Question

 

Question 1. Compare / Contrast the anginas by creating a chart and then complete a list of 5 clinical manifestations associated with stable angina, unstable angina, and MI

Question 2. Create a patient teaching handout that incorporates a list of modifiable and nonmodifiable risk factors for coronary artery disease (CAD). Have students include pertinent teaching information about how patients could modify behaviors to address modifiable risk factors.

Question 3.Discuss at least 5 ways to help educate community members about the prevention of shock or sepsis, recognizing hypovolemic shock, and pre-hospital actions to take.

Answer 1

1.Compare and contrast the clinical manifestations of stable angina, unstable angina, and MI.

Angina pectoris is defined as chest pain caused by a temporary imbalance between the coronary arteries’ ability to supply oxygen and the cardiac muscles demand for oxygen. Chronic stable angina (CSA) is chest discomfort that occurs with moderate or prolonged exertion in a familiar pattern. The frequency, duration and intensity of the pain remain the same for long periods of time, usually months. Stable angina is usually easily relieved with nitroglycerin or rest/ cessation of the precipitating event. Chronic angina presents as a depressed ST segment on ECG.Unstable angina is chest pain that occurs at rest or with exertion but, unlike stable angina, but causes severe activity limitations. Unstable angina usually occurs when there is a change in frequency or intensity of stable angina. Unstable angina has a longer duration and can last as long as 15 minutes and responds less to nitroglycerin and rest. Different kinds of angina are encompassed under the term unstable angina, and they include, new-onset angina, variant angina, and pre-infarction angina. Unstable angina also presents with a depressed ST segment on ECG but all angina lacks the presence of cardiac enzymes unlike a true MI.A myocardial infarction occurs when myocardial tissue is abruptly and severely deprived of oxygen. There are two types of MI seen upon ECG. A non-ST-segment elevation MI does not have an ST segment elevation (although there are some changes to the ST segment seen) indicating ischemia of the heart muscle. Cardiac enzymes increase over 3 to 12 hours. Causes of this type of MI include: coronary vasospasm, spontaneous dissection, and sluggish blood flow secondary to narrowing ofthe coronary artery. A ST-elevation myocardial infarction presents with ST segment elevation in 2 contiguous leads on a 12 lead ECG, indicating necrosis of the heart muscle. This type of MI is caused by rupture of the fibrous atherosclerotic plaque. When the plaque ruptures platelets aggregate at the rupture site eventually causing thrombus formation. Whena blood clot is formed on an already diseased vessel it causes an abrupt 100% blockage.Both angina and myocardial infarction cause pain in the patient. Angina pain causes substernal chest discomfort that radiates to the left arm and is usually precipitated by exertion or stress. This pain may occur at rest for patient with variant angina because it is caused by muscle spasm. The pain from angina is relieved with nitroglycerin or rest. The pain lasts less than 15 mins and there are few other symptoms, if any. Pain from a myocardial infarction causes chest pain or pressure that radiates to the leftarm but there is also pain present in the jaw, back, shoulder, or abdomen. This pain usually occurs without precipitating factors and often time occurs in the morning time. MI pain is not relieved by nitroglycerin and requires opioid analgesics for pain relief. The pain of MI also has a longer duration than angina pain, generally lasting 30 minutes or

Non-Modifiable Risk Factors For Coronary Heart Disease

Non-modifiable risk factors are fixed, unchangeable traits (e.g., age, gender and race-ethnicity). Increasing age and heredity are the two major categories of non-modifiable risk factors for CHD.

