1.NURS 216 Spring 2013 Dr. Smith

2. Reading You must read Chapter 17 for review of the structureand normal function of the cv system. Slides 5-20 inthis lecture should be review from A&P and we willonly briefly discuss them. We will discuss most parts of Chapter 18 except forHTN in special populations. We will discuss most parts of Chapter 19 except forheart disease in infants and children. 3. Objectives Review important concepts of cardiovascular anatomy:layers of the heart, valves, electrical conducting system Review important concepts of cardiovascularphysiology: mechanical function, hemodynamics,regulation of cardiac output and blood flow Review components of the systemic circulation andblood vessels 4. Discuss disorders of arterial function: artherosclerosis,peripheral arterial disorders, aneurysms anddissections Discuss control of blood pressure and hypertension Discuss disorders of venous function: varicose veinsand venous thrombosis Discuss coronary heart disease: chronic and acute Discuss pericardial, myocardial, endocardial, andvalvular disorders 5. Mechanical Functions The hearts job is to pump blood throughout thecirculatory system Cardiac muscle is similar to skeletal, with addition ofintercalated disks Atria and ventricles must be coordinated and healthyto achieve ideal blood flow and circulation 6. Pulmonary circulation: smaller volume,low pressureSystemic circulation:larger volume, high pressure 7. Arterial vs. Venous System Difference in type and thickness of layers Vascular smooth muscle Arterial system: high-pressure resistance vessels,blood moves through b/c of pressure pulsations fromLV Venous system: low-pressure capacitance vessels,blood moves through by muscle pumps-valves-effects of gravity 8. Volume and Pressure One influences the other In the systemic circulation:-pressure is highest in the arteries, lowest in the veins-volume is lowest in the arteries, highest in the veins Veins are extremely compliant and distensible, so theyare able to expand and store large volumes of blood The whole circulatory system is closed, but blood canshift between systemic and pulmonary systems andbetween central and peripheral circulation 9. Pressure, Resistance, and Flow Blood flow (cardiac output) = pressure/resistance-higher pressure gradient means more blood flow-higher resistance means less blood flow Resistance is affected by radius of the vessel and bloodviscosity Ideally, blood flow is laminar, not turbulent Laplace law: P = T/rmay restate: T = P*rVesselradius Intraluminal Wall pressure tension 10. Layers of the Heart 11. Coronary Arteries 12. Conduction System 13. Electrocardiogram (EKG or ECG) 14. Cardiac Cycle During systole, AV valves are closed, semilunar valves open,and ventricles eject their blood into the pulmonary arteriesand aorta During diastole, semilunar valves are closed, AV valvesopen, and atria drop blood down into ventricles At end of diastole, there is an atrial kick End Diastolic Volume (EDV) = volume in ventricles at endof diastole End Systolic Volume (ESV) = volume at end of systole Stroke Volume (SV) = EDV-ESV usually ~ 70 mL Ejection fraction (EF) = SV/EDV usually ~ 60-70% 15. Cardiac Output Determinants Cardiac output (CO) = SV x HR, measured in L/min-varies greatly with metabolic demands, activity-anywhere from 4 to 8 L/min Preload = EDV, volume work or prestretch-to a limit, higher preloads cause a strongercontraction (due to arrangement of muscle fibers) Afterload = pressure that LV must overcome to pumpblood into aorta pressure work (blood pressure) Contractility = increased strength of contractionindependent of preload 16. Control of Cardiovascular Function CV system is innervated by the autonomic nervoussystem (ANS) Effects of sympathetic and parasympathetic systems Vagus nerve SNS is the main controller of blood vessels Autoregulation in the tissue beds-histamine, serotonin, kinins, prostaglandins Endothelial control-nitrous oxide (NO), angiotensin II 17. Arterial Disorders Hyperlipidemia and atherosclerosis (central) Peripheral arterial problems Aneurysms and dissections (usually central) 18. Atherosclerosis The development of fibrous, fatty lesions in the intimaof large and medium-sized arteries (aorta, coronaryarteries, cerebral arteries) MOST COMMON CAUSE OF CORONARY HEARTDISEASE!!! Vessels become narrowed, blood flow decreases, leadsto ischemia (chronic) A portion of the lesion or plaque can break off andcompletely block blood flow (acute) 19. Atherosclerosis