MECHANICAL CIRCULATORY SUPPORTS IN ADVANCED

HEART FAILURE

Dr SHALINI GARG SR II DM CARDIOLOGY

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Adapted from Bristow, MR Management of Heart Failure, Heart Disease: A Textbook of Cardiovascular Medicine, 6th edition, ed. Braunwald et al.

Class III

25% of HF Patients

Frequent hospitalizations

Worsening symptoms despite drug therapy

Significant opportunity for new therapies

Survival RateHospitalizations

Natural History of Heart Failure

Stages of Heart Failure

Addressing Heart Failure in 2013

Katz AM Heart Failure

INTERMACS SCOREInteragency Registry for Mechanically Assisted Circulatory Support

Long-Term LVADIdeal candidates are INTERMACS classes 3-4

Short-Term LVADCandidates are INTERMACS classes 1-2

Not a LVAD CandidateINTERMACS 1 or those with multisystem organ failure

INTERMACS Level Pre-Implantfor 1092 Primary LVAD (June 2006–March 2009)

1 Critical cardiogenic shock

2 Progressive decline

3 Stable but inotrope dependent

4 Recurrent advanced HF

5 Exertion intolerant

6 Exertion limited

7 Advanced NYHA III

Kirklins et al INTERMACS 2. JHLT 2010

Short term Device options

Bridge to recoveryBridge to decision

IABP

ECMO

Tandem Heart

Impella

AbioMed 5000Centrimag

Circulation 112 (3): 438

Intraaortic Balloon Pump (IABP)

Basic principles of counterpulsation

Counterpulsation is a term that describes balloon inflation in

diastole and deflation in early systole. Balloon inflation causes

‘volume displacement’ of blood within the aorta, both

proximally and distally. This leads to a potential increase in

coronary blood flow and potential improvements in systemic

perfusion by augmentation of the intrinsic ‘Windkessel effect’,

whereby potential energy stored in the aortic root during

systole is converted to kinetic energy with the elastic recoil of

the aortic root.

IABP inflates with aortic valve closure:Provides pressurized pulse of blood against closed aortic valve, increasing coronary perfusion

IABP deflates immediately prior to aortic valve opening:Reduces LV afterload

IABP: Physiology

• Inflation at aortic valve closure:• Increases aortic diastolic blood pressure• Increases diastolic coronary perfusion• Net neutral effect on cerebral perfusion• Increases C.O./“runoff” to subdiaphragmatic organs

• Deflation prior to systole:• Reduces impedance to LV ejection (afterload)• Reduces myocardial oxygen consumption

IABP: Physiology

• 2 main beneficial effects:

– 1) Augmented coronary perfusion

– 2) Reduced LV afterload/Increased CO

IABP: Physiology

• 2 main beneficial effects:1) Augmented coronary perfusion

• Only in normal coronary arteries• No augmentation beyond severe stenoses pre PCI• Augmentation beyond severe stenoses post PCI

2) Reduced LV afterload/Increased CO

IABP: Physiology

• 2 main beneficial effects:

– 1) Augmented coronary perfusion

– 2) Reduced LV afterload/Increased CO• Most important of 2 main effects when severe coronary

stenoses present

Hemodynamic Effects of IABP Aorta ↓systolic pressure, ↑diastolic pressure

Left ventricle ↓systolic pressure, ↓end-diastolic pressure, ↓volume, ↓wall tension

Heart ↓afterload, ↓preload, ↑cardiac output

Blood flow ↑→ coronary blood flow

IABP: Indications• Cardiogenic shock: Post cardiotomy, Ass. with acute MI, Mechanical complications of MI• In ass. with CABG Pre op : Pt with severe LV dysfunction Pt with intractable ischemic arrythmias Post op: Post Cardiotomy cardiogenic shock• In ass. With non surgical revascularization.

