Interpret the ECG of a patient with sinus bradycardia, isolated diastolic hypertension, first-degree atrioventricular block (PR interval 212 ms), mild QRS widening (duration 106 ms), normal QTc (404 ms), and normal P‑, QRS‑ and T‑wave axes.

ECG Interpretation: Sinus Bradycardia with First-Degree AV Block and Isolated Diastolic Hypertension

This ECG demonstrates sinus bradycardia (HR 60 bpm) with first-degree atrioventricular block (PR 212 ms), mild QRS widening (106 ms), and isolated diastolic hypertension (BP 130/100 mmHg)—findings that warrant clinical correlation to exclude underlying cardiac pathology, particularly given the association between first-degree AV block and future risk of advanced conduction disease in hypertensive patients.

Primary ECG Findings

Rhythm and Rate Analysis

• Sinus bradycardia at 60 bpm is at the lower threshold of normal and may reflect increased vagal tone, athletic conditioning, or underlying sinus node dysfunction 1
• In non-athletic adults, heart rates ≥30 bpm are generally considered physiologic if asymptomatic, though rates at 60 bpm warrant evaluation for reversible causes 1
• The normal P-wave axis (31°), QRS axis (9°), and T-wave axis (23°) confirm sinus origin with normal ventricular depolarization and repolarization patterns 1

Conduction Abnormalities

First-degree AV block (PR interval 212 ms):

• The PR interval exceeds the normal upper limit of 200 ms, indicating delayed atrioventricular conduction 1
• In hypertensive patients specifically, first-degree AV block carries significant prognostic implications: it independently predicts future advanced AV block (hazard ratio 2.77), atrial fibrillation (hazard ratio 2.33), and left ventricular dysfunction (hazard ratio 1.49) over a mean 9.4-year follow-up 2
• While first-degree AV block is common in athletes (present in 35% of trained athletes) and mediated by increased parasympathetic tone, it resolves with exercise in physiologic cases 1

Mild QRS widening (106 ms):

• The QRS duration of 106 ms represents borderline prolongation (normal <100 ms in adults, though some sources use <110-120 ms) 1
• This degree of widening may reflect early intraventricular conduction delay or incomplete bundle branch block 1
• Combined with first-degree AV block, this suggests potential multi-level conduction system disease 3

QT Interval Assessment

• The QTc of 404 ms is normal (normal range <450 ms in men, <460 ms in women) 1
• This excludes long QT syndrome and drug-induced QT prolongation as contributing factors 1

Clinical Context: Isolated Diastolic Hypertension

The blood pressure of 130/100 mmHg demonstrates isolated diastolic hypertension:

• The diastolic pressure of 100 mmHg is significantly elevated (normal <80 mmHg, hypertension ≥90 mmHg)
• This pattern suggests increased systemic vascular resistance and may reflect chronic hypertensive changes affecting the cardiac conduction system 2
• Hypertension can impair cardiac parasympathetic function and reduce normal respiratory sinus arrhythmia 4

Differential Diagnosis and Risk Stratification

Physiologic vs. Pathologic Bradycardia

Key distinguishing features to assess:

• Symptoms: Absence of syncope, presyncope, dizziness, or heart failure symptoms suggests physiologic bradycardia 1
• Exercise response: Physiologic bradycardia normalizes with exercise and preserves maximal heart rate; failure to do so suggests sinus node dysfunction 1
• Athletic status: In trained endurance athletes, sinus bradycardia and first-degree AV block are common adaptive changes; however, this patient's isolated diastolic hypertension makes athletic conditioning less likely 1

Causes of Combined Bradycardia and First-Degree AV Block

Reversible causes to exclude:

• Medications: Beta-blockers, calcium channel blockers, digoxin, antiarrhythmics, or other AV-nodal blocking agents 1, 4
• Metabolic: Hypothyroidism (though this typically causes more profound bradycardia), electrolyte abnormalities (hyperkalemia) 1
• Increased vagal tone: Sleep, post-prandial state, or vagally-mediated episodes 1
• Ischemia: Inferior wall ischemia affecting the AV node blood supply 4

Intrinsic conduction system disease:

• Age-related degenerative changes (fibrosis of the conduction system) 1, 2
• Hypertensive heart disease with conduction system involvement 2
• Familial conduction disorders (though typically present earlier in life) 3

Recommended Clinical Approach

Immediate Assessment

1. Symptom evaluation: Specifically query for syncope, presyncope, dizziness, exercise intolerance, or heart failure symptoms 1
2. Medication review: Identify and potentially discontinue AV-nodal blocking agents if clinically appropriate 1, 4
3. Physical examination: Assess for signs of heart failure, thyroid disease, or structural heart disease 1

Diagnostic Workup

Essential investigations:

• Exercise stress testing or ambulatory ECG monitoring: Confirm that heart rate appropriately increases with activity and that AV conduction normalizes (resolution of first-degree AV block with exercise confirms functional origin) 1
• Echocardiography: Evaluate for left ventricular hypertrophy, systolic/diastolic dysfunction, and structural abnormalities given the hypertension and increased risk of LV dysfunction with first-degree AV block 2
• Thyroid function tests: Exclude hypothyroidism as a reversible cause 1
• Electrolytes: Check potassium, calcium, and magnesium 1

Consider if clinically indicated:

• 24-hour Holter monitoring: Assess for progression to higher-degree AV block, particularly during sleep when vagal tone is highest 1
• Electrophysiology study: Reserved for patients with symptoms suggestive of conduction disease or if non-invasive testing suggests infranodal block 1

Management Strategy

For asymptomatic patients:

• Hypertension management: Optimize blood pressure control, but avoid or use caution with AV-nodal blocking agents (beta-blockers, non-dihydropyridine calcium channel blockers) given the first-degree AV block 2
• Serial monitoring: Given the 2.77-fold increased risk of advanced AV block in hypertensive patients with first-degree AV block, periodic ECG surveillance (annually or with symptom development) is warranted 2
• Patient education: Counsel regarding symptoms of progressive conduction disease (syncope, presyncope, severe fatigue) that should prompt immediate evaluation 1

For symptomatic patients:

• If symptoms are attributable to bradycardia or conduction disease (documented correlation between symptoms and ECG findings), permanent pacemaker implantation is indicated 1
• Symptomatic bradycardia is defined as documented bradyarrhythmia directly responsible for syncope, presyncope, dizziness, heart failure symptoms, or confusional states from cerebral hypoperfusion 1

Critical Pitfalls to Avoid

1. Dismissing first-degree AV block as benign in hypertensive patients: Unlike in athletes where it is physiologic, first-degree AV block in hypertension predicts adverse outcomes and requires longitudinal follow-up 2

2. Attributing findings to athletic conditioning without confirmation: The presence of isolated diastolic hypertension makes athletic heart syndrome unlikely; verify athletic status and perform exercise testing 1

3. Missing progression to higher-degree AV block: First-degree AV block can progress to Mobitz Type II or complete heart block, particularly in the setting of structural heart disease or multi-level conduction system involvement suggested by QRS widening 1, 2, 3

4. Overlooking medication effects: Many antihypertensive agents (beta-blockers, non-dihydropyridine calcium channel blockers) can cause or worsen bradycardia and AV block 1, 4

5. Failing to correlate symptoms with ECG findings: Asymptomatic bradycardia and first-degree AV block generally do not require intervention, but documented symptom-rhythm correlation mandates treatment 1