CV Final

  1. Why is the ventricular AP very long?
    inward calcium current: L-type Ca2+ channels --> longer plateau phase
  2. What is the trigger for excitation-contraction coupling in cardiac myocytes?
    • calcium-induced-calcium release
    • depolarization --> Na+ influx, triggers voltage-sensitive L-channels
    • calcium entering from T-tubule via L-channels (i.e. dihydropyridine)
    • triggers calcium elease from SR via ryanodine receptors
  3. How does calcium promote muscle contraction?
    • calcium stimulates troponin C
    • troponin C moves --> disinhibition of thick and thin filaments from each other
  4. How does an intracellular calcium burst relate to muscle contraction timing?
    intracellular calcium burst precedes muscle contraction/force generation
  5. What does a non-linear length-tension relationship of myocytes reflect?
    • steeply increasing stiffness with stretching
    • prevents overstretching
  6. What is the dominant component of the diastolic passive elastic property of cardiac muscle?
  7. What cardiac properties is connectin/titin responsible for?
    • diastolic passive elastic property
    • cardiac hypertrophy
    • stress-sensing
    • diastolic stiffening with diastolic heart failure
  8. Why does the force of contraction increase with increased muscle length?
    because of increased sensitivity to calcium
  9. What increases the force of a (cardiac) muscle contraction?
    • increased contractility
    • increased preload
    • increased muscle length
    • increased sensitivity to calcium
    • increased intracellular calcium
    • increased overlap between thick/thin filaments
    • increased passive force
    • increased shortening-velocity
    • increased SNS
    • increased heart rate

    decreased afterload
  10. What component of cardiac muscle is responsible for length dependent calcium sensitivity?
    troponin C
  11. Increase in what parameter results in cardiac dilatation?
    increasing volume
  12. Why is heart failure associated with cardiomegaly?
    heart failure --> decrease in contractility --> heart muscle lengthens to compensate and maintain force of contraction --> cardiomegaly

    i.e. during heart failure the heart takes advantage of the length-tension relationshiop
  13. What is responsible for the cardiac muscle length-tension relationship?
    increased sensitivity to calcium
  14. What determines length of cardiac muscle fibers?
    • preload
    • End Diastolic Volume
  15. What it used as a measure of left heart afterload?
    diastolic BP
  16. What affects stroke volume?
    • preload
    • afterload
    • contractility
  17. True/False: Stroke volume is a function of afterload.
  18. What does heart rate effect?
    • calcium kinetics
    • contractile strength
  19. Can a decreased heart rate ever increase the force of cardiac contraction?
    yes, during rest potentiation a decreased beat frequency may result in increased force of contraction
  20. What would you suspect if a patient has normal cardiac contractility but decreased cardiac performance?
    • leaky valves (i.e. regurgitation)
    • low blood volume
  21. What increases (cardiac) muscle contractility?
    • increased SNS discharge
    • increased epi/norepi
    • increased intracellular calcium
  22. What effects do epi and norepi have on cardiac myocytes?
    • increased contractility
    • increased rate of relaxation
    • increased force of contraction
    • increased peak force
    • increased rate of force develpment
  23. What effect does contractility have on stroke volume?
    increasing contractility increases the amount of shortening --> increased stroke volume
  24. When does the ejection fraction change?
    • systolic heart failure
    • increasing afterload --> decreasing ejection fraction
    • increasing contractility --> increasing efection fraction
    • changing preload --> no effect on efection fraction
  25. What are some clinical features of left ventricular systolic failure?
    • stroke volume stabilized by increased preload (i.e. increased muscle fiber length)
    • increased EDV
    • increased EDP
    • decreased Ef
    • unchanged afterload
    • cardiomegaly
  26. How can afterload reduction benefit a patient with severe systolic heart failure?
    decrease afterload --> decrease BP --> increase SV --> increase Ef
  27. Is cardiac myocyte relaxation a passive process?
    no: calcium actively pumped back into SR
  28. What does an ECG record?
    summation of millions of AP's over space/time
  29. What does the P wave signify in a cardiac cycle?
    slight atrial pressure increase
  30. In the cardiac cycle, what is signified by a R wave?
    increased ventricular pressure
  31. In the cardiac cycle, what is signified by a S wave?
    increased aortic pressure (isovolumetric contraction)
  32. In the cardiac cycle, what is signified by a T wave?
    peak aortic/ventricular pressure
  33. In the cardiac cycle, what is signified after the T wave?
    • isovolumic relaxation
    • decreased ventricular pressure (steep)
    • decreased aortic pressure (gradual)
  34. What is happening during isovolumic ventricular contraction?
    • ventricular pressure is still less than aortic pressure, aortic valve closed
    • pressure rises but volume remains constant
    • correlates to S wave on ECG
  35. What is happening during isovolumic relaxation?
    • ventricular pressure lower than aortic pressure and higher than atrial pressure, all valves closed
    • volume remains same as ventricular relaxation continues
  36. When does the ventricle fill with blood at the fastest rate?
    • rapid ventricular filling phase
    • i.e. phase F: ventricular pressure decreases --> atrial P > ventricular P --> mitral valve opens
    • i.e. immediately after mitral valve opens
    • i.e. early diastole
  37. What are the normal heart sounds? What produces them?
    • normal heart sounds are produced by closing of heart valves
    • S1 = AV valves closing
    • S2 = PV and Aortic (i.e. semilunar) valves closing
  38. What produces the atrial "a" wave?
    atrial contraction
  39. What produces the atrial "c" wave?
    ventricular contraction
  40. What is the "v" venous wave from?
    venous filling (relative to atria)
  41. Which closes first, aortic or pulmonic valves?
    aortic valves (esp. during inspiration)
  42. What could cause wide splitting of S2 (i.e. A2/P2) during inhalation and exhalation?
    • Right bundle branch block
    • pulmonic stenosis
  43. What can cause fixed splitting of the S2 heart sounds during inspiration and exspiration?
    atrial septal defect
  44. What could cause paradoxical splitting (i.e. reversal of P2/A2 sounds, splitting during exhalation and not inhalation)?
    • left bundle branch block
    • advanced aortic stenosis
    • Left-sided CHF
  45. What are the common causes of valvular heart disease and what are common risk factors?
    • causes:
    • congenital: aortic and pulmonic stenosis, tricuspid and mitral stenosis (rare), bicuspid aortic valve
    • degenerative: aortic stenosis and insufficiency, mitral insufficiency, mitral valve myxomatous disease
    • rheumatic: mitral sentosis/insufficiency, aortic stenosis/insufficiency
    • infectious: usually tricuspid, mitral, and aortic insufficiency