– Hemodynamically unstable infarct patients– High risk PCI : severe LV dysfunction, complex CAD

• Stabilization of Cardiac Transplant recipient before insertion of VAD• Post Infarction Angina • Ventricular Arrythmias related to Ischemia

IABP: ContraindicationsContraindications FOR IABP

Absolute Relative

Aortic regurgitation Uncontrolled sepsis

Aortic dissection Abdominal aortic aneurysm

Chronic end-stage heart disease with no anticipation of recovery

Tachyarrhythmias

Severe peripheral vascular disease

Technique of insertion and operation

The IABP device has two major components: (i) a double-lumen 8.0–9.5 French catheter with a 25–50 ml

balloon attached at its distal end(ii) a console with a pump to drive the balloon. The balloon is made of polyethylene and is inflated with gas

driven by the pump. Helium is often used because its low density facilitates rapid transfer of gas from console to the balloon. It is also easily absorbed into the blood stream in case of rupture of the balloon

The appropriate balloon size is selected on the basis of pt’s height

PATIENT’S HEIGHT BALLOON VOLUME

< 152 cms 25 cc

152 – 163 cms 34 cc

164 – 183 cms 40 cc

> 183 cms 50 cc

The diameter of the balloon, when fully expanded should not exceed 80–90% of the diameter of the patient’s descending thoracic aorta.

• Once vascular access is obtained, the balloon catheter is

inserted and advanced, usually under fluoroscopic guidance,

into the descending thoracic aorta, with its tip ~ 2 to 3 cm distal

to the origin of the left subclavian artery (at the level of the

carina).

• Intraoperatively, balloon placement can be ascertained using

transoesophageal echocardiography.

• The outer lumen of the catheter is used for delivery of gas to

the balloon and the inner lumen can be used for monitoring

systemic arterial pressure.

• The console is programmed to identify a trigger for balloon

inflation and deflation. The most commonly used triggers are

the ECG waveform and the systemic arterial pressure waveform.

• The balloon inflates with the onset of diastole, which

corresponds with the middle of the T-wave. The balloon deflates

at the onset of LV systole and this corresponds to the peak of the

R-wave.

• Poor ECG quality, electrical interference, and cardiac

arrhythmias can result in erratic balloon inflation.

When intra-aortic balloon pumping is begun, the assist

interval is set on 1:2 (the IAB inflates and deflates every

other systole). This is done so that landmarks can be

identified and the effects of inflation and deflation can be

compared to the baseline hemodynamic status. Later on the

Assist ratio can be changed to 1:1.

PDP/AUG should be higher than the PSP/SYS unless:

• Balloon is positioned too low

• severe cases of hypo volemia

• balloon is too small for patient’s aorta

• low SVR

• improper timing

• catheter partially kinked, in sheath, not unwrapped

Criteria for Assessment of Effective IAB Therapy on the Arterial Pressure Waveform1 ) Inflation occurs at the dicrotic notch.

2) Inflation slope is parallel to the systolic upstroke and is a straight line.

3) Peak Diastolic augmentation should be greater than the unassisted systolic peak.

4) An end-diastolic dip in pressure is created with balloon deflation.

5) Two assisted pressures (systolic and diastolic) should be lower than the unassisted pressures .

Timing is set and changed using two separate controls that

move the timing markers to the left and right. The inflate

control is moved to the left to adjust the inflate time to occur

earlier and to the right to occur later. The deflate control

operates in a similar manner: moved to the left for earlier

deflation, to the right for later deflation.

LATE DEFLATIONWaveform characteristics• assisted aortic end-diastolic pressure may be equal to the unassisted aortic end-diastolic pressure; •rate of increase of assisted systole is prolonged •diastolic augmentation may appear widened.

