Cardiovascular for Pathophysiology

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jdieken22
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Cardiovascular for Pathophysiology
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2011-10-16 22:12:20
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cardiovascular pathophysiology
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cards for cardiovascular system
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  1. What is the Virchow Triad?
    • Venous Stasis
    • Endothelial damage
    • Hypercoagulability
  2. What is an emboli?
    After the thrombus breaks away from the vessel wall
  3. What is a thrombus?
    A blood clot attached to the vessel wall
  4. What is the average heart rate in adults?
    70 beats per minute
  5. Normal Blood pressure
    120/80 or less
  6. Prehypertension
    120-139/80-89
  7. Stage 1 hypertension
    140-159/90-99
  8. Stage 2 hypertension
    greater than or equal to 160/greater than or equal to 100
  9. What are the effects of aging on the cardiovascular system in resting state?
    • Cardiac Output - unchanged or slightly decreased in women only
    • Heart Rate - slight decrease
    • Stroke Volume - slight increase
    • Ejection Fraction - Unchanged
    • Afterload - increased
    • End-diastolic volume - unchanged
    • End-systolic volume - unchanged
    • Contraction - increased because of prolonged relaxation
    • Cadiac dilation - no change
    • VO2 max - N/A
  10. What are the effects of aging on the cardiovascular system during excercise?
    • Cardiac Output - declines because of a decrease in heart rate and stroke volume
    • Heart Rate - increases less than in younger people, possibly becasue of decreased cardiovascular response to catecholamines; overall slight decrease
    • Stroke Volume - slight increase
    • Ejection Fraction - increases less from rest to exercise than in younger people
    • Afterload - uncertain
    • End-diastolic volume - smaller for women
    • End-systolic volume - lesser increase
    • Contraction - decreases with vigorous exercise
    • Cadiac dilation - increases at end-diastole and end-systole
    • VO2 max - declines because of a decline in skeletal muscle mass
  11. What factors affect blood flow?
    • Pressure and Resistance
    • Total Peripheral Resistance
    • Velocity
    • Laminar flow vs Turbulent flow
  12. What does pressure mean pertaining to blood flow?
    The force exerted on the liquid per unit area and is expressed as dynes per square centimeter
  13. What does resistence mean pertaining to blood flow?
    opposition to force, most opposition to blood flow is provided by the diameter and length of the blood vessels themselves
  14. What does Total Peripheral Resistance mean pertaining to blood flow?
    determined primarily by change in the diameter of the arterioles. reflex control of total cardiac output and peripheral resistance includes (1) sympathetic stimulation of heart, arterioles, and veins and (2) parasympathetic stimulation of the heart.
  15. What does velocity mean pertaining to blood flow?
    the distance the blood travels in a unit of time, usually centimeters per second
  16. What does laminar flow mean pertaining to blood flow?
    concentric layers of molecules move "straight ahead"
  17. What does turbulent flow mean pertaining to blood flow?
    where flow is obstructed, the vessel turns, or blood flows over rough surfaces
  18. What are the disorders of arterial flow?
    • Arterial thrombus
    • Periphreal Vascular Disease
    • Hypertension
    • Acute Coronary Syndrome
    • Coronary Artery Disease
    • Myocardial Ischemia
    • Arteriosclerosis
    • Atherosclerosis
    • Aneurysm
    • Embolism
    • Orthostatic (postural) Hypotension
  19. What are the disorders of venous flow?
    • Chronic venous insufficiency
    • Venus thrombus
    • Varicose Veins
    • Superior vena cava syndrome
    • Embolism
  20. What is the pathogenesis of Hypertension?
    • Sympathetic Nervous System (SNS) increases HR and vasoconstriction
    • Renin-angiotension-aldosterone (RAA) system - renal retention of sodium and water, as well as vasoconstriction
    • Natriuretic hormones increase sodium retention
    • Endothelial injury decreases nitrous oxide and increases endothelin
    • Obesity - leptin increases SN and natriuresis
    • Insulin resistance decreases nitrous oxide, increases SNS and RAA
    • Aged - decreases elastin and increases collagen - - decrease elasticity of arteries and increases fibrosis in media and thickening of intima. Thickened intimal layer of vessels -- increased systolic blood pressure
  21. What are manifestations of hypertension?
    • None, except for elevated systemic blood pressure
    • Hard to detect
  22. What disorders are associated with secondary hypertension?
    • Renal failure due to renin-angiotensin; sodium and water retention.
