Tachycardia

Introduction

Tachycardia, at its core, just means a fast heartbeat—over 100 beats per minute at rest—but folks search “tachycardia symptoms,” “tachycardia causes,” or “tachycardia treatment” when their heart feels like it’s sprinting in their chest. Clinically, it can signal anything from harmless caffeine jitters to serious heart disease. This article looks at tachycardia both through modern clinical evidence and real-world patient guidance, so you get the facts and practical tips. We’ll skip the fluff and dive into symptoms, diagnosis, treatments, and more.

Definition

Tachycardia is defined medically as any heart rate consistently above 100 beats per minute when at rest in adults, although thresholds may vary in children. The term itself comes from the Greek "tachy," meaning rapid, and "cardia," referring to the heart. It's important to note that tachycardia isn't a disease per se but rather a symptom or manifestation of underlying cardiac or systemic disturbances.

There are several main subtypes:

• Sinus tachycardia: the normal electrical pathway just running fast, often in response to fever, dehydration, anxiety, or exercise.
• Supraventricular tachycardia (SVT): rapid rhythms originating above the ventricles, often paroxysmal (sudden onset and termination), seen in young adults, sometimes provoked by caffeine or stimulants.
• Atrial flutter and atrial fibrillation with rapid ventricular response: disorganized atrial activity causing irregular or regular rapid heartbeats, common in older adults or those with heart disease.
• Ventricular tachycardia (VT): rapid rhythms originating in the ventricles that can reduce cardiac output and degenerate into ventricular fibrillation, posing immediate danger.
• Other specific arrhythmias: like multifocal atrial tachycardia, junctional tachycardia, and rare genetic channelopathies (e.g., long QT syndrome leading to torsades de pointes).

Clinically, tachycardia matters because sustained rates can compromise cardiac output and oxygen delivery, leading to dizziness, chest pain, syncope, or worse. It also influences long-term outcomes: chronic tachycardia can cause or exacerbate heart failure and increase stroke risk in atrial arrhythmias. Recognizing the type—sinus vs SVT vs VT—is vital for guiding treatment (like vagal maneuvers, medication, or ablation). While most people first notice palpitations or a racing heart, proper medical evaluation distinguishes harmless causes from emergencies.

In children, normal resting rates are higher—sometimes up to 120 bpm in toddlers—so pediatric definitions adjust accordingly. Some people experience inappropriate sinus tachycardia, where their heart accelerates without a clear trigger, and this can be distressing and lead to anxiety or fatigue. In everyday life, you might hear someone say “my heart is pounding,” but only with a proper measurement (like a pulse check or ECG) can tachycardia be confirmed.

Epidemiology

Estimating how common tachycardia is depends on the subtype. Sinus tachycardia is ubiquitous—virtually everyone will have an elevated heart rate during exercise, stress or illness. Persistent inappropriate sinus tachycardia is more rare, affecting about 1% of adults, predominantly women in their 20s and 30s. Supraventricular tachycardias (SVTs) like AV nodal reentrant tachycardia occur in approximately 2.25 per 1,000 persons each year, with lifetime risk estimated around 1 in 250. SVTs often present in adolescence or early adulthood, but can develop at any age.

Atrial fibrillation (AF) and atrial flutter with rapid ventricular rates contribute to tachycardia in older adults: AF affects roughly 2-4% of adults over 60, rising steeply with advancing age—nearly 10% by age 80. Men and women develop AF at similar rates, though men seem slightly higher incidence early on, while women catch up later. Ventricular tachycardia is less common in the general healthy population but more frequent in patients with prior heart attack or cardiomyopathies, seen in up to 10-15% of people with significant coronary artery disease.

Data limitations exist: many episodes of transient tachycardia go unreported if individuals dismiss palpitations as anxiety. Ambulatory monitoring (Holter, event recorders, wearbles) show up to 15% of healthy adults have brief runs of nonsustained ventricular tachycardia, often asymptomatic. Gaps in epidemiology also reflect access to healthcare—undetected arrhythmias are more common in underserved populations. In short, while brief rapid rhythms are widespread, persistent or clinically significant tachycardias are less frequent but carry important health implications.

Etiology

Tachycardia arises from a variety of causes that can be loosely divided into functional (physiologic) and organic (pathologic) categories. Understanding the root is key—are we dealing with a provoked, normal response, or is there underlying heart disease or systemic pathology?

