An atrioventricular block is a loss of the regular function of the cardiac electroconductive pathways linking the sinoatrial node (SA node) and the ventricles via conduction through the atrioventricular node (AV node). Third-degree AV block indicates a complete loss of communication between the atria and the ventricles. Without appropriate conduction through the AV node, the SA node cannot act to control the heart rate, and cardiac output can diminish secondary to loss of coordination of the atria and the ventricles. The condition can be fatal if not promptly treated. Most patients will initially require temporary pacing, followed by a permanent pacemaker.
The underlying cause of AV blocks is varied and the same for all degrees of blocks. These causes include idiopathic fibrosis and underlying chronic cardiac diseases such as structural heart disease, acute ischemic heart disease, medication toxicity, nodal ablation, electrolyte abnormalities, and post-operative heart block such as after surgical or transcatheter aortic valve replacement.[1] Additional causes of AV block include Lyme disease and some systemic diseases such as collagen vascular disorders, amyloidosis, sarcoidosis, and systemic lupus erythematosus.
Drugs associated with third-degree heart block include:
An anterior wall MI with an infranodal complete heart block is a life-threatening condition. About 5 to 10% of patients with an inferior wall MI will develop complete heart block, but this may resolve within 2 to 48 hours. In general, a complete heart block after an acute MI is rare. AV blocks may accompany right coronary artery occlusion and most resolve after revascularization.
AV block can occur after open-heart surgery, septal alcohol infusion, and percutaneous coronary interventions. After aortic valve surgery, complete heart block is more commonly seen in female patients and those with annular calcification.
Although AV blocks are fairly common, third-degree AV block is relatively rare.[2] The incidence in the general population appears to be low, approximately 0.02% to 0.04%.[3] Given the etiology of the disease, the incidence among the apparently healthy and presumptively asymptomatic individuals is as low as 0.001%.[4] Similarly, as one looks at people with a greater disease burden, the incidence increases with a study of patients in the Veterans Health Administration, demonstrating an incidence of 1.1% in those with diabetes mellitus and 0.6% in those with hypertension.[5]
Under its regular function, the AV node receives an impulse from the SA node. That impulse gets delayed in the AV node, assuring the contraction cycle in the atria is complete before a contraction begins in the ventricles. From the AV node, the electrical impulse passes through the His-Purkinje system to activate ventricular contraction. When there is a pathological delay in the AV nodal conduction, it is visualized on an electrocardiogram as an alteration in the PR interval. These delays present in the form of AV blocks, which are of first, second, and third-degree. The third-degree block is also known as complete heart block. As the name implies, no impulses from the SA node get conducted to the ventricles, and this leads to a complete atrioventricular dissociation. The SA node continues its activity at a set rhythm, but the ventricles activate through an escape rhythm that can be mediated by either the AV node (junctional escape), one of the fascicles (fascicular escape), or by ventricular myocytes themselves (ventricular escape rhythm).[1]
The heart rate will typically be less than 45 to 50 beats/min, and most patients will be hemodynamically unstable. This rhythm is unresponsive to atropine and exercise.
Patients with third-degree blocks can have varying clinical presentations. Rarely, patients are asymptomatic. Usually, they may present with generalized fatigue, tiredness, chest pain, shortness of breath, presyncope, or syncope. They may have a significant hemodynamic instability and can be obtunded. The patient's status at the time of presentation can vary depending upon the concurrent disease and the rate of the escape rhythm. Patients with complete AV-block accompanying an acute myocardial infarction often have ischemic symptoms of chest pain or dyspnea. The past medical history will often include the presence of cardiovascular disease and/or its risk factors, including diabetes mellitus, hypertension, dyslipidemia, and smoking, etc.
The physical exam is usually remarkable for bradycardia. JVP examination often demonstrates cannon A-waves owing to the simultaneous contraction of the atria and ventricles. Thus a very large pressure wave is felt up against the vein. Especially with heart rates below 40/min, patients might also present with features consistent with decompensated heart failure, respiratory distress, and hypoprofusion such as diaphoresis, tachypnea, altered mental status, retraction, cool skin, and decreased capillary refill.
