Cardiac/Vascular Nurse Exam Secrets Study Guide (4 page)

Cardiomyopathy diagnostic tools include chest x-ray to determine if heart is enlarged, echocardiogram to assess size and motion of the heart, electrocardiogram to determine the presence of electrical disturbances and blood tests to assess BNP levels. Thyroid levels and serum iron counts are also helpful. Clinical practitioners may also perform cardiac stress testing to assess cardiac muscle function as well as electrical activity when the heart is under physical stress. MRI and PET scans may also be used to evaluate cardiac structures, rhythm, and chemical activity in different areas of the heart.

Other more invasive diagnostic techniques include cardiac angiography and biopsy.

Congestive heart failure

Congestive heart failure is a condition where the heart is unable to pump adequate oxygenated blood throughout the body.

Congestive heart failure is caused by diseases that weaken or stiffen cardiac muscle. It can also be caused by diseases that increase oxygen demand, which the heart is unable to support.

The prevalence of congestive heart failure is approximately 5 million individuals in the United States, with half a million cases diagnosed each year and approximately 300,000 deaths per year. An important prognostic factor associated with congestive heart failure is the development of arrhythmias. Mortality due to congestive heart failure can be attributed to arrhythmias in 50% of patients and progressive heart failure in another 50% of patients.

Congestive heart failure is prevalent in individuals 65 years of age and older. It is also prevalent among African Americans, obese individuals and individuals with type II diabetes. Congestive heart failure is more prevalent among men than women.

Risk factors

Factors that can lead to congestive heart failure include heart muscle weakness, systolic dysfunction, heart valve disorders, viral infections, thyroid disorders, and arrhythmias. The most common causes of congestive heart failure include hypertension and coronary artery disease.

Other risk factors include a family history of congestive heart failure, presence of other comorbid conditions including previous heart attack, diabetes, metabolic disorders, and alcohol consumption.

Additional factors that can attribute to the progression of congestive heart failure include pharmacologic agents such as NSAIDs, corticosteroids, calcium channel blockers and diabetic agents.

Symptoms

Congestive heart failure can be asymptomatic until later stages of the disease. However, some patients may present with fatigue and muscle weakness during earlier stages of the disease.

Symptoms vary among patients and are based on end organ system involvement. With progression of disease, symptoms may include fatigue, weakness, shortness of breath after exertion, swelling of abdomen and extremities, dizziness, fainting, arrhythmias, increased urination, decreased appetite, nausea and palpitations.

These symptoms tend to get worse as the degree and extent of disease progresses. However, the time to progression varies from patient to patient and ranges from sudden onset to a slow progression.

Diagnosis and screening

Physical examination and diagnostic screening tools are typically used in addition to symptoms to screen for congestive heart failure. However, congestive heart failure is typically found when assessing other conditions or during routine examinations.

During physical examination, practicing clinicians aim to uncover excess fluid in the lungs, heart, liver or other end organ systems as well as estimate the level of cardiac function.

Congestive heart failure diagnostic tools include chest x-ray to determine if heart is enlarged, echocardiogram to assess size and motion of the heart, electrocardiogram to determine the presence of electrical disturbances and blood tests to assess BNP levels, thyroid levels and iron counts. Clinical practitioners may also perform cardiac stress testing to assess cardiac muscle function as well as electrical activity when the heart is under physical stress. MRI and PET scans may also be used to evaluate cardiac structures, rhythm, and chemical activity in different areas of the heart. Occasionally, a biopsy of the myocardium is necessary.

