Tachycardia

Hypovolaemia and hypotension

The pathophysiology behind noncardiac causes of tachyarrhythmias depends on the underlying pathology. In the case of hypovolaemia and hypotension, the increase in heart rate is a reflex response to a decrease in cardiac output. Vasodilation or haemorrhaging results in a reduction in the stroke volume (SV) of the heart. A reciprocal change in the heart rate (HR) is implemented to maintain the overall cardiac output (CO) and by extension the blood pressure (BP = CO x TPR; TPR is total peripheral resistance).

Anaemia refers to a decline in the concentration of haemoglobin in the blood. This process may be due to either a haemoglobinopathy (disorder of haemoglobin formation) or a decrease in the concentration of red blood cells in the system. Haemoglobin is responsible for transporting oxygen throughout the body. Therefore, any reduction in the haemoglobin concentration introduces the risk of decreased oxygen tension at the tissue level, i.e. hypoxia. The initial compensatory mechanism performed by the cardiovascular system is increasing the flow rate of blood throughout the system. This is best achieved by increasing the heart rate.

Infections

Infections often times illicit an inflammatory response in an immunocompetent host. A part of the inflammatory response involves the release of lipopolysaccharides, interleukins, prostaglandins and other inflammatory mediators. In addition to promoting vasodilation, chemotaxis and immune cell activation, these inflammatory mediators also promote a febrile response. The associated tachycardia that is seen with febrile illnesses has been attributed to an increased metabolic demand. In this case, the pathophysiology is similar to that seen in hypoxic states. Other theories propose that the cytokines also stimulate cardiac pacemaker cells, resulting in an increase in their automaticity.

Hyperthyroidism

Hyperthyroidism also causes tachycardia on the basis that excess triiodothyronine (T3) enters the cardiac myocytes and incites positive inotropic (force of contraction) and chronotropic (rate and rhythm of contraction) activity. In other words, they result in increased force and rate of contraction of the heart.

Pulmonary embolism

A pulmonary embolism is typically the result of a migrating deep vein thrombus that has occluded a vessel in the lung vasculature. This disorder results in an increase in alveolar dead space (region not participating in gaseous exchange), hypoxaemia (low oxygen concentration in the blood) and hyperventilation (> 22 breaths per minute). The associated tachycardia is an attempt to perfuse viable lung tissue in order to counteract the low oxygen concentration and impending hypoxia.

Abnormalities of impulse formation

Abnormalities of impulse formation occur when the sinuatrial node is no longer the leading pacemaker center for the heart. In these cases, there is abnormal automaticity, and other myocardial cells gain the ability to generate depolarization. If these points, also known as ectopic foci, begin to depolarize at a faster rate than the sinuatrial node, then they will take of the pacemaker function of the heart. This is the basis for ventricular tachycardia and accelerated ventricular rhythm.

Other disorders of impulse formation include early and delayed afterdepolarizations. In early afterdepolarization, the duration of the action potential is prolonged due to opening of sodium and calcium channels that result in the membrane potential of myocardial cells being more positive. As a result, the baseline of the cells is established above the threshold potential, resulting in automatic and continuous depolarization of the cells. Electrolyte imbalances like hypokalaemia are believed to play a role in this process. This is also the rationale behind the progression of QT segment (time between ventricular depolarization and repolarization) prolongation to the more fatal Torsade de Pointes. On the other hand, delayed afterdepolarization occurs between the end of one cycle (repolarization) and the beginning of another (depolarization). Hypercalcaemic conditions as seen in digitalis toxicity and ischaemic injury to the cells may propagate this activity. This is thought to be the pathophysiology behind multifocal atrial tachycardia and atrial tachycardia.

