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170 Cards in this Set
- Front
- Back
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1. What 3 questions should be asked in every focused cardiac examination history of the patient’s present illness? |
Chest pain, shortness of breath and syncope
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2. What three pulmonary symptoms could be asked in the history of present illness to help separate pulmonic from cardiac induced shortness of breath?
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Orthopnea, PND (heart) and productive sputum (lung)
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3. What parameter based questions can you ask the patient to separate episodes of stable angina pectoris from unstable angina?
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Changes in frequency and duration. Pain at rest. If episode of angina last 20 min, the damage process starts
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4. What is the most common cause of death in both men and women in this country?
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Atherosclerosis
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5. How long does myocardial ischemia have to last before myocardial damage (myocardial infarction) begins to occur?
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20 min
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6. List 5 major risk factors for the development of coronary artery disease.
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Age, smoking, age, diabetes, cholesterol, family history, obesity, hypertension
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7. Where in the history, other than family history, would be the place to list the atherosclerotic risk factors in a patient with suspected coronary artery disease
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HOPI
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8. In what part of the history would you list cardiac review of systems in a patient with a cardiac problem?
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HOPI
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9. What is the most common diagnosis for episodic syncope upon standing?
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Orthostatic hypotension/ vasovagal syncope
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10. How would you describe a Stokes Adams attack?
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Sudden block in AV conduction leads to syncope, once ventricles establish their own rhythm, patient regain consciousness
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11. Define congestive heart failure.
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The heart is unable to pump blood at a sufficient rate to meet the metabolic demands or can do so at elevated filling pressure
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12. What relatively rare congenital life threatening conditions should you consider in a 20 year old with suspected cardiac induced syncope?
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Long QT syndrome, Wolf Parkinson Wright "WPW", Hypertrophic obstructive cardiomyopathy. Cardiac #1, slide 33.
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13. What is the usual chief complaint when mitral regurgitation is severe?
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No symptoms until end stage, then SOb. Too late. L ventricle and L atrium dilate until reaches point it cannot anymore, then SOB and severe heart failure occurs. Dr Heibel grand rounds, slide 96 cardiac #2.
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14. What are the 3 presenting symptoms of a patient with severe aortic stenosis?
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a)Dyspnea on exertion "SOB"
b) chest pain c) syncope. Cardiac #2, side 71. |
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15. Which of these 3 complaints in a patient with aortic stenosis is compatable with the shortest life span?
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CHF onset --> death = 3 years, Angina, syncope onset --> death = 5 years. slide 71.
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16. What is the usual chief complaint of patient with severe mitral stenosis?
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SOB, fatigue , gradual onset. Cardiac #2, slide 91
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17. What is the usual presenting symptom of chronic severe AR?
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Asymptomatic then when too late SOB. Heat can no longer compensate with hypertrophy and chamber dilation. Cardiac #2, slide 82.
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18. What is the presentation in the emergency department of acute severe AR or MR?
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Pulmonary edema and shock. (BP low and congestive failure) Cardiac #2, slides 81, 101
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19. What is the range of pressure we call prehypertensive?
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120-139/80-89 Mosbys CE p440
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20. What is the normal pulse pressure?
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Pulse pressure is systolic minus diastolic. Normally 30-40mmHg up to 50mmHg still normal. Mosbys CE p440.
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21. What is the significance of pulsus alternans in a patient?
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Alternating pulse volume- Congestive heart failure. Cardiac #2, slide 68
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22. What is the significance of a 12 mm or greater paradoxical pulse?
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Pulsus paradoxicus= on inspiration your systolic pressure lowers. >12 = tamponade with large or sudden significant pericardial effusion until proven otherwise. Cardiac #2, slide 68. Heibel grand rounds too.
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23. What is the finding on carotid palpation in severe aortic stenosis?
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Parvus and tardus pulse (weak and late) (Cardiac assorted, slide 68)
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24. A patient presents with a murmur, bounding pulses and a pulse pressure of 80. What is your diagnosis?
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Aortic regurgitation (Cardiac assorted, slides 81- 89)
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25. What is top normal size for a point of maximal impulse (PMI)?
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1 - 2 cm (approx size of pad of finger) (Cardiac history and physical exam, slide 55)
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26. In a patient with normal cardiac anatomy, which chamber are you palpating when feeling the PMI?
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Left ventricle (Cardiac history and physical exam, slide 56)
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27. What would be the underlying pathology behind a paradoxical or rocking component of the apical impulse?
