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Mechanical Circulatory Support

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Trattamento dello Shock cardiogeno Contropulsazione Aortica ed Assistenza Meccanica del circolo :

Trattamento dello Shock cardiogeno Contropulsazione Aortica ed Assistenza Meccanica del circolo 20-01-2010 27-01-2010

Slide 3:

Circulatory Shock “Pathophysiologic state in which tissue perfusion is totally inadequate to meet the oxygen or nutritional needs of the cells” Shock described as “momentary pause in the act of death” Shock is not a disease entity in itself, but a response to some assault or injury the body has experienced Whatever the initiating event, the cause of death in irreversible shock is microcirculatory failure and the subsequent depression of cellular metabolism

Slide 4:

Inadequate tissue perfusion resulting from cardiac dysfunction Clinical definition - decreased cardiac output and tissue hypoxia in the presence of adequate intravascular volume Hemodynamic definition - sustained systolic BP < 90 mm Hg, cardiac index < 2.2 L/min/m 2 , PCWP > 15 mm Hg Parrillo, J. 2005 Cardiogenic Shock

Slide 5:

Evolution Of The Disease Frequently, shock develops after presentation for myocardial infarction. - SHOCK Registry • At presentation 25% in shock • Within 24 hours 75% (median delay = 7 hours) - GUSTO Trial • At presentation 11% in shock • After admission 89% SHOCK Registry, Circulation. 1995;91:873-81. GUSTO J Amer Coll Cardiol. 1995;26:668-74 . Cardiogenic Shock

Obiettivo della assistenza meccanica del circolo.:

Obiettivo della assistenza meccanica del circolo. Definizione dello Shock cardiogeno

Emergency treatment:

Emergency treatment The first priority in treating cardiogenic shock is to expand the circulating blood volume with IV fluids, using the PWP or CVP as a basic guide

Starlings law of the heart:

Starlings law of the heart The ability of the heart to increase its output in response to an increase in venous return represents a positive feedback in which altered blood flow to the heart leads to a corresponding change in blood flow leaving the heart.

Slide 10:

Frank-Starling Phenomenon End-Diastolic Pressure Stroke Volume “In the normal heart, the diastolic volume (preload) is the principal force that governs the strength of ventricular contraction.” Otto Frank and Ernest Starling

VENTRICULAR FUNCTION CURVES NORMAL AND FAILING LV:

VENTRICULAR FUNCTION CURVES NORMAL AND FAILING LV

C.O. = Stroke volume x Heart rate:

C.O. = Stroke volume x Heart rate Stroke volume: Preload Myocardial contractility Afterload: systemic and pulmonary resistance blood viscosity Heart Rate Bradycardia Sustained tachycardia

Obiettivo della assistenza meccanica del circolo.:

Obiettivo della assistenza meccanica del circolo. Trattamento dello Shock cardiogeno

DETERMINANTS OF MYOCARDIAL OXYGEN SUPPLY AND DEMAND:

DETERMINANTS OF MYOCARDIAL OXYGEN SUPPLY AND DEMAND MVO 2 Supply Demands Coronary artery anatomy Diastolic pressure Diastolic time O 2 Extraction HBG PaO 2 Heart rate Afterload Preload Contractility

Slide 15:

300 200 100 0 Systole Diastole Left Coronary Artery Right Coronary Artery Coronary Blood Flow (ml/min) Slide courtesy of A.C. Guyton, MD from Textbook of Medical Physiology, Sixth Edition, 1981, W.B. Saunders Company © Datascope Corp.

Slide 16:

OXYGEN DELIVERY DO 2 = Q X CaO 2 DO 2 = Q X (1.34 X Hb X SaO 2 ) X 10 Q = cardiac output CaO 2 = arterial oxygen content Normal DO 2 : 520-570 ml/min/m 2 Oxygen extraction ratio = (SaO 2 -SvO 2 /SaO 2 ) X 100 Normal O 2 ER = 20-30%

Slide 17:

OXYGEN EXTRACTION VO 2 = Q x Hb X 13.4 X (SaO 2 - SvO 2 ) Arterial Inflow (Q) capillary O 2 O 2 O 2 O 2 O 2 O 2 O 2 Venous Outflow (Q) C ell O 2 (Adapted from the ICU Book by P. Marino)

HEMODYNAMIC CHANGES PROGRESSIVE LEFT HEART FAILURE:

HEMODYNAMIC CHANGES PROGRESSIVE LEFT HEART FAILURE Hours

Slide 19:

Fisiopatologia dello Shock cardiogeno Hollenberg Ann Int Med 1999; 131:47-99 When a critical mass of LV is necrotic and fails to pump, stoke volume and CO falls Myocardial and coronary perfusion are compromised causing tachycardia and hypotension Increased LVEDP further decreases coronary perfusion Increase LV wall stress increases myocardial oxygen demand Lactic acidosis worsens myocardial performance

Slide 20:

Fisiopatologia dello Shock cardiogeno Feng et al Circulation 2001;104:700-704

Slide 21:

Cardiogenic shock IS NOT simply the result of severe depression of LV function due to extensive myocardial ischemia/injury. Depressed Myocardial Contractility combined with Inadequate Systemic Vasoconstriction resulting from a systemic inflammatory response to extensive myocardial ischemia/injury results in cardiogenic shock . Pathophysiology of Cardiogenic Shock

The Overproduction of Nitric Oxide May Cause Both Myocardial Depression and Inappropriate Vasodilatation.:

Thus, excess nitric oxide and peroxy nitrites may be a major contributor to cardiogenic shock complicating MI. The Overproduction of Nitric Oxide May Cause Both Myocardial Depression and Inappropriate Vasodilatation.

