Arrow ACAT®1 Operators Manual

Copyright Copyright © 1998 Arrow International, Everett, MA 02149 USA

Document Specification When making reference to or requesting additional copies of this document, please note the following Part Number: IAM-9001, Revision 4.

0123

Table of Contents

CHAPTER 1: Clinical Uses and Function 1.1: Clinical Uses of IABP

1-1 1-3

Physiological Basis of IABP...1-3 Medical Indications...1-4 Mechanical Defects...1-7 Surgical Indications...1-9 1.2: Contraindications and Potential Complications of IABP

1-11

Contraindications...1-11 Potential Complications...1-12 1 . 3 : F u n c t i o n o f t h e A C A T ®1

1-13

CHAPTER 2: Installation Procedures

2-1

2.1: Installation Procedures

2-3

Pre-installation Requirements...2-3 Service Installation...2-4 AC Power...2-5 Time Meter...2-5 CHAPTER 3: Principles of Operation

3-1

3 . 1 : O v e r v i e w o f t h e A C A T ®1

3-3

ACAT®1 Control Module...3-4 Patient Connections...3-8 Storage Compartment...3-9 Pneumatic Drive Module...3-10 System Battery...3-10 Strip Chart Recorder...3-11 3.2: Input and Output Connections

3-12

Input Connections...3-13 Output Connections...3-14 Balloon Connection...3-15 3.3: Control Keys and Function Keys

3-16

Function Control Keys...3-16 Inflate/Deflate Control Keys...3-17 Trigger Control Keys...3-18 Pump Status...3-20 Signal Input Selection...3-21 AP Signal Source Select...3-23 Assist Ratio...3-25 Balloon Volume...3-26

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Table of Contents

Recorder Control Keys...3-27 Alarm System...3-28 Alarm Control Keys...3-32 Cursor...3-33 Help...3-34 Home...3-40 Display Control...3-41 Multi-Function Keys...3-42 AP Scaling...3-43 Recorder Setup...3-44 Weaning Setup...3-45 Show/Hide Stats...3-46 Audio Setup...3-47 Hemodynamic Calculations (Hemo Calcs)...3-48 Clock Setup...3-49 3.4: Balloon Inflation and Deflation Control

3-50

Assist Ratio...3-50 Balloon Volume...3-50 Triggering...3-51 Timing...3-52 CHAPTER 4: Performance and Technical Specifications

4-1

4 . 1 : A C A T ®1 S p e c i f i c a t i o n s

4-3

4 . 2 : A C A T ®1 C l a s s i f i c a t i o n a n d S y m b o l s

4-10

ACAT®1 Classification...4-10 ACAT®1 Symbols and Definitions...4-11 ACAT®1 Outside Labeling Information...4-14 CHAPTER 5: Operating Procedures

5-1

5.1: Operating Instructions

5-3

Summary...5-3 Preparation...5-5 Patient Connections...5-6 Choosing a Trigger Mode...5-10 Initiating Counterpulsation...5-12 Optimizing Inflation/Deflation Timing...5-13 Assessing the Balloon Pressure Waveform...5-17 Maintaining Balloon Pumping...5-18 Freezing and Recording Waveforms...5-20 Weaning the Patient...5-21

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Table of Contents

5.2: Clinical Environments

5-23

ACAT®1 Transport...5-23 The ACAT®1 in the Operating Room or Catheterization Lab...5-26 The ACAT®1 in the Intensive Care Unit...5-28 The ACAT®1 in Emergency Conditions...5-28 CHAPTER 6: Calibration Procedures

6-1

6.1: Calibration of Transducers

6-3

Transducer Calibration...6-3 Changing the Display Range...6-4 CHAPTER 7: Operational Precautions, Limitations and Hazards