Increasing Age

CHD develops over the lifespan of an individual. As people age the more likely they are to develop CHD and suffer a fatal heart attack. After 40 years of age, the lifetime risk of developing CHD is 49% for men and 32% for women. More than four out of five or 81% of the people dying from CHD are 65 years of age or older

As it turns out, research is being conducted on arterial and cardiac aging and why it is that cardiovascular disease (CVD) is more likely in elderly persons. Investigators are attempting to determine the ways in which the structure and function of the cardiovascular system changes over time and how those changes contribute to the risk of developing CHD. One proposed hypothesis is that age-related changes in the structure and function of the cardiovascular system become intertwined with disease-related processes which brought about by such risk factors as hypertension, inflammation, smoking and obesity, among others

Heredity

It is firmly established in the medical literature that heredity plays a significant role in the development of CHD. Heredity represents nature’s involvement in putting people at risk for CHD, while lifestyle is the nurture dimension for developing the disease. As a non-modifiable risk factor, heredity implicates gender, race-ethnicity and family history.   

GENDER

it was mistakenly believed that males suffered predominantly from CVD and CHD was a male disease. However, all of the various diseases of the heart and blood vessels constituting CVD make it the leading cause of death in the U.S. for both men and women. Yet, only approximately 13% of women consider CVD to be the greatest risk to their health.

Just as with females, CHD is the single leading cause of death of males in America. Half of the men who die suddenly from CHD typically do not exhibit previous symptoms, death being their first and last symptom. Between 70%-89% of sudden cardiac deaths are associated with men, with the annual incidence being 3-4 times higher in men compared to wome.

In summary, CHD imposes serious health risks for both men and women. It is the single leading cause of death for both men and women. Thus, CHD is not a disease unique to men. Women are also clearly at risk for CHD and its consequences. Yet, men are even at greater risk when it comes to CHD and heart attacks. They tend to be at a greater risk than women for CHD and they have heart attacks earlier in life than women. Although the risk for women of having a heart attack increases subsequent to menopause, their risk never rises to level that of men.

Race-Ethnicity

Statistical studies indicate that racial-ethnic minorities are at risk for diseases of the heart and blood vessels, especially CHD. CVD is the leading cause of death among African-Americans. African-Americans, Mexican-Americans, American Indians, native Hawaiians and some Asian Americans have a higher risk for CHD than Caucasians. This is the case because non-whites (especially African-Americans) have more risk factors and higher rates of overweight and obesity, diabetes and high blood pressure, which are among the most serious risk factors for CHD.

Number of risk factors. The more risk factors a person has the greater the likelihood of developing CHD. African-American and Mexican-American women have more risk factors for CHD than Caucasian women who share a comparable socioeconomic status. The prevalence of having two or more risk factors for CHD among racial-ethnic minorities is highest among African-Americans, American Indians and Alaska Natives and lowest among Asia.

High blood pressure. HThe prevalence of HBP (hypertension) in African-Americans in America is considered to be among the highest world-wide. African-Americans ages 20-39 exhibit a higher prevalence of pre-hypertension than Caucasians and Mexican Americans. Compared to Caucasians, African-Americans develop full-blown HBP earlier in life and their average blood pressure is considerably higher. “As a result, compared with whites, blacks have a 1.3 times greater rate of nonfatal stoke, a 1.8 times greater rate of fatal stroke, a 1.5 times greater rate of heart disease death and a 4.2 time greater rate of end-stage kidney disease” (American Heart Association, 2006, p. 109). In comparison to Caucasian women, African-American women experience an 85% higher rate of ambulatory medical care visits for HBP.

Overweight and Obesity. Although the obesity-overweight and obesity statistics in Caucasian, African-American and Mexican-American adult males are somewhat similar, African-American and Mexican-American adult females suffer from significantly higher rates of being overweight or obese than adult Caucasian females, putting these minority female groups at greater risk for CHD.

It is important to point out that a higher percentage of African-American and Mexican-American male and female children ages 6-11 and adolescents ages 12-19 suffer from being overweight than their Caucasian counterparts. This of course sets the stage for the children and adolescents from these minority groups to be at an even greater risk for becoming overweight or obese adults than their Caucasian counterparts.