Physiological effects• afterload reduction is essentially absent• increased MVO2 consumption because of the left ventricle ejecting against a greater resistance and a prolonged isovolumetric contraction phase•IAB may impede LV ejection and increase the afterload

1. Inflation -- Just Prior to the Dicrotic Notch (DN) If > 40ms before—EARLY INFLATION If dicrotic notch exposed—LATE INFLATION2. Deflation:-- BAEDP < PAEDPBAEDP = Balloon Aortic End Diastolic PressurePAEDP = Patient Aortic End Diastolic Pressure If BAEDP is higher—LATE DEFLATION may be occuring3. Deflation:Assisted Systole (APSP/ASYS) < Peak Systole (PSP/SYS)SYS/PSP = Peak Systolic PressureASYS/APSP = Assisted Peak Systolic PressureIf both pressures are equal—EARLY DEFLATION can be suspected

BALLOON PRESSURE WAVEFORM During a cycle of inflation/deflation, helium is rapidly moved in and

out of the balloon. The environment within the balloon and the surrounding forces that affect balloon behavior all contribute to a predictable pattern of gas flow and pressure. The gas pressure characteristics are converted into a waveform. This transduced waveform can tell us much about the interaction of the balloon within the patient’s aorta.

• Initial under fill of the intra-aortic balloon• Leak• Auto-fill failure• Balloon disconnected

Auto-vent failure Possible vacuum malfunctionKinked Line

Kinked catheter.

Weaning from the Intra-Aortic Balloon Pump

There are two methods of weaning which may be used independently or in conjunction with one another. Weaning can be accomplished by decreasing the frequency and/or volume of balloon inflation. Weaning by decreasing the frequency is accomplished by decreasing the frequency of assistance from one balloon inflation per cardiac cycle to 1:2, 1:3, 1:4, and 1:8. Weaning can also be accomplished by decreasing the volume delivered to the balloon. Do not reduce the volume delivered to the balloon less than 2/3 the capacity of the balloon, i.e. a 40cc balloon should not have the volume reduced to less than 28cc.

IABP: ComplicationsComplications associated with IABP

Transient loss of peripheral pulse

Limb ischaemia

Thromboembolism

Compartment syndrome

Aortic dissection

Local vascular injury—false aneurysm, haematoma, bleeding from the wound

Infection

Balloon rupture (can cause gas embolus)

Balloon entrapment

Haematological changes, for example thrombocytopenia, haemolysis

Malpositioning causing cerebral or renal compromise

Cardiac tamponade

IABP: ComplicationsRisk Factors

• Odds Ratios for Major complications with IABP therapy:

– PVD: 2.0– Female Gender: 1.7– Small BSA: 1.5– Advanced age: 1.3

(Little Old Ladies!!!)

Ventricular Assist Device (VAD)

Long-Term LVADImplanted surgically with the intention of

support for months to years

Short-Term LVADUtilized for urgent/

emergent support over the course of days to

weeks

A mechanical circulatory device used to partially or completely replace the function of

either the left ventricle (LVAD); the right ventricle (RVAD); or both ventricles (BiVAD)

Ventricular Assist Devices

• There are several many different VADs. All VADs have the following four parts:– An inflow cannula which takes

blood from the ventricular to the pump

– A pump – An outflow cannula that takes the

pumped blood to the ascending aorta

– A power source for the pump

• They are powered by external power sources that connect to the implanted pump via a percutaneous lead (driveline) that exits the body on the right abdomen.

• Pump output flow can be pulsatile or nonpulsatile.

Components of a Ventricular Assist Device

Classification of Ventricular Assist Devices On the basis of period of use: a) Temporary, b) Permanent

On the basis of impaired ventricle: a) LVAD, b) RVAD, c) Bi-VAD

On the basis of Pumping mechanism: a) Pulsatile b) Non pulsatile

On the basis of suspension of rotors: a) Bearing suspension b) Electromagnetic or Hydrodynamic suspension.

Krishnamani, R. et al. (2010) Emerging ventricular assist devices for long-term cardiac support

Nat. Rev. Cardiol. doi:10.1038/nrcardio.2009.222

Pulsatile Devices• Ventricle-like pumping sac device.

