Acute Coronary Disease

According to the CDC, cardiovascular disease claims 614,348 lives in 2014 making it the leading cause of death in the United States, accounting for 46.9% of all deaths in 2014. This percentage is estimated to increase threefold by the end of 2016 (Heron, 2016). This is a significant issue, mainly because, for the most part this is a preventable ailment. If not closely control, this can quickly become an epidemic as the overall death rate increase each year. To fully understand this disease, we need to first look at the root cause, coronary artery disease.

Coronary artery disease remains number one killer of the western civilization despite 40 years of aggressive drug and surgical interventions (Esselstyn). Usually, pharmaceutical drugs, such as statin, are given to try to slow the progression, but may provide uncomfortable side effects. In fact, the majority of patients discontinue statins within 1 year of treatment initiation (Maningat). Furthermore, surgery is performed to circumvent clogged arteries and literally bypass the symptoms. In the last year, 500,000 coronary bypass procedures were performed (Swaminathan et al). However, these surgeries can have significant risks, including the potential to cause further heart damage, stroke, and brain dysfunction. Thus, it is evident that these way of treatments may not be enough on its own, and that getting to the

Coronary artery disease (CAD) is the commonest heart disease in the United States1. Approximately, 29% of patients with Myocardial Infarction ( MI ) present with ST- elevation Myocardial Infarction ( STEMI )2. STEMI is the result of complete occlusion of a major epicardial coronary artery due to thrombus formation. STEMI from a small coronary artery presenting as substantial EKG abnormalities similar to occlusion of a major artery and hemodynamic instability is a rare entity. The epidemiology, typical clinical presentation, outcomes, and optimal management in this group of patients are not sufficiently known.

Heart: has regular rhythm and rate, with no clubbing, cyanosis, or edema of the extremities.

The patient has been diagnosed with atrial defibrillation and congestive heart failure. There is no visible jugular vein distention or pulsations on either side of the neck. The patient was not comfortable with removing her sweater, therefore, pulsations, lifts, or heaves were not seen if present. Palpated and auscultated the carotid arteries for vascular sounds, no bruits heard. Heart sounds were auscultated with the bell and diaphragm of the stethoscope. S1 82/min, even and regular. S2 85/min, even and regular. S3 82/min, even and regular. S4 83/even and regular. No murmurs were heard. The apical pulse rate was 92 bmp, regular and was accessed with patient in sitting position and between the 4th and 5th intercostal space. Patient stated

Cardiovascular. Client denies chest pain, palpitations, murmurs, any arrhythmias, hypertension, awakening at night with shortness of breath, or dizzy spells. Client has not had an electrocardiogram.

In the valvular disease the regurgitation of blood back to the ventricles occurs when the valves fail to close tightly and this will result in ventricular overload and increased muscle stretching. This increases the heart muscles need for oxygen and energy resulting in the cardiac muscles to contract harder (Karch, 2013). The failure of the left ventricle to pump efficiently will lead to pulmonary vessel congestion and in severe cases, pulmonary edema whereas the inefficient pumping of right ventricle will lead to liver congestion and peripheral edema (edema of the legs and feet). The cardiovascular system works as a closed system and therefore, if one-sided failure left untreated, will eventually lead to failure of both sides (Karch, 2013). The American College of Cardiology (ACC)/ American Heart Association (AHA) has incorporated a classification system of heart failure that include four stages. This staging system (stage A to stage D) recognizes that there are established risk factors and structural abnormalities that are characteristics of the four stages of heart failure.

Cardiac movement or pulsations are not usually visible in well-built patients and will be visible in a frail, elderly patient. However, discernable pulsations or newly developed movements may suggest cardiomegaly, hypertrophy, or valvular problems. Marked cardiac pulsations are evident in thyrotoxicosis and hypertension also. For cardiac auscultation to be effective, remember to provide a quiet environment as possible. Although this is difficult, close your eyes to block any visual stimuli and focus on the sound heard. Make sure that there is direct contact with the skin, diaphragm firmly pressed against the skin for high-frequency sounds, and bell lightly against the chest for low-frequency sounds. Listen to one sound at a time and compare the characteristic of this sound in the different areas. Auscultate five areas using the diaphragm, and then with bell of the stethoscope (see Figure 3-2). In an ICU setting, the best position to auscultate is supine and left lateral because left lateral will bring ventricles close to the chest wall. See Table 3-4 for descriptions of the heart sounds ( Murray & White, 1999). Evaluation of the pulses is an important in ICU assessment. Palpation of the most distal pulse, the dorsal pedis pulse, can give an understanding about both cardiac contractility (diminished bilateral pedal) and diminished arterial flow to that limb

Cardiac: rRegular rate and rhythm, no murmurs, rubs, or gallops; no JVD, thrills, or heaves; PMI non-displaced at 5th intercostal space

Coronary heart disease (CHD), also known as ischemic heart disease is the most prevalent form of cardiovascular disease in Australia (Australian Institute of Health and Welfare, 2014). While over 20,000 of deaths in 2011 were attributed to CHD. There were estimated 590,000 Australians 18 years old and above diagnosed with CHD in 2011-2012 (AIHW, 2014; Craft, 2014, pg. 596). Myocardial ischaemia is a common form of CHD. A sufficient coronary artery blood flow is essential to supply oxygen for normal cardiac activities. Myocardial ischaemia develops when there is an insufficient supply of blood and oxygen to support the function of myocardial cells (Craft, 2014, pg. 599). A decrease in blood supply can led to the formation of atherosclerotic plaques by narrowing or occluding the arteries. Other conditions such as hypotension, coronary spasm, dysthymias, hypoxemia and anaemia can also decrease the blood and oxygen supply to the myocardial cells (McCance & Huether, 2014, pg. 1153)

One to two patients presented in the clinic area has heart murmurs heard on auscultation. The patients are asymptomatic, and the primary care will continue to monitor the patient. One particular patient stands out. A 6-year-old child verbalizes she will need a pacemaker as she gets older. She experienced shortness of breath, dizziness, severe fatigue (tiredness), fainting spell, and poor appetite. The child blood works were typical, expect the EKG showed completed heart block. She wore a Holter monitor for 24 hours, and echocardiography from the cardiologist. On assessment, the heart rate was 65pbm and regular, no chest discomfort, dizziness, palpitation or shortness of breath. The mother calms she checked her daughter pulse rate and records

R: yes, patient is not going to be moving and is NPO with fluid restrictions.

must be considered as a red flag, which may be an indication of heart failure. Vital signs

ECG : ventricular rate 54 beats/min, HR varying from 39 to 60 during a 45 minute period of monitoring, infrequent PVCs, ST elevation in leads II, III and avF indicating inferior injury or ischemia secondary to acute MI.

Cardiac: Regular rhythm without murmur, normal S1and S2. One plus edema to bilateral lower extremities. Capillary refills are presents and carotid bruits are absent.