Atrial Kick

Function

Physiological Role of the Atrial Kick and Integration in the Cardiac Cycle

Understanding the physiological significance and clinical implications of the atrial kick requires an examination of the cardiac cycle. This cycle is the complete sequence of myocardial events that includes ventricular filling, isovolumetric contraction, ejection of blood, and myocardial relaxation.

The cardiac cycle is divided into 2 primary phases: diastole and systole. Diastole is the period of ventricular relaxation and filling. Systole is the period of ventricular contraction and ejection. Each phase is further subdivided into periods defined by pressure-volume relationships and valve dynamics.

Phases of Left Ventricular Diastole

Left ventricular diastole occurs in 4 periods: isovolumetric relaxation, early diastolic rapid filling, diastasis, and atrial contraction.[3] Isovolumetric relaxation begins during ventricular systole after the aortic valve closes and the ventricle relaxes, lowering intraventricular pressure without a change in volume. When ventricular pressure falls below left atrial pressure, blood from the left atrium forces open the mitral valve and flows into the left ventricle. Early rapid filling is passive, driven by the pressure gradient, and contributes 70% to 80% of blood transfer during diastole. Continued passive flow across the mitral valve equalizes pressures in the left atrium and left ventricle, halting blood flow. This cessation of flow defines diastasis, which ends with the onset of atrial contraction. The final phase, atrial contraction, is also known as the atrial kick.

The atrial contraction phase is initiated by spontaneous electrical activity from the sinoatrial node located in the right atrium near the opening of the superior vena cava.[4][5][6] Electrical impulses generated by the sinoatrial node spread across the right atrium through 3 internodal pathways: anterior, middle, and posterior. The anterior internodal pathway gives rise to the Bachmann bundle, which transmits electrical activity to the left atrium. Depolarization and subsequent contraction follow the propagation of electrical activity across both atria, driving residual blood through the mitral valve. This phase accounts for 20% to 30% of the total diastolic volume entering the left ventricle.

Issues of Concern

Multiple factors influence blood flow across the mitral valve and the contribution of the atrial kick to left ventricular end-diastolic volume. These factors are either structural, electrophysiological, or physiological in nature.

Structural factors include valvular abnormalities such as mitral or aortic stenosis, as well as left ventricular hypertrophy. In mitral stenosis, the left atrium must generate greater pressure to overcome resistance from a narrowed valve orifice. In left ventricular hypertrophy, the decreased pressure gradient across the mitral valve similarly requires increased atrial force to maintain adequate filling.[7]

Electrophysiological factors include atrial fibrillation, atrial flutter, and abnormalities involving the atrioventricular node, all of which impair coordinated atrial contraction. Physiological factors include conditions such as exercise, pregnancy, and sepsis, which alter hemodynamic demands and modify the relative contribution of the atrial kick to ventricular filling.

Echocardiographic Assessment of Transmitral Velocities: The Role and Importance of the Atrial Kick  

Flow across the mitral valve may be measured using transthoracic echocardiography. During the early rapid filling phase of ventricular diastole, peak transmitral velocity is measured with pulse wave Doppler and is referred to as the "E wave." Flow across the mitral valve during atrial contraction, or the atrial kick, is also visualized and measured, producing the "A wave." Both E and A waves are demonstrated on pulse wave Doppler.[8] The E/A ratio is used to evaluate left ventricular diastolic dysfunction. A normal E/A ratio is less than 0.8. Aging and diastolic dysfunction reduce transmitral flow during early rapid filling and enhance flow during atrial contraction, altering the E/A ratio.[9]

Loss of the Atrial Kick 

The atrial kick may be absent in medical conditions that impair atrial systole. Atrial muscle fibers contract asynchronously due to multiple or disordered pacemaker foci in atrial fibrillation and atrial flutter. These arrhythmias diminish atrial contraction through 2 mechanisms. First, asynchronous contraction prevents effective atrial systole and limits blood propulsion across the mitral valve. Second, rapid ventricular depolarization shortens diastole, reducing the time available for passive filling. Both mechanisms decrease left ventricular filling and reduce cardiac output.

