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Clinical ECG Interpretation

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  1. Introduction to ECG Interpretation
    6 Chapters
  2. Arrhythmias and arrhythmology
    24 Chapters
  3. Myocardial Ischemia & Infarction
    22 Chapters
  4. Conduction Defects
    11 Chapters
  5. Cardiac Hypertrophy & Enlargement
    5 Chapters
  6. Drugs & Electrolyte Imbalance
    3 Chapters
  7. Genetics, Syndromes & Miscellaneous
    7 Chapters
  8. Exercise Stress Testing (Exercise ECG)
    6 Chapters
Section 2, Chapter 12
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Sinus tachycardia & Inappropriate sinus tachycardia

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Sinus tachycardia: causes, ECG, normal variants & pathological variants

Sinus tachycardia is the most common tachyarrhythmia (tachycardia). Sinus tachycardia is the result of an increased rate of depolarization (i.e increased automaticity) in the sinoatrial node. This simply means that the sinoatrial node discharges electrical impulses at a higher frequency than normal. Similar to sinus rhythm, the rhythm is regular with a positive P-wave in lead II, but the heart rate exceeds 100 beats per minute.

Although sinus tachycardia is the most common tachyarrhythmia, it may not always be straight forward to diagnose on the ECG. Moreover, many clinicians remain uncertain about the implications of sinus tachycardia. A crucial task is to distinguish three types of sinus tachycardia. These types differ fundamentally in terms of pathophysiology, prognosis and treatment. The types of sinus tachycardia are as follows:

  • Normal (physiologic) sinus tachycardia: The automaticity (rate of spontaneous depolarization) in the sinoatrial node is increased during physical activity, stress and nervousness. This is due to altered tone in the autonomic nervous system, with increased sympathetic input (leading to stimulation of beta-adrenergic receptors) and parasympathetic withdrawal.
  • Sinus tachycardia secondary to disease and medications: A wide range of diseases and medications may cause sinus tachycardia; e.g congestive heart failure, lung disease (e.g COPD), fever, infections, anemia, myocardial ischemia/infarction, pulmonary embolism, pheochromocytoma, hyperthyroidism, hypovolemia, pharmacological substances (alcohol, amphetamine, coffee, anticholinergic drugs, beta-adrenergic agonists). In all of these conditions, sinus tachycardia is merely an expression of an underlying disease or substance effect, which may require attention. Therefore, management of sinus tachycardia always requires that each of these causes be assessed thoroughly, as many of the causes require prompt treatment.
  • Inappropriate sinus tachycardia: When all the abovementioned causes have been ruled out and the sinus tachycardia persists without any known cause, it may be classified as inappropriate sinus tachycardia. This diagnosis can only be established after all other causes have been ruled out. Inappropriate sinus tachycardia is presumably more common than previously thought and the condition may hamper the quality of life substantially.

Thus, management of sinus tachycardia is aimed at finding secondary causes that may and must be treated or, when no cause can be found, establish a diagnosis of inappropriate sinus tachycardia. Although there are no evidence-based treatments for inappropriate sinus tachycardia, patients frequently benefit from obtaining a diagnosis, because it justifies their suffering and symptoms (treatment alternatives are discussed below).

ECG in sinus tachycardia

Sinus tachycardia fulfills all criteria for sinus rhythm but the heart rate is faster than 100 beats per minute. Thus, the ECG criteria for sinus tachycardia follows.

ECG criteria for sinus tachycardia

  • Regular rhythm with ventricular rate >100 beats per minute.
  • P-wave with constant morphology preceding every QRS complex.
  • The P-wave is positive in lead II.
Figure 1. ECG showing sinus tachycardia. Paper speed 25 mm/s. Calculate the heart rate by dividing 300 by the number of large boxes between R-waves. There are approximately 3 large boxes between the R-waves; 300/3 equals 100 beats per minute.
Figure 1. ECG showing sinus tachycardia. Paper speed 25 mm/s. Calculate the heart rate by dividing 300 by the number of large boxes between R-waves. There are approximately 3 large boxes between the R-waves; 300/3 equals 100 beats per minute.

Noteworthy ECG characteristics of sinus tachycardia

Note that at heart rates above 140 beats per minute it may be difficult to discern the P-waves from the previous T-wave, particularly if the paper speed is 25 mm/s (using 50 mm/s may be advised). Always search carefully for the P-wave as it may be very discrete and only cause an irregularity of the contour of the T-wave. Finding the P-wave is a requirement for establishing a diagnosis of sinus tachycardia.

On the contrary to many paroxysmal supraventricular tachyarrhythmias (e.g AVNRT, AVRT, or atrial tachycardia), sinus tachycardia has a gradual onset and the patient can often report that the palpitations accelerated gradually. Note that the mode of onset (abrupt vs. gradual) is an important piece in the puzzle to determine which type of arrhythmia a patient suffers from. Abrupt onset suggests that the tachyarrhythmia is AVNRT, AVRT, atrial tachycardia, atrial flutter or atrial fibrillation. It may, however, also be a special form of sinus tachycardia referred to as SANRT (discussed below).

Long-Standing sinus tachycardia may lead to ST-segment depressions on the ECG. Such ST-segment depressions may be seen anywhere but most commonly in leads V3, V4, V5 and V6. The ST-segment tends to be either horizontal or upsloping. Long-standing sinus tachycardia may also cause diminished T-wave amplitude on the ECG. This occurs in the same leads that display ST-segment depressions. These ST-segment depressions and diminished T-wave amplitude should disappear rapidly (within minutes) after the sinus tachycardia has resolved. Otherwise, one must suspect other causes of ST-segment depression (e.g acute myocardial ischemia).