– Blood enters via the inflow cannula and fills a flexible pumping chamber.

– Electric motor or pneumatic (air) pressure collapses the chamber and forces blood into systemic circulation via the outflow cannula.

• Can be LVAD, RVAD, or BiVAD• First-generation devices (in use since early 1980s)• Patients will have a palpable pulse and a measurable blood pressure.

Both are generated from the VAD output flow.• Pulsatile VADs emulated the real contraction phenomenon of

ventricles while Advanced VADs use continuous flow mechanisms

FEATURES• is a short-term uni- or

biventricular support system .

• comprised of two 100 mL polyurethane blood sacs.

• the inlet and outlet portions of which are guarded by polyurethane valves

The Abiomed BVS 5000i

NEWER ADVANCES IN HEART FAILURE DEVICE THERAPY

HeartMate XVE

• Has a titanium-alloy external housing, with inflow and outflow conduits that use porcine xenograft valves.

• Internal blood-contacting surface is made of textured titanium that results in the development of a pseudo-neointima on which thrombus formation is greatly reduced, thereby decreasing the need for anticoagulation.

NEWER ADVANCES IN HEART FAILURE DEVICE THERAPY

Non-Pulsatile Devices• Continuous-flow devices

Impeller (spinning turbine-like rotor blade) propels blood continuously forward into systemic circulation.

Axial flow: blood leaves the pump in the same direction as it enters (boat motor propeller).

Key features of nonpulsatile VAD

• Most implanted devices are LVADs only.

• Are quite and cannot be heard outside of the patient’s body. Assess VAD status by auscultation over the apex of the LV. The VAD should have a continuous, smooth humming sound.

• The Patient may have a weak, irregular, or non-palpable pulse

• The Patient may have a narrow pulse pressure and may not be measurable with automated blood pressure monitors. This is due to the continuous forward outflow from the VAD.

• The Mean Arterial Pressure is the key in monitoring hemodynamics. Ideal range is 65-90 mmHg.

Heartware HVAD

Patient Selection: Who benefits from a VAD

Recommendations in pt with severe Heart Failure ineligible for transplant

Mechanical Circulatory Support

VADRECOVE

RY

CANDIDACY

DESTINATION THERAPY

TRANSPLANT

Mechanical Circulatory SupportINDICATION NOMENCLATURE DEFINITION

Bridge to transplantation Patient is listed for heart transplantation

Bridge to candidacy

Patient initially deemed ineligible for heart transplantation because of comorbidity (cardiorenal syndrome or pulmonary hypertension), which improves during mechanical support

Bridge to recoveryPatient with a potentially reversible cause of cardiac decompensation (acute myocarditis, postcardiotomy syndrome, peripartum cardiomyopathy)

Bridge to decision Patient in whom the potential for transplantation or recovery is yet unclear

Destination therapy Patient in whom recovery or transplantation is not feasible

Indications for Use:Pulsatile vs. Continuous Flow

• Pulsatile Devices– PVAD– IVAD– Heartmate XVE

LVAD• Continuous Flow

– Heartmate II LVAD

– Heartware HVAD

FDA Approved Devices for Bridge to Transplant

PVAD/IVADHeartmate XVE LVADHeartmate II LVADHeartware HVAD

FDA Approved Device for Destination Therapy

Heartmate XVE LVADHeartmate II LVAD

• Score of 0-8 is low risk and predict 3 months survival of 87.5% while greater than 19 is very high risk with survival of 13.7%

• This Risk Score is not validated for Cont. flow device implanted for destination therapy

RISK FACTORS FOR 3 MONTHS MORTALITY AFTER VAD IMPLANT

RISK FACTORS SCORE

Platelet Count < 148 X 103 per uL 7

Serum Albumin < 3.3 g/dL 5

INR > 1.1 4

Vasodilator treatment 4

Mean PAP < 25mm Hg 3

SGPT > 45 units/ml 2

HCT < 34% 2

BUN > 51U/dL 2

No IV Inotropes 2

Anti Coagulation is must

• Optimal INR for cont. flow device is 1.5 to 2.5• Higher degree of anti coagulation is required in AF, prior

thromboembolic events , known LA or LV thrombi and if there is low assist device flow rate < 3 l/min.

