circulation & cardiovascular

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Author:
lacey0133
ID:
48168
Filename:
circulation & cardiovascular
Updated:
2010-11-21 22:33:49
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pathophysiology
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Description:
disorders of circulation & cardiovascular
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  1. blood path
    left side of heart-arteries-arterioles-capillaries-venules-veins-right side of the heart
  2. arteries
    • walls composed of elastin connective tissue, fibrous connective tissue, and smooth muscle
    • Elastic arteries located in aorta and major branches
    • muscular arteries located in medium/small arteries
  3. Capillaries
    • very thin walls, making exchange of substrates, metabolites, and other products possible
    • products pass through via junctions, fenestration, vesicles of active transport, diffusion
  4. Veins
    • More numerous than arteries
    • thin walled fibrous, less elastic tissue, larger diameter, few smooth muscle fibers, valves to reduce back flow
    • 60% of blood is in veins
    • contains muscle pumps, skeletal muscle contraction compresses deep vein muscles to aid in flow of blood to heart
  5. Factors affecting blood flow
    amount of blood moved per unit of time (mL/min)
  6. pressure
    pressure: force exerted on the liquid per unit area (mm Hg)
  7. resistance
    Resistance: the opposition of force (radius/length, viscosity (dehydrated vs hypotonic), arrangement (sequential vs parallel), cross sectional area)
  8. velocity
    velocity: distance blood travels in unit of time (cm/sec)
  9. turbulent v laminar flow
    smooth or bumby
  10. compliance
    Compliance: increase in vessel volume to accommodate for increase in pressure
  11. total peripheral resistance
    • total resistance in the systemic circulation
    • determined primarily by changes in arterioles
    • Reflex control: sympathetic (heart arterioles veins), parasympathetic (heart)
    • autoregulation: smooth muscle activity by vasodilators and vasoconstrictors
  12. Reflex control in arteries
    • smooth muscle layer innervated my sym nervous system
    • a1adrenergic receptors: cause vasoconstriction of vessel
    • b2 adrenergic receptors: induce smooth muscle relaxation
    • vasodilators mainly act locally
    • vasoconstrictors are systemic (raas)
  13. shunting
    • shock: shut down everthing but heart and brain
    • exercise after eating
    • fight or flight
  14. arteriosclerosis
    • chronic disease of arterial system
    • abnormal thickening and hardening of vessel walls
  15. atherosclerosis
    • soft deposits of intra-arterial fat and fibrin in vessels which harden over time
    • the most common form af arteriosclerosis
    • leading cause of coronary artery and cerebrovascular disease
  16. steps of atherosclerosis
    • injury to arterial wall
    • macrophages/immune cells bind to injury site
    • inflammation releases oxygen radicals that oxidize ldl (foam cells)
    • macrophages engulf foam cells which penetrates into intima
    • lesion is created (fatty streak)
    • collagen migrates over fatty streak, forming a fibrous plaque
  17. risk factors of atherosclerosis
    • Standard american diet, Mcdonalds
    • smoking
    • cholesterol
    • lack of exercise
    • glucose intolerance
    • htn
  18. partial obstruction
    • due to narrowing caused by plaque
    • wen severe enough to cause inadequate oxygenation-produces ischemia
  19. total obstruction
    • stroke (cva), heart attack (myocardial infarction)
    • may be due to thrombu, or embolus that follow flow of blood to eventually block an artery
  20. aneurysms
    • outpouching or dilation of a vessel wall or cardiac chamber due to weakened area (changes in collagen and elastin that make the vessel more vulnerable to pressures)
    • burst causes bleeding: often asymptomatic until rupture
    • examples: abdominal aorta 3/4, brain (berry aneurysms)
  21. aneurysm risks
    • atherosclerosis most common cause: formation erodes vessel wall
    • htn increases wall stress
    • collagen vascular disorders (marfans)
    • infections that affect arterial walls (syphilis)
  22. chambers functions
    • atria: collecting chambers that feed ventricles
    • left arium: collects blood from lungs
    • Right atrium: collects blood from body
    • Ventricles: pump
    • Left ventricle: directs blood to body
    • Right ventricle: directs blood to lungs
  23. valves
    • between atria and ventricles (tricuspid-right; mitral -left)
    • semilunar valves between ventricles and arteries (pulmonic- right; aortic - left0
  24. cardiac cycle
    • hearts contraction and relaxation that follows it