Sinus tachycardia with strong sympathetic activation has a bathmotropic effect on the conduction system. This implies that the speed of impulse conduction is increased. Therefore, the PR interval may be slightly (but not significantly) reduced. Long-standing and rapid sinus tachycardia, on the other hand, may exhaust the atrioventricular node and bring about a slowing of conduction that prolongs the PR interval (again, not significantly).

Maximum heart rate

It is often difficult to differentiate sinus tachycardia from other supraventricular tachycardias (e.g atrial flutter, AVNRT etc). Many of these tachycardias have a tendency to present themselves with a particular heart rate. There is an age-dependent upper limit for the impulse frequency of the sinoatrial node. The maximal discharge rate in the sinoatrial node diminishes with age (due to diminishing sensitivity to catecholamines). Hence, using the individual expected maximum sinus rate may help differentiate sinus tachycardia from other arrhythmias. Any tachycardia with rate faster than the age expected maximum rate is probably not a sinus tachycardia.

Maximum discharge rate in the sinoatrial node is estimated using the following formulas:

Sinus tachycardia & Inappropriate Sinus Tachycardia
Formula 1: Estimation of maximal heart rate in relation to age and sex.

Note that at maximal exercise capacity, the sinus rate may be somewhat higher than the formulas estimate. Also note the third formula, which is necessary to estimate a maximum frequency in patients using beta-blockers (which diminish the discharge frequency of the sinoatrial node).

Normal range for sinus rhythm

The lower limit of sinus tachycardia is 100 beats per minute and this is an arbitrary and questioned figure. The main reason for this is that observational studies (both retrospective and prospective) and randomized controlled clinical trials have shown that the association between heart rate and mortality is linear, and the mortality increases gradually at heart rates above 60 beats per minute. Moreover, studies in recent years show that resting heart rate is actually a strong predictor of overall and cardiovascular mortality.

Inappropriate sinus tachycardia

Inappropriate sinus tachycardia is a condition where sinus tachycardia is present at rest and the sinus rate is usually excessively high during physical activity. The condition has been recognized for more than seven decades but many clinicians are still unaware of it. A large body of science suggests that inappropriate sinus tachycardia is caused by increased automaticity in the sinoatrial node. The cause of the increased automaticity, however, remains elusive. Theories suggest hypersensitivity to catecholamines, disturbance in the autonomic nervous system etc. Inappropriate sinus tachycardia may only be diagnosed when all other causes of sinus tachycardia have been ruled out.

Patients with sinus tachycardia present with resting heart rate above 100 beats per minute. They also tend to have an excessive increase in heart rate during all sorts of physical activity. Their heart rate during sleep is higher than the average individual. For some unexplained reason women, particularly health care workers, are overrepresented. Pre-syncope, syncope, chest discomfort, dyspnea, anxiety and fatigue are also common symptoms.

No clear evidence points to any increased mortality in inappropriate sinus tachycardia. This is somewhat unexpected given that tachycardia is a well-known risk factor for cardiomyopathy (tachycardia induced cardiomyopathy). It is not unlikely that individuals with inappropriate sinus tachycardia will be at greater risk of cardiovascular disease but the evidence is yet lacking.

Treatment of inappropriate sinus tachycardia

Inappropriate sinus tachycardia is treated with oral beta-blockers (bisoprolol 5-10 mg once daily), calcium channel blockers or ivabradine. Ivabradine acts by reducing the heart rate via specific inhibition of the funny channel (If), a mechanism different from that of beta-blockers and calcium channel blockers. The use of ivabradine in inappropriate sinus tachycardia is off-label. Referral to a cardiologist should be considered.

High resting heart rate

As mentioned above there is a strong association between resting heart rate and cardiovascular as well as all-cause mortality. The risk of death and cardiovascular disease increases already at resting heart rates above 60 beats per minute. This means that there is considerable mortality difference within the normal reference range 50–100 beats per minute. The Framingham Heart study demonstrated that individuals with a heart rate in the highest quintile had 5 times as great a risk of sudden cardiac death as compared with individuals in the lowest quintile.

The explanation for this finding is most likely multifaceted, but some straight forward causes exist. High heart rate increases myocardial oxygen consumption (because of increased workload) while impairing oxygen delivery. The impairment of oxygen delivery is due to shortening of diastole at higher heart rate; the coronary arteries perfuse the heart during diastole, which means that reduced length of diastole causes reduced myocardial perfusion. High resting heart rate is associated with a significantly increased risk of hypertension, arrhythmias, aortic dissection, atherosclerotic heart disease (ischemic heart disease), congestive heart failure and sudden cardiac death. This applies to healthy persons as well as those with established heart disease.

Treatment of high resting heart rate

Sinus Tachycardia

Sinoatrial nodal re-entrant tachycardia (SANRT) is caused by a re-entry circuit located in or by the sinoatrial node. It is recognized on the ECG (typically requires ECG monitoring for a longer period) as abruptly starting sinus tachycardia. Normal sinus tachycardia does not start abruptly, but rather gradually. The P-wave in SANRT is identical to the sinus P-wave. Other terms used for this condition is sinus node reentry or sinus node reentrant tachycardia.


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