M1P7.pdf

1/9/24, 1:04 AM herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9a… Premature Atrial Complex A PAC is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus n...

1/9/24, 1:04 AM herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9a… Premature Atrial Complex A PAC is a single ECG complex that occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus node. The PAC may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium (e.g., as in hypervolemia), anxiety, hypokalemia (low potassium level), hypermetabolic states (e.g., with pregnancy), or atrial ischemia, injury, or infarction. PACs are often seen with sinus tachycardia. PACs have the following characteristics (see Fig. 22-9): Ventricular and atrial rate: Depends on the underlying rhythm (e.g., sinus tachycardia) Ventricular and atrial rhythm: Irregular due to early P waves, creating a PP interval that is shorter than the others. This is sometimes followed by a longerthan-normal PP interval, but one that is less than twice the normal PP interval. This type of interval is called a noncompensatory pause QRS shape and duration: The QRS that follows the early P wave is usually normal, but it may be abnormal (aberrantly conducted PAC). It may even be absent (blocked PAC) P wave: An early and different P wave may be seen or may be hidden in the T wave; other P waves in the strip are consistent PR interval: The early P wave has a shorter-than-normal PR interval, but still between 0.12 and 0.20 seconds P:QRS ratio: Usually 1:1 PACs are common in normal hearts. The patient may say, “My heart skipped a beat.” A pulse deficit (a difference between the apical and radial pulse rate) may exist. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9aojXmGqF3r… 1/7 1/9/24, 1:04 AM herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9a… Atrial Fibrillation Atrial fibrillation is a very common arrhythmia; between 2.7 and 6.1 million Americans are living with atrial fibrillation (Centers for Disease Control and Prevention [CDC], 2017). Atrial fibrillation is a serious public health concern because it is associated with aging, and the older adult population is increasing in the United States (Chen, Chung, Allen, et al., 2018). Atrial fibrillation can result from diverse pathophysiologic etiologies and risks. Atrial fibrillation results from abnormal impulse formation that occurs when structural or electrophysiologic abnormalities alter the atrial tissue causing a rapid, disorganized, and uncoordinated twitching of the atrial musculature (January, Wann, Alpert, et al., 2014; January, Wann, Calkins, et al., 2019). Both the extrinsic (central) and intrinsic cardiac autonomic nervous systems (CANS) are thought to play an important role in the initiation and continuance of atrial fibrillation (Qin, Zeng, & Liu, 2019). Separate from the extrinsic (central) nervous system, which includes the brain and spinal cord, the CANS consists of a highly interconnected network of autonomic ganglia and nerve cell bodies embedded within the epicardium, largely within the atrial myocardium and great vessels (pulmonary veins). Hyperactive autonomic ganglia in the CANS are thought to play a critical role in atrial fibrillation, resulting in impulses that are initiated from the pulmonary veins and conducted through to the AV node. The ventricular rate of response depends on the conduction of atrial impulses through the AV node, presence of accessory electrical conduction pathways, and therapeutic effect of medications. Lack of consistency in describing patterns or types of atrial fibrillation has led to the use of numerous labels, such as paroxysmal (i.e., sudden onset with spontaneous termination), persistent, and permanent. The use of the term “chronic atrial fibrillation” is no longer included in the classification system, due to a lack of consensus on what constitutes chronicity (January et al., 2014, 2019). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9aojXmGqF3r… 2/7 1/9/24, 1:04 AM herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9a… https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9aojXmGqF3r… 3/7 1/9/24, 1:04 AM herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9a… Atrial fibrillation has the following characteristics (Fig. 22-10): Ventricular and atrial rate: Atrial rate is 300 to 600 bpm; ventricular rate is usually 120 to 200 bpm in untreated atrial fibrillation. Ventricular and atrial rhythm: Highly irregular QRS shape and duration: Usually normal, but may be abnormal P wave: No discernible P waves; irregular undulating waves that vary in amplitude and shape are seen and referred to as fibrillatory or f waves PR interval: Cannot be measured P:QRS ratio: Many:1 Patients with atrial fibrillation are at increased risk of heart failure, myocardial ischemia, and embolic events such as stroke (January et al., 2014, 2019). A rapid and irregular ventricular response reduces the time for ventricular filling, resulting in a smaller stroke volume. Because atrial fibrillation causes a loss in AV synchrony (the atria and ventricles contract at different times), the atrial kick (the last part of diastole and ventricular filling, which