#12, 13, 14 cardiovascular-1


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#12, 13, 14 cardiovascular-1

  1. 1. NURS 216 Spring 2013 Dr. Smith
  2. 2. Reading You must read Chapter 17 for review of the structure and normal function of the cv system. Slides 5-20 in this lecture should be review from A&P and we will only briefly discuss them. We will discuss most parts of Chapter 18 except for HTN in special populations. We will discuss most parts of Chapter 19 except for heart disease in infants and children.
  3. 3. Objectives Review important concepts of cardiovascular anatomy: layers of the heart, valves, electrical conducting system Review important concepts of cardiovascular physiology: mechanical function, hemodynamics, regulation of cardiac output and blood flow Review components of the systemic circulation and blood vessels
  4. 4.  Discuss disorders of arterial function: artherosclerosis, peripheral arterial disorders, aneurysms and dissections Discuss control of blood pressure and hypertension Discuss disorders of venous function: varicose veins and venous thrombosis Discuss coronary heart disease: chronic and acute Discuss pericardial, myocardial, endocardial, and valvular disorders
  5. 5. Mechanical Functions The heart’s job is to pump blood throughout the circulatory system Cardiac muscle is similar to skeletal, with addition of intercalated disks Atria and ventricles must be coordinated and healthy to achieve ideal blood flow and circulation
  6. 6. Pulmonary circulation: smaller volume, low pressureSystemic circulation: larger volume, high pressure
  7. 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 from LV Venous system: low-pressure “capacitance” vessels, blood moves through by muscle pumps -valves -effects of gravity
  8. 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 they are able to expand and store large volumes of blood The whole circulatory system is closed, but blood can shift between systemic and pulmonary systems and between central and peripheral circulation
  9. 9. Pressure, Resistance, and Flow Blood flow (cardiac output) = Δ pressure/resistance -higher pressure gradient means more blood flow -higher resistance means less blood flow Resistance is affected by radius of the vessel and blood viscosity Ideally, blood flow is laminar, not turbulent Laplace law: P = T/r may restate: T = P*r Vessel radius Intraluminal Wall pressure tension
  10. 10. Layers of the Heart
  11. 11. Coronary Arteries
  12. 12. Conduction System
  13. 13. Electrocardiogram (EKG or ECG)
  14. 14. Cardiac Cycle During systole, AV valves are closed, semilunar valves open, and ventricles eject their blood into the pulmonary arteries and aorta During diastole, semilunar valves are closed, AV valves open, and atria drop blood down into ventricles At end of diastole, there is an “atrial kick” End Diastolic Volume (EDV) = volume in ventricles at end of 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. 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 stronger contraction (due to arrangement of muscle fibers) Afterload = pressure that LV must overcome to pump blood into aorta “pressure work” (blood pressure) Contractility = increased strength of contraction independent of preload
  16. 16. Control of Cardiovascular Function CV system is innervated by the autonomic nervous system (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. 17. Arterial Disorders Hyperlipidemia and atherosclerosis (central) Peripheral arterial problems Aneurysms and dissections (usually central)
  18. 18. Atherosclerosis The development of fibrous, fatty lesions in the intima of large and medium-sized arteries (aorta, coronary arteries, cerebral arteries) MOST COMMON CAUSE OF CORONARY HEART DISEASE!!! Vessels become narrowed, blood flow decreases, leads to ischemia (chronic) A portion of the lesion or plaque can break off and completely block blood flow (acute)
  19. 19. Atherosclerosis Why? Response-to-injury hypothesis The intima is damaged (HTN + high LDL = danger) Injury to the endothelium changes the permeability and causes an inflammatory response Monocytes and platelets are attracted to the injury Monocytes and oxidized LDL molecules burrow under intima Lesion under intima grows, core may become necrotic, may harden due to calcium deposits Thrombosis, hemorrhage, or rupture of fibrous cap may occur
  20. 20. Hyperlipidemia Types of lipoproteins are categorized by the amount of fat (density) “bad” and “good” Levels affected by diet, activity level, and liver function
  21. 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 <100 mg/dL -TC < 200 -HDL > 60
  22. 22. Xanthomas
  23. 23. Atherosclerosis Always monitor risk factors, work with patient to improve/reduce them If patient develops s/sx: -exercise/stress test -cardiac catheterization May need angioplasty, stents, or coronary artery bypass grafting (CABG)
  24. 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. 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 of pulses, ultrasound Address risk factors, avoid injury, medications May need a stent
