**Tachyarrhythmia case**
- Middle-aged patient admitted with septic shock on norepinephrine. Home meds include metoprolol 100 qday.
- Baseline rhythm: sinus at HR ~100.
- STAT call to bedside for HR in 170s-180s with escalating norepi requirements.
- The monitor screenshot:
1/
2/ -Initial read: narrow-complex tachycardia.
-First therapy: Adenosine
-Result: rhythm not converted but adenosine confirms underlying P-waves with atrial rate of ~180
-Interpretation: SVT at rate of ~180 with 1:1 conduction
-Differentials considered: sinus tach vs atrial tach.
3/ - Further history: RN confirms that "HR has been ~100 all day". Such high rate makes sinus tachycardia less likely.
- Next step: amio 150 bolus: worsened hypotension but rhythm persists.
- Due to hemodynamic instability, decision made to cardiovert --> was unsuccessful x2!!
4/ Next step: Quick review of trends on telemetry. Looks like the HR gradually escalated from ~100 over a few minutes! (images)
This is quite unusual for a tachyarrhythmia to do that. So is this indeed sinus tachycardia?
But the HR is 180!?!
~~~
Let's pause and analyze:
5/ Technically, this is a long RP NCT. Other than sinus tach & atrial tach, the differential includes:
(iii)Atypical (slow-slow) AVNRT: However, a re-entrant arrhythmia should have been terminated by adenosine/cardioversion, so less likely. (More on this:litfl.com/avnrt-for-two/)
6/ (iv)PJRT: a rare form of AVRT. Since this is a reentrant arrhythmia as well, it should have been terminated with adenosine/cardioversion
Hence, we are indeed left with 2 options: sinus tach vs atrial tach
-An important feature to make this distinction is the P-wave morphology
7/ Let's review the telemetry in further detail:
The most likely point of tachycardia origin is identified in the attached image. Note the subtle difference in P-wave morphology in lead I.
However, this difference could not be picked up in any other monitor leads.
8/ The telemetry ECGs typically have aggressive filters and hence may miss subtle changes in morphology.
A 12-lead ECG will have higher precision. In the image, subtle changes in P-wave morphology can be appreciated in both lead I and III
The all other leads look about the same
9/ This is highly suggestive of ectopic (non-sinus) focus of atrial excitation. Since the difference in P-wave morphology is difficult to identify & the P-axis is about the same, the location of the ectopic focus is likely close to the SA node.
Provisional diagnosis: Atrial tach
10/ (Focal) atrial tachycardias (ATs) can be further classified as:
(a)Automatic ATs: due to enhanced automaticity
(b)Non-automatic ATs: due to microreentry or triggered activity
Automatic ATs have some unique characteristics:
(i)They don't terminate with adenosine/cardioversion
11/ ... ,while non-automatic ATs do
(ii) Automatic ATs often accelerate over several seconds (warm-up): this was seen in our case {image}. Also, they gradually slow down on termination (cool-down).
Hence, the mainstay of treatment in automatic AT is sympathetolysis.
12/
Back to the case...
Norepi was switched to phenylephrine. As this was happening, the tachyarrhythmia converted back to sinus rhythm while exhibiting a "cool-down" behavior (HR reduced over several seconds).
/End
(This is my interpretation but I may be missing something)
This generated some great discussion. Now let's do a deep dive
The first odd thing here is the Paw waveform. Traditional teaching is that in VC with continuous flow, the initial ⬆️in Paw corresponds to the pressure required to overcome resistance (as lung filling is minimal)
Since flow is constant, this 'resistive pressure' remains constant throughout the breath as revealed by the post-inspiratory pause (image 1)
Hence, the height of the initial Paw spike should equal the height of PIP - Pplat. This is not the case in our patient!
2/
In our patient, the initial ⬆️ in Paw is >> PIP - Pplat (let's call this pattern X). This implies that in the beginning of the breath, pressure is being spent not just to overcome the resistive load, but also on something else. But what?
Paging ENTtwitter & AirwayTwitter. Had a patient with moderate subglottic stenosis s/p recent dilation Intubated twice post-dilation for episodic stridor. During the second episode, scope showed laryngospasm. How common is this in non-OR (ICU) setting? Any tips on prevention/Rx?
Further clarification -
Patient was fine immediate post op. First episode occurred the next day. Extubated after 2 days - did fantastic for 10 minutes and then raging stridor. ?Precipitated by deep oral suctioning.
Scope showed laryngospasm. Improved some with PPV but needed RSI
**Volumetric capnography: data points & equipment**
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There are three major reasons for limited utilization of volumetric capnography (VCap): (1) Lack of education/training (2) Lack of understanding of the data (3) (Perceived) lack of equipment
Lets try to address 2 & 3
Let's start with a TL;DR of what VCap is:
Conventional capnography is 'time-based': Time on the X-axis and pCO2 on the Y-axis.
VCap has volume on the Y-axis.
VCap requires simultanoues measurement of exhaled pCO2 and expiratory flow.
*VCap data points*
VCap provides several data points: some more useful than others.
(i) PECO2: Mixed expired CO2 pressure (mmHg):
This is simply the “volume-averaged” CO2 of the pCO2-volume curve: the mean pCO2 of expired gas.
(ii) VTCO2: Volume of CO2 expired in a breath (cc):
..In this case, the 'gauge' refers to the luminal diameter (image 1),
B. By convention, the size label of a percutaneous sheath introducer (PSI) (e.g. Cordis) refers to its inner diameter. This is because the whole purpose of a PSI is to allow introduction of another catheter...
...Hence, the size label of a PSI serves as a guide for the size of the catheter that should be introduced through it
Take the example of a MAC introducer. Although the label reads 9Fr, this is in fact the inner diameter of the bigger lumen. The outer diameter is actually ~14Fr!