Pathophysiology and Pathophysiology of AF

David Ramsey, 76 years old is lying on the bed and I, an ambulance paramedic, has just arrived at his home. I find his partner attending to him. When told to describe what his problem is, David explains that he has been feeling unwell for some time and that his heart seems to be jumping out of his chest. Moreover, David denies having any chest pains or nausea but ascertains something is wrong with him. At times, he is unable to catch his breath and says the same had happened earlier, but he could not remember what the doctor had said about it. David past medical history is unknown, but he had regular blood tests. He is currently taking aspirin, warfarin, and digoxin. There is no known family history recorded.

Diagnosis

On diagnosis, David presents the following vital signs. His heart rate matches the normal ECG. His respiration rate is 24, and no respiratory sounds are observed. Both blood glucose and pressure stands at 4.7mmol and 136/90 respectively. His temperature is normal (370C) and skin slightly pale. Oxygen saturation stands at 93%RA with the rate of fluid passage through the circulatory system to tissues being 2s. The pupils functioning are equal and reactive. The Glasgow Coma Scale indicates a conscious level of 15 with the ECG image printout showing an irregular heartbeat rate. David’s blood pressure is high (136/90), he has an irregular heartbeat rhythm (arrhythmia), there are no P Waves, and thus PR intervals cannot be measured. QRS complexes are wide due to the anomalies within the intraventricular conduction system. After diagnosis and following the provisional diagnosis on the ECG, I establish that David is suffering from Atrial Fibrillation (AF), a condition characterised by an irregular heart rate and sometimes it can be very fast.

Epidemiology

Atrial Fibrillation (AF) was first discovered in 1909 and has continued attracting attention as it mainly affects the elderly (Silverman, 2009). Currently, AF affects about 2.2 million people in U.S. and is the leading rhythm disorder in patients hospitalised with a primary diagnosis of arrhythmia. Concerning impacts on mortality and morbidity, the developing epidemic of AF is linked to several conditions such as thromboembolism, ageing, hypertension, haemorrhage, and the left ventricular dysfunction (Sumeet & Bernard, 2011). Presently, the natural history and epidemiology of AF constitute every aspect in the clinical management of the condition. Discovering the genetics of AF offers a ground to understand the electrical and structural phenotypes that result from genetic mutation, where strategies are being invented to treat arrhythmia at the cellular level. Therefore, the existing adverse trends are associated with the background of rapidly growing understanding on potential therapeutic options in existence.

Etiology

In AF, the chambers of the heart undergo irregular contraction that is occasionally so fast that makes the heart muscles unable to contract correctly between these contractions (National Health Services, 2017). Consequently, the performance and efficiency of the heart are reduced. AF occurrence is prevalence in particular groups of people and is sometimes triggered by certain habits such as too much alcohol or smoking. However, the leading causes of damage to the structures of the heart that leads to atrial fibrillation include heart attacks, high blood pressure, abnormal heart valves, coronary artery disease, congenital heart defects and metabolic imbalances due to conditions such as hyperactive thyroid glands (Mayo Clinic, 2017). Others include; being exposed to stimulants such as caffeine, medications, alcohol or tobacco, lung disease, sick sinus syndrome previous heart surgeries, sleep apnea, viral infections and stress associated with pneumonia, surgeries, or other ailments (Mayo Clinic, 2017).

Pathophysiology of Atrial Fibrillation

The onset of AF is linked to the heightened electrical action of the pulmonary vein cardiomyocyte covers, whereas sources of pulmonary vein become incredibly significant when AF persists for long (Ferrari, et al., 2016). Afterward, AF is maintained through a primary driver mechanism that can either be the focal ectopic source or quick local re-entry into the vulnerable substrate. In the re-entry process, a substrate and a trigger are required (Nattel, Burstein, & Dobrev, 2008). Excitations advance via the vulnerable substrate having a spiral or circular wavefronts known as rotors and hence maintenance of AF and the modification of atrium (substrate) structures. Sustainment of AF using atrial rhythms at 350-600 bpm causes electrophysiology remodelling that comprises of outward K+ current (Ito), L-type Ca2+ and ultra-rapid delayed rectifier K+ current (Ikur). This results in a parallel increase in the inward rectifiers K+ current (Ik1), reduced components of delayed rectifier K+ current (Iks), and agonist-independent forms of acetylcholine dependent K+ current (Ik, Ach). The outcomes of these variations in current cause effective refractory period and action potential to shorten causing maintenance of AF (Nattel, Burstein, & Dobrev, 2008).

Significantly, the remodelling of electrophysiological is associated with the abnormal Ca2+ prevalence and an increase in the incidence of potential proarrhythmic Ca2+
discharge cycles from the sarcoplasmic reticulum following diastole that compromises contraction of the atria triggering ectopic activities (Ferrari, et al., 2016). The remodelling process of electrophysiology becomes absent during the sinus rhythm of the heart. The processing frequency reduces in a paroxysmal AF as a result of reversibility that occurs between AF-free intervals. The remodelling process takes weeks, days, or even hours following arrhythmia onset and relies on the ion channels. During maintenance of AF, remodelling of atria structures occurs (fibrosis and hypertrophy). In comparison to electrophysiological remodelling, atrial remodelling takes long to months or years and is linked to hypertension, age, and other comorbid heart conditions. This is the reason for aggressive and early treatment of linked factors like heart failure, hypertension, and coronary diseases that may come before AF.