7-1

7 . 1 : W a r n i n g s a n d C a u t i o n s f o r t h e A C A T ®1

7-3

7 . 2 : H a z a r d s A s s o c i a t e d w i t h t h e A C A T ®1

7-8

7.3: System Malfunction and Pump Shutdown

7-9

CHAPTER 8: Maintenance and Service 8.1: Routine Maintenance Procedures

8-1 8-3

ACAT®1 System Maintenance Schedule...8-3 Operational Checkout...8-4 Cleaning and Disinfection...8-7 Condensate Removal...8-8 Recorder Paper Installation...8-9 Helium Tank Replacement...8-10 Fuse Replacement...8-12 System Shutdown...8-12 Sealed Lead Acid Battery Maintenance...8-13 Battery Load Test...8-15 Battery Replacement Procedure...8-16 8.2: Service and Ordering Information

8-17

Service Information...8-17 Ordering Parts, Supplies, Options and Accessories...8-17 8.3: Warranty

8-20

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Table of Contents

CHAPTER 9: Troubleshooting 9 . 1 : T r o u b l e s h o o t i n g t h e A C A T ®1

9-1 9-3

Common Operational Problems...9-3 Diagnostic Alarms...9-6 Automatic Response Alarms...9-6 Information Only Alarms...9-11 Troubleshooting ESIS...9-13 Balloon Pressure Waveform...9-15 Squared Waveform...9-16 Reduced Augmentation...9-17 Baseline Below Zero...9-18 Leak Testing and Tubing Repairs...9-19 APPENDIX: Common Abbreviations

A-1

GLOSSARY

G-1

REFERENCES

R-1

ADDRESS INFORMATION

R-3

iv

ILLUSTRATIONS

3.1: 3.2 3.3: 3.4: 3.5: 3.6: 3.7: 3.8 3.9: 3.10: 3.11: 3.12: 3.13: 3.14: 3.15: 3.16: 3.17: 3.18:

The ACAT®1 IABP System Configuration...3-3 Screen Area Definitions...3-5 The ACAT®1 LCD and Control Function Keypad...3-7 The ACAT®1 Connector Panel and Power Switch...3-8 Top Panel Storage Compartment...3-9 The Strip Chart Recorder...3-11 Input and Output Connectors...3-12 Front Panel of Control/Display Module...3-16 Adjustment of Internal Trigger Rate via the Multi-Function Keys...3-19 ECG Lead Selection (3 lead cable) via ECG Select Key and Multifunction Keys 3-21 ECG Lead Selection with Manual Gain Control...3-22 ECG Lead Selection via Multi-Function Keys...3-22 Transducer Zero and Calibration Functions...3-24 AP Sensitivity when CAL is Pressed...3-24 Initial Display of Volume Change...3-26 Example of IAB Volume Change to less than Full Volume...3-26 ALARMS OFF time (in minutes) for duration of ALARMS OFF...3-28 ALARMS OFF time (minutes) Selections...3-32

4.1

The ACAT®1 IABP System...4-3

5.1: 5.2: 5.3: 5.4a: 5.4b: 5.4c: 5.4d: 5.4e: 5.5a: 5.5b: 5.6:

ECG Electrode Placement, 3- or 5-Lead...5-7 ECG Connectors...5-8 Typical Arterial Pressure Waveform...5-9 Arterial Pressure Waveform (Optimum Timing)...5-14 Early Inflation...5-15 Late Inflation...5-15 Early Deflation...5-16 Late Deflation...5-16 Normal Balloon Pressure Waveform...5-17 Properly Timed Arterial Pressure Waveform...5-17 Placement of ECG and ESU Cables...5-27

8.1: 8.2: 8.3: 8.4: 8.5:

The Condensate Collection Bottle...8-8 Condensate Bottle Behind Helium Tank...8-8 The Strip Chart Recorder...8-9 Helium Tank Installation with Disposable Tank...8-11 Helium Tank Installation with Refillable Tank...8-11

9.1a: 9.1b: 9.2: 9.3: 9.4:

Normal Balloon Pressure Waveform...9-15 Properly Timed Arterial Pressure Waveform...9-15 Squared Balloon Pressure Waveform...9-16 Balloon Pressure Waveform Reflecting Reduced Augmentation...9-17 Balloon Pressure Baseline Below Zero...9-18

