Cardiology 7

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  1. Beck TRIAD of Tamponade
    HYPOtension, Elevated jugular venous pressure, Small quiet/ muffled heart
  2. Atrial Fibrillation TRIAD
    Coronary artery disease, Mitral stenosis, Hyperthyroidism
  3. Aortic Stenosis TRIAD
    Chest pain/ angina, SOB (or CHF), Syncope
  4. Virchow TRIAD (predisposed to venous thrombosis/ Pulmonary Embolism)
    Local trauma to vessel wall (intimal damage), State of hypercoagubility, Venous stasis
  5. Endocarditis TRIAD
    Fever, Murmur, Septicemia
  6. More common in left iliac vein than right
  7. J wave on EKG
  8. Acute endocarditis
    Staph aureus
  9. Subacute endocarditis
    Strep viridans
  11. PE
    conventional pulmonary angiography
  12. CHF
  13. MI
    cardiac enzymes
  14. DDx: CP, hypotension and shock with distended neck veins
    Myocardial Ischemia, Cardiac Arrhythmia (brady or tachy), Cardiac Tamponade, Massive Pulmonary Embolism, Tension Pneumothorax
  15. DDx: chest pain and hypovolemia: shock due to hypovolemia
    Myocardial infarction, Aortic Dissection, Leaking AAA
  16. What is Beck’s triad a diagnosis of?
    Cardiac Tamponade
  17. What is Beck’s triad composed of
    JVD from an elevated central venous pressure (CVP), Hypotension, muffled heart sounds.
  18. What kind of chest pain is worse with inspiration
    Pleuritic CP
  19. What is the most common symptom of a pulmonary embolism?
    Dyspnea; others: pleuritic and non pleuritic CP, anxiety, cough & syncope
  20. Tracheal deviation is an indication of what?
  21. What are the SS of a pneumothorax?
    Tracheal dev, pleuritic pain, hyper resonance with decreased breath sounds unilaterally
  22. Who typically gets pneumothorax?
    Tall, thin, athletes
  23. What are the SS of pneumonia?
    Pleuritic pain with associated SOB, cough, fever, sputum production, rales & dullness (infection)
  24. Wheezing is typically a symptom of what?
  25. What are the SS of pulmonary edema?
    severe respiratory distress, frothy pink or white sputum, rales, S3/S4, PND, orthopnea, edema
  26. What is meant by flash edema?
    Rapid onset of SOB - edema
  27. What is S3 usually associated with?
  28. What is S4 associated with?
    HTN – L ventricular hypertrophy
  29. What is pleurisy?
    inflammation of pleurae
  30. What is pleurisy usually caused by?
    Infection or connective tissue/ inflammatory dz
  31. What are the SS of pleurisy?
    Friction rub and low grade fever
  32. What are the SS of pulmonary HTN?
    pleuritic CP – Loud P2, right ventricular lift
  33. What are GI causes of CP?
    GERD, Esophageal perforation, Mallory- Weiss, PUD, Cholecystitis, Pancreatitis
  34. What kind of pain is GERD associated w?
    Substernal or epigastric; squeezing or pressure- like; exertional or at rest; radiating; post-prandial ; postural changes; spasm
  35. What relieves GERD pain?
    Antacids / NTG
  36. Why is GERD pain similar to cardiac CP?
    Innervation for heart, esophagus & stomach are similar, so symptoms may be similar
  37. How does esophageal perforation present?
    Acute, severe, unrelenting & diffuse pain in chest, neck or abdomen (“worst pain of life”). May radiate to back or shoulders & swallowing may exacerbate pain
  38. How does a Mallory Weiss tear present?
    hematemesis with or without prior vomiting episode
  39. What is a Mallory –Weiss tear?
    A laceration in the mucus membrane of the lower part of the esophagus or upper part of stomach – usually from vomiting or coughing
  40. What are SS of PUD?
    burning epigastric pain, post-prandial sx, relieved with food; , may present as N & V, wt loss, anorexia & bleeding (especially in geriatric pts)
  41. How does cholecystitis present?
    epigastric/RUQ “visceral” pain + fever, chills, N & V, anorexia…may radiate to back or scapular region
  42. What are SS of pancreatitis?
    midepigastric, piercing pain, constant, radiates to back, associated with N & V, abdominal distention & exacerbation in supine position; Low- grade fever, tachycardia & hypotension may be present
  43. How does musculoskeletal CP present?
    Sharp pain, worse with movement/palpation (also 5-10% of MI pts have reproducible chest wall tenderness…be aware!)
