**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)

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with Aman Thind

Aman Thind Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

More from @Thind888

20 Sep 20
1/ **Septal kinetics in acute cor pulmonale (ACP)**

I'm glad @load_dependent brought this up. I think it's helpful to analyze the mechanistic reasoning behind why 'diastolic' flattening is seen in ACP

In general, septal position depends on the relative RV/LV pressures.
2/
Normally, LV pressures during the entire cardiac cycle are higher than RV pressures so the curvature of septum is towards the RV.

Now let's consider what happens in acute massive PE:
(i) Acute pressure overload results in prolongation of RV systole, compared to LV systole.
3/
This has been shown in multiple clinical studies (e.g. PMID: 19561027), but I have not been able to track down the precise mechanism (?altered calcium cycling with increased afterload).

In any case, this leads to a brief *early-diastolic* septal flattening: first sign of ACP.
Read 7 tweets
14 Jul 20
contd

Part 2B:
*Transmural and intramural pressures*
– More on tendencies for pulmonary congestion vs pulmonary edema

Part A recap: Changes in ITP affect pulmonary post-capillary (venous) pressures and PCWP equally --> do not affect the gradient for pulmonary venous return.

1/
2/ Therefore, the best way to assess tendency for pulmonary congestion is to measure PCWP when ITP is close to zero (at end-expiration), or normalize PCWP for ITP (PCWP – Ppl).

Let’s try now to dig a bit deeper into ‘tendency for pulmonary edema’ using the example of obesity.
3/Example 1: Obesity
We first have to appreciate basic respiratory mechanics in obesity. Extra chest and abdominal weight pushes on the chest wall causing a positive ITP during expiration (say ~10 cmH20). Mechanically, this is actually quite similar to forceful expiration (image) Image
Read 19 tweets
4 Jul 20
Part 2A:
*Unique effects of transmural(tm) pressure and intramural(im) pressures*
–Introduction and basic concepts

Some of these ideas are quite convoluted so I’m splitting them up for clarity.

(NB: Some interpretations are a bit personalized so I can’t guarantee accuracy!)

1/
2/
Definitions:

Consider a hollow organ located in a pressurized compartment.
- The pressure inside the organ = intramural pressure.
- The pressure outside = extramural pressure. -
- The pressure across the wall of the organ is transmural pressure ('mural' = wall).

(See image)
3/
*Transmural pressure*

Effect: This is the true distending pressure. As mentioned in the previous thread, LVEDP is an excellent marker of LV preload but the biggest caveat is that it's the transmural pressure that matters.

So what's the extramural pressure of the heart?
Read 18 tweets
29 Jun 20
Part 1:
*Defining ventricular preload*

The conceptual definition of preload is quite straightforward: end-diastolic myocardial load/stretch. At the microscopic level, it's the sarcomere length we are interested in, which would increase with higher end-diastolic load (preload)
1/
2/
The importance of preload is in effecting the Frank-Starling mechanism: increase in ventricular performance with ⬆️ preload. The basis of F-S relationship is primarily the sarcomere Force-Length relation.

At sarcomere length of ~2.3 μm, actin-myosin interaction is optimized.
3/
Any further increase in sarcomere length does not improve ventricular performance (flat part of F-S curve).

So when we give fluids, what we're really trying to achieve is an ⬆️in the average sarcomere length.

~~~
The clinical definition of preload is much more controversial!
Read 14 tweets
27 Jun 20
*** PCWP in Muller's maneuver || Poll ***

Muller's maneuver (forced inspiration with closed mouth) is an excellent way to study heart-lung interactions.

In the experiment below, compare PCWP before and a few seconds into the maneuver (2 blue boxes) and take the poll below 👇 Image
Compared to baseline, estimated LV preload near the end of the maneuver is ...

(Feel free to comment!)
The results are quite spread out and for good reason!

This is a tough one so I plan to deal with this in multiple discussion threads over the next few days.

We have to start with the basics - defining preload. So here's thread no. 1/n -

Read 5 tweets
9 May 20
1/
**Doppler knobology microskills: Wall filter**

I realized I haven't done an ultrasonography post for a while now so here goes.

Spectral doppler knobology is often overlooked but the basic settings include (i) Doppler Gain (ii) Scale (PRF) (iii) Sweep speed, and (iv) Baseline
2/ Just like B-mode ultrasound, doppler settings should be optimized to get the best tracing.

Here I'll talk about the less recongnized setting of "wall filter" and give a clinical example of how it may be useful to adjust.

But first, let's briefly review doppler physics.
3/ When ultrasound encounters a moving interface, the frequency of the reflected waves is "phase shifted" proportional to the velocity of the interface.

The direction of the phase shift depends on the direction of the object (positive if moving towards the ultrasound): image
Read 15 tweets

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Too expensive? Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal Become our Patreon

Thank you for your support!

Follow Us on Twitter!

:(