This case study discusses the management of a 68 year old male who presented with chest palpitations secondary to rapid trial fibrillation. Trial fibrillation is a common cardiac arrhythmia with serious complications if not treated correctly. This essay will discuss the initial clinical presentation of the patient and examine the management and outcome of the interventions applied. The significance of trial fibrillation including its pathologically and etiology will also be discussed. Description of the case:
A 68 year old male presented to the emergency department at 0800 hours via ambulance after experiencing chest discomfort and intermittent palpitations since 3500 hours. Prior to presentation, the patient stated he was fit and well, taking only aspirin and Stool daily to manage his trial fibrillation which had been diagnosed in late 2004. The patient had no other medical history and was managed by his local doctor. Based on the Australian Triage Scale a category three (urgent) was allocated indicating that the patient should be reviewed by a medical officer within thirty minutes (McCollum, 2006).
Due to his rapid heart rate and potential risk of becoming humiliatingly unstable as well as the associated chest discomfort/ palpitations he was allocated to the high dependency area within the department. On initial assessment the patient was gauged as lethargic but orientated, with a Glasgow Coma Scale of 1 5/15. He was spontaneously breathing, speaking in short sentences, not visibly distressed but moderately short of breath. His skin was warm but sweaty and heart rate irregular on radial palpation.
The patient complained of intermittent chest palpitations, similar to previous episodes of rapid trial fibrillation UT denied chest pain. Chest auscultation revealed equal air entry with normal breath sounds. He was not experiencing any dizziness or nausea at the time of assessment. The initial vital signs were as follows: heart rate (HRS) 125 beats per minute blood pressure (BP) 113/43 oxygen saturation (Esp.) 100% room air respiratory rate (OR) 20 breaths per minute temperature 35 C.
Interventions and rationale: Initially, several nursing interventions were implemented whilst waiting for a medical officer to review the patient. A complete set of vital signs was recorded and the attain placed on cardiac monitoring, allowing a cardiac rhythm to be determined. As the patient was maintaining adequate blood pressure he was considered stable enough to remain in the allocated triage category. The patient became anxious due to shortness of breath. Low flow oxygen was applied via nasal prongs to increase the meme of circulating oxygen.
This provided reassurance and his anxiety and shortness of breath subsided. Secondly, a twelve lead electrocardiogram (EGG) was obtained to determine the cardiac ran Hoyt and possible underlying triggers such as chemical. On examination of the EGG it was evident that the patient was in rapid trial fibrillation with a fluctuating heart rate of between 100-148 beats per minute. EGG characteristics included a rapid ventricular and trial rate, absent P waves and an irregular ventricular rhythm. The SIRS complex presented as normal and there Nas no PR interval (Hussar, 2002).
An eighteen gauge intravenous canola was inserted into the cubical Foss allowing venous bloods to be obtained. Intravenous access for fluid and pharmacological intervention was established in case of rapid deterioration. Bloods were sent to pathology to view the patients urea and electrolytes, full blood count, coagulation count and cardiac enzymes. Abnormal results would indicate a potential cause for the sudden onset of trial fibrillation. A chest x-ray was ordered to establish if the event was triggered by a chest infection, pulmonary embolism or other cause.
The primary focus once the initial interventions Nerve obtained was to maintain stable vital signs, in particular blood pressure and heart rate. As time progressed the patient became hypertensive whilst still in a rapid rhythm. He had a blood pressure of 97/47 and a heart rate of 119 beats per minute hen assessed by the medical officer. Medical involvement included pharmacological intervention. An infusion of Stool MGM was administered intravenously at proxy 0930 over thirty minutes with continuous cardiac monitoring.
Stool, an antilogarithms drug, depresses the sinus heart rate, decreases theoretically conduction, decreases cardiac output and decreases systolic and diastolic blood pressure (Bryant, Knights, & Saleroom, 2003). As the patient was already humiliatingly compromised, a bolus of fluid (Seclusion malls) was administered prior to the Stool infusion. The aim was to increase the circulating meme and raise blood pressure. Vital signs remained stable during the infusion, however the heart rate was neither converted to sinus rhythm or reduced to a normal rate.
At 1130 a second antilogarithms drug, Emendation 1 MGM, was administered via intravenous infusion. Its action is unknown however is thought to prolong the action potential duration (Sideway, 2003). Similar to the Stool no effect Nas noted with the rate or rhythm. The patients blood pressure remained low, 96/67 and heart rate fluctuating between 100-130 beats per minute. The patient was asymptomatic with his blood pressure but remained sweaty and lethargic. He received further intravenous fluids whilst the medical officer discussed his presentation with the cardiology team.
