Dealing with quasi-stable patients can be tricky by Deborah Gesensway
Published in the April 2012 issue of Today's Hospitalist
ONE OF THE SCARIEST SITUATIONS hospitalists regularly encounter is patients with unstable arrhythmias. At a recent hospital medicine conference, Gregory M. Marcus, MD, an electrophysiologist and assistant professor of medicine at the University of California, San Francisco (UCSF), shared insights on how hospitalists can be more confident treating these patients.
When a patient is unstable due to a tachyarrhythmia, "It doesn't really matter what the rhythm is," Dr. Marcus told the audience at UCSF's management of the hospitalized patient conference last fall. "You just shock them."
But hospitalists also have to determine if
"Remember all the other potential causes of arrhythmias before you order invasive treatments."
–Gregory M. Marcus, MD University of California, San Francisco
the rhythm is supraventricular vs. ventricular and regular vs. irregular. For essentially any rhythm other than ventricular fibrillation, the shock needs to be "synchronized," Dr. Marcus noted. Typically, this is simply a matter of selecting a button—and if that button is not selected, shocking a supra ventricular arrhythmia or regular ventricular tachycardia can actually cause ventricular fibrillation. When shocking ventricular fibrillation or a very irregular (polymorphic) ventricular tachycardia, "synch" should not be turned on to avoid any delay in delivering the shock.
The much trickier issue is when someone is only quasi-stable. "Clearly, if they are unconscious, that's easy: Go ahead and shock them," Dr. Marcus said.
But the real problem is a patient who is quasi-stable with altered mental status or ongoing chest pain "because you're going to cause a lot of pain by shocking them." Physicians have to make a judgment call, he added, and it's not unusual for doctors to feel as if they are in a kind of "twilight zone" when making that call.
What can help? According to Dr. Marcus, one strategy for making decisions in that grey zone is to think about each type of arrhythmia separately.
Tachyarrhythmias: Supraventricular tachycardia
With supraventricular tachycardia (SVT), one of the first things Dr. Marcus advised hospitalists to consider is a manual maneuver, "especially while everybody is getting their drugs ready." Vagal maneuvers that block the AV node can be useful in these patients.
First, consider the carotid sinus massage. Find the carotid pulse, Dr. Marcus said, and make sure you push hard enough, like you are going to "dent a tennis ball." Hold that pressure for a count of five seconds; if that doesn't work, go to the other side and hold again for five seconds.
An alternative is to have the patient bear down and do a Valsalva maneuver, which "sometimes will work when carotid sinus massage doesn't." Studies have shown that these manual maneuvers can help about 20% of patients.
"It's not fantastic, but it's certainly easy and inexpensive, and it can be rapid," Dr. Marcus pointed out. If you are worried that a patient is at high risk of having a carotid plaque and that you could cause a stroke by pressing on the carotid, "don't do this." It's a matter of clinical judgment.
Adenosine is another treatment mainstay for quasi-stable patients with SVT. But hospitalists need to keep in mind that adenosine is metabolized by red blood cells and the endothelium, Dr. Marcus said, so as soon as the drug hits a patient's vein, it's starting to be metabolized.
That means that nurses administering the drug must give it rapidly and follow immediately with a flush, ideally with a three-way stopcock. The first dose should be 6 mg IV with a 20 cc flush. If that doesn't work, Dr. Marcus said, give 12 mg IV twice. Warn patients that they are going to "feel funny," he noted, with perhaps some chest pain and flush, "but reassure them that it's going to last only a few seconds."
If patients don't report feeling anything like that, however, and if you don't see any change in their rhythm, you need to consider that the drug is not being flushed rapidly enough. If patients report feeling horrible but have no rhythm changes, that's a sign that you have probably given enough adenosine.
And when a quasi-stable patient has SVT, make sure you have a 12-lead electrocardiogram ready before initiating any other treatment or even calling a consult. When called for these patients, cardiologists and electrophysiologists will want to examine the 12-lead ECG obtained at the time of the adenosine effect to see flutter waves, for instance, or arrhythmia termination.
Once you terminate the abnormal rhythm, the next step is to figure out what you can do to cure the SVT causing it. More than 95% of the time, Dr. Marcus said, SVT can be cured with ablation.
