Ch23FlashCards.txt

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radracer43
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278064
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Ch23FlashCards.txt
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2014-07-02 22:54:12
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CRNA
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A&P Test 4
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A&P Chapter 23
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  1. What is the first heart sound (S1) associated with?
    • Closure of the AV valves at the beginning of systole
    • Mitral and tricuspid
    • R-wave on EKG
  2. What is the second heart sound (S2) associated with?
    • Closure of the semilunar valves at the end of systole
    • Aortic and pulmonic
    • End of QRS complex
  3. What is the third heart sound (S3) associated with?
    • Blood entering and distending a relatively noncompliant LV
    • Ventricular diastolic gallop indicates significant LV dysfunction and may be the first sign of CHF
    • Weak rumble heard during the second 1/3 of diastole
    • Corresponds to T-wave
  4. What is the 4th heart sound (S4) associated with?
    • Late diastolic atrial contraction causes a rushing of blood into ventricles
    • Almost never heard with stethascope except in hypertensive patients with a thick LV
    • Corresponds to P-wave
  5. What anitomical location are S3 and S4 heard?
    Apex of the heart
  6. What are the 4 main causes of murmurs?
    • 1) Rheumatic fever
    • 2) Bacterial endocarditis
    • 3) Congenital defects
    • 4) Degenerative defects
  7. What leads to the greatest number of valvular lesions?
    Rheumatic fever
  8. What is the organism responsible for rheumatic fever?
    Group A hemolytic streptococci
  9. What is the mechanism by which group A strep. causes valvular lesions?
    Typically initiates an antibody response which can persist up to 1 year. This ultimately leads to autoimmune/immunologic damage
  10. What valves are most frequently affected by rheumatic fever?
    • MV most frequently
    • AV second most frequently
  11. What are typical causes of bacterial endocarditis?
    • 1) IV drug abuse
    • 2) Dental decay
  12. What are 2 congenital defects of valves that may cause murmurs?
    • 1) Stenosis
    • 2) Lack of 1 or more leaflets; congenital bicuspid AV
  13. What type of defect would calcific aortic stenosis be?
    Degenerative defect
  14. What are pressure overload lesions caused by?
    Stenotic valves
  15. What are volume overload lesions caused by?
    Regurgitant valves
  16. What type of murmur is produced by AS?
    • Systolic ejection murmur that may be transmitted into the neck
    • "Woosh-dub"
  17. What is the normal area of the AV?
    2.5-3.5cm2
  18. What are criteria for surgical repair of AS?
    • 1) Pressure gradient >50mmHg or
    • 2) Valve area <1cm2
  19. How high may LV pressure be in severe AS? What about aortic root pressure?
    LV pressure may be as high as 300mmHg with normal aortic root pressure
  20. What type of LV changes may be caused by AS?
    Concentric LV hypertrophy as sarcomeres are added in parallel
  21. Angina pectoris, DOE, and syncope are the classic triad of what valvular lesion?
    Aortic stenosis
  22. What is the life expectancy without surgery of a patient presenting with aortic stenosis?
    5 years
  23. What type of lesion is AS?
    Pressure overload
  24. How do you manage hypotension in a patient with aortic stenosis?
    Neosynepherine or vasopressin; increasing contractility will not increase BP due to stenotic, small orifice in AS
  25. What happens to SV in AS?
    Net SV is reduced
  26. What type of murmur is AR?
    • "Blowing" murmur of relatively HIGH PITCH with swishing quality
    • Heard maximally over LV during diastole
    • "lub-woosh"
  27. What is especially important regarding a short duration blowing murmur over the LV during diastole?
    Severe aortic regurgitation - blood is flowing back rapidly into LV
  28. What happens with SV during AR?
    Decreased net stroke volume as a large amount of blood immediately rushes back into the LV
  29. What type of LV changes may be caused by AR?
    Eccentric hypertrophy (big floppy heart) as sarcomeres are added in series
  30. What type of LV change may lead to some signs and symptoms of IHD? Why?
    • Eccentric hypertrophy, seen in AR.
    • s/s of IHD because the thin LV wall allows compression of endocardium/subendocardial arteries during LV filling
  31. What type of lesion is AR?
    Volume overload
  32. What type of murmur is MR?
    • High-pitched blowing murmur heard throughout systole (holosystolic)
    • Transmitted strongly to the LA, but LA is deep in the chest and difficult to hear the murmur
