Acute cardiac unloading

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Acute cardiac unloading
Acute Unloading Interupt Spiral.png
Current treatment paradigms for increasing cardiac output after the heart has been damaged often increase the stress placed on the heart and cause more damage leading to a progressive cycle into functional decompensation. Acute unloading removes the heart from this cycle by increasing cardiac output through mechanical means.
Specialty cardiology

Acute cardiac unloading is any maneuver, therapy, or intervention that decreases the power expenditure of the ventricle and limits the hemodynamic forces that lead to ventricular remodeling after insult or injury to the heart. This technique is being investigated as a therapeutic to aid after damage has occurred to the heart, such as after a heart attack. The theory behind this approach is that by simultaneously limiting the oxygen demand and maximizing oxygen delivery to the heart after damage has occurred, the heart is more fully able to recover. This is primarily achieved by using temporary minimally invasive mechanical circulatory support to supplant the pumping of blood by the heart. Using mechanical support decreases the workload of the heart, or unloads it.

Contents

Cardiac traumas such as myocardial infarction (commonly called a heart attack), myocarditis,  peripartum cardiomyopathy, cardiogenic shock  , and takotsubo cardiomyopathy result in an impaired ability of the heart to pump blood. Without proper blood flow the person will ultimately die. Maintaining sufficient cardiac output is the primary objective of therapeutic approaches treating these cardiac conditions. However, many therapies aimed at increasing cardiac output place further stress on the heart. In this way a well-document vicious cycle begins in which increased cardiac output is required, but in order to achieve this the heart must work harder. This exacerbated stress leads to poorer outcomes. [1] With the exception of cardiopulmonary bypass, current therapeutic approaches do not allow the heart to rest and recover. The workload of the heart (pumping blood) is never uncoupled from heart function. Acute cardiac unloading is able to functionally uncouple [2] the heart from cardiac output, allowing the heart to rest and recover from damage.

Power expenditure

ESPVR and EDPVR are dynamic properties of the myocardium. End Systolic Pressure Volume Relationship.jpg
ESPVR and EDPVR are dynamic properties of the myocardium.

The pumping of blood is considered the workload of the heart and requires power expenditure. Acute cardiac unloading is any maneuver, therapy, or intervention that decreases the power expenditure of the ventricle while maintaining cardiac output. Oxygen consumption (MVO2) is a direct measure of the total energy requirements of the heart, including the energy needed to pump blood. [3]

MVO2

The pressure-volume area (PVA) is the total mechanical energy generated by ventricular contraction. Pressure Volume Area.jpg
The pressure-volume area (PVA) is the total mechanical energy generated by ventricular contraction.

Pressure-volume (PV) loop analysis provides a framework for understanding how acute cardiac unloading reduces MVO2 in the heart. [4] [5] The PV loop characterizes the events occurring during a single cardiac cycle (a single heartbeat). The total area bound by the PV loop is the mechanical energy (pressure-volume work) used to actively pump blood every beat, measured in mmHg·mL (aka, a joule  ). This is known as the stroke work (SW). The remaining area bound by the ESPVR and EDPVR that is outside of the loop is the potential energy (PE) that resides in the myofilaments that was not transduced into the work of pumping blood. The sum of these two areas (PE + SW) is known as the pressure-volume area (PVA). PVA is a first order approximation of MVO2. [3]

Acute cardiac unloading decreases the workload of and the oxygen demand of the heart. This can be visualized as an overall decrease in the PVA of the PV loop. [3] [2] Mechanical unloading of the heart by a percutaneous ventricular support device such as the Impella device can achieve this in two ways. First, the device is a continuous flow device. It directly aspirates blood from the ventricle into the aorta. This decreases the preload and results in a left-shift and loss of the normal isovolumic contraction line. [2]

Under conditions of mechanical support, mean aortic pressure (MAP) is maintained independent of native ventricular function, and ventricular and aortic pressures become uncoupled. [2]

Myocardial infarction

As the level of support increases, aortic pressure is maintained independent of ventricular function. Perfusion pressure is uncoupled from heart function (1-4). Complete Unloading Figure.png
As the level of support increases, aortic pressure is maintained independent of ventricular function. Perfusion pressure is uncoupled from heart function (1-4).