    • risk factors:
    • age
    • atherosclerosis risk factors
    • family history
    • hypertension
  46. What heart valves do rheumatic diseases generally affect?
    • mitral valve
    • aortic valve
    • usually both at same time
  47. What is the most common etiology of aortic stenosis today vs 30 years ago?
    • today: degenerative valvular disease
    • 30 years ago: bicuspid aortic valve (i.e. congenital)
  48. What is the least common etiology of aortic stenosis vs 30 years ago?
    • today: post-infectious (Group A Strep)
    • 30 years ago: degenerative valvular disease
  49. How can you measure added pressure load on heart in stenotic patients?
    measure pressure gradient across aortic valve (i.e. between LV and Aorta)
  50. What would you expect on clinical exam with a patient with aortic stenosis?
    • diminished and delayed upstroke = pulsus parvus et tardus
    • difference between systolic blood pressures of LV and aorta (i.e. increased LV afterload)
    • harsh diamond-shaped systolic murmur: RUSB radiating to carotids
    • S4: increased stiffness
    • strong PMI
    • pulmonary congestion
  51. What are the clinical consequences of aortic stenosis?
    • outflow obstruction:
    • unable to increase SV with decrease in SVR, i.e. resistance does not drop normally
    • syncope

    • LV wall stress:
    • increased O2 demand
    • chest pain

    • LV thickness:
    • ECG and echo findings
    • impaired diastolic function

    • LA size:
    • atrial fibrillation

    • PV pressure:
    • pulmonary congestion/edema
    • dyspnea on exertion
  52. What are the 3 main components of the Bernoulli equation and which is most important with stenotic valves?
    • 1. convective acceleration
    • 2. flow acceleration
    • 3. viscous friction

    stenotic valves: convective acceleration component predominates
  53. What is useful about the Bernoulli equation and CV?
    can calculate effects of increased flow rates through valves/vessels
  54. What are some pathological causes of a change in cardiac output?
    • stenosis
    • shock
    • fever
    • anemia
  55. What are some normal causes of a change in cardiac output?
    • pregnancy
    • exercise
  56. What are some common treatments for aortic stenosis?
    • aortic stenosis = mechanical problem, treatment = mechanical solution
    • mechanical valve replacement
    • valve grafts
    • balloon valvuloplasty

    anticoagulation therapy (prevent thrombus)

    treatment usually only for symptomatic patients
  57. What are the clinical consequences of mitral stenosis?
    • valve gradient:
    • need for long diastolic period
    • sensitivity to high heart rates
    • dyspnea onexertion

    • LA enlargement:
    • atrial fibrillation
    • stasis
    • thrombus formation
    • emboli

    • pulmonary venous congestion:
    • shortness of breath
    • dyspnea on exertion

    • physical exam:
    • harsh diastolic murmur (apex)
    • opening "snap"
  58. In a patient with aortic stenosis, what is the average survival rate for a person with angina, syncope, CHF, and/or atrial fibrillation?
    • angina: 5 yrs
    • syncope: 3 yrs
    • CHF: 2 yrs
    • Atrial fibrillation: 6 mo
  59. What are some common treatments for mitral stenosis?
    • many non-surgical options, unlike with aortic stenosis
    • maintenance of sinus rhythm: medication
    • balloon valvulplasty
  60. What are some common etiologies of mitral insufficiency?
    • myxomatous degeneration
    • mitral annular dilation
    • ruptured mitral chordae tendinae
    • ventricular dilation
    • ischemic disease
    • leaflet/chord abnormality (congenital, rheumatic, infectious)

    (mitral valve prolapse: CT disorders, Marfan's, myxomatous degenerative disease)
  61. What are some common clinical findings for mitral regurgitation?
    • increased PVP --> pulmonary congestion, dyspnea
    • right-heart failure uncommon
    • holosystolic murmur at apex
    • ECG: LA enlargement, AF
    • CXR: LA and LV enlargement
    • rate of progression is highly variable
  62. How is mitral regurgitation treated?
    • trace/mild mitral regurgitation = common normal variant
    • main treatment = diuretics
    • i.e. main treatment = reduce afterload

    • severe:
    • 45% 5 yr survival
    • surgical repair of valve
  63. What are common etiologies of mitral valve prolapse?
    • genetic CT disorders: Marfan's, Ehlers-Danlos
    • myxomatous degeneration
    • normal variant
  64. What are common etiologies for aortic insufficiency?
    • rheumatic
    • congenital: bicuspid aortic valve
    • degenerative
    • infectious
    • annular dilation: from asc. aorta dilation
  65. How does left ventricular pressure relate to coronary artery flow?
    increased LV pressure --> decreased cornary artery blood flow
  66. What are common clinical findings of aortic insufficiency?
    • dyspnea (most common)
    • angina/palpitations (less common)
    • wide pulse pressure (Corrigan's pulse)
    • head bob (de Musset)
    • capillary pulsations (Quincke's sign)
    • diastolic flow reversal (Duroziez's sign)
    • diastolic, decresendo murmur
    • CXR: cardiomegaly

