Cardiac Conduction System and Atrial Flutter Essay

The heart is critical to the body as it pumps oxygen-rich blood that is necessary for normal functioning to other organs (Bugnitz & Bowman, 2016). The heart must keep pumping blood to prevent it from clotting as clots can cause severe conditions, including stroke. The cardiac cycle is controlled by the cardiac conduction system, which produces and directs electrical signals that enable this function (Laske et al., 2016).Cardiac Conduction System and Atrial Flutter Essay. This system consists of the sinus or sinoatrial (SA) node, the atrioventricular (AV) node, the AV bundle, or bundle of HIS, and the bundle branches called Purkinje fibres.

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The upper wall of the right atrium contains the SA node, which is the heart’s anatomical pacemaker. The central nervous system activates the electrical signals that are sent from the sinus node throughout the atria until they reach the AV node found in the centre of the heart just above the right atrioventricular valve (Laske et al., 2016). The AV node regulates these impulses before they pass to the ventricles via the bundle of His to ensure that the atria fully contracts before the lower chambers are activated to pump blood out of the heart (Kennedy et al., 2016).

Understanding how a heartbeat is represented on an electrocardiogram (ECG) is crucial to deciphering the cardiac cycle. The elements of an ECG are the P wave, PQ segment, QRS complex, ST segment, and the T wave. In a normal ECG, during the p wave, the SA node releases electrical pulses causing the atria to contract (van Weerd & Christoffels, 2016). In the PQ segment, the AV node receives impulses from the SA node and begins transmission to the AV bundle (Kennedy et al., 2016).  In the QRS complex, depolarization of the ventricles occurs in three stages. The Q wave depolarises the intraventicular septum, the R wave acts on the main ventricular mass, and the S wave represents the final depolarization phase at the base of the heart (van Weerd & Christoffels, 2016). In the ST segment, the ventricles contract and pump blood out of the heart, and during the T Wave, the ventricles repolarize and relax before the cycle repeats. Cardiac Conduction System and Atrial Flutter Essay.

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Tachycardia is any condition that causes a rapid heartbeat that cannot be explained by factors such as age, emotional state, or physical activity. Atrial flutter is a supraventricular tachycardia as it affects the upper chambers of the heart (Cosío, 2017). It is dangerous because it stops the atria from filling with enough blood before they contract, thus reducing blood flow to the rest of the body.  Atrial flutter causes rapid contractions of up to 250-300 beats per minute (bpm) while the ventricles contract at a standard rate, thus creating an arrhythmia.

In case the sinus node fails at its pacemaking function, automaticity foci located in the atria send electrical signals as a backup (Cosio, 2017). During atrial flutter, an irritable automaticity focus beats at a rate of 250-300bpm, sending electrical impulses in circular patterns. When the signal is sent to the AV node, the ventricles regulate by reducing it by a half or fourth to between 75 – 150 bpm. Additionally, the AV node has a refractory period so that an amount of time must pass before it transmits another electrical impulse, which causes the ventricles to maintain a normal pace (Bugnitz & Bowman, 2016; Cosio, 2017). On an ECG, the heartbeat presents as regularly regular with equidistant intervals between R-waves and a series of sawtooth-like P-waves.

Atrial fibrillation is the most common chronic arrhythmia, characterized by erratic atrial electrical activity with atrial rates of 400 to 600 beats per minute. The P wave is absent on the surface electrocardiogram and can, at times, be replaced with “fibrillatory waves.”

Atrial flutter is similar to atrial fibrillation in regards to symptoms and thromboembolic risk, including stroke. However, the pathophysiology and management differ.

The symptoms of atrial fibrillation are related to the loss of atrial mechanical activity (atrial contraction) and rapid ventricular heart rates, both of which can reduce cardiac output and lead to congestive heart failure. Thromboembolism frequently causes stroke in patients with atrial fibrillation.

Atrial fibrillation is classified into paroxysmal, persistent or permanent — the three Ps.

Paroxysmal atrial fibrillation is self-limiting, and sinus rhythm restores spontaneously. Paroxysmal atrial fibrillation lasts for less than 7 days and does not require intervention such as electrical or chemical cardioversion to convert to a normal rhythm.

Persistent atrial fibrillation lasts for greater than 7 days. The term persistent is used when there is a plan to use a rhythm control strategy and return the patient to sinus rhythm.

Permanent atrial fibrillation is present when atrial fibrillation is present 100% of the time for greater than 7 days, and there are no interventions planned to restore sinus rhythm.

The term “chronic atrial fibrillation” and the abbreviation “PAF” are no longer recommended for use. Cardiac Conduction System and Atrial Flutter Essay. The term “lone atrial fibrillation” is used when structural heart disease is not present. Atrial fibrillation has also been classified as valvular vs. nonvalvular in etiology. Atrial fibrillation is termed “recurrent” when there have been two or more episodes.