When the heart is damaged by a myocardial infarction a portion of muscle is permanently lost. The heart has a limited innate ability to replace dead muscle with new, functional muscle. [6] The dead heart muscle is replaced by non-contractile fibrotic tissue, forming the myocardial scar. Scar tissue does not contract, and it does not help the heart pump blood. This persistently stresses the heart and increases the workload of the lasting myocardium as measured by MVO2. Clinical research indicates that as the size of the myocardial scar increases, so does the likelihood of the patient to develop heart failure. [7] Acute cardiac unloading decreases cardiac MVO2 and has been demonstrated to limit the amount of scar tissue that forms, thus preserving heart function after a heart attack. [8] [9]

Related Research Articles

<span class="mw-page-title-main">Cardiology</span> Branch of medicine dealing with the heart

Cardiology is the study of the heart. Cardiology is a branch of medicine that deals with disorders of the heart and the cardiovascular system. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease, and electrophysiology. Physicians who specialize in this field of medicine are called cardiologists, a sub-specialty of internal medicine. Pediatric cardiologists are pediatricians who specialize in cardiology. Physicians who specialize in cardiac surgery are called cardiothoracic surgeons or cardiac surgeons, a specialty of general surgery.

<span class="mw-page-title-main">Ventricular fibrillation</span> Rapid quivering of the ventricles of the heart

Ventricular fibrillation is an abnormal heart rhythm in which the ventricles of the heart quiver. It is due to disorganized electrical activity. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by sudden cardiac death in the absence of treatment. Ventricular fibrillation is initially found in about 10% of people with cardiac arrest.

<span class="mw-page-title-main">Systole</span> Part of the cardiac cycle when a heart chamber contracts

Systole is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood.

<span class="mw-page-title-main">Ventricle (heart)</span> Chamber of the heart

A ventricle is one of two large chambers located toward the bottom of the heart that collect and expel blood towards the peripheral beds within the body and lungs. The blood pumped by a ventricle is supplied by an atrium, an adjacent chamber in the upper heart that is smaller than a ventricle. Interventricular means between the ventricles, while intraventricular means within one ventricle.

<span class="mw-page-title-main">Mitral regurgitation</span> Form of valvular heart disease

Mitral regurgitation (MR), also known as mitral insufficiency or mitral incompetence, is a form of valvular heart disease in which the mitral valve is insufficient and does not close properly when the heart pumps out blood. It is the abnormal leaking of blood backwards – regurgitation from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts. Mitral regurgitation is the most common form of valvular heart disease.

<span class="mw-page-title-main">Cardiac catheterization</span> Insertion of a catheter into a chamber or vessel of the heart

Cardiac catheterization is the insertion of a catheter into a chamber or vessel of the heart. This is done both for diagnostic and interventional purposes.

<span class="mw-page-title-main">Cardiogenic shock</span> Shock due to heart dysfunction

Cardiogenic shock is a medical emergency resulting from inadequate blood flow to the body's organs due to the dysfunction of the heart. Signs of inadequate blood flow include low urine production, cool arms and legs, and decreased level of consciousness. People may also have a severely low blood pressure and heart rate.

The intra-aortic balloon pump (IABP) is a mechanical device that increases myocardial oxygen perfusion and indirectly increases cardiac output through afterload reduction. It consists of a cylindrical polyurethane balloon that sits in the aorta, approximately 2 centimeters (0.79 in) from the left subclavian artery. The balloon inflates and deflates via counter pulsation, meaning it actively deflates in systole and inflates in diastole. Systolic deflation decreases afterload through a vacuum effect and indirectly increases forward flow from the heart. Diastolic inflation increases blood flow to the coronary arteries via retrograde flow. These actions combine to decrease myocardial oxygen demand and increase myocardial oxygen supply.

<span class="mw-page-title-main">Amrinone</span> Chemical compound

Amrinone, also known as inamrinone, and sold as Inocor, is a pyridine phosphodiesterase 3 inhibitor. It is a drug that may improve the prognosis in patients with congestive heart failure. Amrinone has been shown to increase the contractions initiated in the heart by high-gain calcium induced calcium release (CICR). The positive inotropic effect of amrinone is mediated by the selective enhancement of high-gain CICR, which contributes to the contraction of myocytes by phosphorylation through cAMP dependent protein kinase A (PKA) and Ca2+ calmodulin kinase pathways.

<span class="mw-page-title-main">Takotsubo cardiomyopathy</span> Sudden temporary weakening of the heart muscle

Takotsubo cardiomyopathy or takotsubo syndrome (TTS), also known as stress cardiomyopathy, is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the muscular portion of the heart. It usually appears after a significant stressor, either physical or emotional; when caused by the latter, the condition is sometimes called broken heart syndrome.

