Atrial Kick

Article Author:
Rahul Kurapati
Article Editor:
Steve Bhimji
Updated:
10/27/2018 12:32:04 PM
PubMed Link:
Atrial Kick

Introduction

Atrial kick describes the part of the cardiac cycle during which the atrial systole occurs. The atrial systole occurs at the end of the ventricular diastole by the depolarization of the atrial muscle cells which causes the P wave of the electrocardiogram. This depolarization results in atrial contraction, increase in atrial pressure and the transfer of blood from atrium to the ventricle, thus completing the period of ventricular filling. 

Atrial kick can be better explained when described as a part of the cardiac cycle. By convention, the cardiac cycle begins at end diastole. Systole can be divided into 2 phases, isovolumetric contraction, and the ejection phase. At end diastole the left ventricular (LV) systole begins, and LV contraction leads to increase in pressure with no change in the LV volume (isovolumetric phase). Once the LV pressure exceeds the aortic pressure, the aortic valve opens leading to the ejection phase of the systole which terminates with the emptying of the LV and the closure of the aortic valve; this marks the beginning of the diastole.

Issues of Concern

The LV diastole can be divided into four phases:

  1. Isovolumetric relaxation
  2. Early diastolic/rapid filling
  3. Diastasis
  4. Atrial contraction or kick

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 LA to LV pressure gradient is created propelling the blood into the LV. During this phase, about 20% to 30% of the LV 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 contribution can become significant, especially if it occurs immediately after the rapid filling phase when the AV pressure gradient is maximal. Thus atrial contraction becomes very 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 non invasively using echocardiography. During the early diastolic filling phase, the flow across the mitral valve is depicted as "E" and the flow across the MV during the atrial kick as "a." E/a ratio can be used to evaluate for diastolic dysfunction of the LV. When an individual has diastolic dysfunction due to impaired ventricular relaxation, the 'E' phase of filling decreases leading to an increased dependence on the atrial kick part of LV filling. In severe (grade III) diastolic dysfunction there is a reversal of the E/a ratio.

Clinical Significance

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 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

Mitral Stenosis 

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.

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 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.

Catheter Ablation

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.

Other Issues

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.