Atrial kick describes the part of the cardiac cycle during which the atrial systole occurs. It occurs during the late inflow portion of the cardiac cycle where blood is moving from the left atrium to the left ventricle. The purpose of the atrial kick is to increase the pressure gradient across the mitral valve to allow more blood to be present in the LV at the end of diastole. In normal patients the atrial kick is responsible for about 20-30% of the volume of blood in the LV at the end of diastole. 
Issues of Concern The LV diastole can be divided into four phases:
After the aortic valve closes, the ventricle starts to relax, and the ventricular pressure falls with no change in the volume (isovolumetric relaxation) until the LV pressure is lower than the left atrial (LA) pressure resulting in the mitral valve opening, and the early rapid filling phase begins. LV filling during the early rapid filling phase is a passive process during which the blood flow across the MV is driven by the pressure gradient between the left atrium and the LV. Around 70% to 80% of the LV volume is filled passively during the early rapid filling phase; this period ends with the equalization of pressures across the mitral valve resulting in a period during which there is no blood flow between the LA and LV, this phase of the diastole is known as diastasis. The final phase of diastole is the atrial contraction, or the atrial kick which occurs during atrial systole resulting in an increased LA to LV pressure gradient propelling the blood into the LV. During this phase, about 20% to 30% of the LV end diastolic volume moves across the MV.
However, its contribution to LV volume is governed by the heart rate and the structure of the AV valves. During tachycardia, diastasis is shortened, and atrial contraction becomes more important in rapidly propelling blood to fill the ventricle during this brief period of the cardiac cycle..
Echocardiographic Evaluation of the Function of Atrial Kick
The 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 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 utilized with tissue doppler when looking at either the lateral or septal mitral valve annulus.
Loss of Atrial Kick
In conditions such as atrial fibrillation and atrial flutter, the atrial systole is not initiated by a single pacemaker (sinus node) but by independent unsynchronized nodal firing resulting in the loss of uniform contraction/systole of the atrium needed for the generation of the atrial kick. In atrial fibrillation and atrial flutter, when the atrial impulse is conducted to the ventricle, it can lead to a rapid ventricular response. During these periods of tachycardia, the ventricular diastole is shortened resulting in increased dependence on the atrial kick for adequate LV filling. However, in the atrial fibrillation and atrial flutter due to the unsynchronized atrial contraction, there is the obliteration of the atrial kick resulting in potential inadequate filling of LV, and this sometimes may cause a syncopal episode.
The rationale for the treatment of atrial fibrillation and atrial flutter by either rate control agents or rhythm control is to restore the length of ventricular diastole by decreasing heart rate, thus leading to decreased dependence on atrial kick through rhythm control or by converting to sinus rhythm restoring the atrial kick.
Scenarios with Increased Dependence on Atrial Kick
Narrowing of the mitral valve orifice results in hemodynamic changes in the left atrium and left ventricle. Flow across the mitral valve in the impaired by the narrow mitral valve opening results in inadequate LV filling; this results in increased residual blood in the left atrium and increased dependence on the atrial kick/systole for adequate LV filling. Stenosis of the mitral valve also results in pressure changes upstream in the left atrium leading to left atrial remodeling and left atrial dilatation. Long-term effects of MS include LA dilation and atrial fibrillation. During exertion due to shortened diastole, the dependence of atrial kick increases and the left atrial pressure also increases, and this can result in flash pulmonary edema in severe cases and in mild to moderate stenosis. It can result in exertional dyspnea and limitation of physical activity.
With severe aortic stenosis the stenotic orifice of the aortic valve is the limiting factor of flow from the LV to the aorta. In these patients it is important to keep to the LV full at end diastole so that as much blood as possible is ejected. In patients with AS the atrial kick can be responsible for up to 40% of the LV end diastolic volume.
Heart Failure with Preserved Ejection Fraction
Ventricular diastolic dysfunction (impaired relaxation and increased diastolic stiffness) that is present at rest or induced by stress is the central perturbation in heart failure with preserved ejection fraction. This diastolic stiffness results in incomplete LV filling during early rapid filling and diastasis resulting again in increased dependence on the atrial systole to augment the LV filling and therefore cardiac output.
The clinical significance of atrial systole in HFpEF is seen particularly in patients with concomitant AF and HFpEF where the loss of “atrial kick” can impact patient functional status as well as adversely affect long-term clinical outcomes. 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 HF patients with rhythm control.
Restoring Atrial Systole/Kick
Several Methods have been employed attempting to restore atrial kick and to decrease the dependence on the atrial kick.
Pharmacological Rate Control (Beta-blockers, non-dihydropyridine calcium channel blockers)
By controlling the heart rate, we can increase the duration of diastole, especially the early diastolic filling, thereby decreasing the dependence on the left atrial kick to augment cardiac output. In patients with heart failure, this method can be utilized as the first line before attempting pharmacological, electrical, or surgical rhythm control.
AV Nodal ablation with Permanent Pacemaker Placement
Patients most likely to benefit are those with rare ventricular control refractory to medical therapy. This approach is usually limited to elderly patients because it leads to pacemaker dependence; however, long-term outcomes have not been beneficial when contrasted to patients who underwent PVI for AF.
Pharmacological Rhythm control (Class III Antiarrhythmic: Amiodarone, Dofetilide, and Sotalol)
These agents are used to convert atrial fibrillation into sinus rhythm restoring atrial systole. However, limitations of rhythm control are a recurrence of atrial fibrillation, and frequent monitoring of ECG for side effects such as QT prolongation with sotalol, dofetilide, noncardiac side effects of amiodarone, and other significant drug interactions due to Cytochrome P450 isoenzyme inhibition.
Direct current cardioversion is recommended for patients with atrial fibrillation or atrial flutter if pharmacological cardioversion is unsuccessful and if the rapid ventricular rate does not respond to pharmacological therapies and contributes to ongoing myocardial ischemia, hemodynamic instability, and heart failure.
Is useful for symptomatic, paroxysmal, atrial fibrillation in young individuals without structural heart disease if intolerance to at least 1 class of antiarrhythmics is seen and also in patients with recurrent atrial fibrillation.
Surgical Maze Procedures
Surgical procedures are recommended in patients with atrial fibrillation undergoing cardiac surgery for other indications and in patients in whom symptomatic atrial fibrillation is recurrent and not managed well with all the approaches mentioned above.
Future Research Directions
All the methods described above have been proven to convert the patient to sinus rhythm and restore atrial conduit function. However, there is a lack of evidence and sufficient knowledge regarding the reasons for recurrence of atrial fibrillation and the reasons behind the lack of recovery of complete atrial kick/systole following conversion to sinus rhythm.
The atrial kick is an often over looked, but very important part of the cardiac cycle. To maximize LV EDV the atrial kick is necessary. It is imperative that health care professionals are able to recognize the loss of the atrial kick (loss of P wave on EKG). There should be investigation as to the cause of this and attempts should be made, with expert consultation, to restore the native cardiac rhythm.