Tachyarrhythmias are abnormal heart rhythms with a pulse rate of >100 beats per minute (bpm). This can be due to a variety of causes, including physiological and pathological, and is a commonly encountered issue whilst on the wards – a patient’s heart rate contributes to their NEWS score (National Early Warning Score) and thus may be a reason (alongside other observations) as to why you’re asked to see a patient.
It is useful to remind ourselves of the physiology of the heart at this point, and appreciate the relevance of a raised heart rate (HR). Remember, the mean arterial blood pressure (MAP) is very important when considering organ perfusion. The MAP is a function of the cardiac output (CO) and the systemic vascular resistance (SVR), where the CO is determined by the stroke volume (SV) multiplied by the heart rate.
MAP = CO x SVR, CO = SV x HR
As such, if there is a change in one of these parameters (SVR, SV, or HR), then we can expect any of the other values to compensate to maintain an appropriate blood pressure. The classic example is during sepsis, where infection causes vasodilation and a fall in the SVR, thereby causing a rise in the HR to prevent haemodynamic collapse. Therefore, if a patient has a raised HR, always consider why this may be occurring from a haemodynamic perspective.
In the normal heart, the heart rate (HR) is determined by the sinoatrial node (SAN), and the interaction between the sympathetic and parasympathetic nervous systems. At rest, the parasympathetic nervous system predominates, and the resting HR is set between 60-100 bpm. Where there is an increase in the sympathetic outflow, therefore, or a reduction in parasympathetic stimulation to the heart, there will be an increase in the HR to cause sinus tachycardia (a HR >100 bpm where the pacemaker impulse originates from the SAN).
Causes of increased sympathetic outflow
• ‘Fight or flight’ response
• Emotion: fear, anger, nervousness, excitement, bereavement
• Stress response
• Pain and discomfort
Causes of reduced parasympathetic outflow
• Respiratory-induced sinus arrhythmia (inspiration phase)
• Post cardiac transplant – absence of vagal stimulation, owing to nerve severance, leads to a HR set by the ‘natural’ internal pacemaker of the transplanted heart’s sinoatrial node (SAN) at 100-110 bpm
There are various pathological causes of tachycardia, and these can be thought of as intrinsic (cardiac) causes, and extrinsic (non-cardiac) causes. Moreover, it is helpful to subclassify cardiac causes into regular-and-irregular, and narrow-and-broad complex tachycardias. The latter is further classified into monomorphic and polymorphic tachycardias (see the flow chart, and table, below).
Intrinsic causes of tachyarrhythmias are usually due to an abnormal electrical focus (located in the atria, conducting system, or the ventricles) that overrides the rate set by the SAN, or due to a reentry circuit within the heart – remember, the HR will be determined by any pacemaker / electrical focus that is depolarising at the fastest rate.
Risk factors associated for developing a tachyarrhythmia include: cardiac ischaemia (i.e., previous MI, ischaemic heart disease), presence of an accessory pathway, age, smoking, alcohol, left ventricular systolic dysfunction (LVSD) and recreational drug use (sympathomimetics, i.e., cocaine)
The flow chart below shows the potential causes of tachycardia. Sinus tachycardia is not included in this flow chart, but would otherwise cause a narrow complex, regular tachycardia in the absence of any conduction abnormalities.
AF: atrial fibrillation, AV: atrioventricular, AVNRT: atrioventricular nodal re-entry tachycardia, AVRT: atrioventricular re-entry tachycardia, SVT: supraventricular tachycardia, VT: ventricular tachycardia
SVT*: any cause of regular tachycardia originating from above the ventricle
Aberrancy**: any form of abnormal conduction of the electrical impulse (i.e., left bundle branch block)
For those who prefer tables, below is another way to think about the cardiac causes of tachycardia. Similarly, sinus tachycardia is not included in this table.
|Narrow complex tachycardia||Broad complex tachycardia|
|Regular rhythm||Atrial tachycardia|
Atrioventricular re-entrant tachycardia (AVRT)
Atrioventricular nodal re-entrant tachycardia (AVNRT)
|Monomorphic ventricular tachycardia |
Supraventricular tachycardia* with aberrancy**
|Irregular rhythm||Atrial fibrillation with rapid ventricular response|
Multifocal atrial tachycardia
Atrial flutter with variable AV block
|Atrial fibrillation with aberrancy |
Multifocal atrial tachycardia with aberrancy Polymorphic ventricular tachycardia
*A supraventricular tachycardia (in this context) is used to describe any regular, abnormal tachycardia that originates from above the ventricles (i.e., atrial tachycardia, AVRT, AVNRT)
**The term aberrancy (or aberrant conduction) describes an abnormality of conduction through the ventricles that cause a widened QRS complex (broad complex).
Remembering back to fundamental physiology, we can derive multiple reasons as to what would cause a non-cardiac origin of the tachycardia. However, further causes can be seen below and, although not comprehensive, the mnemonic: ABCDEFG HIT can be a helpful memory aid.