• Functional (Physiologic) Causes
  • Exercise or Physical Activity: Increases demand for oxygen, triggering sinus tachycardia.
  • Emotional Stress or Anxiety: Releases adrenaline (epinephrine), accelerating heart rate.
  • Fever or Infection: Body’s metabolic rate ramps up, adding 10-20 bpm for each degree Fahrenheit elevation.
  • Dehydration or Hypovolemia: Lower blood volume prompts compensatory tachycardia to maintain perfusion.
  • Pregnancy: Elevated blood volume and hormonal changes raise resting heart rate by 10-20 bpm.
  • Postural Orthostatic Tachycardia Syndrome (POTS): Excessive heart rate increase (>30 bpm) upon standing, often in younger women.
• Organic (Pathologic) Causes
  • Cardiac Ischemia or Coronary Artery Disease: Damage to heart muscle can disrupt electrical pathways and trigger tachycardias.
  • Cardiomyopathies: Dilated, hypertrophic, or restrictive changes create arrhythmogenic foci.
  • Valvular Heart Disease: Mitral valve prolapse or stenosis lead to atrial enlargement and arrhythmias.
  • Electrolyte Abnormalities: Low potassium or magnesium can provoke SVT and VT—common in paitients on diuretics.
  • Thyroid Dysfunction: Hyperthyroidism classically causes sinus tachycardia or AF, sometimes with rates over 140 bpm.
  • Drug and Substance Effects: Caffeine, nicotine, alcohol binges, stimulants (cocaine, amphetamines), and over-the-counter decongestants.
  • Medications: Beta agonists (asthma), theophylline, certain antipsychotics, and digitalis toxicity.
  • Genetic Channelopathies: Long QT, Brugada syndrome, catecholaminergic polymorphic VT—rare but high risk.
  • Infiltrative Disorders: Sarcoidosis or amyloidosis affecting conduction system.

Often, multiple factors apply. For example, an anxious patient with mild hyperthyroidism may have overlapping triggers. Some causes are reversible—treating dehydration, correcting electrolyte imbalances or stopping stimulants can normalize heart rate, whereas others like cardiomyopathy may require lifelong management. Always, thorough evaluation is needed to identify which etiology is driving tachycardia in an individual.

Pathophysiology

The heart’s electrical system is like a finely tuned orchestra. In normal sinus rhythm, the sinoatrial (SA) node fires impulses at a regular rate, traveling through atrial tissue to the atrioventricular (AV) node, down the His-Purkinje pathways, and causing coordinated ventricular contraction. Tachycardia occurs when any part of this conduction system discharges too rapidly or when circuits develop that bypass usual delays.

Sinus Tachycardia: Here, the SA node itself accelerates its firing rate, usually under control of sympathetic nervous system upregulation or parasympathetic withdrawal. Fever increases metabolic demands—cells need more oxygen so heart rate goes up by around 10 bpm for every degree Celsius rise. Anxiety and pain also elevate catecholamines, bumping rates into the 100s. Sinus tachycardia is generally smooth, with P waves before each QRS complex on ECG, and a gradual onset and offset.

Reentrant Tachycardias: In SVT and some forms of VT, electrical impulses loop in circuits rather than following the standard pathway. An idealized example is AV nodal reentrant tachycardia (AVNRT), where the impulse travels down one pathway in the AV node and returns via another, creating a loop that repeats up to 250-300 bpm. On ECG this looks like narrow-complex tachycardia with absent or buried P waves. In real life, I once saw a 25-year-old yogi collapse when her AVNRT hit 220 and her BP plummeted.

Triggered Activity and Afterdepolarizations: Certain conditions like digitalis toxicity or electrolyte abnormalities produce abnormal afterdepolarizations in myocardial cells that can precipitate tachycardia. Early afterdepolarizations may lead to torsades de pointes, a polymorphic VT that twists around the ECG baseline.

Enhanced Automaticity: Some myocardial cells outside the SA node (ectopic foci) can gain pacemaker activity when exposed to high catecholamine levels, hypoxia or ischemia. They fire spontaneously and override the SA node, leading to atrial tachycardias or junctional tachycardias.

Structural and Electrical Remodeling: Chronic pressure overload, volume changes, or infarction cause fibrosis and stretching in the myocardium. These alterations break uniform conduction, creating slow pathways and obstacles around which reentry circuits form. Long-standing AF patients develop atrial enlargement; the dilated tissue fosters more ectopic beats, perpetuating a vicious cycle of tachycardia and remodeling.

