Introduction
Bradycardia, or low heart rate (below 60 beats per minute in adults), can range from normal to immediately life-threatening. It is therefore important to promptly and effectively assess patients who are bradycardic. A symptomatic bradycardia may represent pre-cardiac arrest, and should be treated aggressively, especially if patients are unstable.
The Case of Philip W.
Philip W. is a 69 year-old man who comes to his doctor feeling ‘weak’. He has felt this way for the past few hours, but it is getting worse. As a part of the assessment, Philip’s doctor checks his pulse and finds it to be 38.
- what further questions should his doctor ask?
- what should he do next?
Differential Diagnosis
Causes of bradycardia include:
physiologic
medications:
electrolyte and metabolic abnormalities
|
toxins
heart disease
infectious diseases:
other
|
Heart Blocks
With first degree block, there is a delay of over 0.2 sec (5 boxes) between the PR interval. However, the 1:1 relationship is maintained between atrial and ventricular contractions. Impairment is usually in the AV node.
Reversible causes include:
- heightened vagal tone
- ischemia, myocardial infarction
- drugs that suppress conduction
- digitalis
- beta blockers
- calcium channel antagonists
- other antiarrhythmic medications
Mobitz Type I block (also known as Wenckebach),results in a gradual lengthening of PR interval until an impulse is completely blocked. It is usually benign and is commonly seen in athletes, children, and people with high vagal tone.
Mobitz type II block is characterized by the sudden intermittent loss of AV conduction, without a gradual PR lengthening. The block may persist for two or more atrial beats. It is usually caused by block distal to the AV node. It usually indicates severe disease, and can lead to third degree block.
Third degree block can lead to life-threatening arrhythmias.
History and Physical Exam
Symptomatic bradycardia is defined by signs and symptoms due to slow heart rate. These can include:
- chest pain or discomfort
- shortness of breath
- weakness or fatigue
- decreased level of consciousness, dizziness, presyncope, syncope
Consider, however, that symptoms may be due to conditions other than bradycardia (ie myocardial ischemia).
Other questions should include:
- past medical history, especially ischemic heart disease, heart failure, valvular disease
- previous infections, as described above
- medications, especially as described above
- toxic exposures
Examine the patient for the following:
- level of consciousness
- pallor
- diaphoresis
Listen to lung fields, measure jugular venous pressure, and assess for ankle edema to look for evidence of congestive heart failure.
A cardiovascular exam should be done, paying particular attention to murmurs.
Investigations
- electrolytes, especially glucose, potassium, and calcium
- creatinine
- troponin
- digoxin levels (as appropriate)
- TSH
Cardiac monitoring is recommended initially, especially if the patient is symptomatic or is manifesting 2nd degree block type II or 3rd degree block.
Management
If the bradycardia is recognized incidentally, is not leading to symptoms, and is explanable by factors such as being an athlete, or beta blocker administration, the patient can be discharged with instructions on warning signs to watch for.
Monitoring
In patients who are symptomatic, or in whom the bradycardia is not explainable, monitoring is warranted in an emergency room setting. This should include vital signs and ECG tracing.
Obtain IV access and provide oxygen if warranted. Establish pacing pads on the patient.
Treatment
There is no need to provide treatment unless the patient is showing evidence of hypoperfusion. If this is occurring, however, treatment should be pursued.
Idenfify and correct electrolyte abnormalities.
If the heart block is not Mobitz type II or third degree, IV atropine may be given.
If atropine is not successful, IV infusions of epinephrine or dopamine may be used.
Transcutaneous pacing may be necessary with Mobitz Type II or third degree block, or if medications fail. Sedation is suggested, given the pain associated with the treatment. A permanent pacemaker may also be required.
If digoxin toxicity is suspected, DIGIBIND is an anti-digoxin antibody that may be used.
Pathophysiology
main article: electrical control of the heart
If the SA node is sufficiently impaired, escape rhythms can emerge from the AV node, bundle of His, or ventricles. Junctional escape beats have no P waves and have normal, narrow QRS complexes, with a rate of 40-60 bpm. Retrograde P waves can sometimes be observed. Ventricular escape rhythms are slow – 30-40 bpm – and have widened QRS complexes. Morphology depends on area of origin.
Escape rhythms occur when an unstable ventricular region begins contracting independently. This is especially common with ischemia, but can also occur with electrolyte abnormalities or acidosis.
PVCs or ventricular tachycardia can occur.
Resources and References
North Carolina EMS Bradycardia protocol
Topic Development
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