Clinical Pearls: Tachycardia
One of the most common calls you’re going to get as an ICU provider is regarding tachycardia. Nurses are trained to monitor and report abnormalities, particularly life threatening ones. And this is a good thing. The best nurses have astute pattern recognition and can piece together impending badness. (The “he just doesn’t look good” call is one you do not ignore.)
Your role as the provider is to make the decision on whether or not this is something to worry about, and this is often what I find students and new providers struggle with. So in this post I’m going to discuss my approach to the evaluation of tachycardia in the ICU and an argument for why you might want to consider leaving them alone among the treatment options.
First things first, while you’ll get something like … “Room 21’s heart rate is 132, do you want to give some Metoprolol” you’ll be missing 9/10 of the story if you reply with a simple yes. My caution to new providers is to make sure you are treating a diagnosis not a symptom because you can do more harm than good.
Why? Well tachycardia is often a normal physiologic compensatory mechanism for a body that is in a state of stress (aka emotional or physical distress; aka trying to heal itself; aka decompensating; aka dying - could be any one of these). Unless you have a pretty good idea which of those it is, you probably shouldn’t blunt the body’s natural response. If you do you just knock out their drive to stay alive and then there is the risk of them, well, not being alive.
So here’s the order in which I approach this:
What is the rhythm? Get an EKG stat if you don’t know. Is this wide complex (in which case put some pep in your step). I’m not going to discuss VT as that goes beyond the focus of this post. Just be aware if you have VT on your hands treat it like the emergency it can be. If it’s a narrow complex, distinguish what type of SVT this is (commonly seen Afib/flutter, MAT or other atrial tachycardias, SR with PAC’s/PVC’s versus ST). Treatment algorithms differ. If this is unstable SVT you need to act quickly. First order of business is to identify the rhythm; this is where Adenocard can be helpful. If it’s unstable cardiovert, push an anti-arrhythmic, start a drip, call a cardiologist.
What are the other vitals? Particularly BP. But I raise the argument that hypoxia induces tachycardia. What is the RR; are they labored? If one can’t breathe the HR will jump. Fever? Fever is a number one consideration for etiology in the pt with ST.
What does the pt look like? Are they suddenly unconscious or confused? Are they having shortness of breath or chest pain? Palpitations? Any other signs of poor end organ perfusion or acute coronary syndrome? Are they having pain or anxiety? Do they look toxic or pale?
What have we done to or taken away from this patient recently? If this is someone who is vented and we have been undergoing sedation wean? This could likely be your explanation (I notice this frequently with weaning of Precedex). Conversely, is this someone we just added Ketamine to the mix? Ketamine will induce a hyperdynamic state and you’ll often see a jump in bp or hr. Is this someone who normally has afib and takes all the rate reducing drugs in all the land and we held them on admission 2/2 shock and now they’re all better and we haven’t resumed their normal meds (that was a long run on, but a necessary addition to the story). Honestly, you should do a thorough med review, lots of drugs can increase hr including nebs.
Once I’m sure it is Afib with RVR and the pt is non-symptomatic/stable. Check the volume status. Overload and dehydration both play a role here. Treat that. Try vagal maneuvers, if intubated, suction them (this works more than you’d think). Do a med review. If the BP will tolerate I will try a BB or even start a drip like Esmolol (easy on/off and to titrate). Check a magnesium level or just add some mag (natural BB). Check your electrolytes and treat accordingly. Then there’s the ole standard Amiodarone or possibly Cardizem but beware the BP drop.
Once I am sure it is ST I look at etiology and treat the underlying symptom. Sinus Tachycardia is a compensatory response. Sometimes it is compensating for (mostly) harmless reasons: exercise, anxiety, pain, side effect of other drugs, fever, anemia, SA node issues, POTS, hypothyroidism, drug or alcohol withdrawal. In this case rate lowering drugs won’t hurt but their effects will be fleeting and you’ll constantly be chasing it. It’s far better to treat the problem. Anxiety - benzos or other sedatives or off label meds. Pain - pain meds. Side effects - change or reduce (looking at you q2h nebs including atrovent). And so forth.
If it’s ST and it is compensating for impending death here’s where slowing the rate without addressing the problem will make things exponentially worse. The human body is exceptionally good at compensating for badness in an attempt to keep itself alive. ST often occurs in the ICU in response to decomensation: sepsis, all forms of shock, MI, PE, hypoxemia, high work of breathing. In these instances taking away that drive can make them much sicker, quicker. Granted, sustained ST is also a problem (reduced filling time, decreased CO) so action should be taken to address the cause.
Moral of the story: Diagnose the rhythm/etiology before treating!