The exact molecular processes that constitute AF have not been fully unravelled, even though interstitial fibrosis, observable through cardiomyocyte-myofibroblast interactions have been evoked (Ferrari, et al., 2016). In fact, AF results to the distinction of a fibroblast into a myofibroblast that produces more collagen compared to fibroblast and expression of specific cardiac channels such as Ikur and exertion of paracrine activities on the cardiomyocyte. These associations are pivotal to both structural and electrophysiological remodelling that entails preservation of substrates that are re-entering. The primary challenge is the difficulty in reliable identification and quantification of atrial fibrosis in vivo (Davies, Jin, & Shen, 2014).

Assessment

AF presents in any health condition and encompasses a broad range of non-specific symptoms as observed in David’s case. In most scenarios, AF is commonly diagnosed with instances of breathlessness, palpitations, dizziness, syncope, and chest discomfort (Dewar & Lip, 2006). The manifestation of an irregular pulse rate is an indication of AF, and patients are supposed to find immediate treatment. Taking regular blood pressure and pulse checks for patients with palpitations, dyspnea, breathlessness, chest discomfort and dizziness is critical. Moreover, the majority of interventions depends on individual circumstances that at times calls for comprehensive clinical assessment once someone is diagnosed with AF. It is essential to determine clinical patterns of the condition such as the persistent nature of paroxysmal, onset time, probable aetiology, underlying complications, and any co-existing disorders. A full history of the patient (David Ramsey) and his family will offer valuable information for assessment and diagnosis of the patient. However, this was lacking. The availability of blood tests made it easier to assess the pattern of the patient’s blood pressure and pulse rates. For secondary care, echocardiography is critical for optimal management of the condition (Dewar & Lip, 2006).

Treatment

During emergency treatment of AF diagnosed in David Ramsey, it is essential to understand that acute AF converts to sinus rhythm between 16 to 48 hours where cardioversion should be done. This procedure should not be done after 48 hours due to increased risks of thromboembolism. Either electrical or pharmacological cardioversions can be used for the treatment of AF. However, due to adverse inotropic effects of pharmacological cardioversion (propafenone, flecainide, amiodarone, vernakalant, ibutilide), electrical cardioversion is the best intervention method. For long-term control of AF, verapamil, beta-blockers, and digitalis can be used to lower ventricular rates. Controlling AF rhythm denotes attempts to restore the sinus rhythm. Any of anti-rhythmic drugs can be used and include sotalol, propafenone, amiodarone, dronedarone, and flecainide. If paroxysmal AF is identified, catheter ablation can be used (ECGWaves.com, 2017).

Transport Options

Given the urgency of the situation, the patient’s difficulty in breathing and a feeling of discomfort in the chest, the best means of transport is an ambulance with a forced breathing device (C-PAP) and other heart-related emergency medical supplies. The ambulance has a bed to lay the patient, first aid supplies and will travel first to the hospital where further medical checkups will be performed.

References

Davies, L., Jin, J., & Shen, W. (2014). Mkk4 is a negative regulator of the transforming growth factor beta 1 signaling associated with atrial remodeling and arrhythmogenesis with age. Journal of American Heart Association, 3(1).

Dewar, R. I., & Lip, G. Y. (2006). Identification, diagnosis and assessment of atrial fibrillation. Journal of heart, 93(1), 25–28. doi: 10.1136/hrt.2006.099861

ECGWaves.com. (2017, October). Atrial Fibrillation:definations, causes, risk factors, ECG diagnosis, and management. Retrieved from ECGWaves.com: https://ecgwaves.com/atrial-fibrillation-ecg-ekg-causes-classification-management/

Ferrari, R., Bertini, M., Blomstrom-Lundqvist, C., Dobrev, D., Kirchhof, P., & Ravens, U. (2016). An update on atrial fibrillation in 2014: From pathophysiology to treatment. International Journal of Cardiology, 1(1), 22–29.

Mayo Clinic. (2017, October). Atrial fibrillation. Retrieved from Mayo Clinic: https://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/symptoms-causes/syc-20350624

National Health Services. (2017, October). Causes of atrial fibrillation. Retrieved from NHS: http://www.nhs.uk/Conditions/Atrial-fibrillation/Pages/Causes.aspx

Nattel, S., Burstein, B., & Dobrev, D. (2008). Atrial remodeling and atrial fibrillation: mechanisms and implications. Circ. Arrhythm. Electrophysiol, 1(1), 62-73.

Silverman, M. (2009). From rebellious palpitations to the discovery of auricular fibrillation: Contributions of Mackenzie, Lewis and Einthoven. American Journal of Cardiology, 73(1), 384-389.

Sumeet, S. C., & Bernard, J. G. (2011). Epidemiology and natural history of atrial fibrillation: clinical implications. Journal of the American College of Cardiology, 37(2), 371-378. Retrieved from https://doi.org/10.1016/S0735-1097(00)01107-4