patients. The American Heart Association states, as a general rule, if you cannot synchronize the QRS complexes with your eye, the defibrillator also will not be able to synchronize them. In these instances, and if allowed by protocol, perform unsynchronized cardioversion at high energy levels: 360 joules for monophasic defibrillators; 150–200 joules for biphasic defibrillators.

ENERGY LEVEL SELECTION

     When performing synchronized cardioversion with a monophasic defibrillator, use stepped increases in energy levels, delivering the first cardioversion at 100 joules. If additional cardioversion attempts are necessary, deliver the energy at 200, then 300 and finally 360 joules.

     When using a biphasic defibrillator, use the manufacturer's recommended energy level, which is normally between 120–200 joules. There is no need to increase the amount of energy with each cardioversion attempt when using a biphasic defibrillator.⁴

POST-CONVERSION

     Once the ventricular tachycardia has converted, recheck the patient's airway, breathing and circulation, determine the level of consciousness and perform a neuro exam as necessary. Begin an IV infusion of an antiarrhythmic to decrease the chances of a recurring dysrhythmia.

SUMMARY

     Ventricular tachycardia represents ectopic cells within the ventricles stimulating the heart to contract. Many conditions cause ventricular tachycardia, including myocardial muscle deterioration and drug stimulation. The symptom most suggestive of unstable ventricular tachycardia is a change in mental status or loss of consciousness. Stable ventricular tachycardia is managed with antiarrhythmic medications, while unstable ventricular tachycardia requires immediate cardioversion. After converting ventricular tachycardia to a sinus rhythm, administer an antiarrhythmic infusion.

References

1. Compton S. Ventricular Tachycardia. Emedicine.com. www.emedicine.com/med/topic2367.htm.

2. Ernoehazy W. Ventricular Tachycardia. Emedicine.com. www.emedicine.com/emerg/topic634.htm.

3. The American Heart Association. Part 5: Electrical Therapies: Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing. Circulation 112: IV-35–46, 2005.

4. The American Heart Association. Part 7.3: Management of Symptomatic Bradycardia and Tachycardia. Circulation 112: IV-67–77, 2005.

5. Tomlinson DR, et al. Emerg Med J 25(1):15, Jan 2008.

6. Marill KA, et al. Ann Emerg Med 47(3):217, March 2006.

7. The American Heart Association. Part 7.2: Management of Cardiac Arrest. Circulation 112: IV-58–66, 2005.

     Kevin Thomas Collopy, BA, CCEMT-P, NREMT-P, WEMT, is a flight paramedic for Spirit Medical Transportation Service in central Wisconsin. He is the author of numerous magazine articles, textbook chapters, and flash-based CE lessons. He is an adjunct EMS faculty member for Mid-State Technical College, a consultant with Emergency Preparedness Systems, LLC, and a lead instructor for Wilderness Medical Associates. You can contact him at kcollopy@colgatealumni.org.