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A rocking apical impulse could indicate dyskinesis due to myocardial ischemia. It could also indicate a severely dilated left ventricle or ventricular aneurysm.
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28. Which venous pulse can you use to estimate right atrial filling pressure?
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Jugular venous pulse (Cardiac history and physical exam, slide 48)
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29. What is the explanation for the a wave seen in the internal jugular pulses?
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Brief backflow of blood to the vena cava during right atrial contraction (pg. 430)
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30. In what heart rhythm abnormality would the a wave disappear?
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Atrial fibrillation (pg. 451)
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31. Which heart sound signifies the onset of systole?
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S1 (pg.398)
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32. Diastole begins with what heart sound?
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S2 (pg.398)
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33. Why is the S1 sound usually much softer than S2
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The pressure gradients causing the tricuspid and mitral valves to close is less than the pressure gradients causing the pulmonary and aortic valves to close (pg.398)
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34. Where would P2 be most easily heard?
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P2 is the sound created from the pulmonic valves closing. P2 is heard loudest at Second Pulmonic auscultatory area. (Table 14-2, CE pg398)
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35. Why is A2 louder than P2?
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A2 is the sound created by the closure of aortic valve. A2 is louder due to higher pressure in aorta causing the valves to close with greater force than P2. A2 contributes to most of the sound of S2
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36. What cardiac event occurs to cause the S4 sound?
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In the second phase of ventricular filling, vibration is the valves, papillae, and ventricular walls produce S4.
Note: Because it occurs do late in diastole, S4 may be confused with a split S1. (CE pg400) |
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37. When does an S3 gallop occur and what does it signify in an adult?
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When S3 becomes intense and easy to hear, the resultant sequence of sounds stimulates a gallop; this is the protodiastolic gallop rhythm. S3 may be louder if filling pressure is increased or if ventricular compliance is reduces. Best heard when the patient is in left lateral decubitus position. (CE 400)
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38. What abnormalities could cause reverse splitting of A2P2?
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Paradoxic (Reversed) splitting occurs when P2 is heard before A2 during expiration and disappears during inspiration. This can be caused during left bundle branch block.
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39. What valves are responsible for early systolic clicks?
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Opening snap of semilunar valves (CE pg 401)
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40. What valve is responsible for mid systolic clicks?
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Mitral valve prolapse (CE pg 401)
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41. What is the pathophysiologic explanation of a diastolic snap?
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Mitral valve stenosis (CE pg 401, Asked Dr. Heibel)
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42. Where, and with what part of your stethoscope, do you listen for left sided cardiac gallops?
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Bell, at apex. (CE pg 402, table 14-3)
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43. What is the response of gallops when you increase pressure on the bell of your stethoscope?
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High pressure would cause bell to behave like a diaphragm losing the ability to hear gallops. ( Title: Practical cardiac Auscultation; Journal: critical care nursing quarterly)
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44. At what heart rate does the patient develop a summation gallop?
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Summation Gallop is a loud gallop that occurs in patients with tachycardia. One in which the third (S3) and fourth (S4) sounds are superimposed, appearing as one loud sound; usually associated with cardiac disease. ( I could not find a cut off number in any reputable sources) (Evidence Based Physical Diagnosis: Page 337)
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45. How loud does a murmur have to be to cause a thrill?
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A thrill is a fine palpable, rushing vibration, a palpable murmur, often, but not always, over the base of the heart in the area of the right or left second intercostal space. A murmur at the grade IV level or more can be felt as a thrill. It may be appreciated in systolic or diastolic.
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46. In addition to the cardiac examination, what other areas of physical examination would be of most interest to you in a cardiac problem? List 4
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Vascular, Pulmonary, MSK, Neural, GI. (Cardiac emergencies slide 21)
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47. What other factors or major organ dysfunction can cause peripheral edema?
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• Increased capillary pressure
o Kidney retention of salt/water o High venous pressure/venous constriction Heart failure Venous obstruction Failure of venous pumps o Decreased arteriolar resistance Excessive body heat Insufficiency of sympathetics Vasodialator drugs • Decreased plasma proteins o Loss of proteins in kidneys o Loss of protein from burns or wounds o Failure to produce proteins Liver failure Malnutrition • Increased capillary permability o Toxins from inflammation chemicals, bacteria or ischemia o Vitamin C deficiency • Blockage of lymph return o Cancer, infections, surgeries |
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48. What leg statistically swells first in edema?