  26. 26. Aneursyms and Dissections Atrophy or weakness of the medial layer causes a dilation of the artery Can occur in any artery of the body, commonly abdominal aorta Degeneration caused by atherosclerosis, connective tissue disorders, increased blood pressure around a stenotic area Example types: berry, fusiform, saccular, dissection
  27. 27. Aneursyms and Dissections Increasing radius at the weakened spot increases tension 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. 28. Blood Pressure definitions BP is measured in an artery, usually the brachial Measured in mmHg BP is the pressure inside an artery caused by the movement of blood through it BP = CO * PVR
  29. 29. Short-Term Regulation of BP Neural -baroreceptors: pressure sensors, in carotids and aortic arch -chemoreceptors: chemical sensors, in carotids and aortic arch Humoral -RAA System (renin is released by the kidneys) -vasopressin/ADH: released in response to decreased BP or increased osmolality of blood
  30. 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 into angiotensin II in the lungs Angiotensin II effects: -vasoconstriction of arterioles (short-term control) -stimulates aldosterone release, causing Na and water retention (longer-term control)
  31. 31. Long-Term Regulation of BP Mainly by the kidneys via their control of ECF volume ECF excess causes higher rates of Na and H2O excretion ECF deficit causes lower rates of Na and H2O excretion Many blood pressure medications work through changing kidney function
  32. 32. Essential Hypertension Aka “primary” HTN, accounts for 90-95% of HTN Normal BP = <120 and <80 HTN = >140 or >90 Biological risk factors: Lifestyle risk factors: Criteria for HTN diagnosis: at least 2 separate readings Treatments: lifestyle modifications, medications
  33. 33. Manifestations of Hypertension “the silent killer” Target Organ Damage Major risk factor for  Heart: LVH (LV atherosclerosis hypertrophy), angina, Increases workload of MI, prior stents/CABG, the LV heart failure  TIA or strokes in brain  Chronic kidney disease  Peripheral vascular disease  retinopathy
  34. 34. Secondary Hypertension d/t another condition, correcting that condition often improves BP Kidney disease Excess aldosterone or glucocorticoids Pheochromocytoma – tumor usually in the adrenal medulla Coarctation of the aorta Malignant HTN
  35. 35. 3D reconstruction of CT angiography of an infant with coarctation of the aorta http://www.biij.org/2006/2/e11/
  36. 36. Orthostatic Hypotension AKA postural hypotension SNS reflexes don’t work properly BP quickly drops, decreasing CBF -> dizziness & syncope With position change, see BP drop and HR increase
  37. 37. Orthostatic Hypotension Causes Reduced blood volume Medications Aging Immobility, extended bed rest Autonomic nervous system dysfunction Treatment depends on identifying a cause
  38. 38. Coronary Arteries
  39. 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. 40. Varicose Veins
  41. 41. Chronic Venous Insufficiency Commonly caused by reflux/backflow through damaged veins Worsened by prolonged standing s/sx: varicose veins, tissue congestion, edema, eventual impaired nutrient delivery to tissues (necrosis, dermatitis, stasis ulcers, thin/shiny skin) Most common in lower legs
  42. 42. Venous Disorders - DVTs Deep Vein Thrombosis (DVT) Risk factors: blood stasis, vessel wall injury, increased coagulability (Virchow’s triad) -what clinical conditions could lead to these risk factors? May be asymptomatic when small, but gradually tend to increase in size S/sx: pain, swelling, tenderness (usually unilateral, often in calf) Complications?
  43. 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. 44. Cardiac Tamponade
  45. 45. Pericarditis Acute – can be after infections or trauma -increased capillary permeability allows exudate into pericardial 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. 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 of death in the United States for men and women Projected costs of CHD in 2010: 316.4 billion (direct and indirect) (CDC data)
  47. 47. Coronary Arteries
  48. 48. An Oxygen Problem The balance between myocardial oxygen supply and demand must be maintained! Demand influenced by: HR, contractility, muscle mass, ventricular wall tension (afterload) Supply influenced by: coronary blood flow, O2 carrying capacity, vascular resistance Remember that blood flow (perfusion) is necessary for oxygen delivery Effect of reduced oxygen: ischemia Effect of absent/acute lack of oxygen: infarction
  49. 49. Myocardial Ischemia Ischemia occurs when O2 demand is greater than supply O2 shortage forces myocardium to use anaerobic metabolism -> pain (angina pectoris) Mild increases in HR and BP usually occur before chest pain – the SNS is compensating Possible EKG changes All changes are reversible if O2 supply is restored
  50. 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 of the coronary arteries, unpredictable, often at night, often associated with cocaine use
  51. 51. Acute Coronary Syndromes AKA myocardial infarction, “heart attack” Sudden blockage of one or more coronary arteries stops 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 ON LOCATION OF CORONARY ARTERY BLOCKAGE
  52. 52. Signs and Symptoms of an MI Angina pectoris, chest pressure, possibly radiating down left arm Diaphoresis Nausea Women often experience non-traditional symptoms!
