The heart has the enormous responsibility of circulating blood throughout the entire body. It is able to achieve this feat with timed, rhythmic contractions without conscious effort. Cardiac myocytes have the ability to depolarize without an extrinsic stimulus. A specialized group of cardiac myocytes located in the rostral aspect of the right atrium (adjacent to the insertion of the superior vena cava), known as the sinoatrial node, sets the heart’s rate, rhythm and regularity at which the cells depolarize. As a result, the sinoatrial node is referred to as the pacemaker of the heart.
The heart rate (HR), as well as the stroke volume (SV) – volume of blood ejected from the heart with each contraction – both directly affect the cardiac output:
- CO=HR ×SV
The major problem with cardiac dysrhythmias is that they alter the cardiac output. In the case of tachyarrhythmias, the heart is beating too fast to allow adequate filling of the ventricular chambers. Consequently, it is unable to eject sufficient blood to supply the organs of the body (especially the brain, kidneys and lungs).
The normal flow of electrical activity across the heart is such that depolarization of the sinoatrial node result in a spread of electrical current across the right and left atria (P wave on ECG). Once the wave of depolarization arrives at the atrioventricular node (at the insertion of the septal leaflet of the tricuspid valve in the right atrium), it passes through the bundle of His. Shortly thereafter, the electrical activity is conducted along the left and right bundle branches and then into the Purkinje fibers (QRS complex on ECG). Synchronous contraction of the myocardium is made possible by the presence of tight junctions at the cellular level that facilitate rapid conduction of electrical signals across the heart.
The normal range for adult heart rates (at rest) goes from 60 to 100 beats per minute (bpm). It is important to note that the defined ranges for abnormal heart rates vary by age for neonates through to adolescents, as follows:
- 0 - 7 days: 95 - 160 bpm
- 1 - 3 weeks: 105 - 180 bpm
- 1 - 6 months: 110 - 180 bpm
- 6 - 12 months: 110 - 170 bpm
- 1 - 3 years: 90 - 150 bpm
- 4 - 5 years: 65 - 135 bpm
- 6 - 8 years: 60 - 130 bpm
- 9 - 16 years: 60 - 110 bpm
- > 16 years: 60 - 100 bpm
An individual with a heart rate below their respective lower limit would be experiencing bradycardia. On the other hand, if the patient’s heart rate is elevated above the normal upper limit, then they would be experiencing tachycardia. However, it should be noted that individuals who are athletic may have a normal heart rate in the mid-50s, which is normal for that individual (i.e. physiologic bradycardia).
Collectively, tachycardia and bradycardia fall under a much larger umbrella term referring to the rate, rhythm and regularity of the heart rate known as dysrhythmias. They can be classified by aetiology (physiological, pharmacological or pathological tachycardia), by regularity (regular or irregular) or by electrocardiographic changes in the QRS complex (narrow < 0.12 ms; wide > 0.12 ms). Recall that the QRS complex on electrocardiogram depicts the time taken for the ventricles to contract. This article will be focusing on some of the different types of tachydysrhythmias that exist, the underlying pathophysiology as well as the treatment and possible complications of the same.
As previously stated, tachycardia refers to an abnormal increase in heart rate above the upper limit of normal for the patient’s age range. A patient who presents with tachyarrhythmias may not have any intrinsic abnormalities of the heart. However in some patients, there may be an underlying pathology that is affecting myocardial conductivity. The term tachyarrhythmia is more suitable as it includes disorders that are both abnormally fast and may have an abnormal rhythm.