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Right side, due to left side not pumping adequately enough to return blood to the right atrium, increase in venous/capillary pressure (hydrostatic pressure) causes fluid to leak. (closest reference phys 298, spent over an hour looking for a better reference online)
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49. What differentiates lymphedema from edema secondary to fluid retention?
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Lymphedema doesn’t resolve with elevation of affected area, edema does. Edemua can sometimes be alleviated by diuretics, diuretics do not help lymphedema. (clinical pg 232)
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50. Describe an aortic stenosis mumur.
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Mid systolic (ejection) murmur, medium pitch, coarse, diamond shaped, crescendo-decrescendo.
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51. In what auscultation site and what position would aortic stenosis be expected to be loudest?
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2nd right intercostals space in systole (page 395 clinical)
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52. What is the radiation pattern of an aortic stenosis murmur?
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Radiates along the left sterna border and bilaterally up to the carotids and may produce a thrill.
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53. Does loudness of AS usually correlate with severity?
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Yes, the smaller the diameter for blood to flow the louder it is. This is a harsh murmur and gets louder and harsher the worse it is until it progresses to CHF (Cardiac assorta slide 72) Also anything that increases blood flow ie exercise will increase murmur loudness.
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54. What has occurred when the murmur of severe aortic stenosis decreases?
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The heart contractility and ability to contract enough to meet the bodies needs has decreased. The aortic stenosis has progressed to CHF
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55. The etiology of dilated cardiomyopathy is:
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Myosin heavy chain abnormalities, autosomal dominant, usually presents in teens-50s (slide 77 assorted cardiac)
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56. Describe the murmur of mitral regurgitation and its location?
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Heard best at apex (IC5) and radiate to the axilla. Holosystolic, plateau shaped intensity, high pitch, harsh blowing quality, often so loud it may obliterate the S2 sound. (page 407 clinical).
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57. Does loudness of MR correlate with severity?
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Loudness of MR does not correlate, some of the worst MR is not very loud. More severe MRs have a systolic intensity that decrescendos, and mild MR has a murmur that crescendos
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58. What skeletal abnormalities are associated with mitral valve prolapse?
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Ehlers-Danlos, Marfans(wiki)
Pectus Excavatum(Mosby 408) |
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59. What maneuver will move the click of mitral valve prolapse later into systole?
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Increased venous return elevate the legs or supine position
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60. The murmur of mitral regurgitation will radiate toward the high sternum with an abnormality of which leaflet of the mitral valve?
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Anterior leaflet
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61. What are the other sounds associated with a murmur in mitral valve prolapse?
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a mid-systolic click, followed by a late systolic murmur heard best at the apex is common
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62. What would you expect to find on palpation of the PMI of a patient with severe chronic MR
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It would be more to the left and down due to ventricular hypertrophy secondary to MR
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63. What is the usual causative factor in the development of mitral stenosis?
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Often occurs with MR and can be caused by rheumatic fever or cardiac infection
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64. If someone presents with mitral stenosis in their teens, what can you surmise?
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They had rheumatic fever as a child after a strep infection
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65. Which sex far predominates in the development of mitral stenosis?
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Females
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66. What is the best position and location to hear the murmur of mitral stenosis?
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Heard with the bell at the apex
Patient in left pateral decubitus position |
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67. Which head of the stethoscope do you use to hear mitral stenosis?
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Bell
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68. Describe the mitral stenosis murmur.
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Heard with bell at apex; pt in left lateral decubitus position; low frequency diastolic rumble’ doesn’t radiate’ palpable thrill at apex in late diastole;
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69. What would happen to mitral stenosis murmur if the patient developed atrial fibrillation?
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In individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrial kick. The loss of the atrial kick due to atrial fibrillation can cause a precipitous decrease in cardiac output and sudden congestive heart failure.[citation needed]
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70. What is the response of mitral stenosis to exercise?
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The symptoms of mitral stenosis (palpitations, PND, orthopnea, palpitations, chest pain) may be revealed or accentuated with exercise.
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71. Describe the position of the patient and the locations where the murmur of aortic regurgitation is best heard.
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• “heard with diaphragm, patient sitting and leaning forward, ejection click heard in second intercostal space;
• early diastolic, high pitch, blowing, often with diamond shaped midsystolic murmur; • sounds often not prominent, and duration varies with blood pressure; • low pitched rumbling murmur at apex is common • early ejection click sometimes present; • S1 soft,S2 split may have a tambour like quality • S1-S4 gallop common |
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72. What is implied if the murmur of chronic aortic regurgitation is heard best on the right of the sternum?
