Atrial Fibrillation
Atrial fibrillation is the most encountered cardiac rhythm disorder in clinical practice. It affects <1% of persons aged <60 years. This prevalence increases to 10% in persons aged >80 years (Amerena, Walters, Mirzaee and Kalman, 2013). Atrial fibrillation is a key differential diagnosis in patients presenting with chest pain, palpitations, shortness of breath, light-headedness, and syncope (Cruickshank, 2008). This paper will examine the differential diagnosis, pathophysiology, and paramedic implications of atrial fibrillation in relation to the case of a 43-year old male who presents with features and ECG findings of atrial fibrillation. It will first examine the provided information and identify the key information and other information required.
The information known about the patient includes his age, gender, presenting complaints, physical assessment findings, past medical history, and family history. The patient is a 43 year old male who has complains of shortness of breath, severe chest discomfort, palpitations, anxiety, and hotness of body. The findings of the ABCDE survey are provided. On airway, the patient is alert hence it is most likely that his airway is patent. On breathing, he has mild respiratory distress with a slightly raised respiratory rate of 22 breaths per minute and reduced SpO2 of 94%. On circulation, his heart rate and blood pressure are raised at 145 beats per minute and 170/80 mmHg respectively. His capillary refill time is normal at 2 seconds. He, however, has features of hemodynamic instability that are shortness of breath, severe chest discomfort, and diaphoresis. On disability, the client is alert and oriented to person, time, and place. Findings of the rest of the physical assessment include normal pupil size EARRL size 4 anicteric and atrial fibrillation on ECG. Auscultation reveals no heart murmurs and bibasilar rales in the lungs. On palpation, his abdomen is soft and non-tender. He also has a fever of 38.80C which is suggestive of an infection. His past medical history is significant for depression, hypertension, and paroxysmal atrial tachycardia. He has no known allergies. He is on paroxetine, amiodarone, and hydrochlorothiazide. His family history is insignificant. He smokes, and indulges in ethyl alcohol occasionally. He denies use of recreational drugs.
The key information known about this patient includes the findings of the ABCDE survey, ECG findings, past medical history, and medications the patient is taking currently. An ABCDE survey should be performed on all patients even on patients who appear stable initially. It is essential for recognition of the rapidly deteriorating patient and determination of baseline parameters. The ECG findings of atrial fibrillation are important as they determine a need for urgent transfer of the patient to a hospital and risk for rapid deterioration of the patient. The other key information provided about the patient is his medication history. The patient is on amiodarone which is used for the treatment of supraventricular and ventricular arrhythmias and is presenting with atrial fibrillation (Erven and Schalij, 2010). The patient is also on a diuretic, hydrochlorothiazide, which can cause hypokalemia. The patient has a past medical history of paroxysmal atrial tachycardia. This information is vital as it is essential to determine the evolution of symptoms for patients presenting with atrial fibrillation. This helps to distinguish between paroxysmal, persistent, and permanent atrial fibrillation and consequently, treatment of the patient (Markides and Schilling, 2003). The other information required with regards to this patient includes his adherence to medication. It is essential to determine whether the patient has been taking his medications as prescribed particularly amiodarone as it is supposed to prevent atrial fibrillation. It is also vital to determine whether his blood pressure has been well controlled as hypertension is one of the causes of atrial fibrillation.