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TABLES

Input Connectors...3-13 Output Connectors...3-14 Data Connectors...3-14 Inflate/Deflate Control Keys...3-17 Trigger Mode Control Keys...3-19 Pump Status Control Keys...3-20 Assist Ratio Control Keys...3-25 Recorder Setup Control Keys...3-27 Class 1 (Automatic Response) Alarms...3-29 Class 2 (Automatic Response) Alarms...3-30 Class 3 (Information Only) Alarms...3-31 Alarm Control Keys...3-32 Display Control Key...3-41 Recorder Scaling – AP Waveform...3-44 Inflation and Deflation Ranges for Trigger Modes...3-53 ACAT®1 Technical Specifications...4-4 ACAT®1 Symbols and Definitions...4-11 Standard Lead Configurations...5-7 Recommended IABP Triggers...5-11 Display Scale Recorder Values...6-4 System Maintenance Schedule...8-3 Ordering Information...8-18 Common Operational Problems...9-3 Automatic Response Alarms...9-6 Information Only Alarms...9-11 Troubleshooting ESIS...9-13

vi

1. Clinical Uses and Function

Intra-Aortic Balloon Pumping (IABP), or counterpulsation, is a widely accepted therapeutic method of temporarily supporting patients with impaired left ventricular function. Impaired left ventricular function causes low cardiac output and inadequate coronary perfusion. Counterpulsation helps to balance the myocardial oxygen supply and demand in these patients. The hemodynamic effects of counterpulsation are immediate, predictable, and most importantly, decrease morbidity and mortality. The IABP can be initiated rapidly. For this reason, the IABP has become an important therapeutic tool in a variety of clinical settings, including Emergency Departments, Cardiac Catheterization Labs, Operating Rooms, and Intensive Care Units. This chapter provides an overview to the clinical uses of the IABP and the functions of the ACAT®1 IABP System. The details of how the ACAT®1 works is described in Chapter 3, Principles of Operation. The contents of this chapter include: 1.1: Clinical Uses of IABP

1-3

Physiological Basis of IABP...1-3 Medical Indications...1-4 Mechanical Defects...1-7 Surgical Indications...1-9 1.2: Contraindications and Potential Complications of IABP

1-11

Contraindications...1-11 Potential Complications...1-12 1 . 3 : F u n c t i o n o f t h e A C A T ®1

1-13

Clinical Uses and Functions 1-1

1. Clinical Uses and Function 1.1: Clinical Uses of IABP

Physiological Basis of IABP The overall goal of IABP is to provide cardiac support to patients whose myocardial oxygen supply and demand are imbalanced. Counterpulsation achieves this goal by increasing coronary and systemic perfusion, decreasing afterload (myocardial work) and decreasing preload. The IABP exerts its effect by rapidly shuttling helium gas in and out of the balloon chamber. At a precisely timed interval, the gas enters the balloon chamber within the aorta. As the gas is shuttled into the balloon, it occupies a space within the aorta equal to its volume. The usual adult balloon volume is 40cc although alternate sizes (30 and 50cc) may be better tolerated clinically. The sudden occupation of space by the gas upon inflation causes blood to be moved from its original position. The blood is moved superiorly and inferiorly to the balloon. Along with the movement of blood is a sharp increase in the pressure in the aorta. Since the volume in the aorta is suddenly increased and the aortic wall is fairly rigid, the intra-aortic pressure increases sharply. With deflation of the IAB, the sequence of its effects is reversed. A sudden 40cc fall in aortic volume causes a sudden decrease in aortic pressure within that localized area. In response to the fall in pressure, the blood in adjacent areas moves to equalize the pressure within the aortic cavity as a whole. The evacuation of 40cc of volume from the aorta is timed to occur precisely prior to ventricular ejection (systole). Displacement of blood volume (both away from the balloon on inflation and toward the balloon on deflation) is the mechanism by which the IABP alters the patient’s hemodynamic state. To alter the hemodynamic state for the greatest benefit, the IABP must be set so that inflation and deflation of the balloon occur at the optimal times. To provide maximum benefit to the patient, the IABP must be provided with a reliable trigger so that the assist occurs consistently in each cardiac cycle. ECG triggering utilizing the R-wave or the QRS complex is usually the simplest way to accomplish this, and is the preset mode used by the IABP. In addition, inflation and deflation points must be timed very precisely. Optimum timing results in increased Peak Diastolic Pressure (PDP) and decreased Balloon Aortic End-Diastolic Pressure (BAEDP). If the balloon is inflated too early, Stroke Volume (SV) may be reduced. Late inflation will result in smaller increases in PDP and perfusion. If the balloon is deflated too early, BAEDP (and thus workload) is not decreased. Late deflation is more serious, because BAEDP (i.e. workload) may be increased, causing a further imbalance in myocardial oxygen supply and demand. After you have optimized timing, the ACAT®1 automatically adjusts for most variations in the patient’s heart rate and for arrhythmias. Extensive clinical experience shows that Intra-Aortic Balloon Pumping is a safe and effective method of providing cardiac assist to appropriate patients20. By increasing coronary and systemic perfusion and decreasing preload and afterload, the IABP can stabilize critically ill cardiac patients. It is important to initiate IABP as quickly as possible to help minimize further damage to the myocardium. Medical and surgical indications for IABP are described in the following section.