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• In chronic AR, for many years the left ventricle hypertrophies and dilates to handle the increasing ventricular volume
• The murmur of AR due to dilated aortic root is often heard best to the Right of the sternum • Murmur due to valvular AR usually heard best Left side of sternumside |
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73. Why is the murmur of AR decreshendo?
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The configuration of the aortic regurgitation murmur is usually decrescendo because the magnitude of regurgitation progressively declines. The murmur is high-frequency and has a "blowing" character. Occasionally the murmur can be musical in quality (diastolic whoop); this has been attributed to a flail everted aortic cusp. The "whoop" can be mid, late, or pansystolic
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74. In AR and MR what is the best indication of severity.
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• Length of murmur = severity, worse disease
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75. Hypertrophic cardiomyopathy in 50% of people has a familial transmission, describe:
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Hypertrophic cardiomyopathy (HCM) is a genetically determined heart muscle disease most often (60 to 70 percent) caused by mutations in one of several sarcomere genes that encode components of the contractile apparatus. Most familial DCM is transmitted in an autosomal dominant inheritance pattern, although all inheritance patterns have been identified (autosomal recessive, X-linked, and mitochondrial). During the past 15 years, familial DCM genetic studies have identified mutations in over 30 genes.
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79. What physical examination sign is pathognomic of atherosclerotic heart disease?
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Pathognomonic means characteristic for a particular disease and its presence means that a particular disease is present beyond any doubt. (WIKI) uncure about answer. Could be MI, periphereal vascular disease, stroke.
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80. Which vessel is the most likely cause of an inferior wall MI?
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Right coronary artery (30% to 40%): infarcts involving the inferior/posterior wall of left ventricle, posterior portion of ventricular septum, and the inferior/posterior right ventricular free wall in some cases
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81. Which vessel is the most likely cause of a lateral MI?
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Left circumflex coronary artery (15% to 20%): infarcts involving the lateral wall of left ventricle except at the apex.
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82. Which vessel is the most likely cause of an anterior wall MI?
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Left anterior descending coronary artery (40% to 50%): infarcts involving the anterior wall of left ventricle near the apex; the anterior portion of ventricular septum; and the apex circumferentially.
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83. What is the most common abnormality in congenital heart disease?
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Incomplete closure of the ventricular septum, allowing free communication of blood between the left to right ventricles, is the most common form of congenital cardiac anomaly.
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84. What is the most common form of congenital heart disease in adults?
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The most common lesions seen in adults are atrial septal defect and tetralogy of Fallot.
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85. What is the most common cause of an extracardiac shunt?
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Embryo Chapter 13: VSDs are the most common type of congenital heart disease. Most people with a large VSD have massive left-to-right shunting of blood.
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86. Which congenital heart disease is more common in women:
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Chapter 13 Embryo: PDA, a common anomaly, is two to three times more frequent in females than in males.
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87. Which congenital heart diseases occur most commonly in males?
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Embryo Chapter 13: VSDs are the most common type of CHD, accounting for approximately 25% of defects. VSDs occur more frequently in males than in females.
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88. Which congenital heart disease has the largest male predominance?
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Embryo Chapter 13: VSDs are the most common type of CHD, accounting for approximately 25% of defects. VSDs occur more frequently in males than in females.
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89. Which conditions demonstrate increased incidence of patent ductus arteriosus?
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Embryo Chapter 13: The embryological basis of PDA is failure of the DA to involute after birth and form the ligamentum arteriosum. Failure of contraction of the muscular wall of the DA after birth is the primary cause of patency. There is some evidence that the low oxygen content of the blood in newborn infants with respiratory distress syndrome can adversely affect closure of the DA; for example, PDA commonly occurs in small premature infants with respiratory difficulties associated with a deficiency of surfactant.
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90. Describe the murmur and location of a PDA murmur.
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PDA produces a characteristic continuous harsh murmur, described as “machinery-like”. heard in 1st to 3rd intercostal spaces on the left side.
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91. What will occur in a child with a patent ductus arteriosus with elevated pulmonary vascular resistance?
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If a large PDA is not closed, then increased flow will lead to increased pressure in the pulmonary arteries and can lead to Eisenmenger`s syndrome. This is a situation in which a reversal of flow (a right to left shunt) occurs.
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92. In older children and adults, what is the relationship between the size of a VSD and the murmur?
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A smaller defect causes a louder murmur and a more easily felt thrill than a large one. (p.419 Mosby’s PE)
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93. On examination of a newborn, how does a small VSD present?