After discussion with the patient regarding other methods of treatment he was transferred to the resuscitation cubicles in order to have an elective electrocardiogram. He was a suitable candidate as he had been fasting since early morning and was failing to revert with pharmacological intervention alone. The patient was sedated and shocked twice at kick] and 1 ask] respectively. On the second shock he reverted to a sinus brickyard. He was given further Seclusion to maintain his blood pressure and remained in sinus rhythm. He patient was discharged home several hours later with instructions to his local general practitioner to organize a cardiologist review and potential trial electrical ablation. His cardiac enzymes were normal, as were all other diagnostic studies. No specific trigger was identified for the sudden onset of trial fibrillation. He was advised to continue on his medications and to represent if experiencing similar symptoms. The patient was discharged none at 1 ours that evening into his Knife’s care as he was deemed competent to monitor his own condition.
Anatomy and physiology: ere heart is a muscular, hollow organ which has the primary function of pumping blood around the body through coordinated nerve impulses and rhythmic muscular contractions. The heart can be divided into right and left sides and is composed of cardiac muscle. The left side is responsible for pumping oxygenated blood into the aorta and various parts of the body. The right side of the heart receives De- oxygenated blood and pumps it into the pulmonary arteries (Tractor ; Derricks, 2006).
Blood flow through the heart is regulated by a series of valves Inch prevent back flow and overfilling of the chambers. In the normal operation of the heart, electrical conduction allows an impulse generated by the senatorial node SIS), found in the right atrium, to be transmitted to the theoretically node (VA), located between the atria and ventricles. The impulse from the AS node spreads over the atria causing contraction of the muscle. The VA node slows the impulse slightly Inch then continues down the bundle of HIS, stimulating left and right ventricle interaction.
Coordinated contraction of the atria and ventricle results in efficient ejection of blood around the body (Tractor ; Derricks, 2006). Specializes cardiac muscle fibers termed authoritarian fibers are the source of electrical activity as they are self excitable and generate action potentials causing muscle contraction. These fibers form a conduction system which ensures each chamber is stimulated and contracts in a coordinated and organized way maintaining an effective pumping action. Trial fibrillation (OAF) is a common cardiac arrhythmia which can be detrimental if not controlled.
It involves rapid irregular firing from multiple octopi pacemaker cells of the atria as well as irregular and often rapid ventricular responses. There is no coordinated trial deportation and contraction. The heart muscle cannot produce strong, efficient contractions and instead is a quivering mass of muscle (Tangential, Keller ; Stickpins, 2004). Trial fibrillation can result from cardiac and non cardiac causes and its pathologically is not fully understood. Cardiac causes can include post cardiac surgery, hypertension and material exaggeration whilst non cardiac causes can include infections of the chest or urinary tract.
On the other hand, trial fibrillation can also be present in some individuals Ninth no identified risk factors, and can be considered idiopathic (Marketed ; schilling, 2003). Signs, symptoms and pathologically: Clinical presentations of OAF can vary dramatically in individuals. Generally patients can experience dizziness, fatigue, chest discomfort, palpitations and shortness of breath. A heart beating in a rhythm of trial fibrillation is not pumping enough blood Ninth each beat. Stroke volume is the amount of blood ejected with each heart beat. He decreased filling of the ventricles and loss of trial kick decreases the stroke meme. As a result cardiac output is decreased and a drop in blood pressure, despite a rapid heart rate, occurs. The body has several mechanisms to maintain blood pressure but can only maintain it for a short period. Vessels can be constricted and encourage the pooling of blood to important organs to maintain perfusion. When ¶load pressure decreases significantly cerebral b tool can be diminished and feelings of light headiness, fatigue and weakness can be experienced.
Chest pain can result from trial fibrillation due to the excess stimulation of the atria and ‘intricate. Decreased cardiac output can cause decreased oxygen supply to the tissues and muscles, resulting in angina type pain. It can often be reduced by applying supplemental oxygen. Patients with complex cardiac histories such as hypertension, myocardial infarct and other risk factors such as smoking and diabetes are more likely to develop trial fibrillation as a result of their commodities (Gharry & Mantel, 2002). Palpitations experienced by the patient in rapid trial fibrillation an be uncomfortable and cause anxiety and distress.