    • Endocrine disorders: hyperaldosteronism, excess cortisol from adrenal cortex, pheochromocytoma from adrenal medulla
    • Vascular disorders: arteriosclerosis
  23. What disorders are associated with chronic or complicated hypertension?
    • Cardiac - increases work load of the heart, myocardium eventually hypertrophies
    • Vascular - causes shearing force of endothelium causing tissue damage and atherosclerosis in medium to large sized vessels; increased pressure contributes to aneurysms
    • Renal - atherosclerosis narrows renal arteries causing necrosis of renal arteries, atrophy, and finally renal failure
    • Brain - atherosclerosis narrows vessels to brain causing cerebral infarctions, transient ischemic attacks (TIA) and perhaps a cerebrovascular accident (CVA) or cerebral aneurysm
    • Eyes - atherosclerosis causes ischemia to retinal veins causing retinal vascular sclerosis leading to blindness and/or hemorrhage
  24. What is the pathophysiology of cardiogenic shock?
    • decreased cardiac output (leads to)
    • compensatory renin-aldosterone, ADH (leads to)
    • adequate or increased blood volume (leads to)
    • increased preload, stroke volume, and HR (leads to)
    • systemic and pulmonary edema (leads to)
    • Dyspnea
    • --or--
    • increased preload, stroke volume, and HR (leads to)
    • increased myocardial oxygen requirements (leads to)
    • decreased cardiac output, decreased ejection fraction (leads to)
    • decrease BP (leads to decreased tissue perfussion) or decreased tissue perfussion (leads to)
    • impaired cellular metabolism
    • --or--
    • decreased cardiac output (leads to)
    • catecholamine compensatory release (leads to)
    • increased SVR (leads to)
    • increased pre-load, stroke volume, and HR (look at above detail below this to see what the rest (leads to))
  25. What is the pathophysiology of hypovolemic shock?
    • decreased intravascular volume (leads to)
    • decrease cardiac output (leads to)
    • Shift of interstitial fluid or aldosterone, ADH or splenic discharge (all together leads to)
    • increased volume (leads to)
    • increased cardiac output (leads to)
    • more volume loss (leads to)
    • decreased cardiac output (leads to)
    • decreased systemic and pulmonic pressures(leads to decreased tissue perfusion) "or" decreased tissue perfusion (leads to)
    • impaired cellular metabolism
    • --or--
    • decreased cardiac output (leads to) (look at above reaction)
    • catecholamine release (leads to)
    • increased HR, contractility (leads to increased cardiac output (look from there above)) --or-- increased SVR (leads to decreased cardiac output (look from there above))
  26. What is the pathophysiology of neurogenic shock?
    • decreased sympathetic and/or increased parasympathetic stimulation (leads to)
    • decreased vascular tone (leads to)
    • massive vasodilation (leads to)
    • decreased SVR (systemic vascular resistence) (leads to)
    • inadequate cardiac output
    • decreased tissue perfusion
    • impaired cellular metabolism
  27. What is the pathophysiology of anaphylactic shock?
    • Antigen (allergen) (leads to) "or" activates antibody (IgE)
    • complement, histamine, kinins, prostaglandins (leads to)
    • increased capillary permeability (leads to) "or" peripheral vasodilation (leads to) "or" constriction of extravascular smooth muscle (bronchoconstriction, laryngospasms, gastrointestinal cramps)
    • --increased capillary permeability--
    • extravasation of intravascular fluids (leads to)
    • edema --or-- relative hypovolemia (leads to)
    • decreased cardiac output (leads to)
    • decreased tissue perfusion (leads to)
    • impaired cellular metabolism
    • --peripheral vasodilation--
    • decreased SVR (leads to)
    • relative hypovolemia (leads to)
    • decreased cardiac output (leads to)
    • decreased tissue perfusion (leads to)
