cardio exam 1

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cardio exam 1
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  1. what encloses the heart and roots of the great vessels
    a fibroserous sac called the pericardium
  2. the inner serosal layer that adheres to the external wall of the heart is known as the what
    visceral pericardium
  3. what does the pericardium attach to
    sternum and mediatstinal portions of the R and L pleura
  4. this is shaped by the R atrium and ventricle
    anterior surface of the heart (the L atrium and ventricle lie more posterior so contributes only to a small tip of the anterior)
  5. this is shaped by both ventricles (mainly the left)
    inferior surface of the heart
  6. which area of the heart lies on the diaphragm
    inferior surface (diaphragmatic surface)
  7. what are the 2 basic rules of normal cardiac anatomy
    • 1) right sided structures lie mostly anterior to their left sided counterparts
    • 2) atrial chambers are located mostly to the right of their corresponding ventricles
  8. what lines the heart valves and interior surface of the chambers
    a single layer of endothelia cells (endocardium)
  9. which parasympathetic nerved innervates the heart and great vessels
    vagus nerve
  10. explain S1 and where it is best heard
    it is best heard at the apex (listening for closure of mitral valve)

    S1= systole and the aortic and pulmonic are open and mitral and tricuspid are closed
  11. explain S2 and where it is best heard
    best heard at the base

    S2= diastole and the aortic and pulmonic are closed and the mitral and tricuspid are open
  12. why would you have an accentuated S1
    • shortened PRI (WPW)
    • mild mitral stenosis
    • increased cardiac output or tachycardia
    • (ie: exercise or anemia)
  13. why would you have a diminished S1
    • prolonged PRI= 1st degree heart block
    • mitral regurgitation
    • severe mitral stenosis
    • "stiff" left ventricle
  14. explain a widened S2 split and what causes it
    RBBB or stenotic pulmonic valve

    there is a delayed closure of the pulmonic valve
  15. what is the common cause of a fixed S2 split
    ASD
  16. explain a paradoxical S2 spilt and what is the most common cause
    it is the delayed closure of the aortic valve, heard best with expiration

    LBBB is the main cause
  17. when is a physiological S2 split heard
    on inspiration
  18. explain the pathophys behind an ejection click
    presence of aortic or pulmonic valve stenosis or dilation of the pulmonary artery or aorta

    the sound occurs as the valve reaches max accent into the great vessels and reaches elastic limit and the decelerates rapidly
  19. where is an aortic ejection click heard best and how does it differ from a pulmonic ejection click
    heard at both base and apex

    DOES NOT VARY WITH INSPIRATION
  20. where is a pulmonic ejection click best heard and how does it differ from an aortic click
    heard only at base

    INTENSITY DIMINISHES DURING INSPIRATION
  21. an opening snap is heard with what and what is this usually associated with
    mitral or tricuspid stenosis

