The 4 Physiologic Etiologies of Shock, and the 3 Etiologies of Cardiogenic Shock

A 60-something presented with hypotension, bradycardia, chest pain and back pain.

She had a h/o aortic aneurysm, aortic insufficiency, peripheral vascular disease, and hypertension.  She had a mechanical aortic valve.  She was on anti-hypertensives including atenolol, and on coumadin, with an INR of 2.3. 

She was ill appearing.  BP was 70/49, pulse 60.

A bedside echo showed good ejection fraction and normal right ventricle and no pericardial fluid.

Here is the initial ECG:

What do you think?

This ECG actually looks like a left main occlusion (which rarely presents to the ED alive):  ST Elevation in aVR, but also in V1, and what appears to be "coving" of the ST segment in aVL, which suggests ST Elevation in that lead as well.

There is bradycardia, which is ominous in such a sick patient.  This may be due to atenolol, but could simply be a sign of severe illness.

Whereas ST elevation in aVR is usually reciprocal to the the ST depression of subendocardial ischemia, with a negative ST vector towards leads II and V5, and may be accompanied by STE in V1 (which is in the same direction as aVR), when there is also STE in aVL it implies a more directly superior ST axis (supported by ST depression in all of II, III, aVF).

When the ST axis is directly superior, there may actually be transmural ischemia of the "base" of the heart (the base is actually the top of the heart, which really does not have a wall -- the ventricles have openings to the atria at the base, and so no complete wall).  However, the anterior, lateral, posterior, and septal walls all have a superior portion that may result in ST elevation in a superior direction if all walls have subepicardial ischemia, as in left main occlusion.

It is important to remember that an ECG like this represents possible left main occlusion only if it is a result of ACS!! 

Knotts et al. found that such ECG findings only represented left main ACS in 14% of such ECGs: 
Only 23% of patients with the aVR STE pattern had any LM disease (fewer if defined as ≥ 50% stenosis). Only 28% of patients had ACS of any vessel, and, of those patients, the LM was the culprit in just 49% (14% of all cases).  It was a baseline finding in 62% of patients, usually due to LVH. 

Reference: Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.    

Case continued:

The chest X-ray was consistent with pulmonary edema, and the ultrasound showed a "plump" inferior vena cava.  (This data is all consistent with high right and left sided filling pressures, which is the hallmark of cardiogenic shock -- not obstructive, distributive, or hypovolemic)

Aortic dissection was considered (with involvement of the coronary arteries and aortic outflow obstruction), but a CT scan was negative for dissection.

The cath lab was activated.

It is a very long story, but I will make it brief:

The angiogram could not be done because of inability to access the arterial system (unexplained).

The interventionalist listened to the heart and heard both a systolic flow murmur across the valve and a diastolic murmur.

A formal echo showed aortic insufficiency, then TEE showed a mass on the aortic valve, and surgical exploration showed aortic valve thrombosis.  

This was not ACS.  This was not Left Main occlusion.

Comment:

Shock has 4 basic etiologies:

1. Obstructive (pulm embolism, tension pneumothorax, tamponade, atrial myxoma, etc.)
These were all ruled out
2. Distributive (sepsis, neurogenic, beriberi, etc.).  The patient showed no signs of high output
3. Hypovolemic (dehydration, hemorrhage, third spacing)  The IVC was plump

4. Cardiogenic -- the likely culprit

Cardiogenic shock has 3 basic physiologic etiologies:

1. Poor pump function (diastolic or systolic)  The bedside echo showed good pump function, though that does not completely rule out diastolic dysfunction.
2. Dysrhythmia (too fast or too slow to adequately fill and pump)  There was only some mild bradycardia
3. Valvular.  The pump works but the blood goes the wrong way.  This is what we are left with: Valvular etiology is frequently forgotten.  Any valve dysfunction can result in shock, especially aortic, mitral, or tricuspid (I have never seen a case of acute pulmonic valve dysfunction and cursory search found nothing)

Aortic valve thrombosis should be considered in any patient who has a prosthetic aortic valve, especially a mechanical one.  It is a catastrophic complication, which is why we are so careful to maintain a high therapeutic INR on these patients.

One could say that this case is a hybrid of cardiogenic and obstructive shock, but since it is all valvular, let's call it cardiogenic.

Suffice it to say that one should suspect valvular thrombosis in patients with artificial valves who have:

1. Dyspnea
2. New or worsening heart failure
3. Hypotension or shock

One should listen for muffled heart sounds or a new murmur, but this is not sensitive.

One should be suspicious especially if the INR is not at the goal of:

2.5  - for bi-leaflet or current-generation single tilting disk mechanical aortic valves is 2.5 if they have no risk factors for thromboembolism 

3.0  - if they have a ball-cage mechanical valve (because of the associated higher risk of thrombosis) or risk factors for thromboembolism such as atrial fibrillation, left ventricular systolic dysfunction, prior thromboembolism or hypercoagulable state.

