part man, part machine…

the case.

48 year old male is bought to the Emergency Department via ambulance following a syncopal episode. They are unable to obtain a blood pressure & describe ‘some sort of device coming out of his chest’ !!

He has a past medical history of a severe, familial dilated cardiomyopathy (LVEF ~18-20%) & atrial fibrillation and is awaiting cardiac transplantation. Six months ago he was implanted with a left ventricular assist device.

He has recently felt systemically well, however today he reports collapsing without prior warning shortly after getting out of his chair. Following a brief loss of consciousness, he quickly returned to his normal self.

[DDET Firstly, what is a left ventricular assist device ?!?]

Left ventricular assist device [LVAD]

These are intricate mechanical pumps utilised in the management of end-stage cardiac failure refractory to aggressive medical therapy, typically bridging a patient to cardiac transplantation.

The first implantation of an LVAD occurred back in 1984, however their technology and success have markedly improved since then. The landmark REMATCH paper demonstrated significant survival increase [52% vs 25% at 1 year, p=0.002] with an improved quality of life. Currently over 90% of LVAD-supported patients will survive to 1 year post-implantation.

Indications.

• Bridge to cardiac transplant.
• Bridge to recovery – potential reversible myocardial pathology.
• Destination therapy – long-term assistance for patients ineligible for transplant

The components.

• Inflow cannula.
  • placed within the left-ventricle
  • draws blood from the LV into the pump.
• The pump.
  • is located at the apex of the LV.
  • houses the impeller – a frictionless rotor which is magnetically levitated. This rotates at speeds of >3000 rpm & can generate up to 10 litres per minute of blood flow.
• Outflow graft.
  • flexible & gel-impregnated
  • conveys blood from the pump to the ascending aorta.
• Driveline.
  • tunneled subcutaneously from the pump & exits typically in the patients epigastrium or right-upper quadrant
  • contains wires from external controller.
• Controller.
  • regulates power, monitors VAD performance & displays alarms,
  • displays battery life & function.
  • allows data to be downloaded for analysis.
• Batteries.
  • at least two rechargeable lithium-ion batteries are carried at all times
  • the device is also capable of recharging on standard power supply.

What do they look like ?

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[DDET Outline your assessment of this patient ?]

The assessment of a patient with a VAD begins like any other; a primary survey !! However, there are a few specifics we should mention.

1) BLOOD PRESSURE MEASUREMENT.

Due to diminished [& sometimes absent] peripheral pulses in the continuous-flow VADs, standard non-invasive blood pressure is difficult [perhaps impossible] to obtain.

Blood pressure can be measured with (1) a manual sphygmomanometer & (2) Doppler ultrasound over the radial or brachial artery. Cuff pressure is gradually reduced until a constant sound is heard – signifying the mean arterial pressure. Alternatively, in a critically ill patient just place an ultrasound-guided arterial line !

 

 

 

 

 

 

 

In this case the patients’ mean arterial pressure was measured at 59 mmHg. He normally runs at 70-80mmHg.

2) ASSESSING DEVICE FUNCTION.

• Check that the pump is running. Auscultate the epigastrium/precordium for a continuous noise ! This is the pump operating.
• Check the controller for;
  • BATTERY FUNCTION !
  • Flow
  • Power etc…

3) A BEDSIDE ECHO CAN BE A VERY POWERFUL TOOL.

• VAD malfunction can result in catastrophic consequences & marked haemodynamic instability.
• ECHO will allow rapid assessment of RV:LV chamber size comparison.
  • Small RV: consider Hypovolaemia [check IVC also]
  • Large RV: consider Pulmonary hypertension [correct hypoxia & acidosis]
  • Large RV + LV: consider VAD-thrombus !!
• ECHO will also allow assessment of IVC diameter & collapsibility as well as the presence of pericardial effusion ± tamponade.
  • Will also confirm the correct positioning of the inflow cannula [which can migrate or kink overtime].

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[DDET The golden rule of LVADs !!]

Call your nearest LVAD or Cardiac-transplant centre as soon as possible for assistance in the care of these complex patients !!

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[DDET What could be causing his hypotension ??]

It is important to acknowledge that these devices are

1. preload dependent &
2. afterload sensitive.

Any physiological or pathological influence on either of these can significantly alter pump-efficiency and result in hypotension !!

