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25 Cards in this Set
- Front
- Back
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57. Aortic regurg murmur?
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a. Immediate high-pitched “blowing” diastolic murmur.
b. Wide pulse pressure when chronic. c. Can present w/bounding pulses and head bobbing. |
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58. Causes of Aortic regurg?
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a. Often due to:
1. Aortic root dilation 2. Bicuspid aortic valve 3. Rheumatic fever. |
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59. What DECREASES intensity of aortic regurg murmur?
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a. Vasodilators.
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60. Mitral Stenosis murmur?
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a. Follows opening snap.
b. (Opening snap due to tensing of chordae tendineae). c. Delayed rumbling late diastolic murmur. d. LA>>LV pressure during diastole. |
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61. What is Mitral Stenosis MS often secondary to?
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a. 2º to rheumatic fever.
b. Chronic MS can result in LA dilation |
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62. What enhances Mitral stenosis murmur?
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a. Enhanced by maneuvers that ↑ LA return (eg expiration).
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63. PDA murmur?
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a. Continuous machine-like murmur.
b. Loudest at S2. c. Often due to congenital rubella or prematurity. |
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64. When does calcium enter cardiac myocytes and what is its effect?
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a. Enters during plateau (phase 2) of action potential and stimulates calcium released from the SR (calcium-induced calcium release).
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65. Phase 0 of Ventricular action potential?
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a. Rapid upstroke.
b. Voltage-gated Na channels open. |
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66. Phase 1 of Ventricular action potential?
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a. Initial repolarization.
b. Inactivation of voltage-gated Na channels. c. Voltage gated K channels begin to open. |
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67. Phase 2 of Ventricular action potential?
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a. Plateau.
b. Ca+ influx through voltage-gated Ca2 channels balances K+ efflux. c. Ca2+ triggers Ca release from SR and myocyte contraction. |
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68. Phase 3 of Ventricular action potential?
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a. Rapid depolarization
b. Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca channels. |
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69. Phase 4 of Ventricular action potential?
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a. Resting potential.
b. High permeability through K+ channels. |
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70. Phase 0 of Pacemaker action potential (occurs in SA and AV nodes)?
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a. Upstroke- opening of voltage-gated Ca channels.
b. These cells lack fast voltage-gated Na channels. c. Results in a slow conduction velocity that is used by the AV node to prolong transmission from atria to ventricles. |
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71. Phase 2 of Pacemaker action potential (occurs in SA and AV nodes)?
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a. Plateau is absent.
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72. Phase 3 of Pacemaker action potential (occurs in SA and AV nodes)?
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a. Inactivation of Ca2+ channels and ↑ activation of K+ channels.
b. Causes ↑ K efflux. |
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73. Phase 4 of Pacemaker action potential (occurs in SA and AV nodes)?
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a. Slow diastolic depolarization.
b. Membrane potential spontansouly depolarizes as Na conductance ↑ (If different from INa above). c. Accounts for automaticity of SA and AV nodes. d. The slope of phase 4 in the SA node determines Heart rate! |
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74. Affect of ACh/adenosine vs. catecholamines on phase 4 of the Pacemaker action potential?
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a. ACh/Adenosine ↓ rate of diastolic depolarization and ↓ HR.
b. Catecholamines ↑ depolarization and ↑ HR. c. Sympathetic stim ↑ the chance that If channels are open. |
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75. PR interval?
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a. <0.20 seconds.
b. Conduction delay through AV node. |
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76. QRS complex?
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a. Ventricular depolarization (not contraction)
b. <.12 seconds. |
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77. What happens during the QT interval?
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a. Contraction of ventricles.
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78. T wave?
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a. Ventricular repolarization.
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79. T wave inversion indicates?
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a. Recent MI.
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80. 2 causes of U wave?
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a. Hypokalemia
b. Bradycardia. |
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81. Torsades de pointes?
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a. Ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG.
b. Can progress to V-fib. |
