An abnormal pulse rhythm refers to an irregular expansion and contraction of the arterial walls, detectable at peripheral sites such as the radial or carotid arteries. It may be persistent or sporadic, rhythmic or arrhythmic. Patients often report palpitations, fluttering, or skipped beats.

Abnormal pulse rhythms are important clinical clues that indicate underlying cardiac arrhythmias, which range from benign to life-threatening. They may be associated with cardiovascular, renal, respiratory, metabolic, and neurologic disorders, as well as medication effects, diagnostic tests, or treatments. Prompt recognition and intervention are critical to prevent decreased cardiac output, hypotension, syncope, or sudden cardiac death.

Classification

Pathophysiology

Abnormal pulse rhythms result from disruptions in the heart’s electrical conduction system:

1. Automaticity disturbances – Enhanced or ectopic pacemaker activity (e.g., atrial or ventricular ectopy).

2. Conduction delays or blocks – Interrupted propagation through AV node or His-Purkinje system (e.g., AV block, bundle branch block).

3. Reentry circuits – Circular electrical pathways cause repeated activation of myocardium (e.g., atrial flutter, ventricular tachycardia).

4. Electrolyte or metabolic imbalances – Abnormal potassium, calcium, or magnesium levels can alter conduction and excitability.

5. Drug effects or toxicity – Digoxin, antiarrhythmics, sympathomimetics, caffeine, and alcohol can precipitate arrhythmias.

History and Physical Examination

History

• Onset, frequency, and duration of palpitations or skipped beats

• Associated symptoms: chest pain, dizziness, syncope, shortness of breath, fatigue

• Past history of heart disease, arrhythmias, hypertension, or heart failure

• Medication history, including antiarrhythmics, digoxin, or sympathomimetics

• Lifestyle factors: caffeine, alcohol, tobacco, illicit drugs

Physical Examination

• Assess radial, carotid, femoral, and apical pulses

• Compare apical and peripheral rates to detect pulse deficit

• Auscultate heart sounds: long pauses (conduction defects), faint S1 (atrial fibrillation/flutter), or close S1-S2 beats (premature contractions)

• Monitor for signs of low cardiac output: hypotension, pallor, diaphoresis, confusion, decreased LOC, oliguria

• Evaluate for signs of heart failure: crackles, edema, jugular venous distention

• Observe respiratory rate and effort

Emergency interventions

• Assess for decreased LOC, hypotension, or dizziness

• Begin continuous cardiac monitoring and obtain ECG

• Insert IV line for emergency medications

• Provide supplemental oxygen as needed

• Keep emergency intubation, cardioversion, defibrillation, and suction equipment ready

• Consider sedation before cardioversion if indicated

• Collect blood for electrolytes, cardiac enzymes, and drug levels

• Prepare for chest X-ray, 12-lead ECG, or 24-hour Holter monitoring

• Compare with prior ECGs if available

Medical causes

Special considerations

• Continuous monitoring for bradycardia, tachycardia, hypotension, or altered LOC

• Bed rest or assisted ambulation as appropriate

• Raise side rails to prevent falls

• Maintain accurate intake/output records and daily weight

• Educate patient on keeping a symptom/activity diary to correlate with arrhythmia episodes

Patient counseling

• Avoid caffeine, tobacco, and alcohol which may exacerbate arrhythmias

• Emphasize adherence to prescribed antiarrhythmic therapy

• Teach pulse monitoring at home

• Encourage reporting of palpitations, syncope, chest pain, or worsening symptoms

Pediatric pointers

• Arrhythmias also cause abnormal pulse rhythms in children

• Common pediatric causes include congenital heart disease, myocarditis, and electrolyte disturbances

• Monitor children carefully, especially if symptomatic with palpitations or syncope

References

1. Buttaro TM, Tybulski J, Bailey PP, Sandberg-Cook J. Primary care: A collaborative practice. St. Louis (MO): Mosby Elsevier; 2008. p.444–447.

2. Colyar MR. Well-child assessment for primary care providers. Philadelphia (PA): F.A. Davis; 2003.

3. Sommers MS, Brunner LS. Pocket diseases. Philadelphia (PA): F.A. Davis; 2012.

4. McCance KL, Huether SE, Brashers VL, Rote NS. Pathophysiology: The biologic basis for disease in adults and children. 7th ed. Maryland Heights (MO): Mosby Elsevier; 2014.

5. Goldberger ZD, Bonow RO, Mann DL, Zipes DP. Braunwald’s heart disease: A textbook of cardiovascular medicine. 12th ed. Philadelphia (PA): Elsevier; 2021.