Cardiogenic Shock – EM Reflections December 2021

 

Authored and Copyedited by: Dr. Mandy Peach

Big thanks to Joanna Middleton for leading this month’s discussion

All cases are imaginary but highlight important learning points.

Case

A 70 yo female presents via EMS with potential syncope accompanied by nausea/vomiting. She describes feeling weak for 2 days and hasn’t eaten or drank much. She got up to go to the washroom and her ‘legs gave out’. She felt diaphoretic after and vomited. She denies any other GI symptoms, abdominal pain or fever. She denies any recent chest pain, shortness of breath, headache or neurological symptoms. You confirm she has had no med changes recently.

Her PMH includes: DM, HTN, DLP, GERD, cholecystectomy.

Her medications include: metformin, ramipril, atorvastatin and pantoprazole.

Her vitals are: BP 108/72 HR 58 RR 20 O2 96% on RA T 37.4 glucose 8.2

On exam, she appears pale and slightly clammy but overall perfusion is normal. Her cardiac and respiratory exam is unremarkable. Her abdomen is soft and non tender. Her neuro exam is grossly normal with no obvious deficits or focal weakness. Aorta scan on PoCUS is determinant and negative, the cardiac views are suboptimal, and IVC appears minimally collapsible.

As per usual, the department is in overcapacity and there are a number of critically ill patients. You begin a small fluid bolus, treat the patient’s nausea and order labs.

What is the differential for this vague presentation in a geriatric patient?

HUGE.

Weakness in the elderly can associated with a number of diagnoses¹:

Focal weakness – ICH, CVA, SAH, tumor, SCI

Acute Non focal weakness -delirium, metabolic, infectious, cardiac

Chronic non focal weakness – anemia, meds, inflammatory disease, deconditioning, malignancy

This patient sounds like she may have had a vagal episode – she could be dehydrated, her anti-hypertensives may now be too high, she may have underlying infection…

Since you don’t see any glaring red flags you await lab work up and continue to see other patients.

An hour has passed and you review her labs: her CBC, CRP, VBG, electrolytes and extended electrolytes are normal. Renal function looks down from previous. You reassess but despite some fluids and Zofran your patient still feels nauseous and lightheaded. Her feeling of generalized weakness has not improved. She now appears drowsy, but responds to voice, and her extremities are now cooler than before. Her BP is lower at 98/68 and HR 56. Other vitals are otherwise unchanged.

Something doesn’t fit.

The ECG tech hands you the ECG that was ordered at triage for ‘syncope’ but was delayed in getting done due to the back log.

Gulp. An inferior STEMI

What do you see²?

ST elevation in the inferior leads (II, III, aVF)

ST elevation in V1, V2 and V3 – V1 is the only lead that looks directly at the RV.

Reciprocal ST depression in lateral leads (I, aVL and V6)

*ST depression in aVL is a sensitive marker for inferior infarct – it truly is the only lead that is reciprocal to the inferior wall.  91% of ‘subtle’ inferior ST elevations that don’t quite meet STEMI, but have ST depression in aVL, have occlusion on PCI⁴.*

What changes suggest RV involvement²? Where is the culprit lesion?

ST elevation in V1 – ST elevation in this lead should always make you think of RV involvement, especially if it exceeds STE in V2

If STE is isoelectric, look for ST depression in V2

ST elevation in lead III > lead II (lead III is more rightward facing)

The majority of RV infarcts(80%) occur secondary to occlusion of the proximal RCA before the marginal branches break off to supply the RV and give the expected ECG findings above. A small percentage (18%) are left sided dominant, with the circumflex artery supplying the RV⁴. Those with chronically occluded RCAs may also develop collateral left sided circulation.

If left sided circulation is occluded leading to RV infarct expect changes in the lateral part of the inferior wall

• ST elevation in lateral leads: I and V5-6.
• STE lead II = lead III
• Absence of reciprocal ST depression in lead I.

“One quarter to one third of inferior STEMIs are associated with RV infarction, and nearly 90% of RV infarctions occur with coexistant inferior MI².”

So – if you have an inferior MI – look for the RV infarct. You order right sided leads

Sure enough – there is elevation in V4.

Are there any signs/symptoms that could have tipped off this patient was having an RV MI³?

Bradycardia in the absence of any beta blockers, especially with hypotension, is a red flag. Patient’s presenting with RV MI can have AV node dysfunction from ischemia – or vagal excess – resulting in bradycardia, AV block or hypotension with clear lungs. They can exhibit more vagal symptoms like nausea, vomiting, diaphoresis, and pallor.

