Ventricular tachycardia is a life threatening rhythm. It falls into a class of rhythms called wide complex tachycardias (WCT's) and accounts for 80% of all WCT's. The characteristics of the rhythm can be defined by:
1. wide QRS complex
2. Rate greater than 100 beats per minute
3. AV dissociation (atrium and ventricles are not synchronized)
4. QRS is the same and consistent
5. Rhythm lasts for at least 30 seconds
Ventricular tachycardia starts or originates in the ventricular myocardium outside of the normal conduction system. The QRS complex is wide since the signal the ventricles get is slow and proceeds in a different sequence. Ventricular tachycardia can be a cause of sudden cardiac death (SCD). 450,000 people die annually in the united states of unexpected SCD. 50% of SCD occur as a first event in people thought to be low risk. VT is more common when a person has a structural heart disease such as:
1. Coronary heart disease (CHD) with prior heart attack
2. Hypertrophic cardiomyopathy
3. Dilated cardiomyopathy
4. Mitral valve prolapse
5. Aortic stenosis
6. Complex congenital heart disease
7. Cardiac sarcoidosis
8. Arrhythmogenic RV cardiomyopathy
CHD is a major risk factor for SCD accounting for 70% or 300,000 deaths per year in the united states. Common drugs associated with the onset of VT are cocaine and digoxin, quinidine or procainamide toxicity.
Symptoms can be mild such as palpitations, lightheadedness, weakness, sweating, abnormal sensation in the chest and polyuria (frequent urination). Worsening symptoms would be that the person is now developing low blood pressure and can lead to dizziness, presyncope (feeling of passing out) syncope (passing out), unconsciousness (e.g. Cardiogenic shock), seizures. The major problem with ventricular tachycardia is blood pressure stability otherwise known in medicine as hemodynamic compromise. The reason the heart is unable to sustain proper blood pressure is usually based on 1 or a combination of 5 factors:
1. Ventricular rate (too fast to be an effective pump)
2. Presence and severity of preexisting heart disease
3. Left ventricular function
4. Presence of AV asynchrony (Atrium out of sync with ventricles)
5. Location of the initiation of left ventricular activation
AV asynchrony is normal atrial function that does not coincide with ventricular function. Presence of such asynchrony strongly suggests VT as the diagnosis, but it's absence does not help define the diagnosis. AV asynchrony can be assessed 2 ways. On examination of the jugular vein in the neck. The practitioner can look for extra pulsations in the neck as the atria tries to pump blood through the closed AV valve. Since the ventricles are beating faster than the atria. In this case the atria are ineffective in moving the blood into the ventricle. The ventricles "beat, beat, beat" to the atria's one "beat". So it's hit and miss for the atria. In this case the atria and ventricles are not synchronized the top chambers are doing one thing and the bottom chambers are doing quite another. Secondly, through interpretation of the ECG by the presence of fusion or captured complexes. The P waves "march" through the QRS complexes.
The diagnosis of ventricular tachycardia can be tricky, as other fast rhythms can mimic VT. When a person already has a widened QRS complex normally or has a ICD, if SVT develops it can look like VT on the monitor. The treatment of the two rhythms are quite different. So it is imperative the clinician diagnose accurately. The doctor will presume it to be VT in absence of contrary evidence and treat accordingly. Studies have shown this approach to be appropriate since VT accounts for 80% of all WCT'S and treating SVT when someone has VT can cause cardiac arrest. However, treating as if it were VT has no ill effects and can be effective. So if someone were in SVT and got treatment for VT it could restore normal sinus rhythm. However, if someone was in VT and got treatment for SVT cardiac arrest could ensue. So always thinking VT is the best approach. Diagnosing VT is usually based on the interpretation of a rhythm of an ECG or monitor in the emergency setting. Having symptoms such as passing out could land someone in the emergency department, however the ECG could be normal and all the blood work could all be normal. Until the event is actual captured on the monitor there would be no way for health professionals to diagnose the VT. Through good history and risk factors for VT the doctors could set up some out patient testing or just send someone to the cardiologist then he or she could do the testing. The aim is to rule out structural heart defects and observe the rhythm over time like a holter monitor or doing a cardiac stress test that will monitor the heart under stress.
First, we would want to make sure the rhythm is VT and not artifact. Notice in the image below the QRS complexes "marching" through the rhythm. Before treatment can begin the rhythm needs to be verified.
The treatment of VT is dependent on how the patient presents or the symptoms the patient has at the time of treatment. It is the determination of a patient of either being stable or unstable that denotes how fast treatment will take place. A stable patient has normal vital signs or perfusable blood pressure. A blood pressure greater than 60 systolic is able to deliver oxygen and nutrients to the organs or perfuse the organs. The patient is awake and generally appears to be unstressed. An unstable patient has a blood pressure close to or below 60 systolic is unconscious or going unconscious. The person would be distressed looking, having active chest pain and possibly sweating. Once this determination is made usually within seconds of arrival, treatment begins. A stable patient means a clinician has time to review history, ECG's and try drugs first or if drugs fail to convert we will proceed to synchronized cardioversion. Any change along the way means the clinician needs to switch gears and follow the unconscious patient route. An unstable patient means the clinician has minutes to act. We don't usually worry about detailed history or ECG interpretation. If the monitor shows a VT like rhythm and the patient is unstable or pulseless we prepare to shock the heart back into rhythm. We don't generally worry about synchronized cardioversion in unstable patients, we just shock, shock, shock the heart into rhythm.
We start by placing pads to the right upper chest. On a hairy chest we might need to quickly shave first to make there is good contact from the gel on the pads to the skin. The second pad placement can be in two places the first place is on the side of the left chest centering to the midline of the armpit and just below the nipple. The second placement is to "sandwich" the heart with the two pads one on the front the other on the back. Generally the first placement works best for synchronized cardioversion. The synchronization comes into play when the monitor is told to identify the QRS complexes so a shock does not "land" on the complex and create further problems.
Possibly magnesium or has low magnesium if torsades de point
Potential causes especially if patient is unstable with no pulse:
1. Hypovolemia (low volume of blood)
2. Hypoxia (low oxygen)
3. Acidosis (increased acid in blood)
4. Hypo-hyperkalemia (low-high potassium)
5. Hypoglycemia (low blood sugar)
6. Hypothermia (low body temperature)
8. Cardiac tamponade
9. Tension pneumothorax
10. Thrombosis (blood clot)
Exercise stress test
Holter monitoring, continuous testing as the patient wears a monitor for 24 or 48 hours
Blood tests (magnesium and potassium, plus routine cardiac blood tests such as troponin and CK)