Why? Response-to-injury hypothesis The intima is damaged (HTN + high LDL = danger) Injury to the endothelium changes the permeability andcauses an inflammatory response Monocytes and platelets are attracted to the injury Monocytes and oxidized LDL molecules burrow underintima Lesion under intima grows, core may become necrotic, mayharden due to calcium deposits Thrombosis, hemorrhage, or rupture of fibrous cap mayoccur 20. Hyperlipidemia Types of lipoproteins arecategorized by theamount of fat (density) bad and good Levels affected by diet,activity level, and liverfunction 21. Hypercholesterolemia Specifically, too-high levels of LDL or Total Cholesterol Primary (familial) or secondary Measure with a fasting lipid profile/panel Treat with diet, exercise, then medications More aggressive depending on other CHD risk factors Goal levels: -LDL 60 22. Xanthomas 23. Atherosclerosis Always monitor risk factors, work with patient toimprove/reduce them If patient develops s/sx:-exercise/stress test-cardiac catheterization May need angioplasty, stents, or coronary arterybypass grafting (CABG) 24. CHD Risk Factors Biologic: male gender, increasing age, family history Modifiable: hyperlipidemia, hypertension, smoking,diabetes mellitus, obesity, sedentary lifestyle Negative risk factor: high HDL-C 25. Peripheral Arterial Disease Can also have atherosclerosis in peripheral arteries,often superficial femoral and popliteal Same risk factors as CHD Blood flow to the extremity is reduced Intermittent claudication Diagnose by signs of hypoxia in limb, palpation ofpulses, ultrasound Address risk factors, avoid injury, medications May need a stent 26. Aneursyms and Dissections Atrophy or weakness of the medial layer causes adilation of the artery Can occur in any artery of the body, commonlyabdominal aorta Degeneration caused by atherosclerosis, connectivetissue disorders, increased blood pressure around astenotic area Example types: berry, fusiform, saccular, dissection 27. Aneursyms and Dissections Increasing radius at the weakened spot increasestension inside artery (LaPlace Law) Danger of eventual rupture Abdominal aortic aneurysm:-usually over age 50, increase with age-often asymptomatic, possible pulsating mass Aortic dissection:-most common site is the ascending aorta-rupture, hemorrhage into vessel wall-abrupt, intense pain, BP quickly falls usu FATAL 28. Blood Pressure definitions BP is measured in anartery, usually thebrachial Measured in mmHg BP is the pressure insidean artery caused by themovement of bloodthrough it BP = CO * PVR 29. Short-Term Regulation of BP Neural-baroreceptors: pressure sensors, in carotids and aorticarch-chemoreceptors: chemical sensors, in carotids andaortic arch Humoral-RAA System (renin is released by the kidneys)-vasopressin/ADH: released in response to decreasedBP or increased osmolality of blood 30. RAA System Renin release stimulated by:-increased SNS activity-decreased BP, ECF volume, or ECF Na concentration Renin changes to angiotensin I in the blood, then intoangiotensin II in the lungs Angiotensin II effects:-vasoconstriction of arterioles (short-term control)-stimulates aldosterone release, causing Na and waterretention (longer-term control) 31. Long-Term Regulation of BP Mainly by the kidneys via their control of ECF volume ECF excess causes higher rates of Na and H2Oexcretion ECF deficit causes lower rates of Na and H2O excretion Many blood pressure medications work throughchanging kidney function 32. Essential Hypertension Aka primary HTN, accounts for 90-95% of HTN Normal BP = 90 Biological risk factors: Lifestyle risk factors: Criteria for HTN diagnosis: at least 2 separate readings Treatments: lifestyle modifications, medications 33. Manifestations of Hypertension the silent killer Target Organ Damage Major risk factor for Heart: LVH (LVatherosclerosis hypertrophy), angina, Increases workload of MI, prior stents/CABG,the LVheart failure TIA or strokes in brain Chronic kidney disease Peripheral vasculardisease retinopathy 34. Secondary Hypertension d/t another condition, correcting that condition oftenimproves BP Kidney disease Excess aldosterone or glucocorticoids Pheochromocytoma tumor usually in the adrenalmedulla Coarctation of the aorta Malignant HTN 35. 