Principles of the IABP:

Principles of the IABP http://www.fda.gov/cdrh/medicaldevicesafety/tipsarticles/balloonpump.gif A flexibile catheter is inserted into the femoral artery and passed into the descending aorta. Correct positioning is critical in order to avoid blocking off the subclavian, carotid, or renal arteries. When inflated, the balloon blocks 85-90% of the aorta. Complete occlusion would damage the walls of the aorta, red blood cells, and platelets.

Slide 24:

Arterial Pressure Balloon Pump Console © Datascope Corp.

Slide 25:

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Slide 27:

Slide 28:

The System 97e is a helium charged, mobile, Intra-Aortic Balloon Pump (IABP). 6/20/2011

Slide 29:

Haemodinamic effects of the IABP

Hemodynamics:

Hemodynamics Helium is rapidly pumped into and out of the balloon (about 40ccs). When inflated, this balloon displaces the blood that is in the aorta. This is known as counter pulsation Helium is used because it is a soluble gas and will not cause an embolus if the balloon ruptures This sudden inflation moves blood superiorly and inferiorly to the balloon. When the balloon is suddenly deflated, the pressure within the aorta drops quickly.

Why Helium?:

Why Helium? Helium is 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.

Which Size of Balloon?:

Which Size of Balloon? for a patient <152 cm in height, a balloon volume of 25 cc is appropriate; for height between 152 and 163 cm, balloon volume 34 cc; for height 164-183 cm, balloon volume 40 cc, and for height >183 cm, balloon volume 50 cc). Smaller balloons are available for paediatric use. The diameter of the balloon, when fully expanded, should not exceed 80-90% of the diameter of the patient's descending thoracic aorta.

Hemodynamics (cont.):

Hemodynamics (cont.) Inflation of the balloon occurs at the onset of diastole. At that point, maximum aortic blood volume is available for displacement because the left ventricle has just finished contracting and is beginning to relax, the aortic valve is closed, and the blood has not had an opportunity to flow systemically. The pressure wave that is created by inflation forces blood superiorly into the coronary arteries. This helps perfuse the heart. Blood is also forced inferiorly increasing perfusion to distal organs (brain, kidneys, tissues, etc.)

Slide 34:

Intraaortic balloon pump counterpulsation

Hemodynamics (cont.):

Hemodynamics (cont.) The balloon remains inflated throughout diastole. At the onset of systole, the balloon is rapidly deflated. The sudden loss of aortic pressure caused by the deflation reduces afterload. The left ventricle does not have to generate as much pressure to achieve ejection since the blood has been forced from the aorta. This lower ejection pressure reduces the amount of work the heart has to do resulting in lower myocardial oxygen demand.

IAB Inflation:

IAB Inflation It inflates immediately following aortic valve closure to to augment diastolic coronary perfusion pressure. The balloon should be inflated at the start of diastole, just prior to the Dicrotic Notch

Slide 37:

37 and demand (DPTI:TTI ratio) 6/20/2011

IAB Deflation:

IAB Deflation The balloon rapidly deflates just before ventricular systole to reduce Left Ventricular work Deflation creates a "potential space" in the aorta, reducing aortic volume and pressure

Arterial Waveform Variations During IABP Therapy:

Diastolic Augmentation  Coronary Perfusion Assisted Aortic End- Diastolic Pressure  MVO 2 Demand Assisted Systole Un assisted Systole Balloon Inflation Un assisted Aortic End-Diastolic Pressure 140 120 100 80 60 mm Hg Arterial Waveform Variations During IABP Therapy © Datascope Corp.

Review of Arterial Pressure Landmarks in 1:2 Assist:

41 Review of Arterial Pressure Landmarks in 1:2 Assist PAEDP = Patient aortic end diastolic pressure, this is the patient's unassisted diastole PSP = Peak systolic pressure, this is the patient's unassisted systole PDP/DA = Peak diastolic pressure or diastolic augmentation, this is the pressure generated in the aorta as the result of inflation BAEDP = Balloon aortic end diastolic pressure, this is the lowest pressure produced by deflation of the IAB APSP = Assisted peak systolic pressure, this systole follows balloon deflation and should reflect the decrease in LV work 6/20/2011 41

Preload vs. Afterload:

Preload vs. Afterload Preload refers to the amount of stretch on the ventricular myocardium prior to contraction. Starling’s law described how an increase of volume in the ventricle at the end of diastole resulted in an increase in the volume of blood pumped out. Preload is often referred to as “filling pressure”. Afterload is the resistance to ventricular ejection which takes several forms: The mass of blood that must be moved, measured by the hematocrit The higher the mass, the more inertia that must be generated. Aortic end diastolic pressure (AEDP). If the AEDP is 80 mm/hg, then the left ventricle must generate 81 mm/hg in order to open the aortic valve and generate blood flow. Arteriole resistance

Physiologic Effects of IABP:

Physiologic Effects of IABP Maccioli, GA, et al; Journal of Cardiothoracic Anesthesia 1988 June; 2(3):365-373

Slide 47:

No improvement in blood flow distal to critical coronary stenosis No improvement in survival when used alone May be essential support mechanism to allow for definitive therapy Intra-aortic Balloon Counterpulsation

Slide 48:

