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Emergency and Acute Medicine – Bradyarrhythmias
Overview and Definitions
Bradyarrhythmias are defined as a ventricular heart rate <60 beats />in. Sinus bradycardia may be a normal physiologic variant, whereas all other bradyarrhythmias are considered pathologic. Patients may be asymptomatic or present with hypotension, altered mental status, fatigue, nausea, syncope, or cardiac arrest. Management depends on ECG findings and the patient’s clinical stability rather than heart rate alone.
Etiology and Pathophysiology
Bradyarrhythmias may be idiopathic or secondary to intrinsic or extrinsic causes. Idiopathic causes include healthy, well-conditioned athletes. Intrinsic cardiac causes include sinus node dysfunction (e.g., sick sinus syndrome with brady–tachy variants), atrioventricular (AV) block with junctional or ventricular escape rhythms, infiltrative diseases (amyloidosis, sarcoidosis, hemochromatosis), collagen vascular diseases (SLE, scleroderma, rheumatoid arthritis), congenital or acquired anatomic abnormalities (postsurgical, post-transplant, postradiation), muscular disorders (myotonic dystrophy), and myocardial contusion from trauma.
Extrinsic causes include myocardial ischemia or infarction (RCA infarction → sinus bradycardia; LAD infarction → high-grade AV block), acidemia, medications and toxins (β-blockers, calcium channel blockers, digoxin, clonidine, antiarrhythmics, lithium, organophosphates), electrolyte abnormalities (hypo-/hyperkalemia, hypoglycemia, hypo-/hypercalcemia, hypermagnesemia), hypoxia, hypothermia, hypotension or severe hypertension, endocrine disorders (hypothyroidism), infections (Lyme disease, Chagas disease, diphtheria, endocarditis, myocarditis), and neurologic conditions (increased intracranial pressure, increased vagal tone, carotid sinus hypersensitivity, spinal cord injury). Vagal triggers include micturition, defecation, coughing, vomiting, ocular pressure, and other Valsalva maneuvers.
Special Populations
In children, hypoxia is the most common cause of bradycardia. During pregnancy, maternal SLE may result in congenital complete heart block.
Clinical Presentation
Many patients are asymptomatic. Symptomatic presentations include lightheadedness, confusion, fatigue, decreased level of consciousness, dyspnea, cyanosis, pallor, chest pain or pressure, diaphoresis, hypotension, syncope, hypothermia, or cardiac arrest.
History and Physical Examination
Key historical elements include recent medication changes, urine output patterns suggesting electrolyte disturbances, trauma (intracranial injury or myocardial contusion), and activity at symptom onset suggesting increased vagal tone. Physical examination focuses on respiratory status, perfusion and pulses, rhythm regularity, mental status with full neurologic assessment, body habitus, skin/hair/nails, and temperature.
Essential Evaluation
Immediate evaluation includes ECG with continuous cardiac monitoring, pulse oximetry, blood pressure monitoring, and bedside glucose and electrolyte assessment.
Diagnostic Tests and Interpretation
Laboratory testing may include serum glucose, electrolytes, BUN/creatinine, cardiac enzymes, digoxin level, thyroid function tests, rheumatologic markers (ANA, RF), Lyme titers, and iron studies. Imaging includes chest radiograph and CT head for altered mental status.
ECG findings define the rhythm: sinus bradycardia with normal P–QRS relationship; sinoatrial block; sinus arrest; AV block (first degree, Mobitz I, Mobitz II, complete heart block); junctional rhythm; and idioventricular rhythm with wide QRS complexes.
Differential Diagnosis
Normal physiologic bradycardia, cardiac ischemia, medication or toxin effects, pacemaker malfunction, hypoxia, hypothermia, electrolyte disturbances, renal failure, hypothyroidism, infection, rheumatologic disease, neuromuscular disease, increased intracranial pressure, and myocardial contusion.
Prehospital Management
Treat the patient rather than the heart rate. Provide oxygen for all patients. In hypothermia, rewarm gently and avoid pacing; administer magnesium as indicated. Use atropine or epinephrine only for hypotension or altered mental status. Initiate transcutaneous pacing if other measures fail.
Initial Stabilization in the ED
Address ABCs, administer oxygen, apply pacing pads, establish IV access, and begin continuous cardiac monitoring.
Emergency Department Management
Asymptomatic bradycardia requires monitoring and evaluation. Symptomatic or unstable bradycardia is treated with oxygen, atropine for symptomatic sinus bradycardia and low-grade AV block, epinephrine, and pacing. High-grade AV block typically requires pacing. Definitive care targets the underlying cause.
Medications
Atropine, epinephrine, calcium gluconate, dextrose, digoxin immune Fab, glucagon, insulin, and pacing are used based on etiology and stability. First-line therapy includes atropine, epinephrine, and pacing; second-line therapy addresses the specific cause.
Disposition
ICU admission is required for hemodynamic instability, Mobitz II or complete heart block, pacing or vasopressor needs, or acute ischemia. Telemetry admission is appropriate for stable cases. Asymptomatic sinus bradycardia may be discharged.
Follow-Up and Referral
All patients except those with isolated asymptomatic sinus bradycardia require cardiology follow-up. Specialty referral is indicated for underlying systemic causes.
Key Clinical Insights and Common Errors
Sinus bradycardia without symptoms is the only potentially normal bradyarrhythmia; all others warrant evaluation or follow-up. Ensure oxygenation, IV access, ECG, and continuous monitoring in all cases. Pediatric bradycardia is most often due to hypoxia. Pacing pads should be readily available for symptomatic patients. Definitive management hinges on identifying and correcting the underlying cause rather than focusing solely on heart rate.