Loss of the atrial kick may be identified on electrocardiography (ECG) by the absence of regular P waves. The presence of fibrillation waves or the classic sawtooth pattern of atrial flutter indicates the absence of synchronized atrial contraction. In patients with chronic atrial fibrillation and preserved ejection fraction, elevated pulse rates may serve as a compensatory mechanism to counter reduced cardiac output.[10] On echocardiography, diminution of the atrial kick is demonstrated by the absence of the A wave.

In healthy individuals, suppression of the atrial kick may not cause clinical symptoms. However, absence of atrial contraction in the presence of structural, electrophysiological, or physiological cardiac alterations may result in dyspnea on exertion, pulmonary edema, or, in some cases, syncope.

Clinical Conditions with Increased Dependence on the Atrial Kick

The atrial kick plays a disproportionately large role in preserving hemodynamics in certain structural and functional cardiac disorders. Some frequently encountered conditions are explained below.

Mitral stenosis  

A stenotic mitral valve reduces the cross-sectional area available for blood flow, thereby limiting transmitral filling. Impaired flow results in residual blood within the left atrium after the early rapid filling phase and increases dependence on the atrial kick to complete left ventricular filling. Shortened diastole caused by physiological factors such as tachycardia or pregnancy, and by pathological factors such as atrial fibrillation or atrial flutter, can precipitate flash pulmonary edema. This presentation often manifests as exertional dyspnea and reduced exercise tolerance. Mitral stenosis was historically regarded as an independent risk factor for atrial fibrillation, although the relationship more accurately reflects an association among atrial fibrillation, mitral stenosis, and rheumatic heart disease.[11]

Aortic stenosis 

Aortic stenosis can increase dependence on the atrial kick due to upstream effects of impaired ventricular systolic and diastolic function. Aortic stenosis obstructs left ventricular outflow, leading to an increase in left ventricular end-systolic volume, concentric hypertrophy, and elevated left ventricular end-diastolic pressure.[12][13] The resulting ventricular remodeling produces diastolic dysfunction, which decreases the transmitral pressure gradient and reduces filling during early diastole. These changes are reflected in alterations of the left atrial volume index and the E/e′ ratio, where e′ represents early diastolic mitral annular velocity measured by tissue Doppler. Together, these indices demonstrate increased reliance on atrial contraction for adequate ventricular filling.[14]

Heart failure with preserved ejection fraction 

Heart failure with preserved ejection fraction (HFpEF) arises from impaired relaxation of the left ventricle, resulting in diastolic stiffness and loss of compliance. Reduced compliance increases dependence on the atrial kick to preserve end-diastolic volume. Heart failure with preserved ejection fraction is particularly detrimental in patients with concurrent atrial arrhythmias, as the absence of atrial systole eliminates the ability to compensate for reduced compliance. Loss of atrial contraction has been shown to decrease cardiac output by 20% to 30%, a finding of particular significance in diastolic dysfunction. Restoration of sinus rhythm improves forward flow and contractility, as demonstrated by hemodynamic improvement in patients with heart failure managed with rhythm control.[15]

Clinical Significance

Patients who rely on the atrial kick to maintain adequate ventricular filling may experience symptomatic and prognostic benefits from the treatment of atrial arrhythmias. Management of these cardiac disturbances may be achieved through 2 approaches: rate control and rhythm modulation.