Physiological Basis of IABP 1-3

1. Clinical Uses and Function 1.1: Clinical Uses of IABP

Medical Indications Cardiogenic Shock2,6,9,10,13,14,17,27,28,29 Cardiogenic shock is a physiological derangement of circulatory failure due to severe depression of myocardial function. Cardiac Output (CO) is markedly depressed and the compensatory mechanisms that usually maintain CO (e.g., increased Heart Rate [HR], increased preload and increased contractility) are no longer sufficient to return systemic perfusion to a life supporting level. CO is further compromised by the loss of contributing myocardium to the contractile process. During cardiogenic shock, further deterioration occurs as a result of dysfunctional compensatory mechanisms, resulting in a vicious cycle that increases the stress on an already over stressed myocardium. Cardiogenic shock may result from several conditions, the most common is following Myocardial Infarction (MI). Hemodynamic variables are manipulated with pharmacologic agents to break the cycle of cardiogenic shock. It is generally accepted that pharmacologic agents should be used as a first line of therapy. Drug intervention, however, cannot cause increased perfusion to the coronary artery system. In an ischemic state, the coronary arteries are already maximally dilated and are totally dependent on the perfusion gradient. The ability to autoregulate coronary flow is lost. IABP can help to increase coronary perfusion. The reduction in afterload and the increase in systemic perfusion pressure are also advantageous. Most practitioners agree that early use of IABP increases the probability of survival. IABP should be considered if first line medical therapies do not improve the patient’s clinical status within two to three hours. Further losses of viable myocardium can occur if inadequate perfusion is allowed to continue. The ACAT®1 should only be used under supervision of qualified medical personnel. An external patient monitor must be used with the ACAT®1. The external monitor must have alarms for high and low blood pressure enabled. Pre-shock Syndrome2,13 Pre-shock syndrome is a condition of deteriorating cardiac function secondary to myocardial ischemia, infarction or mechanical defects. The hallmark signs are decreasing CO, increasing afterload resulting from initial compensatory mechanisms, increasing preload caused by failing cardiac function and the initial signs of generalized systemic myocardial ischemia. IABP therapy is indicated if first line therapies do not reverse the condition and the patient is still salvageable. Myocardial cells are at risk for irreversible damage. Time is critical because the IABP may prevent further deterioration and provide time for the myocardium to heal before infarction occurs.

