Introduction:
This paper will provide an academic paper on case study of one Mr. Curtis who is a 74-year-old man with a history of hypertension and acute myocardial infarctions.
Cardiac Arrhythmia :
Mr. Curtis’ Electrocardiogram (ECG) shows that he has a fast heart rate HR of 150 to 200 beats per minute (bpm). Heart rate is calculated by counting each square between R waves (Shah, 2011). Furthermore, fibrillatory waves are seen and no P waves. Therefore, the PR interval cannot be measured. QRS complexes are normal. The ECG shows an irregularly irregular rhythm due to Atrial fibrillation (AF). In AF electrical impulse travel frequently in a disorderly manner in the atria. These rapid impulses affect the AV node and abnormal ventricular contractions occur (Tai, Lo, Lin, & Chen, 2012). Hence, irregular R to R intervals are observed.
According to Mr. Curtis ECG results and past medical history, the three reasons for Atrial fibrillation (AF) rhythm to occur are acute myocardial infarction (AMI), hypertension and hypoxemia. According to a study, atrial fibrillation can be observed in the patients with different heart disease such as AMI and CHF (Crandall et al., 2009). Acute myocardial infarction indicates that the heart tissues have been damaged which promotes the electrical disorganization of atrial depolarization (Crandall et al., 2009). These changes affect SA and AV node which are responsible for the arrhythmias. Atrial fibrillation is a most usual arrhythmia observed in acute myocardial infarction (Crandall et al., 2009). Due to AMI, the lack of oxygen supply to the working myocardium is depleted and hypoxemia is developed. Hence, the low level of oxygen in the blood starts structural and electrical remodeling which affects electrical conduction (Ohashi, Mitamura, & Ogawa, 2009). Subsequently, a patient with hypertension has also a higher risk of having a atrial fibrillation (Tao et al., 2014). It is because high blood pressure pushes blood with more power than usual, which over the time can damage artery walls. Hence, continuous pressure will start to narrow and limit the blood flow which is managed by electrical impulses. Therefore, coordination of electrical impulses will decrease, eventually leading to atrial fibrillation.
The three treatment options for atrial fibrillation for Mr. Curtis would be pharmacological, elective cardioversion and balancing electrolytes. Firstly, pharmacologically atrial fibrillation can be treated by treating symptoms. For instance, slowing the heart rate and maintaining normal rhythm can be achieved by medicines such as Digoxin (helps in contractility), Beta Blockers and some calcium channel blockers. Beta-blockers blocks the effects of adrenaline to lower the heart rate (Shojaee, Feizi, Miri, Etemadi, & Feizi, 2017). Subsequently, calcium channel blockers block absorption of calcium which helps in contractions (Shojaee et al., 2017). Hence by decreasing the contractions, ventricles have the time to fill the blood fully before they contract and spread to other body parts. Moreover, Anticoagulants such as warfarin and apixaban are prescribed to treat clot formation which can reduce the cerebrovascular accident and prevent embolization (Jelonek, Gorczyca, Bączek, Kośmider, & Wożakowska-Kapłon, 2018). Secondly, elective cardioversion therapy is initiated where the heart is given an electrical shock to restore a normal heartbeat (Hellman et al., 2017). Lastly, the balance of electrolytes is important in treating atrial fibrillation (Sultan et al., 2012). As ions such as calcium, magnesium and potassium plays a vital role in cardiac conduction. Patient’s with atrial fibrillation are usually magnesium deficient (Sultan et al., 2012). Magnesium is one of the electrolytes that plays a vital role in the heart’s electrical functioning. According to a study, intravenous administration of magnesium in the treatment of atrial fibrillation can reduce heart rate to below 100bpm and helps to convert irregular rhythm into normal sinus rhythm (Wang, 2012). Potassium is also very vital in the treatment, as it extends the time the heart take rest in between beats, thus maintaining normal sinus rhythm.
