Mechanical Support of the Failing Cardiorespiratory System Mr David J McCormack Consultant Cardiothoracic Surgeon Waikato Cardiothoracic Unit

Acknowledgements Previously Presented at the Royal Society of Medicine - Cardiology Section With thanks to Henry Bishop – Lead Perfusionist – Imperial College Healthcare NHS Trust who supplied many of the slides and valuable teaching

Today’s talk.. Options for mechanical support IABP ECMO VADs

Considerations Indications Application Physiology Potential complications

Rationale for mechanical support ? Rationale for mechanical support

Short Term Devices IABP ECMO VADs VA ECMO VV ECMO Pneumatic pumps Centrifugal pumps Axial pumps

Complications common to devices Bleeding CPB time if post-cardiotomy Pharmacology if post PCI Thrombocytopenia Clot/embolus formation Anti-coagulation Haemolysis (not IABP) Immobility (usually) Infection Connection to console

Intra Aortic Balloon Pump Counter Pulsation

Counterpulsation Therapy The IABP was pioneered during the early 1960s by Dr. Adrian Kantrowitz The first clinical implant was performed at, Brooklyn, N.Y. in Oct., 1967 The patient, a 48 year old woman, was in cardiogenic shock and unresponsive to traditional therapy. An IABP was inserted by a cut down on the left femoral artery. Pumping was performed for approximately 6 hours. Shock reversed and the patient was discharged

Indications 1. Refractory Unstable Angina 2. Impending Infarction 3. Acute MI 4. Refractory Ventricular Failure 5. Complications of Acute MI 6. Cardiogenic Shock 7. Support for PCI 8. Ischaemia related intractable ventricular arrhythmias 9. Septic Shock 10. Intraoperative pulsatile flow generation 11. Weaning from bypass 12. Cardiac support for non-cardiac surgery 13. Prophylactic support in preparation for cardiac surgery 14. Post surgical myocardial dysfunction/low cardiac output syndrome 15. Myocardial contusion 16. Mechanical bridge to other assist devices 17. Cardiac support following correction of anatomical defects

The Application of Counterpulsation Therapy Balloon catheter selection Catheter size Balloon volume

cc 50 cc 40 cc 34 cc 25 > 6’ [183 cms] 5’4”- 6’ [163 - 183 cms] 5’- 5’4” [152 - 163 cms] cc 25 < 5’ [152 cms]

Intra-aortic Balloon Catheter Placement: • Ideally should be inserted using fluoroscopy. • Tip of the IAB catheter should be positioned 1 to 2 cms distal to the left subclavian artery. An x-ray should be taken as soon as possible after insertion to correctly identify placement (TOE can also verify position). IAB Arterial pressure transducer line Helium gas line to the balloon pump console

IAB Catheter should be positioned between the second and third intercostal space

Left Ventricular Failure MVO2  Demand  Supply

Diastole: IAB Inflation . Increase coronary perfusion Increase MAP

Systole: IAB Deflation . Decrease cardiac work . Decrease myocardial oxygen consumption . Increase cardiac output

Primary Effects of Counterpulsation Therapy IAB Deflation  Demand Supply = Demand IAB Inflation MVO2  Supply

Sympathetic tone LV Dysfunction Inotropes Revascularization Coronary occlusion Ischaemia Contractile mass Arterial pressure Coronary flow Vasoconstriction Na & H2O retention Sympathetic tone RAS Pathophysiology of Cardiogenic shock due to acute myocardial infarction: The pathophysiology of Cardiogenic Shock involves a downward spiral: ischemia causes myocardial dysfunction, which in turn, worsens ischemia. Left ventricular [LV] dysfunction leads to increased sympathetic tone and activation of the renin-angiotensin system [RAS] causing vasoconstriction and sodium retention, two factors which promote further LV dysfunction. Patients in shock often have obstruction of a major coronary vessel, with resultant extensive loss of contractile mass, which leads to decreased arterial pressure. A significant drop in arterial pressure may be profound enough to cause a decrease in coronary blood flow, aggravating myocardial ischemia and further compromising LV function. Initially, the dysfunction is reversible but persistent hypotension leads to irreversible permanent cellular injury and necrosis, organ dysfunction, and can ultimately lead to death. In general, three treatment strategies have been aimed at reversing the vicious cycle of cardiogenic shock. 1. Inotropic and pressor agents have been used to counteract LV dysfunction and hypotension. These agents are generally temporizing measures to stabilize a patient until other therapeutic measures can be instituted. They do not improve survival. 2. The use of intra-aortic balloon counterpulsation therapy to improve coronary blood flow, enhance collateral circulation, and improve hemodynamics by increasing cardiac output. Survival benefits have been demonstrated. 3. Revascularization, which is the ultimate goal. IABP Therapy Barry WL, et al, Clin. Cardiol. 21, 72-80 [1998]