They occur as a result of the chaotic and irregular firing and stimulation of the cardiac muscle. Often the patient feels as though their heart is beating in their chest and that they cannot catch their breath. Physical and emotional stress can lead to a sympathetic response from the body. Airways dilate allowing more airflow in and out of the lungs, vacillation of specific vessels that feed the important organs such as skeletal and cardiac muscle occurs, and sweating can increase to regulate temperature changes secondary to the
Increased workload on the body (Tractor & Derricks, 2006). Evidence: There are three types of trial fibrillation; paroxysmal, persistent and permanent. Paroxysmal often has a spontaneous onset and self resolves. Patients can fluctuate between normal sinus rhythm and trial fibrillation often experiencing little to no symptoms. Treatment is not required unless symptoms cause aggravation for the patient. Persistent OAF requires intervention as it will not self resolve and the patient has the potential to become humiliatingly unstable.
Pharmacological intervention may be required with antilogarithms drugs, or elective electrocardiogram’s may be deemed appropriate. Permanent OAF however is non- responsive to treatment and sinus rhythm cannot be restored. The primary focus shifts from rhythm control to rate control and often the patient needs anticoagulation therapy to prevent fatal complications such as stroke (Lee, 2006). The initial management of OAF is dependent on the type of, severity of symptoms and commodities of the patient.
Literature agrees that maintenance of sinus rhythm produces a better outcome than rate control interventions (Gharry ; Mantel, 2002). The most common complication of OAF is stroke. Chaotic and irregular contractions of the heart can leave blood to pool and clot in the atria. This clot can eventually be expelled and lodge in other vessels, or block blood flow causing chemical (Ballad, Gelded ; Crisis, 2002). Permanent trial fibrillation often requires coagulation therapy to prevent such events from occurring.
Permanent OAF can also weaken the heart muscle and lead to cardiac failure which compromises the amount of blood flow circulating and compromising specific body organs and functions. Appropriate intervention is necessary to ensure these complications are minimized. Despite a wide variety of drugs being available, one is not identified as being superior or more effective in the treatment of trial fibrillation. As discussed, two antilogarithms drugs were used, Stool and Emendation. Stool is often well tolerated and commonly used within this setting to establish sinus rhythm.
Emendation is not as preferable in use and is oaten used as a second or last choice as it has a number of adverse reactions and a long half life. In this situation neither drug was effective in reverting the patient to sinus rhythm and compromised the blood pressure of the patient. Electrical carnivores to establish normal sinus rhythm is decided based on several factors including, likelihood of success, potential risk factors, benefits of a successful revert and hemorrhagic stability of the patients. He patient is lightly sedated and an electrical shock is applied at a low voltage to stop the hearts electrical activity for a split second. While the heart is stopped the conduction system has a chance to resume a normal pathway and achieve sinus rhythm (Tangential, Keller ; Stickpins, 2004). Commonly a second shock at a higher voltage is required. Despite this method being invasive and painful, it has less complications than many of the antilogarithms drugs used. In this situation it was ‘ere effective and reverted the patient to sinus rhythm after two shocks.
Evaluation and conclusion: Cardiac arrhythmias can be detrimental if ignored or misdiagnosed. The implementation of pharmacological intervention is often a less traumatic experience for the patient and preferred within the emergency department if the patient is not considered seriously humiliatingly unstable. However, in this case the patient Nas unresponsive to antilogarithm drugs. He reverted to sinus rhythm only after electrocardiogram. Legally, the patient was required to be consented for treatment and failure to do so would have been considered assault.
The risks and procedure Nas well explained by the medical officer allowing the patient to ask questions and refuse the treatment if he felt it was inappropriate (Staunton & Hepburn, 2002). Nursing implications for the management of a patient in trial fibrillation would include the following: constant monitoring of vital signs to identify potential deterioration understanding of the pharmacological interventions, their expected outcomes, side effects and adverse reactions continually re-evaluating the patients response to the intervention.
Despite a wide variety of literature being available on trial fibrillation there is not a uniform method of treatment. Interventions are based on clinical presentation and currently support the concept of rhythm control rather than rate control. Further research is required into the specific actions of some drugs used in treating trial fibrillation as their action is not fully understood. Recent studies examining the mechanisms of trial fibrillation will allow revision of current therapeutic Interventions. The patient discussed in this case study was previously healthy with a DOD quality of life.