  53. 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. 54. Myocardial Infarction Left main coronary artery Left anterior descending coronary artery (LAD)
  55. 55. Zones of necrosis and ischemia
  56. 56. Effects of an MI Reduced contractility & compliance Abnormal wall motion Reduced SV & EF dysrhythmias These changes combine to depress overall ventricular function Severity depends on: -function of the uninvolved myocardium -collateral circulation -general compensation of the cardiovascular system
  57. 57. Compensatory Mechanisms SNS will react to < CO and cause vasoconstriction of systemic arteries and veins SNS also causes > HR and > contractility (HR and BP usually maintained) Kidneys retain Na and water The increased preload increases ventricular contractility to a point (Frank Starling) The body’s compensations for decreased ventricular function are limited The ventricles (LV) gradually dilate and hypertrophy due to increased volume and workload
  58. 58. Worst-Case Scenario Outcomes Cardiogenic shock – when MI affects > 40% of LV, the severe drop in systemic and cardiac circulation causes death Papillary muscle rupture – usually affects mitral valve Cardiac rupture – the necrotic area of the ventricle wall ruptures, leads to massive bleeding into pericardium MIs often result in heart failure
  59. 59. Myocardial Disorders All the other causes of myocardial dysfunction besides CHD Myocarditis: inflammation of myocardium, usually d/t infection -wide variation of s/sx -diagnose by EKG changes, cardiac enzymes, biopsy Cardiomyopathies -primary and secondary -dilated, hypertrophic, restrictive
  60. 60. Hypertrophic Cardiomyopathies(HCM) Ventricular wall enlargement “enlarged heart”, walls become stiff and less compliant -> heart failure Common in young adults, cause of sudden cardiac death 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. 61. Dilated Cardiomyopathies(DCM) Pathogenesis: a gradual enlargement (dilation) of the ventricle 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. 62. Infective Endocarditis Rare but life-threatening Often d/t bacteria that invade the endocardium and valves -> common cause of valve disorders Staphylococci, streptococci, enterococci Requires an already-damaged endocardium and an organism 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. 63. Acute Rheumatic Fever Multisystem inflammatory disease that may occur after group A β-hemolytic streptococcal pharyngitis Theory is that the infection causes a systemic autoimmune response Rheumatic Heart Disease (RHD) is the cardiac manifestation of RF, may involve all three layers of the heart Autoantibodies react with host tissue – cause damage to the valves, both stenosis and regurgitation Progression is gradual
  64. 64. Valvular Heart Disease A problem with any of the four heart valves creates abnormal blood flow and increases cardiac work Normal valves allow unidirectional and unimpeded blood flow Regurgitation: valve doesn’t close properly and allows backflow – creates volume work Stenosis: valve opening is restricted, preventing forward flow – creates pressure work Both problems can occur together in the same valve Regurg or stensosis cause murmurs
  65. 65. Pathogenesis of Valve Disease Destruction by infective endocarditis (ex: rheumatic fever) 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 of damage, rapidity of onset, any compensatory mechanisms
  66. 66. Mitral Valve Stenosis Resistance to blood flow from LA->LV, LA must work harder Pressure from LA backs up into pulmonary circulation, pulmonary pressures rise Increased pressure may travel through pulmonary system to the RV -> RV hypertrophy -> R heart failure Sx appear at ~50% stenosis Increasing exertional dyspnea, tachycardia, atrial dysrhythmias
  67. 67. Mitral Regurgitation During systole, some blood flows backward into LA instead of all moving forward through aortic valve Causes: RHD, mitral valve prolapse LA dilates to accommodate backflow, eventually fails and pressures in pulmonary circuit rise -> L heart failure LV will become dilated and hypertrophied Acute mitral regurg usually fatal
  68. 68. Aortic Stenosis Narrowed aortic valve obstructs blood flow into aorta from 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