Alteration in Cardiovascular Function PDF

Disease of the Arteries and Veins Laminar (smooth) vs Turbulent (rough) blood flow • Hemostatsis: Correct blanace of formation and dissolution of clots • Thrombus: Blood clot that remains attached to the vessel wall • Thromboembolus: Circulating clot • Arterial thrombus: Clots blocking an artery •...

Disease of the Arteries and Veins Laminar (smooth) vs Turbulent (rough) blood flow • Hemostatsis: Correct blanace of formation and dissolution of clots • Thrombus: Blood clot that remains attached to the vessel wall • Thromboembolus: Circulating clot • Arterial thrombus: Clots blocking an artery • Venous thrombus: Clots blocking a vein • Thrombophlebitis: Inflammation caused by a clot in a vein Venous & Arterial Thrombosis Venous thrombosis and arterial thrombosis develop when 1. Conditions prommote activation of coagulation 2. There is stasis of blood flow Or Both Ex. • • • • • • • • Irritation or roughening (surgical procedures) Traumatic injury Inflammation Infection Low blood pressure Anatomical CHanges in an artery (aneurysm) Medications Genetic conditions Thrombus formation Diseases of the veins Venous thrombi are more common than arterial thrombi Deep venous thrombosis • Occurs near a venous valve • Inflammation around the thrombus promotes further platelet aggregation (grows) • Obstruction of venous flow increases venous pressure (edema) Triad of virchow • Venous stasis • Venous endothelial damage • Hypercoagulable states (other: cancer, orthopdic surgery/ trauma, heart failure, immobility) S&S • Pain and redness- inflammation • Deep in leg - no pain but edema • Untreated cause pulmonary embolis Tx: • Anticoagulation therapy • Low molecular-weight heparin & warfarin Varicose Veins • Vein in which blood has pooled • Distended, tortuous, and palpable veins • Caused by trauma o gradual venous distention Risk factors: • Age • Female gender • Family history • Obesity • Pregnancy • Deep veiin thrombosis • Prior leg injury Chronic Venous insufficiency • Inadequate venous return over a long period due to varicose veins or valvular incompetence • Venous stasis ulcer Embolism Obstruction of a vessel by an embolus • Bolus of matter circulating in blood Ex. • • • • • • • Dislodged thrombus Air bubblr Aggregate of aniotic fluid Fat Bacteria Cancer cells Foreign substance Travels until it gets tuck and causes ischemia/infraction • pulmonary emboli originate from venous side • Arterole emboli mostly originate from the left side of the heart Hypertension: Sustained systolic blood pressure > 140 mm Hg or diastolic pressure > 90 mm Hg Cardiac output: amount of blood pumped by the heart per minute Peripheral vascular resistance: resistance to blood flow in the blood vessels Primary Hypertension: • Essential or idiopathic HTN • Genetic and environmental factors • Affects 92%-95% of individuals w/ HTN Risk factors: • obesity • Insulin resistance • Natriuretic peptide abnormalities • High sodium intake Isolated systolic HTN - becoming prevalent in all age groups • Elevations of systolic pressure are caused by increases in cardiac output, total peripheral vascular resistance, or both Shift in the pressure-Natriuresis Relationship Secondary Hypertension • Caused by a systemic disease process that raises peripheral vascular resistance or cardiac output • Renal artery stenosis, renal parenchymal disease, tumor (phenochromocytoma), and drugs (oral contraceptives, corticosteroids, antihistamines) • If underlying cause can be removed - may return to normal Complicated hypertension • Chronic hypertensive damage to the walls of systemic blood vessels • Cardiac smooth muscle cells undergo hypertrophy and hyperplasia w/ fibrosis of the tunica intima and media • Affects heart, kidneys, retina • Can result in transient ischemic attack/stroke, cerebral thrombosis, aneruysm, dementia Orthostatic (postural) hypotension • Decrease in both systolic and diastolic blood pressure upon standing • Lack of normal blood pressure compensation in response to gravitational changes on the circulation Acute orthostatic HTN • Prolonged immobility, starvation, exhaustion, blood volume depletion, venous pooling Chronic orthostatic HTN • Secondary to disease or idiopathic/primary • Increased fluid and salt • Compression stockings, vasoconstrictors, mineralocorticoids Aneurysm • Local dilation or outpouching of a vessel wall or cardiac chamber True Anuerysm • Fusiform aneruryms • Circumferential vs saccular aneruysms False Aneyrysms Aorta most susceptible, especially