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Arterial pulse is small and jugular venous pulse is unaffected. A loud, coarse and high-pitched Holosystolic murmur heard along sternal border in the 3rd to 5th intercostal spaces. Distinct lift along left sternal border and the apical area. The smaller defect causes an extra loud murmur and more intense thrill than a large one. There would be LESS (As opposed to MORE in a LARGE VSD but these symptoms are still possible) presentation of rapid breathing, poor growth, CHF. Many small defects close during the first 2 years of life. (p.419 Mosby’s PE)
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94. What is the term used to describe the development over time of pulmonary hypertension in congenital heart disease?
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Eisenmenger syndrome is term used to describe a physiologic state that begins with the presence of a left- to-right shunt. This results in a net increase in pulmonary blood flow eventually leading to the development of pulmonary vascular disease and increased pulmonary vascular resistance. The increase in pulmonary vascular resistance results in a rise in pulmonary artery pressure. Pulmonary arterial hypertension causes reversal of flow through the shunt because right heart pressure exceeds left heart pressure and right-to-left shunting of blood occurs. With right-to-left shunting, de-oxygenated blood returning to the right side of the heart, passes through a communication such as a VSD or PDA to the left side of the heart and is pumped to the body resulting in cyanosis. (Pathology p.540)
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95. In the fetus where is the highest percentage oxygen saturation?
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umbilical veins
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96. What is the most common congenital cardiac defect as a cause of early post birth presentation of congestive heart failure?
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Large VSD with irreversible pulmonary hypertension. (Path p.541 and Mosyb’s p.419)
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Hypoxemia at birth resulting in pulmonary vascular disease, usually presents first as
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: lethargy, anxiety, irritability citation needed
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98. If this condition persists it presents later with:
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Central cyanosis path 540
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99. A male child presents to clinic with dysmorphic facies, mental retardation, bleeding and pulmonic stenosis. Your diagnosis is:
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Trisomy 21 path 161-162
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100. Define Kartagener’s syndrome:
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Kartagener syndrome results from patients having an underlying primary ciliary dyskinesia disease (an autosomal recessive syndrome causining and absence/shortening of dynein arms impairing cilia this leads to retention of secretions, recurrent infections progressing to bronchiectasis). Kartagener syndrome manifests as comorbidity of ciliary dyskinesia, bronchiectasis, sinusitis and situs inversus/partial lateralizing disorders (path p.692)
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101. You are examining a young female patient who is of short stature , has low set ears, broad chest with wide nipples, and a early systolic ejection click and a systolic ejection murmur. What is your diagnosis?
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turners syndrome single X chromosome
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102. What is the chromosomal abnormality associated with this condition? turners syndrome
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A single X chromosome.
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103. What heart lesions are often associated with turners syndrome
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coartication of the aorta
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104. We are seeing a child in pediatric cardiology with a short, flattened facies, upslanted palpebral fissures and mental retardation. What is your diagnosis?
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Down's syndrome
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105. What is the most significant risk factor for the development of this condition?
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advanced age of the mother
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106. What are the cardiac conditions most often associated with this condition?
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Endocardial Cushion Defect: AV canal
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107. A thirty five year old man is in your office with chest pain. He is tall, with long limbs, loose ligaments, arachnodactyly, lens dislocation, and aortic regurgitation. What is your diagnosis?
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Marfan’s Syndrome
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108. What is the term for a clot that arises from the veins, passes usually thru an ASD to lodge arterial circulation?
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Paradoxical embolus
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109. What congenital syndrome is most commonly associated with endocardial cushion defect (atrioventricular canal defect)?
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Down Syndrome
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110. What 2 structures does the patent ductus usually connect and in what location?
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Connects the pulmonary artery with the arch of the aorta
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111. What condition would you suspect in a child when you hear a systolic murmur best posteriorly between the scapulae?
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Coarctation
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what are the forms of coartication of the aorta
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. Postductal coarctation occurs after left subclavian (typical):
- Hypertension in upper extremities with normal to low blood pressure in lower extremities - Radial-femoral pulse delay 1b. Postductal coarctation occurs before left subclavian - Weaker radial pulse on left than right and radial-femoral pulse delay 2. Ductal Coarctation 3. Preductal Coarctation - Blood flow depends on patent ductus arteriosus (see question 115) - Life threatening |
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113. What would you expect upon blood pressure readings in a child with coarcticcation of the aorta
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Elevated blood pressure in upper extremities with low blood pressure in lower extremities
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114. What congenital abnormality has a high incidence of coarctation of the aorta
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Turners Syndrome (45XO) associated with preductal coarctation
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115. What happens to a newborn baby born with severe coarctation of the aorta if the associated PDA closes?