The presence of any new murmurs should be noted as a strong association exists between complete AV block and cardiomyopathies, mitral calcification, aortic calcification, or endocarditis. If there is coexistent heart failure evidenced by S gallop, peripheral edema, or hepatomegaly, then immediate pacing is a crucial part of management.
Attention should be paid to any signs of infection or skin rashes, such as rheumatic fever, Lyme disease, and endocarditis, which cause heart blocks.
Patients in complete heart block might present in significant distress. After stabilizing the patient, the most important component of the evaluation is the electrocardiogram. The electrocardiogram will have completely independent atrial and ventricular activity with no relation between the P wave and the QRS complex. The atrial rate, demonstrated by the P wave, should be faster than the ventricular rate, as demonstrated by the QRS complex. Depending on the location of the block, the QRS complex might be a narrow morphology (junctional escape QRS complex) or a wide morphology (ventricular escape QRS complex). An ECG should also have an evaluation for signs of ischemia. A basic metabolic panel should be obtained to correct electrolyte abnormalities and to evaluate and correct the glucose, which might be low in beta-blocker toxicity. Troponin should also be evaluated and trended to check for myocardial infarction. In patients who take digoxin, a digoxin level must be obtained to exclude digoxin toxicity. A chest radiograph and complete blood count is necessary to evaluate for concomitant diseases.
The initial management of bradycardic patients that are symptomatic usually begins with the use of intravenous atropine as per the advanced cardiac life support recommendations. Unfortunately, atropine acts at the AV node and, as such, is rarely effective in raising the heart rate in patients with complete heart block. Subsequently, medical options for the treatment of symptomatic bradycardia include dopamine and epinephrine, but both may serve as a temporary supporting measure only and might also be unsuccessful in improving the patient's heart rate in third-degree AV block. Often patients in third-degree heart block will require pacing. Transcutaneous pacing is more rapid, although both electrical and mechanical capture must be assured.
If transcutaneous pacing is not successful, a transvenous pacemaker is necessary. In stable patients, a cardiologist/electrophysiologist consultation for placement of a permanent pacemaker is most appropriate. Pacing may not be successful if underlying diseases causing the heart block do not receive treatment; this is particularly true in drug toxicity. In these patients, although the clinician might attempt pacing, the priority should be to treat the underlying cause. In patients with heart block secondary to an acute myocardial infarction, temporary pacing is a consideration in the cath lab. In patients with acute inferior infarct secondary to an occluded right coronary artery, timely restoration of arterial perfusion may often lead to improvement of the complete heart block. On the contrary, complete heart block related to an anterior infarction is more likely to eventually require placement of a permanent pacemaker than patients with inferior infarction. In a large recent study utilizing the National Inpatient Sample databases in patients with STEMI, the incidence of complete heart block was found to be approximately 2.2% in acute ST-elevation MI patients. It demonstrated that the in-hospital mortality was significantly higher in patients with complete heart block than those without it. Although the use of temporary pacing was higher in inferior MI patients, the need for an eventual permanent pacemaker was significantly higher in anterior MI patients.[6]
Regardless, cardiac catheterization and attempt for successful restoration of perfusion should not be delayed in patients with acute MI and complete heart block. Timely perfusion increases the likelihood of native rhythm restoration.
Third-degree heart block is often a straightforward diagnosis on the 12-lead ECG. It is characterized by the presence of a complete AV-dissociation, with an atrial rate being faster than the ventricular rate. It is crucial to differentiate complete heart block from AV dissociation related to other causes such as in idioventricular rhythms where the ventricular rate is faster than the atrial rates. Sometimes, second-degree heart block and high-degree AV blocks may masquerade as complete heart block. Repeating ECGs or longer rhythm strips are often helpful in making such a distinction.