Cor Pulmonale

By definition, cor pulmonale is failure of the right heart not caused unrelated to left heart failure. Cor pulmonale is a disease that affects the structure and function of the right ventricle due to respiratory system abnormalities such as prolonged pulmonary hypertension. Pathophysiologic mechanisms that can lead to cor pulmonale include pulmonary vasoconstriction, compromise of vascular bed due to lung disease such as emphysema and interstitial lung disease, increased blood viscosity due to diseases like sickle cell anemia and primary pulmonary hypertension. The disease can present as a chronically evolving condition, but can also occur acutely due to pulmonary embolism or acute respiratory distress syndrome. In the United States, the prevalence of cor pulmonale associated with adult onset cardiac disease is approximately 6% to 7%. Nearly half of these cases are due to underlying chronic bronchitis, chronic obstructive pulmonary disease, or emphysema. Acute pulmonary embolism is the most common cause of death in patients with cor pulmonale. Of the 50,000 patients that die of acute pulmonary embolism in the United States, nearly half are associated with cor pulmonale. Of those patients with chronically evolving disease due to chronic obstructive pulmonary disease, 30% have a chance of surviving 5 years.

Causes

Cor pulmonale is caused by any condition that leads to prolonged pulmonary hypertension and can occur secondary to an array of cardiopulmonary diseases. Chronic pulmonary diseases that can put patients at a predisposition for cor pulmonale include COPD, obstructive sleep apnea, central sleep apnea, cystic fibrosis, primary pulmonary hypertension, pneumoconiosis, kyphoscoliosis, interstitial lung disease, chronic thromboembolic pulmonary disease, pulmonary vascular disease and pulmonary hypertension.

Acute causes of cor pulmonale include massive pulmonary embolization and exacerbation of chronic cor pulmonale.

Chronic causes of cor pulmonale include COPD, loss of lung tissue due to trauma or surgery, Pierre Robin sequence and end stage pneumoconiosis.

Cor pulmonale is caused by several mechanisms including pulmonary vasoconstriction, anatomic changes in vascularization, increased blood viscosity, and idiopathic or primary pulmonary hypertension.

Symptoms

The symptoms associated with Cor Pulmonale are typically nonspecific and can be associated with a variety of cardiopulmonary diseases. The symptoms of the disease also depend on whether the disease presents chronically or acutely due to pulmonary embolism or acute respiratory distress syndrome.

The symptoms of cor pulmonale include shortness of breath, coughing, wheezing, swelling of feet and ankles, fluid retention, exercise intolerance, tachypnea, hemoptysis, labored respiratory efforts with retractions of chest wall, hoarseness and chest pain or discomfort. Additionally, neurological symptoms may occur due to decreased cardiac output and hypoxemia.

Screening and diagnosis

Physical examination and diagnostic screening tools are typically used to diagnose cor pulmonale. Patients typically present with a bluish hue to their skin as well as distension of the neck veins caused by elevated right side heart pressures. Other indicators of the disease include abnormal fluid collection in abdomen, liver enlargement, increased chest diameter, prominent a or v waves, cyanosis, ankle and foot swelling as well as abnormal heart sounds.

Diagnostic tools used to diagnose the disease include echocardiogram, chest x-ray, CT scan, pulmonary angiography, magnetic resonance imaging, ECG-gated CT scanning, pulmonary function tests, ventilation/perfusion lung scans, arterial blood gas measurements, antibody testing and brain natriuretic peptide measurements. Additionally, more invasive diagnostic approaches include Swan-Ganz catheterization and lung biopsy.

Type I, II and Gestational Diabetes Mellitus

Type I diabetes occurs in approximately 10% of all cases of diabetes mellitus. The condition can affect both adults and children, but is referred to as juvenile diabetes because it typically affects adolescents. The incidence of type I diabetes is approximately 15 cases per 100,000 individuals annually.

Type II diabetes is the most common type of diabetes mellitus, approximately 90% of all cases of diabetes mellitus. Additionally, more than half of patients diagnosed with type II diabetes are obese. It is also more common in patients over 40 years of age, but can occur in young adults and adolescents. It is also more prevalent in Hispanics, Native Americans, African Americans, and Asians/Pacific Islanders than in Caucasians.

Gestational diabetes occurs in approximately 2% to 5% of all pregnancies and is treatable with careful supervision throughout pregnancy. Of those women affected with gestational diabetes, approximately 20% to 50% develop type II diabetes.

