Management of a Cardiac Arrhythmia - Case Study Example

 «Management of a Cardiac Arrhythmia» A case study is made on a patient having cardiac arrhythmia which occurs in different forms. This researcher being an emergency practitioner on ambulance service ideally selects a patient to whom she is competent to give emergency treatment. Rationale for choice of this patient: Arrhythmia occurs as tachycardia and bradycardia both associated with heart rhythm problems. It is proposed to discuss a patient presented with suspected bradycardia for which emergency medicines were readily available before being admitted for further investigation and treatment. Case history The patient on ambulance was 62-year old woman with chest pain and reported to be having a cardiac history. The pain started one hour before she was taken into the ambulance. Her relative informed that the patient was unable to stand steadily since one week due to dizziness. The patient had high blood pressure also. She had no breathing trouble, perspiration or vomiting. Skin was pale and no respiratory distress. Vital signs: BP 90/56, pulse 50 and regular, RR 20/M, pulse oximetry 90 %. Pupils were equal, round and reactive. Blood sugar 88. Persistent enquiry revealed that the patient had been on weight loss programmes. Her body temperature was 86 °. Oxygen through NASLA cannula at 3 LPM. ECG: 12 lead ECG reveals Sinus Bradycardia at 50 PM. QT interval was prolonged without acute ST segment or depressions. Before discussing the case further, it would be worthwhile to have a brief look physiology of arrhythmia and other connected issues such ECG readings etc. Brief account of physiology of arrhythmia The term arrhythmia was coined by Heidenhaim in 1872 to denote irregular cardiac rhythm (Kass and Clancy, 2006 p3). However, understanding of the complication has still not been complete and been evolving. Arrythmogenesis involves two mechanisms of ion disruption and abnormalities in conduction both of which however overlap. The irregular rhythm is caused by irregular movement of ions across muscle membranes of the heart. Electrical conduction in the heart becomes irregular particularly affecting homogeneity of the depolarizing wave. The ions movement across the membranes produce measurable electrical charging in terms of voltage. This movement of electric current is called action potential. The action potential facilitates entry of calcium into cardiac cell. The entry of calcium is for contraction of the cell which in turn results in the heart ejecting blood. Thus the concentration of ions on the sides of the membrane determines the velocity of movement of ions across the membrane. The following table 1 is illustrative of this. (Khan, 2006). The action potential has five phases ranging from 0 to 4. When the myocardial membrane is negative within and positive outside during diastole, the electrical state at rest is said to be polarized when the cell cannot contract. Hence, depolarization takes place to enable the cell to contract by making cell membrane positive inside and negative outside. Sodium ions enter the cell for making the cell positive inside. The steep concentration gradient enables sodium gush into the cell on its membrane becoming permeable. Electricity which comes from sino-arterial (SA) node is what acts as stimulator for opening up ion channels. The artificial pace-maker can also provide the electricity. Thus, entry of sodium ion channels makes the voltage in the cell membrane change from negative value to positive value. This is phase 0. And the phase 1 witnesses more of positive voltage in cell membrane as more calcium membrane channels allow calcium into the cell. Since in phase 1, both the channels are opened because of voltage, they are called voltage-sensitive channels. At this stage, membrane becomes fully polarized. In phase 2, muscle fibres contract because of interaction between liberated calcium and contractile protein called myocin. The contraction continues as long as there is free calcium inside. To stop further calcium entry, the cell is made negative by opening of potassium channels which are positively charged. As the potassium channels come out of the cell, positive charges fall rapidly with no use of energy. This is phase 3. Calcium also is flushed out of the cell thus making the membrane negative inside as the 4 th phase known as repolarisation of the cell which stops from contracting. The depolarized myocardial cell cannot be again depolarized till the completion of the action potential. This is refractivity. The above explained action potential makes the myocardium refractive to another depolarization (contraction) till the action potential is complete. Thus myocardium, is completely refractive during phases 0, 1, and 2 If myocardium is not stable, it can be stimulated by an abnormal stimulus (ectopic) (Khan, 2006). Sinoatrial