Intra-aortic Balloon Pump Counterpulsation and Mechanical Circulatory Support

1. Intra-aortic Balloon Pump Counterpulsationand Mechanical Circulatory Support

2. Arrow Intra-Aortic Balloon Pump Cardiac Assist technology with proven reliability and performance, effectively decreases the workload of a weary heart Decreases oxygen consumption Increases cardiac output, perfusion, pressure and volume to Coronary Artries Made in U.S.A. with over 35 years of proven technology

3. Counterpulsation: A technique that synchronizes the external pumping of blood with the heart's cycle to assist the circulation and decreasing the work of the heart. Counterpulsation pumps when the heart is resting to increase blood flow and oxygen to the heart. Counterpulsation stops pumping when the heart is working to decrease the heart's workload and lessen oxygen demand

4. Intra-Aortic Balloon Pump (IABP) - A device used to reduce left ventricular systolic work, left ventricular end-diastolic pressure, and wall tension. • It is inserted into the descending aorta via the femoral artery either percutaneously or by surgical cut-down. • The balloon rapidly deflates just before ventricular systole to reduce the impedance (A measure of the total opposition to current flow in an alternating current circuit) to left ventricular ejection.

5. It then rapidly inflates immediately following aortic valve closure to augment (To make (something already developed or well under way) greater, as in size, extent) diastolic coronary perfusion pressure.

6. Intra-aortic Balloon Counter Pulsation Pump (IABP)

7. The balloon is inflated during diastole in sync with the closure of the aortic valve. The blood in the aortic arch above the level of the balloon is pushed backward providing increased coronary artery blood flow and increased myocardial oxygen supply.

8. The balloon is deflated just before systole which helps to decrease afterload. The space where the balloon was inflated creates an empty space where the blood doesn't have to flow against any resistance.

9. IABP support is used until the heart function is improved enough to work on its own. • The patient is gradually weaned from the IABP by reducing the pumping rate from 1:1 (augmentation (the amount by which something increases) with every beat) to 1:2 (augmentation with every other beat) to 1:4 (augmentation with every fourth beat). • Cardiac function is assessed at each stage and IABP is removed if heart function is satisfactory.

10. Intra-aortic balloon pump (IABP) • If a patient is unable to be weaned from CPB (Cardiopulmonary bypass (CPB) is a technique that temporarily takes over the function of the heart and lungs during surgery), an intra-aortic balloon pump can be used to decrease afterload and increase myocardial blood flow.

11. Harken and colleagues of Boston originally described the concept of counterpulsation in 1958 when, in an attempt to increase coronary artery perfusion, they used femoral access to remove blood during systole and replace it during diastole. • Intra-aortic balloon pump (IABP) counterpulsation was first introduced clinically by Kantrowitz and associates in 1967.

12. This therapeutic approach was instituted for treatment of two patients with left ventricular failure after AMI. • Since that time, IABP has become a standard treatment for medical and surgical patients with acute left ventricular failure that is unresponsive to pharmacological and volume therapy

13. Therapeutic goals are directed toward increasing oxygen supply to the myocardium, decreasing left ventricular work, and improving cardiac output. • Before IABP, no single therapeutic agent was capable of meeting these three goals. • IABP counterpulsation is designed to increase coronary artery perfusion pressure and blood flow during the diastolic phase of the cardiac cycle by inflation of a balloon in the thoracic aorta.

14. Deflation of the balloon, just before systolic ejection, decreases the impedance (The total opposition that a circuit offers to the flow of alternating current or any other varying current at a particular frequency) to ejection (afterload) and thus left ventricular work, with subsequent decreased myocardial oxygen consumption. • Inflation and deflation counterpulse (To move or act in opposition to; oppose) each heart beat. • With improved blood flow and effective reduction in left ventricular work, the desired results are increased coronary artery perfusion and decreased afterload with subsequent increase in cardiac output.

15. Physiological Principles • Greater work is required to maintain cardiac output in the failing heart. • With this added work requirement, oxygen demand increases. • These circumstances may occur at a time when the myocardium already is ischemic and coronary artery perfusion is unable to meet the oxygen demands.

16. As a result, left ventricular performance diminishes even further, resulting in decreased cardiac output. • A vicious cycle ensues (To follow as a consequence or result) that is difficult to interrupt. Without interruption of the cycle, cardiogenic shock may be imminent (close in time; about to occur).

17. This cycle can be broken with IABP therapy by increasing aortic root pressure during diastole through inflation of the balloon. • With increased aortic root pressure, the perfusion pressure of the coronary arteries is increased. • Effective therapy for the patient in left ventricular failure also involves decreasing myocardial oxygen demand. • Four major determinants of myocardial oxygen demand are afterload, preload, contractility, and heart rate.