  44. What is musculoskeletal pain typically relieved with
  45. This can present with fleeting chest pain, variable onset/duration (usually > 30 min & persistent) & often reproducible on palpation (but not with exertion)
    Panic disorder / anxiety
  46. What is the “typical” presentation of an acute MI
    New, sudden onset CP/pressure with associated SOB, nausea, diaphoresis
  47. When should an EKG be performed
    Goal is within 10 minutes
  48. What other diagnostic studies should be performed for angina?
    CXR, Cardiac biomarkers, CBC, D-dimer, PT-PTT, ECHO, V/Q scan, CT
  49. When is a d-dimer helpful?
    When it is very positive
  50. Is a d-dimer specific?
  51. Why get a PT/PTT?
    In case pt goes to cath
  52. What do you look for in an echo?
    LV and valvular function, WMA (wall motion abnormalities), effusion/septal defects
  53. Who goes to CPU (chest pain observation units)
    Patients at low risk of acute MI
  54. What do you do monitor in CPU?
    Rule out MI with serial ECGs & cardiac biomarkers (CK/MB, Troponin levels)
  55. Continuous telemetry monitoring
  56. Is myoglobin specific?
  57. Which are the most helpful cardiac markers?
    Troponin and CK-MB
  58. Which is released first: troponin or CK-MB?
  59. Who usually presents with atypical cardiac symptoms?
    Elderly, women, diabetic
  60. What is the definition of angina pectoris?
    chest discomfort or other related symptoms caused by myocardial ischemia
  61. What is stable angina?
    Deep, pressure-like pain in substernal region, may radiate to jaw, neck or left shoulder/arm, Frequently associated SOB, Transient – lasting 2-30 minutes, Precipitated by physical exertion or emotional stress, Responsive to rest or SL NTG
  62. Is the physical exam in stable angina usually normal or abnormal?
  63. What are some possible PE findings secondary to risk factors?
    Elevated BP +S4, arterial bruits, Retinal changes (AV nicking, Papilledema, cotton wool spots), Corneal arcus. Xanthelasma (skin)/Xanthomas(joints), CHF +S3 (transient LV dysfunction), Murmurs (transient papillary muscle dysfunction, typically MR), Elevated cholesterol, Elevated glucose
  64. Would cardiac enzymes be elevated in stable angina?
    NO- should be normal – there is blockage but still perfusing
  65. Would an CXR be normal in stable angina?
    Yes, often normal
  66. What are some EKG findings in stable angina when no CP is present ?
    1/3 normal / non specific changes, Non specific ST-T wave changes (elevation = closer to MI), Q waves = evidence of prior MI, Conduction abnormalities: *LBBB (high association with CAD), RBBB (can be normal), fascicular blocks (*stronger association)
  67. What would you see in unstable angina during angina in an EKG?
    ST segment depression/possibly elevation, *T wave inversion
  68. What is the treatment of stable angina?
    Lifestyle modification!, 81 – 325mg ASA daily – dose depends on other comorbidities, Beta blocker, ACE Inhibitor – low LV fx or diabetic, Nitrates (PRN or long acting), Statins/Lipid Agents, Consider Revascularization (PCI/Stent vs. CABG) palliative
