Chapter 24: Alterations of Cardiovascular Function

Diseases of the Veins

• Varicosities are enlarged veins, commonly in the saphenous veins, caused by valve damage or chronic venous distension.
• Chronic Venous Insufficiency (CVI) is impaired venous return over time, causing tissue damage in the affected area.
• Venous Stasis Ulcers appear as a result of CVI due to compromised cell metabolism in the extremities.
• Deep Venous Thrombosis (DVT) arises from blood stasis, endothelial damage, or hypercoagulability. Pulmonary embolism is a serious DVT complication.
• Superior Vena Cava Syndrome is a progressive blockage of the superior vena cava leading to fluid buildup in the upper body. It is generally associated with cancer and considered an oncological emergency.

Diseases of the Arteries

• Hypertension is elevated systemic arterial blood pressure caused by increased cardiac output, total peripheral resistance, or both.
• Primary Hypertension has unknown causes, while Secondary Hypertension is linked to underlying diseases.
• Risk Factors for Hypertension include family history, age, gender, race, obesity, sodium intake, and lifestyle habits.
• Pathophysiology of Primary Hypertension involves potential factors such as overactive SNS, RAAS, kidney dysfunction, and hormonal imbalances.
• Clinical Manifestations of Hypertension stem from damage to various organs and tissues, such as retinal changes, heart disease, kidney disease, stroke, and dementia.
• Management of Hypertension involves reducing blood volume and peripheral resistance through non-pharmacological and pharmacological interventions.
• Orthostatic Hypotension (OH) is a decrease in blood pressure upon standing due to inadequate vasoconstriction and blood pooling in the lower body.
• Clinical Manifestations of OH include fainting, cardiovascular symptoms, and potential bowel and bladder dysfunction.
• Aneurysm is a localized dilation of a vessel wall, commonly affecting the aorta.
• Thrombus is a stationary blood clot attached to a vessel wall. Embolus is a mobile clot or other substance that can obstruct blood flow.
• Sources of Embolism include thrombus, air, amniotic fluid, bacteria, fat, and foreign matter.
• Common Sources of Arterial Embolism are the heart, often due to valvular disease, fibrillation, or myxomas. Affected areas include the lower extremities, brain, and heart.
• Emboli in Central Organs can lead to tissue death in the lungs, kidneys, and mesentery.
• Peripheral Vascular Diseases include Buerger's disease and Raynaud phenomenon, affecting arterioles in the extremities.
• Atherosclerosis is a type of arteriosclerosis, a leading cause of coronary artery disease (CAD) and cerebrovascular disease.
• Atherosclerosis is an inflammatory process starting with endothelial injury.
• Atherogenesis Stages include vasoconstriction, macrophage adherence, inflammation, LDL oxidation, foam cell formation, fatty streak development, and fibrous plaque formation.
• Plaque Rupture can lead to clot formation, vasoconstriction, and lumen obstruction, compromising tissue oxygenation.
• Ischemic Heart Disease commonly results from CAD and reduced myocardial blood supply.
• Peripheral Artery Disease develops from atherosclerotic plaques in the arteries supplying the extremities, causing pain and ischemia in the affected limb.
• Coronary Artery Disease (CAD) arises from atherosclerotic plaque that narrows or ruptures in the coronary arteries.
• Risk Factors for CAD include traditional factors like dyslipidemia, smoking, hypertension, diabetes, obesity, and sedentary lifestyle, as well as non-traditional factors like elevated C-reactive protein, hyperhomocysteinemia, and adipokine changes.
• Stable Angina Pectoris is predictable chest pain caused by myocardial ischemia due to increased demand.
• Prinzmetal Angina is caused by coronary artery vasospasm.
• Silent Ischemia is asymptomatic myocardial ischemia, a risk factor for acute coronary syndromes.
• Acute Coronary Syndromes (ACS) are caused by sudden obstruction due to thrombus formation. These syndromes include unstable angina, non-STEMI, and STEMI.
• Unstable Angina results in reversible myocardial ischemia.
• Myocardial Infarction (MI) is prolonged ischemia leading to myocardial cell death and tissue necrosis.
• Complications of MI include dysrhythmias and cardiac failure.
• Non-STEMI and STEMI are classified based on ECG findings showing subendocardial or transmural damage.
• Plasma Enzyme Levels like CK-MB, troponins, and LDH-1 indicate MI occurrence and severity.
• Treatment of MI involves revascularization, antithrombotics, ACE inhibitors, beta-blockers, pain management, and fluid management.