3.0  - (range, 2.5 to 3.5) for patients with mechanical mitral valves 

3.5 to 4.0 -  for patients with mechanical tricuspid valves. 

Transesophageal echo may be necessary for diagnosis.

Always think about doing Doppler on the valves during POCUS.  It is not that difficult to see regurgitation.  Had that been seen, the diagnosis would have been made much earlier.

Complications of aortic thrombosis include, of course, severe obstruction of aortic outflow (with shock), aortic insufficiency and regurgitation, and embolism to any artery in the tree, resulting in stroke, myocardial infarction, or other catastrophic infarction.

The combination of outflow obstruction (decreased cardiac output) and regurgitation (low diastolic pressure) results in severe coronary ischemia.  The coronaries are perfused during diastole when the myocardium is not contracting.

There is no reason to write more about this complication, as there are many good articles on the topic.  See this one:
https://www.mayoclinic.org/medical-professionals/cardiovascular-diseases/news/prosthetic-valve-thrombosis-time-is-critical/mac-20430866

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Comment by KEN GRAUER, MD (11/30/2018):

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Interesting case with an excellent discussion and timely reminder by Dr. Smith of the principal etiologies of shock and cardiogenic shock. I limit my comments to the initial ECG, which I’ve reproduced for clarity in Figure-1.

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Figure-1: Initial ECG on a woman in her 60s, presenting with shock (See text). 

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My interpretation of the ECG in Figure-1 was as follows:

• Baseline artifact. This is most marked in leads I and III, suggesting the cause might be the right upper extremity.
• Sinus bradycardia at a rate just over 50/minute. All intervals (PR, QRS, QT) are normal. Slight leftward axis, though not quite leftward enough to qualify for LAHB (since the QRS complex is still predominantly positive in lead II).
• Probable LVH (See below).
• Diffuse ST-T wave depression, with especially deep T wave inversion in leads V4-thru-6 — and biphasic T waves in leads III, aVF and V3. Significant ST elevation in leads aVR and V1, with fatter-than-they-should-be T wave peaks in these leads, and a pattern for the ST-T waves in leads aVR and V1 that looks “reciprocal” to the ST-T wave depression in many of the other leads.

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IMPRESSION: Sinus bradycardia with probable LVH + ST-T wave changes suggestive of LV “strain” + diffuse subendocardial ischemia. Urge clinical correlation.

• Why “probable” LVH? The ECG is an imperfect tool for assessment of LVH. At best — sensitivity of the ECG for picking up LVH is no more than 55%. Echo is far superior to the ECG for assessment of chamber enlargement. That said, when the clinical situation is “right” — and, voltage criteria for LVH are met — and, ST-T wave repolarization changes of LV “strain” are present — then specificity of the ECG for detecting LVH may be more than 90-95%! Admittedly, voltage criteria for LVH are not met in Figure-1 (ie, the R wave in lead V6 falls shy of the 18-20 mm needed in this lead). But, given the high prevalence clinical situation (ie, this patient has known hypertension plus aortic insufficiency) + nearly enough R wave amplitude in lead V6 (16mm) + ST-T wave changes consistent with LV “strain” in all lateral leads (ie, leads I, aVL, V4-6) — true chamber LVH is likely (CLICK HERE — for more on the ECG diagnosis of LVH).
• It would be extremely interesting to see a baseline ECG on this patient, taken at a time when she is not in acute cardiogenic shock! My GUESS as to what such a “baseline” ECG on this patient would show is: i) ST-T wave changes of LV “strain” in the same 5 lateral leads with similar shape for the ST-T waves, but with less J-point depression than the 2-4mm seen in leads V4-thru-V6 in Figure-1; ii) much less (if any) ST elevation in leads aVR and V1; iii) possibly an upright T wave in lead V2, with a shape reciprocal to the ST-T wave depression seen in the lateral chest leads in Figure-1 (ie, LV “strain” often results in mirror-image upright ST-T waves in anterior leads, compared to the ST-T depression seen in lateral chest leads); iv) much less (if any) ST depression in leads II, III, aVF and V3 (with loss of biphasic T waves); and, v) possibly greater R wave amplitude in lateral chest leads (sometimes ischemia reduces R wave amplitude ... ).
• Without the luxury of seeing this patient’s “baseline ECG” — we are reduced to educated guessing about which ECG findings in Figure-1 are “new” vs “old” vs “new on-top-of old”. My hunch is that what we are seeing in Figure-1, is a combination of longstanding LVH with LV “strain” + superimposed diffuse subendocardial ischemia in this patient with acute cardiogenic shock from complications of her valvular heart disease. Cardiac catheterization would have told us if significant underlying coronary disease was also contributing to the subendocardial ischemia.

Our THANKS to Dr. Smith for presentation of this interesting case.