abdominal • Causes include atherosclerosis, hypertension —- Weaken the walls and increased stress • Can lead to aortic dissection or rupture Cardiac aneurysms most comm. form after myocardial infraction when intraventricular tension streches the non-contracting infracted muscle Peripheral Artery Disease Raynaud Phenomenon and Raynaud disease • Episodic vasospasm in arteries and arterioles of the fingers, less commonly the toes • Raynaud disease is a primary vasospastic disorder of unknown origin Raynaud phenomenon is secondary to other systemic disease or conditions: • Collagen vascular disease • Smoking • Pulmonary hypertension • Myxedema • Cold environment Manifestations include pallor, cyanosis, cold, pain Arteriosclerosis Chronic disease of the arterial system • Abnormal thickening and hardening of the vessel walls • Smooth muscle cells and collagen fibers migrate to the tunica intima Atherosclerosis • Form of arteriosclerosis • Thickening and hardening cause by accumulation of lipid-laden macrophages in the arterial wall • Plaque development Progression 1. Inflammation of endothelium 2. Cellular proliferation 3. Macrophage migration and adherennce 4. LDL oxidation (foam cell formation) 5. Fatty streak 6. Fibrous plaque 7. Complicated plaque Risk factors: hyperlipidemia/ dyslipidemia, diabetes, smoking, hypertension Results: inadequate perfusion, ischemia, necrosis Fatty Streak • Increase production of O2 radicals • Lipid accumulation Tx: • Decrease LDL may reverse the process • Statins-Crestor, Zocor, Lipitor Fibrous plaque • Microphages release growth factors • Smooth muscle cells proliferate and migrate over the fatty plaque • Plaque May calcify • Protrudes into the vessel lumen Treatment • Stabilize and reverse plaques before rupture ‘Unstable’ plaques are prone to rupture Peripheral artery disease • Atherosclerotic disease of the arteries that perfuses the limbs • Risk factors same as atherosclerosis —- prevalent in individuals with diabetes • ischemia can be gradual or acute • Doppler to measure blood flow and detect the obstructed region Tx: • Vasodialtors and antiplatelet or antithrombotic mediications • Cholesterol lowering medications to reverse dyslipidemia • Excerise and rehabilitation • Emergent percutaneous procedures or surgical revascularization be needed (stent or bypass) Coronary Artery Disease (CAD) • Any vascular disorder that narrows or occludes the coronary arteries leading to myocardial ischemia • Atherosclerosis is the most comm. cause • CAD LAD bad Risk factors: Major: • Increased age • Family history • Male gender or female post menopause Modifiable: • Dyslipidemia • Hypertension • Cigarette smoking Diabetes mellitus • Obesity/sedentary lifestyle • Atherogenic diet Coronary Artery Disease Coronary arteries supply blood flow to meet the 02 demands of the myocardium Myocardial ischemia • local, temporary deprivation of the cornorary blood supply — 50% narrowing is enough to hamper cellular metabolism when the demand increases • stable angina • Prinzmetal angina • Silent ischemia Angiogensesis: chronically under-perfused tissues might develop collateral circulation from pre-existing blood vessels. Stable Angina • Cause by gradual luminal narrowing and hardening of the arterial walls — affected vessels cannot dilate in response to increased myocardial demand • Chest discomfort, heaviness/pressure to moderately severe —Radiation - afferent sympathetic fibers (neck, jaw, tooth, shoulder ,either arm (more often left) back, pallor, diaphoresis, dypnea • women may not present with typical pain — Palpitations, severe fatigue, sense of unease • Treatment — nitroglycerine Prinzmetal angina • Variante angina • Unpredictable and often occurs at rest or during the REM sleep cycle • Usually a benign ocndiditon but can occasionally cause serious dysrhythmias Silent ischemia • May not cause detectable symptoms such as angina • Indiividuals complain of fatigue, dyspnea or a felling of unease CAD:Myocardial Ischemia Evaluation • Many individuals with reversible myocardial ischemia will have normal physical examination • Rapid pulse rate of extra heart sounds (gallops or murmurs), pulmonary congestion (crackles) —-indicate left ventricle dysfunction • Peripheral or carotid artery bruits • Xanthelasmas (small fat deposits) —— suggests dyslipidemia and possible atherosclerosis TX: Medication for life • Manipulate the O2 demand —Manipulation of blood pressure, HR, contactility, and left ventricle volume Drugs: increase coronary flow and