Cardiogenic Shock

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.


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?


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
  2. Nickson, C. 2022. ROSC, hypotension and an ECG exigency. Life in the fast lane. Retrieved April 2, 2022 from
  3. Levin T, Goldstein J. 2021. Right ventricular myocardial infarction. Uptodate. Retrieved April 4, 2022 from
  4. Buttner R, Burns E. 2021. Inferior STEMI. Life in the fast lane. Retrieved April 4, 2022 from
  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. 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, 1st EM Ottawa Blog. Retrieved April 11 2022 from
  9. Tintinalli, JE. (2016). Cardiogenic Shock (8th ed.) Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (pages 349-352). New York: McGraw-Hill.
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Nar’ pump, mo’ problems

Nar’ pump, mo’ problems, a case on cardiogenic shock

Resident Clinical Pearl (RCP) – June 2017

Mandy Peach, R2 FMEM, Dalhousie University, Saint John, New Brunswick

Reviewed/Edited by Dr. David Lewis and Dr. Kavish Chandra

It’s 11 pm, you’re doing the overnight shift and EMS calls in to report a patient with an ETA of 3 minutes: “80 yo female, found on floor in apartment by husband after reportedly feeling unwell for 2 days. Decreased LOC but arousable and responding appropriately. BP 82/36, HR 120, RR 22, Afebrile, oxygen sat 86% on 6L nasal cannula.”

You hear the vitals, and many differentials run through your mind – PE, sepsis, hemorrhage, tamponade. Your main concerns are: this person needs more airway support and they are in shock, and when you think shock you think ‘fluids’.

EMS rolls in with your patient and she looks awful – pale, mottled extremities and drowsy. She is being re-assessed, RT is present to switch to a face mask, IV access is being established and you’re about to pound her with fluids when you are handed her ECG:


This lady clearly is having an inferior STEMI – there is marked ST elevation in II, III and aVF with early Q wave formation.


Take home point #1: In any Inferior STEMI, you must suspect RV involvement

Look for ST elevation in V1 and depression in V2, or ST elevation in lead III > lead II. If these are present – get a 15 lead ECG.1

On closer look at our patient’s ECG there is ST elevation in V1-V2 and the elevation in lead III is indeed larger than lead II. You order the 15 lead.


Look for ST elevation in right sided leads V3-V6, but the money is on V4R – ST elevation in this lead has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83% for RV infarction2. Our patient does have RV infarction seen by ST elevation in V4R.


Take home point #2: RV involvement is associated with increased risk of cardiogenic shock and death with a mortality of 50% within the first 48 hours3. If there is RV involvement, giving nitroglycerin for chest pain is CONTRAINDICATED

Due to a poorly functioning RV, patients are pre-load sensitive2. If you decrease the pre-load then they have even less to pump, further worsening the hypotension.

So we have diagnosed this lady with cardiogenic shock secondary to AMI (the most common cause of cardiac related shock) and we determined she has RV involvement. We know we can’t give her nitroglycerin. Let’s reassess her status – the basic ABC’s.

Airway & Breathing – the RT has since advanced her to a non-rebreather with a sat level in the high 80’s. You suggest trying Optiflow or BiPAP as a temporizing measure – this lady is going to need to be intubated.


Take home point #3: Positive pressure ventilation requires a stable, cooperative patient – which is often not the case in cardiogenic shock

Positive pressure can decrease pre-load and potentially worsen hypotension3. It is a temporizing measure only. The majority will require endotracheal intubation to maintain their saturation as their work of breathing is a large expenditure of energy.

You successfully complete a RSI and the saturation improves to 94-98%.

Circulation – Repeat BP is 82/36. You complete a cardiac point-of-care-ultrasound (PoCUS) and see poor contractility, but no pericardial effusion or large clots suggesting chordae or papillary rupture. IVC is > 50% collapsible.


Take home point #4: On PoCUS, heart failure caused by acute ischemia will show a large RV and small LV secondary to low filling pressures, which is best seen on the apical 4 chamber view3

Your patient continues to be hypotensive – you give a small 500 cc bolus; you don’t want to overload a poorly pumping heart with fluid it can’t handle. However you anticipate that this will not be enough to improve her BP, and as she continues to be hypotensive her myocardial ischemia worsens, which subsequently worsens her pump dysfunction in a vicious cycle. She needs pressure support.


Take home point #5: Cardiogenic shock requires vasopressor support

If systolic BP > 90: Start with dobutamine for inotropy. Double up on agents – likely will need to add a vasoconstrictor. Dopamine is usually the next to add.

If systolic BP < 90: Can still use dobutamine, but need to add norepinephrine for vasoconstriction. Dopamine alone will worsen BP as it is a vasodilator.

3Tintinalli’s Comprehensive Guide to Emergency Medicine.

You start dobutamine and dopamine peripherally with the intention of obtaining central venous assess once stabilized.

In the meantime, cardiac labs and portable CXR are pending, you treat this patient as any other STEMI in terms of dual anti-platelet and anti-coagulation loading.


Take home point #6: Do not give beta blockers

Do not give beta blockers in RV infarcts as high risk of bradycardia and AV block due to ischemia of the AV nodal artery3.

You consult cardiology to activate the cath lab.


Take home point #7: Early revascularization in ischemic related cardiogenic shock is key

Early revascularization has a long term mortality benefit, preferably if done within 6 hours4.  Catheterization or CABG is the preferred method over thrombolytic therapy.

You consult cardiology to activate the cath lab.

Back to our patient –

This lady did go on to the cath lab and had stenting of her RCA, however her infarct likely occurred > 48 hours before presentation. Unfortunately, despite aggressive vasopressor therapy and revascularization, she coded immediately after the procedure and resuscitation attempts were unsuccessful, emphasizing the poor prognosis associated with ischemia related cardiogenic shock.


Bottom line for cardiogenic shock: fluid bolus 500 cc 0.9% NaCl, vasopressor support and RSI. Early revascularization is key – catheterization is preferred. Despite these interventions, the diagnosis portends a poor prognosis.



  1. Inferior STEMI – Life in the Fast Lane
  2. Right Ventricular Infarction – Life in the Fast Lane
  3. Tintinalli, JE. (2016). Cardiogenic Shock (8th ed.) Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (pages 349-352). New York: McGraw-Hill.
  4. Cardiogenic Shock – Literature Summary – Life in the Fast Lane


This post was copyedited by Kavish Chandra @kavishpchandra

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