Atrial fibrillation can be caused by a number of conditions. The possible causes of atrial fibrillation in this patient are pneumonia, electrolyte imbalance, and hypertension. The most likely diagnosis for this patient is atrial fibrillation complicating hypertension. Atrial fibrillation occurs due to anomalies in the heart’s electrical signaling pathway. In atrial fibrillation, signals are not triggered systematically by the sino-atrial node (SAN). Rather, they are produced all over the atria and they do not follow a regular coordinated pathway. The signals so generated and transmitted lead to fibrillating or quivering uncoordinated atrial activity. Therefore, the pathophysiology of atrial fibrillation involves an interaction between initiating triggers and anomalies in atrial tissue substrate that are capable of maintaining arrhythmia. Triggers of atrial fibrillation are often in the form of fast firing ectopic loci located within one or more pulmonary veins. They can also be a single localized reentry circuit or multiple functional reentry circuits differing in time and space. Paroxysmal forms of atrial fibrillation are often caused by local triggers especially from the pulmonary veins. Reentry substrates which are functional initially then structural predominate as the atrial fibrillation becomes persistent then eventually permanent. The mechanisms underlying ectopic firing are enhanced automaticity, early afterdepolarizations, and delayed afterdepolarizations (Markides and Schilling, 2003).
Sustained atrial fibrillation causes electrophysiological remodeling of the atrium begetting more atrial fibrillation. Long-standing hypertension can cause structural heart disease. The mechanisms through which these changes lead to generation of abnormal foci are, however, yet to be fully elucidated. Atrial fibrillation is associated with a high risk of thromboembolism. When the atrium is fibrillating, it is unable to empty the atrium fully leading to accumulation of blood in the atrial appendage, an area of increased atrial mass within the left atrium that forms a sac. The stagnated blood can form clots which can break away causing an embolic stroke. Patients with atrial fibrillation can also progress into cardiac arrest due to loss of atrial contraction and fast and irregular ventricular rate. Atrial fibrillation causes an increase in ventricular rate as the atrio-ventricular node is unable to filter the excess signals coming from the atrium (Iwasaki, Nishida, Kato and Nattel, 2011).
On the implications for paramedic practice, it is important for paramedics to understand the pathophysiology of atrial fibrillation as they are caused by both cardiac and non-cardiac causes. In addition, they should be able to accurately identify and classify patients with atrial fibrillation by their presenting features and ECG and to initiate management rapidly. This is especially more so as atrial fibrillation is the most common cardiac arrhythmia. More importantly, paramedics should be able to identify features that indicate hemodynamic instability in patients presenting with atrial fibrillation. These features include shortness of breath, chest pain, light headedness, and diaphoresis. This is because such patients require prompt electric cardioversion to restore sinus rhythm. Lastly, paramedics need to familiarize themselves with Australian resuscitation guidelines and standards on atrial fibrillation (Ministry of Health of New South Wales, 2011).
In summary, this paper has examined the differential diagnosis, most likely cause, and pathophysiology of atrial fibrillation in relation to the case of a 43-year old male patient who presents with features suggestive of atrial fibrillation confirmed by ECG. Atrial fibrillation can be caused by a host of factors including heart disease, hypertension, and infections like pneumonia. Atrial fibrillation in this patient is likely the result of structural remodeling of the heart due to hypertension. Because of the heightened risk for stroke and death, it is vital for paramedics to be able to identify features of atrial fibrillation, to identify atrial fibrillation on ECG, and initiate management promptly.
References
Amerena, J. V., Walters, T. E., Mirzaee, S. and Kalman, J., 2013. Update on the management of atrial fibrillation. The Medical Journal of Australia, 199(9), pp. 592-597.
Cruickshank, J., 2008. Initial management of cardiac arrhythmias. Australian Family Physician, 37(7), pp. 516-521.
Erven, L. and Schalij, M. J., 2010. Amiodarone: An effective antiarryhtmic drug with unusual side effects. Heart, 96, pp. 1593-1600.
Iwasaki, Y., Nishida, K., Kato, T. and Nattel, S., 2011. Atrial fibrillation pathophysiology: implications for management. Circulation, 124(20), p. 2264.
Markides, V. and Schilling, R. J., 2003. Atrial fibrillation: Classification, pathophysiology, mechanisms and drug treatment. Heart, 89(8), pp. 939-943.
Ministry of Health New South wales, 2011. Chest pain evaluation. [Online] Available at: <http://www0.health.nsw.gov.au/policies/pd/2011/pdf/pd2011_037.pdf> [Accessed 1 September 2016].
