Heart block, First Degree INTRODUCTION Background: First degree heart block, or first degree AV block, is a condition that results in prolongation of the PR interval on electrocardiogram (ECG) to >0.20 seconds. The PR interval is defined as the time from the initial deflection of the P wave from baseline to the beginning of the QRS complex. A normal PR interval is from 0.12 - 0.20 seconds. Pathophysiology: Electrophysiological studies have shown that first degree heart block may be due to conduction delay in the AV node, the His-Purkinje system, or a combination. AV nodal dysfunction accounts for the bulk of cases. However in the subset of patients with first degree heart block and bundle branch block, conduction delay in the His-Purkinje system is the more likely cause. Frequency: Internationally: The prevalence in the young adult population ranges from 0.65-1.1% . Higher prevalences have been reported in studies of trained athletes (8.7%) and medical students (8%). The incidence is 1.13 per thousand person-lives. Mortality/Morbidity: Morbidity and mortality from heart disease appears to be unaffected by the presence of first degree block. CLINICAL History: First degree heart block is generally an incidental findings noted on ECG without any particular associated symptoms. Patients may have a past history of heart disease, including myocardial infarction or myocarditis. They may be highly conditioned athletes with a high degree of vagal tone or they may be on medications that slow conduction through the AV node (see below). Causes: First degree heart block is most commonly caused by intrinsic AV nodal disease, enhanced vagal tone, acute myocardial infarction (particularly acute IMI), myocarditis, electrolyte disturbances, and drugs. The most common drugs that cause first degree heart block are those drugs that increase the refractory time of the AV node, therby slowing AV conduction. These drugs include calcium channel blockers, beta blockers, and digitalis glycosides. WORKUP Lab Studies: Routine laboratory testing is not indicated in the evaluation of first degree heart block, unless there is a suspicion of metabolic derangement or drug toxicity. In these situations, electrolyte and drug screens can be ordered. Imaging Studies: Routine imaging studies are not indicated. Other Tests: Follow-up ECG's may be indicated in patients who are treated with AV nodal agents while in the ED and for patients with concomitant myocardial infarction. The remainder of the evaluation of first degree heart block can be conducted on an out-patient basis. TREATMENT Emergency Department Care: No specific therapy is required. However, patients with concomitant myocardial infarction should receive appropriate therapy. FOLLOW-UP Further Inpatient Care: First degree heart block in and of itself does not require hospital admission unless there is associated myocardial infarction. Electrolyte annormalities should be identified and corrected. Offending medications, if any, should be withheld. Further Outpatient Care: In the absence of a disease process that requires admission, patients with first degree AV block may be followed as out-patients. They will need follow-up ECG's over time to assess for progression to higher grade AV block. Patients with first degree heart block and co-existent bundle branch block should be particularly closely followed. Consideration should also be given to switching to medications other those that slow AV nodal conduction. Complications: Patients with first degree heart block may occasionally progress to higher grade block, often with accompanying hemodynamic instability. This occurs primarily in patient with acute myocardial infarction or myocarditis, although it may also be drug-related, especially in the setting of an acute overdose. In addition, it should be understood that the administration of drugs, even in appropriate doses, that slow AV nodal conduction will increase the risk of progression to higher degrees of heart block. These drugs should be given with great caution. Prognosis: The prognosis for first degree heart block is very good. Heart block, Second Degree INTRODUCTION Background: Second degree heart block, or second degree AV block, refers to a cardiac conduction system disorder in which some P waves fail to conduct to the ventricle and generate a QRS complex. It is divided into 2 types: Mobitz I and Mobitz II. Mobitz I second degree AV block, or Wenckebach block, is characterized by progressive prolongation of the PR interval causing progressive RR interval shortening until a P wave fails to conduct to the ventricle. Mobitz II second degree AV block is characterized by sudden unexpected blocked P waves without variation or necessarily even prolongation of the PR interval. Pathophysiology: Mobitz I Wenckebach block is