decrease myocardial demand ——-Nitrates, beta blockers, Ca channel blockers Progression of atherosclerosis may tak years and year but when we have a sudden coronary obstruction from thrombus.. Acute coronary syndrom: • Unstable angina ——result of reversible myocardial ischemia and means impending myocardial infraction • STEMI (ST segment elevation MI) —complete blockage of a coronary artery • NSTEMI (NON-stemi) — partial blockage of a coronary artery Sudden cardiac death can occur as a result of any of the acute coronary syndromes Heart Wall Myocardial Infraction Sudden and extended obstruction of the mycardial blood supply • • • • • • • • Vessle blockage -> decreased O2 supply Anoxia - total lack of 02 Decreased aerobic metabolism Decrease in pH Decreased ATP prodution Failure of Na+/K+ pump Cellular swelling & vaculation Necrosis of cardiac tissue (infraction) Cellular Injury • 8-10 seconds of decreased blood flow the affected myocardium becomes cyanotic and cooler • Myocardial oxygen reserves are depleted (8 sec) Cellular death • 20 min before irreversible hypoxic injury causes cellular death (apoptosis) and tissue necrosis Hormonal effects • Catecholamines • RAAS DAMPs and inflammation • Cytokines Heart Failure and Shock Sudden Cardiac Death • Ischemia • Left ventricular Dysfunction • Electrical Instability Structural and Functional Changes Myocardial Stunning Hours to days - loss of contractility post reperfusion Hibernating myocardium Tissue that is persistently ischemic and undergoes metabolic adaptation to prolong survival unit perfusion can be restored Myocardial remodeling Myocyte hypertrophy and loss of contractile function Severity of impairment depends on size of lesion and site of infarction Repair • Mycocardial infarction causes severe inflammatory response that ends with would repair • After 6 weeks the necrotic area is completely replaced by scar tissue • Strong but cannot contract and relax like healthy myocardial tissue Subendocardial infarction • Thrombus disintegrates, but some damage to the vessel • Small MI Transmural infaction • Damage across the entire muscle • Marked by ST elevation on ECG-STEMI Myocardial Infarction Manifestations: • Sudden severe chest pain; may radiate • Nausea, vomiting • Diaphoresis • Dyspnea Complications: • Sudden cardiac arrest due to ischemia, left ventricular dysfunction, and electrical instability Treatment: Evaluation: • 02 History • Nitroglycerin Physical exam • Aspirin • Increased BP • Morphine • Extra heart sounds • Thrombolytic therapy or heparin infusin • Pulmonary • Inotropes - affects contraction • Congestion • Percutaneous coronary interventions • Diaphoretic but feels cold (angioplasty, stent implantation) • Clammy • BEd rest for 24hr then slow rehabilitation ECG-narrows down affected area • Stool softeners- prevent straining Serial cardiac biomarker alterations —- Can percipitate bradycardia followed by • Troponin I and T - most specific indicator of MI increased venous return to the heart - cardiac overload — Hyperglycemia is treated with insulin Heart Failure General term used to describe several types of cardiac dysfunction that result in inadequate perfusion of tissues with blood-borne nutrients • Common reason for hosp admission for ppl 65 +, w/ congestive HF affecting nearly 10% of this pop. Key risk factors: • Ischemic heart disease • HTN • Obesity • Diabetes • renal failure • Valvular heart disease • Cardiomyopathies • Myocarditis • Congenital heart disease • Excessive alcohol intake • • • Genetic polymorphisms linked to increased HF risk Dysfunction can occur in either ventricle, but left ventricular dysfunction is more common In some cases, inadequate perfusion despite normal or elevated cardiac output. Left Heart Failure (congestive Heart Failure) Systolic Heart Failure • inability of the heart to generate adequate cardiac output to perfuse tissues • Ventricular remodeling • Causes included myocardial infarction, myocarditits, cardiomypoathy Diastolic heart failure • Pulmonary congestion despite normal stroke volume and cardiac output • Causes include myocardial hypertrophy and ischemia, diabetes, valvular and pericardial disease Manifestations of Left heart failure • Result of pulmonary vascular congestion and inadequate perfusion of the systemic circulaion S&S: • Dyspnea • Orthopnea • Cough of frothy sputum • Fatigue • Decreased urine output • Edema Physical findings: • pulmonary edema • Cyanosis • Inspiratory cackles • Pleural effusions • Hypotension/hypertension • S3 gallop • Evidence of underlying CAD or HTN Right Heart Failure • Most commonly caused by a diffuse hypoxic pulmonary disease • Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation High output failure • inability of the heart to supply the body w/ blood-borne nutrients, despite adequate blood volume and normal or elevated myocardial contractility • Causes include anemia, hyperthyroidism, septicemia Dysrhythmias (Arrhythmias) • Disturbance of the heart rhythm • Range from occasional ‘missed’ or rapid beats to severe disturbances that affect the pumping ability of the heart • Can be caused by an abnormal rate of impulse generation or abnormal impulse conduction Ex. • Tachycardia, flutter, fibrillation, bradycardia, premature ventricular contractions (PVCs), premature atrial contractions (PACs), asystole Shock • Cardiovascular system fails to perfuse the tissues adequately • Leads to impaired cellular metabolism — Impaire oxygen use — Impaired glucose use • Manifestations vary based on stage but often include hypotension, tachycardia, increased respiratory rate Types of Shock Cardiogenic • Decreased cardiac output and evidence of tissue hypoxia Hypovolemic • Loss of whole blood — hemorrhage, plasma (burns), severe dehydration Neurogenic • Widespread massive vasodilation Anaphylactic • Widespread hypersensitivity reaction Septic • Infection, bacteremia, systemic inflammatory response syndrome (sepsis) Multiple Organ Dysfunction Syndrome Progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury Causes: • Most common: sepsis, septic shock • Other: any severe injury (trauma, burns, major surgery) Manifestations: • Respiratory • Hepatic • Renal • Gi • Myocardial failure Disorders of the heart wall Disorders of the pericardium Acute pericarditis • Idiopathic, viral, MI, trauma, neoplasm, surgery, uremia, bacterial infection Pericardial effusion • Accumulation of fluid in pericardial cavity • Tamponade-pressure from fluid doesnt allow proper filling of atria • • • • • Inflammatory exudate (most common) Serous (water): hypervolemia Sanguineous (blood): trauma Serosanguineous (water +blood): TB, radiation, uremia Chyle (lymphatic fluid): trauma to thoracic duct Constrictive pericarditis Fibrotic pericardium encases the heart in a rigid shell • Mostly idiopathic, sometimes associated with:TB, radiation, rheumatoid arthritis Diisorders of the Myocardium Cardiomyopathies: • Dilated cardiomyopathy (congestive cardiomyopathy) • Hypertophic cardiomyopathy —Asymmetrical septal hypertrophy —Hypertensive (valvular hypertrophic) cardiomyopathy —Restrictive cardiomyopathy Disorders of the Endocardium Valvular dysfunction: Valvular stenosis • Aortic stenosis • Mitral stenosis Valvular regurgitation • Aortic regurgitation • Mitral regurgitation • Tricuspid regurgitation Mitral valve prolapse syndrome (MVPS) Valvular Dysfunction C-Hemodynamic effect of mitral stenosis • The stenosis valve is unable to open sufficiently during left arterial systole, inhibiting left ventricular filling D-Hemodynamic effects of mitral regurgitation • The mitral valve does not close completely during left ventricular systole, permitting blood to re-enter the left atrium Acute rheumatic fever & rheumatic heart disease Rheumatic Fever • Systemic, inflammatory disease caused by a delayed immune response to pharyngeal infection by the group A betahemolytic streptococci • Febrile illness —inflammation of the joints, skin, nervous system, and heart If left untreated, rheumatic fever causes rheumatic heart disease Manifestations: • Feve Lymphadenopathy • Arthralgia • Nausea/vomiting • Tachycardia • Abdodminal pain • Epistaxis —bleeding from the nose Major clinical manifestations: Carditis • cardiac inflammation and scarring Polyarthritis • involves 5 or more joints simultaneously Chorea • abnormal involuntary movement disorder Erythema marginatum • Pink, erythematous macules on trunks Infective endocarditis Inflammation of the endocardium Agents: • Bacteria • Viruses • Fungi • Rickettsiae • Parasites Pathogenesis: • Damaged (prepared) endocardium • Blood-borne microorganism adherence • Proliferation of the microorganism (vegetations) Manifestations: Classic findings • fever • New/changed cardiac murmur • Petechal lesions of the skiin, cojunctiva, and oral mucosa Characteristic physical findings: • Osler nodes (painful erythematous nodules on the pads of the fingers and toes) • Janeway lesions (nonpainful hemorrhagic lesions on the palms and soles) Other: weight loss, back pain, night sweats, and heart failre