    • impaired cellular metabolism
  28. What is shock?
    • cardiovascular system fails to perfuse tissues
    • impaired cellular metabolism
  29. Cardiogenic shock
    decreased cardiac output and evidence of tissue hypoxia in presence of adequate intravascular volume
  30. Hypovolemic Shock
    loss of whole blood (hemorrhage), plasma (burns), or interstitial fluids (diaphoresis, diabetes mellitus, diabetes insipidus, emesis, diarrhea, or diuresis) in large amounts
  31. Neurogenic Shock
    widespread vasodilation from parasympathetic overstimulation and sympathetic understimulation
  32. Anaphylactic Shock
    wide spread type 1 hypersensitivity reaction, called anaphylaxis
  33. Septic Shock
    one component of systemic inflammatory response syndrome (sirs) with bacteremia, then sepsis, then septic shock, and then multiple organ dysfunction syndrome (mods)
  34. What is the pathophysiology of septic shock?
    • Bacteremia (leads to)
    • Gram-negative organism (leads to) --or-- Gram-positive organism (leads to)
    • --Gram-negative organism--
    • release of endotoxins, proteases, and other products (leads to)
    • acts as triggering molecules and result in activation of (look below gram-positive organism)
    • --Gram-positive organism--
    • release of exotoxins and enzymes
    • acts as triggering molecules and result in activation of (leads to)
    • complement system --or-- coagulation cascade --or-- kinin system --or-- neutrophil, endothelial, and monocyte-macrophage cell activity (all leads to)
    • Release of central endogenous mediators (leads to)
    • Tumor necrosis factor (TNF); interleukin - 1 (IL-1) (leads to)
    • release of proinflammatory cytokines (leads to)
    • endothelial cell damage (leads to)
    • hypotension --or-- decreased systemic vascular resistance --or-- depressed myocardial function --or-- lactic acidosis --or-- leukopenia --or-- thrombocytopenia --or-- vascular leakage --or-- pulmonary congestion --or-- tissue necrosis (all lead to)
    • organ dysfunction
  35. Manifestations of Cardiogenic Shock are?
    impaired mentation, elevated preload in systemic and pulmonary vasculature, systemic and pulmonary edema, dusky skin color, marked hypotension, oliguria (diminished capacity to form and pass urine), ileus (an obstruction of the intestines), and dyspnea (distressful, uncomfortable breathing)
  36. Manifestations of Hypovolemic Shock are?
    SVR (systemic vascular resistance), poor skin turgor, thirst, oliguria, low systemic pulmonary preloads, rapid heart rates, thready pulse, mental status deterioration
  37. Manifestations of Neurogenic Shock are:
    decrease in vascular tone, space containing blood has increased, low SVR, brachycardia, decrease cardiac output, hypotension, underperfusion of tissues
  38. Manifestations of Anaphylactic Shock are:
    anxiety, difficulty breathing, gastrointestional cramps, edema, hives, sensations of burning or itching skin, decreased blood pressure, impaired mentation, decreased SVR, high or normal cardiac output, oliguria, vasodilation, peripheral pooling, relative hypovolemia
  39. Manifestations of Septic Shock are:
    low arterial pressure, low SVR from vasodilation, systemic edema, alteration in oxygen extraction by all cells, tachycardia, decreased myocardial contractility, temperature instability, deranged renal function, gastrointestinal mucosa changes, jaundice, clotting abnormalities, deterioration of mental status, ARDS (adult respiratory distress syndrome), inflammation, and immune reactions
  40. What are the complications of Cardiogenic Shock?
    myocardial infarction, left heart failure, arrhythmias, acute valvular dysfunction, ventricular or septal rupture, myocardial or pericardial infections, heart failure resulting from drug toxicity, and death
  41. What are the complications of Hypovolemic Shock?
    hypothermia and coagulopathies (blood can't coagulate)
  42. What are the complications of Neurogenic Shock?
    trauma to the spinal cord or medulla, conditions that interrupt supply of oxygen, depressive drugs, anesthetic agents, severe emotional stress or pain, bradycardia
  43. What are the complications of Anaphylactic Shock?
    vasodilation, increased vascular permeability, peripheral pooling, tissue edema, constriction of extravascular smooth muscle, death
  44. What are the complications of Septic Shock?
    bacteremia, sepsis, multiple organ dysfunction, death, tachycardia, inflammation, hypotension, hypofusion, tissue hypoxia, necrosis, apoptosis leading to MODS