accounts for 25% to 30% of the cardiac output) is also lost. As a consequence, although some patients with atrial fibrillation are asymptomatic, others experience palpitations and clinical manifestations of heart failure (e.g., shortness of breath, hypotension, dyspnea on exertion, fatigue. In addition, a high ventricular rate of response during atrial fibrillation (greater than 80 bpm) can eventually lead to mitral valve dysfunction, mitral regurgitation, intraventricular conduction delays, and dilated ventricular cardiomyopathy. Patients with atrial fibrillation may exhibit a pulse deficit—a numeric difference between apical and radial pulse rates. The shorter time in diastole reduces the time available for coronary artery perfusion, thereby increasing the risk of myocardial ischemia with the onset of anginal symptoms. Decreasing the ventricular rate may avoid and correct these effects. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9aojXmGqF3r… 4/7 1/9/24, 1:04 AM herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9a… The erratic nature of atrial contraction, alterations in ventricular ejection, and atrial myocardial dysfunction promote the formation of thrombi, especially within the left atrium, increasing the risk of an embolic event. The origin of embolisms resulting in stroke for patients with nonvalvular atrial fibrillation is most often the left atrial appendage (LAA) (Schellinger, Tsivgoulis, Steiner, et al., 2018). A therapeutic approach to addressing the role of the LAA in atrial fibrillation, left atrial appendage occlusion (LAAO). Assessment and Diagnostic Findings The clinical evaluation of atrial fibrillation should include a history and physical examination that identifies the onset and nature of signs and symptoms, including their frequency, duration and any precipitating factors, and any response to medications. Whether or not the patient has a known history of heart disease or other risks is identified (see Chart 22-2). A 12-lead ECG is performed to verify the atrial fibrillation rhythm, as well as to identify the presence (or absence) of left ventricular (LV) hypertrophy, bundle branch block, prior myocardial ischemia, or other arrhythmias. The RR, QRS, and QT intervals are analyzed to verify the effectiveness of any prescribed antiarrhythmic medications (January et al., 2014, 2019). A transesophageal echocardiogram (TEE) can identify the presence of valvular heart disease, provide information about LV and right ventricular (RV) size and function, RV pressures (to identify pulmonary hypertension, which may exist concomitant with atrial fibrillation), LV hypertrophy, and presence of left atrial thrombi (January et al., 2014, 2019). Blood tests to screen for diseases that are known risks for atrial fibrillation, including thyroid, renal, and hepatic function, are assessed in the patient with a new onset of atrial fibrillation, as well as when the ventricular rate is difficult to control (January et al., 2014, 2019). Additional tests may include a chest x-ray (to evaluate pulmonary vasculature in a patient suspected of having pulmonary hypertension), exercise stress test (to exclude myocardial ischemia or reproduce exercise-induced atrial fibrillation), Holter or event monitoring, and an EPS (January et al., 2014, 2019). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9aojXmGqF3r… 5/7 1/9/24, 1:04 AM herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9a… Atrial Flutter Atrial flutter occurs because of a conduction defect in the atrium and causes a rapid, regular atrial impulse at a rate between 250 and 400 bpm. Because the atrial rate is faster than the AV node can conduct, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV node. This is an important feature of this arrhythmia. If all atrial impulses were conducted to the ventricle, the ventricular rate would also be 250 to 400 bpm, which would result in ventricular fibrillation, a lifethreatening arrhythmia. Atrial flutter risk factors mirror those for atrial fibrillation (Fuster et al., 2017. Atrial flutter has the following characteristics (see Fig. 22-12): Ventricular and atrial rate: Atrial rate ranges between 250 and 400 bpm; ventricular rate usually ranges between 75 and 150 bpm. Ventricular and atrial rhythm: The atrial rhythm is regular; the ventricular rhythm is usually regular but may be irregular because of a change in the AV conduction. QRS shape and duration: Usually normal, but may be abnormal or may be absent. P wave: Saw-toothed shape; these waves are referred to as F waves. PR interval: Multiple F waves may make it difficult to determine the PR interval. P:QRS ratio: 2:1, 3:1, or 4:1 Atrial flutter is treated with antithrombotic therapy, rate control, and rhythm control in the same manner as atrial fibrillation (January et al., 2014, 2019). Electrical cardioversion is often successful in converting atrial flutter to sinus rhythm. . https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9aojXmGqF3r… 6/7 1/9/24, 1:04 AM herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9a… https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbusjeLUzRyumZIEGwikvZDA89aMIS3TVE3sojJO9aojXmGqF3r… 7/7