Contraindications

– End-stage lung, liver, or renal disease– Metastatic disease – Medical non-adherence or active drug

addiction– Active infectious disease– Inability to tolerate systemic anticoagulation

(recent CVA, GI bleed, etc.,)– Moderate to severe RV dysfunction for some

LVADs

• RV dysfunction is an important source of morbidity and mortality after LVAD insertion.

• Predictors of post implant RVF are CVP/PCWP > 0.63, BUN > 39 mg/dL, and preop mechanical ventilatory support.

• RV failure is reversible with inotropes or PDEI. • If RV function does not improve and LVAD flow still

suboptimal (<2.4 L/min/m2 ) with CVP > 16 mm Hg then RVAD insertion is necessary which can be short term or long term.

• Recent data demonstrates that early planned institution of RV support can mitigate the potential adverse consequences of RV dysfunction after LVAD placement.

Basic VAD Management ALL VADs are:

Preload-dependent EKG-independent Afterload-sensitive Anticoagulated Prone to:

• infection• bleeding• thrombosis/stroke• mechanical malfunction

Key differences depend on pulsatile vs. non-pulsatile device

Variations of Short-Term VADs

• Impella 2.5 and 5.0• Tandem Heart• CentriMag• ECMO (V-A)

Impella 2.5 and 5.0• Utilized for LV support only; not

appropriate to use with RV failure• Impella 2.5 can be inserted through

the femoral artery during a standard catheterization procedure; provides up to 2.5 L of flow

• Impella 5.0 inserted via femoral or axillary artery cut down; provides up to 5L of flow

• The catheter is advanced through the ascending aorta into the left ventricle

• Pulls blood from an inlet near the tip of the catheter and expels blood into the ascending aorta

• FDA approved for support of up to 6 hours

Effect of IABP and Impella 2.5 device on important hemodynamic parameters

NEWER ADVANCES IN HEART FAILURE DEVICE THERAPY

Algorithm for device selection.

TandemHeart pVAD• Used for LV support; not

appropriate in RV failure• Cannulas are inserted

percutaneously through the femoral vein and advanced across the intraatrial septum into the left atrium

• The pump withdraws oxygenated blood from the left atrium and returns it to the femoral arteries via arterial cannulas

• Provides up to 5L/min of flow

• Can be used for up to 14 days

CentriMag

• Can be used for LV and/or RV support

• Cannula are typically inserted via a midline sternotomy

• Capable of delivering flows up to 9.9 L/min

• Can be used for up to 30 days

ECMO (VA)

• Used for patients with a combination of acute cardiac and respiratory failure

• A cannula takes deoxygenated blood from a central vein or the right atrium, pumps it past the oxygenator, and then returns the oxygenated blood, under pressure, to the arterial side of the circulation

• Can be used for days to weeks

TOTAL ARTIFICIAL HEART

NEWER ADVANCES IN HEART FAILURE DEVICE THERAPY

Artificial Heart

Effects of Chronic Hemodynamic Unloading with Ventricular Assist Devices

Structural• Regression of myocyte hypertrophy.• Reduction in neurohormonal activation• Normalization in expression of contractile proteins .• Enhanced electron transport chain respiratory function• Decreased apoptosis and cellular stress markers

Functional Provide mechanical circulatory support to restore the circulation of blood flow to the

body.• Decreases preload• Decreases cardiac workload• Increases systemic circulation & tissue perfusion• Decreases neurohormonal response

•Thank you