  45. What are the risk factors of Coronary Artery Disease?
    • Nonmodifiable: advanced age, male gender or women after menopause, family history, race
    • Modifiable: dyslipidemia, hypertension, cigarette smoking, diabetes and insulin resistence, obesity, sedentary lifestyle, atherogenic diet
    • Non-traditional: inflammation, thrombosis, hyperhomocysteinemia, infection
  46. What are the etiologies of coronary artery disease?
    advanced age, family history, race, dyslipidemia, hypertension, diabetes & insulin resistence, obesity, sedentary lifestyle, atherogenic diet, infection, inflammation & thrombosis, & hyperhomocysteinemia
  47. What leads to acute coronary syndrome?
    Coronary Artery Disease
  48. What are the etiologies of acute coronary syndrome?
    unstable agina, myocardial infarction, persistent ischemia,complete occlusion of coronary artery
  49. What is SNS?
    Sympathetic Nervous System
  50. What is the pathophysiology of coronary artery disease?
    imbalance between the supply and the demand for oxygen
  51. What is the pathophysiology of acute coronary syndromes?
    myocardial ischemia and myocyte necrosis
  52. What are the manifestations of Coronary Artery Disease?
    angina
  53. What are manifestations of Acute Coronary Syndrome?
    sudden severe chest pain; radiation to the neck, jaw, back, shoulder, or left arm; nausea; vommiting; skin cool & clammy; decreased BP; SNS is activated resulting in increased HR & BP; abnormal heart sounds; pericardial friction rub; cardiac murmurs; dullness to percussion & inspiratory crackles in lungs
  54. What are the etiologies of Left Heart Failure?
    hypertension, coronary heart disease, valvular disease, cardiomyopathy, left ventricular hypertrophy, myocardial infarction, myocarditis myocardial ischemia, myocardial workload
  55. What is the pathophysiology of Left Heart Failure?
    • Myocardial Dysfunction (myocardial infarction, ischemic heart disease, hypertension, other) (leads to)
    • decreased cardiac output & decreased systemic blood pressure (leads to) or decreased perfusion to kidneys (leads to) (see below vasoconstriction)
    • Baroreceptors activated (left ventricle, aortic arch, carotid sinus) (leads to)
    • Vasometer regulatory centers in medulla stimulated (leads to)
    • Sympathetic nervous system activated (leads to)
    • Increased catecholamines (epinephrine and norepinephrine) (leads to)
    • Vasoconstriction (leads to) (look below next set to see what comes next)
    • --decreased perfusion to kidneys--
    • Renin-angiotensin-aldosterone system activated (leads to)
    • Affects Kidneys, Liver, and Lungs
    • Increased angiotensin II and increased aldosterone (leads to)
    • Retain sodium and water, arginine vasopression, endothelin, cytokines (tumor necrosis factor-a) (all lead to)
    • Vasoconstriction (leads to)
    • --Vasoconstriction--
    • Increased afterload, Increased BP, Increased HR (leads to)
    • Ventricular remodeling (hypertrophy and dilation of ventricle, genetically large cells, impaired contractility
  56. What are the manifestations of Left Heart Failure?
    Dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, edema, cyanosis, rales, pleural effusions, hypotension, hypertension, S3 gallop
  57. What are the etiologies of Right Heart Failure?
    Left Heart Failure, Chronic Obstructive Pulmonary Disease (COPD), Cystic Fibrosis, Adult Respiratory Distress Syndrome (ARDS), Myocardial Infarction, cardiomyopathies, pulmonic valvular disease
  58. What is the pathophysiology of Right Heart Failure?
    • Lung Disease (leads to)
    • Increase in Pulmonary vascular resistance (leads to) --or-- decreased oxygen supply (leads to) (see oxygen supply below)
    • --Increase in Pulmonary vascular resistance--
    • Increased force of right ventricular (RV) contraction (leads to)
    • Increased RV oxygen demand (leads to)
    • RV hypoxia (leads to)
    • decreased force of RV contraction (leads to)
    • increased RV end-diastolic pressure (leads to)
    • increased RV preload (leads to)
    • increased RA preload (leads to) --or-- increased RV oxygen demand (see up above)
    • Periphreal Edema
    • --decreased oxygen supply-- (see above)
    • RV hypoxia (see above)
  59. What are the manifestations of Right Heart Failure?
    Periphreal Edema and hepatosplenomegaly (enlargement of the spleen and liver)