Pathophysiology and Treatment:
ABG results of Mr. Curtis indicates that he has a pH of 7.32 meaning an acidic blood. This means that H+ concentration is high in the blood (Lynch, 2009). As paco2 is 55 which is higher than the normal range of 35-45mmHg. It means that there is an increase in dissolved carbon dioxide (CO2). This increased range of paco2 with acidic pH indicates that Mr. Curtis has respiratory acidosis, due to the inadequate elimination of CO2 from the blood (Woodrow, 2010). Also, moderate hypoxemia is observed due to the rate of pao2 which is 64. The HCO3 rate is 26, which is in normal range showing the concentration of bicarbonate ions. The bicarbonate ion is regulated by kidneys and it assists in determining the disturbance of acid-base whether its metabolic or respiratory (Woodrow, 2010). Furthermore, SaO2 of 91% is a bit low in Mr. Curtis’s ABG results. SaO2 shows the percentage of oxygenated hemoglobin. The relation between SaO2 and PaO2 is crucial to understand as PaO2 is the partial pressure of oxygen present in the blood. Nearly 97% of oxygen in the blood is taken up by hemoglobin as oxyhemoglobin (HbO2). This oxyhemoglobin is shown in the measurement of SaO2 (Rogers & McCutcheon, 2013). While some of the oxygen is dissolved in the blood and that dissolved O2 is shown as Pa02. Hence, the higher the 02 is dissolved in the blood or higher the Pa02 value the higher the Sa02 will be as oxygen in the blood will combine with hemoglobin. Thus, 100% SaO2 will show hemoglobin is saturated completely (Rogers & McCutcheon, 2013).
The pathophysiology of Acute pulmonary oedema (APO) is crucial to understand in the case of Mr. Curtis. APO patients have a mortality rate of 65% who die within their first year of diagnosis (Rahmawati, 2018). APO is defined as an accumulation of fluid in the lungs which is forced into the pulmonary circulation (Yan, Zhiyang, Xuefeng, Yanhua, & Huixia, 2018). APO is categorized into two themes such as non-cardiogenic and cardiogenic. Precipitating factors for non-cardiogenic edema are anaemia, burns, head injury, pulmonary embolus, lung injury, and high altitude are some of the factors. As Mr.Curtis has a past medical history of AMI, he has acute cardiogenic pulmonary oedema (ACPO). ACPO can be caused by increased pulmonary pressure from left-sided heart failure. It can occur from systolic or diastolic heart failure (Yan et al., 2018). Diastolic heart failure can decrease the ability of the left ventricle to dilate completely between contractions, thus less ventricular filling can decrease cardiac output. Subsequently, systolic heart failure can diminish the power of the left ventricle in maintaining normal cardiac output. There are other factors which can affect heart failure such as AMI, hypertension, coronary artery disease and arrhythmias (AuCoin, 2011). Subsequently, decreased cardiac output will eventually start compensatory mechanisms by retaining fluid and vasoconstriction to improve cardiac output. Hence, the compensatory mechanism will elevate the after-load eventually damaging cardiac muscle even more. These changes will put more pressure in pulmonary veins and thus leading increase pressure in the capillary collection of fluid in alveoli and interstitial spaces of the lung. The collection of fluid in the lungs will then decrease lungs capacity to exchange gases, hence causing respiratory distress. Due to fluid collection in lungs crackles can be heard as well. Clinical manifestations can include shortness of breath, orthopnea, and anxiety because of the suffocating feeling (AuCoin, 2011).
