Tony Breu Profile picture
Aug 7 16 tweets 7 min read
1/16
🤔Why does subarachnoid hemorrhage lead to deep/inverted "cerebral T-waves"?

This ECG finding is so dramatic. But as we will see, these patients often have normal hearts.

Why does an issue in the brain manifest on a test of the heart?
2/
Cerebral T-waves have been observed for decades.

🔑Though they have been seen in multiple forms of stroke, subarachnoid hemorrhage (SAH) is most closely linked with their appearance.

pubmed.ncbi.nlm.nih.gov/13313536/
3/
In 1960, Cropp reported a case of T-wave inversions (TWI) secondary to SAH. Surgery was delayed for fear of myocardial infarction (MI).

An autopsy showed no evidence of MI or chronic coronary artery disease.

💡Something else was causing the TWI.

pubmed.ncbi.nlm.nih.gov/13812988/
4/
Many theories have been proposed to explain cerebral T-waves.

🔑An increase in sympathetic tone, either systemically or localized to the heart, are part of most theories.

pubmed.ncbi.nlm.nih.gov/12138415/
5/
A 1991 study found that in patients with subarachnoid hemorrhage, high norepinephrine levels were associated with inverted T-waves.

pubmed.ncbi.nlm.nih.gov/2057973/
6/
But not all studies agree. Others have found that plasma norepinephrine concentrations do not parallel electrocardiographic abnormalities.

💡Maybe the sympathetic activity is local, not systemic.

pubmed.ncbi.nlm.nih.gov/8891057/
7/
This possibility was suggested in 1969.

Patients with SAH were found to have myocardial necrosis. But instead of being centered around coronary arteries, it was found near intracardiac nerves!

The damage appeared neural, not ischemic, in origin.

pubmed.ncbi.nlm.nih.gov/5782382/
8/
The results of the study in tweet 7 were felt to be mediated by the LOCAL release of norepinephrine from nerve endings.

🔑Whether systemic or local, sympathetic activation appears to be part of the genesis of cerebral T-waves.

pubmed.ncbi.nlm.nih.gov/5782382/
9/
The question then becomes: how does bleeding into the subarachnoid space lead to sympathetic activation?

To answer this question, we need to examine adjacent structures that might be susceptible to injury after SAH.
10/
The hypothalamus is one structure adjacent to the subarachnoid space.

Given its role in the autonomic nervous system, one hypothesis suggests that hypothalamic irritation after SAH leads to sympathetic activation and cerebral T-waves.

pubmed.ncbi.nlm.nih.gov/7359184/
11/
This is supported by animal studies from the 1960s showing that direct electrical stimulation of the hypothalamus leads to ECG changes (including TWI).

pubmed.ncbi.nlm.nih.gov/13843556/
12/
Another structure that may be affected by SAH is the insular cortex, an area that lies buried in the sylvian fissure beneath the frontoparietal and temporal lobes.

🔑The insular cortex also plays a role in sympathetic regulation.

ncbi.nlm.nih.gov/pmc/articles/P…
13/
Just as with the hypothalamus, the insular cortex is susceptible to injury after SAH.

💡It may be that damage to the insular cortex leads to sympathetic activation resulting in cerebral T-waves.

pubmed.ncbi.nlm.nih.gov/19813104/
14/
Additional support for the sympathetic activation hypothesis comes from another condition associated with elevated catecholamines and deep/inverted T-waves:

⚡️Takotsubo (stress) cardiomyopathy⚡️

The TWIs are often identical in appearance.

pubmed.ncbi.nlm.nih.gov/25981361/
15/
Cerebral T-waves in subarachnoid hemorrhage are just one example where sympathetic activation leads to deep TWI.

In the coming days, I'll add some other examples of what might be more accurately termed "sympathetic T-waves".
16/16
☞ Subarachnoid hemorrhage is associated with deep/inverted "cerebral T-waves"
☞ Cerebral T-waves are the result of sympathetic activation, either from injury to the hypothalamus and/or insular cortex

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More from @tony_breu

Aug 8
1/4 - The Mystery

A doctor is on overnight call in the hospital. They are also hooked up to continuous ECG monitoring.

