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Explain me what tachycardia is

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Explain me what tachycardia is

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ECG showing sinus tachycardia

This diagnostic image series presents three successive 12-lead electrocardiograms (ECGs) documenting the evolution of cardiac rhythm and repolarization in a clinical case. Panel A displays a baseline ECG showing a sinus rhythm with prominent ST-segment depressions, most notable in the precordial leads V3 through V5, suggesting acute subendocardial ischemia or NSTEMI. Panel B illustrates a subsequent tracing characterized by a rapid supraventricular tachycardia, showing frequent QRS complexes and persistent baseline oscillations. Panel C demonstrates a follow-up ECG where the rhythm has returned to sinus tachycardia with a partial resolution of the previous ST-segment abnormalities, although minor depressions remain visible in the anterior leads. These images are essential for teaching the interpretation of dynamic ECG changes associated with acute coronary syndromes and tachycardia-induced ischemia in an emergency or critical care setting.

This diagnostic image series presents three successive 12-lead electrocardiograms (ECGs) documenting the evolution of cardiac rhythm and repolarization in a clinical case. Panel A displays a baseline ECG showing a sinus rhythm with prominent ST-segment depressions, most notable in the precordial leads V3 through V5, suggesting acute subendocardial ischemia or NSTEMI. Panel B illustrates a subsequent tracing characterized by a rapid supraventricular tachycardia, showing frequent QRS complexes and persistent baseline oscillations. Panel C demonstrates a follow-up ECG where the rhythm has returned to sinus tachycardia with a partial resolution of the previous ST-segment abnormalities, although minor depressions remain visible in the anterior leads. These images are essential for teaching the interpretation of dynamic ECG changes associated with acute coronary syndromes and tachycardia-induced ischemia in an emergency or critical care setting.

Two-part 12-lead electrocardiogram (ECG) comparison demonstrating drug-induced arrhythmia. (a) Initial ECG showing sinus bradycardia at approximately 40 bpm. Findings include narrow QRS complexes, prolonged QT interval, and T-wave abnormalities (inversions in inferior leads II, III, and aVF). This baseline demonstrates common findings in patients on QT-prolonging agents like sotalol. (b) ECG recorded during a syncopal event, displaying a transition from sinus rhythm into a polymorphic ventricular tachycardia (Torsades de Pointes). The tachycardia is characterized by wide QRS complexes (duration >120ms) with a shifting axis, rotating around the isoelectric line at a rapid rate of 150-200 bpm. The visual sequence illustrates the clinical progression from drug-induced QT prolongation to life-threatening ventricular arrhythmia. Educational focus is on identifying bradycardia, QT prolongation, and the morphology of polymorphic ventricular tachycardia in the context of syncope.

Two-part 12-lead electrocardiogram (ECG) comparison demonstrating drug-induced arrhythmia. (a) Initial ECG showing sinus bradycardia at approximately 40 bpm. Findings include narrow QRS complexes, prolonged QT interval, and T-wave abnormalities (inversions in inferior leads II, III, and aVF). This baseline demonstrates common findings in patients on QT-prolonging agents like sotalol. (b) ECG recorded during a syncopal event, displaying a transition from sinus rhythm into a polymorphic ventricular tachycardia (Torsades de Pointes). The tachycardia is characterized by wide QRS complexes (duration >120ms) with a shifting axis, rotating around the isoelectric line at a rapid rate of 150-200 bpm. The visual sequence illustrates the clinical progression from drug-induced QT prolongation to life-threatening ventricular arrhythmia. Educational focus is on identifying bradycardia, QT prolongation, and the morphology of polymorphic ventricular tachycardia in the context of syncope.

This composite medical visual contains two primary elements: diagnostic neuroimaging and a cardiovascular tracing. The top panel (A) displays a sequence of five axial T2-weighted brain MRI scans ranging from the cranial vault to the base of the skull. These images depict normal neuroanatomy, including the cerebral cortex, subcortical white matter, lateral ventricles, basal ganglia, brainstem, and cerebellum, with no visible intracranial pathology or structural abnormalities. The bottom panel (B) is a standard 12-lead electrocardiogram (ECG) printed on grid paper. The tracing shows a narrow-complex rhythm with a visible P wave preceding each QRS complex, consistent with sinus rhythm. The heart rate is notably elevated, approximately 115 beats per minute, indicating sinus tachycardia. The combination of normal brain imaging and an ECG showing sinus tachycardia is used in a clinical context to evaluate post-traumatic autonomic dysfunction, such as postural orthostatic tachycardia syndrome (POTS) or other dysautonomias following a traumatic brain injury (TBI).