    *rheumatic heart dz
  22. explain the "a" wave in the cardiac cycle
    it represents transient venous distention caused by back pressure from RA contraction
  23. what does the "c" wave represent in the cardiac cycle
    a small rise in atrial pressure as the tricuspid and mitral valves close and bulge into their respective atria
  24. what does the "v" wave represent in the cardiac cycle
    it is a result of passive filling of the RA from the systemic veins during systole, when the tricuspid is closed
  25. the faster the heart beat, the shorter the ______ phase
    diastolic
  26. what is an easily obtainable way to measure the right heart function
    JVP
  27. what does the "y" mean in the cardiac cycle
    a fall in RA pressure due to filling of the ventricle
  28. if you see a prominent "a" in the cardiac cycle, what could be the etiologies (pg 31)
    RVH, TS
  29. if you see a prominent "v" in the cardiac cycle, what could be the etiology (pg 31)
    TR
  30. if you see a prominent "y" in the cardiac cycle, what could be the etiology
    constrictive pericarditis
  31. what is a normal JVP measurement
    ≤ 9cm
  32. why wouldn't you use the external jugular vein to measure JVP
    because it contains valves that interfere with venous return to the heart
  33. why would you hear a split between the closure of the mitral and tricuspid valves, where there is a delay in closure of the tricuspid (pg 32)
    RBBB
  34. what are the 3 factors that determine the intensity of S1
    • 1) the distance separating the leaflets of the open valves at the onset of ventricular contraction
    • 2) the mobility of the leaflets (normal, or rigid because of stenosis)
    • 3) the rate of rise of ventricular pressure
  35. this is heard when the PR interval is shorter than normal because the valve leaflets do not have sufficient time to drift back together and are therefore shut from a relatively wide distance
    accentuated S1
  36. what determines the intensity of S2
    it depends on the velocity of blood coursing back toward the valves from the aorta and pulmonary artery after the completion of ventricular contraction, and the suddenness with which that motion is arrested by the closing valves
  37. what would cause an accentuated S2
    in systemic or pulmonary HTN, the diastolic pressure in the respective artery is higher than normal, such that the velocity of the blood surging toward the valve is elevated
  38. what will cause a diminished S2
    severe aortic or pulmonic valve stenosis
  39. what is the cause of an S3 heart sound in a middle-aged or older adult
    it indicated volume overload owing to CHF, or increased transvalvular flow that accompanies advanced mitral or tricuspid regurgitation
  40. if there is an S4 heart sound, when does it occur and what does it coincide with
    it occurs in late diastole and it coincides with contraction of the atria (atrial kick)
  41. what is the etiology behind an S4 heart sound
    it specifically indicates a decreased ventricular compliance which typically results from ventricular hypertrophy or myocardial ischemia
  42. what is the hallmark sign of constrictive pericarditis (pg 38)
    the abrupt cessation of ventricular filling in early diastole which is known as the pericardial knock
  43. what grade is a systolic murmur that is barely audible
    1/6
  44. what grade is a systolic murmur that is faint but immediately audible
    2/6
  45. what grade is a systolic murmur is easily heard
    3/6
  46. what grade is a systolic murmur easily heard and associated with a palpable thrill
    4/6
  47. what grade is a systolic murmur that is very loud; heard with a stethoscope lightly on the chest
    5/6
  48. what grade is a systolic murmur that is audible without the stethoscope directly on the chest wall
    6/6
  49. what grade is a diastolic murmur that is barely audible
    1/4
  50. what grade is a diastolic murmur that is faint but immediately audible
    2/4
  51. what grade is a diastolic murmur that is easily heard
    3/4
  52. what grade is a diastolic murmur that is very loud
    4/4
  53. a systolic ejection murmur is typical of what
    aortic or pulmonic valve stenosis
  54. what is the "shape" of the systolic ejection murmur
    crescendo- decrescendo type
  55. what are the causes of pansystolic murmurs
    • mitral regurgitation
    • tricuspid regurgitation
    • VSD
  56. what are the reasons for a late systolic murmur
    mitral valve prolapse
  57. this murmur is heard best at the apex and is a high pitched and "blowing" in quality, it often radiates to the L axilla (pg 41)
    pansystolic murmur of advanced mitral regurgitation
  58. this murmur is best heard at the fourth to sixth left intercostal spaces, is high pitched, and may be associated with a thrill (pg 41)
    VSD
  59. which radiological study is performed when greater structural detail is required (pg 50)
    transesophageal imaging