  60. What are the etiologies of Systolic Heart Failure?
    Myocardial infarction, renal failure, hypertension
  61. What is the pathophysiology of Systolic Heart Failure?
    • Myocardial Infarction (leads to)
    • decreased contractility (leads to)
    • decreased ejection fraction & increased ventricle end-diastolic volume (LVEDV) (leads to) --or-- decreased renal perfusion & increased renin and angiotension (leads to) (see below)
    • increased pre-load (leads to)
    • decreased contractility
    • --renal perfusion & renin and angiotension-- (see above)
    • increased afterload (leads to)
    • decreased contractility
    • --end of Myocardial Infarction--
    • Renal Failure (leads to)
    • Increased preload (leads to)
    • decreased contractility
    • --end of renal failure--
    • Hypertension (leads to)
    • increased afterload (leads to)
    • decreased contractility
  62. What are the manifestations of Systolic Heart Failure?
    Dyspnea (uncomfortable breathing), orthopnea (must sit or stand to breathe deeply or comfortably), cough of frothy sputum, fatigue, decreased urine output, edema, cyanosis, rales, pleural effusions, hypotension, hypertension, S3 gallop (third heart sound)
  63. What are the etiologies of Diastolic Heart Failure?
    Systolic Heart Failure, Gender - Women, Pulmonary Edema, hypertension-induced myocardial hypertrophy, myocardial ischemia, aortic valvular disease, mitral valve disease, pericardial disease, cardiomyopathies, diabetes
  64. What is the pathophysiology of Diastolic Heart Failure?
    • Myocardial infarction (leads to) --or-- Hypertrophy (leads to) (below)
    • increased stiffness (leads to)
    • elevated left atrial pressure and size (leads to)
    • --Hypertrophy--
    • abnormal relaxation and increased stiffness (leads to)
    • elevated left ventricular filling pressures (leads to)
    • elevated left atrial pressure and size (leads to) (see above)
    • atrial fibrillation and decreased cardiac output (leads to)
    • reduced exercise tolerance and signs of congestive heart failure (leads to)
    • diastolic heart failure
  65. What are the mainifestations of Diastolic Heart Failure?
    dyspnea on exertion, fatigue, pulmonary edema (auscultation and pleural effusions), coronary disease, hypertension, valvular disease
  66. What is the etiology of Mitral Stenosis?
    • postinflammatory scarring from rheumatic heart failure and aging increases rigidity and thickening of valves
    • decreased preload
    • decreased contractility
    • 0 affect on afterload
  67. What is the pathophysiology of Mitral Stenosis?
    Impairs blood flow from the left atrium to the left ventricle. Left atrium dialates, may hypertrophy. Increases risk of atrial fibrillation and thrombi. Mitral valve is damaged and thickened.
  68. What are the manifestations of Mitral Stenosis?
    • *Rheumatic Heart Disease
    • *Left atrial hypertrophy and dilation with fibrillation, followed by right ventricular failure
    • *Pulmonary edema; dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, predisposition to respiratory infections, hemoptysis, pulmonary hypertension
    • * Neural deficits only associated with emboli (hemiparesis)
    • *Atypical chest pain
    • *Low rumbling diastolic murmur heard best at the apex and radiating to the axilla, accentuated first heart sound, opening snap
  69. What are the etiologies of Aortic Stenosis?
    • Postinflammatory scarring from rheumatic heart disease and age-related calcification
    • increased preload
    • increased afterload
  70. What is the pathophysiology of Aortic Stenosis?
    Decreased HR, faint pulses, resistance to flow leads to systolic heart murmur at the right parasternal second intercostal space, left ventricular hypertrophy develops due to increased workload, increases myocardial oxygen demand
  71. What are the manifestations of Aortic Stenosis?
    • *Congenital bicuspid valve, degenerative (calcific) changes with aging, rheumatic heart disease
    • *Left ventricular hypertrophy followedby left heart failure; decreased coronary blood flow with myocardial ischemia
    • *Pulmonary edema; dyspnea on exertion
    • *Syncope (loss of consciousness), especially on exertion
    • *Angina Pectoris
    • *Systolic murmur heard best at the right parasternal second intercostal space and radiating to the neck