Although that shouldn't be news to anyone, "we see a lot of patients who have had five visits to the ER and keep getting referred out or keep getting admitted before they come to see us," Dr. Marcus said. "We ablate them, and they never have another episode. It's some thing we as electrophysiologists love to see because it's very gratifying that we can so definitively help these patients."
For a quasi-stable patient with atrial fibrillation and a rapid ventricular response, Dr. Marcus said that the first-line treatment is either a non-dihydropyridine calcium channel blocker like diltiazem (Cardizem, Tiazac, Dilacor and others) or verapamil (Calan, Verelan and others). Alternatively, you can give these patients any beta-blocker. There are no data to show that beta-blockers work better than calcium channel blockers here, he said.
But one problem to watch for is that these antihypertensives can often lower blood pressure to a dangerous level. The first step in such a situation is to address patients' underlying condition, particularly what is causing them to be hypotensive. At times, the primary cause may simply be the fast ventricular response, so administering these antihypertensive AV nodal blockers can actually raise blood pressure. You can determine that by starting with low doses, Dr. Marcus advised, and then titrating up, depending on the patient's blood pressure response.
If patients remain hypotensive but need more ventricular rate control, esmolol (Brevibloc) can help. But it is not a particularly potent drug, and it often requires a heavy load of fluids to go with it.
Digoxin can be a good addition for patients with hypotension, particularly those having a heart failure exacerbation. Another drug you can add to control the heart rate without substantially reducing blood pressure is amiodarone, which does not work particularly well for acute conversion of atrial fibrillation, but is effective for rate control. Typically, amiodarone is given as 50 mg over 10 or 20 minutes, but it can be given over an hour if you are worried about alpha-receptor blocker-induced hypotension.
And hospitalists should know, Dr. Marcus added, about recent safety concerns with one drug used in these patients: dronedarone (Multaq), an analog of amiodarone. Recent data suggest you probably shouldn't give it to patients with permanent afib or those with heart failure.
Atrial fibrillation with WPW
When you see a patient with rapid atrial fibrillation in the setting of WPW (Wolff-Parkinson-White syndrome), Dr. Marcus said it is important to avoid AV nodal blockers, especially calcium channel blockers. Those can increase the possibility of patients going into ventricular fibrillation.
When these patients are unstable, they should be shocked. But if they are quasi-stable, the best course of treatment is to give them potassium channel blockers such as procainamide IV or ibutilide (Corvert).
These drugs block potassium channels and help by increasing the refractory period of the accessory pathway, so the ventricle receives fewer rapid signals from the atrium. And procainamide actually enhances AV node conduction, Dr. Marcus said. Once again, ablation therapy is ultimately the best treatment for these patients and, in this circumstance, may actually be life-saving.
In cases of ventricular tachycardia, Dr. Marcus noted, amiodarone is probably the most effective drug, al though it can pose problems. The first concern is that amiodarone can cause bradycardia, a problem that may be significant in a hemodynamically compromised patient. In addition, it can hinder electrophysiology studies, and these patients can be potentially cured with radio frequency ablation.
Alternatives include lidocaine or procainamide. Lidocaine is not the best choice for people with liver failure, and there are concerns about its neurotoxicity and relationship to seizures in the event of an overdose.
With procainamide, hospitalists have to watch out for hypotension and a prolonged QT. Getting an EP consult can be very helpful for these patients, Dr. Marcus said, because a 12-lead ECG can show if a patient is likely to respond to beta-blockers (such as in right ventricular outflow tract ventricular tachycardia) or calcium channel blockers (as is classically observed in "fascicular tachycardias"), or be amenable to ablation.
Dr. Marcus reminded hospitalists that when making many ECG diagnoses such as long QT syndrome, 12 leads are necessary. Some aspects of the 12-lead ECG can pro vide clues as to certain electrolyte deficiencies—such as hypokalemia, hypomagnesaemia and hypocalcaemia— and/or certain congenital syndromes.
The concern about patients with a long QT is that they can develop a fast and potentially lethal ventricular rhythm known as torsades de pointes. The first line of treatment for patients with torsades de pointes is often IV magnesium, then isoproterenol to increase the sinus rate and prevent a bradycardic dependent pause, and transvenous pacing to keep the heart rate up. If tachyarrhythmia persists and results in hemodynamic instability, he said, shock the patient.