Medical Indications 1-4

1. Clinical Uses and Function 1.1: Clinical Uses of IABP

Threatening Extension of MI16,17,18,23 If signs of myocardial ischemia continue after an infarction, a portion of the myocardium is in jeopardy. IABP may salvage viable myocardium in these patients. The IABP can be used to alleviate the hemodynamic instability caused by myocardial ischemia while the physician evaluates further intervention options (e.g., coronary bypass surgery). Early intervention is important. Unstable Angina18 Angina is a sign that oxygen supply to the heart is inadequate. Angina sometimes becomes resistant to usual modes of therapy, and the pain continues. Patients with intractable angina often find dramatic relief within 15 minutes of instituting IABP support. This allows time for further evaluation of patient symptoms. Intractable Ventricular Dysrhythmias Ventricular irritability may result from islands of ischemic myocardium. Cell membranes of the hypoxic cells become unstable and discharge electrical currents in a disorganized manner. IABP can relieve the hypoxic environment of the irritable cells by increasing coronary artery perfusion. Reduced myocardial oxygen demand may also help patients with these dysrhythmias. Septic Shock Syndrome21 Septic shock is a state of vascular collapse due to a fall in systemic blood pressure. Bacterial endotoxins paralyze the pre-capillary sphincters, causing a fall in blood pressure. These pre-capillary sphincters are paralyzed in the open position and are unable to maintain a driving pressure for tissue perfusion. At the onset of septic shock syndrome, CO is very high (maintained by elevated Stroke Volume [SV] and HR) and Systemic Vascular Resistance (SVR) is very low. Late in the course of septic shock, profound vasoconstriction increases SVR and decreases CO. Also, it is thought that circulating myocardial depressant factors begin to impair myocardial contractility in the later stages of this syndrome. CO falls, and the patient’s condition deteriorates rapidly. In addition, the tissues become unable to utilize the oxygen that is delivered, and increased arteriovenous shunting of oxygen occurs. The IABP has been employed in some cases of septic shock, generally when the patient is known to have compromised myocardial function. In the early stages of the syndrome, when coronary perfusion is low due to arterial vasodilatation, the IABP may help to increase Coronary Perfusion Pressure (CPP) and supply the heart with extra oxygen. In the late stages, IABP may benefit the patient by reducing afterload when vasoconstriction becomes prominent.

Medical Indications 1-5

1. Clinical Uses and Function 1.1: Clinical Uses of IABP

Cardiac Contusion26 Contusion with subsequent infarction of the myocardium can occur with trauma to the chest wall. The majority of cases of myocardial contusion result from automobile accidents and other blunt chest trauma. Aneurysms involving the contused area can occur. The necrosis of contused cardiac tissue is very similar to infarction from Coronary Artery Disease (CAD). The acute phase of contusion is characterized by hemodynamic instability, and cardiogenic shock is not uncommon in severe cases. These patients benefit from IABP in much the same way that patients with cardiogenic shock caused by a coronary event benefit from IABP. However, many patients with cardiac contusion are young and without coronary disease. The infarction involves a discrete area and is much less diffuse than infarction caused by coronary obstruction. The long-term prognosis is far better in patients with necrosis caused by contusion if they survive the acute phase. IABP is indicated if conservative measures do not restore hemodynamic stability. Prophylactic Support During Diagnostic Interventional and Non-surgical Procedures3,8,12 Patients undergoing ischemic events are sometimes candidates for cardiac catheterization, coronary angioplasty stents, thrombolytic therapy or coronary atherectomy. Cardiac catheterization is necessary to identify the obstructed arteries that may be successfully treated by coronary bypass surgery. In hemodynamically unstable patients, the catheterization procedure can be hazardous because coronary artery supply is temporarily interrupted during injection of the radio opaque dyes. This interruption of the already inadequate oxygen supply can precipitate sudden deterioration of myocardial functions. Use of IABP increases the probability that angiographic studies can be completed in a controlled manner. Coronary angioplasty may be contraindicated in a hemodynamically unstable patient with an otherwise correctable lesion. Inflation of the angioplasty balloon temporarily obstructs coronary blood flow. The use of IABP may help to stabilize the patient’s hemodynamic condition and increase coronary reperfusion by increasing CPP. In addition, studies have shown that IABP use after emergency or high risk primary PTCA for acute MI reduces reocclusion and may add strength to reperfusion and improvement of LV function10,14,15,22. Coronary atherectomy may be indicated in specific types of coronary lesions. IABP may support this interventional procedure24.