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Nothing if PDA is postductal, since PDA is not required for blood flow
If preductal, PDA is required to shunt blood to the aorta distal to the coarctation - baby will not survive |
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116. What is the underlying pathology in a 40-70 year old man who presents with symptoms of severe aortic stenosis?
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Midsystolic ejection murmur, radiates along left sterna border and to carotid with a palpable thrill. S1 at apex disappears, followed by ejection click; S2 soft or absent.
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117. Where would you expect to hear the murmur of a VSD?
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Along left sterna border, 3rd-5th intercostals space. Pg 419.
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118. What is the correlation between loudness of a VSD murmur and VSD size?
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Smaller causes louder murmur, thrill may be easily felt.
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120. What is the mother’s underlying condition in a baby born with Ebstein’s anomaly?
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Bipolar disorder
ebsteins is when the opening of the tricuspid valve is displaced towards the apex of the heart |
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121. What agent has been thought to increase the development of
Ebstein’s? |
lithium during the first trimester of pregnancy
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122. How would you describe the anatomical problem in Ebsteins?
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heart defect in which the opening of the tricuspid valve is displaced towards the apex of the right ventricle of the heart. There’s subsequent 'atrialization' of a portion of the morphologic right ventricle (which is then contiguous with the right atrium). This causes the right atrium to be large and the anatomic right ventricle to be small in size.
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123. What is the usual early presentation of the severe form of ebsteins
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• S3 heart sound
• S4 heart sound • Systolic murmur of tricuspid regurgitation • Middiastolic murmur along the lower left sternal border • Right atrial hypertrophy • Right ventricular conduction defects • Wolff-Parkinson-White syndrome often accompanies |
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Why should pregnancy be avoided in a female patient with congenital heart disease with Eisenmenger’s physiology?
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Cardiac output, heart rate, and blood volume all increase substantially with pregnancy. Systemic vascular resistance decreases during pregnancy but will increase dramatically at the time of delivery. Delivery also results in a sudden increase in venous return. Cyanotic patients are at increased risk of fetal complications including spontaneous abortion and intrauterine growth retardation. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768916/)
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125. What is the gender of a child born with Noonan syndrome? What is the associated cardiac abnormality?
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Based on several sources, states that this is seen in BOTH sexes although it used to be considered the male version of TURNER SYNDROME.
About 80 percent of people with Noonan syndrome have congenital heart disease, accounting for some of the key signs and symptoms. Pediatric cardiologists may be the first doctors to see children with Noonan syndrome. Some forms of congenital heart disease associated with this disorder include: Valve disorders. Pulmonary valve stenosis is a narrowing of the pulmonary valve, the flap of tissue that separates the lower right chamber (ventricle) of your heart from the artery that supplies blood to the lungs (pulmonary artery). It's the most common heart problem seen with Noonan syndrome. The defect may occur by itself, or there can be additional associated defects. Thickening of the heart muscle (hypertrophic cardiomyopathy). This is abnormal growth or thickening of the heart muscle that affects more than 20 percent of people with Noonan syndrome. Other structural defects. People with Noonan syndrome often have structural defects of the heart. The defects involve a hole in the wall that separates the two lower chambers of the heart (ventricular septal defect), or a condition that causes a narrowing of the arteries that carry blood to the lungs for oxygen (pulmonary artery stenosis). |
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126. What are the four congenital lesions which can present with cyanosis at birth and are considered cardiac emergencies in a new born?
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Tetralogy of Fallot, Transposition of Great Vessels, Truncus arteriosus, tricuspid atresia, Total anomalous pulmonary venous return. (Rapid Review Pathology, Goljan 175). Also in Heibel’s PPT “Cardiac Part II” Slide 8
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which deadly congenital heart lesion is most common
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teratology fo fallot
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128. Describe the heart shape of truncus arteriosis on X-ray:
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The normal mediastinum is largely contributed to by the “x-like” crossing of the pulmonary artery and aorta. In truncus arteriosus (TA) there is a single great vessel (truncus) resulting in a narrow mediastinum. In addition, many patients with TA have DiGeorge syndrome, where there is small or no thymus gland, further contributing to the appearance of a narrow mediastinum. The size and origin of the pulmonary arteries can be quite variable in this lesion and may be speculated at in this view by the amount of flow noted to each lung segment (Fig. 2.13).2 • Cardiomegaly • Right aortic arch (33%) • Concave pulmonary artery segment • Enlarged left atrium in 50%
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129. What is expected on examining an X-ray of a patient with tricuspid atresia?