    • "Woosh-lub" that is less harsh than AS
  33. Where is MR best heard?
    Apex of the heart
  34. What valvular lesion allows blood from LV to be ejected back into the LA during systole?
    MR
  35. What is the cause of atrial fibrillation and pulmonary edema due to heart valve problems?
    Increased LA pressures
  36. What type of lesion is MR?
    Volume overload
  37. What will happen with PA and PCWP during MR?
    They will be elevated
  38. What are associated characteristics of acute MR?
    • 1) Papillary muscle rupture/ischemia due to LAD infarction
    • 2) High LA pressure
  39. What are associated characteristics of chronic MR?
    • 1) Rheumatic fever
    • 2) Bacterial endocarditis
    • 3) Increased likelihood of A-fib
    • 4) Dilated LA with normal pressure
  40. What type of murmur is MS?
    • Described as a low rumbling "thrill" heard during last 1/3 of diastole over the apex of the heart
    • "Kentucky" - "lub-dub-purr"
  41. What is the normal MV orifice area?
    4-6cm2
  42. At what change of MV opening do patients typically become symptomatic in MS?
    50% decreased orifice size
  43. MS causes what change in LVEDP? Why?
    Decreased LVEDP because flow from LA to LV is decreased
  44. MS can result in what changes in the pulmonary system? How does this affect the RV?
    May result in decreased pulmonary compliance causing increased RV pressures and subsequent RV failure
  45. What physiologic changes occur to the LV as the result of MS?
    • None, the LV is normal
    • CO and MAP do not decrease nearly as much as with AS
  46. What type of lesion is MS?
    Pressure overload
  47. What valvular lesions cause a net reduced movement of blood from LA to LV?
    MS and MR
  48. What congenital abnormalities are outflow obstructions?
    • 1) Coarctition of the aorta
    • 2) Pulmonic stenosis
    • 3) Aortic stenosis
  49. What congenital abnormalities cause left-to-right shunting?
    • 1) ASD
    • 2) VSD
    • 3) PDA
    • TOF and hypoplastic left heart are congenital abnormalities causing what type of shunting?
    • Right-to-left
  50. What are examples of "cyanotic" heart defects?
    • Any abnormality causing a right-to-left shunt
    • 1) TOF
    • 2) Hypoplastic left heart
    • 3) Tricuspid atresia
    • 4) Transposition of the great vessels
  51. What are examples of "acyanotic" heart defects?
    • 1) ASD
    • 2) VSD
    • 3) PDA
    • 4) Coarctition of the aorta
    • 5) Pulmonic stenosis
  52. What makes a PDA a left-to-right shunt?
    • Blood flows from left side to right side of heart, bypassing systemic circulation
    • Will see an increase in PA pressures
  53. What is the murmur of PDA?
    Machinery murmur more intense during systole, less intense during diastole. Waxes and wanes with each heartbeat
  54. What congenital heart defect can lead to recirculating of blood through lungs? What can this cause?
    • PDA; can cause decreased respiratory reserve and pulmonary edema
    • Increased pulmonary flow can lead to RV hypertrophy
  55. What is the treatment for PDA?
    For babies, indomethacin or surgical ligation
  56. What is the frequent cause of ASD?
    Failure of the foramen ovale to close
  57. What is the prevalence of ASD?
    About 1/3 of the population has ASD, but increased LA pressures force it close and many people are asymptomatic
  58. What is the murmur of ASD?
    Systolic murmur over pulmonic valve that is very mild and often not detected
  59. What frequently undiagnosed congenital heart defect can lead to MI or CVA in the event of a venous air embolism (VAE)?
    • ASD; air can shunt to arterial circulation
    • What are the 3 variations of ASDs?
    • 1) Ostium secundum
    • a. About 75% of all ASDs
    • 2) Ostium primum
    • a. Endocardial cushion defect
    • 3) Sinus venosus
  60. What EKG changes may be seen as the result of ASD?
    Right axis deviation and RBBB
  61. What arrhythmias are associated with ASD?
    a-fib and SVT
  62. What may be seen on a chest X-ray in a patient with ASD?
    Prominent pulmonary arteries due to left-to-right shunting increasing pulmonary flow
  63. What is the most common congenital heart defect?
    25-35% of congenital heart disease
  64. What congenital heart defect usually spontaneously closes by the age of 2?
    VSD
  65. What is the murmur of VSD?
    • Holosystolic murmur at the left sternal border is heard UNLESS the hole is closed during contraction
    • Small VSDs may not produce a murmur
  66. How can a VSD go from left-to-right shunting to right-to-left shunting?
    • Early pathophysiologic changes reflect increased pulmonary flow. With chronic increases of pulmonary flow, PVR may become > SVR reversing the shunt
    • When a VSD is chronic, it becomes a cyanotic defect due to right-to-left shunting
  67. What is unique of CXR and EKG with small VSD?
    They are normal
  68. What physiologic changes are seen with moderate to large VSD?
    LA and LV enlargement
  69. What EKG changes are seen with VSD causing pulmonary hypertension?
    • Right axis deviation
    • Lead I - Lead aVF +
    • this indicates RA and RV enlargement
  70. What congenital heart defect is the most common "cyanotic" defect?
    TOF
  71. What 4 anatomical defects characterize TOF?
    • 1) Aortia originates from RV instead of LV or overrides the septum
    • 2) PA stenosis causes preferential flow from the RV through the path of least resistance which is the VSD to the aorta
    • 3) VSD
    • 4) RV hypertrophy secondary to increased afterload of both pulmonary stenosis and systemic afterload
  72. What is the usual treatment for TOF?
    Surgical repair
  73. What diagnostic tools are available to identify murmurs?
    • 1) Stethascope or phonocardiogram
    • 2) EKG to identify hypertrophic axis deviation
    • 3) Echocardiography
    • 4) Chest radiography
    • 5) Cardiac catheterization

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