    • Pink frothy sputum
    • dry cough
    • orthopnea
    • will look like left-sided heart failure
    • crackles
    • shortness of breath
  72. What are the etiologies of Mitral Insufficiency or Regurgitation?
    • Postinflammatory scarring from rheumatic heart disease
    • Infective endocarditis - inflammation of outer layer of heart
    • Mitral valve prolapse - falls into the ventricle
    • Increased preload
    • increased contractility
    • 0 affect on afterload
  73. What is the pathophysiology of Mitral Insufficiency or Regurgitation?
    • Valves will be flapping instead of closing
    • preload will increase
    • cardiac output will drop
    • right atrium will hypertrophy
    • will require valve replacements
  74. What are the manifestations of Mitral Insufficiency or Regurgitation?
    • *Mitral valve prolapse
    • *Left atrial hypertrophy and dilation, followed by left heart failure
    • *Pulmonary edema with dyspnea on exertion
    • *Atypical chest pain
    • *Murmur throughout systole heard best at the apex and radiating to the axilla
  75. What are the etiologies of Aortic Insufficiency or Regurgitation?
    • Postinflammatory scarring from rheumatic heart disease and infective endocarditis
    • Increased preload
    • increased contractility
    • decreased afterload
    • hypertrophy
  76. What is the pathophysiology of Aortic Insufficiency or Regurgitation?
    During systole, blood is ejected from the left ventricle into the aorta. During diastole, some of the ejected blood flows back into the left ventricle. Volume overload occurs in the ventricle becasue it receives blood from both the left atrium and from the aorta during diastole. over time, the end-diastolic volume of the left ventricle increases, and myocardial fibers stretch to accommodate the extra fluid. compensatory dialation permits the left ventricle to increase its stroke volume and maintain cardiac output. Ventricular hypertrophy also occurs as an adaptation to the incread volume and becasue of increased afterload created by the hihg stroke volume and resultant systolic hypertension. ventricular dilation and hypertrophy eventually cannot compensate for aortic incompetence.
  77. What are the manifestations for Aortic Insufficiency or Regurgitation?
    • *Widened pulse pressure
    • *Decrescendo murmur heartbeat in second, third, or fourth intercostal spaces parasternally and may radiate to the neck
    • *Prominant carotid pulsations and bounding peripheral pulses (corrigan pulse)
    • *Dysrhythmias and endocarditis
    • *Infective endocarditis; aortic root disease (connective tissue diseases, Marfan syndrome); dilation of the aortic root due to hypertension and aging
    • *Left ventricular hypertrophy and dilation, followed by left heart failure
    • *Pulmonary edema with dyspnea on exertion
    • *Syncope
    • * Angina pectoris
  78. What is the etiology of Atrial Septal Disease (ASD)?
    Alcohol, High Altitude, cri du chat, turner syndrome, klinefelter variant
  79. What is the manifestations of Atrial Septal Disease (ASD)?
    • Left to right shunt, usually asymptomatic, rare cases may have pulmonary overcirculation and slow growth
    • Older children and adults: shortness of breath w/activity, pulmonary hypertension and stroke, systolic ejection murmur, widely split second heart sound, right ventricle hypertrophy
  80. What are the etiologies of Ventricular Septal Disease (VSD)?
    Diabetes, alcohol, increased maternal age, prematurity, eisenmenger syndrome (a condition in which shunting of blood is reversed because of high pulmonary pressure and resistance (right to left shunt w/cyanosis)), cri du chat, trisomy 13, trisomy 18, trisomy 21 (down syndrome))
  81. What are the manifestations of Ventricular Septal Disease (VSD)?
    • Left to right shunt, may have no symptoms, congestive heart failure, poor growth (failure to thrive), tachypnea, holosystolic (pan-systolic) mumur
    • Child: at risk for pulmonary hypertension and endocarditis
  82. What are the etiologies for Patent Ductus Arteriosus (PDA)?
    • Left to right shunt
    • Infection intrauterine, systemic viral, rubella, phenylketonuria (PKU), prematurity, high altitude, cri du chat, trisomy 13, trisomy 18, klinefelter variant
  83. What are the manifestations for Patent Ductus Arteriosus (PDA)?
    asymptomatic, pulmonary overcirculation (dyspnea, fatigue, poor feeding), machinery like murmur, low diastolic blood pressure, widened pulse pressure, bounding pulses, bacterial endocarditis, rarely develop pulmonary hypertension
  84. What are the etiologies of Coarctation of the Aorta (COA)?
    Infection Intrauterine, systemic viral, rubella, phenylketonuria (PKU), Turner Syndrome
