You will likely encounter, whether on a call shift or on your CCU rotation, a wide complex tachycardia. A wide complex tachycardia (WCT), defined by A widened QRS (≥120 msec) represents a unique clinical challenge for two reasons:
Patients may be unstable at the onset of the arrhythmia or deteriorate rapidly at any time. Therapeutic decisions are further complicated by the risks associated with giving therapy for an SVT to a patient who actually has VT. Since having the correct diagnosis is imperative to providing the most appropriate care, we want to go over some case scenarios.
- Diagnosing the arrhythmia is difficult – Although most WCTs are due to ventricular tachycardia (VT), the differential diagnosis includes a variety of supraventricular tachycardias (SVTs)
- Urgent therapy is often required
Patients may be unstable at the onset of the arrhythmia or deteriorate rapidly at any time. Therapeutic decisions are further complicated by the risks associated with giving therapy for an SVT to a patient who actually has VT. Since having the correct diagnosis is imperative to providing the most appropriate care, we want to go over some case scenarios.
Case #1: unstable ventricular tachycardia with a pulse. A 67 year old male with a CHF exacerbations has shortness of breath and his blood pressure drops from 119/85 to 84/42 mmHg. During the exam, he has chest pain. He is alert and oriented only to person, although previously he has been A & O to person, place, and time. The EKG is obtained and reveals a monomorphic WCT. You diagnose Ventricular Tachycardia.
What should you do next: Vasovagal maneuvers? Adenoxing 6 mg IV? Chest compressions? Emergent synchronized cardioversion? Vasovagal maneuvers followed by an IV Beta Blocker?
This patient is classified as unstable V Tach with a pulse. Thus the best thing to do is give a synchronized shock of 100 - 200 joules if you are using a monophasic machine or 50 - 100 joules if you are using a biphasic machine.
What should you do next: Vasovagal maneuvers? Adenoxing 6 mg IV? Chest compressions? Emergent synchronized cardioversion? Vasovagal maneuvers followed by an IV Beta Blocker?
This patient is classified as unstable V Tach with a pulse. Thus the best thing to do is give a synchronized shock of 100 - 200 joules if you are using a monophasic machine or 50 - 100 joules if you are using a biphasic machine.
Case #2: unstable ventricular tachycardia without a pulse. A 70 year old woman with a COPD exacerbation becomes pulseless, so a Code Blue is called. Your pager goes off and you rush into the room. She is unresponsive and pulseless when you get there. The cardiac monitor has been hooked up by the nursing staff and shows Ventricular Tachycardia.
What do you do next: cardioversion? synchronized or unsynchronized? vasovagal maneuvers? page the attending? page the cardiologist? give dobutamine? give epinephrine?
Unfortunately, this 70 year old woman has pulseless ventricular tachycardia. You need to treat her by following the VT/VF algorithm from ACLS. You start with defibrillation with 200 joules, then give epinephrine 1 mg Q 3 - 5 minutes, all while doing chest compressions. There are a few proven therapies in the literature for pulseless V Tach: chest compressions, defibrillation, amiodarone IV, and epinephrine IV. Amiodarone takes 10 minutes to have any effect and it has a half-life of 50 - 100 days. With amiodarone, there are two doses, one for the living (150 mg) and one for the dead (300 mg).
What do you do next: cardioversion? synchronized or unsynchronized? vasovagal maneuvers? page the attending? page the cardiologist? give dobutamine? give epinephrine?
Unfortunately, this 70 year old woman has pulseless ventricular tachycardia. You need to treat her by following the VT/VF algorithm from ACLS. You start with defibrillation with 200 joules, then give epinephrine 1 mg Q 3 - 5 minutes, all while doing chest compressions. There are a few proven therapies in the literature for pulseless V Tach: chest compressions, defibrillation, amiodarone IV, and epinephrine IV. Amiodarone takes 10 minutes to have any effect and it has a half-life of 50 - 100 days. With amiodarone, there are two doses, one for the living (150 mg) and one for the dead (300 mg).
Case #3: stable ventricular tachycardia. A 63 year old woman who is admitted for COPD exacerbation has a past medical history significant for type 2 diabetes, hypertension, gout, and chronic kidney disease with a GFR of 32. You are paged by the nursing staff about a telestrip that reveals a sustained, monomorphic wide-complex tachycardia. Her previous EKG from admission this morning reveals tall T-waves in addition to a long QT, a prolonged PR interval, and absent P waves. When frantically reviewing her lab results, you notice that her potassium level is 8.0.
What should you do next: give her kayexalate? give her a beta blocker? try vasovagal maneuvers? give a calcium channel blocker? give calcium bicarbonate? give calcium chloride?
Treatmetn of hyperkalemia with a conduction abnormality is serious business, and you can potentially save a life if you know what to look for. There is a characteristic EKG finding with high potassium (see the page on EKGs). Calcium chloride is the drug of choice because it is eight times more potent than calcium gluconate. Regular insulin 10 units in an amp of D 50 can be given to help move potassium into the cells, but this is of secondary importance. Also, bicarbonate and albuterol can help move potassium into cells and out of the circulation. Hemodialysis and kayexalate are other options as well, but will not work so well in the emergent setting.
What should you do next: give her kayexalate? give her a beta blocker? try vasovagal maneuvers? give a calcium channel blocker? give calcium bicarbonate? give calcium chloride?
Treatmetn of hyperkalemia with a conduction abnormality is serious business, and you can potentially save a life if you know what to look for. There is a characteristic EKG finding with high potassium (see the page on EKGs). Calcium chloride is the drug of choice because it is eight times more potent than calcium gluconate. Regular insulin 10 units in an amp of D 50 can be given to help move potassium into the cells, but this is of secondary importance. Also, bicarbonate and albuterol can help move potassium into cells and out of the circulation. Hemodialysis and kayexalate are other options as well, but will not work so well in the emergent setting.
Case #4: a 53 year old man is admitted to the hospital with shortness of breath. He has a known history of atrial fibrillation. On the floor, he has an acute episode of worsening SOB accompanied by dizziness and palpitations. His heart rate is fluctuating between 155 and 170 when you come into the room. When you take a look at his EKG, the PR interval appears to be short and you see a slurred upstroke in the QRS complex.
What to do Doctor! What to do! Give adenosine? give a calcium channel blocker? call your senior? give metoprolol? page the cardiologist?
What is that slurred upstroke? Some might call it a Delta Wave and it is part of Wolff-Parkinson-White Syndrome .
For starters, do not give an drugs that will block the AV node!!! do not give beta blockers or calcium channel blockers like diltiazem or verapamil. These drugs can make WPW worse because they block the AV node and force the electrical activity through the pre-excitation pathway. This can cause unstable ventricular arrhythmias, especially in the face of atrial fibrillation or atrial flutter, where there may be 1 to 1 conduction of electrical impulses. The best thing to do at this point is to get an expert cardiologist.
What to do Doctor! What to do! Give adenosine? give a calcium channel blocker? call your senior? give metoprolol? page the cardiologist?
What is that slurred upstroke? Some might call it a Delta Wave and it is part of Wolff-Parkinson-White Syndrome .
For starters, do not give an drugs that will block the AV node!!! do not give beta blockers or calcium channel blockers like diltiazem or verapamil. These drugs can make WPW worse because they block the AV node and force the electrical activity through the pre-excitation pathway. This can cause unstable ventricular arrhythmias, especially in the face of atrial fibrillation or atrial flutter, where there may be 1 to 1 conduction of electrical impulses. The best thing to do at this point is to get an expert cardiologist.