This is the conclusion to 83 year old male CC: "Cardiac patient in distress". You may wish to check out the previous post for details about the patient's clinical presentation.
Let's take another look at the 12-lead ECG.
This ECG shows a regular narrow complex tachycardia at a rate of 170.
Could it be sinus tachycardia? One of the "rules of thumb" for the maximum sinus rate is 220 minus age. This patient is 83 years old. 220 – 83 = 137. Granted, this is just a rule of thumb so I'm sure expections exist but 170 is a good distance from 137.
I agree with some commenters that atrial fibrillation can appear regular at very fast heart rates. However, a trained eye can still pick up on some irregularity with rates < 200. You can also use calipers or fold the ECG paper in half and line up the R-waves to verify that the rhythm is regular.
In this case the rhythm is clearly regular which rules out atrial fibrillation but not 2:1 atrial flutter.
In lead V1 we can see atrial complexes (inverted or "retrograde" P-waves) after the QRS complex. We're narrowing in on the mechanism of this tachycardia. If we play the odds there's a good chance this is AV nodal reentrant tachycardia (AVNRT). However, it could still be 2:1 atrial flutter or the less common (but not uncommon) orthodromic AVRT.
You will recall that the paramedics documented "cannon waves" that corresponded to the heart rhythm. Some of you asked, "What are cannon waves?" Cannon waves are pulsations that are visible in the external jugular veins when the right atrium contracts against a closed AV valve.
Normally atrial systole is an end-diastolic event (the so-called "atrial kick"). When the P-waves follow the QRS complexes the pressure generated by ventricular systole have already forced the AV valves shut. Hence, the atria contract against closed AV valves and back pressure creates a visible "wave" or pulsation that is transmitted back up the superior vena-cava and to the external jugular veins.
Here's an example to give you an idea although this patient's external jugular veins are severely distended and the heart rate is much slower. For the current case study the patient's cannon waves were fast, regular and visible just above the clavicle on the right side.
Does determining the exact mechanism of the tachycardia matter in the field? No, because that's not possible. We don't have an EP lab. However, we can carefully document the arrhythmia before and after treatment on those occasions where the patient is not critically unstable!
The first thing the treating paramedics did was put this patient in a supine position and place him on oxygen which perked him up a little bit. Remember, BLS before ALS. I am aware of the controversy associated with placing a patient in Trendelenberg. However, I think we can all agree that lying flat is better than sitting or standing when you're hypotensive!
Vagal maneuvers were attempted (the patient was asked to "bear down" and blow into an empty syringe) with no effect to the tachycardia. An IV was started but unfortunately the only good peripheral access was a 20 G IV in the back of the left hand.
Many (perhaps most) lf you recommended synchronized cardioversion for this patient. I have no quarrel with that. However, I do know that it's easier to say than do when you have a conscious, talking patient in the back of the ambulance. It also helps if you carry the right drugs and don't have to play "mother may I" with online medical control.
In this case paramedics pushed the PRINT button and gave 6 mg of adenosine followed by a 5 ml "flush" of 0.9% NS. It took more than 30 seconds to have an effect (Clinical tip: always follow adenosine with a minimum of a 20 ml flush) but here's what happened. The next four strips are continuous.
With the conversion to sinus rhythm the patient felt much better.
Vital signs were re-assessed.
- RR: 18
- Pulse: 100
- NIBP: 138/81
- SpO2: 100
A post-conversion 12-lead ECG was captured.
The patient was transported to the hospital in a position of comfort.
No further information is available.