caused by conduction delay in the AV node in 72% of patients and by His-Purkinje system conduction delay in the other 28%. The presence of a narrow QRS complex makes the site of delay even more likely to be at the AV node. Wenckebach block and a wide complex QRS may be due to AV nodal or infranodal conduction delay. Mobitz II block is due to infranodal His-Purkinje system conduction delay, electrophysiological studies have proved. It is generally associated with a wide QRS complex except in some of the patients with delay localized within the His bundle. Frequency: Internationally: The prevalence of second degree heart block in the young adult population is reported to be 0.003%. Higher rates (2.4%) are observed in trained athletes undergoing routine ECG. Mortality/Morbidity: Mobitz I block localized to the AV node is believed by most investigators to have no significant associated morbidity or mortality in the absence of organic heart disease. Type I block localized to the His-Purkinje system has the same risks of Type II block. Mobitz II block carries a high risk of progression to complete heart block, often with associated cardiovascular collapse. CLINICAL History: Mobitz I Wenckebach block is generally asymptomatic. Uncommonly patients may experience dizzyness, lightheadedness, or syncope. Patients may have associated symptoms of myocardial ischemia or myocarditis. They may also have a prior history of organic heart disease. Mobitz II block may be asymptomatic but is more likely to present with dizzyness, lightheadedness, or syncope. Patients may also have associated symptoms of myocardial ischemia and a prior history of organic heart disease. Physical: The physical examination in second degree heart block will reveal an irregular heart rate and often accompanying bradycardia but is otherwise generally unremarkable. In symptomatic patients there may be evidence of hypoperfusion, including hypotension and altered mental status. In patients with concomitant myocardial infarction, there may be signs evident on examination related to the acute MI. Causes: Mobitz I Wenckebach block can be caused by acute inferior myocardial infarction, states of vagal stimulation or enhanced vagal tone, or toxicity relating to digitalis, beta-blockers, or calcium channel blockers. Mobitz II block is most commonly caused by acute myocardial infarction (anterior or inferior). WORKUP Lab Studies: For the evaluation of patients with second degree heart block, serum electrolytes may be checked and a digoxin level is indicated for those patients on digoxin. Cardiac enzymes are indicated for any patient with suspected myocardial ischemia, paticulary those with type II block. Imaging Studies: Routine imaging studies are not required, although a chest radiograph may be appropriate for those with associated signs and symptoms of myocardial ischemia. Other Tests: Follow-up ECG's and cardiac monitoring are appropriate for patients with second degree heart block. TREATMENT Prehospital Care: Second degree heart block requires no specific prehospital therapy, unless the patient is symptomatic from a resulting bradycardia. In this case, standard ACLS guidelines should be followed, including the use of atropine and transcutaneous pacing. Emergency Department Care: Mobitz I Wenckebach block requires no specific ED therapy. Those patients with associated myocardial ischemia should be treated with appropriate anti-ischemic medications. Those on AV nodal agents should have them withheld. Those with symptomatic bradycardia should be treated with atropine and transcutaneous pacing, per standard ACLS guidelines. Caution should be used in administering atropine to a patient with suspected acute myocardial infarction because atropine has been reported to precipitate VT/VF in this situation. Mobitz II block requires more aggressive ED therapy. Certainly, AV nodal agents should be withheld and anti-ischemic therapy delivered where appropriate. In addition, given the propensity for progression to complete heart block, these patients should have transcutaneous pacing patches applied and tested, even when asymptomatic. Those with symptoms and those in whom transcutaneous pacing is tested unsuccessfully should have urgent cardiac consultation for the placement of a temporary transvenpous pacing wire. Some experts recommend transvenous pacing in all patients with new type II block, although this practice varies from institution to institution. Unstable patients may also be treated with atropine, although this is much less likely to be successful in Mobitz II block and caution should be used in administering atropine in the setting of a suspected acute myocardial infarction. Unstable patients for whom cardiology consultation is not available in a timely fashion should undergo temporary