3D reconstruction of CT angiography of aninfant with coarctation of the aortahttp://www.biij.org/2006/2/e11/ 36. Orthostatic Hypotension AKA posturalhypotension SNS reflexes dont workproperly BP quickly drops,decreasing CBF ->dizziness & syncope With position change,see BP drop and HRincrease 37. Orthostatic Hypotension Causes Reduced blood volume Medications Aging Immobility, extended bed rest Autonomic nervous system dysfunction Treatment depends on identifying a cause 38. Coronary Arteries 39. Venous Disorders Varicose Veins Legs contain superficial and deep veins Varicose veins dilated, enlarged superficial veins Occur due to impaired or blocked flow in deep veins, increased pressure is superficial veins More common after age 50, in obese persons & women Long-term increased venous pressures eventually weaken valves, worsening the vein distension Support stockings, surgical repair 40. Varicose Veins 41. Chronic Venous Insufficiency Commonly caused by reflux/backflow throughdamaged veins Worsened by prolonged standing s/sx: varicose veins, tissue congestion, edema, eventualimpaired nutrient delivery to tissues (necrosis,dermatitis, stasis ulcers, thin/shiny skin) Most common in lower legs 42. Venous Disorders - DVTs Deep Vein Thrombosis (DVT) Risk factors: blood stasis, vessel wall injury, increasedcoagulability (Virchows triad)-what clinical conditions could lead to these riskfactors? May be asymptomatic when small, but gradually tendto increase in size S/sx: pain, swelling, tenderness (usually unilateral,often in calf) Complications? 43. Pericardial Disorders Pericardial effusion -accumulation of fluid in the pericardial cavity -can compress heart, lower SV -diagnose with ultrasound/echo -pericardiocentesis -cardiac tamponade 44. Cardiac Tamponade 45. Pericarditis Acute can be after infections or trauma-increased capillary permeability allows exudate intopericardial cavity-S/sx: chest pain, pericardial friction rub, EKG changes Chronic exudate may remain for months, years-often due to systemic diseases-symptoms usually minimal-still needs to be monitored 46. Coronary Heart Disease Heart disease due to impaired coronary blood flow,usually d/t atherosclerosis-stable plaque (usually leads to ischemia/angina)-unstable plaque (often leads to MI) CHD (MIs, heart failure, etc) is the leading cause ofdeath in the United States for men and women Projected costs of CHD in 2010: 316.4 billion (directand indirect) (CDC data) 47. Coronary Arteries 48. An Oxygen Problem The balance between myocardial oxygen supply anddemand must be maintained! Demand influenced by: HR, contractility, musclemass, ventricular wall tension (afterload) Supply influenced by: coronary blood flow, O2carrying capacity, vascular resistance Remember that blood flow (perfusion) is necessary foroxygen delivery Effect of reduced oxygen: ischemia Effect of absent/acute lack of oxygen: infarction 49. Myocardial Ischemia Ischemia occurs when O2 demand is greaterthan supply O2 shortage forces myocardium to useanaerobic metabolism -> pain (angina pectoris) Mild increases in HR and BP usually occurbefore chest pain the SNS is compensating Possible EKG changes All changes are reversible if O2 supply isrestored 50. Angina Pectoris Stable predictable onset, pain is constricting,pressure-like, subsides with rest or medication Silent ischemia without angina Variant or vasospastic due to spasmodic narrowing ofthe coronary arteries, unpredictable, often at night,often associated with cocaine use 51. Acute Coronary Syndromes AKA myocardial infarction, heart attack Sudden blockage of one or more coronary arteriesstops blood flow to a part of the myocardium The myocardium quickly begins to die:infarction/necrosis MIs are most common in the LV Locations: Anterior, inferior, lateral, septal LOCATION AND SIZE OF INFARCT DEPEND ONLOCATION OF CORONARY ARTERY BLOCKAGE 52. Signs and Symptoms of an MI Angina pectoris, chest pressure, possiblyradiating down left arm Diaphoresis Nausea Women often experience non-traditionalsymptoms! 53. Diagnosis of an MI Blood markers: cardiac enzymes (troponin) EKG changes (ST elevation STEMI) Cardiac catheterization Treatment: -medications -reperfusion (usually angioplasty and/or stent) 54. Myocardial Infarction Left main coronary arteryLeft anteriordescendingcoronaryartery (LAD) 55. Zones of necrosis and ischemia 56. Effects of an MI Reduced contractility & compliance Abnormal wall motion Reduced SV & EF dysrhythmias These changes combine to depress overall ventricularfunction Severity depends on:-function of the uninvolved myocardium-collateral circulation-general compensation of the cardiovascular system 57. Compensatory Mechanisms SNS will react to < CO and cause vasoconstriction