Cardiovascular Disorders Part 1 & 2 PDF (SN 300 Fall 2024)

Cardiovascular Disorders Part 1 SN 300 – Pathophysiology I Kara Morriseau MN, BScN, RN Fall 2024  Content & Required Readings Week 10 Cardiac Diseases Part 1 Quiz 4 in Class (5%) – Week 9 Content Nov 11 (CLO 5.0 – 5.3, 8.0 – 8.2) Chapter 23 – S...

Cardiovascular Disorders Part 1 SN 300 – Pathophysiology I Kara Morriseau MN, BScN, RN Fall 2024  Content & Required Readings Week 10 Cardiac Diseases Part 1 Quiz 4 in Class (5%) – Week 9 Content Nov 11 (CLO 5.0 – 5.3, 8.0 – 8.2) Chapter 23 – Structure and function of the Cardiovascular and Lymphatic System Chapter 24 – Alterations of Cardiovascular Function  Specific Diseases Diseases of the arteries and veins: varicose veins, chronic venous insufficiency, thrombus formation in veins, superior vena cava syndrome, hypertension, hypotension, aneurysm, thrombus formation, embolism, thromboangiitis obliterans (Buerger’s disease), raynaud’s phenomenon, arteriosclerosis, peripheral arterial disease, shock Review of Cardiovascular System Heart Structure Right heart Pulmonary circulation → Pumps blood through the lungs Left heart Systemic circulation → Pumps blood through the body The Heart Heart wall Three layers enclosed in the pericardium Epicardium Outer layer Myocardium Composed of cardiac muscle Endocardium Inner lining Pericardium Pericardial sac Pericardial cavity Pericardial fluid Structure of the Heart Right atrium Left atrium Right ventricle Left ventricle Atrioventricular valves: Tricuspid valve Mitral valve Semilunar valves: Pulmonic semilunar valve Aortic semilunar valve Valves of the Heart  Great Vessels Superior and inferior venae cavae Pulmonary artery Right and left pulmonary arteries Pulmonary veins Aorta  Blood Flow and Cardiac Cycle Cardiac cycle Diastole Systole Phases of the cardiac cycle  Coronary Vessels Right coronary artery Conus Right marginal branch Posterior descending branch Left coronary artery Left anterior descending artery Circumflex artery Collateral arteries Coronary capillaries Coronary veins: Coronary sinus Great cardiac vein Posterior vein of the left ventricle Lymphatic vessels Structures That Control Heart Action Cardiac action potentials Conduction system Sinoatrial node (SA) Atrioventricular node (AV) Bundle of His (AV bundle) Right and left bundle branches Purkinje fibres  Structures That Control Heart Action Propagation of cardiac action potentials Resting membrane potential Depolarization Repolarization Hyperpolarization Refractory period Electrocardiogram Automaticity Rhythmicity  Myocardial Cells Nearly identical to skeletal muscle cells Differences important for cardiac function Sarcomeres Intercalated discs Actin, myosin, and the troponin–tropomyosin complex A band, I bands, Z line, M line Troponin T, I, and C Myocardial metabolism Myocardial oxygen consumption  Myocardial Contraction and Relaxation Cross-bridge theory of muscle contraction Excitation-contraction coupling Calcium channel L-type (calcium channel blocker medications) T-type Myocardial Contraction and Relaxation Myocardial Contraction and Relaxation Cardiac Performance Cardiac output Preload Volume/pressure inside ventricle at end of diastole Left ventricular end-diastolic volume Laplace’s law Starling’s law of the heart Afterload Resistance to ejection of blood from left ventricle Load muscle must move after it starts to contract Determined by system vascular resistance in aorta Cardiac Performance Myocardial contractility Stroke volume and preload Inotropic agents Oxygen and carbon dioxide levels Cardiac output Volume of blood flowing through either the systemic or pulmonary circuit in litres per minute Ejection fraction Cardiac Output Cardiac Performance Heart rate Cardiovascular vasomotor control centre Excitatory and inhibitory centres Neural reflexes Baroreceptor reflexes Atrial receptors Brainbridge reflex Hormones and biochemicals Systemic Circulation Arteries Arterioles Capillaries Venules Veins Structure of Blood Vessels Lumen Tunica intima Tunica media Tunica externa (adventitia) Structure of Blood Vessels (Cont.) Factors Affecting Blood Flow Pressure Force exerted on a liquid per unit area Resistance Opposition to force Diameter and length of the blood vessels contribute to resistance Poiseuille’s law Neural control of total peripheral resistance Change in diameter of the vessels Baroreceptors Arterial chemoreceptors Baroreceptor and Chemoreceptors Modified from Patton, K.T. (2019). Anatomy & physiology (10th ed.). Elsevier. Baroreceptor and Chemoreceptors Modified from Patton, K.T. (2019). Anatomy & physiology (10th ed.). Elsevier.  