    **left ventricular dilation/dysfunction
  67. How do the effects of vasodilators differ from aortic and mitral insufficiencies?
    • vasodilators: reduce afterload
    • mitral insufficiency: vasodilators relieve symptoms
    • aortic insufficiency: vasodilators slow progression of disease
  68. What is the prognosis for someone with severe aortic insufficiency?
    • severe AR but normal LV and asymptomatic: good 10 year prognosis
    • angina: 4 year survival
    • CHF: 2 year survival
    • vasodilators can
    • diuretics can reduce symtpoms
    • surgical options
  69. What are the pathological heart sounds? What causes them? Can they ever be "normal"?
    • S3 = early ventricular filling, always pathological
    • S4 = atrial filling, can be normal
  70. How are heart murmurs described?
    • timing: systolic, diastolic, continuous
    • intensity: systolic grade +3 = pathological , diastolic grade +1 = pathological
    • pitch/character: high frequency = high gradient
    • shape: de/crescendo
    • location: near source
    • radiation: direction of flow
    • maneuvers
  71. What are some common correlates to cardiac output?
    • CO is dependent on SV and HR
    • decreases with age
    • decreases with supination (i.e. sitting/standing up)
  72. What can cause an error in calculating Fick cardiac ouput?
    • anything that can change the oxygen content of blood/air of vlume of air
    • improper technique
    • perforated ear drums
    • change in resting lung volume
    • small air bubbles in syringes
  73. What is the effective cardiac output and how is it measured?
    • effective cardiac output = amount of blood actually being pumped throughout the body
    • measured by Fick equation (i.e. O2 consumption)
  74. How is cardiac output determined?
    • 1. effective cardiac output: effective transport (Fick equation), dilution method (temp. indicator)
    • 2. stroke volume: volumetric techniques (imaging), flow techniques (Doppler)
  75. What are the common causes of acute rheumatic fever?
    • causes:
    • autoimmune complication of Strep pyogenes Group A beta-hemolytic pharyngitis
    • bacterial glycoproteins similar to cardiac antigens (valve glycoproteins, sarcolemmal/smooth muscle)
    • possibly direct toxic effect by bacteria endotoxins
  76. What are common clinical features of acute rheumatic fever?
    • pancarditis: all layers of the heart
    • pericarditis: effusions, fibrin deposition
    • myocarditis: lymphocyte/macrophage infiltration
    • Aschoff bodies: fibrinoid necrosis, myocyte loss, lymphocyte/marophage infiltration
    • endocarditis: ulceration, collagen damage
  77. What are some common causes of chronic rheumatic heart diseae?
    • causes:
    • develops 10-30 years after initial episode of rheumatic fever
    • chronic inflammation and scarring of cardiac valves and chordae tendinae
    • mitral valve > mitral + aortic > aortic > tricuspid > pulmonic
  78. What is the most common cause of mitral stenosis?
    chronic rheumatic heart disease
  79. What is the most common cause of mitral regurgitation?
    (asymptomatic) mitral valve prolapse
  80. What are some common clinical features of chronic rheumatic heart disease?
    • inflammation/scarring of (mitral/aortic) valves and chordae tendinae
    • fusion of valvular commissures
    • fusion/shortening of chordae tendinae
    • valvular stenosis: fusion of valves
    • valvular regurgitation: rigid leaflets, short chordae

    • complications:
    • atrial fibrillation
    • thrombosis
    • pulmonary hypertension
    • right- and left- sided heart failure
  81. What are some common findings with mitral valve prolapse?
    • genetic CT disorders: Marfan's, Ehler's-Danlos
    • myxomatous tissue degeneration --> gelatinous appearance
    • fragmentation of collagen fibers
    • redundant valvular leaflets
    • myxomatous tissue in CT
  82. What is clinically significant about calcification of the mitral valve annulus?
    • common in elderly, usually asymptomatic
    • can interfere with valve closure
    • can cause regurgitation
    • can affect valvular leaflets and interventricular septum
  83. What are the 3 main ways a myocardial infarction can cause mitral regurgitation?
    • 1. dilation of mitral valve annulus
    • 2. papillary muscle rupture
    • 3. papillary muscle dysfunction/scarring
  84. What are the main pathological findings of fibrocalcific aortic stenosis?
    • nodular fibrosis of leaflets
    • marked calcification
    • inflammatory cell accumulation
    • serum-derived lipids
  85. What are common complications of fibrocalcific aortic stenosis?
    • aortic stenosis
    • aortic regurgitation
    • LV hypertrophy
    • myocardial ischemia --> MI
    • arrhythmias
    • sudden death
  86. What are the common features of Marfan's syndrome?
    • genetic CT disorder: autosomal dominant
    • genes: fibrillin, microfibrils
    • musculoskeletal abnormalities (e.g. arachnodactly)
    • CV structural complications
    • mitral valve prolapse
    • mitral regurgitation (kids)
    • aortic regurgitation (adults)
    • aneurysms
    • **cystic medial degeneration
  87. What is tricuspid stenosis usually from?
    • rheumatic disease
    • mitral disease
  88. What usually causes tricuspid regurgitation?
    • dilation of tricuspid annulus: pressure/volume overload
    • (i.e. rarely a primary valvular disease)
  89. What usually causes pulmonary valve stenosis?
    congenital abnormailty: Tetralogy of Fallot, isolated pulmonary stenosis
  90. What usually causes pulmonary valve regurgitation?
    • dilation of the valve annulus
    • severe pulmonary hypertension
  91. What is the most common cause of infectious endocarditis? rarest?
    • most common: bacterial endocarditis
    • rarest: fungal endocarditis
  92. What are predisposing factors to developing infectious endocarditis?
    • abnormal valves (e.g. bicuspid aortic valve, congenitally stenotic valves, rheumatic valves, MVP, fibrocalcific valves)
    • prosthetic valves
    • IV drug use (S. aureus most common)
    • Iatrogenic bacteremia (e.g. dental procedures, urinary catheterization)
  93. What are common clinical features of infectious endocraditis? complications?
    • vegetations
    • inflammed myocardial tissue