This composite medical visual contains two primary elements: diagnostic neuroimaging and a cardiovascular tracing. The top panel (A) displays a sequence of five axial T2-weighted brain MRI scans ranging from the cranial vault to the base of the skull. These images depict normal neuroanatomy, including the cerebral cortex, subcortical white matter, lateral ventricles, basal ganglia, brainstem, and cerebellum, with no visible intracranial pathology or structural abnormalities. The bottom panel (B) is a standard 12-lead electrocardiogram (ECG) printed on grid paper. The tracing shows a narrow-complex rhythm with a visible P wave preceding each QRS complex, consistent with sinus rhythm. The heart rate is notably elevated, approximately 115 beats per minute, indicating sinus tachycardia. The combination of normal brain imaging and an ECG showing sinus tachycardia is used in a clinical context to evaluate post-traumatic autonomic dysfunction, such as postural orthostatic tachycardia syndrome (POTS) or other dysautonomias following a traumatic brain injury (TBI).

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tachycardia

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Tachycardia

Tachycardia simply means a fast heart rate - defined as a resting heart rate greater than 100 beats per minute in an adult (normal resting rate is roughly 60-100 bpm) - Guyton and Hall Textbook of Medical Physiology.

Why it happens

The sinoatrial (SA) node is the heart's natural pacemaker, and anything that increases its excitability or firing rate speeds up the heart. Common causes include:
  • Fever - each 1°F rise in body temperature raises heart rate by about 10 bpm (about 18 bpm per °C), because higher temperature speeds up the metabolic rate of the SA node itself. This trend reverses only at very high temperatures (~105°F/40.5°C), where the heart muscle starts to weaken.
  • Sympathetic nervous system stimulation - stress, pain, exercise, or reflex responses to low blood pressure (e.g., after severe blood loss) can push the heart to 150-180 bpm.
  • Dehydration or blood loss/anemia - the heart compensates for reduced blood volume or oxygen-carrying capacity by beating faster.
  • Toxic or metabolic conditions of the heart - e.g., thyrotoxicosis, certain drugs/stimulants.
  • Weakened myocardium - a failing heart pumps less blood per beat, lowering blood pressure and triggering sympathetic reflexes that raise rate to compensate.
(Guyton and Hall Textbook of Medical Physiology, p. 1358-1359)

Clinical classification

Tachycardias are broadly split by where they originate and QRS width on ECG:
  • Sinus tachycardia - normal P-wave-before-QRS pattern, just faster (physiologic response to fever, pain, exercise, anemia, hyperthyroidism, etc.)
  • Supraventricular tachycardia (SVT) - arises above the ventricles (atrial or AV-nodal); typically narrow QRS (<0.12 sec)
  • Ventricular tachycardia (VT) - arises in the ventricles; wide QRS (≥0.12 sec), more dangerous, can degenerate into ventricular fibrillation
  • Torsades de pointes - a specific polymorphic VT linked to QT prolongation (e.g., from certain drugs), which can cause syncope or sudden cardiac arrest
Clinical management follows an ACLS-style algorithm: assess airway/breathing/circulation, give oxygen, get a 12-lead ECG, then branch based on whether the QRS is narrow or wide and whether the rhythm is regular or irregular - guiding use of vagal maneuvers, adenosine, or rate-controlling drugs like beta-blockers/calcium channel blockers (The Washington Manual of Medical Therapeutics, p. 7635-7658).
Here's an ECG example showing sinus tachycardia (narrow QRS, P wave before every QRS, rate ~115 bpm):
ECG showing sinus tachycardia alongside normal brain MRI in a post-traumatic autonomic dysfunction workup

Recent evidence note

A 2024 systematic review of registered trials found the current evidence base for ventricular tachycardia treatments (especially catheter ablation) still has gaps in study design and long-term outcome data (PMID: 38821759), and a separate 2024 systematic review reported promising early outcomes for pulsed-field ablation as a newer VT treatment option (PMID: 39350646). These relate specifically to the more serious ventricular tachycardia subtype rather than the general definition above, and don't contradict the core physiology.
If you want, I can go deeper into any specific type (SVT, VT, atrial fibrillation with rapid ventricular response) or into how it's diagnosed/treated in a particular clinical setting.
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