    • systole: ventricular contraction that ejects blood into aorta
    • diastole: muscle relaxation: filling of ventricles
  25. systole
    • LUB
    • ventricular contraction increasing pressure and forcing blood into aorta
    • ventricle=aorta pressure
    • semilunar valve opens
  26. Diastole
    • DUB
    • ventricle relaxes completely
    • Ventricles < aorta pressure
    • semilunar valve closes
  27. Cardiac Output
    • CO=SV*HR
    • normal adult: 5 L/min
    • Factors: Preload, afterload and myocardial contractibility
  28. myocardial contractility
    • inotopic state; force of contraction affected by
    • changes in stretching of ventricular muscle due to volume of blood
    • alterations in sympathetic activation of ventricles
    • adequate oxygen supply
  29. inotropy
    the force or energy of muscle contractions
  30. heart rate regulators
    • neural humoral (body fluids)
    • ANS: sympathetic increases hr, parasympathetic decrease hr (vasovagal, syncope)
    • hormones and biochemicals: Norepinephrine increases hr, Growth hormone thyroid and adrenal hormones decreases hr
    • atrial receptors: influence hr and volume retention
  31. Mean arterial pressure
    • MAP=Pd+1/3(Ps-Pd)
    • MAP=CO*SVR
    • normal: 80-120 mmHg
  32. Baroreceptors
    • location: Carotid sinus, atrial walls, vena cava, aortic arch
    • Sense change in pressures
    • when stretched it signals high pressure and decreases CO (HR and SV)
  33. arterial chemoreceptors
    • location: carotid, aortic arteries
    • sense changes in o2 co2 and ph
    • \/ o2 ph ^ pressure
    • ^ co2 ^ pressure
  34. SVR controls
    • systemic vascular resistance
    • a1 adrenergic receptors: vasoconstriction
    • b2 adrenergic receptors: smooth muscle relaxation
    • histamines prostaglandins and RAAS
  35. aldosterone
    retains sodium and water in kidney
  36. osmoreceptors
    neurons in hypothalamus: stimulate ADH
  37. ADH
    • antidiuretic hormone
    • retains free water, induce thirst and vasoconstriction
  38. natriuretic peptides
    regulate sodium excretion, diuresis, vasodilation, and antagonize RAAS
  39. hypertension
    • systolic > 120 or diastolic > 80
    • increases risk for stroke, left vent hypertrophy, renal failure
    • interventions ace inhibitors, diuretics, beta blockers, calcium channel blockers, nitrates
  40. hypotension
    • cause: loss of blood volume, excessive demand (heat stroke/sepsis), heart failure
    • response to hypotension: ^ hr via sns, ^ heart contractility via sns, ^ svr direct blood to essential areas (heart brain), increase preload
  41. orthostatic hypotension
    • vasoconstricting slow/absent with change to position resulting in blood pooling
    • altered body chemistry, drug action, prolonged immobility, starvation, phys exhaustion, volume depletion, venous pooling
  42. increase preload
    • deep breaths to increase thoracic pump
    • constriction of veins by activation of sns
    • conserve and attempt to renew blood volume (thirst, water conservation by secreating adh)(decrease urine output via RAAS)
  43. atherosclerosis
    • soft deposits of intra-arterial fat and fibrin in vessels whch harden over time
    • most common form of arteriosclerosis
    • leading cause of coronary artery and cerebrovascular disease
    • ischemia/hypoxia
  44. ischemia
    insufficient blood flow to tissues that may result in hypoxia (can result in cell injury and or death)
  45. Hypoxia
    Insufficient oxygen levels
  46. atherosclerosis outcomes
    angina, myocardial infarction, sudden cardiac death, heart failure, stroke, pvd
  47. atherosclerosis risk factors
    age gender family history diabetes smoking hypertension cholesterol sedentary lifestyle obesity
  48. inflammatory response hypothesis of atherosclerosis
    • 1. risk factors cause chronic injury of endo and result in endo dysfuntion
    • 2. injured endo allow lipids to enter intima and elicits ongoing inflam response
    • 3. inflam response attempts to repair damage but also contributes to plaque formation
    • 4. dysfunctional endo secretes growth factors that promote plaque growth and vesssel remodeling
  49. complication (athero)
    continued inflammatory response weakens fibrous cap/ leads to rupture at shoulder of plaque/ leads to rapid clot formation
  50. fatty streak
    • macrophages engulf foam cells and penetrate into intima; smooth muscle cells also migrate into intima
    • does not obstruct blood flow
    • develops in more advanced lesions
  51. foam cells
    oxidized lipids (mostly ldl chol)
  52. fatty plaque
    • intermediate between fatty streak and fibrous plaque
    • accumulations of lipids smooth muscle cells & collagen, macrophages, lymphocytes
  53. Fibrous plaque