Coronary Blood Flow (ml/min) 300 200 100 Systole Diastole Left Coronary Artery Right Coronary Blood Flow (ml/min) Slide courtesy of A.C. Guyton, MD, Textbook of Medical Physiology, Sixth Edition, 1981 W.B. Saunders Company

Aortic Pressure Waveform Dicrotic Notch Mean Pressure Systolic Pulse Pressure Diastolic 120 100 80 Systole Diastole mm Hg

Timing Assessment Increased Coronary Artery Perfusion 120 C D F mm Hg B E F Reduced Myocardial O2 Demand 120 100 80 Inflation and deflation of the IAB change the configuration of the arterial pressure waveform. A properly timed balloon will inflate at the dicrotic notch, which will appear as a sharp “V” configuration between the systolic pressure and the diastolic augmentation. The peak diastolic augmentation represents the maximum pressure in the aorta with balloon inflation during diastole. Deflation of the balloon at the end of diastole is reflected in an assisted aortic end-diastolic pressure lower than the unassisted aortic end-diastolic pressure. Proper deflation will also reduce the systolic pressure that follows balloon deflation. The next systolic beat is called the assisted systole. A = One complete cardiac cycle B = Unassisted aortic end diastolic pressure C = Unassisted systolic pressure D = Diastolic Augmentation E = Reduced aortic end diastolic pressure F = Reduced systolic pressure

Contraindications Severe aortic insufficiency Abdominal or thoracic aortic aneurysm Severe calcific aorta-iliac disease or peripheral vascular disease Sheathless insertion with severe obesity, scarring of the groin

Timing Assessment Increased Coronary Artery Perfusion 120 C D F mm Hg B E F Reduced Myocardial O2 Demand 120 100 80 Inflation and deflation of the IAB change the configuration of the arterial pressure waveform. A properly timed balloon will inflate at the dicrotic notch, which will appear as a sharp “V” configuration between the systolic pressure and the diastolic augmentation. The peak diastolic augmentation represents the maximum pressure in the aorta with balloon inflation during diastole. Deflation of the balloon at the end of diastole is reflected in an assisted aortic end-diastolic pressure lower than the unassisted aortic end-diastolic pressure. Proper deflation will also reduce the systolic pressure that follows balloon deflation. The next systolic beat is called the assisted systole. A = One complete cardiac cycle B = Unassisted aortic end diastolic pressure C = Unassisted systolic pressure D = Diastolic Augmentation E = Reduced aortic end diastolic pressure F = Reduced systolic pressure

Timing Errors - Early Inflation Assisted Systole Diastolic Augmentation Assisted Aortic End- Diastolic Pressure Unassisted Inflation of the IAB prior to aortic valve closure Waveform Characteristics: • Inflation of IAB prior to dicrotic notch • Diastolic augmentation encroaches onto systole (may be unable to distinguish) Physiologic Effects: • Potential premature closure of aortic valve • Potential increase in LVEDV and LVEDP or PCWP • Increased left ventricular wall stress or afterload • Aortic regurgitation • Increased MVO2 demand

Timing Errors - Late Inflation Assisted Systole Diastolic Augmentation Dicrotic Notch Assisted Aortic End- Diastolic Pressure Unassisted Inflation of the IAB markedly after closure of the aortic valve Waveform Characteristics: • Inflation of the IAB after the dicrotic notch • Absence of sharp V • Sub-optimal diastolic augmentation Physiologic Effects: • Sub-optimal coronary artery perfusion

Timing Errors - Early Deflation Assisted Systole Diastolic Augmentation Assisted Aortic End-Diastolic Pressure Unassisted Aortic Premature deflation of the IAB during the diastolic phase Waveform Characteristics: • Deflation of IAB is seen as a sharp drop following diastolic augmentation • Sub-optimal diastolic augmentation • Assisted aortic end-diastolic pressure may be equal to or less than the unassisted aortic end-diastolic pressure • Assisted systolic pressure may rise Physiologic Effects: • Sub-optimal coronary perfusion • Potential for retrograde coronary and carotid blood flow • Angina may occur as a result of retrograde coronary blood flow • Sub-optimal afterload reduction • Increased MVO2 demand

Timing Errors - Late Deflation Diastolic Augmentation Assisted Aortic End-Diastolic Pressure Unassisted Systole Widened Appearance Prolonged Rate of Rise of Assisted Systole Deflation of the IAB as the aortic valve is beginning to open Waveform Characteristics: • Assisted aortic end-diastolic pressure may be equal to the unassisted aortic end-diastolic pressure • Rate of rise of assisted systole is prolonged • Diastolic augmentation may appear widened Physiologic Effects: • Afterload reduction is essentially absent • Increased MVO2 consumption due to the left ventricle ejecting against a greater resistance and a prolonged isovolumetric contraction phase • IAB may impede left ventricular ejection and increase the afterload