Rate stabilization reduces the ventricular response, thereby prolonging diastole and decreasing reliance on the atrial kick. Rhythm correction restores sinus rhythm, reestablishing synchronized atrial contraction and optimizing ventricular filling.[16]

Modalities That Stabilize Cardiac Rate

β-blockers and nondihydropyridine calcium channel blockers are 1st-line agents for rate control. Slowing the ventricular rate increases the duration of diastole, allowing greater passive early diastolic filling. The resulting hemodynamic changes reduce dependence on the atrial kick, improve end-diastolic volume, and augment cardiac output. Pharmacological rate regulation is the preferred strategy in asymptomatic adults older than 80 years with low cardiovascular risk.[17]

Atrioventricular nodal ablation with pacemaker implantation is reserved for patients with ventricular responses refractory to pharmacological rate and rhythm modulation or recurrent atrial tachyarrhythmias despite catheter ablation. This approach is used sparingly due to its invasive nature and the induction of ventricular dyssynchrony from right ventricular pacing, which may necessitate additional interventions to address pacing-induced dyssynchrony.[18][19]

Therapies That Regulate Rhythm

Rhythm control is the preferred strategy for restoring sinus rhythm in patients who are symptomatic or have elevated cardiovascular risk.[20][21] Rhythm restoration synchronizes atrial and ventricular contraction, thereby optimizing ventricular filling and improving cardiac output.

Cardioversion 

Direct cardioversion is often the initial approach to achieve rhythm regulation. Some patients do not respond to this modality, while others experience recurrence of atrial fibrillation or atrial flutter following initial conversion to sinus rhythm. Long-term management depends on symptom burden and cardiovascular risk.

Patients with low symptom burden and low cardiovascular risk are generally treated with rate-modulating agents and anticoagulation, whereas younger patients with significant symptom burden or high cardiovascular risk are offered catheter ablation or pharmacological rhythm-regulating therapy. Anticoagulation must be established before cardioversion, or transesophageal echocardiography must confirm the absence of thrombus in the left atrial appendage, as restoration of sinus rhythm can dislodge atrial thrombi and precipitate arterial thromboembolism.[22][23]   

Pharmacological treatment

Pharmacological rhythm control may be achieved with several antiarrhythmic agents. The presence or absence of structural heart disease largely guides selection. Flecainide, dofetilide, propafenone, dronedarone, amiodarone, and sotalol are generally preferred in patients without structural abnormalities.[24][25] Propafenone and flecainide are avoided in the presence of structural heart disease because of the increased risk of ventricular tachycardia and other malignant arrhythmias, including torsade de pointes. Sotalol, dronedarone, dofetilide, and amiodarone are appropriate options for patients with structural heart disease but preserved systolic function. Amiodarone and dronedarone are the primary pharmacological choices for patients with heart failure.[26]

Catheter ablation 

In younger patients without structural heart disease, catheter ablation may be offered as 1st-line therapy for paroxysmal atrial fibrillation because it provides lower recurrence rates with comparable adverse event rates.[27][28] Radiofrequency ablation achieves rhythm regulation by electrically isolating the pulmonary veins, which account for approximately 90% of ectopic foci.[29] The procedure preserves the sinus node as the primary pacemaker to maintain atrioventricular synchrony. Reported 1-year success rates at high-volume centers range from 60% to 80%.[30]

Surgical maze procedures

Surgical maze procedures may be considered in patients undergoing cardiac surgery for other indications. These procedures involve the creation of atrial scar tissue using various techniques. Electrically inert scar tissue interrupts abnormal conduction circuits, reducing the likelihood of nonsinus atrial arrhythmias.[31]

Other Issues

Available therapeutic strategies can restore sinus rhythm and reestablish atrial function. Despite these advances, limited evidence exists regarding the mechanisms underlying the recurrence of atrial fibrillation and the incomplete recovery of the atrial kick following rhythm conversion. Future research should focus on identifying structural and electrophysiological predictors of recurrence and clarifying the determinants of atrial mechanical recovery.

Enhancing Healthcare Team Outcomes

The atrial kick is an essential component of the cardiac cycle, as it contributes to maximizing left ventricular end-diastolic volume. Recognition of its absence is clinically important, and identification of the underlying etiology should guide further evaluation. Restoration of sinus rhythm, ideally in consultation with cardiologists or cardiac electrophysiologists, is the primary therapeutic objective when feasible.