Overall, tachycardia emerges from a dynamic interplay of cellular electrophysiology, autonomic influences, and structural heart characteristics. Clinicians use ECG patterns—QRS width, P wave morphology, rate variability, and response to maneuvers or drugs—to piece together the mechanism, since targeted treatment depends on knowing if it’s reentry, automaticity, or sinus node acceleration.

Diagnosis

Diagnosing tachycardia involves piecing together history, physical exam, and often ECG-based testing. Patients typically report palpitations (“butterflies” or a “thumping chest”), dizziness, shortness of breath, or even chest discomfort. In some cases, people feel fine and the tachycardia is discovered on routine check or an incidental monitor finding.

History-Taking: I ask about onset (sudden vs gradual), triggers (exercise, caffeine, stress), duration (seconds vs hours), accompanying symptoms (syncope, sweating, anxiety), and relief methods (vagal maneuvers, breath-holding). Alcohol binge history might hint at “holiday heart” syndrome—AF after drinking.

Physical Examination: Check vital signs, including orthostatic heart rates. Observe neck for jugular venous pulsations—cannon A waves suggest AV dissociation in VT. Listen for murmurs (structural disease), signs of heart failure (rales, edema), or thyroid enlargement.

Electrocardiogram (ECG): A 12-lead ECG is the gold standard for documenting rhythm. Look for narrow or wide QRS complexes, P wave presence, PR interval, and rate regularity. SVT usually has narrow QRS and regular rhythm at 150-250 bpm; VT is often wide QRS >120 ms at 100-250 bpm.

Ambulatory Monitoring: Holter monitors and event recorders help catch intermittent episodes. Implantable loop recorders may be used for infrequent, recurrent palpitations or unexplained syncope, recording up to years of data.

Labs and Imaging: Basic labs include electrolytes (K, Mg, Ca), thyroid function tests, and drug levels if digitalis or antiarrhythmics are used. Echocardiography assesses structural heart disease—ventricular function, valve abnormalities, chamber size. In select cases, stress testing or coronary angiography rules out ischemia.

Differential Considerations: Anxiety disorders, hyperthyroidism, anemia, or dehydration can mimic or coexist with tachycardia. Factitious tachycardia (e.g., induced by stimulants) deserves consideration. Ultimately, the clinician synthesizes findings—history, exam, ECG patterns, labs—to assign a subtype and plan management. Sometimes, electrophysiology studies are needed to confirm complex arrhythmias.

Differential Diagnostics

When a patient presents with tachycardia, doctors methodically rule out alternative explanations to pinpoint the exact cause. The differential spans benign, transient conditions to life-threatening emergencies.

• Sinus Tachycardia vs. SVT: Sinus tachycardia has normal P waves and gradual onset/offset, whereas SVT begins and ends abruptly and may hide P waves within QRS complexes.
• SVT vs. Atrial Flutter: Flutter often shows sawtooth flutter waves between QRS complexes at a rate of 250-350 bpm, with variable ventricular response.
• SVT vs. Ventricular Tachycardia: Widened QRS complexes (>120 ms) suggest VT; AV dissociation and capture beats further confirm VT.
• Atrial Fibrillation vs. Multifocal Atrial Tachycardia (MAT): AF has no distinct P waves and irregularly irregular RR intervals; MAT shows at least three distinct P wave morphologies and irregular rhythm, often linked to COPD exacerbations.
• Physical Conditions: Hyperthyroidism (tremor, heat intolerance), anemia (pallor, fatigue), sepsis (fever, hypotension) often present with sinus tachycardia; labs can distinguish these.
• Anxiety and Panic Attacks: Palpitations, sweating, hyperventilation can mimic SVT. Look for hyperventilation signs and ask about panic triggers. Beta blockers may help confirm if tachy is anxiety-induced vs true arrhythmia.
• Medication Effects: Sympathomimetic substances (decongestants, stimulants, digoxin toxicity) need careful history, and sometimes tox screens.

By combining targeted history questions—like “did your heart rate suddenly jump” or “how do you feel when standing up”—with focused ECG interpretation and basic labs, clinicians can separate major categories. If doubt persists, electrophysiology testing can map reentry circuits or ectopic foci. This systematic approach avoids misdiagnosis, ensuring patients receive the right regimen—whether simple hydration and reassurance or prompt cardioversion in unstable ventricular tachycardia.

