Arrhythmias - Heart blocks: Nursing
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Notes
| ARRHYTHMIAS - HEART BLOCKS | ||
| KEY POINTS | NOTES | |
| DEFINITION |
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| PHYSIOLOGY |
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| CAUSES AND RISK FACTORS |
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| PATHOPHYSIOLOGY |
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| SIGNS AND SYMPTOMS |
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| DIAGNOSIS |
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| TREATMENT |
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| MANAGEMENT OF CARE |
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| PATIENT AND FAMILY TEACHING |
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Transcript
Arrhythmias are irregular heartbeats that occur due to any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical impulse, which can affect the heart’s ability to effectively pump blood throughout the body.
Now a heart block, or atrio-ventricular block, occurs when there is delay or disturbance in the conduction of cardiac electrical impulse from the atria to the ventricles. There are three types of atrio-ventricular block or AV block, for short: first degree AV block, second degree AV block which is further divided into Mobitz type I and Mobitz type II, and lastly, third degree AV block.
The cardiac conduction system is made of specialized myocardial cells that create and transport electrical potential which play a role in regulating heart rate and rhythm. They possess automaticity which is the ability to generate an impulse, excitability or the ability to respond to a stimulus by initiating stimulus, conductivity or the ability to send that impulse, and contractility or the ability to shorten fiber length.
Now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. From the atrium, electrical activity goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood.
From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles, causing them to depolarize. This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations, and it’s represented by the QRS complex on an ECG. Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on an ECG, ventricular repolarization will create a T wave, while the pause between ventricular depolarization and repolarization is represented by the ST segment. Sometimes, immediately after the T wave, there’s a U wave, which represents late repolarization of the ventricles.
Okay, now let’s look at AV blocks, which are typically caused by any kind of structural damage or fibrosis to the electrical conduction system.
This damage is strongly associated with several risk factors, particularly cardiac surgery or underlying heart conditions. These include ischemic heart disease, previous or recent myocardial infarction, congenital heart disease, myocarditis, as well as rheumatic fever. Other risk factors include drug toxicity, typically with digoxin, calcium channel blockers or beta blockers. Finally, elderly clients, as well as athletes are at a higher risk for developing AV blocks.
Okay, the pathology of an AV block starts when any of these factors impair the function of the electrical conduction system. Now, a first degree AV block is technically not really a block, because it’s more of a delay as the cardiac electrical impulses still make it to the ventricles, but result in a delayed ventricular contraction.
On the other hand, second degree AV block has two subtypes: Mobitz type I and Mobitz type II. In Mobitz I, each atrial impulse encounters a longer and longer delay until one of them does not make it through to the ventricles, and you get what’s called a “dropped beat.” When a signal doesn’t make it from the atria to the ventricles, and if a long enough time passes, then the ventricles’ pacemaker cells kick in, sort of as a fail-safe mechanism, called a ventricular escape beat.
Like Mobitz I, the heart also drops a beat in Mobitz II, except this time, conduction through the AV node is all-or-nothing. Either the atrial impulse goes through with no delay, or it doesn’t at all. A lot of times, a ratio for the overall number of beats conducted to not-conducted is given, like 2:1 Mobitz II AV block, but it’s important to remember that the dropped beats happen fairly randomly so we can’t really predict exactly when the next beat will get dropped. Mobitz II can be dangerous and may result in severe bradycardia and decreased cardiac output.
Lastly, there is third degree or complete AV block, where the signal is completely blocked when moving from the atria to ventricles, every time. Because the atria and the ventricles each have their own pacemakers, they now contract independent of one another, which is called AV dissociation.
So, in terms of clinical manifestations, most clients with a first degree AV block and Mobitz type I don’t have symptoms, but occasionally patients feel lightheadedness, dizziness, and syncope. In contrast, most clients with Mobitz type II have symptoms like fatigue, confusion, dyspnea, chest pain, and syncope, though the severity can vary from client to client. In third degree AV block, these symptoms become more severe and without treatment may lead to cardiac arrest and even death.
The diagnosis of an AV block starts with the client's history and physical assessment, followed by a 12-lead electrocardiogram. In first degree AV block, the PR interval is greater than 200 milliseconds. In Mobitz type I AV block, also called Wenckebach block, the PR interval gets progressively longer with each beat until a P wave is blocked completely. So, maybe the first PR interval is 200 milliseconds, then the next is 260 milliseconds, then 300 milliseconds, and finally the next one doesn’t make it to the ventricles.
In Mobitz type II AV block, there is no progressive prolongation of the PR interval. Instead, there are a couple of normal PR intervals followed by a dropped beat. Lastly, in third degree AV block, the P-waves and QRS complexes have nothing to do with each other, each appearing at their own rates. The atrial rate is 60 to 100 beats per minute, whereas the ventricular rate usually ranges between 30 to 45 beats per minute. The QRS complex is normal if the escape rhythm starts at the bundle of His or above. It is widened if the escape rhythm starts below the bundle of His.
Now, treatment of AV block may vary depending on the cause, types and severity of symptoms. No treatment is required if the client is asymptomatic like in the first degree or Mobitz type I AV block. Now, in a symptomatic client, the underlying cause of the AV block should be identified and treated, when possible. Additional treatment depends on the type of block as well as whether or not the client is hemodynamically stable.
Sources
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- "Lewis’s medical-surgical nursing: Assessment and management of clinical problems" Elsevier (2020)
- "Saunders Comprehensive Review for the NCLEX-RN Examination" Elsevier (2017)
- "Fundamentals of Nursing" Elsevier (2021)
- "Contralateral pneumothorax and pneumopericardium after dual-chamber pacemaker implantation: Mechanism, diagnosis, and treatment" HeartRhythm Case Reports (2018)
- "Right Bundle Branch Block: Current Considerations" Current Cardiology Reviews (2021)