48 Intra-Aortic Balloon Pump Support Improvement in cardiac output and coronary blood flow Essential as a support device for PCI or bridge to CABG ACC-AHA Class I recommendation IABP support was associated with a ↓ in mortality: * NRMI-2 with lysis, from 67% to 49% 2 * SHOCK Trial, from 63% to 47% 1 Hollenberg Ann Int Med 1999; 131:47-99 2 Barron AHJ 2001; 141:933

Left Ventricular Failure:

Left Ventricular Failure MVO 2  Demand  Supply

Primary Effect of IAB Therapy:

Primary Effect of IAB Therapy MVO 2  Supply - IAB inflation  Demand - IAB deflation Supply Demand

Indications:

Indications 1. Refractory ventricular failure 2. Cardiogenic shock 3. Unstable refractory angina

Indications:

Indications 4. Impending infarction 5. Mechanical complications due to acute myocardial infarction 6. Ischemia related intractable ventricular arrhythmias

Indications:

Indications 7. Cardiac support for high-risk general surgical and coronary angiography/ angioplasty patients 8. Septic shock 9. Weaning from cardiopulmonary bypass

Indications:

Indications 10. Intraoperative pulsatile flow generation 11. Support for failed angioplasty and valvuloplasty

Pazienti che possono giovarsi dell’IABP:

Pazienti che possono giovarsi dell’IABP Scompenso cardiaco acuto da miocardite Scompenso cardiaco acuto in pz con cardiomiopatia cronica

Indication for IABP:

Indication for IABP

IABP:

IABP Intra-aortic balloon pump (IABP) remains the most widely used circulatory assist device in critically ill patients with cardiac disease. The National Centre of Health Statistics estimated that IABP was used in 42 000 patients in the USA in 2002.

History:

History Kantrowitz described augmentation of coronary blood flow by retardation of the arterial pressure pulse in animal models in 1952. In 1958, Harken suggested the removal of some of the blood volume via the femoral artery during systole and replacing it rapidly in diastole as a treatment for left ventricular (LV) failure, so called diastolic augmentation.

History _2:

History _2 Four years later, Moulopoulos and colleagues developed an experimental prototype of an IABP whose inflation and deflation were timed to the cardiac cycle. In 1968, Kantrowitz reported improved systemic arterial pressure and urine output with the use of an IABP in two subjects with cardiogenic shock, one of who survived to hospital discharge.

1986:

1986 Percutaneous IABs in sizes 8.5-9.5 French (rather than 15 French used earlier) were introduced in 1979, and shortly after this, Bergman and colleaguesdescribed the first percutaneous insertion of IABP. The first prefolded IAB was developed in 1986.

BenchmarkSM Counterpulsation Outcomes Registry*:

Benchmark SM Counterpulsation Outcomes Registry* * Results as of 1/2000

BenchmarkSM Counterpulsation Outcomes Registry*:

Benchmark SM Counterpulsation Outcomes Registry* * Results as of 1/2000

Slide 66:

66 Reversible Myocardial Dysfunction Myocardial stunning represents persistent myocardial dysfunction that occurs despite the restoration of normal flow. Develops as a result of alterations in calcium homeostasis, oxidative stress, and decreased myofilament responsiveness to calcium Hibernating myocardjum is a persistent state of myocardial dysfunction at rest because of severely reduced coronary flow. Develops as an adaptive response to hypoperfusion Both conditions may indicate recovery over time as reperfusion occurs Hollenberg Ann Int Med 1999; 131:47-99

Slide 67:

Wall motion abnormality during occlusion Wall motion abnormality From Kloner RA. Am J Med. 1986;86:14. Gradual return of function (hours to days) Persistent wall motion abnormality (despite reperfusion and viable myocytes) Coronary occlusion Coronary reperfusion Return of function Clamp Schematic Diagram of Stunned Myocardium

Slide 68:

Atherosclerotic narrowing Wall motion abnormality due to chronic ischemia without infarction Wall motion abnormality From Kloner RA. Am J Med. 1986;86:14. Hibernating Myocardium

Slide 69:

Pre-operative 8 Months Postoperative CONTROL LVEDV = 128 EF = 0.37 POST NTG LVEDV = 101 EF = 0.51 LVEDV = 104 EF = 0.76 Patient Coronary Bypass Graft to L.A.D. Single vessel disease - Occluded L.A.D. End-Diastole End-Systole From Rahimtoola SH, et al. Circ. 1992;65:225. Hibernating Myocardium

Slide 70:

Cell death Significant residual stenosis Reperfusion Segments with myocardial stunning Segments with both stunning and hibernation Segments with hibernating myocardium Relief of ischemia Inotropic support No return of function Return of myocardial function Ischemic Myocardium

Timing:

Timing Inflation and deflation timing is critical in order to obtain the maximum benefits from the pump. Incorrect timing can result in poor patient outcomes. During a cardiac arrest, the IABP can provide very effective perfusion in conjunction with external compressions. Since there is no ECG signal and no arterial pressure wave to trigger the pump, an internal trigger is selected. This trigger detects the flow of blood caused by compressions and inflates the balloon providing improved circulation. Good, consistent compressions are a must for this to work! Use of the Autopulse in these situations has not been studied.