In the below, we have included congestive cardiac failure (CCF) in the mnemonic, as acute decompensation of CCF can often be caused by non-cardiac issues (i.e., infection). It also helps with the mnemonic. However, it is worth remembering that having severe LVSD (left ventricular systolic dysfunction) in itself is a very arrhythmogenic state, even when not decompensated (whether from LV dilatation or scar tissue from previous infarcts, etc)- this is why implantable cardioverter defibrillators (ICDs) are implanted into these types of patients. Severe LVSD tends to cause a lot of ventricular arrhythmias, and it can be an arrhythmia that causes decompensation in the first place. This is why LVSD is also included in the cardiac causes above.
|Blood loss||Anaemia, acute blood loss (i.e., secondary to trauma)|
|Congestive cardiac failure* (Pulmonary oedema)||During acute decompensation in an attempt to maintain CO|
|Drugs||Aminophylline, atropine, salbutamol, caffeine, nicotine, sympathomimetics (i.e., cocaine, MDMA)|
|Fever||Causes an increase in the basal metabolic rate, increasing metabolic demand and need for O2 delivery1|
|Glucose||Hypoglycaemia, DKA, HHS|
|Hyper / hypo –||Hypovolaemia, hyperthyroidism (thyrotoxicosis)|
|Infection (sepsis)||Causes vasodilation and reduces the SVR|
|Trauma||Cardiac tamponade*, pain and / or blood loss, tension pneumothorax|
History and symptoms
When taking a history, it is important to be comprehensive and to proceed in a structured manner, asking first with the presenting complaint. Then proceed through the history up to, and including, the system’s review.
Tachycardia does not always cause symptoms alone, and it may manifest via another underlying issue (i.e., left leg cellulitis causing leg pain). However, particularly in instances of a cardiac cause, common and important features you should always enquire about include:
• Chest pain (and if relieved with GTN)
• Shortness of breath/dyspnoea
• Dizziness/syncope / light-headedness
The above symptoms would be even more concerning for cardiac disease if they occurred in conjunction with exercise.
Other features to consider include other causes of tachycardia, as outlined earlier, and these should be included in the general history taking. For example, when exploring the patient’s social history, you can enquire about the acute use of alcohol and sympathomimetics / illicit drug use, or if the patient complains of a productive cough, this would raise concerns for an underlying chest infection.
Examination – signs
All patients presenting with an elevated HR should be approached using an A-E examination. The standard examination is not always informative, but certain features in the examination may be indicative of particular diagnoses / causes / precipitating factors. Cardiac-specific signs include2:
• Cannon-a-waves in the JVP
• Features of heart failure (i.e., pulmonary oedema, SOB, pitting oedema, etc.)
• Features of shock (i.e., cold, clammy, confused, haemodynamic compromise / low blood pressure / raised shock index, etc.)
• Parasternal right ventricular (RV) heave – a PE may cause RV strain
• S3 – added heart sound due to blood filling against a very compliant LV wall
• Syncope (loss of consciousness)
• Variability of the sound of S1 – suggestive of AV dissociation
The main diagnostic investigation that all patients should have is a 12-lead ECG. The ECG can offer a huge plethora of information and is vital in helping determine underlying causes.
Diagnostic investigations, alongside a focused history and examination, should include2:
|1st line investigations||Further investigations (to consider)|
|12 lead ECG||24hr Holter monitor|
|Full blood screen*||Event recorder / loop recorder|
The management of tachycardia should first be determined by the clinical status of the patient using an A-E approach. In any patient with haemodynamic instability and / or ‘life-threatening features’ (shock, syncope, myocardial ischemia, or heart failure), they should be managed as part of the Resuscitation Council UK’s guidelines3, as seen further below.
It should be remembered that most tachycardias are a symptom of an underlying condition i.e., sepsis. If the patient is haemodynamically stable, then waiting for the treatment of the trigger to work i.e., antibiotics is usually the best approach. This is not to say, however, that all tachycardias are due to an underlying, non-cardiac condition (as we have discussed above).
It is important to involve senior support early in patient management, especially if a cardiac cause is suspected, as this would need to be escalated to cardiology.
The Resuscitation Council UK Guidelines 2021
Image sourced from Resuscitation Council UK: 2021 Resuscitation Guidelines from URL: https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf
- Launey Y, Nesseler N, Mallédant Y, Seguin P. Clinical review: fever in septic ICU patients–friend or foe?. Crit Care. 2011;15(3):222. doi:10.1186/cc10097.
- Assessment of Tachycardia. BMJ Best Practice. [Internet]. Accessed June 2022. Available from URL: https://bestpractice.bmj.com/topics/en-gb/830/diagnosis-approach
- BMJ Best Practice: Assessment of Tachycardia
- CV Physiology Cardiovascular Concepts
- Patient UK: Narrow complex tachycardias
- Patient UK: Broad complex tachycardias
- Resuscitation Council UK: 2021 Resuscitation Guidelines
Written by Dr Steven Scholfield (FY3)
Reviewed and edited by Dr Lucy Priestner (Cardiology ST4)
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