Disorders of the Heart Wall

• Pericarditis is inflammation of the pericardium, commonly caused by infection, trauma, surgery, or neoplasm. Although uncomfortable, it is not life-threatening.
• Pericardial Effusion is fluid buildup in the pericardial sac, potentially impairing cardiac function if rapid and excessive.
• Cardiomyopathies are primary myocardial disorders involving remodelling, neurohumoral responses, and hypertension. Types include dilated, hypertrophic, and restrictive cardiomyopathy.
• Cardiac Valve Disorders can be congenital or acquired, leading to stenosis, regurgitation, or both.
• Identification of Valve Disorder is aided by heart sounds, murmurs, and symptoms.
• Mitral Valve Prolapse Syndrome (MVPS) involves improperly positioning mitral valve leaflets during systole. It can be asymptomatic or lead to unpredictable symptoms.
• Rheumatic Fever is an inflammatory response to streptococcal infection, usually resolving without complications if treated.
• Rheumatic Heart Disease is a potential complication of untreated or severe rheumatic fever, leading to cardiovascular dysfunction.
• Infective Endocarditis is infection and inflammation of the endocardium, particularly the valves.
• Consequences of Infective Endocarditis include impaired valve function, bacteremia, and systemic emboli.
• HIV and AIDS can lead to cardiac abnormalities like myocarditis, endocarditis, pericarditis, and cardiomyopathy.

Manifestations of Heart Disease

• Heart Failure (HF) is broadly classified into reduced ejection fraction (systolic) and preserved ejection fraction (diastolic).
• Common Causes of Left Ventricular Failure are MI and hypertension.
• HF with Reduced Ejection Fraction (Systolic) arises from increased preload, decreased contractility, or increased afterload. These factors lead to elevated left ventricular end-diastolic volume and pressure, causing pulmonary congestion and edema.
• Neuroendocrine Response in HF includes SNS and RAAS activation, exacerbating the condition. Diuretics, beta-blockers, and ACE inhibitors are part of treatment.
• HF with Preserved Ejection Fraction (Diastolic HF) is characterized by HF symptoms, preserved ejection fraction, and abnormal diastolic function.
• Diastolic Dysfunction causes increased LVEDP even with normal volume and cardiac output.
• Right Ventricular Failure can be caused by left ventricular failure or pulmonary disease.
• Dysrhythmia (Arrhythmia) is irregular heart rhythm, ranging from occasional missed beats to life-threatening disturbances.
• Causes of Dysrhythmias include abnormal impulse generation or conduction.

Shock

• Shock is a widespread metabolic impairment leading to MODS through positive feedback loops.
• Types of Shock include cardiogenic, hypovolemic, neurogenic, anaphylactic, and septic.
• Final Common Pathway in Shock is impaired cellular metabolism, shifting from aerobic to anaerobic metabolism.
• Consequences of Anaerobic Metabolism include inflammatory response activation, decreased blood volume, and lowered pH.
• Impaired Glucose Utilization in shock leads to glycogenolysis, gluconeogenesis, and lipolysis for energy production.
• Gluconeogenesis depletes structural proteins, further impairing cell metabolism while contributing to lactic acid, uric acid, and ammonia buildup.
• Cardiogenic Shock involves decreased cardiac output, tissue hypoxia, and adequate intravascular volume.
• Hypovolemic Shock is caused by significant blood or fluid loss, leading to reduced tissue perfusion despite compensatory mechanisms.
• Neurogenic Shock is caused by massive vasodilation, resulting in relative hypovolemia despite high cardiac output.
• Anaphylactic Shock is triggered by an allergic reaction leading to massive vasodilation and fluid shifts, causing relative hypovolemia.
• Septic Shock begins with impaired cellular metabolism due to uncontrolled septicemia, triggering inflammation and immune responses, further disrupting tissue and cellular function.
• Multiple Organ Dysfunction Syndrome (MODS) is the progressive failure of two or more organs due to severe illness or injury.
• MODS Pathophysiology involves stress response, vascular endothelial changes, complement and coagulation protein release, and inflammatory processes.
• Consequences of MODS include maldistributed blood flow, hypermetabolism, hypoxic injury, and myocardial depression.
• Clinical Manifestations of MODS include inflammation, tissue hypoxia, and hypermetabolism. All organs can be affected.