Diabetes Mellitus. Based on a Medline search of 290 articles on diabetes, the U.S. Department of Health and Human Services Public Health Service through its Agency for Healthcare Research and Quality or AHRQ (2001) found that the burden of diabetes on minorities is greater than it is on Caucasians. Specifically, AHRQ (2001) reported that (1) all minorities, except for Alaska Native, are 2-6 times more likely to have Type 2 diabetes than Caucasians, (2) African Americans are from 1.4 – 2.2 times more likely to contract diabetes than Caucasians, (3) Hispanic-Americans have a higher prevalence of diabetes than non-Hispanics, (4) the prevalence of diabetes among American Indians is 2.8 times the overall rate, (5) primary groups within the Asian and Pacific Islander communities (i.e., Japanese Americans, Chinese Americans, Filipino Americans & Korean Americans) have higher prevalence rates for diabetes than Caucasians and (6) death rates related to diabetes for African-Americans, Hispanic Americans and American Indians were higher than those for Caucasians. In sum, given that it afflicts them in a sigificant way and given that it is major risk factor for the development CHD, there is little doubt that diabetes puts racial-ethnic minorities at risk for CHD.

Family History

Certain families seem to be more plagued with and predisposed to diseases of the heart and blood vessels than do other families. Medical researchers have devoted considerable attention to unraveling the ways in which family history becomes implicated with the different forms of CVD, including CHD. They have established that people are at a significantly increased risk for CVD when they have family members (especially first degree relatives & even second degree relatives) who have a history of (1) CVD (e.g., CHD, stroke, heart failure, angina pectoris, hypertension, etc.), (2) cardiac related events (e.g., myocardial infarction/heart attack & sudden death).

In an effort to understand the risk-raising connection of family history to CVD, medical researchers have attempted to identify those genes that predispose people to diseases of the heart and blood vessels. For example, there are studies focusing on genetically transmitted cardiovascular diseases such as hypertrophic cardiomyopathy, Long-QT syndrome and Marfan syndrome that have a deleterious effect on the anatomic structure (heart size) and function (heart rate/muscle contraction) of the heart .

There are also studies devoted to genes affecting the metabolic functioning of lipids and other bio-markers that have the potential to make people more susceptible bio-chemically and predisposed statistically to CHD and other types of CVD. For example, researchers have learned that certain gene mutations or variations can result in (1) high LDL cholesterol levels (2) low HDL cholesterol levels, (3) iron overload in the blood, (4) elevated homocysteine levels, (5) high Lp(a) levels,

Modifiable risk factors include hypertension, hyperlipidemia, diabetes, obesity, smoking, poor diet, sedentary lifestyle, and stress. Given the immense healthcare burden of CAD, modifiable, and non-modifiable risk factors were identified to mitigate the resulting economic and disease-related burden.

the prevention of shock or sepsis, recognizing hypovolemic shock, and pre-hospital actions to take.

1. Clear guidance, policies and clinical pathways to be in place for the recognition, management and communication of sepsis and Red Flag Sepsis.

2. All patients with a NEWS score above trigger threshold (or a single NEWS criterion scoring 3), or with physiological abnormality in the presence of clinical suspicion of infection to be screened for sepsis with Sepsis Risk Stratification undertaken, and the outcome of this screening process recorded on the Patient Care Record or electronic Patient Care Record (PCR/ePCR).

3. The PH Sepsis Bundle (or a modified prehospital equivalent) to be used as a delivery method for early sepsis care and to be delivered within 1 hour post diagnosis in ≥95% of cases in collaboration with receiving EDs

4. Definitive, documented decision made and communicated about the presence/ absence of sepsis and the level of severity at time of handover to ED or other clinical group.

5. Mandatory annual sepsis training for all clinical members of staff.

6. A minimum of 80% of permanent staff to have received appropriate sepsis training at any one time point, audited at least biannually.

7. A nominated clinical Sepsis lead within the prehospital providers organization.

8. Interdisciplinary meetings to be undertaken between the ED and prehospital service staff together with managers and commissioners as appropriate, with remit to refine care pathways for sepsis and ensure compatibility between clinical areas. This work should be undertaken within the remit of, or fed back to, the organization’s Sepsis Group

9. Voluntary reporting of performance data into the public domain.