    • complications:
    • valve perforation
    • CHF
    • septic embolization
    • immune complex glomerulonephritis
  94. What is non-bacterial thrombotic endocardosis?
    • a.k.a. Marantic (Wasting) Endocarditis
    • sterile vegetations
    • vegetations can be colonized --> infectious endocarditis
    • unknown mechanism
    • associated with wasting syndromes, end stage cancers
  95. What causes carcinoid heart disease?
    • neuroendocrine tumors
    • overproduction of serotonin, bradykinin, histamine, prostaglandins
    • stimulate fibroblastic cells in endocardium, chordae, valve leaflets

    i.e. overproduction hormones resulting in overproduction of ECM in myocardium
  96. What are the common clinical features of carcinoid heart disease?
    • fibrosing valvular disease
    • fusion of chordae
    • fibrous plaques on leaflets
    • lesions are predominantly right-sided
  97. How do carcinoid heart disease, drug-induced valvular disease, and chronic rheumatic heart disease present differently clinically?
    • carcinoid heart disease: predominance of right-sided lesions
    • drug-induced valvular disease: predominance of left-sided lesions
  98. What causes drug-induced valvular disease?
    • serotonergic drugs: methylsergide, ergotamines
    • appetitie suppressants: fenfluramine
  99. What physical factors determine the rate of fluid flow (i.e. resistance) through a tube?
    • viscosity of the fluid
    • radius of the tube
    • length of the tube
  100. How does the Poiseuille equation relate to CV?
    • shows the relationship between flow and resistance
    • flow occurs only when there is a pressure difference
    • small changes in radius result in large changes in resistance
  101. What does the ascending limb of the arterial pulse wave represent?
    rapid ventricular ejection
  102. What does the incisura/dicrotic notch of the arterial pulse wave represent?
    • aortic valve closure
    • end of systole
  103. What does the apex the arterial pulse wave represent? the nadir?
    • apex = systolic pressure
    • nadir = diastolic pressure
  104. What is the pulse pressure?
    pulse pressure = systolic - diastolic pressure = apex - nadir of arterial pulse wave
  105. How is mean arterial pressure determined?
    • MAP = average pressure over time
    • MAP = baseline of arterial pulse wave
    • sphygmomanometer on brachial artery
    • MAP = diastolic pressure + 1/3 pulse pressure
  106. How does the heart make peripheral blood flow less pulsatile?
    • arterial tree is distensible (Windkessel effect)
    • elastic recoil of arteries preparing for diastole
    • artery recoil ejects part of stroke volume that remains after systole
  107. Why does pulse pressure increase with age?
    • inreasing age relates to decreasing arterial compliance
    • i.e. increasing age relates to increasing hardening of arteries
  108. What are the Korotkoff sounds when using a sphygmomonometer?
    • 1st sound = cuff pressure falls below systolic pressure, intermittent systolic squirts
    • 1st sound increases in amplitude until muffled during diastole
    • 2nd sound = disspearance of 1st sound, diastolic pressure
  109. What is mean transmural pressure?
    • meaured with a sphygmomanometer
    • equal to blood pressure when the subject is lying down
    • affected by hydrostatic effect if not meaured at heart level
  110. Does the arterial pulse wave amplitude increase or decrease as it travels down the arterial tree?
    • increases with arterial tree progression
    • increase in systolic pressure, decrease in diastolic pressure
    • **mean pressure declines
  111. Why is the total resistance of the capillary bed less than the arteriolar bed even though they are narrower?
    capillary bed = several parallel resistor systems
  112. What are the 3 harmonic changes in the arterial pulse wave as it progresses through the arterial tree?
    • reflections: increase systole, decrease diastole
    • harmonic dispersion: high frequency waves faster than low frequency
    • elastic tapering: decreased compliance relates to increased amplitude
  113. True/False: It is normal for the ankle systolic pressure to be less than or equal to the systolic pressure measured in the upper arm.
    • False
    • It is normal the ankle systolic pressure to be 20mmHg higher than the systolic pressure of the upper arm.
  114. True/False: Intracellular free Ca2+ can occur both with and without changes inthe membrane potential.
    • True
    • electromechanical coupling
    • pharmacomechanical coupling
  115. How is the effect of caclium on muscle contraction different for smooth muscle and skeletal/cardiac muscle?
    • skeletal/cardiac muscle: calcium --> troponin C disinhibits actin --> faster ATP consumption
    • smooth muscle: calcium --> calmodulin --> activates/phosphorylates myosin --> slower ATP consumption
  116. Through which range of arterial pressure is autoregulation active?
  117. Which cranial nerve innervates the carotid sinus?
    CN IX: glossopharyngeal
  118. What happens when the carotid sinus baroreceptors are stretched?
    • decrease in heart rate
    • arterial pressure reflexively decreases
  119. How is the SA node innervated?
    • PNS: CN X
    • SNS: bulbospinal pathway
  120. What areas of the heart are supplied by the left coronary artery?
    • anterior portion of interventricular septum
    • anterior wall of RV
    • LA
    • LV
  121. What areas of the heart are supplied by the right coronary artery?
    • posterior portion of the interventricular septum (dominant right coronary artery)
    • RA
    • posterior RV
  122. What are Thebesian veins?
    • veins that drain directly into the ventricular and atrial chambers wihtout passing through an epicardial vein
    • shunts with unknown functions
  123. How is coronary blood flow regulated?
    • autoregulation (60-140mmHg)
    • strong metabolic control: flow higher for greater level of metabolism
    • below 60mmHg: maximal dilation: small drop in pressure decreases flow greatly
    • large during diastole, small during systole: myocardium squeezes on own blood flow during systole
    • small flow during systole: increased aortic pressure
    • subendocardium perfused first, then subepicardium: tissue pressure gradient, waterfall third pressure
    • Nitric Oxide --> increases cGMP --> vasodilation
  124. What can threaten subendocardial perfusion?
    • decreases in diastolic pressure difference across aortic valve (e.g. hypotension)
    • shortened diastole (e.g. tachycardia)
    • prevention of autoregulatory vasodilation
    • decrease in coronary blood flow (e.g. atherosclerosis)
  125. Why is cardiac oxygen consumption almost the same as overall myocardial metabolism?
    barely any anaerobic respiration, even in resting cardiac muscle
  126. Where does the most blood oxygen extraction occur in the body?
    coronary artery flow: 70% of oxygen extracted by myocardium
  127. What is clinically useful about the "double product"?
    • double product = Heart Rate x Systolic BP
    • i.e. = heart rate x tension development