transvenouspacing wire placement in the ED. A chest radiograph should be obtained to confirm placement and exclude complications of the procedure, including pneumothorax and hemothorax. Consultations: Mobitz I Wenckebach block: A cardiology consultation is indicated for symptomatic patients or those with concomitant myocardial ischemia. Cardiology consultation also may be useful in asymptomatic stable patients, particularly with regard to disposition decisions. Mobitz II block: A cardiology consultation is indicated for all these patients, regardless of symptoms. MEDICATION Drug therapy in second degree heart block is aimed at vagolysis, with atropine being the only currently available agent. The goal is to improve conduction through the AV node by reducing vagal tone via atropine-induced receptor blockade. This is only effective if the site of block is within the AV node. For patients with infranodal second degree heart block, atropine will be generally ineffective. Drug Name Atropine - Enhances sinus node automaticity. Blocks the effects of acetyl choline at the AV node, thereby decreasing refractory time and speeding conduction through the AV node Insufficient doses may cause paradoxical further slowing of heart rate. Adult Dose 0.5-1 mg rapid IV push q 3-5' (maximum 0.04 mg/kg) Can also be given via the endotracheal tube although absorption may be unreliable Pediatric 0.02 mg/kg IV push Minimum dose 0.1 mg IV Maximum single dose: 0.5 mg (child), 1.0 mg (adolescent) Maximum total dose 1.0 mg (child), 2.0 mg (adolescent) Can also be given via the endotracheal tube, although absorption may be unreliable. Contraindications Absolute: none Relative: concomitant acute myocardial infarction/ischemia. Interactions Decreased effect: Levodopa, phenothiazines, antihistamines with cholinergic mechanisms decrease anticholinergic effects of atropine. Increased toxicity: Thiazides increase effects. Amantadine increases anticholinergic effects. Pregnancy C - Safety for use during pregnancy has not been established Precautions Large doses may cause tachycardia, flushing, blurred vision, ataxia, and altered mental status. FOLLOW-UP Further Inpatient Care: Mobitz I Wenckebach block requires admission if symptoms of bradycardia are present or if there is concomitant acute myocardial ischemia. Admission should be to a unit that has telemetry monitoring and available transcutaneous pacing capabilities. Mobitz II block uniformly requires admission to a monitored bed. Transcutaneous and/or transvenous pacing capability should be available. Permanent pacemaker implantation should be determined by the admitting cardiologist. Further Outpatient Care: Those patients who are discharged from the ED with Wenckebach block should have prompt follow-up with a primary care physician or cardiologist. Complications: The most important complication of second degree heart block is progression to complete heart block with associated cardiovascular collapse. This is much more commonly seen with Mobitz II block than with Wenckebach block. Prognosis: Wenckebach block carries a good prognosis, with appropriate follow-up and treatment. Mobitz II block is a more dangerous entity, as it more frequently progresses to complete heart block and cardiovascular collapse. It is also commonly associated with acute myocardial infarction and its attendant risks. Heart block, Third Degree INTRODUCTION Background: Third degree heart block, also referred to as third degree AV block or complete heart block, is the cardiac conduction system disorder with complete absence of AV conduction. No P waves conduct to the ventricle and there is complete AV dissociation. The ventricular escape mechanism may originate from the AV node, His bundle to the bundle branch-Purkinje system. Not all patients with AV dissociation have complete heart block. For example, a patient with an accelerated junctional rhythm that is faster than his native sinus rate has AV dissociation but not complete heart block, as there is no disorder of AV conduction. Pathophysiology: Third degree heart block is caused by conduction block at the level of the AV node, the His bundle, or the bundle branch-Purkinje system. Block below the His bundle accounts for the majority of cases, approximately 61%, while block within the AV node accounts for 21% and block within the His bundle represents 14-18%. The duration of the escape QRS complex is dependent on the site of the block and the site of the escape rhythm pacemaker. Pacemakers above the His bundle produce a narrow QRS complex escape rhythm while those at or below the His bundle produce a wide QRS complex. When the block is at the level of the AV node, the escape rhythm generally arises from a junctional pacemaker with a rate between 45-60 per minute. Such patients are frequently stable and