  69. What are acute coronary syndromes?
    Unstable angina: NSTEMI, STEMI
  70. What is the presentation of a NSTEMI/ USA?
    New, sudden onset CP/pressure with associated SOB, nausea, diaphoresis. Chest Pain at greater frequency, severity or with less activity. Chest Pain at rest or nocturnally. Chest Pain previously controlled with nitrates, now refractory
  71. What are the EKG findings in NSTEMI/ USA
    EKG similar to stable angina but more likely to show acute ischemic changes (ST depression & T wave inversion)
  72. Are cardiac enzymes positive in USA?
    No, they are negative
  73. Are cardiac enzymes positive in NSTEMI
  74. What does MOAN stand for?
    Morphine, O2, ASA, NTG
  75. What is the diagnosis and treatment of USA/NSTEMI
    Admit/monitor, bed rest. MONA (Morphine, O2, NTG, ASA). Serial EKG & cardiac enzymes. ASA, Beta Blocker, NTG, ACE & anticoagulation (heparin/LMWH vs Platelet GP IIb/IIIa Inhibitors). Cardiac risk stratification with cardiac catheterization preferred. Plavix (clopidigrel) following cath
  76. What causes acute STEMI?
    thrombotic obstruction of epicardial coronary arteries
  77. What is the prognosis of STEMI?
    1/3 don’t survive – half deaths occur w/in first hour, 1/5 don’t recognize symptoms
  78. How does STEMI present?
    Sudden onset CP associated with nausea, diaphoresis & SOB
  79. CP persists > 30 min; may not respond to NTG
  80. What are PE findings of STEMI?
    HTN or hypotension, Tachycardia or bradycardia, S3 or S4 or both, Signs of CHF, Systolic murmurs (MR, VSD), Friction rub (usually day 2 or 3)
  81. Why are EKG’s performed on STEMI
    To id the site of infarct vessel
  82. What are EKG findings in a STEMI?
    Early Peaked T waves (0 – 6 hrs), ST segment elevation (0- 18 hrs), Q waves (takes ~ 18 hrs to “Q” out) & may remain lifelong or later disappear, Extent of ST deviation & QRS duration correlate with risk of adverse outcomes
  83. What EKG findings are indicative of an MI
    ST elevation at the J point in 2 or more contiguous leads
  84. Do EKG’s always indicate Acute MI?
    NO, Initial ECG is negative or non-diagnostic in up to 40% of patients having an AMI. Repeat ECG…if possible during CP episode
  85. What leads correspond with an inferior MI
    II, III, AVF
  86. What leads correspond with an anterior MI?
    (V2-V5) or (V1-V4)*
  87. Lateral MI?
    (I, aVL, V5-V6)
  88. Inferolateral
    (II, III, aVF, I, aVL)
  89. Anterolateral?
    (V4-V6, I, aVL)
  90. When is PCI the treatment of choice for a STEMI?
    Emergent PCI preferred if early presentation (< 3 hr from sx onset) & skilled team available (door to balloon time < 90 minutes
  91. When are lytics the preferred Rx of choice?
    Lytics within 12 hr of onset & no PCI option
  92. What are the ABSOLUTE contraindications to lytic therapy?
    any prior intra-cranial hemorrhage, cerebral AVM, malignant neoplasm, active bleeding, suspected aortic dissection, ischemic CVA in past 3 months or closed head trauma, severe uncontrollable HTN
  93. What other meds do you give STEMI?
    ASA, Beta Blockers, Oxygen, NTG +/- Morphine, ACE Inhibitors, Heparin/LMWH, GP IIb/IIIa Inhibitors, Statins, Aldosterone Inhibitors
  94. What are complications of STEMI?
    Arrhythmias (VT, VF or heart block), CHF/ Cardiogenic Shock, RV infarction, Ventricular Free Wall Rupture, Ventricular Septal Rupture, Mural thrombus/ embolus, CVA, Pericarditis, Postinfarction angina
  95. What is sudden cardiac death?
    unexpected non-traumatic death in clinically well or stable patients who die within 1 hour after onset of symptoms
  96. What is the most causative rhythm in SCD?
    ventricular tachycardia except in the setting of acute ischemia or infarction (then VF arrest)