Overview and Definitions
Bradyarrhythmias are defined as a ventricular heart rate <60 beats />in. Sinus bradycardia may be a normal physiologic variant, whereas all other bradyarrhythmias are considered pathologic. Patients may be asymptomatic or present with hypotension, altered mental status, fatigue, nausea, syncope, or cardiac arrest. Management depends on ECG findings and the patient’s clinical stability rather than heart rate alone.
Etiology and Pathophysiology
Bradyarrhythmias may be idiopathic or secondary to intrinsic or extrinsic causes. Idiopathic causes include healthy, well-conditioned athletes. Intrinsic cardiac causes include sinus node dysfunction (e.g., sick sinus syndrome with brady–tachy variants), atrioventricular (AV) block with junctional or ventricular escape rhythms, infiltrative diseases (amyloidosis, sarcoidosis, hemochromatosis), collagen vascular diseases (SLE, scleroderma, rheumatoid arthritis), congenital or acquired anatomic abnormalities (postsurgical, post-transplant, postradiation), muscular disorders (myotonic dystrophy), and myocardial contusion from trauma.
Extrinsic causes include myocardial ischemia or infarction (RCA infarction → sinus bradycardia; LAD infarction → high-grade AV block), acidemia, medications and toxins (β-blockers, calcium channel blockers, digoxin, clonidine, antiarrhythmics, lithium, organophosphates), electrolyte abnormalities (hypo-/hyperkalemia, hypoglycemia, hypo-/hypercalcemia, hypermagnesemia), hypoxia, hypothermia, hypotension or severe hypertension, endocrine disorders (hypothyroidism), infections (Lyme disease, Chagas disease, diphtheria, endocarditis, myocarditis), and neurologic conditions (increased intracranial pressure, increased vagal tone, carotid sinus hypersensitivity, spinal cord injury). Vagal triggers include micturition, defecation, coughing, vomiting, ocular pressure, and other Valsalva maneuvers.
Special Populations
In children, hypoxia is the most common cause of bradycardia. During pregnancy, maternal SLE may result in congenital complete heart block.
Clinical Presentation
Many patients are asymptomatic. Symptomatic presentations include lightheadedness, confusion, fatigue, decreased level of consciousness, dyspnea, cyanosis, pallor, chest pain or pressure, diaphoresis, hypotension, syncope, hypothermia, or cardiac arrest.
History and Physical Examination
Key historical elements include recent medication changes, urine output patterns suggesting electrolyte disturbances, trauma (intracranial injury or myocardial contusion), and activity at symptom onset suggesting increased vagal tone. Physical examination focuses on respiratory status, perfusion and pulses, rhythm regularity, mental status with full neurologic assessment, body habitus, skin/hair/nails, and temperature.
Essential Evaluation
Immediate evaluation includes ECG with continuous cardiac monitoring, pulse oximetry, blood pressure monitoring, and bedside glucose and electrolyte assessment.
Diagnostic Tests and Interpretation
Laboratory testing may include serum glucose, electrolytes, BUN/creatinine, cardiac enzymes, digoxin level, thyroid function tests, rheumatologic markers (ANA, RF), Lyme titers, and iron studies. Imaging includes chest radiograph and CT head for altered mental status.
ECG findings define the rhythm: sinus bradycardia with normal P–QRS relationship; sinoatrial block; sinus arrest; AV block (first degree, Mobitz I, Mobitz II, complete heart block); junctional rhythm; and idioventricular rhythm with wide QRS complexes.
Differential Diagnosis
Normal physiologic bradycardia, cardiac ischemia, medication or toxin effects, pacemaker malfunction, hypoxia, hypothermia, electrolyte disturbances, renal failure, hypothyroidism, infection, rheumatologic disease, neuromuscular disease, increased intracranial pressure, and myocardial contusion.
Prehospital Management
Treat the patient rather than the heart rate. Provide oxygen for all patients. In hypothermia, rewarm gently and avoid pacing; administer magnesium as indicated. Use atropine or epinephrine only for hypotension or altered mental status. Initiate transcutaneous pacing if other measures fail.
Initial Stabilization in the ED
Address ABCs, administer oxygen, apply pacing pads, establish IV access, and begin continuous cardiac monitoring.
Emergency Department Management
Asymptomatic bradycardia requires monitoring and evaluation. Symptomatic or unstable bradycardia is treated with oxygen, atropine for symptomatic sinus bradycardia and low-grade AV block, epinephrine, and pacing. High-grade AV block typically requires pacing. Definitive care targets the underlying cause.
Medications
Atropine, epinephrine, calcium gluconate, dextrose, digoxin immune Fab, glucagon, insulin, and pacing are used based on etiology and stability. First-line therapy includes atropine, epinephrine, and pacing; second-line therapy addresses the specific cause.
Disposition
ICU admission is required for hemodynamic instability, Mobitz II or complete heart block, pacing or vasopressor needs, or acute ischemia. Telemetry admission is appropriate for stable cases. Asymptomatic sinus bradycardia may be discharged.
Follow-Up and Referral
All patients except those with isolated asymptomatic sinus bradycardia require cardiology follow-up. Specialty referral is indicated for underlying systemic causes.
Key Clinical Insights and Common Errors
Sinus bradycardia without symptoms is the only potentially normal bradyarrhythmia; all others warrant evaluation or follow-up. Ensure oxygenation, IV access, ECG, and continuous monitoring in all cases. Pediatric bradycardia is most often due to hypoxia. Pacing pads should be readily available for symptomatic patients. Definitive management hinges on identifying and correcting the underlying cause rather than focusing solely on heart rate.
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