  85. What are the manifestations of Coarctation of the Aorta (COA)?
    • if severe-low cardiac output, acidosis, hypotension, weak or absent femoral pulses w/poor perfusion
    • Asymptomatic later unexplained hypertension, leg pain or cramping on exercise, rarely experience dizziness, headaches, fainting, epistaxis from hypertension
  86. What are the etiologies of Tetralogy of Fallot (TOF)?
    Alcohol, increased maternal age
  87. What are the manifestations of Tetralogy of Fallot (TOF)?
    some acutely cynotic at birth, others hypoxia and cyanosis gradual over 1st year may occur after crying or feeding, clubbing of the fingers, squatting, poor growth, at risk for emboli, cerebrovascular disease, brain abscess, seizures, loss of consciousness, sudden death
  88. Arteries
    main transporters of oxygenated blood
  89. Arterioles
    diameter is adjusted to regulate blood
  90. Capillaries
    diffusion occurs across thin walls
  91. What does SNS (sympathetic nervous system) regulate?
    Peripheral vascular resistance
  92. Norepinephrine
    vasoconstriction via alpha1 receptors located in vascular smooth muscle walls
  93. Epinephrine
    • Increases heart rate
    • enhances myocardial contractility
    • Increases venous return to the heart
  94. Veins
    large diameter vessels with some smooth muscle in wall
  95. Valves
    only in veins and prevent blood from flowing backward
  96. Chronic Venous Insufficiency
    • valves unable to maintain forward blood over a long period of time
    • flow and pressure in deep veins increases
  97. What is the pathophysiology of Chronic Venous Insufficiency?
    • Increased pressure in superficial veins transmitted to deep veins, that become distended
    • Increased pressure and stasis increase pressure on arteries causing tissue hypoxia, leads to inflammatory reaction in vessels, leads to fibrosclerotic remodeling of skin and then ulceration
    • Poor perfusion leads to delayed healing, other signs of arterial insufficiency
  98. What are the manifestations of Chronic Venous Insufficiency?
    • peripheral edema
    • pitting edema below the knees
    • Brown leather skin (hyperpigmentation of skin)
    • venous stasis ulcers - so muc fluid it seeps from the skin from all the water
    • can become an arterial problem because it will start to press on arteries
  99. Thrombus Formation
    a blood clot that attaches to vessel wall
  100. What are the etiologies of Deep Vein Thrombosis (DVT)?
    • Virchow Triad
    • 1. Venous Stasis (immobility, age, heart failure)
    • 2. Endothelial damage (trauma, intravenous infusions)
    • 3. Hypercoagulability (inherited disorders, malignancy, pregnancy, oral contraceptives, hormone replacement)
    • Inherited disorders - prothrombin mutations, deficiencies in protein C, protein S, and antithrombin
  101. What is the pathophysiology of Deep Vein Thrombosis?
    • Accumulation of clotting factors and platelets leads to thrombus formation in vein
    • Inflammation around thrombus promotes further platelet aggregation, thrombus grows proximally
  102. What are the manifestations of Deep Vein Thrombosis?
    • Initially no signs or symptoms
    • Pain and redness
    • Edema when significant obstruction to venous flow
    • DVT travels to right side of heart (lungs) creating pulmonary emboli causing hypoxia, increased heart and respiratory rates
    • Inflammation
    • May hurt when walking
    • One leg may be bigger than the other
  103. What is the pathophysiology of Arterial Thrombus?
    • Activation of clotting factors (inflammation, trauma)
    • Stasis of blood flow (low blood pressure)
    • Anatomic change (calcification or vegetation on heart valves)
  104. What are the manifestations of Arterial Thrombus?
    • Ischemia from occluded artery (cerebral arteries)
    • Arterial emboli originate in the left heart after MI, valvular disease, left heart failure, or dysrhythmia
  105. What are the manifestations of Peripheral Arterial Disease (PAD)?
    • Pulseless
    • pallor
    • erythema (red)
    • paresthesia
    • pain
    • poikliothermia
    • skin shiny
    • hair is absent (very noticable on men with no hair in one spot of their legs)
    • leg cramping when walking relieved by rest
    • intermittent claudication versus leg cramping not relieved by rest - rest pain
    • Big black ulcers (necrosis)