Pathophysiology – Atrial Fibrillation

Atrial fibrillation occurs when irritable foci cause rapid action potentials that result in an atrial heart rate between 400 and 600 bpm. The foci are commonly located in the superior pulmonary veins; this is important in regards to the approach to atrial fibrillation ablation — also known as pulmonary vein isolation. Less commonly, the foci of atrial fibrillation can be within the right atrium; rarely, they are in the superior vena cava or coronary sinus.

Atrial tissue in patients with atrial fibrillation is well known to remodel, showing pathologic changes of fibrosis and inflammation ― the exact mechanism of which remains unclear. Any cardiac condition that results in left atrial enlargement will increase the risk for atrial fibrillation because the above-mentioned remodeling is more prominent in this setting. The left atrium will enlarge whenever the left atrial pressure is increased, as in congestive heart failure, chronic hypertension and valvular heart disease. The larger the left atrium, the higher the risk for atrial fibrillation. Likewise, the larger the left atrium, the less likely that maintaining sinus rhythm after cardioversion will be successful, especially without antiarrhythmic drugs.

Fortunately, not all 400 to 600 atrial action potentials during atrial fibrillation conduct to the ventricles in normal individuals due to the actions of the atrioventricular node. The AV nodal refractoriness inhibits more than half of these action potentials from reaching the ventricles; thus, the typical ventricular heart rate in patients with atrial fibrillation — in the absence of AV blocking medications — is about 100 to 170 bpm. Cardiac Conduction System and Atrial Flutter Essay.

In patients with Wolff-Parkinson-White syndrome who develop atrial fibrillation, an “accessory pathway” is present, electrically connecting the atrium to the ventricles (separate from the AV node) and allowing many more action potentials to reach the ventricles — resulting in ventricular rates greater than 200 bpm. Blocking the AV node with medications such as beta-blockers or calcium channel blockers paradoxically increases the ventricular heart rate because more atrial action potentials can conduct through the accessory pathway, which commonly has a short refractory period (can conduct quite fast). This paradoxical increase in ventricular heart rates can lead to ventricular fibrillation (ventricular rates of 400-600 bpm) and death. Procainamide or electrical cardioversion is recommended in patients with WPW with AF for this reason.

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The development of thrombi in the left atrial appendage can result in embolus, causing stroke in susceptible individuals. When AF is present, flow velocities are significantly decreased in the atrium including the left atrial appendage. This allows coagulation and thrombus formation. Certain predictors can be used to identify those at higher risk for thromboembolism; see the CHADS₂ Score Topic Review, the CHA₂DS₂-VASc Score Topic Review and the American College of Cardiology/American Heart Association guidelines.

Etiology – Atrial Fibrillation

Identifying the cause of atrial fibrillation must not be under emphasized as the treatment of the cause is frequently necessary to eliminate atrial fibrillation. The classic mnemonic “PIRATES” encompasses a vast majority of the causes of atrial fibrillation:

Pulmonary embolus, pulmonary disease, post-operative, pericarditis
Ischemic heart disease, idiopathic (“lone atrial fibrillation”), intravenous central line (in right atrium)
Rheumatic valvular disease (specifically mitral stenosis or mitral regurgitation)
Anemia, alcohol (“holiday heart”), advanced age, autonomic tone (vagally mediated atrial fibrillation)
Thyroid disease (hyperthyroidism)
Elevated blood pressure (hypertension), electrocution
Sleep apnea, sepsis, surgery

Historically, hypertension was thought to be the most common cause of atrial fibrillation, however obstructive sleep apnea is present in about 40% of patients with atrial fibrillation, and it is well known that obstructive sleep apnea causes hypertension.Cardiac Conduction System and Atrial Flutter Essay.  The exact proportion of atrial fibrillation resulting directly from obstructive sleep apnea remains unclear.

Diagnosis – Atrial Fibrillation

Diagnosing atrial fibrillation (AF) is done predominantly on the surface ECG. Sinus P waves are absent and sometimes no atrial activity can be identified. Frequently, coarse “fibrillatory waves” can be seen representing the erratic atrial activity that occurs in the setting of atrial fibrillation.

The QRS complexes are “irregularly irregular” as there is no pattern to their frequency. This is commonly described as varying R-R intervals.

Note that there are three rhythms originating from the atrium that can be irregularly irregular: Atrial fibrillation, atrial flutter with variable conduction and multifocal atrial tachycardia.

The ventricular rate is frequently elevated; when significantly so (> 150 beats per minute), it is often difficult to distinguish atrial fibrillation from atrial flutter, atrial tachycardia, or atrioventricular nodal reentrant tachycardia (AVNRT). In this situation, giving adenosine will transiently slow the ventricular rate in patients with atrial fibrillation, allowing a more definitive diagnosis to be made. This should not be done in patients with Wolff-Parkinson-White syndrome (as described above) because this paradoxically increases the ventricular rate in this setting, leading to ventricular fibrillation, which can be fatal. Cardiac Conduction System and Atrial Flutter Essay.