There is an eclectic collection of causes of tachyarrhythmias. It may be easier to think of these causes as those originating outside the heart (non-cardiac) and those caused by a disease process within the heart (cardiac). However, the specific cause of the tachyarrhythmia (if one exists) is often dependent on the type of tachyarrhythmia the patient has. Some general non-cardiac causes of tachyarrhythmias are listed below; aetiologies due to cardiac abnormalities will be discussed further under pathophysiology. However, this is not an exhaustive one, as there are many other possible causes for an abnormally elevated heart rate:
- Physiological Causes
- Pathological Causes
- Pulmonary embolism
- Pharmacological Causes
Pathophysiology of Non-Cardiac Causes of TachycardiaAlthough the heart has innate automaticity, its contractility is influenced by extracardiac factors (such as the automatic nervous system and pharmacological agents) as well as loop feedback mechanisms to maintain cardiac output. Physiological increase in heart rate associated with exercise is intended to increase the cardiac output in order to keep up with the body’s oxygen demand. Emotional changes (fear, anxiety and euphoria) stimulate the sympathetic response which results in the release of catecholamines. These catecholamines act on adrenergic receptors at the sinoatrial node and subsequently increase the automaticity (i.e. frequency of depolarization) of the sinoatrial node cells and by extension, increases the rate of contraction of the heart.
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 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 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.
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.
Pathophysiology of Cardiac Causes of Tachycardia
Cardiac causes of tachyarrhythmias may either be a result of disturbance in the formation of an electrical impulse (i.e. abnormality of the sinoatrial node) or an alteration of the conduction of the same (e.g. bundle branch block, Wolf-Parkinson-White syndrome).
Abnormalities of impulse formation
Abnormalities of impulse formation occur when the sinoatrial 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 sinoatrial 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.
It should be noted that there are two sets of fibers that conduct impulses from the sinoatrial 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 sinoatrial 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.
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.
Types of 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 sinoatrial 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.
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 commonly 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.
The management of any patient presenting for emergent care is to assess their Airway, Breathing and Circulation. Any abnormalities noted in these three fundamental systems should be addressed and stabilized urgently. Intravenous (IV) accesses should also be sited and the patient should be connected to essential monitors, including blood pressure, electrocardiogram and pulse oximetry. At the time of IV placement, complete blood count, and urea and electrolytes can be taken off to asses for any haematological cause of the tachydysrhythmia.
An easy way to remember cardiac causes of tachyarrhythmias is to think of them in terms of regularity and QRS wave morphology. This classification system will further guide the mode of treatment for these disorders. Tachyarrhythmias may either be regular or irregular; furthermore, the electrocardiographic representations of the heart’s electrical activity may reveal a narrow QRS complex (normal ventricular depolarization) or a widened QRS (prolonged ventricular depolarization):
- Narrow QRS
- Sinus tachycardia
- Atrial tachycardia
- Junctional tachycardia
- Atrial flutter
- Atrial fibrillation
- Atrial flutter with variable block
- Multifocal atrial tachycardia
- Premature atrial contraction
- Wide QRS
- Supraventricular tachycardia with aberrancy
- Ventricular tachycardia
- Atrial fibrillation with bundle branch block
- Polymorphic ventricular tachycardia (Torsade de Pointes)
- Premature ventricular contraction
Narrow complex tachycardiaFor 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 manoeuvres (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 atropine into a large vein. Atropine 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.
One of the biggest skills that a clinician has is the ability to take a thorough history. The patient’s experience during their time of illness will clue the physician into what could possibly be the problem. Tachycardia by itself is not a diagnosis, but rather a sign of an underlying disorder. Therefore it is imperative that a thorough history is taken so that any potentially life threatening causes of tachycardia (usually associated with chest pain, shortness of breath and a history of heart disease) can be addressed immediately. Pay particular attention to:
- a history of palpitations
- the onset of tachyarrhythmia
- regularity of tachyarrhythmia
- speed of the tachyarrhythmia
- shortness of breath
- chest pain
- loss of consciousness
Patients who present to the emergency room or general practitioner inadvertently will have their vital signs checked on that visit. It’s during this time the clinician may notice that the patient has an elevated heart rate. This can either be done with monitors such as a pulse oximeter or electrocardiogram, or clinically by palpating the peripheral or central pulses and counting the number of beats within a minute. When clinically assessing the pulses, it is important to compare peripheral pulses with each other (i.e. left and right radial pulses) as well as with a central pulse (i.e. right radial with carotid pulse). This is done to verify whether or not the pulse rate is regular or irregular.