    • no ability to heal
    • skin shiny
    • cool to touch
  106. Aneurysm
    localized dilation of an arterial wall, usually aorta
  107. What are the etiologies of an Aneurysm?
    • Congenital weakness of a vessel
    • Atherosclerosis - plaque formation erodes vessel wall, causes inflammation
    • Hypertension - increases vessel wall stress
    • Trauma
  108. What is the pathopysiology of an Aneurysm?
    changes in collagen and elastic making vessel vulnerable to intravascular pressures
  109. Cerebral aneurysm - Saccular
    in the head where if it bursts, it is a hemorraghic stroke
  110. What are the manifestations of an Aortic Aneurysm?
    sudden, severe chest pain; cadiogenic shock; renal failure (descending); decreased level of consciousness (ascending)
  111. What are the manifestations of an Abdominal Aortic Aneurysm?
    • Pulsatile mass or bruit
    • Compression of lumbar nearves causes back pain
    • Compression on the bowel causes gastric discomfort
  112. What is the pathogensis of Ischemia?
    • Cellular effects begins within 10 sec of occlusion
    • decreased ATP production by hypoxic mitochondria to Glycolysis to
    • Anerobic metabolism to lactate formation to
    • Decreased intracellular pH (acidosis)
    • Acidosis makes myocardium more vulnerable to lysosomal enzymes
    • Failure of ATP dependent pumps (Na+, K+ & Ca++ pumps) (cells will shrink)
    • Loss of intracellular potassium, calcium, and magnesium reduce myocardial contractility
    • Increase of intracellular sodium (Na+) makes
    • Catecholamines released to increase glucose
    • Angiotensin II released during myocardial ischemia
  113. Preload
    The amount of blood in the left ventricle in diastolic pressure
  114. Afterload
    is the pressure that the heart has to push against to get the blood through the aorta into the body
  115. Respiratory Acidosis
    • pH = low
    • CO2 = high
    • Bicarb = normal to high
    • pH = 7.35 - 7.45
    • CO2 = 35 - 45
    • Bicarb = 22 - 26
    • Mental capability - menti
    • mechanical ventilations
    • Retain CO2
    • Headache restlessness
    • Apprehension
    • Lethargy
    • Coma
    • Disryhthemias
    • Hypoventilation
  116. Respiratory Akalosis
    • pH = high
    • CO2 = low
    • Bicarb = normal to low
    • parasthesias (due to hypocalcemia)
    • lightheadedness and dizziness
    • confusion
    • seizures
    • coma
    • hyperventilation with severe anxiety or hysteria
    • Hypoxemia from pulmonary disease (rapid, deep respirations)
  117. Varicose Veins
    • Tortous dark superficial veins
    • When valves begin to fail blood backs up and creates varicose veins
  118. What is arterialsclerosis?
    • Leads to huge problems of the heart
    • Damage to the arteries brings inflammation eventually a thrombus is formed, activation of clotting factors, blood stasis
    • Most self-induced
    • hypertension - (HTN) - will sheer the vessel walls
    • Hyperlipidemia - builds plaque around vessels
    • Viruses/Toxins
    • Increased vascular resistance
  119. If we are thinking arterial side think ......
    Brain
  120. What is claudication?
    pain that goes away after rest
  121. What are the 5 P's?
    • Pulseless
    • Palor
    • Pain
    • Paresthesia (numbness, tingling, "pins and needles")
    • Poikliothermia (red, scaley, skin)
  122. What is Berger's Syndrome?
    • affects small and medium size of arteries in hands and feet
    • smoking constricts the vessels
    • manifestations same as the 5 P's
    • Hands turn white when cold
  123. What is Reynold's Disease?
    affects small and medium sized arteries in the hands
  124. Remember what, when it comes to the order of the valves?
    • Toilet = Tricuspid Valve
    • Paper = Pulmonary Valve
    • Meets = Mitral Valve
    • Ass = Aortic Valve
  125. What is corpulmonale?
    • Right-sided heart failure because of fluid problem
    • Cystic Fibrosis
    • Emphysemia
    • Chronic Bronchitis
    • juggler vein distention
    • Edema - LOTS
    • will back into peripheries
    • liver and spleen enlarged
    • Chronic
  126. What is diastolic pressure?
    is a filling issue, pulmonary hypertension, corpulmonale
  127. What is Systolic pressure?
    inability to pump blood a contraction problem, increased afterload
  128. What is forward effects?
    • decreased CO = RAA (aldosterone = increased Na and water)
    • vasoconstriction
    • increased BP
    • increased HR

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