Cardiovascular 10: Bradycardia Treatment Portal
General Key Points
- Treat the patient, not the monitor.
- A heart rate of 65 may be a relative bradycardia if the BP is low.
- Look for adverse clinical manifestations with the bradycardia, including symptoms (such as chest pain, shortness of breath) and signs (such as decreased LOC, hypotension, CHF, and PVCs) in the setting of MI and shock.
- Make sure that the patient’s signs and symptoms are due to the slow heart rate. Hypovolemia or myocardial dysfunction may cause hypotension associated with a bradycardia, but the patient may not have a conduction system abnormality or an autonomic problem.
With bradycardia and heart block, consider both:
- The site of the heart block
- The degree of the heart block
The heart block may occur at the AV node or be infranodal (ie, at or below the His-Purkinje level), such as in the bundle of His or in the bundle branches. First-degree AV block normally occurs at the AV node.
Type I Second-Degree (Wenckebach's) Block occurs at the level of the AV node. This frequently is due to increased parasympathetic tone or dig-effect, such as from digitalis, beta blockers, or verapamil. Wenchebach manifests as having a regular atrial rhythm, but an irregular ventricular rhythm, with progressive elongation of the PR interval with shortening of the R to R interval and with the R to R interval that brackets the non-conductive P wave as being < 2 times a normal cycle.
Type II Second-Degree Block occurs below the AV node, either at the bundle of His (uncommonly) or in the bundle branch (most common). PR intervals tend to be of equal length, but there can be more than one non-conductive P wave in a row. This is associated with organic lesions in the conduction pathway and is rarely due just to increased parasympathetic tone or drug affect. Therefore, this block has:
- A poorer prognosis
- A greater chance of developing a third-degree heart block
Most of these blocks are at the level of the bundle branches. The PR interval may be normal or prolonged. To drop a beat, we need to have a complete block of one bundle, either the right or the left, and intermittent interruption of the conduction in the contralateral bundle. Therefore, Type II second-degree block is usually associated with a wide QRS complex. When the block is at the bundle of His, the QRS complex is not wide since the ventricular conduction is not disturbed or blocked.
Third-Degree Heart Block can be at the level of the AV node, bundle of His, or the bundle branches. The distinction is important since the pathogenesis, treatment, and prognosis vary depending on the anatomical level of the block.
When the block is at the AV node, a junctional escape pacemaker frequently initiates the ventricular depolarization. The QRS complex is a narrow complex with a stable rate and rhythm of 40 to 60 bpm. This is because the block is above the bundle bifurcation. This location of third-degree block is common in inferior MIs, toxic drug effects (from digitalis or Inderal), or from damage to the AV node. This is usually transient, and the prognosis is good.
Third-degree blocks at the infranodal level most often are due to blocks involving both bundle branches. This indicates extensive infranodal conduction symptom disease, often from coronary disease, which is frequently associated with an extensive anterior wall MI. These usually do not result just from increased parasympathetic tone or from drug effects. The only natural escape mechanism for pacing the heart is the ventricle distal to the blockage. This is an unstable rhythm with a rate < 40 bpm and has a high frequency of becoming asystolic. These complexes are wide in nature.
Key Points to Remember in Treating Bradycardia1
If the patient has a bradycardia or heart block and has signs and symptoms from this bradycardia, initiate and perform treatment quickly and decisively.
These patients' conditions may be pre-cardiac arrest and merit aggressive intervention, including a number of interventions together, such as transcutaneous pacing, atropine IV, and preparation for an epinephrine infusion.
If the symptoms are fairly mild, atropine 0.5 mg IV to a maximum dose of 0.03 to 0.04 mg/kg (3 mg, total cumulative adult dose) may be given with dosing intervals of 3 to 5 minutes.3 The severity of the patient's symptoms determines the interval of dosing. Thus, use the 3-minute dosing interval in severe clinical situations.
Dopamine IV starting at rates of 2 μg/kg/min may be given and increased rapidly up to 20 μg/kg/min for hypotension.1
Severe clinical symptoms may necessitate epinephrine infusion1 at 2 to 10 μg/min or (PEDS) 0.1 to 1 μg /kg/min.
