Thanks
This is a talk about the broken heart, and I’m going to give a brief overview of Management of CS, with particular focus on advanced MCS options available
As intensivists we commonly resuscitate and support patients with many kinds of circulatory shock. Treatment varies depending on cause, stage, and end- organ effects.
Cardiogenic shock can be defined in simple terms as
‘pump’ problem: Low CO (index< 2.2L/min) despite normal or ELEVATED preload (normal circulatory volume, PCWP> 15-18mmHg with
2. End- organ hypoperfusion (lactate, UO, mental state, peripheries etc). May include definitions such as SBP< 90mmHg for >30mins, or catecholamines required to keep SBP> 90mmHg
CS: Very heterogenous group. Acute MI most common, homogenous population, most commonly studied.
Decomp HF (acute/ chronic, many causes). Myocarditis (many causes)
Cardiogenic shock complicates up to 15% of AMI, translating to 50,000 patients/ year in USA, 70,000/ year in Europe.
Mortality overall remains unacceptably high at 40%
I’d like you to think of cardiogenic shock as a spectrum. Treatment options will depend on severity and what has been initiated already.
Samuels et al 1999.
Werden 2014 EHJ. Prognostically relevant components of shock complicating MI.
In addition to micro-and-macro circulatory effects of systolic and diastolic dysfunction, SIRS +/- sepsis may resultMODS. Cytokines also shown to influence outcome (up arrow means levels increased in non-survivors….down arrow means reduced in NS)
Treatment options: Divided into medical Tx, revascularisation, mechanical support.
Current evidence from RCT’s for CS in the PCI era.
This is a talk about MCS for CS, therefore not going into details of medical therapy. BUT if we look at current evidence in CS in the PCI era: only intervention to show significant benefit (NNT= <8), mortality benefit at 6months, 1 yr, 6 yrs.
Catecholamines: balance of increasing BP+ end- organ perfusion vs impairing micro-circulation and increasing myocardial O2 consumption
Despite lack of good quality evidence, vasoactive meds are our bread and butter in ICU, and cardiology guidelines recommend vasoconstrictor as first choice agent, followed by inotrope of choice (depending on flavour de jour in your unit….milrinone v dobutamine, adrenaline, levo, not dopamine. But vasoconstrictor and adrenergic effects of these drugs are helpful only up until a point, with downregulation of receptors, tachyarrhymias, microcirculatory dysfunction all attributed to excessive doses. So how much is too much? Well, no –one knows and institutions will vary in threshold of when to introduce MCS device. But increasing consensus that earlier MAY be better.
MCS can be thought of as providing a Bridge: to recovery, bridge to destination (transplant), bridge to bridge (LVAD), bridge to decision, bridge to nowhere??
When thinking of mechanical circulatory support for CS, consider several things: temporary vs prolonged, percutaneous vs surgical approach, timing of insertion, level of support the device can provide, potential complications with each device.
Considerations for choice of device. Timing crucial. Comes back to pathology of MODS, and high mortality rate once this is established. Devices work in different ways, and support RV and LV with varying levels. Axial/ centrifugal flow, pulsatile vs non-pulsatile flow considerations.
Axial pump consists of a propeller in a pipe. Ability to generate higher flow rates, relatively, compared to centrifugal pumps. But less efficient. And more likely to cause haemolysis due to crude nature of flow generated.
Centrifugal pumps work on principle of generating rotational kinetic energy to hydrodynamic energy of fluid flow. (often driven by electromagnetic force)
Surgical VAD’s require careful consideration and work-up prior to insertion. Technical surgical procedures, performed in limited centres. Funded as bridge to transplant in Australia.
Not usually an option in the acute/ emergent setting of VAD: LVAD, BiVAD, mini-LVAD. (Heartware LVAD pictured). As bridge to transplant (in USA as destination therapy). Total artificial heart.
IABP: 8F placed in descending aorta via fem artery. Support of 0.5-1L/min
Impella: Axial pump placed across aortic valve, retrograde, using 12F cannula via femoral artery (Impella 5 uses femoral cutdown, 21F cannula). Support of 2.5- 5L/min
VA ECMO: 21-23F inflow from RA via fem vein, outflow to descending aorta via fem artery. Support >4.5L/min
Tandemheart uses 21F inflow into LA via femoral vein and transeptal puncture. Outflow via 15-17F cannula into femoral artery (Centrifugal). Support up to 4L/min
Aim is to improve CO, and unload critically damaged ventricle (either pre-load or afterload reduction). Each device has a different mechanism, or several mechanisms, and can be thought of working as….
The balloon, or Intra-aortic balloon counterpulsation has been around for long time, works on principle of diastolic augmentation. Helium driven balloon, pneumatic principle, increasing diastolic coronary perfusion pressure, reducing afterload, and reducing myocardial work as a result.
Used for many indications: AMI with CS, high risk PCI, high risk sternotomy, difficulty weaning from CPB.
Most cardiologists familiar with insertion techniques and management. Complication rates are generally low, but include ischaemia, thrombosis etc.
Despite widespread use…..Not evidence based!
IABP-SHOCK 2 (Thiele et al NEJM 2012). 600 patients with CS post AMI
IABP vs no IABP. All received early revascularisation plus optimal medical therapy. No difference in mortality. No difference in secondary outcomes: lactate, renal failure, catecholamine doses, ICU LOS
Then Thiele et al Lancet 2013: 1 yr F/U. ESC guidelines downgraded to 3a recommendation for routine IABP use in CS (previously class 1)
So what are the other options?
Impella has gained popularity in USA an Europe: axial rotary pump, placed across AV providing transvalvular assistance (volume unloading).
Comes as 2.5 and 5. 2.5 requiring access via femoral artery (12F or 21F), cutdown required for 5.
Complications as for IABP, with additional risks of introducing to cardiac chambers (perforation etc).
Short term use only (4 days ish)
Studies have demonstrated safe and haemodynamically effective in high- risk PCI patients.
But studies looking at Impella 2.5 in pre-shock STEMI population (IMPRESS), and haemodyamically unstable STEMI population (RECOVER-2) were terminated due insufficient patient enrolment.
ISAR- SHOCK: IMPELLA 2.5 vs IABP in AMI CS patients: 26 patients total. Improvement in CI, MAP, lactate in Impella group. No difference in 30d mortality or complications.
VA ECMO has been used to support all kinds of CS. Peripheral approach has gained familiarity amongst Intensive Care community.
Access via femoral vein (21-23F, tip in RA), with return in distal aorta (15-19F).
Requirement for distal limb perfusion cannula (‘Backflow’ cannula).
Small data numbers……
Top 2 studies were with IABP as control: 1st one was progressive CS after successful PCI. 2nd one STEMI with ‘profound’ CS.
Impella included cardiac arrest.
Overall better survival with ECMO vs IABP (thought heterogenous group and small numbers), BUT no long- term survival or neuro outcome figures.
Important to get basics right (Fluid status, vasoactives, rhythm/ rate control etc)
Earlier MCS is probably better (balancing risks vs benefits) to avoid spiral into MODS which is usually irretrievable
IABP will continue to be used by most (familiarity, practical purposes, availability etc)
VA ECMO increasingly used in select centres ?Future