Diabetes mellitus is a condition resulting in high blood glucose level. The condition is caused by metabolic dysfunction due to either low levels of insulin or abnormal resistance to insulin combined with inadequate levels of insulin secretion.

Type I diabetes is also known as juvenile diabetes or insulin dependent diabetes. It is a chronic metabolic disorder that results in high blood glucose levels due to low levels of insulin. In type I diabetes, the pancreas does not produce enough insulin, resulting in high blood glucose levels.

Type II diabetes is also known as adult onset or noninsulin dependent diabetes. It is a chronic metabolic disorder that results in high blood glucose levels due to insulin resistance and/or low secretion of insulin. In type II diabetes, the body is resistance to insulin, which in turn results in high blood glucose levels. Early in the disease, insulin levels may actually be greater than normal, but eventually the beta cells in the pancreas “burn out” and insulin levels are lower than normal.

Gestational diabetes is not a chronic condition and typically occurs during pregnancy and resolves upon birth. The condition results in high blood glucose levels due to low insulin secretion and responsiveness.

Causes and risk factors

Individuals with type I diabetes typically have a genetic predisposition for the condition. Therefore, individuals with a parent or sibling with the disease have a higher risk for developing the condition. The causes and risk factors for type I diabetes are poorly understood, aside from some individuals having a predisposition for the disease.

It remains unclear why individuals develop type II diabetes, but the disease is associated with certain predisposing risk factors. Risk factors that increase the risk for developing type II diabetes include obesity, physical inactivity, family history, increasing age, prediabetes, and gestational diabetes. Also, individuals of African American, Hispanic, Native Americans, and Asian American descent are at higher risk for developing type II diabetes.

Medical conditions associated with a higher risk for developing type II diabetes include high blood pressure, elevated cholesterol levels, coronary artery disease, polycystic ovary syndrome, chronic pancreatitis, liver dysfunction, hemochromatosis, and cystic fibrosis.

Symptoms

The symptoms of type I diabetes include increased thirst, frequent urination, extreme hunger, weight loss, fatigue and blurred vision. Patients diagnosed with type I diabetes may also present with diabetic ketoacidosis, which may include altered mental status, coma, hyperventilation, and abdominal pain. The symptoms associated with type I diabetes tend to develop rapidly over a short period.

The symptoms of type II diabetes also include increased thirst, frequent urination, extreme hunger, weight loss, fatigue and blurred vision. The condition also includes slow healing sores or frequent infections. Also, patients diagnosed with type II diabetes may present in a hyperosmolar nonketotic state. The symptoms associated with type II diabetes develop over time and may be mistaken for other conditions or go unrecognized.

Diagnosis and screening

The diagnosis of both type I and type II diabetes is suggested by physical examination, patient symptoms, and diagnostic tools. Type I diabetes diagnosis is suggested by the sudden onset of symptoms. A fasting glucose greater than 126 mg/dL or random glucose greater than 200 mg/dL on 2 different occasions is diabetes. Age, family history, comorbidities, and demographics help suggest type I, II, or gestational diabetes. Additionally, C-peptide levels serve as a marker for insulin production. Elevated C-peptide suggests type II and low C-peptide suggests type I.

The diagnosis of type II diabetes is typically made during ordinary health examinations, but diagnosis can be made by detection of hyperglycemia during other examinations or based on the presence of secondary symptoms such as fatigue or vision changes. In many cases, type II diabetes is not diagnosed until the patient experiences a complications caused by the condition including heart attack, neuropathy, vision problems and/or foot ulcers. Diabetes screening tools include random blood glucose testing, fasting blood glucose testing, and more-formal blood glucose tolerance testing. Other lab studies include urine glucose and ketones as well as renal function tests. Blood tests include glycated hemoglobin, islet cell antibodies, thyroid function tests, antithyroid antibodies, lipid levels, and antigliadin antibodies.

Metabolic syndrome