node (SA node) Located in the right atrium, SA node is made up of specialised cell groups having the feature of what is known as automaticity capable of generating an action potential (current) explained elsewhere (Opie,1998; Huszar,2001; Marirot and Conover,1998). This automaticity takes place as a result of continuous entry of positive ions into the cell (Waldo and Wit, 2001). The automaticity in SA node is triggered by several mechanisms which include autonomic nervous system and hormone. The SA has the automaticity in the heart at 60-100 impulses per minute and it is considered as the physiological pace-maker of the heart (Khan, 2004). Internodal pathways known as atrial pathways serve to conduct impulse generated by SA node. Three such pathways are in the right atrium and one in the left atrium. Those on the right transport electrical impulses from SA Interpretation of the ECG It has become necessary for nurses to have basic understanding of the ECG even for non-cardiac cases such as cases involving Q-T interval-prolonging effect of medicines meant for mental health disorders (Booker et al, 2003, Hennessy et al, 2002 and O’Brien and Oyebode, 2003). The waves PQRST have an interesting history. It was Augustus D Walter (1856-1922) who first discovered that human heart generated current. But Williem Eithnoven (1860-1927) expanded on the Augustus’ discovery and is said to have labelled the waves as PQRST anticipating there might be some more waves yet to be discovered by reserving some of the alphabets before and after (Hurst, 1998). He subsequently found the U wave (Smellen, 1995). The foregoing pages have explained the impulse conduction in the heart through specialised modified muscle tissues which act 2-3 times faster than myocardium does (Levick, 2000). The conduction system consists of “SA node, atrial conduction pathways, the atrioventriclular (AV) node and ventricular conduction pathways “(Khan, 2004, p 441) as seen in the figure below. (above Khan, 2004). Bradycardia In simple terms, bradycardia is slow heart rhythm. Symptoms of bradycardia are fatigue, light-headedness, dizziness and fainting. Bradycardia is characteristic of slow pumping resulting in low blood pressure. This may cause faintness in the patient. Bradycardia characterised by slow heartbeat can occur in healthy persons after some activity. Thus, athletes or those who are in deep relaxation may experience bradycardia. This is normal where condition of the pacemaker is healthy. However, the slow heart-beat can be abnormal with the symptoms of light-headedness or blacking out in otherwise unhealthy patients (A-A Executive Committee, 2010). The heart rhythm coming from the sinus node of heart is at the rate of less than 60 bpm in a bradycardia condition. Diagnostic criteria are “P wave of sinus origin (normal mean axis of the P wave., constant and normal P-R interval of 0.12.--.20 second, constant P wave configuration in each given lead, rate of 45-59 bpm (cyclic length > 1 second) and regular or slightly irregular P-P (R-R) cycle” (Chung, 2000. p 170). It may be noted that sinus bradycardia is different from other conditions of slow heart rhythms as result of many other mechanisms known as “AV JER, second degree or advanced AV block, frequent blocked APCs, SA block and sinus arrest” (Chung,2000, p 170). One should look for upright P-waves in lead II and inverted in a VR for the condition of sinus bradycardia which may also be characterised by more than one Av junctional escape beats (Chung, 2000). In one case, patient had a fall resulting in hypothermia and non-responding to atropine administered for severe bradycardia with a prominent J wave called Osborn waves. The patient was 85-year old with a history of Alzheimer disease with recurrent falls. He had lastly fallen from his bed on a wooden floor and was brought for treatment. As he was combative, initial ECG was interpreted as sinus bradycardia with a bpm of 38. There was ST elevation in the inferior and lateral leads. It was thought to be of symptomatic bradycardia but the two doses of atropine did not increase the heart rate. When the ECG was further analysed, prominent J waves were noticed in II, III, a Vf, and V3-V6 leads. As he was agitated, body temperature could not be checked earlier. Now with these ECG findings, when temperature was checked, it was found to be 88 ° F. After treatment for hypothermia with rewarming, heart rate increased to 64 bpm.and the ST elevation indicated as prominent J wave disappeared. Hypothermia must therefore be watched for to avoid severe bradycardia (Quadir and Kanjwal, 2010). (figure above)Initial ECG showing sinus bradycardia with prominent J waves. (Quadir and Kanjwal, 2010) (figure above: subsequent ECG after treatment for Hypothermia seen without prominent J waves and sinus rhythm instead (Quadir and Kanjwal, 2010). Krantz and Mehler (2004) have