Long-term prognosis of third-degree AV block is not well studied (as it often requires treatment in acute settings). The prognosis likely is dependent on the patient's underlying disease burden and severity of the clinical presentation on arrival. Complete heart block is sometimes reversible in settings such as acute MI by restoring coronary perfusion and in conditions such as Lyme disease by treatment with antibiotics. Historically, high-grade AV blocks have been considered a marker of poor prognosis in patients with ST-segment elevation myocardial infarction, and more recent studies indicate that this continues to be true in the era of percutaneous coronary intervention.[7] As previously mentioned, the presence of a complete heart block in acute MI is an independent predictor for increased mortality in these patients. Complete heart block occurs more frequently in patients with inferior MI than anterior MI. Although the use of temporary pacing was higher in inferior MI patients, the need for an eventual permanent pacemaker was significantly higher in anterior MI patients. Also, the mortality associated with complete heart block is higher in patients with anterior MI compared to inferior MI.[6]
The recommendation is that a pacemaker is placed in patients with a persistent third-degree AV block, although the term "persistent" is often a matter of clinician judgment.[8] An Italian survey of just over 24000 patients found that 21% received pacing for third-degree AV blocks.[9] Although pacemaker is the definitive treatment for patients in third-degree AV block, it does carry some burden of heart failure itself. A 2017 study concluded that patients with AV blocks are more prone to develop heart failure than those without an AV block, both acutely (over 6 months) and chronically (6 months to 4 years), which may be related to the dependence of frequent RV pacing.[10]
Patients with third-degree heart blocks are vulnerable to decreased perfusion related to symptomatic bradycardia and decreased cardiac output. Patients may experience syncope related falls and head injuries. Critically ill patients may be unable to protect their airway and may develop nausea, possibly aspirate, and may have delirium. Treatment-related complications in the short term are malposition or dislodgement of a pacemaker lead and cardiac perforation in the short term and pacemaker associated heart failure in the long term. As is true for the prognosis of third-degree heart block, complications will frequently be dependent on a patient's overall health and compensatory mechanisms.
A cardiology consultation should be sought in all patients suffering from third-degree atrioventricular (AV) block. In patients with coexistent acute myocardial infarction, congestive cardiac failure, or symptoms of hypoperfusion, an emergent cardiologic consultation is indicated. An electrophysiologist should also be consulted whenever appropriate.
Patient education should focus on diminishing the overall disease burden. Although not directly causative, underlying cardiac risk factors like diabetes mellitus and hypertension, as discussed above, are associated with an increased prevalence of third-degree AV block. Generally speaking, a focus on the overall cardiac health would be expected to improve the prognosis.
After implantation of a permanent pacemaker, patients should have counseling about wound care and receive post-operative instructions. The patients should often refrain from driving for about 2 to 3 weeks and should use an arm-sling during the night and intermittently during the day to prevent any arm movement above the shoulder level. They should receive education regarding devices known to cause significant electromagnetic interference with the pacemaker, although this is less of a concern with newer-generation pacing devices available in the market. Patients should also be educated about periodic pacemaker check-ups, including but not limited to lead function, lead thresholds, and battery life evaluation.
The management of patients with third-degree AV block requires interprofessional care coordination. The initial diagnosis often starts with the hospitalist, intensivist, or emergency department physician. The initial phase of stabilization of the critically ill patient with third-degree AV block requires close coordination and communication of the physician, nurses, and ancillary healthcare workers to carry out the principles of the bradycardia algorithm of advanced cardiac life support. If the patient is not currently in a critical care setting, the care teams must coordinate appropriate transportation to a critical care facility.
Nursing will assist with care irrespective of whether it is medical treatment or if the pacing is the choice of therapy. If medical, the nurses will coordinate with the pharmacist, who will verify all dosing and perform medication reconciliation, and report any concerns. Nursing staff will administer drugs (e.g., epinephrine) as well as monitor for effectiveness or adverse events.
Treatment of critically ill patients with third-degree AV block should be in either the emergency department, intensive care unit, or the cardiac catheterization laboratory. During and following the initial patient stabilization, coordination, and communication among physicians, nurses and ancillary staff is of utmost importance as the patient will require close monitoring and possibly rapid interventions if the clinical scenario changes. The primary care team needs to coordinate with consulting physicians, usually the intensivist and the cardiologist or electrophysiologist, to place the patient in a monitored setting or place a temporary intravenous pacer until an evaluation of the underlying etiology is done and the decision can be made to implant a permanent pacemaker. No evidence was discovered outlying the specific goals or practices to improve healthcare team performance, but typical procedures and policies used to activate critical care teams are necessary as appropriate to the healthcare setting.
Ultimately, third-degree AV block cases require an interprofessional team approach, including physicians, specialists, specialty-trained nurses, and pharmacists, all collaborating across disciplines to achieve optimal patient results. [Level V]
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