    • consists of an extracellular lipid core in addition to smooth muscle cells, macrophages, and extracellular matrix found in fatty streak
    • lipid core covered by fibrous cap of collagen and smooth muscle cells
    • calcification of plaque may occur which can invade the vessel lumen and obstruct blood flow
  54. vulnerable plaque
    • thin cap more likely to rupture
    • has increased conc of macrophages and tcells
    • once ruptured clot cascade initiated and rapid clot formation occur
  55. steps of athero
    damage, fatty streak, fatty plaque, fibrous plaque, complicated lesion
  56. partial obstruction vessels
    transient ischemic events (exercise, stress)
  57. complicated lesion
    may result in complete obstruction= tissue infarction (formation of tissue infarct (death/necrosis) due to lack of o2
  58. order of electrical activity
    sinatrial node (pacemaker) - atrioventricular node, bundle of his, bundle branches, purkinje fibers
  59. fibrillation
    small sections of heart acting independently
  60. 3 main coronary arteries
    • right coronary artery RCA supplies right ventricle: supplies the sinus node in 55%
    • left anterior descending LAD branches off the left main, supplies the left ventricle
    • Circumflex: branches off the left main, supplies posterior left ventricle: Supplies sinus node in 45%
  61. ischemia
    demand 02 exceeds supply
  62. stable angina pectoris
    • discomfort lasts 3-5 min (activities)
    • no permanent change/damage if blood flow is restored
    • caused by gradual narrowing and hardening of vessel (stable plaque) (cannot dilate when demand increases
    • pain releived by rest and nitrates
  63. angina
    chest pain caused by ischemia
  64. unstable angina pectoris
    • discomfort lasts 15-20 min without cause and with increasing severity
    • caused by unstable plaque, prone to rupture
    • vessels become blocked with blood clots that dissolve within 20 min
    • does not respond to nitrates
    • increased risk for heart attacks
  65. acute coronary syndrome
    • sudden obstruction causing ischemia, usually blood clot formation over unstable/vulnerable plaque
    • can cause mi and death: prolonged ischemia
    • symptoms: 1st=sudden severe chest pain (heavy crushing) radiating to neck back shoulder and left arm; nausea vomiting; soa; diaphoresis
    • women symptoms: fatique, sleep distubance, soa, indigestion, anxiety
    • treatment: clot busters, platelet inhibitors or angioplasty (balloon or stent)
  66. pathogenesis of acute coronary syndrome
    • plaque ruptures, spontaneously, induced by PCL (percutaneous coronary interventions)
    • platelet adhesion at site of rupture
    • more platelet activation
    • platelet aggregation
    • activation of clotting cascade
    • clot formation at site
    • obstruction from clot
  67. myocardial infarction
    • 90% caused by thrombus in coronary arteries
    • 40% fatal (usually from ventricular fibrillation)
    • 10% due to prolonged coronary vasospasm
  68. valve dysfunction
    • can be congenital.. or acquired: inflammatory, ischemic, traumatic, degenerative, infectious, endocarditis
    • stenosis: valve opening constricted and narrowed
    • regurgitation: valve leaflets/cusps fail to close completely
    • management: valve replacement, longterm anticoagulation, prophylaxis for endocarditis PRN
    • murmurs are heard
  69. pericardium
    sac enclosing heart
  70. pericarditis
    • inflammation of pericardium causing membranes to become rough
    • 90% due to viruses
  71. pericardial effusion
    • accumulation of fluid in the pericardial cavity
    • occur with paricarditis
    • if fluid accumulation is rapid can cause cardiac compression (fluid in sac displaces preload)
  72. cardiac tamponade
    rapid fluid accumulation causing cardiac compression
  73. cardiomyopathy
    • heart wall muscle doesnt function well
    • most due to ischemia and htn, some idiopathic, primary:genetics, secondary:diseases toxins infections
    • 3 types: dilated (congestive): big boggy heart , Hypertrophic: so much muscle it blocks outflow , restrictive: stiff small venticles
  74. heart failure
    • cardiac dysfunction resulting in inadequate perfusion of tissues
    • 10% adults over 65
    • commonly left vent: syst & diast heart failure
    • right vent: pulmonary disease
  75. left heart failure
    • congestive heart failure
    • systolic heart failure: decreased cardiac output, affected contractility, preload/afterload
    • diastolic heart failure: preserved systolic function, due to decreased compliance of left vent and abnormal diastolic relaxation (increased lvedp)
    • fluid retention lungs
  76. right heart failure
    • can result form left heart failure: because of back up of blood in pulmonary circulation
