ECG criteria
- Sinus bradycardia: HR less than 60 bpm, P wave of normal morphology before each QRS; an inconstant sign
- Low QRS voltage: maximum QRS amplitude less than 5 mm in all standard limb leads and/or less than 10 mm in all chest leads
- Non-specific T wave flattening or ST-T changes: evaluated in all leads taking the clinical context into account; there is no hypothyroidism-specific distribution across leads; marked T wave inversion is not specific for hypothyroidism and requires ruling out ischemia, hypertrophy, and electrolyte disturbances
- Prolonged QT/QTc interval: QTc is calculated using Bazett's formula — QTc = QT / √RR, or Fridericia's formula — QTc = QT / ∛RR (RR in seconds). Approximately, a QTc of more than 450 ms in men and more than 460 ms in women is considered prolonged, and a QTc of 500 ms or more indicates a substantially increased risk of torsades. In bradycardia, Bazett's formula tends to overestimate the interval (yielding an falsely elevated QTc), so Fridericia's formula or another validated method is preferred
- Possible ST segment depression or T wave inversion: the changes are non-specific; if symptoms or ECG dynamics are present, the patient should be evaluated using ACS algorithms rather than interpreting the changes as benign based on a single tracing
- Electrical alternans in concomitant significant pericardial effusion: requires urgent clinical assessment and echocardiography
What it looks like on ECG
The ECG in hypothyroidism is non-specific, with no strict obligatory pattern. Several elements should be checked sequentially.
| Element | Parameter | Leads |
|---|---|---|
| Rhythm | sinus bradycardia is possible | II, rhythm strip |
| QRS | low voltage is possible | limb and/or chest |
| T wave | flattening or non-specific changes are possible | all leads |
| QT interval | sometimes prolonged | II, V5 |
| PQ interval | sometimes slightly prolonged | II |
The rhythm is usually sinus and may be slowed, but marked bradycardia is not mandatory. The P wave is preserved. The QRS complex is usually narrow in the absence of concomitant conduction defects, although bundle branch block and QRS widening are possible, especially in severe disease—this requires separate evaluation and should not be automatically attributed to hypothyroidism. QRS amplitude may be reduced in some leads, but does not have to be low across all lead groups simultaneously; the low voltage criterion is assessed based on the maximum QRS amplitude separately in limb and chest leads. Voltage reduction in hypothyroidism may be related to decreased myocardial metabolic activity, the accumulation of hydrophilic mucopolysaccharides in the interstitium, and concomitant pericardial effusion—the latter is not inflammatory pericarditis, simply fluid in the pericardial cavity that enhances the low voltage effect. Furthermore, low voltage is multifactorial: obesity, pulmonary emphysema, and infiltrative myocardial diseases all contribute, so the finding cannot be automatically linked to hypothyroidism alone. The T wave may be flat or mildly negative; marked or dynamically changing T wave inversion is not considered typical for hypothyroidism and requires evaluation considering symptoms, previous ECGs, and indications for ischemia workup. The ST segment is usually on the isoelectric line, with occasional minimal depression. QTc is prolonged in a subset of patients; clinically significant prolongation does not occur in everyone, and the risk of torsades de pointes is higher with a QTc of 500 ms or more, bradycardia, hypokalemia, hypomagnesemia, and the use of QT-prolonging medications. In severe hypothyroidism with a large pericardial effusion, electrical alternans may occur—it arises from a significantly mobile effusion, especially one close to tamponade, but its absence does not rule out tamponade, and the finding requires urgent echocardiography.
Mechanism
Thyroid hormone deficiency decreases the expression and activity of cardiomyocyte ion channels and Na+/K+-ATPase. Sinus node automaticity and chronotropic response are reduced, and AV node conduction may also be altered (a slight PQ prolongation in some cases) alongside ventricular repolarization. Myocardial contractility and metabolic activity are reduced, which, together with the accumulation of hydrophilic mucopolysaccharides in the interstitium (myxedema) and frequent pericardial effusion, can decrease the total cardiac electrical vector—hence the potential for low QRS voltage. Repolarization changes can lead to T wave flattening and sometimes prolongation of the QT/QTc interval, though the severity of these changes varies significantly among patients.
Causes
- Primary hypothyroidism (Hashimoto's autoimmune thyroiditis, postoperative, post-radioactive iodine therapy)
- Secondary (pituitary) and tertiary (hypothalamic) hypothyroidism
- Iodine deficiency
- Drug-induced hypothyroidism (amiodarone, lithium, antithyroid drugs)
Severe decompensated hypothyroidism can be complicated by myxedema coma—a rare, life-threatening condition characterized by hypothermia, altered mental status, and profound bradycardia.
