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Cardiogenic Shock - Talk One

Ineffective cardiac output caused by a primary cardiac disorder with evidence of hypoperfusion

Not all hypoperfusion is hypotension! Not all hypotension is hypoperfusion!

The majority of trials use a Systolic of 90-

Classification

Diagnosis

Sometimes obvious, sometimes less so (like de novo HF, or in myocarditis)

Grouping

Cold-Wet

Usually decompensated CHF patients with evidence of congestion, the younger patients can be more subtle Pitting Oedema/Pulmonary Oedema Congestive LFTs, Abdominal Swelling Orthopnoea, Sinus Tachy, Raised Lactate

Cold-Dry

These are more difficult to notice, they can be more shut down and appear like they are dehydrated. Can have very vague symptoms, including GI symptoms.

So these patients may get loads of fluids, as if they're dehydrated, but get super sick.

CVP could be useful in these patients, as it'll show a really high number.

These patients need frequent reassessment

Warm Wet

These are decompensated without shock, or post MI cardiogenic (with inflammation looking sepsisy), or a mixed picture like cardiogenic septic shock with sepsis

Thesell be the patients with minimal response to fluids, or high dose vasopressors, or persistent lactate.

Investications

  • ECG -Bloods - Inc Endocrine TFTs, Lactate -ABG -Mixed Venous Gas from Central Line -CXR - Cardiac Border and Oedema -Echo

What about quantifying congestion?

  • Clinical Exam - JVP
  • CVP
  • Swan Ganz - Could just be temporary
  • Dilated IVC
  • Atrial Size and atrial filling

Making Diagnosis

  • Patients should have an echo at first line.
  • All patients admn to critical care with shock should prob have an echo.
  • B Lines - Cardiologist was less of a fan
  • After initial echo should get a comprehensive echo ASAP
  • For valvular stuff
    • Like AR
    • Like planning for mechanical support

Remember patients often present oddly, sometimes hypoperfusion could just be confusion or GI upset or persistent unexplained tachycardia.

Aetiology

ACS causes about a third Non ACS Decompensated HF causes another third Everything else is the rest Valves Endocrine Tumours

Around 1 in 10 to 1 in 20 ACS have cardiogenic shock,

1/3 of these at admission, 2 /3 during admission

More common in stemi but also occers in NSTEMI

Occurs cos of acute and irreversible loss of myocardial tissue

These patients are generally older with diabetes and vascular disease.

The treatment is urgent revascularisation, initially it was fully revascularisation. But Culprit-SHOCK, the study showed that you should only go for culprit vessel rather than all vessels. Reduces mortality and dialysis. Do the rest later.

The other support is IABP, study for this is IABP-SHOCK II showed no real reduction in mortality (2019), But could be useful in mechanical complications such as VSD and MR. Cardiologists are still a fan.

Pharmacological agents. Cardiologists are more supportive of dobutamine, but does increase risk of arrhythmias.

But if you've an RV infarct, youll be really hypotensive with raised JVP but clear lungs. These patients need really high filling pressures and loads of fluid.

Management in Non-ACS

Will depend on the aetiology.

You need to think about the exit strategy here, what's the reversibility, what possibility of support or transplant.

Sometimes are hypovolaemic and do need fluids but do be careful.

Dobutamine, milrinone, and levosimenden are cardiologists options in CCU.

Again, IABP show now mortality benefit but do improve coronary perfusion. Again cardiologists are a fan.

Decompensated Chronic HF

This can be particularly difficult in terms of exit strategy, as if not transplant candidate may be palliation.

Myocarditis

Serial troponins can be useful for prognosis.

Possibly may need mechanical support.

Steroids can be lifesaving with giant cell myocarditis

Discuss patients with transplant early

Takutsubo

Transient high afterload, dynamic LVOT obstruction

Caused possibly by high catecholamines endogenously, and IABP can make the LVOT worse.

So levosimenden and milrinone may be more useful here.

Palliative Care

Consider if not reversibility Think about device deactivation so not shocked after death

Don't automatically stop diuretics, as if signs of congestion, death w/ pulm oedema won't be nice.

Acute Heart Failure in Critical Care - Andrew Sinclair - Talk Two

Acute Heart Failure is about 5% of emergency admissions in the 65+ age group

The mortality is around 40%

The ESC guidelines are hypotension despite adequate filling status with signs of hypoperfusion.

There is an interventional cardiology group that attempted classification.

Look at the SCAI Document, the clinical expert consensus statement in the classification of cardiogenic shock.

Stage A - At risk Stage B - Beginning hypotension Stage C - Hypotension and Hypoperfusion Stage D - Failure To Respond, Periarrest, Arrest

Assessment

Look for evidence of hypoperfusion and for congestion

Investigations

echo: - Is there a cardiac cause - How severe is cardiac impairment - What is physiological effect - is reversible cause?

The ESC recommendations is all patients with suspected cardiogenic shock, should get immediate ECG and echo.

FUSIC scans Lung USS - B lines, pulmonary congestion

Venous Excess Ultrasound - Is there evidence of venous congestion. One thing is IVC 20mm+

cardiac output monitoring - Benefits help confirm diagnosis and titrate medications, and identify patients who may benefit from escalation - Options include - PA Catheter - Calibrated Pulse Contour Analysis

Management

There is no RCT which shows significant improvement at 30d mortality. Noradrenaline appears preferable to dopamine (due to arrhythmias) and adrenaline (due to refractory shock)

Norad starts at 0.05micro/kg/min following echo You would titrate up to 0.25 Vasopressin would be added after, then methylene blue Then mechanical cardiac support.