Week 2 Cardiac - Student
Alterations in Perfusion: Overview
This note discusses critical concepts from chapters 34, 37-39 of Lewis 12th Edition that provide a detailed understanding of perfusion and heart function.
What is in Blood?
Red Blood Cells (Erythrocytes): These cells transport oxygen from the lungs to tissues and carry carbon dioxide back to the lungs for expulsion.
White Blood Cells (Leucocytes): These are crucial components of the immune system, fighting infections and foreign invaders.
Platelets: Essential for hemostasis, platelets initiate clot formation to prevent excessive bleeding from injuries.
Plasma: This liquid component of blood is primarily composed of water (about 90%), but also contains proteins, electrolytes, hormones, nutrients like amino acids and glucose, as well as waste products.
Thrombocytopenia (Chapter 34)
Definition: Thrombocytopenia is characterized by a low platelet count, defined as fewer than 150,000 platelets per microliter of blood.
Normal Hemostasis: The process relies on the integrity of vascular endothelium, adequate platelets, and functional coagulation factors. Any disruption in these components can lead to bleeding disorders or thrombosis.
Etiology and Pathophysiology of Thrombocytopenia
Thrombocytopenia leads to abnormal hemostasis, resulting in an increased risk of prolonged or spontaneous bleeding. Common causes include:
Drug-induced thrombocytopenia (e.g., some antibiotics, diuretics).
Autoimmune conditions affecting platelet lifespan.
Clinical Manifestations of Thrombocytopenia
Many individuals remain asymptomatic until the platelet count falls below 50,000/μL, at which point the risk of life-threatening bleeding increases significantly.
Symptoms may include:
Mucosal bleeding, such as gum or nosebleeds.
Skin manifestations like petechiae (small red dots), purpura (larger areas of bleeding), and ecchymosis (bruising).
Internal bleeding can present with symptoms such as weakness, fainting, dizziness, tachycardia, abdominal pain, and hypotension.
Causes of Thrombocytopenia
Common Acquired Causes:
Immune Thrombocytopenic Purpura (ITP): This is the most prevalent form and is characterized by the immune system mistakenly destroying platelets.
Thrombotic Thrombocytopenic Purpura (TTP): Associated with microangiopathic hemolytic anemia and is linked to deficiency in the ADAMTS13 enzyme.
Heparin-induced Thrombocytopenia (HIT): A complication of heparin therapy where antibodies against heparin-platelet factor 4 complexes lead to platelet activation and thrombosis.
Immune Thrombocytopenic Purpura (ITP)
This condition often arises in contexts of other autoimmune diseases like lupus or chronic infections such as HIV. Platelets become coated with antibodies, leading to their destruction primarily in the spleen.
Diagnostic Studies for ITP:
A platelet count of less than 150,000/μL is diagnostic.
A peripheral blood smear may reveal small-sized platelets along with a comprehensive medical history.
Treatments for ITP:
Initial Treatment: Corticosteroids (e.g., prednisone) are often the first line of treatment to reduce immune system activity.
Other Medications: Romiplostim and eltrombopag enhance platelet production in the bone marrow.
High-dose IV immunoglobulin (IVIG) can mitigate the action of antiplatelet antibodies, and rituximab reduces the formation of B-cells that produce these antibodies.
Platelet transfusions are reserved for severe bleeding emergencies and not used as a primary treatment.
Splenectomy: Surgical removal of the spleen may be considered in persistent cases where medical treatment fails to restore normal platelet levels.
Thrombotic Thrombocytopenic Purpura (TTP)
This condition features a pentad of symptoms: microangiopathic hemolytic anemia, thrombocytopenia, neurological symptoms, renal dysfunction, and fever.
The primary etiology often involves a significant deficiency of the von Willebrand factor-cleaving protease, ADAMTS13.
Treatment for TTP: The mainstay of treatment is plasmapheresis to remove antibodies and replenish ADAMTS13.
Heparin-Induced Thrombocytopenia (HIT)
HIT typically occurs five to ten days following heparin administration and can precipitate both arterial and venous thrombosis.
Interprofessional Care: When diagnosed with HIT, all heparin treatment must cease immediately, and anticoagulation alternatives must be initiated post-recovery, usually starting with warfarin.
Acute Coronary Syndromes (Chapter 37)
Angina: A clinical manifestation of myocardial ischemia characterized by an imbalance between myocardial oxygen demand and supply.
Types of Angina:
Stable Angina: Pain that is predictable and occurs with exertion; usually relieved by rest.
Unstable Angina: This presents at rest and may worsen, indicating the risk of an impending myocardial infarction.
Myocardial Infarction (MI): This condition results from the complete or partial obstruction of a coronary artery, and can be classified into types such as ST-Elevation Myocardial Infarction (STEMI) and Non-ST-Elevation Myocardial Infarction (NSTEMI).
Clinical Manifestations of Myocardial Infarction
Classic presentation includes severe chest pain not relieved by rest or nitroglycerin, which may radiate to the neck, jaw, back, or left arm.
Associated symptoms often include diaphoresis, tachycardia, shortness of breath, nausea, and potentially altered mental status due to reduced cardiac output.
Laboratory Tests for MI
Cardiac Enzymes: Elevated levels of creatine kinase-MB (CK-MB) and troponins I & T are indicative of myocardial injury.
Diagnostic Procedures: Changes noted on an ECG, like ST-segment elevation, help confirm the diagnosis of an MI.
Heart Failure (Chapter 38)
Heart failure is defined as the heart's inability to meet the oxygen demands of peripheral tissues, leading to efficient circulation.
Classification: Heart failure can be categorized as systolic (impaired contractility) or diastolic (impaired filling).
Signs and Symptoms: Patients may experience fatigue, tachycardia, dyspnea especially on exertion, and symptoms of fluid retention including edema in the legs and pulmonary congestion.
Risk Factors: Common predisposing factors include hypertension, coronary artery disease, diabetes, and sedentary lifestyle choices.
Compensatory Mechanisms: Neurohormonal pathways such as the renin-angiotensin-aldosterone system (RAAS) may exacerbate heart failure through fluid retention and increased vascular resistance.
Nursing Management of Heart Failure
Key nursing interventions include monitoring respiratory status, ensuring adequate oxygenation, patient's positioning for comfort, and educating patients about dietary modifications (such as low sodium diets) and prudent activity levels to manage their condition effectively.