Regulation of Blood Pressure Arterial pressure Mean arterial pressure (MAP) Effects of cardiac output Effects of total peripheral resistance Effects of hormones Epinephrine and norepinephrine Antidiuretic hormone, renin-angiotensin-aldosterone system, and atrial natriuretic peptides Effects of other mediators Nitric oxide Adrenomedullin Venous pressure Regulation of Blood Pressure Cardiovascular Disease Cardiac Diseases Diseases of the arteries and veins: varicose veins, chronic venous insufficiency, thrombus formation in veins, superior vena cava syndrome, hypertension, hypotension, aneurysm, thrombus formation, embolism, Thromboangiitis obliterans (Buerger’s disease), Raynaud's phenomenon, arteriosclerosis, peripheral arterial disease, shock  Varicose Veins A vein in which blood has pooled Pathophysiology: Caused by trauma or gradual venous distension (typically saphenous vein) Clinical Manifestations: → Distended, tortuous, and palpable veins → edema of surrounding tissue (due to increased hydrostatic pressure that pushes plasma through the vessel wall) Risk factors: Age, Female gender, Family history, Obesity, Pregnancy, Deep vein thrombosis, Prior leg injury This can lead to chronic venous insufficiency  Chronic Venous Insufficiency Inadequate venous return over a long period due to varicose veins or valvular incompetence Pathophysiology: Venous hypertension, circulatory stasis, and tissue hypoxia cause an inflammatory reaction in vessels and skin ulcerations. Circulation to the extremities can be so sluggish that metabolic demands of the cells to obtain O2 & nutrients and remove waste are barely met → venous stasis ulcers Venous stasis ulcers→ trauma or pressure can therefore lower the O2 supply and cause cell death and necrosis Clinical Manifestations: Edema of lower extremities (can extend to knees), hyperpigmentation of the skin of feet and ankles.  Venous Thrombus Formation Thrombus formation in veins → thrombus is a blood clot that remains attached to a vessel wall Thromboembolism: detached thrombus Venus is more common than arterial (flow & pressure of veins are lower) Pathophysiology: Obstruction of venous flow leading to increased venous pressure → accumulation of clotting factors and platelets leads to thrombus formation near venous valve → inflammation around thrombus promotes further platelet aggregation → obstructs Three Factors promote it (Triad of Virchow) 1. Venous stasis → immobility, age, heart failure 2. Venous endothelial damage → trauma, intravenous medications 3. Hypercoagulable states → inherited disorders, malignancy, pregnancy, use of oral contraceptives, or hormone replacement therapy Other (cancer, orthopedic surgery/trauma, heart failure, immobility) increased the likleyhood of DVT → Deep vein thrombosis primarily in lower extremities Clinical manifestations: can be asymptomatic, or pain, redness, edema Can break off and cause pulmonary embolism  Superior Vena Cava Syndrome Progressive occlusion of the superior vena cava that leads to venous distension of upper extremities and head Causes: Cancer (bronchogenic cancer (75%), lymphoma, and metastases of other cancers), TB, mediastinal fibrosis, and cystic fibrosis, pacemaker wires, central venous catheters, and pulmonary artery catheters with associated thrombosis can cause SVCS Pathophysiology: SVC is a low-pressure vessel within a closed thoracic compartment susceptible to compression by tissue expansion. Onset slow Clinical Manifestations: edema and venous distension in upper extremities and face, c/o of fullness in head or tightness in shirt collars, necklaces, and rings → cerebral edema can cause visual disturbances, headaches, and impaired consciousness → skin may be purple, taut, and prolonged cap refill → respiratory distress due to edema of bronchial structures Diagnostics: Chest Xray, CT Thorax, MRI, Doppler studies  Hypertension Consistent elevation of systemic arterial blood pressure Sustained systolic blood pressure of 140 mm Hg or greater or a diastolic pressure of 90 mm Hg or greater (nonautomated office BP measurement) – out of office measurements preferred Risk Factors: Age, DM, CKD, diet, sedentary lifestyle, ancestry White coated 140 mm Hg, Life-threatening organ damage  Hypertension Pathophysiology: sustained increase in peripheral resistance (arteriolar vasoconstriction), an increase in circulating blood volume or both. Inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance contribute to increased peripheral resistance and increased blood volume Increased vascular volume is due to a decrease in renal excretion of salt shifting pressure-natriuresis relationship (less salt in urine) Increased SNS leads to increased HR and systemic vasoconstriction → increased BP: causes changes in blood vessels (vascular remodelling), renal sodium retention, insulin resistance, increased renin and angiotensin levels, and procoag effect RAAS System → Salt and water retention & increased vascular resistance 1) Damage: Release of renin, Synthesis of angio II through ACE, the section of aldosterone. Angio II and aldosterone contribute to hypertension hypertrophy, fibrosis of heart muscle, decreased contractibility, increased arrhythmias and HR, systemic vasoconstriction, renal salt and water retention, stimulate tissue growth and inflammation Angio II contributes to endothelial dysfunction, insulin resistance, remodelling of blood vessels, and platelet aggregation 2) Protection: ACE synthesizes angiotensin I from Angio II which stimulates receptors in the brain, blood vessels, heart, kidneys, gut, pancreas, and inflammatory cells and has vasodilatory, antiproliferative, antifibrotic, and antithrombic effects to lower blood pressure, limit vascular inflammation and clotting, and decrease tissue remodelling and damage to main organs Inflammation → activation of innate and adaptive immunity damages endothelial cells → endothelial injury and tissue ischemia resulting in the release of vasoactive inflammatory cytokines (acute inflammation protective but chronic bad) → chronic decreased vasodilators, vascular remodeling, and smooth muscle contraction  Hypertension Clinical Manifestations Silent disease: early stages no CM other than elevated BP Complications that damage organizes and tissues outside of the vascular system Heart disease, renal insufficiency, CNS dysfunction, impaired vision, impaired mobility, vascular occlusion, or edema Diagnostic Tests/Labs 24h BP monitoring CBC, UA, lytes, extended lytes, glucose, cholesterol, triglycerides, ECG  Orthostatic (postural) Hypotension Decrease in both systolic (20mm Hg) and diastolic blood pressure upon standing (10mm Hg) within 3 minutes of standing. Primary (idiopathic): No known cause often related to neurogenic or autonomic function Pathophysiology: Lack of normal blood pressure compensation in response to gravitational changes in the circulation (ie. Baroreceptors do not mediate reflex of arteriolar and venous constriction and increase HR compensation for gravity changes ) Acute orthostatic hypotension → altered body chemistry, medication action (anti-hypertensives, anti-depressants), prolonged immobility, starvation, physical exhaustion, volume depletion (dehydration, diuresis), or venous pooling (pregnancy, VV) Chronic orthostatic hypotension → endocrine disorders, metabolic disorders, diseases of CNS or PNS, cardiovascular autonomic neuropathy Clinical manifestations → Dizziness, blurring, loss of vision, syncope, fainting  Aneurysm Local dilation or outpouching of a vessel wall or cardiac chamber True aneurysms (all three layers) of arterial wall and weakening of vessel wall Types: Fusiform, Circumferential, Saccular, False aneurysms (Extravascular hematoma that communicates with the intravascular space) Occur usually in thoracic or abdominal aorta. Can lead to aortic dissection or rupture Risk Factors: Genetics, smoking, diet (atherosclerosis) Clinical Manifestations: aortic (asymptomatic → rupture → severe pain/hypotension), thoracic → dysphagia and dyspnea, cerebral → increased ICP or stroke if leaking, heart → dysrhythmias, HR, clots Diagnostics/Labs: CT, MRI, US, or angiography Aneurysm  Arterial Thrombi Thrombus formation → Blood clot that remains attached to the vessel wall Thromboembolic → clot circulating Arterial thrombi → clot in artery Risk factors: intimal injury/inflammation, obstruction of flow, pooling (stasis) Pathophysiology → inflammation of endothelium leads to activation of clotting cascade causing platelets to adhere readily Changes to anatomy like an aneurysm can lead to thrombus formation Valves of heart – if calcified or bacterial vegetation can lead to thrombi Septic Shock → systematic inflammation activates intrinsic and extrinsic pathways leaving microvascular thrombi Thrombus can 1) occlude artery causing ischemia and/or 2) dislodge becoming thromboembolism Diagnostics: US doppler or angiography  Embolism Bolus of matter that is circulating in the bloodstream that can obstruct a vessel Types: Dislodged thrombus, Air bubble, Amniotic fluid, Aggregate of fat, Bacteria, Cancer cells, Foreign substance Travels until it cant pass → eventually lodges in systemic or pulmonary vessel Pulmonary emboli (venous side) of systemic circulation or in right heart Arterial emboli → left heart, thrombi after MI, valvular disease, LV failure, endocarditis, or dysthymias Can cause ischemia or infarction in the tissues distal to the obstruction, organ dysfunction, or pain → can lead to necrosis Thromboangiitis obliterans (Buerger’s disease) Inflammatory disease of the peripheral arteries (Strongly associated with smoking) Autoimmune Characterized by the formation of thrombi filled with inflammatory and immune cells Thrombi become organized and fibrotic and result in permanent occlusion and obliteration of portions of small- and medium-sized arteries in feet and sometimes hands Clinical Manifestations: pain and tenderness of affect part, rubor and cyanosis (sluggish blood flow), chronic ischemia → thin and shiny skin, nails thickened and malformed.  Raynaud’s phenomenon Episodic vasospasm in arteries and arterioles of the fingers, less commonly the toes Primary → Vasospastic disorder of unknown origin Secondary → Secondary to other systemic diseases or conditions: Collagen vascular disease, Smoking, Pulmonary hypertension, Myxedema, Cold environment Pathophysiology: endothelial dysfunction with an imbalance of endothelium-derived vasodilators and vasoconstrictors leads to vasospastic attacks as a result of ischemia change sto skin color and sensation. Clinical Manifestations: pallor, cyanosis, cold, pain, numbness, tends to be bilateral, tips of digits to proximal phalanges, paresthesia until blood flow returns  Arteriosclerosis Chronic disease of the arterial system Abnormal thickening and hardening of the vessel walls Risk factors: diabetes, smoking, increased LDL and decreased HDL, and autoimmunity Atherosclerosis( Form of arteriosclerosis) → Thickening and hardening caused by accumulation of lipid-laden macrophages in the arterial wall leading to the formation of a lesion called a plaque Clinical Manifestations → inadequate tissue perfusion can cause transient ischemic events, tissue infarction, ishcemia, obstruction of arteries can lead to pain, coronary artery disease, stroke  Arteriosclerosis Pathophysiology Injury to endothelial cells (see risk ractors) of artery walls causing lesions that develop to fatty streak to the fibrotic plaque to complicated lesion Inflammation of endothelium – atherogenesis (cannot make normal cytokines) Cellular proliferation – expires adhesion molecules that bind to macrophages and other inflammatory/immune cells Macrophage migration and adherence (from the release of inflammatory cytokines including CRP) LDL oxidation (foam cell formation) – toxic free radicals cause oxidation of LDL (lipid-laden macrophages) Fatty streak (lesion formed by lipid-laden macrophages) - (fatty streak produces more free radicals, recruits T cells leading to autoimmunity, secretion of more anti-inflammatory mediators) Fibrous plaque - is caused by macrophages releasing growth factors that stimulate smooth muscle growth, producing collagen and migrating over fatty streaks leading to fibrous plaque. Plaque calcifies, protruding vessel lumen, and obstructs blood flow to distant tissues Complicated plaque- ruptured plaques resulting in platelet adhesion, clotting cascade, and thrombus formation.  