<span class="mw-page-title-main">Myocardial rupture</span> Medical condition

Myocardial rupture is a laceration of the ventricles or atria of the heart, of the interatrial or interventricular septum, or of the papillary muscles. It is most commonly seen as a serious sequela of an acute myocardial infarction.

Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.

The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.

<span class="mw-page-title-main">Myocardial infarction</span> Interruption of cardiac blood supply

A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing infarction to the heart muscle. The most common symptom is retrosternal chest pain or discomfort that classically radiates to the left shoulder, arm, or jaw. The pain may occasionally feel like heartburn.

<span class="mw-page-title-main">Acute decompensated heart failure</span> Medical condition

Acute decompensated heart failure (ADHF) is a sudden worsening of the signs and symptoms of heart failure, which typically includes difficulty breathing (dyspnea), leg or feet swelling, and fatigue. ADHF is a common and potentially serious cause of acute respiratory distress. The condition is caused by severe congestion of multiple organs by fluid that is inadequately circulated by the failing heart. An attack of decompensation can be caused by underlying medical illness, such as myocardial infarction, an abnormal heart rhythm, infection, or thyroid disease.

A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot. A number of methods have been determined for measuring PV-loop values experimentally.

Myocardial infarction complications may occur immediately following a myocardial infarction, or may need time to develop. After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.

Impella is a family of medical devices used for temporary ventricular support in patients with depressed heart function. Some versions of the device can provide left heart support during other forms of mechanical circulatory support including ECMO and Centrimag.

<span class="mw-page-title-main">Protected percutaneous coronary intervention</span>

Protected percutaneous coronary intervention, abbreviated as Protected PCI, is a heart procedure that involves a ventricular assist device that is used to treat patients with cardiovascular disease, including advanced heart failure.

<span class="mw-page-title-main">Pathophysiology of heart failure</span>

The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction, hypertension and cardiac amyloidosis. Over time these increases in workload will produce changes to the heart itself:

References

  1. ↑ Minicucci MF, Azevedo PS, Polegato BF, Paiva SA, Zornoff LA. Heart failure after myocardial infarction: clinical implications and treatment. Clinical Cardiology. 2011;34(7):410-414.
  2. 1 2 3 4 5 D. S. Burkhoff, G.; Doshi, D., Uriel, N., Hemodynamics of Mechanical Circulatory Support. Journal of the American College of Cardiology66, 2663-2674 (2015).
  3. 1 2 3 Suga, H. Total mechanical energy of a ventricle model and cardiac oxygen consumption. The American Journal of Physiology 236, H498-505 
  4. ↑ Burkhoff D., Dickstein M. HARVI: Cardiovascular Physiology & Hemodynamics. Part I. Basic Physiological Concepts (Version 2.0.0) [Mobile application software]. 2012. Updated 2014. Available at: https://itunes.apple.com/gb/app/harvi/id568196279?mt¼8. Accessed October 2, 2015. 10. 
  5. ↑ Burkhoff D. HARVI: Cardiovascular Physiology & Hemodynamics. Part II. Advanced Physiological Concepts (Version 2.0.0) [Mobile application software]. Available at: https://itunes.apple.com/gb/ app/harvi/id568196279?mt¼8. Accessed October 2, 2015.
  6. ↑ Murry, C. E. & Lee, R. T. Development biology. Turnover after the fallout. Science324, 47-48, doi : 10.1126/science.1172255 (2009).
  7. ↑ Stone, G. W. et al. Relationship Between Infarct Size and Outcomes Following Primary PCI: Patient-Level Analysis From 10 Randomized Trials. Journal of the American College of Cardiology 67, 1674-1683, doi : 10.1016/j.jacc.2016.01.069 (2016).
  8. ↑ Kapur, N. K. et al. Mechanically unloading the left ventricle before coronary reperfusion reduces left ventricular wall stress and myocardial infarct size. Circulation128, 328-336, doi : 10.1161/CIRCULATIONAHA.112.000029  
  9. ↑ Sun, X. et al. Early Assistance With Left Ventricular Assist Device Limits Left Ventricular Remodeling After Acute Myocardial Infarction in a Swine Model. Artificial organs, doi : 10.1111/aor.12541 (2015).
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