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Normal-sized heart • Decreased pulmonary vessels (60-70%) • Flat/concave pulmonary artery • Small ASD ␣ enlarged RA square shaped heart
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130. Transposition is noted by the rapidity of the development of what post birth.
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They usually have: VSD, cyanosis, no murmur, loud single S2 (Heibel PPT Cardiac Part 2 – slide 12)
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131. Closure of any of PDA, VSD or patent foamen ovale in complete transposition induces:
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Initial defects include: aorta rising out of the right ventricle, pulmonary artery rises out of the left ventricle, left and right atria are normal. CARDIOPROTECTIVE SHUNTS ASD in right atrium increases SaO2 in right ventricle for delivery to tissues via the aorta. VSD shunts blood into left ventricle for oxygenation in the lungs via pulmonary artery. PDA shunts blood into the pulmonary artery for oxygenation of the lungs. If any of these closes, it will produce CYANOSIS and DEATH. (Rapid Review Pathology – Goljan pg 175).
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132. Transposition x-ray appearance:
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egg on side Heibel PPT “Cardiac Part 2” slide 12
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133. Where is the connection of the pulmonary veins in total anomalous pulmonary venous return if a baby is presenting 12 hours after birth with cyanosis and tachycardia and no murmur?
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Total anomalous pulmonary venous connection (TAPVC) consists of an abnormality of blood flow in which all 4 pulmonary veins drain into systemic veins or the right atrium with or without pulmonary venous obstruction. Systemic and pulmonary venous blood mix in the right atrium. An atrial defect or foramen ovale (part of the complex) is important in left ventricular output both in fetal and in newborn circulation (http://emedicine.medscape.com/article/899491-overview)
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134. Describe the heart shape on X-ray of tetrology of Fallot:
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Couer en Sabat: boot shaped heart, with decreased lung vascularity Heibel PPT “Cardiac Part 2” slide 9
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135. What are the components of Tetrology of Fallot?
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• Stenotic pulmonary valve
• Ventricular septal defect • Overriding aortic valve (destroposition of the aorta) • Hypertrophy of right ventricle |
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136. What is the usual cause behind the development of ventricular fibrillation and death?
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Acute myocardial ischemia is the most common trigger for fatal arrhythmias
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137. What underlying conditions cause ventricular tachycardia in the absence of structural heart disease?
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I cannot find this question ANYWHERE. I checked online and in all our books. I’ll talk to Heibel tomorrow and update this with what he tells me
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139. Three findings that should suggest a possible diagnosis of infective endocarditis:
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Fever, fatigue, murmur, sudden onset of congestive heart failure, signs of neurological dysfunctions, Janeway lesion (small erythematous or hemorrhagic macules appearing on the palms and soles), Osler nodes (appear on the tips of fingers or toes and are caused by septic emboli, roth spots (necrosis with central clearing on fundoscopy)
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140. Which bacterial endocarditis occurs most commonly on previously abnormal valves?
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Subacute bacterial endocarditis, caused by streptococci viridans or by an enterococci. These organisms can only colonize on damaged heart valves. Compare this to acute endocarditis in which the organisms colonize on healthy heart valves
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141. What cardiac abnormality is the most common one to develop endocarditis?
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Endocarditis is associated with congenital heart defects Big Path 565-8
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142. What is the most common presentation of a patient with severe acute endocarditis?
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High grade fever, chills, and rapid onset congestive heart failure
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143. Characterize the fever pattern in subacute endocarditis.
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For subacute endocarditis they have all the symptoms of acute endocarditis but is characterized by additional symptoms of anorexia, back pain, and weight loss with an additional history of endocarditis
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144. Endocarditis occurs predominately on left sided valves with one exception:
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S. Aureus infections in IV drug users affects the tricuspid
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145. What is the most common organism which causes acute endocarditis?
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S. Aureus
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146. What is the organism most likely responsible for subacute bacterial endocarditis?
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Streptococci viridans
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147. What are 2 major criteria for making a diagnosis of endocarditis?
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▬ Positive blood culture
▬ echo ID of valve damage |
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148. What is the recommended number of and timing of obtaining blood cultures?
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▬ 2 positive cultures, >12 hrs apart
▬ 3 positive cultures or a majority of ≥4 positive cultures, >1 hr apart |
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149. What dermatologic findings can be seen on physical examination in endocarditis?