Triggering:

72 Triggering It is necessary to establish a reliable trigger signal before balloon pumping can begin The computer in the IAB console needs a stimulus to cycle the pneumatic system, which inflates and deflates the balloon The trigger signal tells the computer that another cardiac cycle has begun 6/20/2011 72

ECG Trigger:

73 ECG Trigger Since triggering on the R wave of the ECG is preferred, it is very important to give the IABP a good quality ECG signal and lead 6/20/2011 73

Poor ECG Choices:

74 Poor ECG Choices Note: changing QRS morphology may cause wandering timing Note: tall T waves may cause double triggering or may alter previously set timing points Note: wandering baseline may cause skipped trigger Note: artifact may cause inappropriate triggering 6/20/2011 74

ECG Gain:

75 ECG Gain In addition to selecting a lead with a QRS morphology that provides consistent, appropriate triggering, it is important to ensure the QRS complex has adequate amplitude The computer has a minimum height requirement to recognize the initial deflection as an R wave, whether upright or negative in configuration 6/20/2011 75

Slide 76:

40 Arterial Pressure Curve Isovolumetric Contraction Isovolumetric Relaxation 0 120 100 60 Electrocardiogram Ventricular Pressure Arterial Pressure Approx. Time 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 80 10 AV Valve Opens AV Valve Closes Semi-Lunar Valve Closes Semi-Lunar Valve Opens Pressure (mm Hg) Ventricular Systole Atrial Systole Diastole T R P Q S Ventricular Filling Ventricular Ejection Phase Atrial Systole © Datascope Corp.

Aortic Pressure Waveform:

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

The rule of inflation is: inflate just prior to the Dicrotic Notch :

78 The rule of inflation is: inflate just prior to the Dicrotic Notch To accomplish the goals of inflation, the balloon must be inflated at the onset of diastole The result of properly timed inflation is a pressure rise PDP/DA = Peak diastolic pressure or diastolic augmentation, this is the pressure generated in the aorta as the result of inflation 6/20/2011 78

Slide 79:

Slide 80:

Slide 81:

Slide 82:

Slide 83:

Slide 84:

84 Zero Baseline (on console) Balloon Pressure Baseline Rapid Inflation Peak Inflation Artifact Balloon Pressure Plateau (IAB fully inflated) Rapid Deflation Balloon Deflation Artifact Return to Baseline (IAB fully deflated) Duration of Balloon Cycle 6/20/2011

Normal Waveform Variations:

85 Normal Waveform Variations Tachycardia Bradycardia Hypertension Hypotension 6/20/2011

Abnormal Waveform Variation: Wide Inflation and/or Deflation Artifact:

86 Abnormal Waveform Variation: Wide Inflation and/or Deflation Artifact Note the wide inflation and deflation artifacts. This is generally indicative of something impeding the rapid inflation and deflation of the IAB, such as kinking of the gas lumen. This may result in poor augmentation and/or poor afterload reduction. It may also lead to helium/gas loss alarms in higher Heart Rates when in a 1:1 assist ratio. It may precede high pressure/kinked line alarms. The goal is to eliminate the partial obstruction, if possible, to enable the IABP to assist the patient better by moving the helium more rapidly. 6/20/2011 86

Abnormal Waveform Variation: Helium Loss / Gas Loss / Gas Leakage Alarms :

87 Abnormal Waveform Variation: Helium Loss / Gas Loss / Gas Leakage Alarms Note the BPW baseline is below 0. This indicates that a portion of the gas that went out to the balloon did not return to the pump. 6/20/2011 87

Abnormal Waveform Variation: High Pressure / Kinked Line Alarm :

88 Abnormal Waveform Variation: High Pressure / Kinked Line Alarm Note that the plateau pressure is still greater than 250mmHg when it is time to deflate. This indicates that not all of the gas could enter the balloon. It is generally due to a kink in the catheter, either internal to the patient or external . 6/20/2011 88

Abnormal Waveform Variation: High Baseline / Fill Pressure :

89 Abnormal Waveform Variation: High Baseline / Fill Pressure Indicates too much gas in the system. 6/20/2011 89

Factors Affecting Diastolic Augmentation:

Factors Affecting Diastolic Augmentation 1. Patient Hemodynamics Heart Rate Stroke Volume Mean Arterial Pressure Systemic Vascular Resistance

Factors Affecting Diastolic Augmentation:

Factors Affecting Diastolic Augmentation 2. Intra-aortic Balloon Catheter IAB in sheath IAB not unfolded IAB position Kink in IAB catheter IAB leak Low Helium concentration

Factors Affecting Diastolic Augmentation:

Factors Affecting Diastolic Augmentation 3. IABP Timing Position of the IAB augmentation control

Slide 94:

94 It consists of a catheter and a drive console. The catheter has a long balloon mounted on the end. It should be positioned so that the tip is approximately 1 to 2 cm below the origin of the left subclavian artery and above the renal arteries. On chest x-ray the tip should be visible in the 2nd or 3rd intercostal space 6/20/2011 94

IABP correct placement:

95 IABP correct placement 6/20/2011

Slide 96:

Key Insertion Steps:

Key Insertion Steps Preparation of the Insertion Site Puncture the artery - angle of insertion < 45° Insert the guidewire - use the supplied guidewire Make a small incision at the exit of the guidewire Dilate the artery Insert the introducer (sheathed insertion) Spread the subcutaneous tissue with a clamp (sheathless insertion)

Key Insertion Steps (continued):

Key Insertion Steps (continued) Preparing the IAB Catheter Connect the one - way valve and the 60cc syringe to the male luer fitting of the IAB catheter Aspirate 30 cc from the IAB catheter Remove the catheter from the tray - pull the membrane straight out of the tray

Key Insertion Steps (continued):

Key Insertion Steps (continued) Intra-aortic Balloon Insertion Remove the stylet from the central lumen Advance the catheter over the guidewire Insert the catheter to the proper position Position the tip of the IAB approximately 2 cm distal to the origin of the left subclavian artery