You urgently reassess and begin going through contraindications for thrombolysis. As you are questioning the patient she says she doesn’t feel well and is now experiencing chest pain– her HR has dropped to 45, it appears to be sinus. Her BP is now 80/56. 

How do we treat her symptoms?

Certainly, you can treat the pain, but improving her perfusion will improve her symptoms.

Avoiding nitroglycerin is a bit of a no brainer when the BP is this low, but on initial presentation when her SBP was above 100, one still has to avoid nitroglycerin – these patients are preload dependent. How sensitive depends on the extent of the infarct of the RV. Large infarcts lead to dyskinesis of the free wall, poor filling and poor cardiac output despite intact systolic function³. Optimize the preload as much as possible with judicious fluids – considering reassessing the lungs first with PoCUS for signs of pulmonary edema.

Maintaining her heartrate – stroke volume of the RV is relatively fixed, so in addition to improving filling with fluids, the heartrate has to be maintained to ensure cardiac output³. Depending on the rhythm (ie. Normal sinus vs AV block) atropine may not be beneficial. Consider early pacing if atrophine is not beneficial or there is complete heart block.

Improving her blood pressure with vasopressor agents if fluid alone isn’t suffice. Typically start with an alpha-agonist agent (norepinephrine). There is evident that norepinephrine improves survival benefit in patients with LV related cardiogenic shock, but no studies support RV infarct related shock³.

The ultimate way to improve her symptoms is reperfusion.

You have initiated pressors, another small fluid bolus and atropine as the rhythm is normal sinus. You are preparing pacing pads as you finish questioning on contraindications for thrombolysis – she has none. Anti-platelets and anti-coagulants are being prepared.

Should you thrombolyse this patient?

We know reperfusion is what she needs, but should that be with lysis or PCI?

In an ideal world PCI is first line for everyone, but realistically we work peripherally in smaller areas or STEMIs present after cath lab hours. We also don’t really know the onset of this event since the patient has such vague symptoms – presumably it started yesterday.

You need to decide if the patient is truly in cardiogenic shock – for those in shock the first line treatment is PCI/CABG. Early revascularization has been shown to have a mortality benefit 6 months out from the event.⁵

What defines cardiogenic shock⁶?

Reduced contractility resulting in a SBP < 90mmHg, or the need for vasopressors to support BP AND evidence of end organ dysfunction.

Keep in mind patient’s with a lower BP that is above 90mmHg may still be in occult shock if there are signs of end organ dysfunction – have a high suspicion.

Signs of end organ dysfunction:

Skin assessment	Cool, mottled, prolonged cap refill
Mental status	Ranges from drowsy, ALOC , comatose
Urine output	Oliguria often
PoCUS findings	Advanced measurements if within your scope of practice: Splenic doppler resistive index Renal doppler resistive index Portal vein pulsatility index

 

Your patient’s skin assessment and mental status are altered on your last assessment and she is requiring vasopressor support. This patient is in cardiogenic shock secondary to an acute inferior STEMI involving the RV.

As decreased cardiac contractility is the cornerstone of cardiogenic shock you repeat cardiac views with the patient positioned in the left lateral decubitus. You get this parasternal long view:

How can you assess cardiac function⁷?

If you are unable to accurately assess all these, eyeball the size and ‘squeeze’ of the LV – are all the walls thickening uniformly?

An easy way to roughly gauge ejection fraction is to look at the mitral valve – if the anterior leaflet touches off the wall of the LV when it opens the EF is likely normal. If not you can measure the E point septal separation (EPSS) in M mode. EPSS >7mm is 100% sensitive for a severely depressed EF < 30%⁸.

On PoCUS, heart failure caused by acute ischemia will typically show a large RV and small LV secondary to low filling pressures, which is best seen on the apical 4 chamber view⁹.

You determine the EF to be decreased.

You urgently call interventional cardiology to discuss and arrange cath lab. Currently the cardiologist just started a case and isn’t immediately available but will take the patient to the cath lab as soon as they are finished.

What are the other priorities of care in a patient with cardiogenic shock⁶?

First is determining the cause to optimize the overall management -here we suspect acute coronary syndrome and this patient needs reperfusion, but in other patient’s without obvious ACS consider:

• Mechanical issues like valvular problems, free wall rupture or endocarditis
• Myocarditis
• Progressive non-ischemic heart failure

Next optimize oxygenation, usually this is done with NIPPV but caution in patient’s with RV failure – too much positive pressure can increase RV afterload. The patient’s recent O2 sat was above 90% – you apply oxygen via nasal cannula and reassess again – there are still clear lungs on auscultation and no B lines on PoCUS.