In patients with severe signs and symptoms from the bradycardia, consider the immediate use of transcutaneous pacing. Do not wait for IV access or for the atropine to become effective.1
Transcutaneous pacing may be effective but painful, and the patient may need anesthesia.1
The prognosis in AV block is related to the site of the infarction (anterior vs. inferior), the site of the block (intranodal [proximal or above the His Bundle]or infranodal [distal or below the His Bundle]), the nature of the escape rhythm, and the hemodynamic consequences.
Transplanted (denervated) hearts will not respond to atropine. The treatment of symptomatic bradycardia in these patients will require catecholamine infusion, pacing, or both.1
PEDS: Bradycardic children with signs of severe hypoperfusion require chest compressions even if a pulse is present.
Medications and Treatments for Bradycardia
A. Atropine
Mechanism
of Action. Atropine is a parasympatholytic drug that
enhances both the
sinus node automaticity and the AV conduction via its direct vagolytic
action.
Indications.4 Atropine reverses decreases in heart rate, systemic vascular resistance, and BP mediated by parasympathetic (cholinergic) activity. Atropine is useful for treating symptomatic sinus bradycardia and may be beneficial in the presence of AV block at the AV node level or for ventricular asystole. Atropine is most effective for sinus bradycardia occurring within 6 hours of the onset of acute MI. Sinus bradycardia at this time may be related to ischemia, reperfusion (Bezold-Jarisch reflux), ischemic type chest discomfort, or morphine or nitroglycerin therapy. Atropine is also effective for profound sinus bradycardia with hypotension associated with thrombolytic therapy (especially with right coronary artery occlusion). Use atropine with caution in the setting of acute MI, because of the protective effect of parasympathetic tone against VF and MI extension.
Dosage and
Administration of Atropine
Adult dose is 0.5 mg IV. PEDS: Pediatric dose is 0.02 mg/kg. This may be repeated in 3 to 5 minute intervals until desired response or a maximum dose of 0.03 to 0.04 mg/kg. This is approximately 2 to 3 mg for an adult.3
Avoid repeated doses of atropine if possible for patients with ischemic heart disease to prevent the detrimental effects of atropine-induced tachycardia or increased myocardial oxygen demand.
In patients in cardiac arrest, 1 mg IV doses at intervals of 1 to 3 minutes may be given up to 0.04 mg/kg.3
Atropine may be given through an ET tube. Recommended adult dose of atropine for ET administration is 1 to 2 mg diluted to a total not to exceed 10 mL of sterile water or NS. PEDS: 0.04 to 0.06 mg/kg ET dose. This produces rapid onset of action similar to IV injection.5 (Vol III—CV4 Endotracheal Drug Delivery)
Adverse Effects of Atropine
Administration of atropine in doses < 0.5 mg can produce a paradoxical bradycardia owing to the central or peripheral parasympathomimetic effects of low doses in adults. This effect can precipitate VF.6
The use of atropine for patients with infranodal AV block may be harmful. When the AV block is at the His Purkinge level or below (Type II AV block and third-degree block with wide QRS complexes), atropine may cause paradoxical slowing of the heart rate.2
Atropine may cause VF or VT6
Atropine may cause anti-cholinergic syndrome of delirium, tachycardia, flushed and hot skin, ataxia, and blurred vision.4
B.
Transcutaneous Pacing (TCP)
TCP
is a Class I intervention for all symptomatic bradycardia and is
particularly useful if atropine is either contraindicated or is
ineffective.1
Indications for TCP1
Treatment of hemodynamic significant bradycardia that has not responded to atropine therapy or when atropine therapy is not immediately available.
TCP is useful as a short interval bridge until transvenous pacing can be initiated.
TCP can be a bridge until bradyarrhythmias from hyperkalemia or drug overdose can be reversed.
TCP is useful when the patient has received or will receive thrombolytic therapy, and therefore, vascular puncture for transvenous packing is undesirable.
Technique for TCP
Anterior/posterior application. Place an anterior electrode to the left of the sternum centered as close as possible to the point of the maximum cardiac impulse. Place the posterior electrode directly behind the anterior electrode to the left of the thoracic spine column.
Sternal-apex chest wall electrodes include 1 electrode in the right upper chest and a second electrode on the left lateral chest wall.
