Week 2 Cardiac - Student

ALTERATIONS IN PERFUSION (LEWIS 12TH EDITION CHAPTERS 34, 37-39)

• Overview of perfusion alterations in medical-surgical nursing.

COMPONENTS OF BLOOD

• Red Blood Cells (Erythrocytes): Carry oxygen.

• White Blood Cells (Leukocytes): Key players in the immune response.

• Platelets: Essential for blood clotting, preventing excessive bleeding.

• Plasma: Contains nutrients (e.g., amino acids, glucose) and water, serving as the medium for transporting cells and other substances.

THROMBOCYTOPENIA (LEWIS 12TH EDITION CHAPTER 34)

• Definition: A condition characterized by low platelet counts, leading to increased risk of bleeding.

NORMAL HEMOSTASIS

• Involves:

  • Vascular endothelium

  • Platelets

  • Coagulation factors

• All components must function together to prevent hemorrhage and repair vascular injuries.

• Disruption in any element may result in bleeding or thrombosis.

ETIOLOGY AND PATHOPHYSIOLOGY

• Defined as a reduction of platelets below normal levels (normal range not specified).

• Leads to:

  • Abnormal hemostasis

  • Prolonged or spontaneous bleeding

• Commonly acquired from high doses of particular medications.

CLINICAL MANIFESTATIONS

• Patients may be asymptomatic until platelet counts drop below 50,000/μL.

• Symptoms include:

  • Mucosal or cutaneous bleeding

  • Petechiae: Microhemorrhages

  • Purpura: Bruising from multiple petechiae

  • Ecchymosis: Larger areas of hemorrhage

• Prolonged bleeding may occur after routine procedures.

• Possible internal bleeding symptoms: Weakness, fainting, dizziness, tachycardia, abdominal pain, hypotension.

  • Notable concern for hemorrhage, which may be acute or gradual.

CAUSES OF THROMBOCYTOPENIA

• Acquired Causes:

  • Immune thrombocytopenic purpura (ITP)

  • Thrombotic thrombocytopenic purpura (TTP)

  • Heparin-induced thrombocytopenia (HIT)

IMMUNE THROMBOCYTOPENIC PURPURA (ITP)

• Description: Most common acquired thrombocytopenia; results from abnormal platelet production and destruction.

• Associated with autoimmune disorders (like Lupus), infections (H. pylori, HIV).

• Platelets become coated with antibodies, leading to their destruction in the spleen.

DIAGNOSTIC STUDIES

• Reduced platelet count (<150,000/μL).

  • Testing includes peripheral blood smear, ITP antigen-specific assay, medical history evaluation, clinical examination.

TREATMENTS FOR ITP

• Interprofessional Care: Begins if platelet counts drop below 30,000/μL or if symptomatic.

• Initial Treatment: Corticosteroids (e.g., prednisone, methylprednisolone).

• Advanced Treatments:

  • Romiplostim (Nplate)

  • Eltrombopag (Promacta) - can cause liver damage and ineffective with high-calcium foods.

  • High doses of IV immunoglobulin (IVIG) compete with antiplatelet antibodies.

  • Rituximab (Rituxan) targets B cells.

PLATELET TRANSFUSIONS

• Indicated: For life-threatening hemorrhages or when platelet count is very low (<10,000/μL).

• Not used prophylactically due to possible antibody formation.

SPLENECTOMY

• Performed in non-responsive cases or for chronic conditions; it may compromise immunity.

THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP)

• Description: Uncommon syndrome encompassing hemolytic anemia, thrombocytopenia, and various systemic symptoms.

• Microthrombi formation in small vessels leads to complications (notably kidney injury).

CAUSES AND RISK FACTORS

• Deficiency of plasma enzyme ADAMTS13, autoimmune disorders, drug toxicities, pregnancy, infections.

INTERPROFESSIONAL CARE

• Treat underlying conditions; urgent plasmapheresis may be necessary to reverse platelet consumption.

• Corticosteroids and immunosuppressant therapies are sometimes indicated.

HEPARIN-INDUCED THROMBOCYTOPENIA (HIT)

• A serious immune reaction that occurs in some patients after the administration of heparin.

• Symptoms include:

  • Significant drop in platelet counts (≥50%) within 5-10 days of heparin therapy initiation.

  • Major concern for venous and arterial thromboembolic events.

INTERPROFESSIONAL CARE

• Immediate cessation of all heparin; critical notes in medical records.

• Warfarin usage should start only when platelets are stable above 150,000/μL.

• Other treatments for severe cases include plasmapheresis and thrombolytic therapy.

THROMBOCYTOPENIC NURSING MANAGEMENT

• Prevent Hemorrhage: Vigilantly monitor for bleeding and provide safety measures; avoid IM injections when possible.

• Encourage patient education on safety measures to reduce bleeding risks.

• Monitor platelet counts and educate on menstrual blood loss management.

ANGINA AND MYOCARDIAL INFARCTION (ACS)

• Overview: Angina represents ischemia; myocardial infarction indicates irreversibility leading to tissue necrosis.

STABLE ANGINA

• Caused by increased oxygen demand; often linked to underlying atherosclerosis.

UNSTABLE ANGINA & NSTEMI

• New or changing chest pain indicates cardiac ischemia, potential transition to an MI.

STEMI

• Resulting from complete blood vessel occlusion, leading to significant tissue death.

NURSING MANAGEMENT FOR ACS

• Important to assess and provide rapid care during chest pain episodes:

  • Position upright, apply oxygen, monitor VS, conduct ECG, and administer medications as required.

LABORATORY TESTS

• Cardiac Enzymes: Troponin and CK-MB levels used in diagnosis; troponin is particularly sensitive.

HEART FAILURE

• Definition: The heart's incapacity to provide adequate blood to meet physiological demands, leading to systemic complications.

PATHOPHYSIOLOGY OF HF

• Associated with cardiac output issues; dysfunction can arise from left- or right-sided failure, or both.

RISK FACTORS

• Key contributors include hypertension, coronary artery disease, diabetes, and lifestyle factors.

CLINICAL MANIFESTATIONS

• Symptoms such as dyspnea, fatigue, and changes in vital signs indicate worsening heart failure.

NURSING MANAGEMENT

• Constantly monitor respiratory status, administer necessary medications, and educate patients on dietary restrictions.