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

2. 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

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

4. Considerations Indications Application Physiology
Potential complications

5. Rationale for mechanical support?
Rationale for mechanical support

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

7. 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

8. Intra Aortic Balloon Pump Counter Pulsation

9. 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

10. 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

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

14. 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]

15. 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

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

17. Left Ventricular Failure
MVO2
 Demand
 Supply

18. Diastole: IAB Inflation
. Increase coronary perfusion
Increase MAP

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

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

21. 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, [1998]

22. 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

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

25. Timing Assessment Increased Coronary Artery Perfusion 120 C D F mm HgB 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

26. 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

27. Timing Assessment Increased Coronary Artery Perfusion 120 C D F mm HgB 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

28. 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

29. 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

30. 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

31. 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

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

33. 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

34. 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

38. E C M O

39. What is ECMO ?

40. 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.

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

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

43. Ventilator Lung Injury
Oxygen Toxicity
Barotrauma
Volutrauma

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

46. 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

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

51. Ventricular Assist Devices

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

53. Indications Bridge to Recovery Bridge to Transplant
Destination Therapy

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

55. 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

56. 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.

57. 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.

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

64. Axial Pumps Archimedes Screw

65. 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

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

68. 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

69. 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

70. Reitan Catheter Pump

71. 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

72. 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

73. CARDIOHELP Device

76. Thank you