Differential diagnosis
- Pericarditis/effusion without hypothyroidism: low voltage and electrical alternans are similar, but bradycardia is not an obligatory companion; hormonal profile and echocardiography are needed
- Hypothermia: bradycardia and low voltage are also possible, but hypothermia is frequently accompanied by an Osborne wave—which supports the diagnosis, though it is not absolutely specific for it; it is not typical in hypothyroidism
- COPD/pulmonary emphysema: vertical or right electrical axis deviation, low voltage, and signs of cor pulmonale are possible, but the picture is variable and not mandatory; guided by clinical presentation, chest X-ray/CT, and echocardiography as indicated
- Sick sinus syndrome: bradycardia without low voltage and without typical T wave changes
- Hyperkalemia: usually causes tall peaked T waves, and as it progresses, conduction abnormalities and QRS widening; T wave flattening more commonly points toward hypokalemia and other causes rather than hyperkalemia
Clinical significance and management
ECG findings in hypothyroidism are non-specific in most cases, but this does not mean the condition is always benign: marked bradycardia, severe hypothyroidism, significant QTc prolongation (especially 500 ms or more), or a large pericardial effusion can be clinically dangerous and require urgent evaluation. The ECG serves as a reason to suspect thyroid dysfunction, particularly in cases of unexplained bradycardia and low voltage in a patient without CAD or COPD. The main risks are polymorphic ventricular tachycardia (torsades de pointes) in the presence of marked QTc prolongation and unrecognized large pericardial effusion with the threat of tamponade. The physician should: check TSH and free T4 levels, evaluate QTc specifying the formula used (Fridericia is preferred in bradycardia) and rule out concomitant electrolyte disturbances, perform echocardiography if effusion is suspected, and review QT-prolonging medications pending clarification of thyroid status. In the presence of severe bradycardia, syncope, or signs of tamponade, manage according to relevant emergency algorithms rather than confining the patient to observation. Following compensation of hypothyroidism with replacement therapy, some changes may regress—heart rate and certain repolarization abnormalities usually improve, but normalization of low voltage and QT is not guaranteed, as other causes may persist (obesity, effusion, infiltrative diseases, medications, structural heart disease); follow-up ECGs are evaluated on an individual basis.
Common interpretation errors
- Interpreting low voltage as a technical artifact (poor electrode contact) without checking the clinical picture
- Failing to measure QTc in a bradycardic patient and missing the increased risk of torsades de pointes in marked prolongation
- Declaring ST depression or T wave inversion a benign finding of hypothyroidism without assessing symptoms and ACS algorithms
- Confusing low voltage in hypothyroidism with low voltage in COPD, obesity, or amyloidosis without analyzing the clinical picture
- Failing to suspect pericardial effusion when low voltage and electrical alternans are combined
1. Which ECG changes are possible in hypothyroidism without being obligatory or specific?
These changes are described in hypothyroidism, but occur variably and are non-specific; no mandatory diagnostic triad exists.
2. How may the ECG in hypothyroidism differ from the ECG in hypothermia, given that both conditions cause bradycardia and low voltage?
The Osborn wave (an additional deflection at the J point) is characteristic of hypothermia, although described in other conditions as well; it is not typical for hypothyroidism.
3. What clinical action by the physician is most justified when unexplained bradycardia and low QRS voltage are detected in a patient without CAD?
This pattern is a classic indication to rule out hypothyroidism via laboratory testing and to assess the risk of QTc prolongation, rather than immediately resorting to invasive or pharmacological measures.
Frequently asked questions
What is the most frequent sign of hypothyroidism on the ECG?
Sinus bradycardia is most common; low QRS voltage and nonspecific ST-T changes are also possible. None of these signs are specific to hypothyroidism, and no obligatory triad exists.
Is hypothyroidism dangerous for the heart according to the ECG?
The ECG changes themselves are usually nonspecific, but marked bradycardia, QTc of 500 ms or more, syncope, or signs of large pericardial effusion with the threat of tamponade require urgent evaluation. The risk of polymorphic ventricular tachycardia increases substantially mainly with pronounced QTc prolongation combined with bradycardia, electrolyte disturbances, or the use of QT-prolonging drugs, which is why medications and electrolytes should be checked.
How to distinguish low voltage in hypothyroidism from low voltage in COPD?
There are no reliable differentiating criteria. Sometimes in hypothyroidism, low voltage is combined with bradycardia, while in COPD, it is associated with a vertical or right axis deviation and signs of cor pulmonale, but these are only rough tendencies rather than a rule: both combinations are variable and depend on concomitant pathology. Clinical evaluation, verification of recording quality, hormonal profile, and chest X-ray or CT help distinguish between the causes.
Does the ECG normalize after treatment for hypothyroidism?
Some of the changes may regress with replacement therapy: heart rate and certain repolarization abnormalities are more likely to improve. However, normalization of low voltage and QT is not guaranteed if other causes persist — obesity, pericardial effusion, infiltrative diseases, or medications affecting these parameters.
Should hypothyroidism always be suspected when low voltage is present on the ECG?
No, low voltage is a nonspecific sign; it occurs in obesity, COPD, pericardial effusion of any etiology, and amyloidosis. Hypothyroidism is considered in combination with clinical data and other ECG findings, and is confirmed by hormone testing.
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Related terms
More in "Electrolytes and Metabolism"
Sources
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice, 6th ed.
- Goldberger A.L. Clinical Electrocardiography: A Simplified Approach
- Orlov V.N. Guide to Electrocardiography
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.