Optimize fluid status – in RV infarct judicious fluid can help increase preload. However, ideally at time of presentation complete a through fluid assessment for hypervolemia, euvolemia or hypovolemia. PoCUS can be helpful here – consider the following measurements⁶

Up front, as we didn’t suspect cardiac cause, we treated for hypovolemia in the setting of nausea/vomiting and poor intake. She has received fluid to improve pre-load and still appears to have clear lungs.

Improving blood pressure with vasopressors as discussed above⁶ – she is on vasopressors and has received atropine. We are targeting a MAP of 65-80. Norepinephrine is the first line agent – it has been shown to have a lower risk of refractory hypotension compared with epinephrine.

Improving cardiac contractility – can start dobutamine. This is a beta-1 and beta-2 agonist so it has inotropic effects, but it also vasodilates. Therefore – begin norepinephrine before starting dobutamine to avoid worsening hypotension. When comparing dobutamine to other inotropes like milrinone there was no difference in clinical outcome for cardiogenic shock, however dobutamine is shorter acting and may therefore be easier to titrate.

Reassess clinically for improvement in skin perfusion, urine output and mental status.

You reassess your patient – mental status is improving, there has been a temporary improvement in BP and HR. A foley is inserted. She is being prepped for PCI.

If she were to continue to worsen despite your efforts while you await PCI what would be the next management step⁶?

This patient has a clear cause for their shock. You can consider mechanical support to bridge the patient to the intervention, in this case – PCI. Discuss with cardiology and CV surgery early if you suspect you will require mechanical support.  These supports can include intra-aortic balloon pumps (IABP), percutaneous ventricular assist devices (PVAD – Impella, Tandem Heart), and veno-arterial extracorporeal membrane oxygenation (VA-ECMO).

The patient goes on to the cath lab but arrests on the table. Despite these interventions ROSC isn’t achieved.

RV involvement is associated with increased risk of cardiogenic shock and death with a mortality of 50% within the first 48 hours⁸.

To review:

• RV infarcts can present with hypotension with clear lungs, bradycardia, nausea/vomitting, pallor and diaphoresis. Have a low threshold to order an ECG.
• Suspect RV involvement in any inferior MI – get right sided leads. Have a closer look at avL – ST depression in this lead is strongly associated with occlusion MI.
• Cardiogenic shock is SBP < 90mmHg with signs of end organ dysfunction. You can still have ‘shock’ with a BP higher than this. Again, high suspicion.
• Keys points of managing cardiogenic shock
  • Determine cause and if reversible
  • Improve fluid status
  • Improve cardiac contractility
  • Improve blood pressure
  • Improve oxygenation
• Consider mechanical support, like ECMO, as a bridge to interventions. Discuss cases with cardiology and CV surgery early

 

 

References and further reading:

1. Thomas, A. 2018. CRACKCast E181 – Approach to the Geriatric Patient . Retrieved April 4, 2022 from https://canadiem.org/crackcast-e181-approach-to-the-geriatric-patient/
2. Nickson, C. 2022. ROSC, hypotension and an ECG exigency. Life in the fast lane. Retrieved April 2, 2022 from https://litfl.com/rosc-hypotension-and-an-ecg-exigency/
3. Levin T, Goldstein J. 2021. Right ventricular myocardial infarction. Uptodate. Retrieved April 4, 2022 from https://www.uptodate.com/contents/right-ventricular-myocardial-infarction?search=Rv%20infarct&source=search_result&selectedTitle=1~78&usage_type=default&display_rank=1#H267508435
4. Buttner R, Burns E. 2021. Inferior STEMI. Life in the fast lane. Retrieved April 4, 2022 from https://litfl.com/inferior-stemi-ecg-library/
5. Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD, Buller CE, Jacobs AK, Slater JN, Col J, McKinlay SM, LeJemtel TH. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med. 1999 Aug 26;341(9):625-34. PMID
6. Helman, A. Hedayati, T, Tillmann, B. Cardiogenic Shock. Emergency Medicine Cases. January, 2022. https://emergencymedicinecases.com/cardiogenic-shock. Accessed April 5 2022.
7. Atkinson P, Peach M, Lewis D. Just the Facts: The Five F’s of Focused Echocardiography in Shock. CJEM. 2020 Sep;22(5):655-657. doi: 10.1017/cem.2020.440. PMID: 32787986.
8. Wong, M. 2002. Point-of-care echocardiography. A Primer, 1^st EM Ottawa Blog. Retrieved April 11 2022 from https://emottawablog.com/wp-content/uploads/2020/07/DEMEchov3.docx-1.pdf
9. Tintinalli, JE. (2016). Cardiogenic Shock (8th ed.) Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (pages 349-352). New York: McGraw-Hill.