  60. which type of study evaluates blood flow direction and velocity and turbulence. It also permits estimation of pressure gradients within the heart and great vessels
    Doppler imaging
  61. this imaging is particularly helpful in the assessment of aortic and atrial abnormalities, conditions that are less well visualized by conventional transthoracic echo imaging
    transesophageal echocardiography (TEE)
  62. this is the most sensitive noninvasive technique for evaluating perivalvular leaks (pg 54)
    transesophageal echocardiography (TEE)
  63. this imaging study is highly sensitive for the detection of abnormal intracardiac shunts (pg 55)
    contrast echocardiogram
  64. to measure pressures in the right atrium, right ventricle, and pulmonary artery, a catheter is usually inserted through which veins
    femoral, brachial, or jugular vein
  65. pressures in the aorta and left ventricle are measured via the catheters into which arteries (pg 61)
    brachial or femoral
  66. the pulmonary capillary wedge is a direct measurement of what
    it reflects the left atrial pressure
  67. why would you see a cannon "a" wave
    • JVP due to tricuspid stenosis
    • 3rd degree heart block (AV node dissociation)
  68. what are the etiologies of an increased pulmonary artery wedge pressure
    • left-sided CHF
    • mitral stenosis or regurgitation
    • cardiac tamponade
  69. what causes a pulmonary artery wedge pressure "a" wave
    LVH
  70. what causes a pulmonary artery wedge pressure "v" wave
    • mitral regurgitation
    • ventricular septal defect
  71. what is the non-invasive study of choice that gives you the highest precise indirect measurement of the ejection fraction
    MUGA
  72. what is the leading cause of mortality and morbidity in the developed world
    atherosclerosis
  73. what are the 3 layers of the arterial wall
    • intima- closest to the arterial lumen
    • media- middle layer
    • adventitia- outer layer
  74. what are some key components that contribute to the atherosclerotic inflammatory process (pg 121)
    • 1) endothelial dysfunction
    • 2) accumulation of lipids within the intima
    • 3) recruitment of leukocytes and smooth muscle cells to the vessel wall
    • 4) formation of foam cells
    • 5) deposition of extracellular matrix
  75. what are the 3 pathological states of atherosclerosis
    • 1) fatty streak
    • 2) plaque progression
    • 3) plaque disruption
  76. what is the earliest visible lesion of atherosclerosis
    fatty streak
  77. this is known as an endogenous vasodilator, an inhibitor of platelet aggregation, and anti-inflammatory substance
    nitric oxide (NO)
  78. what is the key step in atherogenesis
    recruitment of leukocytes to the vessel wall
  79. what are the modifiable risk factors for atherosclerosis (pg 132)
    • aberrant levels of circulating lipids (dyslipidemia)
    • tobacco smoking
    • HTN
    • DM
    • lack of physical activity and obesity
  80. what are the major nonmodifiable risk factors for atherosclerosis (pg 132)
    • advanced age
    • male gender
    • heredity
  81. what are the major groups of lipid altering agents
    • HMG-CoA reductase inhibitors (statins)
    • niacin
    • fibric acid derivatives
    • bile-acid binding agents
  82. what are the most effective agents to lower LDL
    HMG-CoA reductase inhibitors
  83. what are the coronary artery dz risk equivalents
    • CHD
    • PAD
    • AAA
    • DM (SLE)
  84. which 2 disorders are predisposed to increased TG
    • type II DM
    • hypothryoidism
  85. how long does it take for ventricular remodeling in a transmural infarct
    7+ days
  86. which imaging study can be used to dx the presence of CAD
    stress echo (sees ischemia)
  87. what is the most common cause of secondary HTN
    chronic kidney disease (CKD)
  88. why would you have isolated increased diastolic HTN
    hypothyroidism
  89. what is the most common cause of a compensatory pause
    PAC
  90. what can be the cause of a bisferiens pulse
    aortic regurgitation
  91. what is the class drug of choice for isolated TG >500
    fibrates
  92. what is the most common cause of a SVT
    AVNRT (WPW)
  93. what has been identified as an independent risk factor for CAD (pg 138)
    Lipoprotein (a)
  94. what is the leading cause of death in industrialized nations (pg 141)
    ischemic heart dz
  95. what is the most common manifestation of ischemic heart dz
    angina pectoralis
  96. the supply of oxygen to the myocardium depends on the ______ content of the blood and the rate of ______ ______ flow
    • oxygen
    • coronary blood
  97. when does the predominance of coronary perfusion take place
    diastole
  98. perfusion pressure of the coronary arteries can be approximated by what
    aortic diastolic pressure
  99. these issues can decrease the aortic diastolic pressure which can lead to decreased coronary artery perfusion pressure and may impair myocardial oxygen supply
    • HoTN
    • aortic valve regurgitation