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[DDET LVADs and HAEMORRHAGE…]

The most common adverse event with the first month of implantation. These patients have multiple reasons for bleeding…

1. Anticoagulation: typically warfarin.
2. Antiplatelet therapy: often dual agents.
3. Acquired von-Willebrand syndrome:
4. Increased incidence of AV-malformations & angiodysplasia of the gastrointestinal tract. 

Common sites of bleeding include the GIT, epistaxis, intracerebral haemorrhage & intrathoracic bleeding. Clearly most of these will be clinically obvious, but always consider occult GIT haemorrhage in the hypotensive VAD-patient.

The management of bleeding in VAD-implanted patients is a particularly challenging therapeutic dilemma. If anticoagulation-reversal is undertaken, it should be for as short a time-period as possible. You do not want them going on to have a subsequent embolic/thrombotic event !!

There are multiple case reports regarding the various therapeutic options for life-threatening haemorrhage & they include; prothrombin complex concentrates, FFP, TXA, desmopressin [defective vWF] & Factor VII.

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[DDET LVADs and DYSRHYTHMIAS…]

Every VAD-patient that presents to your department should have a 12-lead ECG as soon as possible….

Both ventricular and atrial dysrhythmias are incredible common amongst patients with VADs. In fact; ventricular dysrhythmias can be surprisingly well tolerated in these patients, with multiple cases reports of very stable patients in both VT & VF !!!

Potential causes for dysrhythmias include;

• Local trauma [VAD comes into contact with endocardium, see Suction Events below]
• Hypovolaemia
• Ischaemia
• Electrolyte disturbances
• other… [remember they have a significantly diseased myocardium to begin with]

Management options;

• Assess volume status & ensure adequate preload. Utilise bedside ECHO…
• Pharmacotherapy:
  • Amiodarone
  • Lignocaine
  • Procainamide
• Electrical cardioversion is safe in these patients…
• At your VAD centre – there may be attempts to reduce VAD-pump speed;  but this is usually performed under guidance of transoesophageal ECHO.

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[DDET LVADs and SUCTION EVENTS…]

A result of large negative pressures within the LV created by continuous-flow LVADs. This results in the LV collapsing on itself, causing marked leftward deviation of the interventricular septum.

Causes of suction events include;

• Right ventricular failure
• Hypovolaemia
• Cardiac tamponade
• Dysrhythmias
• Inflow cannula malposition.

Management;

• IV fluids & maintain preload.
• Obtain and ECG & treat dysrhythmias as above.
• Bedside ECHO
• Again; your VAD-centre may adjust pump-speeds.

[/DDET]

[DDET LVADs and SEPSIS…]

Infections can involve any portion of the VAD including the surgical site, driveline, device pocket & the pump itself !!

Whilst Gram-positive organisms are more commonly implicated in VAD-infections, don’t forget to cover for Gram-negatives & multi-drug resistant organisms. Fungal infections have been documented also.

Culture these patients from every possible site [including exit-site swabs] & maintain a high index of suspicion for occult sepsis in VAD patients present with either hypotension or fever !

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[DDET So what happened to our patient ?]

With his borderline hypotension, he was rather symptomatic with postural changes.

• Afebrile.
• Soft, non-tender abdomen with negative PR.

His results were largely unexciting…

• Normal haemoglobin.
• Electrolytes & renal function normal for him.
• INR 2.4. PLTs 264.
• Inflammatory markers unremarkable. WCC 8, CRP 14.
• 12-lead ECG: atrial sensing, ventricular pacing.
  • No episodes of dysrhythmia whilst on telemetry.
• CXR [seen above].

Here is his bedside ECHO…

PLAX view. Inflow cannula visible in LV-apex. Small RV. No pericardial effusion.

 

Marked respiratory collapse of the inferior vena cava suggesting volume depletion.

Our patient was treated with two small fluid boluses [250mLs of saline] which improved his mean pressure to 74mmHg. At this stage he was admitted under Cardiology to ‘fine-tune’ his medications…

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[DDET References]

1. Partyka, C., & Taylor, B. (2014). Review article: Ventricular assist devices in the emergency department. Emergency Medicine Australasia, 26(2), 104–112. doi:10.1111/1742-6723.12171

I acknowledge that my paper is not Free Open Access; hence why I have put this post together. I am however able [& very keen] to email you a copy upon your request.

So, email me at [email protected] & you’ll get your copy !!

I have since recorded the following presentations for the team at Sydney HEMS…

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