Side Effects and Complications Limb ischaemia Bleeding at the insertion site Thrombocytopenia Immobility Balloon leak Infection Aortic dissection

Limb Ischaemia • Major - loss of pulse, loss of sensation, abnormal limb temperature or pallor, requiring surgical intervention, arterial repair and/or amputation • Minor - anticipated, decreased arterial flow as manifested by diminished pulse that resolves with balloon removal

Bleeding Major - haemodynamic compromise that requires a transfusion of blood or surgical intervention Minor - anticipated, minor haematomas, oozing from puncture site, additional pressure dressing may be used, no medical or surgical intervention required

E C M O

What is ECMO ?

Extra-Corporeal Membrane Oxygenation ECMO A technique of extra-corporeal life support which uses heart-lung bypass techniques for days or weeks to support heart or lung function in the Intensive Care Unit.

Indications Lung disease Acute Life threatening Reversible Unresponsive to conventional therapy Additional cardiac support may be provided

ACUTE INJURY Requires REST not VIGOROUS EXERCISE to HEAL Theory of ECMO Broken Leg Analogy ACUTE INJURY Requires REST not VIGOROUS EXERCISE to HEAL

Ventilator Lung Injury Oxygen Toxicity Barotrauma Volutrauma

Percutaneous cannualtion Two modes Veno-Venous only respiratory support Veno-Arterial (similar to CPB) Full cardiovascular and respiratory support Percutaneous cannualtion

Veno-venous Normal pulmonary flow O2 in pulmonary blood helps dilate vessels, reducing right-sided afterload (pulmonary hypertension Better myocardial oxygenation as less de-oxygenated blood reaches left side Weaning technically easy Venous return mean lungs ‘filter’ Slower to stabilise Recirculation

Veno-arterial Cardiac support Immediate effect LV and coronary arteries receive some poorly oxygenated blood Reduced pulmonary flow Weaning complicated Arterial return - no ‘filter’

Ventricular Assist Devices

Ventricular Assist Devices Different to CPB No oxygenator Left and right treated separately Longer term

Indications Bridge to Recovery Bridge to Transplant Destination Therapy

Breakdown of VADS Pneumatic pumps Centrifugal pumps Axial pumps Open insertion vs percutaneous insertion

LVAD/RVAD Insertion Sternotomy Cannulation RA to PA for RVAD LA or LV to aorta for LVAD Cannulae tunnelled through skin like chest drains Additional monitoring eg LAP line ACT 1.5 x normal to prevent clotting

LVAD LVAD cannulation using a 32FR inflow placed at the junction of the right superior pulmonary vein and left atrium. The 22 FR return cannula is placed in a 8 mm graft sutured to the ascending aorta.

BiVAD LVAD cannulation using a 32FR inflow placed at the junction of the right superior pulmonary vein and left atrium. The 22 FR return cannula is placed in a 8 mm graft sutured to the ascending aorta.

Associated Complications Bleeding 43% - post CPB + continuing heparin Renal failure 38% - haemolysis Infection 14% - lines + complement activation Thrombus/embolus 15%

Axial Pumps Archimedes Screw

Axial Pumps Impella Recover Inserted in femoral artery (9Fr) or directly in aorta Passes through aortic valve Tip in left ventricular apex Pumps 20 cm downstream into aorta

Impella Recover Max 5 l/min Up to 14 days Problems similar to IABP (percutaneous) Aortic aneurysm Aortic-iliac disease Limb ischaemia

Impella – Contraindications Mechanical aortic valves Severe aortic valvular stenosis Hypertrophic obstructive cardiomyopathy Aneurysm or severe anomaly of the ascending aorta Mural thrombus in the LV Ventricular septal defect after MI Anatomic conditions precluding insertion of the pump

Reitan Catheter Pump CardioBridge Folded impeller 14 Fr percutaneous via femoral artery Head in upper descending aorta, pumped downstream Creates pressure gradient within aorta Non-pulsatile, non-sychronised Reduces afterload Increase distal perfusion eg renal arteries

Reitan Catheter Pump

Reitan Catheter Pump Problems similar to IABP 10 Fr in development Aortic aneurysm Aortic-iliac disease Limb ischaemia Not rhythm dependent Not contraindicated in AR 10 Fr in development Left side only

TandemHeart pVAD CardiacAssist Percutaneous Femoral vein – IAS– LA Centrifugal pump Femoral artery <5 l/min Reduces preload Increases MAP Continuous flow 21 F 14 days

CARDIOHELP Device

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