Although the distance between Perfusion and IABP’s has increased over the years due to smarter consoles, auto-timing features, training of Nursing and Cardiac Cath lab personnel, every once in awhile you find yourself at a clinical site that relies more heavily on perfusionists as a resource for Intra-aortic Balloon Pump therapy.
So please excuse this post if it is too rudimentary or “old news” for many of you, it is practical information that requires a little dusting off from time to time to keep us on our toes 🙂
Have an excellent day!
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Basic Principles of Counterpulsation
Counterpulsation is a term that describes balloon inflation in diastole and deflation in early systole. Balloon inflation causes ‘volume displacement’ of blood within the aorta, both proximally and distally. This leads to a potential increase in coronary blood flow and potential improvements in systemic perfusion by augmentation of the intrinsic ‘Windkessel effect’, whereby potential energy stored in the aortic root during systole is converted to kinetic energy with the elastic recoil of the aortic root.
Physiological Effects of IABP Therapy
The primary goal of IABP treatment is to improve the ventricular performance of the failing heart by facilitating an increase in myocardial oxygen supply and a decrease in myocardial oxygen demand. The overall haemodynamic effects of IABP therapy are summarized in Table 1. Although these effects are predominately associated with enhancement of LV performance, IABP may also have favourable effects on right ventricular (RV) function by complex mechanisms including accentuation of RV myocardial blood flow, unloading the left ventricle causing reduction in left atrial and pulmonary vascular pressures and RV afterload. IABP inflates at the onset of diastole, thereby increasing diastolic pressure and deflates just before systole, thus reducing LV afterload.
- Myocardial Oxygen Supply and Demand
Inflation of IAB during diastole increases the pressure difference between aorta and left ventricle, the so-called diastolic pressure time index (DPTI). The haemodynamic consequence of this is an increase in coronary blood flow and, therefore, myocardial oxygen supply. Myocardial oxygen demand is directly related to the area under the LV systolic pressure curve, termed as tension time index (TTI). Balloon deflation during systole causes a reduction in the LV afterload, thereby decreasing TTI. Thus, the ratio of oxygen supply (DPTI) to oxygen demand (TTI), known as the endocardial viability ratio (EVR), should increase if the IABP is working optimally. This can be evidenced by a decrease in coronary sinus lactate.
- Increased Coronary Perfusion Pressure
According to the Hagen Poiseuille principle, flow through a tube is directly proportional to the pressure difference across it and the fourth power of the radius while being inversely proportional to the length of the tube and the viscosity of fluid flowing through it. Hence, in patients with severe coronary artery disease in whom autoregulation is perceived to be absent, coronary blood flow is directly related to diastolic perfusion pressure. Therefore, IABP should theoretically improve coronary flow in these patients.
- Renal Function
Renal blood flow can increase up to 25%, secondary to increase in cardiac output. Decrease in urine output after insertion of IABP should raise the suspicion of juxta-renal balloon positioning.
- AfterLoad Reduction
AfterLoad Reduction is similar to the process of someone opening the door at the very same moment you are about to open it.
The magnitude of these effects depends upon:
- Balloon volume: the amount of blood displaced is proportional to the volume of the balloon.
- Heart rate: LV and aortic diastolic filling times are inversely proportional to heart rate; shorter diastolic time produces lesser balloon augmentation per unit time.
- Aortic compliance: as aortic compliance increases (or SVR decreases), the magnitude of diastolic augmentation decreases.
Indications for IABP RX
Over the years, indications for the use of IABP have developed in clinical practice and are summarized along with contraindications in Table 2.
- Acute Myocardial Infarction
IABP is aimed at achieving haemodynamic stability until a definitive course of treatment or recovery occurs. By decreasing myocardial work and SVR, intracardiac shunting, mitral regurgitation, or both (if present) are reduced while coronary perfusion is enhanced.
Severe mitral regurgitation secondary to papillary muscle dysfunction or rupture after myocardial infarction can lead to significant haemodynamic instability. This can initially be managed by IABP, pending definitive surgery.
- Ventricular Arrhythmias
IABP is also effective in stabilizing patients with refractory ventricular ectopy after myocardial infarction by increasing the coronary perfusion pressure, reducing ischaemia and trans-myocardial wall stress, and maintaining adequate systemic perfusion.
- Cardiogenic Shock
This is life-threatening complication of acute myocardial infarction, is characterized by low cardiac output, hypotension unresponsive to fluid administration, elevated filling pressures and tissue hypoperfusion leading to oliguria, hyperlactaemia, and altered mental status. IABP therapy is considered to be a class I indication (ACC/AHA guidelines) for the management of cardiogenic shock not rapidly reversed by pharmacological therapy.
- Unstable Angina
Unstable angina refractory to drug treatment is an indication for IABP. These patients are at increased risk of developing acute myocardial infarction and death. By improving the haemodynamic condition of these patients, IABP can facilitate further percutaneous interventions or bridge the patient to surgery.
- Refractory Ventricular Failure
IABP has a role in managing patients with refractory ventricular failure outside the setting of acute myocardial infarction, such as those with cardiomyopathy or severe myocardial damage associated with viral myocarditis. This can aid the progression to more definitive treatments such as ventricular assist device or cardiac transplantation.
- Cardiac Surgery
IABP is used for stabilization of patients with acute myocardial infarction referred for urgent cardiac surgery. IABP support is often initiated in the cardiac catheterization laboratory and continued through the perioperative period. Elective placement is considered in high-risk patients such as those with significant left main stem disease, severe LV dysfunction (ejection fraction < 30%), congestive heart failure, cardiomyopathy, chronic renal failure, or cerebrovascular disease. Weaning from cardiopulmonary bypass may be difficult in cases where aortic cross-clamping is prolonged, revascularization is only partially achieved, or pre-existing myocardial dysfunction is present. Separation from cardiopulmonary bypass may be marked by hypotension and a low cardiac index despite the administration of inotropic drugs. The use of IABP in this setting decreases LV resistance, increases cardiac output, and increases coronary and systemic perfusion, facilitating the patient’s weaning from cardiopulmonary bypass
Balloon Pump Timing
Courtesy of MAQUET GETINGE GROUP Click on image to view PDF file
Classic IABP Wave Form
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