18. IABP counterpulsation therapy can have an effect on all these factors. • It decreases afterload directly and affects the other three determinants indirectly as cardiac function improves. • Because IABP therapy assists the left heart, only the left ventricle is discussed here.

19. AFTERLOAD AND PRELOAD • The greatest amount of oxygen required during the cardiac cycle is for the development of afterload • With greater impedance to ejection, afterload increases,thus resulting in increased myocardial oxygen demand.

20. Impedance to ejection is caused by the aortic valve, aortic end-diastolic pressure, and vascular resistance. • Greater aortic end-diastolic pressures require higher afterload to overcome impedance and ejection.

21. Vascular resistance increases impedance when vessels become vasoconstricted. • Vasodilation or lower vascular resistance decreases afterload by decreasing impedance to ejection. • Deflation of the balloon in the aorta just before ventricular systole lowers aortic end-diastolic pressure.

22. This decreases impedance to ejection and decreases left ventricular workload. • In this way, IABP can effectively decrease the oxygen demand of the heart. • A person in acute left ventricular failure has increased volume in the ventricle at end-diastole (preload) as a result of the heart’s inability to pump effectively.

23. This excessive increase in preload increases the workload of the heart. • IABP therapy helps to decrease excessive preload by decreasing impedance to ejection. • With decreased impedance, there is more effective forward flow of blood and more efficient emptying of the left ventricle.

24. CONTRACTILITY • Contractility refers to the velocity and vigor of contraction during systole. • Although vigorous contractility requires more oxygen, it is a benefit to cardiac function because it ensures good, efficient pumping, which increases cardiac output.

25. cardiac function (see Fig. 18-18). ↓  CARDIAC OUTPUT ↓ CONTRACTILITY ↓ ACIDOSIS ↓ ISCHEMIA ↓ AORTIC ROOT PRESSURE ↓ CORONARY PERFUSION ↓ OXYGEN DELIVERY figure 18-18 Cycle leading to cardiogenic shock.

26. In failure, contractility is depressed. • The biochemical status of the myocardium directly affects contractility. • Contractility is depressed when calcium levels are low, catecholamine levels are low, and ischemia is present with resultant acidosis.

27. IABP counterpulsation can increase oxygen supply, thereby decreasing ischemia and acidosis. • In this way, IABP therapy contributes to improved contractility and better cardiac function

28. HEART RATE • Heart rate is a major determinant of oxygen demand because the rate determines the number of times per minute the high pressures must be generated during systole. • Normally, myocardial perfusion takes place during diastole. Coronary artery perfusion pressure is determined by the gradient between aortic diastolic pressure and myocardial wall tension • It can be expressed by the following equation: Coronary perfusion pressure = aortic diastolic pressure -myocardial wall tension

29. Tension in the muscle retards blood flow, which is why approximately 80% of coronary artery perfusion occurs during diastole. • With faster heart rates, diastolic time becomes shortened, with very little change occurring in systolic time. • A rapid heart rate not only increases oxygen demand but decreases the time available for oxygen delivery.

30. In acute ventricular failure, a person may not be able to maintain cardiac output by increasing the volume of blood pumped with each beat (stroke volume) because contractility is depressed. • Cardiac output is a function of both stroke volume and heart rate: Cardiac output = stroke volume × heart rate

31. If stroke volume cannot be increased, heart rate must increase to maintain cardiac output. • This is very costly in terms of oxygen demand. • By improving contractility, IABP therapy helps improve myocardial pumping and the ability to increase stroke volume. • Decreasing afterload also increases pumping efficiency.

32. With improved myocardial function and cardiac output, the need for compensatory tachycardia diminishes. • IABP counterpulsation increases coronary artery perfusion pressure by increasing aortic diastolic pressure during inflation of the balloon, resulting in improved blood flow and oxygen delivery to the myocardium.

33. The physiological effects of IABP therapy are summarized in Box 18-14. • Proper inflation of the balloon increases oxygen supply, and proper deflation of the balloon decreases oxygen demand. • Timing of inflation and deflation is crucial and must coincide with the cardiac cycle.

34. Direct Physiological Effects of IABP Therapy • Inflation • Aortic diastolic pressure •  Aortic root pressure •  Coronary perfusion pressure •  Oxygen supply • Deflation • Aortic end-diastolic pressure •  Impedance to ejection •  Afterload •  Oxygen demand

35. Equipment Features • The intra-aortic balloon catheter and the balloon mounted on the end are constructed of a biocompatible polyurethane material. • Filling of the balloon is achieved with a pressurized gas that enters through the catheter. • Because of its low molecular weight, helium is the pressurized gas of choice. • Balloon size should be determined by the patient’s physical stature (An achieved level; status) to optimize counterpulsation (Table 18-11).