  97. When do most SCD’s occur?
    Early am
  98. What is CHD mostly contributed to in Western cultures?
  99. What are PE findings of MVP?
    Mid-systolic click, inverted T waves inferior leads; unclear etiology of associated CP; myocardial ischemia vs increased systemic arterial pressure
  100. What are PE findings of aortic stenosis?
    Systolic ejection murmur transmitted to carotids. LVH on ECG
  101. What are PE findings for aortic regurgitation?
    Diastolic murmur transmitted to carotid arteries, wide arterial pulse pressure, ECG may show LVH
  102. Who is at increased risk of aortic dissection?
    Men, preggers, patients with connective tissue dz (Marfans), HTN, Bicuspid Aortic Valve or Coarctation of the Aorta
  103. What is an aortic dissection?
    • Intimal tear in aorta creates a false lumen between media & adventitia.
    • May be acute or chronic in nature.
  104. Where do AD’s occur?
    >95% occur in the Ascending aorta just distal to aortic valve or just distal to the left subclavian (fixed points)
  105. What are the two classification systems for AD?
    Debakey, Stanford
  106. What is the difference between debakey and sanford?
    Debakey – 3 parts. I Ascending aorta extending to distal (entire length). II. Ascending aorta only (before left subclavian). III. Descending aorta only (after left subclavian); Sanford – 2 parts: A. Any involvement of ascending aorta. B. Not involving ascending aorta
  107. What are SS of AD?
    Sudden onset retrosternal and back pain. May see infarct pattern on ECG, neurologic deficits/CVA, limb ischemia, syncope, shock, hypertensive. Pulse discrepancies, tamponade possible. Acute AI indicates aortic root involvement. Beware patients with Marfan’s syndrome
  108. What would you see on a CXR for AD?
    Widened Aortic silhouette. Widened mediastinum. Left pleural effusion. 10%-20% normal
  109. When is a CT helpful for AD?
    In acute presentation
  110. When is MRI useful in AD?
    For serial follow up
  111. What would you see on an EKG in AD?
    LVH, non-specific or inferior abnormalities (dissections preferentially extend into Right coronary ostium)
  112. What is the most sensitive & specific diagnostig study for AD?
    Echo- 98% sensitive, 99% specific, +/- pericardial effusion, done bedside
  113. What is the treatment goal for aortic dissection?
    achieve relative hypotension & bradycardia) beta blocker first, then nitroprusside to maintain SBP of 100 -120 mmHg
  114. How do you treat type A AD?
    Surgically (maybe valve replacement)
  115. How do you treat type B AD?
    Medically- except for: Rupture, Limb or visceral ischemia, ongoing pain, Saccular morphology uncontrolled HTN, Marfan’s, or AI (rare)
  116. What is the clinical picture of a AAA?
    Majority are asymptomatic. Prominent aortic pulsation. Pain (if present) described as epigastric fullness or lower back & hypogastric region. Gnawing, hours to days in duration, not positional. Severe back or abdominal pain & hypotension indicate rupture.
  117. When should AAA patients have an emergent vascular surgery consult?
    If diagnosis of rupturing is clear clinically
  118. What test do you use if hemodynamically stable pt?
  119. How do you manage AAA patient?
    Large bore IV, type & cross, monitor closely
  120. What are TAA clinical findings?
    40% of patients are asymptomatic at diagnosis, symptoms dependent on size & position of aneurysm. Pain (if present) substernal, back/neck . Rupture: worsening of pain to severe. Vascular sx: CHF, ischemia, thromboembolism. Mass Effect: SVC syndrome, tracheal deviation, cough, hemoptysis, dysphagia, hoarseness
  121. Is CXR diagnostic?
    Chest X-ray is NOT diagnostic alone (need CT or MRI if suspected & CXR-); stability of patient crucial. CXR + Must differentiate from anterior mediastinal mass (ie thymoma, lung CA)
