Cardiac/Vascular Nurse Exam Secrets Study Guide (12 page)

Neurally mediated hypotension
is a condition that causes a drop in blood pressure after standing for long periods. The symptoms associated with neurally mediated hypotension include dizziness, lightheadedness, heart palpitations, sweating, nausea, confusion, and fainting or syncope. The condition tends to affect younger adults and is caused by a malfunction between the brain and cardiovascular system, which causes blood pooling in the legs and feet leading to sudden blood pressure drops. Lifestyle modifications including the vagal maneuver, increased sodium intake and use of graduated compression stocking may improve symptoms. Pharmacologic agents such as beta-blockers, alpha-adrenergic inhibitors, and agents that maintain salt in the kidneys can improve symptoms.

Causes and risk factors

The causes and risk factors associated with hypotension vary from individual to individual. Athletes and individuals who exercise regularly tend to have lower blood pressure than unfit and/or obese individuals. The main risk factors and causes of hypotension, as outlined by the American Heart Association, include pregnancy; certain pharmacologic agents such as diuretics, beta-blockers, Parkinson disease drugs, tricyclic antidepressants, sildenafil particularly in combination with nitroglycerine, narcotics and alcohol; cardiac conditions such as bradycardia, cardiac valvular disease, myocardial infarction and congestive heart failure, endocrine problems such as hypothyroidism, hyperthyroidism, Addison disease, hypoglycemia and diabetes; blood loss as from major surgery or severe injury; severe infection; allergic reaction; and nutritional deficiencies such as lack of vitamins B-12 and folate; natural aging; and dehydration.

Symptoms

The symptoms of hypotension vary from patient to patient and depend on the extent and degree of the condition. It also depends on the patient’s overall health and presence of other comorbid conditions. Also, some individuals experience more severe symptoms than another, even if their blood pressure is relatively normal. However, patients with relatively low blood pressure may experience few or no symptoms.

Symptoms associated with hypotension include dizziness, lightheadedness, fainting or syncope, lack of concentration or decrease mental capacity, weakness, fatigue, blurred vision, nausea, cold, clammy and/or pale skin, rapid or shallow breathing, depression, and/or thirst.

Diagnosis and screening

Physical examination, medical history, and diagnostic tools are used to diagnose hypotension and determine which type of hypotension a patient presents with. The goal is to determine the underlying cause of hypotension in order to treat the symptoms of hypotension or treat the underlying cause to improve an individual’s blood pressure.

Diagnostic tools used to assess hypotension include blood tests such as red blood cell counts and blood glucose levels, electrocardiogram, echocardiogram, stress test, Valsalva maneuver, and/or tilt-table test.

Compartment syndrome

Compartment syndrome is a condition that involves the compression of nerves and blood vessels within an enclosed space, which leads to decreased blood flow as well as muscle and nerve damage. Compartment syndrome can be acute or chronic depending on the underlying cause. Chronic compartment syndrome can be caused by repetitive activities that lead to swelling such as running or excessive physical activity.

The incidence of compartment syndrome in the United States is relatively low, averaging up to 12%. The mortality rate depends on the time of diagnosis and treatment of the condition. The condition is more common in men than women.

Causes and risk factors

Risk factors and causes of compartment syndrome include swelling due to high-energy trauma from a car accident or surgery, tight bandages or casts with significant swelling. In addition, a variety of physical injuries can lead to compartment syndrome. Compartment syndrome can be caused by increased pressure, swelling and/or decreased compartment size. Increased swelling or fluid buildup can be caused by intensive muscle use, daily physical exertion, burns, intraarterial injection, envenomation, decreased serum osmolarity, infiltrated infusion, and hemorrhage. Decreased compartment size can be caused by military anti-shock trousers, burns, tight bandages, and/or casts. The abdomen can also be a site of compartment syndrome if excessive swelling.