🤔What might cause the following tracing? Image
2/4 - The Answer

📟 Being paged! 📟

This ECG is from a 31-year-old healthy physician just after being aroused by an "alarm call" while on-call in the hospital.

The associated study found that 63% of physicians experienced T-wave inversion when called!

pubmed.ncbi.nlm.nih.gov/9283539/ Image
3/4 - The Explanation

The transient T-wave inversions seen here are felt to reflect increased sympathetic tone.

Anyone who has held a pager overnight can attest to the surge of adrenaline that comes with each chirp, particularly when it wakes you from sleep. Image
Read 4 tweets
Aug 8
1/4 - The Mystery

You are admitting a patient with confusion. As part of the initial work-up, an ECG is obtained.

It is markedly abnormal.

🤔 What vitamin deficiency could lead to this ECG finding? Image
2/4 - The Answer

🧠B1 (thiamine) deficiency!🧠

The ECG is from a 49-year-old who presented with Wernicke’s encephalopathy secondary to B1 deficiency.

An MRI showed abnormal signal in the thalamus, mammillary bodies, and periventricular gray matter.

twtr.to/BXfK Image
3/4 - The Explanation

The authors suggested that the mechanism of these T-wave changes related to inflammation of the adjacent hypothalamus.

This would lead to increased sympathetic outflow to the heart. Image
Read 4 tweets
Jul 2
1/12
🤔Why does iron deficiency cause fatigue, even in the absence of anemia?

I have often equated iron with hemoglobin and oxygen-carrying capacity.

But there is so much more to it!
2/
It has been observed since the 1800s that one can experience fatigue in the setting of iron deficiency, even with a normal hemoglobin value.

And administering iron mitigates these symptoms.

pubmed.ncbi.nlm.nih.gov/13800263/
3/
It wasn't until 1960 that we saw RCT evidence support.

That year, Beutler published a study in which women with hemoglobin >12g/dL were randomized to iron supplementation or placebo.

🔑Those receiving iron had a greater improvement in symptoms.

pubmed.ncbi.nlm.nih.gov/13800263/
Read 12 tweets
Jun 23
1/6 - The Mystery

A patient presents with a serum B12 level above assay.

And yet, the clinician strongly suspects the patient has B12 deficiency.

🤔How might this occur?
2/6 - A Solution

💡Myeloproliferative disorders (e.g., CML, PV, ET) can lead to high B12 levels despite tissue level deficiency.
3/6 - An Explanation

📝The abnormal cells in myeloproliferative disorders secrete haptocorrin. When B12 binds haptocorrin it is less efficiently removed from the body.

Result: increased serum B12 levels

pubmed.ncbi.nlm.nih.gov/5383307/ Image
Read 6 tweets
Jun 21
1/13
🤔Why does multiple myeloma cause anemia and not pancytopenia?

If the issue is infiltration of the bone marrow with plasma cells, wouldn't all cell lines be low?

Let's have a look.
2/
In one review of 1027 with newly diagnosed multiple myeloma...

☞73% had anemia

BUT, only

☞5% had thrombocytopenia
☞20% had leukopenia

pubmed.ncbi.nlm.nih.gov/12528874/
3/
Although an increasing severity is bone marrow infiltration by plasma cells
is associated with worsening anemia, leukocyte and platelet counts remain stable.

This suggests something beyond the replacement of hematopoietic cells is responsible.

onlinelibrary.wiley.com/doi/epdf/10.10…
Read 13 tweets
Jun 12
1/10
Does epinephrine improve outcomes in patients with cardiac arrest?

This is a question with a complex answer. This thread is only meant to scratch the surface and is a follow-up to a recent tweetorial on the use of epinephrine for cardiac arrest.
2/
Although epinephrine has been used for decades questions about its ability to improve outcomes have been around for just as long.

pubmed.ncbi.nlm.nih.gov/14102262/ Image
3/
These concerns were augmented when a large prospective propensity-matched observational study showed:

☞ Rates of survival and good functional outcomes were LOWER in patients receiving epinephrine for out of hospital cardiac arrest.

pubmed.ncbi.nlm.nih.gov/22436956/ Image
Read 11 tweets

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