Treatment

Treatment of tachycardia depends on the type, severity, and patient’s stability. Approaches include self-care maneuvers, medications, procedures, and in emergencies, electrical cardioversion.

Initial Stabilization: Always assess ABCs (airway, breathing, circulation). If a patient is hypotensive, altered, or in chest pain, prepare for immediate synchronized cardioversion.

Self-Care and Vagal Maneuvers: For stable SVT, instruct patients on Valsalva maneuver (bearing down like a bowel movement), carotid sinus massage (gently massage one side of the neck for 5–10 seconds, with caution in elderly), and diving reflex (cold water on face). These increase vagal tone, slowing AV nodal conduction and often breaking the reentry loop.

Medications:

• Beta Blockers (metoprolol, propranolol): reduce sympathetic tone and sinus rate, first-line for inappropriate sinus tachycardia and rate control in AF.
• Calcium Channel Blockers (diltiazem, verapamil): slow AV nodal conduction, helpful in SVT and rapid AF.
• Antiarrhythmics (flecainide, propafenone, amiodarone): for rhythm control in atrial arrhythmias; amiodarone used in acute VT or VF in ACLS protocols.
• Digoxin: less commonly used now but can slow ventricular response in AF with rapid rates.
• Electrolyte Repletion: IV magnesium or potassium for torsades de pointes or QT prolongation-related tachycardias.

Procedures:

• Catheter Ablation: Curative for many SVTs (e.g., AVNRT, accessory pathways) and some ventricular tachycardias, via targeted radiofrequency or cryoablation of aberrant conduction tissue.
• Electrical Cardioversion: Synchronized shock for hemodynamically unstable atrial or ventricular tachycardias; unsynchronized defibrillation reserved for pulseless VT or VF.
• Implantable Devices: Pacemakers for brady-tachy syndromes, implantable cardioverter-defibrillators (ICDs) for high-risk VT or VF survivors.

Lifestyle and Monitoring: Reducing caffeine, alcohol, and managing stress can lessen episodes of benign tachycardia. Wearables and home blood pressure monitors now include heart rate tracking—great for spotting patterns. For POTS, increasing salt and fluid intake, wearing compression stockings, and tailored exercise plans help reform autonomic balance.

When to Seek Supervision: Self-care is ok for known benign SVT breaks, but any chest pain, shortness of breath, syncope, or if tachycardia lasts >15 minutes—seek emergency care. Young patients with suspected inherited arrhythmia syndromes should be referred for genetic counseling and specialist evaluation.

Prognosis

The outlook for tachycardia varies widely based on type, underlying causes, and treatment. Sinus tachycardia related to transient issues like fever or dehydration typically resolves completely once the trigger is addressed. Similarly, episodes of SVT in otherwise healthy individuals often have excellent long-term outcomes—with ablation success rates exceeding 90%, many remain symptom free.

Chronic atrial fibrillation or flutter carries increased risks of stroke, heart failure progression, and requires lifelong management. Rate or rhythm control strategies combined with anticoagulation can reduce stroke risk by up to two-thirds, but patients must adhere to medication and monitoring regimens. Ventricular tachycardia in patients with structural heart disease can be life threatening; however, implantable cardioverter-defibrillators (ICDs) have dramatically improved survival. Some may still experience recurrent shocks and require medication adjustments or repeat ablations.

Factors influencing prognosis include age, comorbid conditions (like hypertension, diabetes, prior myocardial infarction), left ventricular function, and adherence to therapy. Psychological impact—anxiety about recurrent palpitations—can affect quality of life. Overall, with modern diagnostics, tailored treatments, and patient education, most tachycardia sufferers can expect substantial symptom relief and reduced complications. Early intervention and routine follow-ups are key to keeping the heart rate—and worry—under control.

Safety Considerations, Risks, and Red Flags

While many forms of tachycardia are benign, knowing who’s at high risk and recognizing warning signs can be lifesaving. Always watch for:

• Hemodynamic Instability: Weak pulse, low blood pressure, altered mental status—signs of poor perfusion requiring immediate attention.
• Chest Pain or Pressure: Could indicate ischemia or myocardial infarction.
• Syncope or Near-Syncope: Passing out or feeling faint suggests inadequate cerebral blood flow; think ventricular tachycardia or severe brady-tachy syndromes.
• Shortness of Breath or Pulmonary Edema: Rapid rates limit cardiac filling, raising risk of heart failure exacerbation.
• Electrolyte or Drug Imbalances: Hypokalemia, hypomagnesemia, digitalis toxicity—correct these urgently to prevent torsades de pointes or ventricular fibrillation.
• Known Structural Heart Disease: History of cardiomyopathy, valve disease, or coronary artery disease increases risk of life-threatening arrhythmias.
• Genetic Arrhythmia Syndromes: Family history of sudden cardiac death, long QT syndrome, Brugada syndrome—urgent specialist referral recommended.