Symptoms

The main symptom associated with compartment syndrome is severe pain that does not respond to elevation or pain medication. However, in more severe cases, patients may present with decreased sensation, weakness, and paleness of the skin. The degree and extent of symptoms depend on the severity of compartment syndrome and whether or not it is a chronically occurring.

Typically, patients diagnosed with compartment syndrome present with severe pain when a muscle running through a compartment is passively moved or squeezed, such as toe, foot, or leg. The skin covering the compartment being affected will be shiny and swollen.

Diagnosis and screening

Diagnosis of compartment syndrome involves physical examination, medical history, and diagnostic screening tools. A practicing clinician will examine a patient for any swollen toes, legs, or feet. They will also move or squeeze muscle groups potentially affected to see if the patient expresses severe pain.

The diagnosis is made by directly measuring the pressure in the compartment with a needle and pressure meter, which is called the compartment pressure measurement. If the compartment pressure is greater than 45 mmHg or the diastolic blood pressure is within 30 mmHg, then a diagnosis of compartment syndrome is made. Other diagnostic screening tools used include blood tests such as complete metabolic profile, complete blood count, creatine phosphokinase and urine myoglobin, serum myoglobin, toxicity screen, and prothrombin and activated partial thromboplastin time. Urinalysis may also be performed as well as use of imaging tools such as radiography and ultrasonogram.

If chronic compartment syndrome is suspected, then direct blood pressure measurement needs to be determined post–physical exertional activity.

Pulmonary edema

Pulmonary edema is a condition that involves increased blood pressure in the blood vessels of the lungs forcing fluid into the air sacs, which prevents the absorption of oxygen. The elevated pulmonary capillary pressures lead to increased fluid in the interstitial compartment and alveoli. Decreased cardiac output, inadequate tissue perfusion, and acute pulmonary congestion are characteristic of the condition.

Acute pulmonary edema is a serious condition that requires prompt medical attention. However, if treated aggressively and immediately, prognosis is generally good. Yet, delayed intervention can lead to severe complications including death. In the acute care setting, the mortality rate associated with pulmonary edema is as high as 15% to 20%, on average.

Causes and risk factors

The causes and risk factors for pulmonary edema are generally environmental and can be exacerbated by the presence of other comorbid conditions. The causes and risk factors for pulmonary edema include coronary artery disease, congestive heart failure, myocardial infarction, cardiomyopathy, cardiac valve dysfunction, and high blood pressure.

Noncardiac causes and risk factors for pulmonary edema include lung infections, exposure to certain toxins such as chlorine, ammonia and nitrogen dioxide, kidney disease, smoke inhalation, adverse drug reaction to drugs such as illicit drugs and chemotherapy drugs, acute respiratory syndrome, and high altitudes.

Symptoms

The symptoms of pulmonary edema can vary from patient to patient. The symptoms are also dependant on the degree and extent of the condition as well as a patient’s overall general health and presence of other comorbid conditions. However, the most common symptoms associated with pulmonary edema include extreme shortness of breath or difficulty breathing, a feeling of suffocating or drowning, wheezing or gasping for breath, anxiety, restlessness, a sense of apprehension, a cough that produces frothy sputum that may be tinged with blood, excessive sweating, grunting or gurgling sounds when breathing, restlessness, anxiety, nasal flaring, inability to speak, decreased awareness, pale skin, and chest pain.

Symptoms that may develop more gradually include difficulty breathing while lying down, awakening at night out of breath, increased shortness of breath, and significant weight gain.

Diagnosis and screening

Physical examination, medical history, and diagnostic screening tools are used to diagnose pulmonary edema. Acute pulmonary edema requires prompt medical attention for prevention of severe complications. Patients with pulmonary edema typically present with rapid breathing, increased heart rate, crackles in lungs, and pale or blue skin.

