Atrial Kick

Article Author:
Rahul Kurapati
Article Author:
Joseph Heaton
Article Editor:
David Lowery
Updated:
3/25/2020 10:59:49 AM
PubMed Link:
Atrial Kick

Introduction

Atrial kick is the phenomenon of increased force generated by the atria during contraction. This event occurs late in atrial systole when blood flows from the left atrium into the left ventricle. The purpose of the atrial kick is to increase flow across the mitral valve by increasing the pressure gradient. In a healthy patient, the atrial kick can be responsible for 20-30% of the blood transferred to the left ventricle and may be heard as the fourth heart sound.[1][2]

Issues of Concern

During the cardiac cycle, the diastole of the left ventricle occurs in four phases. Namely, isovolumetric relaxation, early diastolic rapid filling, diastasis, and atrial contraction.[3] 

Isovolumetric relaxation occurs after the aortic valve closes, and the ventricle begins to relax, which lowers intraventricular pressure. Due to decreasing pressure without a change in volume status, this phase is isovolumetric. When the pressure inside the ventricle drops below that of the left atrium, blood from the left atrium forces open the mitral valve and allows blood flow into the left ventricle; this early rapid filling phase is passive, as the pressure gradient allows for rapid filling of the left ventricle. 70-80% of blood transferred during diastole occurs during this period.

The continued passive flow of blood across the mitral valve causes pressure in the left atrium and left ventricle to equalize, ceasing the transport of blood. This cessation of flow begins diastasis and concludes when the left atrium contracts. The final phase is the atrial contraction, also known as the atrial kick, when contraction of cardiac muscle in the atrium increases pressure, causing additional blood to flow across the mitral valve. In this last phase, 20%-30% of the total diastolic volume crosses the mitral valve.

The contribution of the atrial kick is dependent on multiple factors. Heart rate and rhythm significantly influence flow from the atrial kick. Tachycardia shortens diastole with a staunch reduction in passive filling time, which allows the atrial kick to contribute a more substantial portion of the volume transferred. Rhythm is also fundamental, as patients in atrial fibrillation and atrial flutter do not have synchronized contractions, which reduces the quantity of volume flowed.[1][4]      

Echocardiographic Evaluation of the Function of Atrial Kick

Flow across the mitral valve can be measured using echocardiography. During ventricular diastole, the flow across the mitral valve is visualized as an "E" and "A" wave utilizing pulse wave doppler (PWD). The E wave is the flow across the MV during the early portion of diastole, and the A wave occurs during the atrial contraction (late diastole). E/A ratio is one method utilized to help evaluate diastolic dysfunction of the LV. Similar measurements can be used with tissue doppler when looking at either the lateral or septal mitral valve annulus.

Loss of Atrial Kick

The atrial kick may be absent due to underlying medical conditions affecting atrial systole. In atrial fibrillation and atrial flutter, the cardiac muscle fibers of the atrium contract asynchronously due to multiple or asynchronous pacemakers. These conditions can diminish the atrial contraction in two ways. First, the asynchronous contraction of the atrium inhibits complete contraction, which hinders the full force potential from being realized. Without adequate compression of the atrial blood, flow across the mitral valve is limited. The second mechanism for diminished atrial kick occurs when the atrial arrhythmia causes rapid ventricular repolarization, which decreases ventricular diastole time. This decrease in time for ventricular diastole reduced the time available for passive filling. Through either mechanism, inadequate filling of the left ventricle can cause a reduction in cardiac output, leading to syncope.

Loss of atrial kick is identifiable on an EKG through a loss of regular P waves. If fibrillation waves or the classic saw-tooth pattern of atrial flutter is present, the heart does not benefit from synchronized atrial contraction. In patients with chronic atrial fibrillation and preserved ejection fraction, increased pulse rates may be a compensatory mechanism used to overcome an otherwise reduced cardiac output state.[5]

Clinical Significance

Treatment of atrial arrhythmias is thus essential to prevent a potentially life-threatening episode. Arrhythmias can be managed pharmacologically by two mechanisms, rate control or rhythm control. Rate control focuses on reducing rapid ventricular responses, while rhythm control attempts to restore sinus rhythm and synchronous atrial contraction.

Anticoagulation is a necessary consideration in atrial fibrillation, due to an increased risk of clot formation.[6] The embolization of a formed clot is also a serious concern, especially after cardioversion.[7] In addition to rate or rhythm control, a provider should consider the use of anticoagulation or device alternatives in patients with atrial fibrillation.[8][9]

Through these treatments, the length of ventricular diastole is improved by decreasing the ventricular rate, which either reduces dependence on an atrial kick or converts an arrhythmia to restore the synchronized atrial contraction.[10]  

Scenarios with Increased Dependence on Atrial Kick

Mitral Stenosis 

A stenotic mitral valve decreases the cross-sectional area available for blood flow. This impedance of flow reduces the quantity of blood that can flow from the atrium to the ventricle. As a result, excess residual blood remains in the left atrium after passive flow, increasing the dependence on the atrial kick to fill the left ventricle. Increased pressures exerted by the atrium to overcome increases in resistance causes atrial remodeling and eventual dilation. Separately, mitral stenosis can also lead to atrial fibrillation.