Delayed treatment of serious tachycardias can lead to cardiogenic shock, stroke (in atrial arrhythmias), or sudden cardiac death. In contrast, minor episodes triggered by stress or caffeine might settle on their own but still warrant evaluation if recurrent. If in doubt always err on the side of caution—getting checked in an emergency department or by a cardiologist quickly can prevent nasty complications.

Modern Scientific Research and Evidence

Contemporary research on tachycardia spans basic electrophysiology to large clinical trials testing new drugs and ablation techniques. Some notable trends:

• Mapping Technology Advances: High-density 3D electroanatomic mapping systems allow operators to visualize circuits in real time during ablation, improving success rates for complex SVTs and ventricular tachycardias.
• Wearable and Remote Monitoring: Smartwatches and wearable ECG patches have become validated tools for detecting atrial fibrillation and other arrhythmias, enabling earlier diagnosis and intervention. A recent study showed patient-generated ECG data led to a 20% increase in early AF detection compared to standard care.
• Catheter Design Innovations: Cryoablation tools and irrigated tip radiofrequency catheters reduce collateral tissue damage and lower complication rates.
• Pharmacologic Developments: New antiarrhythmics like vernakalant for rapid AF conversion, and dronedarone for long-term AF maintenance, have added options beyond amiodarone and sotalol, though each comes with specific safety profiles.
• Genetic and Molecular Insights: Genome-wide association studies (GWAS) have identified genetic variants linked to atrial fibrillation and QT prolongation; this may pave the way for precision medicine approaches in the future.
• Telehealth Impact: Remote device programming and telemetric follow-up in ICD and pacemaker patients reduce clinic visits without compromising outcomes.
• Clinical Trials: Large randomized trials, such as CABANA (atrial fibrillation catheter ablation vs drug therapy), have provided mixed results—highlighting ongoing debates about optimal first-line strategies.

Despite these advances, uncertainties remain: optimal timing for ablation in symptomatic AF, long-term effects of low-level radiation exposure from mapping procedures, and defining the best management for POTS-related tachycardia. Ongoing studies are exploring neuromodulation, gene therapies, and novel biologic agents targeting specific ion channels. In real world, translating cutting-edge science into universally accessible care is the next major hurdle.

Myths and Realities

• Myth: Tachycardia always means heart disease.

  Reality: While it can signal structural issues, sinus tachycardia from fever, stress, or caffeine is common and often benign. Clinical context and ECG patterns clarify the picture.

• Myth: You’ll always feel palpitations if your heart races.

  Reality: Some individuals have “silent” tachycardia discovered only on monitors—no subjective symptoms but potential risk if sustained.

• Myth: Carotid massage is dangerous and never recommended.

  Reality: When done correctly and in the right patient, carotid sinus massage is a safe, effective SVT treatment.

• Myth: All tachycardia needs immediate electrical cardioversion.

  Reality: Only unstable patients—low blood pressure, confusion, chest pain—require emergent cardioversion. Many stable cases respond to meds or maneuvers.

• Myth: Antiarrhythmics cure arrhythmias permanently.

  Reality: Medications often reduce episodes and control rate, but side effects and breakthrough arrhythmias can occur. Ablation may offer more definitive results.

• Myth: Pregnancy tachycardia always harms mother and baby.

  Reality: Mild sinus tachycardia is expected due to increased blood volume and is usually harmless; persistent arrhythmias require evaluation but rarely jeopardize healthy pregnancies.

• Myth: Anxiety-induced palpitations should be ignored.

  Reality: While anxiety can trigger sinus tachycardia, ruling out cardiac causes first is essential—jumping to mental health labeling may delay needed cardiac care.

Separating myth from fact empowers patients: if you hear something online, discuss it with your clinician before assuming the worst or any DIY treatment. Evidence-based guidance beats rumor every time.