36. table 18-11 ■ IABP Balloon Size Guidelines Patient Height Balloon Volume Body Surface Area • <5.430 mL 1.8 • 5.4″–6.0 40 mL >1.8 • >6.0″(or aortic diameter >20 cm) 50 mL >1.8

37. With inflation, the addition of the balloon volume into the aorta acutely increases aortic pressure and retrograde blood flow back toward the aortic valve. • With deflation, the sudden evacuation of the balloon volume acutely decreases aortic pressure. • Catheters have a central lumen with which aortic pressure can be measured from the tip of the balloon.

38. Indications for Intra-aortic Balloon Pump Counterpulsation • Two major applications of IABP therapy are for treatment of cardiogenic shock after myocardial infarction and for acute left ventricular failure after cardiac surgery. • Other applications of IABP therapy for patients with cardiac pathophysiological conditions are noted in Box 18-15.

39. box 18-15 • Indications for IABP Therapy ■ Cardiogenic shock after acute infarction ■ Left ventricular failure in the postoperative cardiac surgery patient ■ Severe unstable angina ■ Postinfarction ventricular septal defect or mitral regurgitation ■ Short-term bridge to cardiac transplantation

40. CARDIOGENIC SHOCK • Treatment of cardiogenic shock is complicated, and the mortality rate remains high. • Cardiogenic shock develops in approximately 15% of patients with myocardial infarction. • Patients initially are treated with various inotropic drugs, vasopressors, and volume.

41. A lack of, or minimal response in, cardiac output, arterial pressure, urine output, and mental status after this therapy indicates a need for assisted circulation with IABP therapy. • Once hypotension is present, the self-perpetuating (To prolong the existence) process of injury is in effect.

42. Control of further injury and improvement in survival require early reversal of the shock state. • Once IABP therapy is instituted, improvement should be observed within 1 to 2 hours. • At this time, steady improvement should be seen in cardiac output, peripheral perfusion, urine output, mental status, and pulmonary congestion. • With improved cardiac function, a decrease in central venous pressure and PAWP also should be seen. • Average peak effect should be achieved within 24 to 48 hours.

43. box 18-15 Indications for IABP Therapy ■ Cardiogenic shock after acute infarction ■ Left ventricular failure in the postoperative cardiac surgery patient ■ Severe unstable angina ■ Postinfarction ventricular septal defect or mitral regurgitation ■ Short-term bridge to cardiac transplantation

44. POSTOPERATIVE LEFT VENTRICULAR FAILURE • Although the best outcomes result when IABP counterpulsation is initiated at least 2 hours before cardiac surgery, a successful reduction in the mortality rate has been achieved by using IABP therapy for patients with acute left ventricular failure after cardiac surgery. • Two major conditions might lead to postoperative pump failure: severe preoperative left ventricular dysfunction and intraoperative myocardial injury.

45. IABP counterpulsation therapy can be used to wean patients from cardiopulmonary bypass and to provide postoperative circulatory assistance until left ventricular recovery occurs. • In these situations, early recognition of failure is evidenced by the heart’s inability to support circulation after cardiopulmonary bypass. • Early recognition and treatment are crucial if left ventricular failure is to be reversed.

46. UNSTABLE ANGINA • IABP counterpulsation therapy may be used during PCI (percutaneous coronary intervention (angioplasty or stent placement) for patients with unstable angina or mechanical problems. In this situation, PCI procedures usually are followed by emergency cardiac surgery. • Patients in this category include those with unstable angina, postinfarction angina and postinfarction ventricular septal defects, or mitral regurgitation from papillary muscle injury with resultant cardiac failure.

47. IABP counterpulsation therapy has been used successfully to control the severity of angina in patients in whom previous medical therapy has failed.

48. The use of IABP therapy for patients with cardiac failure after ventricular septal rupture or mitral valve incompetence aids in the promotion of forward blood flow, which decreases shunting through the septal defect and decreases the amount of mitral regurgitation.

49. Contraindications to Intra-aortic Balloon Pump Counterpulsation • There are few contraindications to the use of IABP therapy. • A competent aortic valve is necessary if the patient is to benefit from IABP therapy. • With aortic insufficiency, balloon inflation would only increase aortic regurgitation and offer little, if any, augmentation of coronary artery perfusion pressure. • In fact, the patient’s heart failure could be expected to become worse.

50. Severe peripheral vascular occlusive disease also is a relative contraindication to the use of IABP therapy. • Occlusive disease would make insertion of the catheter difficult and possibly interrupt blood flow to the distal extremity or cause dislodgement of plaque formation along the vessel wall, resulting in potential emboli.