Contraindications:

Contraindications 1. Severe aortic insufficiency 2. Abdominal or aortic aneurysm 3. Severe calcific aorta-iliac disease or peripheral vascular disease 4. Sheathless insertion with severe obesity, scarring of the groin

Potential Side Effects and Complications:

Potential Side Effects and Complications Limb ischemia Bleeding at the insertion site Thrombocytopenia Immobility of the balloon catheter Balloon leak Infection Aortic dissection Compartment syndrome

BenchmarkSM Counterpulsation Outcomes Registry*:

Outcomes Mortality with IAB in place 11.3% Average length of IABP therapy 59 hours Mean hospital length of stay 14 days Benchmark SM Counterpulsation Outcomes Registry* * Results as of 1/2000

BenchmarkSM Counterpulsation Outcomes Registry*:

Complications IAB related complications 7.1% Severe bleeding 0.9% Minor limb ischemia 2 % Major limb ischemia 1.1% Benchmark SM Counterpulsation Outcomes Registry* * Results as of 1/2000

Vascular Complications:

Vascular Complications Major Complications n=41 (8%) Limb ischemia Aortic Dissection Abdominal aorta perforation Bilateral limb ischemia Arafa, OE, et al; Ann Thorac Surg 1999; 67:645-651

Vascular Complications:

Vascular Complications Minor Complications n=15 (3%) Hematoma requiring operative revision Hemorrhage treated by IAB removal Limb ischemia relieved by IAB removal Local infection and ischemic skin loss Arafa, OE, et al; Ann Thorac Surg 1999; 67:645-651

Vascular Complications:

Vascular Complications Late Complications n=10 (2%) Foot drop Pseudoaneurysm Limb ischemia Arafa, OE, et al; Ann Thorac Surg 1999; 67:645-651

Vascular Complications:

Vascular Complications Arafa, OE, et al; Ann Thorac Surg 1999; 67:645-651

Slide 109:

The primary goal of intra-aortic balloon pump (IABP) treatment is to increase myocardial oxygen supply and decrease myocardial oxygen demand. Decreased urine output after the insertion of IABP can occur because of juxta-renal balloon positioning. Haemolysis from mechanical damage to red blood cells can reduce the haematocrit by up to 5%. Suboptimal timing of inflation and deflation of the balloon produces haemodynamic instability. An IABP is thrombogenic; always anticoagulate the patient. Never switch the balloon off while in situ.

Trattamento dello Shock cardiogeno Contropulsazione Aortica ed Assistenza Meccanica del circolo :

Trattamento dello Shock cardiogeno Contropulsazione Aortica ed Assistenza Meccanica del circolo 10-02-2010

Slide 112:

Timing data were collected from 165 IABP patients from January 1, 2003 to March 31, 2005 using the Datascope series System 97, System 98, and CS100 IABP consoles. Timing criteria used in the evaluation of the IABP in this study included proper inflation, defined as inflation at the dicrotic notch of arterial pressure waveform, and proper deflation, resulting in a presystolic decrease of diastolic pressure by 5-10 mmHg. These parameters were evaluated by examining a printed strip from the IABP console after timing selection stabilization. Before implementation of the CS100, 78.6% of inflations and 53.6% of deflations were correct when using the criteria listed above. After implementation of the CS100, 83.3% of inflations were correct and 44.4% of deflations were correct.

Limb ischemia and IABP:

Limb ischemia and IABP

IABP E TROMBOLISI:

IABP E TROMBOLISI SHOCK CARDIOGENO

Acute MI with Cardiogenic Shock:

Acute MI with Cardiogenic Shock Stomel, R, et al; Chest 1994; 105(4):997-1002 64 Consecutive Patients Group II IABP 29 Patients Group III Thrombolytics + IABP 22 Patients Group I Thrombolytics 13 Patients

Acute MI and Cardiogenic Shock:

Acute MI and Cardiogenic Shock Stomel, R, et al; Chest 1994; 105(4):997-1002

Thrombolysis plus Counterpulsation in Cardiogenic Shock:

Thrombolysis plus Counterpulsation in Cardiogenic Shock Retrospective review of patients with acute myocardial infarction complicated by cardiogenic shock treated with thrombolytic therapy 27 received IABP 19 did not receive IABP Kovack, PJ, et al; J Am Coll Cardiol 1997; 29:1454-1458

Thrombolysis plus Counterpulsation in Cardiogenic Shock:

Thrombolysis plus Counterpulsation in Cardiogenic Shock Kovack, PJ, et al; J Am Coll Cardiol 1997; 29:1454-1458

Concomitant Use of IABC and Streptokinase in Acute MI:

Concomitant Use of IABC and Streptokinase in Acute MI Prospective non-randomized study 45 patients with acute MI received IV streptokinase 20 received streptokinase alone 25 received IABP with the streptokinase Kumbasar, SD, et al; Angiology 1999 June;50(6):465-471

Concomitant Use of IABC and Streptokinase in Acute MI:

Patients with streptokinase and IABP had higher frequency of TIMI grade 3 flow 44% - IABP with streptokinase (p<0.05) 5% - Streptokinase alone Kumbasar, SD, et al; Angiology 1999 June;50(6):465-471 Concomitant Use of IABC and Streptokinase in Acute MI

Slide 124:

We randomized 57 patients with MI complicated by sustained hypotension, possible cardiogenic shock, or possible heart failure to receive either fibrinolytic therapy and IABP or fibrinolysis alone. Of the 27 patients assigned to fibrinolysis alone, 9 deteriorated such that IABP was required.