reported that in anorexia nervosa, patient’s condition may show a resting tachycardia. Actually the underlying condition would be bradycardia. This was case of a 52 year old woman with a chronic anorexia nervosa having been hospitalised for increasing leg pain and weight loss. Her BP was 96/50 mm and resting heart rate was 106 bpm. Although the antibiotic therapy resulted in minimal weight gain, her heart rate decreased to 45 bpm. Thus, their conclusion was bradycardia, a characteristic feature of anorexia nervosa with weight loss and that therefore patient with resting tachycardia should be examined for life-threatening conditions. They state that bradycardia in such conditions would reflect an increased cardiac vagal activity (Galetta et al 2003) which may protect against arrhythmia risk. But resting tachycardia in anorexia nervosa may well be a predictor of arrhythmia and sudden death. Case review As part of the pre-hospital treatment, patient was given Atropine 0.6 mg to bring her heart back to normal rhythm. In response, heart rate increased to 60 PM but later decreased to 40 PM. The patient had to be kept stable before the ambulance could reach a nearby hospital with cardiac invasive facility which was 30minutes away. Poor perfusion was evident in the patient who had also been confused. Her blood pressure remained at 90/56 and hence no second dose of atropine was considered necessary. Previous history was not readily available except that she had cardiac problem. Her heart beat was too slow and there was no conduction of electrical impulses. The signs of jugular venous distension, lung crackles and swollen leg indicated that her vascular volume is not compromised. The above noted poor perfusion needs to be increased but for which at least heart rate of at least 48 beats is required. The signs show that the patient is having bradycardia in view of the apparent low heart beat. Bradycardia treatment decision by the emergency practitioner The Resuscitation Council’s ABCDE approach helped this practitioner to determine appropriate treatment. ABCDE stand for Airway, Breathing, Circulation, Disability and Exposure. This approach has been recommended for assessment. Accordingly, it was ensured that the patient had clear airway and adequate breathing. As the patient was critically ill, she was put on emergency oxygen. No previous medication history was available except that she was a cardiac patient and hence there was no need of withholding of any drug arose. Although the patient was having symptomatic hypoperfusion, there was no apparent deterioration in her condition. Treatment for Bradycardia was started following ABCDE approach. Symptoms suggested are Hypotension, typical heart rate . Booker KJ, Holm K, Drew BJ et al (2003) Frequency and outcomes of transient myocardial ischemia in critically ill adults admitted for non-cardiac conditions. Am J Crit Care 12: 508–16 cited in Khan Eshan (2004). Clinical Skills: the physiological basis and interpretation of the ECG. British Journal of Nursing, 13 (8) 440-446. Chung Edward, K. (2000) Pocket Guide to ECG Diagnosis, Wiley-Blackwell. U.K., USA. Galetta F, Franzoni F, Prattichizzo F, Rolla M, Santoro G, Pentimone F: Heart rate variability and left ventricular diastolic function in anorexia nervosa. J Adolesc Health 2003, 32:416-21 in Krantz Mori, J., and Mehler Philip, S., (2004) Resting tachycardia, a warning sign in anorexia nervosa: case report. 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Huszar JR (2001) Basic Dysrhythmias: Interpretation and Management. 3rd edn. Mosby, St Louis cited in Khan Eshan (2004). Clinical skills: the physiological basis and interpretation of the ECG. British Journal of Nursing, 13 (8) 440-446. Janse, M.J., and Rosen, M.R. (2006) History of Arrhythmias, ed, Kass Robert, S., and Clancy Colleen, E., 2006. Basis and treatment of cardiac arrhythmias. Springer, Germany. Jevon Phil. (2010). How to ensure patient observations lead to effective management of bradycardia.Nursingtimes.net. February 2010, retrieved 28 October 2010 < http://www.nursingtimes.net/nursing-practice-clinical-research/acute-care/how-to-ensure-patient-observations-lead-to-effective-management-of-patients-with-bradycardia-/5010971.article >. Kass Robert, S., and Clancy Colleen, E., 2006. Basis and treatment of cardiac arrhythmias. Springer, Germany. Marriot HJL, Conover MJ (1998) Advanced Concepts in Arrhythmias. 3rd edn. Mosby, St Louis cited in Khan Eshan (2004). 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Waldo L, Wit AL (2001) Mechanisms of cardiac arrhythmias and conduction disturbance. In: Fuster V, Alexander RW, O’Rourke R, Roberts R, King SB III,Wellens HJJ, eds.Hurst’s the Heart. McGraw Hill, New York: 751 cited in Khan Eshan (2004). Clinical skills: the physiological basis and interpretation of the ECG. British Journal of Nursing, 13 (8) 440-446. Read More