Heart rate The release of norepinephrine by the sympathetic nerve endings and epinephrine released from the adrenal gland are the main contributing hormonal factors to heart rate (Banasik & Copstead, 2018; Honan, 2019). Exogenous agents, such as nicotine and caffeine, have a sympathomimetic effect on the heart rate, hence increasing it. Under normal resting conditions, the heart rate is under the influence of the parasympathetic tone, thus maintaining a normal resting heart rate of 70 (Banasik & Copstead, 2018; Honan, 2019). Heart rate control is the first goal of management for AF. This is especially important in patients with ischemic heart disease, since anginal symptoms could be exacerbated with fast heart rates. This can occur because the coronary sinus is perfused during diastole, which could be impaired in atrial fibrillation Stroke volume Stroke volume has three components: preload, afterload, and contractility. Preload is the volume of blood returning to the heart as affected by venous return and compliance. This concept is further described by the Frank-Starling law, which explains that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles. During diastolic filling, myocardial fibers stretch in response to circulating blood volume and this ultimately increases the force of systole or contraction. Thus, when the heart’s volume increases, stroke volume increases (Banasik & Copstead, 2018; Honan, 2019). Clinically, preload can be referred to as the “filling pressures” of the heart, such as central venous pressure (CVP) and pulmonary artery wedge pressure (PAWP). One can decrease preload by giving vasodilators and diuretics. Conversely, preload is increased with fluids or by increasing vascular tone with vasopressors. The next component of stroke volume is afterload. Simply defined, afterload is the pressure the left ventricle must overcome to eject blood. Left ventricular afterload is determined primarily by aortic blood pressure. Hence the resistance, or afterload that the left ventricle must overcome to eject its volume is based on the pressure against the left ventricle from the aortic blood pressure (Banasik & Copstead, 2018; Honan, 2019). The three determinants that create this resistance are aortic impedance (aortic stenosis), systemic vascular resistance (HTN), and volume/viscosity (dehydration). Thus, a patient with HTN has more resistance or a higher afterload to overcome to eject blood from the left ventricle. Therefore, pharmacologic management should focus on decreasing afterload in the appropriate clinical context. Over time, increased afterload can lead to left ventricular hypertrophy and diastolic heart failure. Conversely, patients in septic shock have decreased afterload because of low systemic vascular resistance in response to inflammatory mediators. Therefore, the mainstay treatment for
as diastolic filling is impaired. The faster the heart rate, the shorter the time in diastole and the less time for coronary artery perfusion (Banasik & Copstead, 2018; Honan, 2019). Nursing consideration: Common teaching is that the heart rate of the patient with ischemic heart disease should be kept low to maximize diastolic filling time and coronary artery perfusion. Rather than assessing heart rate alone, the APRN should assess overall clinical status as related to the presence of hypotension, the patient’s report of dizziness, notable changes in fatigue level, functional status, and exercise tolerance, which can be given through the subjective report by the patient or formally with an exercise tolerance test (ETT). septic shock is to maximize volume (preload) by giving fluids, while supporting systemic vascular resistance with vasopressors and treating the underlying cause. The last component of stroke volume is the contractility of the heart. This is often referred to as its “inotropic” action (Banasik & Copstead, 2018; Honan, 2019). Clinically, contractility can be measured as the ejection fraction (EF) using an echocardiogram, transesophageal echocardiogram, or cardiac catheterization. The ejection fraction is the percent of blood ejected from the ventricles with each beat. A normal EF is 50% to 70% (not all blood is ejected from the ventricle at one time). Patients with systolic heart failure have an EF of less than 40%. Documentation of systolic heart failure is commonly noted as heart failure with reduced ejection fraction, or HFrEF. This reduction in systole could result in volume overload, pulmonary congestion, and right-sided heart failure. Active atrial contractions immediately before ventricular systole (ejection) act to increase the efficiency of ventricular ejection second to acutely increasing preload. These atrial contractions are known as the “atrial kick.” Atrial kick accounts for approximately 20% of cardiac output, hence, when patients develop AF with chaotic atrial contractions, they can exhibit clinical manifestations of decreased cardiac output. Nursing consideration: It is crucial to understand cardiac output in the management of the patient that develops atrial fibrillation. Rapid or elevated heart rates can compromise diastolic filling, decreasing coronary artery perfusion and precipitating ischemia. Also, a loss of atrial kick will affect cardiac output by 20%. Patients with reduced ejection fractions will experience greater hemodynamic compromise from this loss of atrial kick. Low volume states could decrease preload (volume) and increase afterload (via resistance), affecting hemodynamic stability.
RISK FACTORS FOR AF
There are numerous risk factors that predispose individuals to developing atrial fibrillation. Structural heart changes to the chambers, valves, and lining of the heart will change the heart’s function, thus changing the electrical excitability. Rather than memorizing the etiologies, think back to the “why” or “how” the heart changes (Table 1). In addition, patients may present with a single risk factor or have multiple comorbidities, which could contribute to the development of new or persistent atrial fibrillation. One co-morbid condition that requires specific attention is the incidence of AF in heart failure (HF). Approximately one-third of all HF patients have AF. More specifically, the prevalence of AF increases with HF severity, ranging from 5% in mild HF to 50% in severe HF. In heart failure with a preserved ejection fraction (diastolic failure), the prevalence of AF is 60% (Patel et al, 2020). Again, the concept of heart structure changing heart function
assists the provider to recall why this disease is so prevalent in the population. Evidence-based practice! A systematic review and meta- analysis were performed on the potential link between obesity and the incidence of AF. This meta-analysis included data from 51 studies, with 626,603 individuals contributing to the data. There was a 29% and 19% greater excess risk of incidence of AF for every five units BMI increase in cohort and case-control studies, respectively. Similarly, there were 10% and 13% greater excess risks of post-operative and post-ablation AF for every five unit increase in BMI, respectively (Wong et al., 2016).
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Book Code: AUS3024
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