    indicates myocardial oxygen consumption
  128. What are the ranges of critical coronary artery stenosis?
    • at rest: 90% diameter narrowing
    • during increased blood flow/exercise: 40% diameter narrowing
  129. What are the 3 main causes of subendocardial ishemia during exertion?
    • 1. exponential pressure drop across a stenosis as a function of flow
    • 2. exhaustion of vasodilation reserve
    • 3. tachycardia during exercise
  130. What causes the majority of CHD events (e.g. heart attack, unstable angina, sudden cardiac death)?
    epicardial coronary atherosclerosis
  131. What are risk factors for developing atherosclerosis?
    age: look at 40yo, esp 50+yo

    gender: male

    • lipid disorders:
    • elevated total cholesterol (more than 240mg/dL)
    • elevated triglycerides (>150mg/dL)
    • elevated LDL
    • elevated LDL:HDL ratio (risk when ration >5)
    • elevated apo B
    • low HDL (less than 40mg/dl for men, less than 50mg/dl for women)
    • low apo A1
    • elevated ratio total cholesterol: HDL (risk when ratio greater than 5-6)
    • elevated ratio of apo B: apo A1
    • elevated lipoprotein and lipoprotein-associated phospholipase A2

    hypertension: SBP above 115mmHg


    diabetes: types I and II

    • obesity:
    • elevated BMI
    • elevated waist to hip ratio (> 1.6)
    • sedentary lifestyle

    • endothelial injury/activation:
    • elevated C reactive protein
    • increased oxidant stress
    • increased physical stress
    • altered shear stress
  132. What are some correlates of low endothelial shear stress?
    • low blood flow
    • increased oxidative sterss on endothelium
    • attenuation of nitric oxide inflammation
    • LDL cholesterol uptake
    • LDL permeability
    • smooth muscle cell migration
  133. When does coronary remodeling take place?
    lumen diameter is maintained until the plaque area increases to 40% of total cross-sectional area

    when plaque area is greater than 40% of lumen, compensatory expansion is overcome and lumen narrows
  134. What predisposes a coronary artery to developing an aneurysm?
    • atherosclerosis
    • lesions with excessive expansive remodeling
    • lesions with thin fibrous cap
    • intense inflammation
  135. What can cause a cornary thrombus?
    • plaque disruption, rupture of fibrous cap
    • endothelial erosion, no fibrous cap disruption
    • intra-plaque hemorrhage, no fibrous cap disruption
  136. What makes a coronary plaque more likely to rupture?
    • thin fibrous cap overlying a large necrotic lipid core
    • presence of inflammatory cells in fibrous cap: foam cells, T-cells --> proteases (MMP); interferon-gamma
    • extensive expansive remodeling
    • minimal/mild lumen narrowing
    • neovessels within plaque
    • pro-thrombotic state
    • previous asymptomatic coronary embolism episodes
    • emotional stress
    • (sudden) physical exertion
  137. True/False: The presence of matrix metalloproteinases (MMP) indicates that a coronary plaque is less likely to rupture.
    • False
    • The presence of matrix metalloproteinases (MMP) indicates that a coronary plaque is MORE likely to rupture.
  138. What is characterized by metabolic syndrome?
    • combination of 3 or more of following:
    • central obesity
    • low HDL
    • elevated triglycerides
    • hypertension
    • glucose intolerance
    • diabetes
  139. According to the Framingham Interheart Study, what are the 9 reasons that 90% of people get myocardial infarctions?
    • elevated apoB/apoA1 ratio (esp. decreased A1)
    • smoking
    • hypertension
    • diabetes
    • central obesity
    • psychosocial stress
    • sedentary lifestyle
    • lower consumption of fruits and vegetables
    • lower consumption of alcohol
  140. What commonly causes stable angina?
    • fixed coronary obstruction: limits maximal coronary blood flow
    • maximal coronary blood flow reduced when coronary lesion exceeds 60-70% diameter stenosis

    marked increase in O2 demand with normal coronary flow: aortic stenosis, hypertrophic cardiomyopathy, dynamic outflow tract obstruction

