Cardiac/Vascular Nurse Exam Secrets Study Guide (13 page)

Other disorders that can lead to second-degree atrioventricular block type I include inflammatory diseases such as endocarditis, myocarditis, Lyme disease, and acute rheumatic fever, infiltrative diseases such as amyloidosis, hemochromatosis, and sarcoidosis, metabolic disorders such as hyperkalemia, hypermagnesemia, and Addison disease, and vascular diseases such as ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, lupus, and Reiter syndrome. Also, acute myocardial infarction has been associated with second-degree atrioventricular block type I.

Symptoms

Individuals who present with second-degree atrioventricular block type I 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 second-degree atrioventricular block type I, heart rate, and atrial rhythm are typically abnormal due atrioventricular node dysfunction. However, some patients may present with lightheadedness, dizziness, decreased cardiac output, activity intolerance, shortness of breath, chest pain, hypotension, bradycardia, heart failure, stroke, and syncope.

Yet, symptoms in patients diagnosed with second-degree atrioventricular block type I can vary greatly depending on the overall health and physical conditioning of the patient as well as presence of other comorbid conditions.

Diagnosis and screening

Physical examination, patient history, and diagnostic screening tools are used to diagnose second-degree atrioventricular block type I. 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.

The condition is diagnosed on electrocardiogram by progressive lengthening of PR interval followed by a p wave without an associated QRS complex. Holter monitor or event recorder can be used to diagnose outpatients. Laboratory tests including serum electrolyte and magnesium levels, serum digoxin levels, and thyroid function tests may be used to find the cause. Other imagining tests may be performed depending on the patient’s symptoms and presence of comorbid cardiovascular conditions. Diagnostic electrophysiologic testing may be necessary to determine the site of block and need for a pacemaker.

Second-degree atrioventricular block type II

Second-degree atrioventricular block type II, also known as Mobitz II, is an intermittent failure of conduction of impulses below the AV node. The condition is often associated with HIS-Purkinje system cardiac disease, which can lead to complications such as complete heart block or ventricular asystole. It occurs most often in adults and is associated with a high mortality rate, as the condition can progress rapidly to a complete heart block.

The condition is highly associated with infra-and intranodal blocks, which indicate the location of the blocks. A small percentage of second-degree atrioventricular block type II occurs due to underlying structural disease. 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 II. The condition is less common than second-degree atrioventricular block type I. Second-degree atrioventricular block type II is associated with a high mortality rate when it occurs with comorbid anterior wall myocardial infarction.

Causes and risk factors

Second-degree atrioventricular block type II can occur due to 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 normal variant or autosomal dominant trait, making the individual genetically predisposed.

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

Other disorders that can lead to second-degree atrioventricular block type II include inflammatory diseases such as endocarditis, myocarditis, Lyme disease and acute rheumatic fever; infiltrative diseases such as amyloidosis, hemochromatosis, and sarcoidosis; metabolic disorders such as hyperkalemia, hypermagnesemia, and Addison disease; and vascular diseases such as ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, lupus, and Reiter syndrome. Also, acute myocardial infarction, congestive heart failure, coronary artery disease, and primary diseases have been associated with second-degree atrioventricular block type II.

Symptoms

Some patients may present with lightheadedness, dizziness, decreased cardiac output, activity intolerance, shortness of breath, chest pain, hypotension, bradycardia, diaphoresis, pauses in pulse, heart failure, stroke, and/or syncope or fainting.

Yet, symptoms in patients diagnosed with second-degree atrioventricular block type I can vary greatly depending on the overall health and physical conditioning of the patient as well as presence of other comorbid conditions.

Diagnosis and screening

Physical examination, patient history, and diagnostic screening tools are used to diagnose second-degree atrioventricular block type II. The condition is typically associated with significant underlying conduction system conditions. Patients often present with hypotension, diaphoresis, and pauses in pulse caused by decreased cardiac output.

The condition is diagnosed by electrocardiogram, Holter monitor, or event recorder. Not every p wave has an associated QRS complex (1:3, etc) and there is NO progressive prolongation of PR interval. Lab tests and echocardiography may be necessary to elucidate further the underlying cause. Also, diagnostic electrophysiologic testing may be necessary to determine the site of the block and need for a pacemaker.

Third-degree atrioventricular block

Third-degree atrioventricular block, also known as complete heart block, involves complete dissociation of impulses between the atria and ventricles. The condition is not well tolerated and most common in adults, but can occur in adolescents with congenital heart disease. The condition can occur intermittently or consistently depending on the underlying cause of the condition.

In the United States, the prevalence of third-degree atrioventricular block is approximately 0.02%. The incidence of third-degree atrioventricular block increases with age, but may occur in infants or adolescents due to congenital complete heart block.

Causes and risk factors

The most common causes of third-degree atrioventricular block include drugs that target the atrioventricular node such as beta-blockers, calcium channel blockers, quinidine, and procainamide; degenerative diseases such as Lenègre disease and Lev disease; infectious causes such as Lyme disease, rheumatic fever, myocarditis, and Chagas disease; rheumatic diseases such as ankylosing spondylitis, Reiter syndrome, relapsing polychondritis, rheumatoid arthritis, and scleroderma; infiltrative processes such as amyloidosis, sarcoidosis, tumors, Hodgkin disease, and multiple myeloma; neuromuscular disorders such as Becker muscular dystrophy and myotonic muscular dystrophy; ischemia or infarction; and metabolic causes such as hypoxia and hyperkalemia.