    • can be due to pulmonary hypertension (from diffuse hypoxic pulmonary disease): copd, cystic fibrosis, ards
    • fluid retention abdomen
  77. causes of heart failure
    • atherosclerotic coronary artery disease
    • untreated hypertension
    • cardiomyopathy
    • hypoxic pulmonary disease, causing pulmonary hypertension
    • valvular disease
  78. physiology of heart failure
    • decreased cardiac output due to decreased stroke volume
    • activates sns to increase hr
    • activates raas
    • increased wall tension leads to myocardial hypertrophy
  79. left forward hearth failure
    • affects systemic circulation
    • results in inadequate oxygen supply to body which results in fatigue
  80. left backward heart failure
    • affects lungs
    • results in pulmonary congestion then increased rv afterload then eventually rv failure
  81. forward right heart failure
    • affects lungs
    • lungs with too little flow causes too little flow in lv
    • decreased cardiac output results in fatigue
  82. backward right heart failure
    • affects veins
    • congestion in veins (jugular disention)
    • abdominal bloating, anorexia, ascites
    • peripheral edema
  83. Diuretics
    • decrease fluid retention (K+ sparring or not)
    • decreases blood volume, which decreases venous return and blood pressure
  84. ACE inhibitors
    Decrease afterload via vasodilation (affecting systolic failure)
  85. B-adrenergic agonists
    Stimulate SNS, increasing calcium flow into myocardial cells causing increased contraction (positive inotrope)
  86. Shock
    • insufficient cardiac output to maintain a blood pressure adequate for functioning
    • Body reacts by saving fluid, increase HR, if possible vasoconstriction, Kussmaul breathing (fast deeep)
    • Signs from SNS: dilated pupils, cool clammy skin, decreased LOC, possible anxiety/panic
    • Vital Signs: Low BP, narrow pulse pressure, Tachycardia, tachypnea, acute renal failure (oliguria, increased BUN and Cr)
  87. Cardiogenic Shock
    • Decreased CO=tissue hypoxia
    • in the presence of adequate intravascular volume
    • MI, cardiomopathy
    • Treatment: inotropic medications, limit infarct size (supply O2), Intra aortic balloon pumps in acute care
  88. Hypovolemic shock
    • loss of whole blood (hemorrhage), plasma (burns), or interstitial fluid (diarrhea, diaphoresis, emesis, diuresis)
    • Treatment: restore volume
  89. Anaphylactic shock
    • A widespread hypersensitivity reaction
    • Vasodilation, peripheral pooling, hypovolemia, causing decreased tissue perfusion, impaired cellular metabolism
    • Treatment: EpiPen- a catecholamine that increases blood pressure and heart contractility and dilates the bronchi
  90. Neurogenic shock
    • widespread and massive vasodilation
    • due to parasympathetic overstimulation or sympathetic understimulation
    • Treatment: remove or treat underlying cause (trauma, drug, stress, pain)
  91. Septic Shock
    • One component of Systemic Inflammatory Response Syndrome SIRS
    • begins with infection (gram- or gram+ bacteria, fungi, or viruses) that progresses to bacteremia, then sepsis
    • 40% in US progress to Multiple Organ Dysfunction Syndrome (MODS) and death
    • Treatment: multiple drug antibacterial therapy, removal of source of infection, fluid sesuscitation, vasoactive mediations to improve hemodynamics
  92. Acute respiratory distress syndrom
    • ARDS: acute lung inflammation and diffuse alveolocapillary injury with pulmonary edema
    • complication of shock
  93. Disseminated Intravascular Coagulation
    • DIC: many micro blood clots form causing tissue dammage and using up the clotting factors (clotting and bleeding occur simultaneously)
    • complication of shock
  94. Multiple Organ Dysfunction syndrome
    • MODS/MOSF: High mortality (2 organs=50%, 3 organs=90%
    • complication of shock
  95. B-adrenergic blockers
    • -lols: propanolol
    • decrease hr, contractility and excitability
  96. ACE inhibitors
    • -prils: lisinopril
    • Blocks ace; prevents vasoconstriction
  97. ARBs
    • -artans: losartan
    • angiotensin II receptor blockers; prevents vasocontriction/ h2o retention
  98. Ca2+ Channel Blockers
    • -dipines: amlodipine
    • block ca2+ from moving into cardiac cells; cause vasodilation and loss of smooth muscle tone
  99. Diuretics
    • -ides: furosemide
    • promote fluid excretion
  100. Nitrates
    • Angina: nitroglycerin
    • cardiac vasodilation
  101. anticoagulants
    • ASA and clopidigrel
    • Prevent clot formation, "thin" the blood
  102. Pressors
    • Dopamine and epinephrine
    • adrengeric effects; cause vasoconstriction

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