Lipid Transport Lipids are transported in combination with proteins. Low-density lipoprotein (LDL) Transports cholesterol from liver to cells Major factor contributing to atheroma formation High-density lipoprotein (HDL) Transports cholesterol away from the peripheral cells to liver—“good” lipoprotein Catabolism in liver and excretion Atherosclerosis Modified from Crawford, M.H., et al. (2010). Cardiology (3rd ed.). Mosby.  Peripheral Arterial Disease Atherosclerotic disease of arteries that perfuse limbs Lower extremity ischemia resulting from artery obstruction - gradual or acute Intermittent claudication – pain with ambulation from gradually increased obstruction to arterial blood flow to less from atherosclerosis in iliofemoral vessels If a thrombus forms over an atherosclerotic lesion, complete obstruction of blood flow can occur acutely causing severe pain, loss of pulses, and skin color changes Symptoms are caused by slow, sluggish blood flow. Causes pain, tenderness in the affected area Can often lead to gangrenous lesions and amputations Peripheral Arterial Disease Most common sites Abdominal aorta Carotid arteries Femoral and iliac arteries Diagnostic tests Blood flow assessed by Doppler studies and arteriography Shock The cardiovascular system fails to perfuse the tissues adequately leading to widespread impairment of cellular metabolism. Impaired oxygen use Cell is not able to use O2 or not receiving adequate O2 Cells go from aerobic or anaerobic (use stores of ATP faster than can be replaced) → cannot operate NA/K pump → Na & Cl accumulate in cell, K goes out of cell → impacts NS and myocardium → decreased resting potential and action potential As Na moved into cell H2O followed (cells swell – cellular edema – injure cells → H20 pulled from vascular space into cell → decreased circulatory volume → inflammatory and clotting cascade activated → acute tubular necrosis, DIC An anaerobic state impacts pH leading to metabolic acidosis → cardiac and skeletal muscles use lactic acid as a fuel sore → acidotic state impacts cell function, repair, and division, reducing O2 carrying capacity of blood Impaired glucose use Impaired glucose delivery or impacted glucose uptake of cells High cortisol levels, thyroid hormone, and catecholamines account for hyperglycemia, insulin resistance, tachycardia, increased cardiac contractility → cells shift to glycogenolysis, gluconeogenesis, and lipolysis to generate fuel to survive → energy costs required for glycogenlysis and lipolysis contribute to cell failure Depletion of protein → gluconeogenesis causes proteins to be used for fuel and protein no longer available for cell structure, function, repair, or replication → protein broken down into alamine (which is converted to pyrvic acid), ammonia, and urea. Protein breakdown weakness skeletal muscle and cardiac muscle leading to muscle wasting Clinical Manifestations: vary based on stage but often include hypotension, tachycardia, increased respiratory rate  Shock The cardiovascular system fails to perfuse the tissues adequately leading to widespread impairment of cellular metabolism. Impaired oxygen use Cell is not able to use O2 or not receiving adequate O2 Cells go from aerobic or anaerobic (use stores of ATP faster than can be replaced) → cannot operate NA/K pump → Na & Cl accumulate in cell, K goes out of cell → impacts NS and myocardium → decreased resting potential and action potential As Na moved into cell H2O followed (cells swell – cellular edema – injure cells → H20 pulled from vascular space into cell → decreased circulatory volume → inflammatory and clotting cascade activated → acute tubular necrosis, DIC An anaerobic state impacts pH leading to metabolic acidosis → cardiac and skeletal muscles use lactic acid as a fuel sore → acidotic state impacts cell function, repair, and division, reducing O2 