Slide 125:

Patients with Killip class III or IV showed a trend toward greater benefit from IABP (6-month mortality 39% for combined therapy versus 80% for fibrinolysis alone; P = 0.05).

Slide 127:

This trial was stopped prematurely because it was unlikely to reach its enrollment targets. The inability to enroll patients who otherwise were eligible for enrollment most likely reflects an inherent bias toward the use of IABP in this population, and thus the corresponding unwillingness to subject patients to the possibility of fibrinolytic treatment alone. Even after enrollment, this bias persisted—one third of the patients randomized to receive fibrinolysis alone crossed over to IABP treatment.

IABP E PTCA (OR CABG):

IABP E PTCA (OR CABG) SHOCK CARDIOGENO

IABP Before Primary PTCA in High-Risk Patients:

IABP Before Primary PTCA in High-Risk Patients This study evaluated 1490 consecutive patients with acute MI treated with primary PTCA without prior thrombolytic therapy. Use of the IAB before intervention in high-risk patients resulted in significantly fewer catheterization laboratory events Brodie, BR, et al; Am J Cardiol 1999; 84:18-23

IABP Before Primary PTCA in High- Risk Patients:

IABP Before Primary PTCA in High- Risk Patients Catheterization laboratory events included: Ventricular fibrillation or tachycardia requiring electrical cardioversion, Cardiopulmonary arrest requiring external cardiac compression or intubation with assisted ventilatory support, or Prolonged hypotension requiring IABC or intravenous pressor agents Brodie, BR, et al; Am J Cardiol 1999; 84:18-23

Catheterization Laboratory Events:

Catheterization Laboratory Events p=0.1 p=0.009 p=0.05 Brodie, BR, et al; Am J Cardiol 1999; 84:18-23

Obiettivo della assistenza meccanica del circolo.:

Incidenza dello shock cardiogeno 4762 patients with AMI who were admitted to 16 hospitals in the Worcester, Massachusetts, metropolitan area between 1975 and 1988. Incidence of and short-term and long-term mortality due to cardiogenic shock in each of six years during this study period. Goldberg et al, NEJM 1991;325:1117-1122 Obiettivo della assistenza meccanica del circolo.

Obiettivo della assistenza meccanica del circolo.:

Obiettivo della assistenza meccanica del circolo. Incidence of CS 7.5%. The overall in-hospital mortality rate among patients with cardiogenic shock was significantly higher than that among patients without this complication (77.7 percent vs. 13.5 percent, P less than 0.001). Long-term survival during the 14-year follow-up period was significantly worse among patients who survived cardiogenic shock during hospitalization than among patients who did not have shock (P less than 0.001). Goldberg et al, NEJM 1991;325:1117-1122

Obiettivo della assistenza meccanica del circolo.:

Obiettivo della assistenza meccanica del circolo. The results of this observational, community-wide study suggest that neither the incidence nor the prognosis of cardiogenic shock resulting from acute myocardial infarction has improved over time. Both in-hospital and long-term survival remain poor for patients with this complication.

Obiettivo della assistenza meccanica del circolo.:

Conclusions: No significant change in the incidence of cardiogenic shock complicating acute myocardial infarction over a 23-year period. However, the short-term survival rate has increased in recent years at the same time as the use of coronary reperfusion strategies has increased. Goldberg et al, NEJM 1999;340:1162-68 Obiettivo della assistenza meccanica del circolo.

Obiettivo della assistenza meccanica del circolo.:

Obiettivo della assistenza meccanica del circolo.

Slide 147:

Slide 149:

Acute coronary syndrome : Constellation of clinical symptoms compatible with acute myocardial ischemia ST-segment elevation MI (STEMI) Non-ST-segment elevation MI (NSTEMI) Unstable angina Unstable angina: Angina at rest (usually > 20 minutes) New-onset of class III or IV angina Increasing angina (from class I or II to III or IV) Braunwald. Circulation 2002; 106:1893-2000. www.acc.org/clinical/guidelines/unstable/unstable.pdf Acute Coronary Syndromes: Definitions

Slide 150:

Inferior Anterior Posterior Multiple Locations 55% 46% 21% 50% Infarct Location in Cardiogenic Shock SHOCK Trial (N=1160) Hochman Circ 1995; 91:873-81

Slide 153:

Recurrent ischemia, Q waves in ≥ 2 leads LAD culprit vessel Chest pain at shock onset ST-segment elevation in two or more leads Multiple infarct locations Inferior MI Left main disease Smoking Shock onset after acute MI occurred within 24 h in 74% of the patients with predominant LV failure Predictors of Early (< 24 h) Cardiogenic Shock Predictors of Late (≥ 24 h) Cardiogenic Shock Webb JACC 2000; 36:1084

Obiettivo della assistenza meccanica del circolo.:

Obiettivo della assistenza meccanica del circolo.