The immediate purpose of treatment for APO is to reduce pulmonary congestion and improve oxygenation (Dominguez-Rodriguez & Abreu-Gonzalez, 2017). Oxygen therapy should be initiated for Mr. Curtis as his saturation is 91%. The continuous positive airway pressure device (CPAP) with 100% oxygen can be helpful in improving oxygenation (Li et al., 2013). Also, the positioning of Mr. Curtis or any patient with APO should be high fowlers position to reduce work of breathing. Mr. Curtis also has a high blood pressure hence glyceryl trinitrate (GTN) should be initiated (Agrawal, Kumar, Aggarwal, & Jamshed, 2016). Moreover, establishing an IV site is necessary for the use of titratable IV nitrates. Nitrates are a better choice of treatment as compared to frusemide and morphine (Dominguez-Rodriguez & Abreu-Gonzalez, 2017). As nitrates do not have side effects of sedation and neurohumoral activating effects of frusemide (Li et al., 2013). Although nitrates help in reducing preload they further reduces the after-load through arteriolar vasodilation which helps in coronary artery perfusion (Nossaman, Nossaman, & Kadowitz, 2010). Furthermore, patients should be on continuous blood pressure monitoring while taking GTN. Distressed patient can be given nitrate sublingually. Moreover, Mr. Curtis should be on continuous pulse oximetry to measure the oxygen saturation. Also, Mr. Curtis should be in Continuous ECG monitoring to detect any further abnormal rhythms. Morphine is not a good idea usually as it reduces the respiratory drive and conscious state but for a patient with anxiety small titrated doses of IV morphine, can be used with strict monitoring (Agrawal et al., 2016). Diuretics should be taken into consideration to decrease cardiac overload (Chigurupati, Reshmi, Gadhinglajkar, Venkateshwaran, & Sreedhar, 2015). Mr. Curtis’s lung sounds should be frequently assessed. Furthermore, signs of restlessness, headache, confusion and dizziness should be noted. It is very crucial to talk to Mr. Curtis and provide reassurance to the patient. The doctor can consider for placing an inserting indwelling catheter to monitor urinary output. Hence, if there is clear evidence of fluid overload frusemide may prove beneficial. Further tests may be necessary such as full blood count, troponin levels, urine test, chest X-ray, blood tests to check arterial blood gas concentrations, electrocardiogram, echocardiogram and cardiac catheterization. Lastly, Nurse should assess pain and involve other multidisciplinary team if necessary.
Systematic Patient Assessment:
Firstly, in the primary survey, Airway should be assessed (Jevon, 2010). If the patient is responding and talking in a normal voice then the airway is patent (Jevon, 2010). Signs of airway obstruction could be stridor which is a high pitched sound during breathing and increased work of breathing. Moreover, excessive movement of the cervical spine should be avoided (Jevron, 2010). Secondly, Assessment of breathing includes counting the respiratory rate, monitoring oxygen rate from the pulse oximeter (Jevron, 2010). Also, assessing ventilation is important as the exchange of gases is crucial to increase oxygen and decrease carbon dioxide from the body. Moreover, lung auscultation should be performed. Positioning of the trachea is also to be maintained. Furthermore, uneven movement of chest wall movement should be observed which can hinder the breathing (Jevron, 2010). Thirdly, circulation is important to maintain tissue perfusion and cellular oxygenation. In circulation pulse rate, blood pressure, electrocardiography monitoring is essential. Subsequently, capillary refill time and heart auscultation should be checked. Alteration in heart rate, peripheral pulses and skin status assessment is also important. If a patient is hypovolemic, changing patient’s position to the supine and elevating leg can help reduce the effects of hypovolemia. Haemodynamic compromised patient who has hypertension, bradycardia or tachycardia can be allocated to higher triage category in Australasian triage system (ATS) for immediate treatment. Subsequently, in disability assessment, conscious level can be quickly assessed using the AVPU method or the Glasgow Coma Score. AVPU means Alert (A), responsive to voice (V), pain (P) and unresponsive (U). Moreover, Movement of limbs, Pupillary light reflexes and Blood glucose level assessment are main elements in the disability section (Jevon, 2010). Lastly, Environment or exposure assessment should be completed where dignity and privacy of the patient should be maintained. A thorough physical examination should be performed for any visible injury such as bleeding, skin reactions or any other trauma possibilities. Evaluation of any subjective data and also assessing temperature as hyperthermia and hypothermia are important clinical indicators (Jevron, 2010).
The three respiratory signs and symptoms of acute pulmonary edema are shortness of breath, crackles, and low oxygen saturation (Yan et al., 2018). As in acute pulmonary edema, the fluid is accumulated in the lungs which makes it harder for the lungs to perform effectively and exchange carbon dioxide and oxygen. Hence, the poor exchange of gases can cause poor oxygenation of blood and thus causing shortness of breath (Yan et al., 2018). Alveoli, the tiny thin air sacs of lungs are responsible for quick gas exchanges into the bloodstream which due to fluid accumulation prevents adequate flow of air and ventilation (Yan et al., 2018). Therefore, low oxygen saturation is recorded. Subsequently, on lung auscultation, the presence of abnormal lung sounds crackles or rales can be heard (Agrawal et al., 2016). This adventitious sound indicates the movement of the air through the fluids in small airways that more commonly heard during inspiration (Agrawal et al., 2016).
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