ofsystemic arteries and veins SNS also causes > HR and > contractility (HR and BPusually maintained) Kidneys retain Na and water The increased preload increases ventricularcontractility to a point (Frank Starling) The bodys compensations for decreased ventricularfunction are limited The ventricles (LV) gradually dilate and hypertrophydue to increased volume and workload 58. Worst-Case Scenario Outcomes Cardiogenic shock when MI affects > 40% of LV, thesevere drop in systemic and cardiac circulation causesdeath Papillary muscle rupture usually affects mitral valve Cardiac rupture the necrotic area of the ventriclewall ruptures, leads to massive bleeding intopericardium MIs often result in heart failure 59. Myocardial Disorders All the other causes of myocardial dysfunction besidesCHD Myocarditis: inflammation of myocardium, usually d/tinfection-wide variation of s/sx-diagnose by EKG changes, cardiac enzymes, biopsy Cardiomyopathies-primary and secondary-dilated, hypertrophic, restrictive 60. Hypertrophic Cardiomyopathies(HCM) Ventricular wall enlargement enlarged heart, wallsbecome stiff and less compliant -> heart failure Common in young adults, cause of sudden cardiacdeath A primary type of cardiomyopathy, genetic Variation in S/sx and prognosis-dyspnea, chest pain, fatigue worse with exertion-arrhythmias Medication and surgical treatments 61. Dilated Cardiomyopathies(DCM) Pathogenesis: a gradual enlargement (dilation) of theventricle chambers (left ventricle) -> heart failure EF drops to 40% or lower A primary type of cardiomyopathy, caused by:-infectious myocarditis-alcohol/drug abuse-NMS diseases-genetic, idiopathic S/sx: dyspnea on exertion (DOE), othopnea, weakness,edema, dysrhythmias Treatment focuses on preventing further damage,maintaining heart function, possible transplant 62. Infective Endocarditis Rare but life-threatening Often d/t bacteria that invade the endocardium andvalves -> common cause of valve disorders Staphylococci, streptococci, enterococci Requires an already-damaged endocardium and anorganism gaining entry into the circulatory system Vegetations often develop on heart valves Pt may have systemic infection s/sx, heart murmur Risk factors: heart disease, IV drug use Diagnose with blood cultures, echo 63. Acute Rheumatic Fever Multisystem inflammatory disease that may occurafter group A -hemolytic streptococcal pharyngitis Theory is that the infection causes a systemicautoimmune response Rheumatic Heart Disease (RHD) is the cardiacmanifestation of RF, may involve all three layers of theheart Autoantibodies react with host tissue cause damageto the valves, both stenosis and regurgitation Progression is gradual 64. Valvular Heart Disease A problem with any of the four heart valves createsabnormal blood flow and increases cardiac work Normal valves allow unidirectional and unimpededblood flow Regurgitation: valve doesnt close properly and allowsbackflow creates volume work Stenosis: valve opening is restricted, preventingforward flow creates pressure work Both problems can occur together in the same valve Regurg or stensosis cause murmurs 65. Pathogenesis of Valve Disease Destruction by infective endocarditis (ex: rheumaticfever) Connective tissue defects Rupture of papillary muscles Damage from an MI Congenital malformations (mitral valve prolapse) Mitral and aortic valves most commonly affected Manifestation variables: valve involved, severity ofdamage, rapidity of onset, any compensatorymechanisms 66. Mitral Valve Stenosis Resistance to blood flow from LA->LV, LA mustwork harder Pressure from LA backs up into pulmonarycirculation, pulmonary pressures rise Increased pressure may travel through pulmonarysystem to the RV -> RV hypertrophy -> R heartfailure Sx appear at ~50% stenosis Increasing exertional dyspnea, tachycardia, atrialdysrhythmias 67. Mitral Regurgitation During systole, some blood flows backward into LAinstead of all moving forward through aortic valve Causes: RHD, mitral valve prolapse LA dilates to accommodate backflow, eventually failsand pressures in pulmonary circuit rise -> L heartfailure LV will become dilated and hypertrophied Acute mitral regurg usually fatal 68. Aortic Stenosis Narrowed aortic valve obstructs blood flow into aortafrom LV during systole Pressure work -> LV hypertrophy Compensation works for a while Sx begin at ~50% narrowing Angina, syncope, LV failure Loud systolic murmur Onset of sx: 5 year survival Usually fatal before causing right heart failure