Steps
1. Decision: Heart rate is < 60 bpm and is symptomatic.
2. Assess and manage the patient using the primary and secondary surveys:
Maintain patent airway.
Assist breathing as needed.
Administer oxygen if oxygen saturation is less than 94% or the
patient is short of breath
Monitor blood pressure and heart rate.
Obtain a 12-lead ECG.
Review patient's rhythm.
Establish IV access.
Complete a problem-focused history and physical exam.
Search and treat possible contributing factors.
3. Answer two questions to help you decide if the patient's signs and symptoms
of poor perfusion are caused by the bradycardia (see Figure 2).
Are the signs or symptoms serious, such as hypotension, pulmonary
congestion, dizziness, shock, ongoing chest pain, shortness of
breath, congestive heart failure, weakness or fatigue, or acute altered
mental status?
Are the signs and symptoms related to the slow heart rate?
4. There may be another reason for the patients symptoms other than the
slow heart rate.
5. Decide whether the patient has adequate perfusion. The treatment
sequence is determined by the severity of the patient's clinical presentation.
If perfusion is adequate, monitor and observe the patient.
If perfusion is poor, move quickly through the following actions:
Prepare for transcutaneous pacing. Do not delay pacing. If no
IV is present pacing can be first.
Consider administering atropine 0.5 mg IV if IV access is
available. This may be repeated every 3 to 5 minutes up to
3mg or 6 doses.
If the atropine is ineffective, begin pacing.
Consider epinephrine or dopamine while waiting for the pacer
or if pacing is ineffective.
Epinephrine 2 to 10 g/min
Dopamine 2 to 10 g/kg per minute
6. Progress quickly through these actions as the patient could be in pre-cardiac
arrest and need multiple interventions done in rapid succession: pacing, IV
atropine, and infusion of dopamine or epinephrine.
General Pharmacology
The vagus (parasympathetic) nerves that innervate the heart release
acetylcholine (ACh) as their primary neurotransmitter. ACh binds to
muscarinic receptors (M2) that are found principally on cells comprising the
sinoatrial (SA) and atrioventricular (AV) nodes. Muscarinic receptors are
coupled to the Gi-protein; therefore, vagal activation decreases cAMP. Gi-
protein activation also leads to the activation of K ACh channels that increase
potassium efflux and hyperpolarizes the cells.
Increases in vagal activity to the SA node decreases the firing rate of the
pacemaker cells by decreasing the slope of the pacemaker potential (phase 4
of the action potential); this decreases heart rate (negative chronotropy). The
change in phase 4 slope results from alterations in potassium and calcium
currents, as well as the slow-inward sodium current that is thought to be
responsible for the pacemaker current (If). By hyperpolarizing the cells, vagal
activation increases the cell's threshold for firing, which contributes to the
reduction the firing rate. Similar electrophysiological effects also occur at the
AV node; however, in this tissue, these changes are manifested as a
reduction in impulse conduction velocity through the AV node (negative
dromotropy). In the resting state, there is a large degree of vagal tone on the
heart, which is responsible for low resting heart rates.
There is also some vagal innervation of the atrial muscle, and to a much
lesser extent, the ventricular muscle. Vagus activation, therefore, results in
modest reductions in atrial contractility (inotropy) and even smaller decreases
in ventricular contractility.
Muscarinic receptor antagonists bind to muscarinic receptors thereby
preventing ACh from binding to and activating the receptor. By blocking the
actions of ACh, muscarinic receptor antagonists very effectively block the
effects of vagal nerve activity on the heart. By doing so, they increase heart
rate and conduction velocity.
Specific Drugs and Therapeutic Indications
Atropine is a muscarinic receptor antagonist that is used to inhibit the effects
of excessive vagal activation on the heart, which is manifested as sinus
bradycardia and AV nodal block. Therefore, atropine can temporarily revert
sinus bradycardia to normal sinus rhythm and reverse AV nodal blocks by
removing vagal influences.
Side Effects and Contraindications
The anticholinergic effects of atropine can produce tachycardia, pupil dilation,
dry mouth, urinary retention, inhibition of sweating (anhidrosis), blurred vision
and constipation. However, most of these side effects are only manifested
with excessive dosing or with repeated dosing. Atropine is contraindicated in
patients with glaucoma.