Symptoms

Most patients diagnosed with third-degree atrioventricular block present with symptoms. However, some patients present with few or no symptoms. Additionally, third-degree atrioventricular block may be an underlying condition in patients who present with sudden cardiac death.

The symptoms associated with third-degree atrioventricular block include fainting or syncope, near-syncope, lightheadedness, fatigue, dyspnea, and chest pain. Patients diagnosed with third-degree atrioventricular block typically present with a series of P-waves and QRS complexes that do not relate to one another. Additionally, atrial heart rate is normal but ventricular heart rate is abnormal.

Diagnosis and screening

Physical examination, medical history, and diagnostic screening tools are used to diagnose third-degree atrioventricular block. Electrocardiogram (ECG), Holter monitor, and event recorders are used to diagnose. On the ECG, there is no association between p waves and QRS complexes. Further tests including echocardiography and lab tests may be necessary to elucidate fully the source of the block.

Cardiogenic shock

Cardiogenic shock is a condition characterized by inadequate perfusion from cardiac dysfunction. It is an emergency situation and requires immediate treatment. Cardiogenic shock is the most common cause of mortality in patients who experience a myocardial infarction.

In the United States, cardiogenic shock occurs in approximately 8.6% of patients experiencing ST-segment elevation myocardial infarction, with about 29% of those presenting to the hospital already in shock. Cardiogenic shock occurs in a smaller percentage of patients with non-ST segment elevation myocardial infarction, occurring in approximately 2% of patients. The condition is the leading cause of mortality in patients experiencing myocardial infarction.

Morality rates vary from 1 race to another, with Hispanics at highest risk, followed by African Americans and then Caucasians and Asians. Women comprise 42% of all patients with cardiogenic shock.

Causes and risk factors

The most common cause of cardiogenic shock is myocardial infarction. However, not every patient who experiences a myocardial infarction goes into cardiogenic shock. The individuals at highest risk for cardiogenic shock include patients who have experience a myocardial infarction, older age, history of congestive heart failure, diabetes, dysrhythmia, and/or coronary artery disease.

Common causes of cardiogenic shock include ventricular septal rupture, papillary muscle infarction or rupture, myocarditis, endocarditis, arrhythmias, pericardial tamponade, and pulmonary embolism.

Other causes of cardiogenic shock include beta-blocker overdose, calcium channel blocker overdose, myocardial contusion, respiratory acidosis, hypocalcemia, hypophosphatemia, ventricular hypertrophy, restrictive cardiomyopathies, aortic stenosis, hypertrophic cardiomyopathy, dynamic outflow obstruction, aortic coarctation, malignant hypertension, mitral stenosis, endocarditis, mitral or aortic regurgitation, atrial myxoma, tamponade, and cardiotoxic drugs such as doxorubicin.

Symptoms

The symptoms associated with cardiogenic shock vary depending on the patient and presence of underlying comorbid conditions. Younger patients in good health tend to present with fewer symptoms than older patients with other comorbid cardiovascular conditions.

The common symptoms associated with cardiogenic shock include confusion, lack of alertness, loss of consciousness, palpitations, sweating, fainting or syncope, pale skin, weak pulse, rapid breathing, shortness of breath, decreased or no urine output, cold hands and/or feet, anxiety, nervousness, weakness, lethargy, fatigue, loss of ability to concentrate, decreased mental status, restlessness, agitation, coma, dizziness, and lightheadedness.

Diagnosis and screening

Physical examination, medical history, and diagnostic screening tools are used to diagnose cardiogenic shock. The condition is treated on an emergency basis and requires prompt attention and is typically diagnosed in the emergency room setting. It is typically diagnosed when a patient has been admitted to the emergency room for a myocardial infarction.

Diagnostic screening tools used to diagnose cardiogenic shock include blood pressure monitoring, electrocardiogram, echocardiogram, chest x-ray, and coronary angiography. Laboratory blood tests that may be performed include arterial blood gas measurement, electrolyte levels, cardiac enzyme levels, renal function, liver function, lactate levels, and thyroid function tests.

Planning and Implementation

CHEST and AHA guidelines for anticoagulation administration

CHEST guidelines promote the use of a systematic protocol for anticoagulation therapy including daily international normalized ratio prothrombin time (INR-PT/INR) monitoring to evaluate dosing levels. Optimal therapeutic INR range while on anticoagulants should be tightly controlled between 2.0 and 3.0. This method requires a high level of accountability in coordinating care and communication with treatment team members as well as the patient regarding test results and rationale behind current dosing levels. The patient should be continuously instructed regarding self-management skills in anticipation for self care. Anticoagulant therapy is contraindicated in the critically ill patient with active—or a high risk for—bleeding. These recommendations are also sanctioned by the American Heart Association.

AHA practice guidelines regarding chronic heart failure

AHA identifies heart disease by four stages: A, B, C and D. Stage A (patients at high risk but without established heart disease) and stage B (patients with measurable damage to the heart who are still currently without symptoms) are the stages where progression to further disease is still preventable. Care is focused on education and prevention measures. ACE inhibitors may be added to the care of patients in stage B.

Stage C (patients with heart disease and symptom complaints) would increase pharmaceutical treatments to also include diuretics. Dietary intervention might include low-salt diets and/or restricted fluid intake.

Stage D (patients who have escalated to end-stage heart disease and require extreme medical measures or end-of-life care) may require surgical interventions on a case-by-case basis, including valve surgery, ventricular assist device (VAD) or transplant. Most patients at this stage do not qualify for such interventions and will enter into care focused on end-of-life comfort.