Conclusion

Tachycardia, simply put, is a heart rate over 100 bpm at rest, but beneath that definition lies a spectrum from harmless sinus responses to potentially lethal ventricular arrhythmias. Recognizing key symptoms—palpitations, dizziness, chest discomfort—and seeking timely evaluation can distinguish occasional benign episodes from emergencies. Diagnosis hinges on ECG patterns, supportive labs, and careful history, illuminating whether it’s sinus tachycardia, an SVT loop, atrial fibrillation, or ventricular tachycardia.

Management ranges from self-care vagal maneuvers for stable SVT to medication therapies—beta blockers, calcium channel blockers, antiarrhythmics—and advanced procedures like catheter ablation or cardioversion in more severe cases. Prognosis varies: many achieve symptom control and excellent long-term outcomes, while chronic atrial arrhythmias and ventricular tachycardia in heart disease require ongoing monitoring and, often, implantable devices.

Importantly, understanding when to call a doctor—persistent rapid heart rate, chest pain, syncope, or significant shortness of breath—can prevent complications like heart failure, stroke, or sudden cardiac death. Continued research is refining tools from wearables to genetic insights, bringing us closer to personalized arrhythmia care. Remember, if something feels off with your heartbeat, professional guidance beats self-diagnosis any day. Stay informed, stay safe, and work with your healthcare team to keep your heart’s rhythm steady.

Frequently Asked Questions (FAQ)

• Q: What exactly is tachycardia?
  A: Tachycardia is a resting heart rate above 100 beats per minute in adults. It’s a sign that the heart’s electrical system is firing too fast, and can be due to many benign or serious causes.
• Q: What are the common symptoms of tachycardia?
  A: Most people notice palpitations, a fluttering or thumping feeling. You might also experience dizziness, chest discomfort, shortness of breath, sweating, or in severe cases, fainting.
• Q: Why does tachycardia occur?
  A: Causes range from normal responses—like exercise, fever, stress or dehydration—to pathologic reasons such as hyperthyroidism, anemia, heart disease, electrolyte imbalances, and drug effects.
• Q: How is tachycardia diagnosed?
  A: Clinicians take a detailed history, perform a physical exam, and record an ECG. Additional tests include Holter monitoring, blood tests (electrolytes, thyroid), and echocardiography.
• Q: When is tachycardia an emergency?
  A: Seek immediate care if you have chest pain, severe shortness of breath, hypotension, confusion, or syncope. These could signal life-threatening arrhythmias like ventricular tachycardia.
• Q: Can lifestyle changes help manage tachycardia?
  A: Yes. Reducing caffeine, alcohol, and stress, staying hydrated, and following a supervised exercise plan can lower episodes of benign sinus tachycardia or POTS.
• Q: What medications treat tachycardia?
  A: Beta blockers, calcium channel blockers, antiarrhythmics (such as amiodarone), and digoxin are common. Electrolyte repletion (magnesium, potassium) also helps certain arrhythmias.
• Q: Is catheter ablation always needed?
  A: No. Many SVTs respond to vagal maneuvers or medications. Ablation is considered when arrhythmias recur, cause significant symptoms, or when drugs are ineffective or poorly tolerated.
• Q: How does atrial fibrillation differ from other tachycardias?
  A: AF shows an irregularly irregular rhythm without clear P waves on ECG. It’s often chronic and linked to stroke risk, requiring both rate/rhythm control and anticoagulation.
• Q: Can children get tachycardia?
  A: Yes. Pediatric resting heart rates are higher, so definitions adjust by age. SVTs are common in infants and children, often presenting as sudden rapid pulses and irritability.
• Q: How long does a tachycardia episode last?
  A: Episodes vary—from seconds in paroxysmal SVT to chronic atrial fibrillation that lasts days or is persistent. Duration helps guide whether to use maneuvers, drugs, or cardioversion.
• Q: Can anxiety cause tachycardia?
  A: Definitely. Anxiety or panic attacks release adrenaline, speeding up the heart. But heart-focused evaluation is important first, to rule out true arrhythmias before attributing to anxiety.
• Q: When should I see a cardiologist?
  A: If tachycardia is recurrent, prolonged, symptomatic, or if initial tests (ECG, labs) are abnormal, getting a specialist opinion helps tailor advanced diagnostics or therapies.
• Q: Is tachycardia hereditary?
  A: Some arrhythmias have genetic links (channelopathies, familial AF). Family history of early sudden death or arrhythmias warrants screening and possibly genetic counseling.
• Q: Can wearables detect tachycardia?
  A: Yes. Many smartwatches and patches continuously monitor heart rate and can alert users to sustained high rates, prompting medical evaluation and early diagnosis.