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Janeway lesion small erythematous or hemorrhagic macules appearing on the palms and soles
Osler nodes appear on the tips of fingers or toes and are caused by septic emboli |
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150. At what age range does acute rheumatic fever usually present?
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▬ Ages 5-15 (childhood)
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151. What are the major criteria for acute rheumatic fever?
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▬ Polyarthritis - temporary migrating inflammation of large joints, usually starting in legs & migrating upward
▬ Carditis - inflammation of the heart or its surroundings ▬ Subcutaneous nodules - painful, firm collections of collagen fibers over bones or tendons; commonly appear on back of wrist, outside elbow & front of knees ▬ Erythema marginatum - long-lasting reddish rash that begins on trunk or arms as macules, which spread outward & clear in the middle to form rings; typically spares the face and is made worse with heat ▬ Sydenham’s chorea (St. Vitus’ dance) - irregular, rapid, uncontrolled, involuntary, excessive movement that seems to flow randomly from one part of the body to another |
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152. Which of the major ARF criteria is the most common?
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▬ Polyarthritis
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153. What are the characteristics of the polyarthritis in acute rheumatic fever?
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▬ Painful, tender, swollen warm joints (2+ joints, primarily ankles, knees, elbows & wrists)
▬ Arthralgia (joint pain) lacks tenderness during passive movement of affected joint (joint can be moved through range of motion) ▬ Usually subsides spontaneous without leaving any sequelae & is non-deforming |
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154. List at least 2 of the findings on physical exam that indicate acute rheumatic carditis.
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▬ inflammation of the heart muscle can manifest as CHF
▬ pericarditis with rub ▬ a new heart murmur |
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155. What layers of the heart are involved with rheumatic carditis?
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▬ All layers of the heart (pancarditis - pericardium, myocardium & endocardium)
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156. What is the pathologic hallmark of rheumatic carditis?
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Aschoff nodules/granulomas/bodies: inflammation of connective tissue of heart
Fibrinoid change Lymphocytic infiltration Occasional plasma cells Abnormal macrophages surrounding necrotic centers ▬ Path 565 |
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157. What part of the body is typically spared in erythema marginatum?
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▬ Face
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158. What exam finding develops late, but is characteristic of ARF?
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Valvular abnormalities (Path pg 565)
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159. What does the onset of Sydenham’s chorea and or mitral stenosis have in common
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they both may occur following streptoccal pharangitis
Sydenham’s chorea: Aimless jerky movements (pg 421 CE)?!? |
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160. What valve murmurs would you expect in the acute phase of rheumatic fever?
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Murmurs of mitral regurgitation and aortic insufficency(pg 421 CE book) affected valves become stenotic and regurgitant.
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161. What organism is responsible for the development of ARF?
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Group A Streptococcal Infection (pg 421 CE book)
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162. What is the current antibiotic regimen in the treatment of ARF?
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Penicillin therapy (10 day oral course) is standard therapy
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163, 164. After an episode of ARF, what valve is the most likely to be significantly damaged long term and what population subset will present with symptoms in the 30-50 age range?
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-mitral valve (path pg 565)
-Im not sure about the 30-50 range....(path 565) incidence and mortality of RHD has declined except in developing countries and in crowded, economically depressed urban areas in the US, its an important public health problem affecting 15 million. -GAS pharyngitis has peak incidence in 5-15 year olds which leads to ARF (microbial disease pg 16, CE pg 421) |
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165. Pressure in the LA is higher than LV pressure during
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Diastole
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166. What would be the lifestyle modifications you would suggest to a patient with high risk for the development of atherosclerosis?
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Staying well: (CE pg 392)
1. Diet that is low in cholesterol, consider oral agents (statins) if diet alone is not sufficient 2. Exercise regularly (even brisk walking) 3. Quit smoking (behavioral programs and newly approved medications may assist) 4. Monitor BP, Blood glucose, inflammatory markers and lipids annually. |
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167. What drug is administered during an episode of angina?
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Nitroglycerine (CE pg389)
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amiodarone SE
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pulmonary fibrosis
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procainamide SE
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pericarditis
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ace inhibitor SE
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dry cough
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cocaine SE
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coronary spasm and MI
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digitalis SE
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heart block
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nitroglycerine SE
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hypotension
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beta blocker SE
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heart block and CHF
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daunorubicin SE
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cardiomyopathy
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methyldopa SE
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AV block
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