    increased afterload
  141. Why do patients with aortic stenosis present with stable angina?
    • elevated ventricular wall stress
    • low diastolic blood pressure
  142. What are clinical features of classic angina?
    • Levine's sign: clenched fist over chest
    • substernal chest pressure/tightness
    • can radiate to arms, neck, jaw
    • associated with dyspnea, nausea, diaphoresis
  143. What exercise test outcomes are associated with high MI risk?
    • poor exercise capacity (<5 METs)
    • poor heart rate repsonse from rest to exercise (chronotropic incompetence)
    • fall in blood pressure during exercise, especially below baseline
    • poor heart rate recovery in the first minute of recovery (<12bpm)
    • exercise-induced ventricular tachycardia
    • high density of PVCs, ventricular couplets, or non-sustained ventricular tachycardia during recovery
  144. What are the variables of the Duke Score of heart disease risk?
    • exercise capacity
    • horizontal/downsloing ST depression
    • angina
  145. How is atherosclerosis diagnosed?
    • clinical history
    • stress test/exercise capacity
    • calcium deposition
    • noninvasive imaging: CT, MRI, angiography, intracoronary ultrasound
  146. Why does coronary angiography miss early-stage atherosclerosis?
    cornary artery lumen narrowing only happens at later stages of atherosclerosis
  147. In the absence of high risk findins, what should be the medical treatment of someone with angina/ischemia?
    • aspirin: reduce risk of ACS
    • nitrates: lower preload, vasodilator
    • beta-blockers: lower HR, lower BP, lower O2 demand
    • calcium-channel blockers: lower HR, lower BP, lower O2 demand
    • sodium-channel blockers: e.g. ranolazine
    • lipid-lowering therapy (e.g. statins): reduce risk of ACS, lower mortality
  148. What are some common complications of MI?
    • embolism
    • ischemia
    • decreased coronary perfusion
    • cardiogenic shock
    • arrhythmias
    • pericarditis
    • papillary muscle infarction/ischemia
    • mitral regurgitation
    • ventricular septal defect
    • ventricular rupture
    • cardiac tamponade
    • CHF
  149. What are the 3 basic components of cardiogenic shock?
    • 1. decreased coronary perfusion
    • 2. ventricular dysfunction: increased ischemia
    • 3. hypotension
  150. What are risk factors for developing NSTEMI?
    • (possible) ECG changes: ST depression, T wave inversion, tansient ST elevation
    • hypotension: hemodynamic instability
    • presentation with heart failure (e.g. pulmonary congestion)
    • recurrent angina despite initial medical therapy
    • elevated cardiac enzymes
  151. What are the vairiable sin teh GRACE Risk Score?
    • age
    • systolic blood pressure
    • heart rate
    • serum creatinine
    • Killip class: symptoms
    • cardiac arrest at admission
    • elevated cardiac enzymes
    • ST segment deviation
  152. What are the 3 basic embyrological principles that determine cardiac development?
    • 1. function of endocardial cushion
    • 2. division of turncus arteriosus
    • 3. role of flow
  153. What is the function of the foramen ovale and ostium secundum in fetal circulation?
    • permits right-to-left flow
    • prevents left-to-right flow
  154. Where are the most common ventricular septal defects?
    membranous septum (last to develop)
  155. Where are the most common atrial septal defects?
    ostium secumdum: last to develop
  156. What structures develop from the endocardial cushion?
    • atrial septum
    • ventricular septum
    • mital valve: anterior leaflet continuity with aorta
    • tricuspid valve
    • offset of AV valves
  157. What are some common endocardial cushion defects?
    • primum atrial septal defect
    • inlet type of ventricular defect
    • cleft anterior mitral leaflet
    • cleft septal tricuspid leaflet
    • AVSD: atrioventricular septal defect
  158. What describes an AVSD?
    atrioventricular septal defect

    • requirements:
    • 1. cleft anterior mitral leaflet
    • 2. cleft septal tricuspid leaflet
    • 3. loss of offset between valves

    also: primum atrial septal defect, inlet ventricular septal defect
  159. What types of complications can arise from dysfunctional truncus arteriosus develpment?
    • septation, no twist:
    • TGA

    • twist, incomplete septation:
    • aorto-pulmonary window

    • displacement of septum:
    • (anterior) Tetralogy of Fallot
    • (anterior) double outlet LV
    • (posterior) double outlet RV
  160. What is related to tricuspic atresia in cardiac develpment?
    hypoplastic RV, Pulmonic valve, PA
  161. What is related to mitral atresia in cardiac develpment?
    hypoplastic LV, Aortic valve, ascending aorta
  162. How does fetal ciculation maintain flow with tricuspic atresia, mitral atresia, and/or other blood flow defects?
    • other "side" of heart still functional
    • ductus arteriosus: right-to-left shunt in pulmonary artery to asc. aorta
  163. What causes hypoplastic left heart syndrome?
    • severe mitral stenosis
    • mitral atresia --> hypoplastic LV, Aortic valve, Asc. Aorta
  164. What causes a "peach-pit" right ventricle?
    • pulmonary stenosis/atresia: right ventricle is exposed to a pressure load while there is little flow
    • simultaneous RV hypoplasia and hypertrophy

    • pulmonary stenosis --> pulmonary atresia:
    • hypoplastic pulmonary vein
    • hypoplastic pulmonary artery
    • hypoplastic right ventricle
    • hypertrophic right ventricle
  165. How does fetal circulation accomodate high vascular resistance in lungs and prevent right ventricular pressure overload?
    • ductus arteriosus: alternate outlet for RV blood flow
    • foramen ovale: prevents backup in RA
  166. What is are the immediate post-partum changes to fetal circulation?
    • first breath:
    • 1. pulmonary vascular resistance decreases
    • 2. lung blood flow increases
    • 3. sytemic blood flow decreases
    • 4. ductus arteriosus shunt reverses to become L-to-R shunt
    • 5. increased pulmonary flow --> increased left atrial pressure --> closure of foramen ovale
    • 6. ductus arteriosus closes (~days)
    • 7. ductus venosus obliterates (~weeks)
    • 8. ductus arteriosus obliterates (~1year)
    • 9. foramen ovale obliterates (~decades)
  167. What is clinically significant about a patent foramen ovale?
    • normal variant
    • prevalence depends on age distribution
    • increased risk for paradoxical embolization
    • increased risk for migraines (?)
  168. What is the most common clinical sign of a congenital heart defect?
    heart murmur (not specific)