  100. what is a reason why the subendocardium is the region most vulnerable to ischemic damage (pg 143)
    when the myocardium contracts, the subendocardium, adjacent to the high intravascular pressure, is subjected to greater force than are the outer muscle layers
  101. any additional oxygen requirement of the heart must be met by what and what controls this
    • an increase in blood
    • autoregulation of coronary vascular resistance is the most important mediator
  102. this is a potent vasodilator and is thought to be the prime metabolic mediator of vascular tone
    adenosine
  103. when adenosine binds to receptors on vascular smooth muscle, what occurs
    it decreases calcium entry into cells which leads to relaxation, vasodilation, and increased coronary blood flow
  104. what are the 3 major determinants of myocardial oxygen demand
    • 1) ventricular wall stress
    • 2) heart rate
    • 3) contractility (also known as inotropic state)
  105. in Laplace's law, the ventricle wall stress is directly proportional to what
    systolic ventricular pressure
  106. in Laplace's law, ventricle wall stress is inversely proportional to what
    ventricular wall thickness because the force is spread over a greater muscle mass
  107. this refers to tissue that, after suffering a period of severe ischemia (but not necrosis), demonstrates prolonged systolic dysfunction even after the return of normal myocardial blood flow
    stunned myocardium
  108. this refers to the tissue that manifests chronic ventricular contractile dysfunction in the face of a persistently reduced blood supply, usually because of multivessel CAD
    hibernating myocardium
  109. what refers to pts with typical symptoms of angina pectoralis who have no evidence of significant atherosclerotic coronary stenosis on coronary angiograms
    syndrome X
  110. what is the sign called for when a pt puts a clenched fist over his/her sternum as if defining the constriction discomfort by that tight group
    Levine sign
  111. when is a stress test considered markedly positive for severe ischemic heart disease
    • 1) ischemic ECG changes develop in the first 3 minutes of exercise or persist 5 minutes after exercise has stopped
    • 2) the magnitude of the ST segment depressions in >2mm
    • 3) SBP decreases during exercise
    • 4) high grade ventricular arrhythmias develop
    • 5) pt cant exercise for at least 2 minutes because of cardiopulmonary limitations
  112. what pharmacologic agents are used in a stress test for pts who can not exercise
    • dobutamine
    • dipyridamile
    • adenosine
  113. what medicatinos are used to decrease the cardiac workload and increase myocardial perfusion
    • organic nitrates
    • B-blockers
    • CCB
  114. which CCBs are potent vasodilators
    nifedipine and amlodipine
  115. which medication has been shown to decrease the frequency of angina episodes and improve exercise capacity in pts with CAD but differs from other anti-ischemic drugs in that it does NOT affect the HR or BP
    ranolazine
  116. what is the typical cause of unstable angina and NSTEMI
    partially occlusive thrombus
  117. this causes more severe ischemia and a larger amount of necrosis, manifesting as a STEMI
    thrombus completely obstructing the coronary artery
  118. this type of infarct spans the entire thickness of the myocardium and result from total, prolonged occlusion of an epicardial coronary artery
    transmural infarct
  119. this type of infarct exclusively involves the innermost layers of the myocardium
    subendocardial infarct
  120. how long does it take for irreversible cell injury in a transmural infarct
    20-24 min
  121. how long does it take for wavy myofibers to form in a transmural infarct
    1-3 hrs
  122. how long does it take for coagulation necrosis, edema in a transmural infarct
    18-24 hrs
  123. how long does it take for tissue necrosis in a transmural infarct
    12-18 hrs
  124. when does ventricular remodeling start to occur
    7+ days
  125. when is fibrosis and scarring complete in a transmural infarct
    7 weeks
  126. how long do troponin levels stay elevated
    10-14 days
  127. what are the preferred serum markers to detect myocardial necrosis
    troponins
  128. when do troponin markers peak after the onset of the MI
    18-36 hours
  129. when do CK-MB markers peak after the onset of the MI
    24 hrs
  130. how long do CK-MB markers stay elevated
    48-72 hrs
  131. what is the management for a STEMI (reperfusion approach, pg 184)
    • ASA
    • Heparin (UFH or LMWH)
    • clopidogrel
    • reperfusion method:
    • - fibrinolytic drug (tnk/tpa)
    • - primary PCI (with GPIIb/IIIa inhibitor)
  132. what is the management for a STEMI in all pts
    • 1) anti-ischemic medications
    • - B-blockers
    • - nitrates
    • - +/- CCB
    • 2) general measures
    • - oxygen (<95%)
    • - pain control (morphine)
    • 3) additional therapies
    • - ACE inhibitors
    • - statin

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