Medical Indications 1-6

1. Clinical Uses and Function 1.1: Clinical Uses of IABP

Mechanical Defects Mechanical defects that impede forward CO are another group of medical indications for IABP. These defects include valvular stenosis, valvular insufficiency and ventricular septal defect. Valvular Stenosis The two types of valvular stenosis are aortic stenosis and mitral stenosis. In aortic stenosis, a narrowed valve opening obstructs left ventricular ejection. The left ventricle must generate a higher pressure for a longer period of time to achieve ejection. The left ventricle hypertrophies in response to chronic systolic pressure overload. The pressure during systole greatly increases wall pressure, but this is offset somewhat by the increased wall thickness. The heart functions at its limits of oxygen supply. Indeed, angina is a hallmark of aortic stenosis. Concurrently, CO becomes “fixed” due to the restricted valve orifice. Patients with symptomatic aortic stenosis are in danger of sudden death, presumably due to an ischemic dysrhythmias. The IABP can be used to maximize coronary artery pressure until surgery can be performed. The value of afterload reduction is limited because orifice size, not aortic pressure, prevents left ventricular ejection. Mitral stenosis causes diastolic ventricular underloading. The mitral valve orifice becomes small and restricts the diastolic filling of the left ventricle. As the valve narrows, blood collects in the left atrium and pulmonary circuit. The ventricle becomes dependent on a high left atrial pressure to facilitate left ventricular filling. CO becomes “fixed” because the amount of blood the left ventricle can empty is restricted by the amount it receives. The high pressures and the blood dammed against the stenotic mitral valve cause respiratory insufficiency. Patients often present with pulmonary hypertension and pulmonary edema. Arrhythmias, which can limit coronary filling and jeopardize the myocardium, are associated with a decompensated state of mitral stenosis. The goal of IABP therapy in mitral stenosis is to maximize coronary artery perfusion while further treatment decisions are being made. Afterload reduction has little value because the heart is incapable of increasing its CO. However, afterload reduction may be desirable following valve replacement if left ventricular failure occurs. Mitral Valvuloplasty In the event that Mitral Valvuloplasty is chosen as a therapeutic intervention, the IABP may be used to maximize coronary artery perfusion and reduce afterload immediately before and/or after the procedure. The IABP mechanisms of action are the same as those described for mitral stenosis.

Mechanical Defects 1-7

1. Clinical Uses and Function 1.1: Clinical Uses of IABP

Mitral Valve Insufficiency The two types of valvular insufficiency are aortic insufficiency (see Section 1.2) and mitral insufficiency. In mitral insufficiency, the leaflets of the valve become unable to seal off the left atrium from the left ventricle during systole. As a result, a portion of the left ventricle’s contents is ejected backward into the left atrium. The left ventricle works under a condition of chronic volume overload and ejects its contents into a relatively low-resistance left atrium. In spite of severe myocardial dysfunction, the heart is able to maintain CO because of the low impedance to ejection. Most of the energy expended is used in fiber shortening instead of tension development. Therefore, the Isovolumetric Contraction (IVC) phase is shortened and myocardial oxygen demand is reduced. Mitral insufficiency causes fatigue and chronic pulmonary vascular congestion. The left atrium becomes dilated and the left ventricle hypertrophies. If mitral insufficiency is sudden, the heart cannot compensate completely and the patient presents with florid pulmonary edema and cardiogenic shock. It is important to reduce afterload because decreased aortic pressure enhances forward CO and minimizes regurgitation into the left atrium. The IABP may be necessary if pharmacologic agents do not reduce afterload adequately. Reduction of afterload by IABP may be the key to survival following valve replacement. When the incompetent valve is replaced, the left ventricle is forced to eject its full SV into the high pressure aorta. Myocardial workload increases dramatically with the increase in the IVC phase. If the myocardium is dysfunctional (which may not be apparent preoperatively), mortality will be high if myocardial workload is not reduced adequately. Ventricular Septal Defect (VSD) In VSD, blood is shunted from the left ventricle to the right ventricle with each ventricular contraction (The pressure on the left side of the heart is greater than that on the right.). As blood is shunted to the right side, the SV ejected into the aorta is decreased and right ventricular pressures rise. Blood begins to pool in the systemic venous circuit because the right ventricle is unable to contain the extra volume it receives from the left ventricle. Systemic venous congestion is the main symptom of VSD. The patient may not show signs of congestive heart failure until the end stages of the disease because there is no obstruction from the pulmonary artery to systemic circulation. IABP increases SV by providing a favorable pressure gradient (with balloon deflation). The left ventricle empties more completely at a lower aortic pressure because less blood is shunted across the septum into the right ventricle. The right ventricle, in turn, is able to empty more completely because the end-diastolic volume is less, relieving wall tension. Right ventricular function is improved and the symptoms of venous congestion lessen.