Shock trial:

Conclusions: In patients with cardiogenic shock, emergency revascularization did not significantly reduce overall mortality at 30 days. However,after six months there was a significant survival benefit. Early revascularization should be strongly considered for patients with acute myocardial infarction complicated by cardiogenic shock. Shock trial

Shock trial:

Shock trial

Shock trial:

Shock trial

Shock trial REGISTRY:

Shock trial REGISTRY

Shock trial REGISTRY:

Shock trial REGISTRY

Shock trial REGISTRY:

Shock trial REGISTRY

Slide 161:

Outcome of patients aged ≥75 years in the SHOCK trial Dzavik et al Am Heart J 2005;149:1128-34

Slide 162:

Dzavik et al AHJ 2005; 149:1128 “The lack of benefit of emergency revascularization in elderly patients with cardiogenic shock may relate to differences in baseline left ventricular function and the smaller sample size” The Elderly with Cardiogenic Shock

Slide 163:

Decade-long experience in prospective registry of consecutive PCIs in Northern New England Characteristics and hospital mortality were compared for elderly ( ≥ 75 years old) versus non-elderly (<75 years old) patients. From 1990 to 2000, a total of 310 patients had PCI for cardiogenic shock, 24% of whom were elderly. Independent predictors of mortality for both groups were older age and the absence of collaterals; During the stent era, significant predictors were lack of stent placement and diabetes mellitus. New England Registry 30-Day Mortality Patients > 75 yrs Dauerman et al J Invasive Card 2003; 15: 380 46%

Slide 164:

Clinical Observations from the SHOCK Trial The classic notion that cardiogenic shock develops only when 40% of the myocardium is irreversibly damaged is inconsistent with: 50% survival in PCI-treated patients Improved LVEF in patients undergoing revascularization NYHA Class I symptoms in 58% of patients after survival of the cardiogenic shock Resolution of the ischemia and neurohumoral-inflammatory mediates may result in resolution of the cardiogenic shock The range of LVEFs, LV size, and SVR in patients with cardiogenic shock indicate that the pathogenesis may be multifactorial. Hochman Circulation 2003; 107:2998

Slide 165:

Clinical Observations from the SHOCK Trial The average LVEF is only moderately depressed (30%) with a wide range of EFs and LV sizes noted - While most patients were on IABP support and inotropes, hemodynamic measurements demonstrated persistent hypotension, low CO, and high filling pressures despite a 30% LVEF The SVR was not markedly elevated in many cases, with the SVR ranging from 1350-1400 dynes-sec-cm -5 despite ionotropic support - Cardiac power = CI x MAP was the most powerful hemodynamic predictor of mortality - The ability to raise SVR may be an important compensatory mechanism to support BP – Endogenous/exogenous vasodilators inhibit this response Hochman Circulation 2003; 107:2998

Slide 166:

Cardiac Power Is The Most Important Mortality Predictor in the SHOCK Trial (Mean Arterial Pressure x Cardiac Output) 451 Cardiac Power = Finke et al JACC 2004; 44:340

PCI vs CABG in the shock-trial:

PCI vs CABG in the shock-trial White et al Circulation. 2005;112:1992-2001

Kaplan-Meier Long-term Survival of All Patients and Those Discharged Alive Following Hospitalization :

Kaplan-Meier Long-term Survival of All Patients and Those Discharged Alive Following Hospitalization Hochman et al JAMA 2006;295:2511-2515

Slide 170:

NRMI STEMI Registry (N=25,311) Age, 69.4 years Women, 42.6% Hypertension, 49.7% Diabetes, 27.2% Prior MI, 23.2% Prior CHF, 15.2% Prior PCI, 9.1% Prior CABG, 12.2% Mortality Rates Over Time Babaev et al JAMA 2005 294:448 1995 2004 60.3% 47.9% P < 0.001

Slide 173:

Patients with ST segment elevation MI who have cardiogenic shock and are less than 75 years of age should be brought immediately or secondarily transferred to facilities capable of cardiac catheterization and rapid revascularization (PCI or CABG) if it can be performed within 18 hours of onset of shock. (Level of Evidence: A) ACC/AHA Class I Indication

Slide 174:

Despite ACC/AHA recommendation to treat patients < 75 years of age aggressively with early mechanical revascularization, in 2001, two years after the guidelines were published, only 41% of patients with cardiogenic shock complicating AMI were treated with primary PTCA and only 3.1% underwent early CABG. These data demonstrate significant underutilization of guideline recommended therapy. Babaev A, et al. Circ. 2002;106(19):1811 (abstract). National Registry of MI Early Revascularization is Underutilized in Cardiogenic Shock

Slide 175:

Average LVEF is only moderately severely depressed (30%), with a wide range of EFs and LV sizes noted. Systemic vascular resistance (SVR) on vasopressors is not elevated on average (~ 1350), with a very wide range of SVRs measured. A clinically evident systemic inflammatory response syndrome is often present in patients with CS. Most survivors (85%) have NYHA functional Class I-II CHF status. Hochman JS. Circ .2003;107:2998-3002. Pathophysiology of Cardiogenic Shock Observations from the SHOCK Trial and Registry that Challenge the Classic Paradigm

Slide 176:

Majority of CS Patients are Class I-II at 1 Year Sleeper et al JACC 2005; 46:266

Slide 177:

In the RV group, cardiac index (CI) and mean arterial pressure (MAP) increased (CI 1.8 +/- 0.2 to 2.8 +/- 0.2, MAP 53 +/- 10 to 73 +/- 8, P < 0.05) within 1 hour after IABP, whereas central venous pressure (CVP) and pulmonary artery wedge pressure (PAWP) decreased ( P < 0.05). 59 patients in the RV group (75 %) could be weaned from IABP successfully and 69 % survived to hospital discharge.

IABP E CABG:

IABP E CABG HIGH RISK PATIENTS

Evaluation of Preoperative IABP Support in High-Risk Coronary Patients:

Evaluation of Preoperative IABP Support in High-Risk Coronary Patients Christenson, JT, et al; Eur J Cardiothorac Surg 1997; 11:1097-1103 Prospective randomized study to evaluate the efficacy and cost benefit of preoperative IABP therapy on cardiac performance, mortality, and morbidity in high-risk coronary surgery patients.