Place regular 3-lead electrodes for monitoring the underlying rhythm.
Set pacer on demand mode.
Initiate TCP at a rate of 60 to 70 bpm.
Initial output from the pacer in the case of bradysystolic arrest should be maximum output, which is 200 mA. With a non-arrest bradycardia, start at a lower power setting and slowly increase the output until achieving capture. Electrical capture usually requires 50 to 100 mA.
Determination of capture may be difficult on a routine monitor because of the wide electrical activity obliterating the cardiac electrical activity on the monitor. A filter is on the pacing monitor, such that capture can usually be determined. Capture also can be assessed by BP determination. If a peripheral pulse is to be obtained, obtain it at the right carotid or right femoral artery, so as not to confuse the jerking of muscle contraction with that of a pulse.
CPR may be administered directly over the insulated electrodes while pacing is going on, without risk to the CPR operator.
Capture success and energy levels are related to electrode placement, patient size, and body size. Large pericardial effusions may inhibit capture.
TCP is painful, and the patient needs analgesia in the form of narcotics and/or sedation with a benzodiazepine.
Pitfalls of TCP
- Failure to recognize the presence of underlying, treatable VF.
- Failure to recognize that the pacemaker is not capturing.
- Induction of arrhythmia, such as VF.
- Skin damage due to prolonged pacing.
C. Dopamine for Bradycardia
- Dopamine is a precursor of norepinephrine that stimulates dopamine,
beta-adrenergic, and alpha-adrenergic receptors.
- Low-dose dopamine (1 to 5 μg/kg/min) causes the dopamine receptors to be stimulated causing renal, mesenteric, and cerebrovascular dilatation and thus, an increase in renal output.4
- Moderate dose of dopamine (5 to 10 μg/kg/min) are cardiac doses which stimulate the beta I and alpha-adrenergic receptors, enhancing the myocardial contractility, increasing cardiac output, and raising the BP. At least 5 μg per kg is needed to help bradycardia.4
- High-dose dopamine (10 to 20 μg/kg/min, a vasopressor dose) causes alpha-adrenergic effect, producing peripheral, arterial, and venous vasoconstriction.4
- For dopamine to be helpful with bradycardia, at least 2 to5 μg/kg/min IV is usually needed. The dopamine may need to be rapidly increased to 5 to 20 μg/kg/min.1
D. Epinephrine
for Bradycardia
Epinephrine infusion can be started instead of dopamine for severe bradycardia with severe hypotension. Epinephrine is the preferred agent for patients close to PEA or even asystole.
Mix epinephrine 1 mg per 500 cc of D5W that produces 2 μg/mL. This is infused at 1 to 10 μg/min (30 cc per hour results in 1 μg per minute; PEDS 0.1 to 1 microgram/kg/min).4
E. Right
Ventricular Infarction With Bradycardia
Identification of a right ventricular infarct requires use of a V4R lead on the ECG.
Relative hypovolemia is common with right ventricular infarctions. A careful fluid challenge of NS IV may be most appropriate to increase the right ventricular filling pressures, which strengthens the right ventricular contractions (based on Starling's law).
Although patients usually develop tachycardia in response to hypovolemia, excessive parasympathetic tone as well as nodal ischemia may be present in patients with inferior or right ventricular infarctions; therefore, these patients may have bradycardia and hypotension. Judicious administration of atropine is often effective in restoring an adequate heart rate.
PEDS: Bradycardia in children is often due to hypoxia and hypoventilation and needs to be treated as a respiratory emergency.
References
- ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3):S748-S750, S887-S888.
- Gunnar RM, et al. ACC/AHA guidelines for the early management of patients with acute myocardial infarction. Circulation. 1990:82:664-707.
- Gonzalez ER. Pharmacologic controversies in CPR. Ann Emerg Med. 1993:22:317-23.
- American Heart Association. Advanced Cardiac Life Support. 1997.
- Prete MR, et al. Plasma atropine concentrations via intravenous, endotracheal, and intraosseous administration. Am J Emerg Med. 1987:5:101-4.
- Dauchot P, et al. Bradycardia after myocardial ischemia and its treatment with atropine. Anesthesiology. 1976: 44:501-18.