Mechanical Defects 1-8

1. Clinical Uses and Function 1.1: Clinical Uses of IABP

Surgical Indications Prophylactic Preparation for Cardiac Surgery5,8,19,20,28 Induction of anesthesia can be stressful to the cardiovascular system. Several drugs can increase myocardial oxygen demand by increasing HR, SVR or contractility. The stress of surgery can cause similar reactions. It may be appropriate to use IABP in patients with limited myocardial reserves, including patients with: • unstable angina • triple vessel disease (all major coronary arteries obstructed) • left main disease (proven to carry higher mortality and morbidity rates) • recent MI (within six weeks) • impending MI • poor LV function (EF <25%)4 The IABP can also be used in conjunction with investigational devices (i.e., LVAD, RVAD, CPS, etc.), if the indication for use of the device is among those listed above as currently approved indications for IABP therapy (e.g., cardiogenic shock, VSD, MI, unstable angina, etc.) Any hemodynamically unstable patient may benefit from IABP, whether undergoing cardiac or non-cardiac surgery5,8. The main objectives are to maintain a margin of safety in myocardial oxygen balance in the pre-bypass or anesthesia induction period and to support the heart in the event of dysfunction in the early postoperative period. Post-surgical Myocardial Dysfunction20 Post-surgical myocardial dysfunction is popularly known as “post-pump syndrome” or “low cardiac output syndrome”. The etiology is not fully known. The low CO following surgery reflects a global depression of myocardial function. Some proposed etiologies include depression caused by drugs, alterations in perfusion from the cardiopulmonary bypass and intraoperative hypotensive occurrences. The syndrome disappears and cardiac function returns in 24 to 36 hours when appropriate therapies are given. Prognosis is generally very good if baseline cardiac function is near normal and intraoperative infarction is absent. Cardiac Support Following Correction of Anatomical Defects Patients undergoing correction of a VSD or mitral valve replacement for mitral insufficiency frequently need cardiac support following surgery. After repair of these defects, the myocardium must overcome a higher afterload in order to eject the SV. IABP support may be more long term if it takes time for myocardial function to return to normal.

Surgical Indications 1-9

1. Clinical Uses and Function 1.1: Clinical Uses of IABP

Maintenance of Graft Patency Post Coronary Bypass Surgery IABP may not be needed to maintain graft patency after coronary bypass surgery. IABP may be appropriate if cardiac function is compromised and graft patency is jeopardized. Pulsatile Flow During Cardiopulmonary Bypass This is not an indication in and of itself. The value of pulsatile flow is debatable and has not been resolved. Some cardiopulmonary bypass machines are capable of providing pulsatile flow or can be adapted to deliver pulsatile flow. In most cases, there must be an additional reason to warrant the use of IABP. Bridge to Left Ventricular Assist Patients who exhibit significant hemodynamic compromise despite IABP therapy, may require more intensive Left Ventricular Support.The IABP may be used until other such devices can be implemented.