Evaluation of Preoperative IABP Support in High-Risk Coronary Patients:

High-risk defined as possessing two or more of the following: Left ventricular ejection fraction (LVEF) < 40% Left main stem stenosis > 70% Redo CABG Unstable angina Christenson, JT, et al; Eur J Cardiothorac Surg 1997; 11:1097-1103 Evaluation of Preoperative IABP Support in High-Risk Coronary Patients

Evaluation of Preoperative IABP Support in High-Risk Coronary Patients:

52 Patients randomized to 3 groups Group I (n=13) received IABP 1 day prior to surgery Group II (n=19) received IABP1-2 hours prior to surgery Group III (n=20) did not receive IABP therapy prior to surgery Christenson, JT, et al; Eur J Cardiothorac Surg 1997; 11:1097-1103 Evaluation of Preoperative IABP Support in High-Risk Coronary Patients

Evaluation of Preoperative IABP Support in High-Risk Coronary Patients:

Use of preoperative balloon pump therapy in high-risk patients undergoing CABG Reduces time on bypass Shortens length of stay in the ICU Lowers in-hospital mortality Christenson, JT, et al; Eur J Cardiothorac Surg 1997; 11:1097-1103 Evaluation of Preoperative IABP Support in High-Risk Coronary Patients

Evaluation of Preoperative IABP Support in High-Risk Coronary Patients:

(p < 0.001) Christenson, JT, et al; Eur J Cardiothorac Surg 1997; 11:1097-1103 Evaluation of Preoperative IABP Support in High-Risk Coronary Patients

Evaluation of Preoperative IABP Support in High-Risk Coronary Patients:

(p < 0.05) Christenson, JT, et al; Eur J Cardiothorac Surg 1997; 11:1097-1103 Evaluation of Preoperative IABP Support in High-Risk Coronary Patients

Evaluation of Preoperative IABP Support in High-Risk Coronary Patients:

Group I & II IABP Group III No IABP (p = 0.004) Mean Length of ICU Stay (days) Christenson, JT, et al; Eur J Cardiothorac Surg 1997; 11:1097-1103 Evaluation of Preoperative IABP Support in High-Risk Coronary Patients

Preoperative IABP - Impact on Postoperative Inotropic Drug Use:

Christenson, JT, et al; Today’s Therapeutic Trends 1999;17(3):217-225 Data pooled from two prospective randomized clinical studies of high-risk coronary patients undergoing myocardial revascularization. 62 patients received preoperative IABP 50 patients did not receive preoperative IABP Preoperative IABP - Impact on Postoperative Inotropic Drug Use

Preoperative IABP - Impact on Postoperative Inotropic Drug Use:

Evaluated total consumption of: Dopamine Dobutamine Norepinephrine Evaluated duration of drug administration Christenson, JT, et al; Today’s Therapeutic Trends 1999;17(3):217-225 Preoperative IABP - Impact on Postoperative Inotropic Drug Use

Preoperative IABP - Impact on Postoperative Inotropic Drug Use:

Conclusion: High-risk patients receiving preoperative IABP have a significantly reduced requirement for inotropic and vasoactive drug therapy. Preoperative IABP - Impact on Postoperative Inotropic Drug Use Christenson, JT, et al; Today’s Therapeutic Trends 1999;17(3):217-225

Preoperative IABP - Impact on Postoperative Inotropic Drug Use:

Preoperative IABP - Impact on Postoperative Inotropic Drug Use Christenson, JT, et al; Today’s Therapeutic Trends 1999;17(3):217-225 P<0.0001 P<0.0001 P<0.0001

Preoperative IABP - Impact on Postoperative Inotropic Drug Use:

Preoperative IABP - Impact on Postoperative Inotropic Drug Use Christenson, JT, et al; Today’s Therapeutic Trends 1999;17(3):217-225 P=0.0002 P=0.0001 P<0.0001

Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients:

Prospective, randomized study conducted to determine optimal timing for preoperative IABP insertion in high-risk patients. Christenson, JT, et al; Annals Thorac Surg 1999; 68:934-939 Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients

Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients:

60 patients enrolled July 1997 - July 1998 Group I (control, n=30) Did not receive preoperative IABP Group II (n=30) Divided into 3 sub groups Received preoperative IABP Christenson, JT, et al; Annals Thorac Surg 1999; 68:934-939 Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients

Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients:

Group II T2 (n=10) received preoperative IABP during 2 hours prior to aortic cross clamp T12 (n=10) received preoperative IABP during 12 hours prior to aortic cross clamp T24 (n=10) received preoperative IABP during 24 hours prior to aortic cross clamp Christenson, JT, et al; Annals Thorac Surg 1999; 68:934-939 Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients

Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients:

High-risk defined as possessing at least two of the following: Left ventricular ejection fraction < 0.30 Unstable angina Left main stenosis > 70% Reoperative CABG Christenson, JT, et al; Annals Thorac Surg 1999; 68:934-939 Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients

Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients:

Preoperative intra-aortic balloon pump support resulted in: Improved cardiac index  ICU and hospital length of stay  length of time on cardiopulmonary bypass  intubation time There was no difference in end points between the subgroups of patients in Group II Christenson, JT, et al; Annals Thorac Surg 1999; 68:934-939 Optimal Timing of Preoperative IABP Support in High-Risk Coronary Patients