Because the sinus rate of atrioventricular node conduction is governed by both the sympathetic and parasympathetic nervous system, Dr. Marcus reminded hospitalists that they should be less concerned about the actual heart-rate number than whether there are symptomatic or hemodynamic consequences of the slow rhythm. ECG-recorded changes, such as lengthening P-P intervals or a pattern of dropped P-waves or QRSs, can help distinguish between vagally-mediated (and, generally, more benign) etiologies and structurally mediated ones that may be less benign.
It may not be necessary, for instance, to order a cardiology consult or put in a pacemaker if patients' heart rate falls to 35 while they are asleep—as long as that rate comes up when they get up and walk around. Their heart rate may have dropped because of something like sleep apnea, he said, or it could simply be related to a healthy amount of vagal tone.
According to guidelines from the American Heart Association on managing symptomatic bradycardia and tachycardia, hospitalists should use this general strategy for a patient with a conduction system problem: Give atropine first and then place external pads. If atropine fails, pace and use dopamine, epinephrine, isoproterenol and a transvenous pacer if needed, or at least order a consult to consider transvenous pacing.
Don't forget the basics
And when it comes to many patients with a potentially scary arrhythmia, Dr. Marcus noted that it is important to not forget the basics. He recalled one patient he saw as a first-year fellow who had a history of heart failure and a pacemaker and had come to the emergency room with a possible acute MI. The patient was diaphoretic and tachypneic, and his oxygen saturation and blood pressure were dropping. His ECG showed a paced rhythm, but with several unusual features.
"We're getting ready to intubate him" and although the initial ECG was read as "uninterpretable" because of ventricular pacing, "we suspected hyperkalemia," Dr. Marcus said. That was based on several ECG clues, especially when compared to a previous ECG from the same patient: Although an atrial pacing artifact was seen, the P waves were more flat, there was a new delay between ventricular pacing and the QRS onset, and the paced QRS was more slurred and delayed than previously.
"We were waiting for the labs and he started to lose ventricular capture with no underlying rhythm," Dr. Marcus recalled. "We then decided based only on those clues from the ECG during ventricular pacing to empirically give him insulin, glucose and sodium bicarbonate, and suddenly his device started capturing. His blood pressure came up. His breathing got better. It turned out that he did have hyperkalemia, which is a cause of failure to capture."
The bottom line, he said, is to compare current ECGs with any previous results you can get. Also, take a good history. In this case, the man had just come back from a trip to Mexico and had had some GI problems, resulting in volume depletion and a resultant decline in renal function. Those, in combination with his ACE inhibitor and aldosterone antagonist, led to his hyperkalemia.
"Remember all the other potential causes of arrhythmias," said Dr. Marcus, "before you order invasive treatments."
Deborah Gesensway is a freelance writer who covers U.S. health care from Toronto.
A new tool for stroke prevention
A NEW ROLE FOR ELECTROPHYSIOLOGY may be in stroke prevention. Speaking at a hospital medicine conference last fall, Gregory M. Marcus, MD, an electrophysiologist and assistant professor of medicine at the University of California, San Francisco, described how his electrophysiology department is having success with an appendage closure device used in atrial fibrillation patients at high risk of having a stroke.
A long-standing problem facing physicians is what to do when a patient on warfarin comes in with catastrophic bleeding or an apparent embolic stroke in atrial fibrillation. If the patient still needs warfarin for atrial fibrillation and has a high CHADS2 score, he said, the question has been, "What are we going to do with these patients going forward?"
The thinking has been that in afib patients with thrombus or thromboembolism, clot formation starts in the left atrial appendage more than 90% of the time, Dr. Marcus said. He and his colleagues are implanting a device and doing a procedure— Percutaneous Left Auricle Closure and Exclusion (PLACE)—to close the appendage related to the problem.
Patients undergoing the procedure, he said, are all being followed in a registry, but so far most patients seem to be having a durable response. Hospitalists may want to consider referring patients like this to electrophysiologists, Dr. Marcus said.