    • cyanosis
    • abnormal heart sounds (e.g. splitting of A2/P2)
    • cyanosis
    • pulmonary edema, dyspnea
    • rales
  169. True/False: Most congenital heart defects involve isolated lesions.
  170. What are the 3 "levels" of congenital heart defects?
    • ASD
    • VSD
    • open ductus arteriosus
  171. What is the most common ASD?
    (ostium) secundum ASD
  172. What are common signs of ASD?
    • RV dilation
    • RA dilation
    • murmur
  173. True/False: Most patients with an ASD are symptomatic.
    • False
    • Most patients with an ASD are asymptomatic.
  174. What is Eisenmenger's syndrome?
    abnormally high blood flow through lungs --> permanent damage of pulmunary arterioles --> permanent elevation of pulmonary vascular resistance --> reversal of shunt to R-to-L

    • direct repair of defect not possible
    • permanent lung damage
  175. Which congenital heart defects are likely to develop Eisenmenger's syndrome?
    • increaesd pulmonary circuit blood flow
    • ASD
    • VSD
    • patent ductus arteriosus
  176. What can keep a ductus arteriosus open?
  177. What promotes ductus arteriosus closure?
    • prostaglandin inhibitors
    • e.g. indomethacin
  178. What is coarctation of the aorta?
    significant narrowing of aorta
  179. What is the most common location for a coarctation of the aorta?
    • juxtaductal coarcatation: area in descending aorta near where the ductus arteriosus is
    • preductal coarctation: hypoplasia of aortic arch
  180. What are long-term complications of coarctation?
    • re-coarctation
    • late hypertension
    • aneurysm
    • cardiac defects
  181. What can lead to an increase in systolic loads (pressure) and cause hypertrophy?
    • RV:
    • pulmonary stenosis
    • peripheral pulmonic stenosis
    • pulmonary hypertension

    • LV:
    • aortic stenosis
    • coarctation
    • systemic hypertension
  182. Which shunts are cyanotic?
    Right to left: mix deoxygenated blood with oxygenated blood
  183. What is the direction of shunt resulting from an isolated, restrictive defect?
    Left to Right: follows normal pressure gradient
  184. What can cause right-to-left shunts or reversal of left-to-right shunts?
    • Eisenmenger's syndrome
    • tricuspid stenosis
    • pulmonary stenosis
    • pulmonary hypertension
    • decreased systemic arterial pressure
    • preductal coarctation (with hypoplasia of aorta)
    • Valsalva effect
    • any condition which raises the RV EDP
    • any condition where QP<QS
  185. What are common consequences of shunts?
    chamber enlargement: ASD --> RA/RV dilation; VSD --> LA/LV dilation

    • L-to-R:
    • pulmonary hypertension --> Eisenmenger's syndrome
    • endocarditis (not ASD)
    • heart failure
    • decreased exercise tolerance (decreased cardiac function, normal O2 sat)

    • R-to-L:
    • systemic emboli
    • polycythemia
    • hyperviscosity
    • decreased exercise tolerance (decreased oxygen saturation)
    • hypoxemic spells
  186. What are the ductus dependent lesions?
    • systemic flow obstruction:
    • mitral atresia
    • coarctation
    • aortic stenosis

    • pulmonary flow obstruction:
    • tricuspid atresia
    • tetralogy of Fallot
    • pulmonary stenosis

    • no other connections:
    • TGA
  187. Which murmurs are usually pathological?
    • diastolic murmurs
    • continuous murmurs
    • >grade3
    • harsh murmurs
    • radiating murmurs
  188. What are some normal murmurs?
    functional/flow murmurs

    • stills
    • pulmonic
    • venous hum
    • subclavian bruit
  189. When should you administer PGE2 to an infant? What are counter-indications?
    clinical signs of ductus dependent congenital heart defect

    • sx:
    • failure to thrive
    • cyanosis
    • shock
    • acidosis
    • murmur
    • differential pulses

    • dx:
    • TGA
    • pulm. stenosis
    • aortic stenosis
    • mitral atresia
    • tricuspid atresia
    • coarctation
    • tetralogy of Fallot

    • counterindications:
    • difficult birth
    • respiratory distress
    • prematurity
  190. What are the 3 main causes of edema?
    • increased capillary hydrostatic pressure: increased venous pressure in heart failure
    • reduced capillary osmotic pressure: nephrotic syndrome, liver disease
    • increased tissue oncotic pressure: filariasis, tissue injury (changes permeability)
  191. How does arteriole pressure change affect capillary pressure?
    • increasing arteriole pressure --> decreases capillary pressure
    • decreasing arteriole pressure --> increases capillary pressure
  192. What part of the heart is most posterior?
    left atrium
  193. Why choose a lateral view of heart with CXR than A-to-P view?
    • lateral view:
    • inspect right ventricle
    • (better) left atrium inspection

    • A-to-P view:
    • right ventricle obscured
  194. What are common radiographic findings in heart failure?
    • cardiomegaly
    • enlarged lung vessels, equalization, rarely cephalization
    • edema: Kerley B lines, "fluffy" or hazy alveolar filling
    • pleural effusions
  195. What are common sites and causes of calcification as seen with CXR?
    • pericardium: viral, TB, other chronic pericarditis
    • coronary artery: atherosclerosis
    • myocardium: remote infarction, rheumatic disease
    • valve: sclerosis, degeneration, rheumatic disease
  196. What is the sequence of the myocardial ischemia cascade?
    • ischemia: perfusion abnormailities
    • diastolic and regional systolic dysfunction: wall motion abnormalities
    • ECG changes: electrical transit abnormalities
    • chest pain: angina, MI, death
  197. Which vessel layers are disturbed in a pseudoaneurysm? true aneurysm?
    • pseudoaneurysm: always t. intima and t. media layers involved, sometimes t. adventitia intact
    • true aneurysm: all layers involved
  198. Where do Berry aneurysms typically develop?
    • cerebral vessels
    • near Circle of Willis
  199. What is the most common cause of pseudoaneurysms?
    • catheter puncture sites: femoral artery
    • break-down of suture lines of bypass grafts swen to femoral arteries
  200. What is the most common cause of peripheral arterial aneurysms?
    • artherosclerosis (not from occlusion; from direct arterial wall degeneration)
    • (genetic CT disorders)
  201. What are common causes of mycotic aneurysms?
    • bacteremia: following dental work
    • cholecystits (Salmonella)
    • syphilis
  202. True/False: Aneurysms are typically lined with thrombi due to blood stasis.
  203. True/False: Arteriograms of a patient with an aneurysm may appear normal.
    • True
    • Arteriograms only demonstrate flowing blood, not stasis
  204. What is the classic triad of aneurysm symptoms indicating surgery?
    • abdominal pain
    • hypotension
    • palpable, pulsatile abdominal mass