carrying capacity of blood Impaired glucose use Impaired glucose delivery or impacted glucose uptake of cells High cortisol levels, thyroid hormone, and catecholamines account for hyperglycemia, insulin resistance, tachycardia, increased cardiac contractility → cells shift to glycogenolysis, gluconeogenesis, and lipolysis to generate fuel to survive → energy costs required for glycogenlysis and lipolysis contribute to cell failure Depletion of protein → gluconeogenesis causes proteins to be used for fuel and protein no longer available for cell structure, function, repair, or replication → protein broken down into alamine (which is converted to pyrvic acid), ammonia, and urea. Protein breakdown weakness skeletal muscle and cardiac muscle leads to muscle wasting → decreased immune system, decreased circulatory volume, decreased O2 and glucose delivery, and decreased waste removal Types of Shock Cardiogenic → Inability of heart to Hypovolemic → loss Neurogenic → Neural maintain cardiac of circulating blood alterations of vascular output to circulation volume smooth muscle tone (HF) Anaphylactic → Immunological Septic → Infection process Cardiogenic Shock Dyspnea, tachypnea, systemic venous and pulmonary edema, dusky skin, hypotension, oliguria) Hypovolemic Shock High systemic vascular resistance, poor skin turgor, thirst, oliguria, low systemic and pulmonary preloads, rapid HR, thready pulse, and deteriorating mental status Neurogenic Shock Relative hypovolemia, SVR decreases, bradycardia, decrease CO, under perfusion of tissues, Anaphylactic Shock  Anaphylactic Shock Hypersensitivity Reactions – Type I Type I hypersensitivity—allergic reactions (Humoral) Common Caused by allergen Skin rashes Hay fever Causative mechanism Exposure to allergen Development of IgEs Mast cells Complications Anaphylaxis Anaphylactic Shock Generalized itching or tingling, especially in oral cavity Coughing Difficulty breathing Feeling of weakness Dizziness or fainting Sense of fear and panic Edema around eyes, lips, tongue, hands, feet Hives Collapse with loss of consciousness  Septic Shock SIRS – Systemic Inflammatory Sepsis can lead to Response Multiple Organ Syndrome Dysfunction Syndrome (MODS) Diagnostic Tests & Lab Tests Electrocardiography Useful in the initial diagnosis and monitoring of dysrhythmias, myocardial infarction, infection, pericarditis Holter Monitor Auscultation Determination of valvular abnormalities or abnormal shunts of blood that cause murmurs Detected by listening through a stethoscope Dobutamine Stress Echocardiography Transesophageal Echocardiogram (TEE) Probe is inserted into the esophagus Uses ultrasound to look closely for blood clots Clear pictures of heart Echocardiography Used to record heart valve movements, blood flow, and cardiac output Diagnostic Tests & Lab Tests Exercise stress tests Used to assess general cardiovascular function Perstantine-Thallium Imaging, Chest x-ray films Used to show shape and size of the heart Nuclear imaging Tomographic studies CT Thorax or MRI Cardiac catheterization Measures pressure and assesses valve and heart function Determines central venous pressure and pulmonary capillary wedge pressure Angiography - Visualization of blood flow in the coronary arteries Can result in a Percutaneous Coronary Intervention  Diagnostic Tests & Lab Tests US Doppler studies Assess blood flow in peripheral vessels Record sounds of blood flow or obstruction Blood tests Assess levels of serum triglycerides, cholesterol, A1C, sodium, potassium, calcium, electrolytes, PTT, PT, D-Dimer Arterial blood gas determination Checks the current oxygen level and acid- base balance  Case Study Ms. Smith is a 75 year old woman presenting with PAD, HTN, DM2. She has smoked for the last 40 years, 1 pack per day. BP 175/92 95 bpm 95% RA 36.8 18R. The patient has a c/o of R leg pain. The physician orders CBC, Lytes, Extended Lytes, CRP, ESR, A1C, ABG, Random glucose, Cholesterol, and Triglycerides. 1. Can you explain the pathophysiology of HTN and PAD. 2. Describe the pathophysiology of Arteriosclerosis and Atherosclerosis. 3. Explain the two laboratory tests of Cholesterol and Triglycerides and their impact on PAD and HTN.