their heart rates will increase in response to exercise and atropine. When the block is below the AV node, the escape rhythm arises from the His bundle or the bundle branch-Purkinje system at rates less than 45 per minute. These patients are generally unstable and their heart rates unresponsive to exercise and atropine. Mortality/Morbidity: Patients with complete heart block are frequently hemodynamically unstable. This may lead to cardiovascular collapse, syncope, and death. CLINICAL History: Complete heart block may present asymptomatically or with minimal symptoms related to hypoperfusion, such as fatigue, dizzyness, or impaired excercise tolerance. Minimal symptoms are more likely to be seen in patients with narrow complex escape rhythms. More commonly, patients are profoundly symptomatic, especially when the escape rhythm is wide and slow. Symptoms may include syncope (Stokes-Adams attack), confusion, or sudden death. Patients may also have associated symptoms of acute myocardial infarction. They may also have a prior history of organic heart disease or be on medications that affect AV nodal conduction, including beta-blockers, calcium-blockers and digitalis glycosides. Physical: The physical examination will be notable for bradycardia, which may be profound. Symptomatic patients will have signs of hypoperfusion, including hypotension, altered mental status, and lethargy. Congestive heart failure may also be present. In patients with concomitant myocardial infarction, there may be signs evident on examination related to the acute MI. Causes: Third degree heart block may be congenital or acquired. Congenital block usually occurs at the level of the AV node as does acquired block due to acute inferior myocardial infarction, profound hypervagotonia, and drug intoxications (digitalis, beta-blockers and calcium blockers). Infranodal block is most commonly caused by acute anterior myocardial infarction. Other causes of third degree heart block include metabolic disturbances and cardiomyopathies. WORKUP Lab Studies: Cardiac enzymes are indicated. Serum electrolytes should be checked, as should a digoxin level when appropriate. Imaging Studies: A chest radiograph should be obtained to evaluate for pulmonary edema. Other Tests: Initial and follow-up electrocardiograms are necessary to make the diagnosis and monitor response to therapy. Procedures: Temporary pacemaker insertion through a central venous introducer may be required in a subset of unstable patients who do not respond to less invasive therapy. TREATMENT Prehospital Care: Asymptomatic patients with third degree block should be rapidly transported to the nearest available facility via ALS with continuous cardiac monitoring. Oxygen should be administered and intravenous access obtained. Maneuvers likely to increase vagal tone should be avoided (valsalva, painful stimuli). In symptomatic patients, transcutaneous pacing is the treatment of choice. Atropine can also be administered (cautiously, if acute myocardial infarction is the underlying cause) but is likely to be ineffective unless the escape QRS complex is narrow. Emergency Department Care: In the ED, the treament initiated in the pre-hospital setting should be continued, including oxygen administration, continuous cardiac monitoring, and frequent blood pressure measurements. Secure large-bore intravenous access should be obtained. AV nodal agents should be withheld and anti-ischemic therapy delivered where appropriate. All patients with third degree heart block should have transcutaneous pacing patches applied and tested. Stable patients who can be transcutaneously paced can be admitted to a telemetry unit and undergo elective placement of a permanent pacemaker at the discretion of the cardiologist. Those patients with symptoms and those in whom transcutaneous pacing is tested unsuccessfully should have urgent cardiac consultation for the placement of a temporary transvenous pacing wire. Unstable patients may also be treated with atropine, although this will be ineffective in patients with wide complex escape rhythms and caution should be used in administering atropine in the setting of a suspected acute myocardial infarction. Unstable patients for whom cardiology consultation is not available in a timely fashion should undergo temporary transvenous pacemaker insertion in the ED by the emergency physician. A chest radiograph should be obtained to confirm placement and exclude complications of the procedure, including pneumothorax and hemothorax. Consultations: Cardiology consultation is indicated for all patients with third degree heart block. The consultation is urgent in patients with concomitant acute myocardial infarction, wide complex escape rhythms, or symptoms of hypoperfusion. MEDICATION Drug therapy in third degree heart