Surgical Indications 1-10

1. Clinical Uses and Function 1.2: Contraindications and Potential Complications of IABP

Contraindications Intra-Aortic Balloon Pumping (IABP) requires an adequate location in which to place the balloon and a functional aortic valve. Further, the clinician must have confidence that the patient will benefit from the procedure. The conditions described below are contraindications.

Absolute Hemodynamically Significant Aortic Valve Insufficiency If an aortic valve is incompetent, inflation of an IAB will result in increased regurgitation into the left ventricle. The flow of blood back into the left ventricle will reduce forward CO, further aggravating the patient’s abnormal hemodynamics. Aortic Aneurysm or Aortic Wall Disease Movement of an IAB may jeopardize the integrity of the aortic wall in a patient with either of these conditions. Rupture of the aortic wall must be avoided.

Relative Atherosclerosis In some patients with severe atherosclerosis, the femoral arteries may be sufficiently plaque-filled and tortuous to prevent placement of the balloon. End-stage Disease Use of IABP may not be justified in some patients with late-stage terminal illness. This is an aggressive and invasive procedure and should be used only if the patient will derive significant clinical benefit.

Contraindications 1-11

1. Clinical Uses and Function 1.2: Contraindications and Potential Complications of IABP

Potential Complications As with any invasive procedure, there are risks associated with IABP use. Potential complications arising from the use of IABP include the following: Limb ischemia may result from obstruction caused by the presence or improper position of the catheter. Aortic wall damage may be caused by stripping of the endothelial surface, improper placement of the catheter or unsuspected aortic wall disease. Thrombosis can occur around the insertion site, on the aortic intima or on the catheter, if it is left dormant in the aorta. Embolus formation may occur from the beginning of insertion to the post-removal phase. Materials known to embolize include thrombi, plaque, gas and air. Infection may result when a debilitated patient is exposed to nosocomial organisms in the critical care setting. Thrombocytopenia may be caused by the presence of the balloon, especially if the balloon totally occludes the aorta during inflation. IAB Rupture and/or Entrapment If calcified plaque is present in the aorta around the area of the IAB, repeated contact with plaque may cause a loss of IAB membrane integrity. This may result in blood in the catheter or in prolonged exposure, clot in the IAB membrane. This may make IAB removal difficult. If blood is present or a leak is suspected, extreme caution must be exercised during IAB removal. Surgical removal should be considered. Bleeding may occur at the IAB insertion site. If anticoagulation (ACT or aPTT), a higher risk of bleeding complications may be noted.

Potential Complications 1-12

1. Clinical Uses and Function 1 . 3 : F u n c t i o n o f t h e A C A T ®1

Function of the ACAT®1 The ACAT®1 IABP System is an advanced microprocessor based system designed for in hospital and transport applications. The ACAT®1 is compact, lightweight and can run with full operational capacity for a minimum of 120/240 minutes on battery power. Precise IAB inflation and deflation is maintained by continuously monitoring the patient’s current physiological data. The ACAT®1 can interface with most monitors, accept inputs from patient cables and transducers and the ACAT®1 is designed to save you time by automating many of the system’s operating functions. The ACAT®1 automatically: • Selects start-up operating parameters that are appropriate for initiating counterpulsation • Purges the pneumatic system for rapid initiation of IABP • Removes water from the pneumatic tubing without interrupting pumping • Refills the IAB line without interrupting pumping • Adjusts timing for most variations in heart rate and arrhythmias • Displays operation on a color LCD (Liquid Crystal Display) and alerts you to potential problems • Shuts down the pump if a malfunction occurs • Switches from AC to battery power when needed • Continuously maintains adequate ECG size for reliable/consistent triggers. These automated operating features make IABP initiation rapid and simple. You can then focus on optimizing IABP support to the patient. Using the system’s controls, you can: • select the sources of the ECG/AP • zero and/or calibrate the transducer • choose from seven trigger modes • select the assist ratio for your patient • set balloon inflation volume • adjust balloon inflation and deflation timing • define recorder settings • use cursor to assess patient and pump parameters • turn alarms on/off • obtain function specific or startup help • set up system clock

Function of the ACAT®1 1-13