    (impending rupture: sudden back/abdominal tenderness)
  205. What is the most common cause of aortic dissection?
  206. Where are the most common sites of aortic dissection? common treatments?
    • sites:
    • most commonly begins beyond the arch vessels
    • spirals down into iliac vessels

    • tx:
    • reduce HTN
    • vasodilators (e.g. nitroprusside)
    • beta antagonists
    • severe: surgical replacement of aorta
  207. What are symptoms of aortic dissection?
    • acute onset of tearing back pain
    • symptoms associated with occlusion of branch vessels
    • involvement of other arteries: stroke, renal failure, mesenteric ischemia

    ascending aorta dissection: acute aortic insufficiency, occlusion of coronary arteries, causing acute myocardial ischemia, dissection into pericardium, pericardial tamponade
  208. What is acute ischemia and what causes it?
    acute ischemia = sudden decrease in blood flow +/- sudden increase in myocardial O2 demand

    • causes:
    • embolism
    • thrombotic occlusion: atherosclerotic plaque
    • aorta dissection
    • traumatic disruption
    • vasospasm: drugs
  209. What are some potential complications of acute ischemia?
    • CHF
    • renal failure
    • collateral circulation: vasculogenesis, angiogenesis
    • loss of limb
  210. What are the 6 P's of acute ischemia?
    • Pain
    • Pallor
    • Poikilothermia (cold)
    • Pulselessness
    • Parasthesia (numbness)
    • Paralysis (weakness)
  211. What are the typical treatments for acute ischemia?
    • anticoagulation therapy: heparin
    • surgical thrombectomy, embelectomy, bypass
    • thrombo-lytic agents: catheter-directed, tissue-plasminogen-activation factor
    • revascularization (systemic and local complications: compartment syndrome, hyperkalemia, etc.)
  212. What causes compartment syndrome? what are its symptoms?
    leaking of capillaries caused by reperfusion injury within muscular fascial compartments

    • symptoms:
    • tense compartment
    • pain on passive stretch
    • loss of sensation
    • motor weakness
  213. How is acute hyperkalemia treated?
    glucose/insulin IV (some bicarbonate)
  214. What is Buerger's disease? What causes it and what are its symptoms?
    Brueger's disease = thromoangitis obliterans = inflammatory process of small/medium blood vessels related to smoking addiction

    causes: occlusion of distal tibial/digital arteries

    symptoms: ulcers of tips of fingers and toes, loss of digits
  215. How is acute myoglobinemia treated?
    • fluid, osmotic diuretics (e.g. mannitol)
    • bicarbonate
  216. True/False: In a patient with intermittent claudication, their chance of losing a limb at 10 years is greater than losing their life.
    • False
    • In a patient with intermittent claudication their chance of losing a limb at 10 years is 22% and chance of losing life is 61%.
  217. What are varicose veins and which veins are commonly affected?
    varicose veins = enlarged superficial veins, veins elongate and widen, benign

    common site: branches of saphenous veins (greater and lesser)
  218. What is Virchow's triad of deep vein thrombosis? How are these related to risk factors?
    • damage to endothelium (e.g. inflammation, smoking)
    • stasis (e.g. sedentary lifestyle, immobilization, aneurysm)
    • hypercoagulable state (e.g. genetic disorders, pregnancy, cancer, etc.)
  219. What are (7) major risk factors for DVT?
    • age
    • prior history of DVT
    • major surgical procedure
    • malignancy
    • genetic procoagulant abnormalities
    • estrogen drugs
    • acute paraplegia
  220. What does a (-) d-dimer test rule out?
    pulmonary embolism
  221. What are the signs/symptoms of a pulmonary embolism?
    • decreased osygenation
    • hyperventilation
    • hypotension
    • intravascular thrombosis
    • (+) d-dimer levels
  222. What is post-thrombotic syndrome?
    post-thrombotic syndrome = long-term result of chronic ambulatory venous hypertension due to valve damage and loss of calf-pump mechanism

    mechanism: increased capillary pressure results in exudation of protein into interstitial space, calf narrows at ankle, RBC infiltrate tissue --> hyperpigmentation
  223. How are venous ulcers different from arterial ulcers?
    arterial ulcers = dry, pale, painful, toes-distal foot

    venous ulcers = moist, pink, ankle-mid calf
  224. What is carotid disease associated with embolization of plaque and not actual arterial occlusion?
    intracerebral circulation has rich collateralization: Circle of Willis
  225. Where does carotid heart disease typically occur and why?
    • common site: bifurcation in neck
    • why: low, oscillating shear
  226. What are the common symptoms of carotid disease?
    • focal, hemispheric neurologic deficits
    • contralateral numbness
    • contralateral weakness
    • aphasia
    • ipsilateral amaurosis fugax (monocular blindness)
  227. When should you intervene on carotid artery disease?
    when >70% stenosis of carotid artery
Card Set
CV Final
CV Final