block is aimed at vagolysis, with atropine being the only currently available agent. Catecholamines have only a limited role. Drug Category: Vagolytics - The goal is to improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade. This is only effective if the site of block is within the AV node. For patients with infranodal block, this therapy is ineffective. Drug Name Atropine - Enhances sinus node automaticity; blocks the effects of acetyl choline at the AV node, thereby decreasing refractory time and speeding conduction through the AV node Insufficient doses may cause paradoxical further slowing of heart rate. Adult Dose 0.5-1 mg rapid IV push q 3-5' (maximum 0.04 mg/kg) Can also be given via the endotracheal tube, although absorption may be unreliable Pediatric 0.02 mg/kg IV push; minimum dose 0.1 mg IV; maximum single dose: 0.5 mg (child), 1.0 mg (adolescent); maximum total dose 1.0 mg (child), 2.0 mg (adolescent) Can also be given via the endotracheal tube although absorption may be unreliable. Contraindications Absolute: none Relative: concomitant acute myocardial infarction Interactions Decreased effect: Levodopa, phenothiazines, antihistamines with cholinergic mechanisms decrease anticholinergic effects of atropine Increased toxicity: Thiazides increase effects, amantadine increases anticholinergic effects Pregnancy C - Safety for use during pregnancy has not been established Precautions Large doses may cause tachycardia, flushing, blurred vision, ataxia, and altered mental status. Drug Category: Catecholamines - Improve hemodynamics by acting via beta-adrenergic receptor stimulation to increase heart rate and contractility and via alpha-adrenergic receptor stimulation to increase systemic vascular resistance Drug Name Dopamine - in low doses (2-5 ug/kg/min), it will act on dopaminergic receptors in the renal and splanchic vascular beds casuing vsaodilatation in these beds In mid-range doses (5-15 ug/kg/min), it will act on beta-adrenergic receptors to increase heart rate and contractility In high doses (15-20 ug/kg/min), it will act on alpha-adrenergic receptors to increase systemic vascular resistance and raise blood pressure Adult Dose 5-20 ug/kg/minute via continuous IV infusion Pediatric 5-20 ug/kg/minute via continuous IV infusion Contraindications Hypersensitivity to sulfites Interactions Dopamine's effects are prolonged and intensified by MAO inhibitors, alpha- and beta-adrenergic blockers, general anesthetics, and phenytoin. Pregnancy C - Safety for use during pregnancy has not been established Precautions Safety in children has not been established. Hypovolemia should be corrected prior to administration. Extravasation may cause tissue necrosis. Mid to high range doses should be delivered through a central venous catheter. Common adverse reactions (>10%) include ectopic heartbeats, tachycardia, vasoconstriction, hypotension, cardiac conduction abnormalities, widened QRS complex, ventricular arrhythmias, headache, nausea, vomiting, and dyspnea. Drug Name Epinephrine - Will stimulate beta-adrenergic receptors predominantly, increasing heart rate, cardiac contractility, and cardiac output. Alpha-adrenergic receptors will also be stimulated to a lesser degree, causing systemic vasoconstriction and increased blood pressure. Adult Dose 2-10 ug/kg/min Pediatric 0.1-1.0 ug/kg/min Contraindications No absolute contraindications Interactions Increased cardiac irritability if administered concurrently with halogenated inhalational anesthetics, beta-adrenergic blocking agents, or alpha-adrenergic blocking agents Pregnancy C - Safety for use during pregnancy has not been established Precautions Use with cautiously in elderly patients and those with acute coronary syndromes. Some products contain sulfites as preservatives. Withhold in the sulfite-allergic patient. Rapid infusion may cause death from cerebrovascular hemorrhage or cardiac arrhythmias. Extravasation may cause tissue necrosis. Administer through a central venous catheter. FOLLOW-UP Further Inpatient Care: Third degree heart block mandates admission to a telemetry unit, preferably the cardiac care unit. The timing of permanent pacemaker implantation will be determined by the admitting cardiologist. In/Out Patient Meds: Cardiac pacing should obviate the need for further required drug therapy. Transfer: Transfer may be necessary when the treating facility cannot provide comprehensive cardiac care. In this case, pacing (transcutaneous or tranvenous), when indicated, should be initiated prior to transfer. Transfer should be via ALS with continuous cardiac monitoring and pacing capability. Complications: Cardiovascular collapse and death Atropine-induced ventricular arrhythmias Hemothorax, pneumothorax, or tamponade resulting from improper placement of the temporary pacmaker wire