Re-entrant circuit

It should be noted that there are two sets of fibers that conduct impulses from the sinuatrial node to the atrioventricular node and His-Purkinje system. One is a slow (α) pathway, while the other is a fast (β) pathway. Normally, waves of depolarization will travel along the β fibers faster than in α fibers. By the time the impulse reaches the atrioventricular node via the α fibers, the node would have already been depolarized by impulses from the β fibers and therefore would not be susceptible to further depolarization until it is out of its refractory state. If the conduction pathway has been increased (dilated cardiomyopathy), there is reduction in the conduction velocity of the β fibers (scar tissue, ischaemia, infarction, hyperkalaemia), or the refractory period of the cells have decreased (sympathomimetic drug), then a re-entrant circuit can be established. If these re-entry circuits are self-sustaining, then a rapid, recurrent depolarization can occur in the affected area.

If the sinuatrial node and associated fibers connecting it to the atrioventricular node is functioning normally, but there is an obstruction along the His-Purkinje pathway, then a partial or complete block may be the cause of the dysrhythmia. This phenomenon can also lead to the establishment of a reentry circuit, which may result in either a tachycardia or a bradycardia. Fibrosis of areas of myocardium, ischaemia or cardiomyocytes in protracted refraction can result in pathway block. Other noncardiac causes such as drugs and trauma may also result in the same problem.

Bypass tracts

As stated earlier, there is usually only one pathway permitting conduction of depolarizing waves from the atria to the ventricles. However, there are congenital and acquired instances in which an accessory bypass tract connects the atria to the ventricles. One such rare congenital disorder is known as the Wolf-Parkinson-White syndrome where an accessory conduction pathway known as the Bundle of Kent allows electrical activity to bypass the atrioventricular node.

Supraventricular tachycardia

There are several other ways to classify tachycardias. If the rhythmic abnormality is proximal to the bundle of His, then it is called a supraventricular tachycardia. Supraventricular tachycardias may either originate at the sinuatrial node, the atrioventricular node or the atria. This abnormality may also be subdivided based on the regularity of the rhythm. Typically, the irregular subtypes usually affect the atria, while the regular subtypes affect both atrial and atrioventricular regions of the heart.

Ventricular tachycardia

On the contrary, if the dysrhythmia occurs distal to the bundle of His it is known as a ventricular tachycardia. Ventricular tachycardia are often referred to as broad complex tachycardias that (as the name suggests) affects the ventricles. The subclassification of these abnormalities are based on the morphology of the waves (monomorphic versus polymorphic) or the duration of the abnormality (sustained versus nonsustained).  

Flutter and fibrillation

Other terms that are commonly used when discussing tachycardias are flutter and fibrillation. The former refers to an unstable rhythm with rates ranging between 250 to 400 beats per minute; depending on whether the flutter occurs in the atria  of ventricles. The latter, however, refers to quivering activity of the myocardium that does not result in blood leaving the heart. Consequently, blood may settle in the chambers of the heart and form clots that have the potential to embolize. Of note, atrial flutter may persist for years without affecting the patient adversely, but ventricular flutter is a worrisome precursor to ventricular fibrillation, which can result in sudden cardiac death.

Narrow complex tachycardia

For narrow complex tachycardia, vagal manoeuvers can result in inhibition of the atrioventricular node, resulting in a reduction of the heart rate. Vagal manoeuvers include carotid sinus massage (manually stimulating the carotid area in the neck) or Valsalva maneuvers (forcefully expiring against a closed glottis stimulate the vagus nerve, which propagates a parasympathetic response. Consequently, a negative inotropic effect is achieved. If manual techniques fail, then chemical cardioversion and negative chronotropic effect can be achieved by the bolus administration of 6 milligrams, IV of adenosine into a large vein. Adenosine also works by blocking the atrioventricular node. The drug is administered simultaneously with a saline flush via a three-way stop cock, with continuous electrocardiogram monitoring. It is important to identify the specific narrow complex tachycardia and treat the patient accordingly.

Wide complex tachycardias

Wide complex tachycardias are quite dangerous and are likely to progress to a fatal rhythm. If it is difficult to identify the underlying rhythm, then the patient should be treated as a ventricular tachycardia patient (since this is the most common cause of broad complex tachycardia). The patient should be connected to a continuous cardiac monitor and a defibrillator should be readily available.