Diagnostic tools used for screening of pulmonary edema include blood tests such as arterial blood gas concentrations, chest x-ray, electrocardiogram, echocardiogram, and transesophageal echocardiography. A more invasive diagnostic approach used to diagnose pulmonary edema when diagnosis is unclear is pulmonary artery catheterization.

First-degree atrioventricular block

First-degree atrioventricular block is defined as a delay in conduction of impulses from the sinoatrial (SA) node to the atrioventricular (AV) node. The condition is typically asymptomatic and undiagnosed. It can occur in individuals of all ages. The disease is typically benign and not associated with an increase in morbidity and mortality.

In the United States, the prevalence of first-degree atrioventricular block varies up to 1.6%. Higher prevalence in younger adults occurs in athletes and medical school students. The condition is more prevalent in African Americans than Caucasian Americans. The condition also increases with natural aging and more prevalent among elderly patients with other cardiovascular comorbid conditions.

Causes and risk factors

Other comorbid conditions that can lead to first-degree atrioventricular block include cardiac ischemia, myocardial infarction, congestive heart failure, coronary artery disease, scarring of atrial tissue in internodal pathways, infiltration by amyloid, sarcoid, Lyme carditis, endocarditis, degenerative diseases, rheumatic cardiac disease, electrolyte imbalances, atrial stretch, increased vagal tone, and inflammatory diseases.

Pharmacologic agents that can lead to first-degree atrioventricular block include digoxin, calcium channel blockers such as nifedipine, amlodipine, verapamil and diltiazem, and beta-blockers.

The condition is characterized by prolonged PR interval (greater than 200 msec), which can also occur as a normal variant in some individuals.

Symptoms

Individuals who present with first-degree atrioventricular block have few or no symptoms and typically are not at risk of developing other comorbid conditions. Diagnosis is typically made during routine physical examination or when being examined for another compliant. In patients with first-degree atrioventricular block, heart rate and rhythm are typically normal, and there may be nothing wrong with the heart. However, some patients may present with fainting and syncope, bradycardia, left ventricular systolic dysfunction, as well as comorbid congestive heart failure.

Many well-trained athletes may present with first-degree atrioventricular block but do not present with symptoms.

Diagnosis and screening

Physical examination, patient history, and diagnostic screening tools are used to diagnose first-degree atrioventricular block. The condition is often hard to diagnose, as patients typically present with few or no symptoms. Many individuals go undiagnosed due to lack of symptoms. Additionally, some individuals have prolonged PR interval due to a normal variant that is typically asymptomatic.

The condition is often diagnosed during routine electrocardiogram screening and is found incidentally. Diagnosis is made by a PR interval greater than 200 msec.

Second-degree atrioventricular block type I

Second-degree atrioventricular block type I, also known as Wenckebach or Mobitz I, is also an asymptomatic dysrhythmia. The condition typically occurs in adults post myocardial infarction or with inferior wall ischemia. It is usually caused by disease of the atrioventricular node.

A small percentage of second-degree atrioventricular block type I occurs due to underlying structural disease. Second-degree atrioventricular block type I is the most common type of second-degree atrioventricular block. The condition occurs in adults and equally both in men and women. There is no correlation between ethnicity and/or race and second-degree atrioventricular block type I.

Second-degree atrioventricular block type I

Second-degree atrioventricular block type I, also known as Wenckebach or Mobitz I, is also an asymptomatic dysrhythmia. The condition typically occurs in adults as post–myocardial infarction or with inferior wall ischemia.

Causes and risk factors

Second-degree atrioventricular block type I can occur due to the presence of structural heart disease. However, structural heart disease does not have to be present for the disease to occur. The condition may also occur due to a normal variant or autosomal dominant trait, making the individual genetically predisposed.

Pharmacologic agents that slow conduction through the atrioventricular node have been shown to cause second-degree atrioventricular block type I. These agents include cardioactive drugs such as digoxin, beta-blockers, calcium channel blockers, and certain antiarrhythmia drugs such as sodium channel blockers (procainamide).