Additionally, as a consequence of mild to moderate mitral stenosis, and in the setting of shortened diastole, flash pulmonary edema can occur. This edema may present as exertional dyspnea with limited exercise tolerance.

Aortic Stenosis

Aortic stenosis can increase the dependence on atrial kick due to upstream sequelae of impaired ventricular systolic function. Similar to mitral stenosis, aortic stenosis impairs outflow. Due to reduced outflow, diastolic filling pressure increases in the left ventricle, which forces the atrium to work harder in transferring blood. In patients with aortic stenosis, the atrial kick can be responsible for up to 40% of the LV end-diastolic volume.

Heart Failure with Preserved Ejection Fraction

Heart failure with preserved ejection fraction (HFpEF) is caused by impaired relaxation of the left ventricle, inducing left ventricular diastolic stiffness. Loss of compliance of the left ventricle reduces the volume available for blood pooling. Decreased compliance increases dependence on the atrial kick to overcome the stiffness and preserve end-diastolic volume.

Heart failure with preserved ejection fraction is especially harmful in patients with concurrent atrial arrhythmias, as there is no ability to overcome the loss of compliance in the left ventricle. Loss of atrial systole has been shown to decrease cardiac output by up to 20% to 30% and is of significance, particularly in diastolic dysfunction. Forward flow and contractility improve with the restoration of sinus rhythm, as evidenced by hemodynamic improvement in heart failure patients with rhythm control.[11]

Restoration of Atrial Systole and Atrial Kick

Pharmacologic and non-pharmacologic methods can help overcome signs and symptoms associated with the loss of a patient's atrial kick. The two approaches focus on the restoration of a synchronized atrial contraction and reducing the dependence of the atrial kick.

Pharmacological Rate Control

Medical Management: Beta-blockers and non-dihydropyridine calcium channel blockers.

Beta-blockers and non-dihydropyridine calcium channel blockers regulate the heart rate, increasing the duration of diastole. Through increases in filling time, the left ventricle can receive more blood during the passive early diastolic filling. Consequently, this decreases the dependence on the left atrial kick for proper end-diastolic volume and cardiac output. Typically, this is the first-line treatment in patients with heart failure. 

AV Nodal ablation with Permanent Pacemaker Placement 

Atrioventricular node ablation with concurrent pacemaker placement is useful for patients with ventricular responses refractory to medical management. This method controls the ventricular rate but is of limited use due to non-superiority.

Pharmacological Rhythm control

Medical Management: Class III Antiarrhythmic: Amiodarone, Dofetilide, and Sotalol

Class III antiarrhythmic medications may convert atrial fibrillation into normal sinus rhythms, thus restoring atrial systole. The use of antiarrhythmic medications should be cautionary as the agents inherently cause arrhythmias, can prolong the QT interval and have significant drug-drug interactions. Amiodarone, in particular, is well known for its complex side-effect profile and long half-life.

Direct Cardioversion

Direct cardioversion is useful in patients with atrial fibrillation or atrial flutter who failed medical management and are experience ongoing myocardial ischemia, hemodynamic instability, and heart failure. Non-acute cases can be potentially dangerous, as clots may form in the atrium and possibly dislodge after cardioversion. 

Catheter Ablation

In young patients without structural heart disease, catheter ablation can be useful in overcoming arrhythmias. Using radiofrequency ablation techniques, an operator can destroy non-sinus junctions which are responsible for the abnormal rhythm. This procedure intends to leave a single pacemaker node intact for synchronization. 

Surgical Maze Procedures

A surgical maze procedure may be beneficial to patients undergoing heart surgery for coexisting cardiac problems. Using various techniques, a surgeon creates scar tissue in the atria. Since scar tissue cannot conduct electricity, a stray current is halted, which reduces non-sinus induced arrhythmias.[12]

Other Issues

Future Research Directions 

All methods described above can convert the patient to sinus rhythm and restore atrial function. However, there is a lack of evidence and sufficient knowledge regarding the reasons for the recurrence of atrial fibrillation and the reasons behind the lack of recovery of complete atrial kick following conversion to sinus rhythm.

Enhancing Healthcare Team Outcomes

Atrial kick is a significant part of the cardiac cycle as it is necessary to maximize left ventricular end-diastolic volume. Health care professionals must be able to recognize the loss of the atrial kick. When detected, a practitioner should attempt to identify etiology and, with expert consultation, restore the native cardiac rhythm.


References

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