  122. How do you manage TAA?
    Same as AAA- Large bore IV, type & cross, monitor closely
  123. An inflammation of the pericardium is usually associated with effusion is…
    Acute pericarditis
  124. What is AP due to?
    ~85% associated with viral or “idiopathic” etiology; remainder are associated with TB/bacterial/fungal infections, neoplastic dz, uremia or collagen vascular dz, or following MI cardiac surgery or irradiation
  125. What does excessive anticoagulation cause?
    hemorrhagic effusion
  126. What are clinical findings of AP?
    Pleuritic, sharp, stabbing CP that radiates to shoulders, back, neck that is worse on deep inspiration or movement, worse supine & relieved by sitting up & leaning forward. Low grade fever, dyspnea, friction rub LLSB & sometimes palpitations or dysphagia
  127. What is seen on EKG of AP?
    Upsloping ST segment
  128. What would be seen on CXR of AP?
    Usually normal- r/o other dz
  129. What labs would you order?
    CBC with diff, BUN/creatinine to r/out uremia, serologies (strep, ANA, viral studies), thyroid to ID underlying cause
  130. What would an echo reveal?
    may reveal effusion
  131. T/F – pericardiocentesis is necessary
    False - usually not necessary
  132. Who would you do a pericardiocentesis on?
    Patients with tamponade. Confirm / exclude purulent pericarditis
  133. Rx for AP?
    Stable pts Rx as OP with NSAIDs for 1 to 3 weeks. Treat underlying cause if identified
  134. Who should be admitted for AP?
    Any pt with myocarditis, uremic pericarditis, enlarged cardiac silhouette on CXR or hemodynamic compromise should be admitted for observation
  135. Why does tamponade occur?
    Tamponade occurs when the pressure in the pericardial sac exceeds normal RV filling pressure, resulting in restricted filling & decreased cardiac output
  136. What are conditions that lead to tamponade?
    Malignancy induced pericarditis. Aortic dissection. MI with Ventricular rupture. Pacemaker perforation during implant
  137. What are the symptoms of cardiac tamponade?
    Shortness of breath & weakness more likely than CP, tachycardia
  138. What would you see on PE when evaluating cardiac tamponade?
    Distended neck veins, pulsus paradoxus
  139. What is the diagnostic gold standard for tamponade?
    ECHO – large pericardial effusion
  140. What would you see on EKG in tamponade?
    Electrical alternans an/or low voltage. El Alt = beat to beat variability in the amplitude of the P & R waves unrelated to inspiratory cycle…really only see ~ 20% of time, but is diagnostic if present
  141. When is the only time CXR is helpful for tamponade?
    If you see a large cardiac silhouette
  142. Is cardiac tamponade an emergency
    YES! - Tamponade is a True Emergency
  143. What are SS of cardiac tamponade?
    Becks triad: hypotension, elevated systemic venous pressures, small quiet heart
  144. What are the treatments of tamponade?
    Volume resuscitation, Pericardiocentesis, Admit & consider Pericardial window
  145. What is the difference between hypertensive urgency / emergency
    Emergency has target organ damage (TOD!!)
  146. What is the Rx for hypertensive urgency?
    Short term Rx with labetalol, clonidine or captopril with outpatient follow up within 72 hrs is recommended
  147. What are the most common causes of hypertensive emergencies?
    CHF with pulmonary edema, cerebral infarction
  148. What is treatment for hypertensive emergencies?
    Goal of treatment is to achieve a controlled, gradual lowering of BP. 10% decrease in first hour, then 15% over next 3 – 12 hrs to BP of no less than 160/110 mmHg. Rapid correction of BP to norm levels puts pt at high risk for worsening cerebral, renal or cardiac ischemia
  149. Malignant htn is a form of hypertensive emergency or urgency
  150. Who is malignant HTN more common in?
    Most common in young adults, prior renal dz, AA males, pregnancy or in collagen vascular dz.
  151. What must be present in malignant HTN?
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Cardiology 7
Cardiology flashcards made by previous students
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