A: Finals: Cardiology

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  1. Outline the conducting pathway of the heart
    • Autonomic and endocrine control
    • Sinu-atrial node (right atrium)
    • Atrioventricular node
    • Bundle of His
    • Left/Right bundle (left has 2 branches, ant/post)
    • Purkinje fibres
  2. What is preload?
    Pressure of blood on the left ventricle after diastole (when passive filling has completed)
  3. What is afterload?
    The amount of systemic pressure that needs to be exceeded by the ventricles to open the aortic/pulmonary valves
  4. What is stable angina?
    • A relatively unchanging reduction in coronary blood flow
    • Insufficient blood flow occurs when heart activity increases
    • No thrombotic pathogenesis
  5. What is unstable angina?
    • Acute reduction in coronary blood flow
    • Typically caused by endothelial rupture in pre-existing stable angina/atheromatous disease
    • Symptoms of this angina occur at rest, with rise in troponin due to clotting involvement
  6. What are the major criteria in the Duke diagnosis of IE?
    • Causative organism in 2 separate cultures
    • Positive echo OR new valve regurgitation detected in auscultation
  7. What investigations are required in suspected IE?
    • ECG: Ischaemia, conduction delay or arrhythmia
    • Blood cultures: S. Viridans/S. Aureaus
    • Echo: Valve function and ejection volume
    • CXR: Valve calcification
  8. What is rheumatic fever?
    • S. Pyogenes infection
    • 'Molecular mimicry' effect
    • Autoimmunity against valves and kidneys
    • Both stenosis and regurgitation occur
  9. What is the lower limit for ST segment elevation?
    • 80ms
    • 2 small boxes
  10. How is heart axis determined on an ECG?
    • Examine QRS in lead I and II
    • Normal = Both are mostly positive
    • Posterior deviation = I positive and II negative
    • Anterior = I is negative, II positive
  11. Briefly describe the normal metabolism of cholesterols
    • Absorbed in GI, enter lymph as chylomicrons
    • In liver, converted to cholesterol then either bile, vLDL or LDL
    • Transported to tissues, which can return it as HDL (which is then converted to bile)
  12. Outline the pathogenesis of atheroma
    • LDL enters sub-endothelial space when high blood content
    • Macrophages consume and oxidise the LDL
    • Cytoplasm enlarges and saturates, making "foam cells"
    • Apoptotis occurs, causing LDL release and inflammation
  13. What is the MoA of statins?
    • Inhibit HMG-CoA reductase activity in liver
    • Reduced cholesterol production from acetyl CoA
    • Liver LDL receptors expressed to remove cholesterol from bloodstream
    • Cholesterol processed into bile salts, excreted and 95% absorbed by bowel
  14. What modifiable risk factors can be managed for primary prevention of cardiovascular events? Give 6
    • Smoking
    • Alcohol consumption
    • Blood pressure
    • BMI/obesity
    • Cholesterol
    • Blood glucose
  15. What are the most common and most dangerous adverse effects of statins?
    Side effects: Muscle/joint pain or cramps, malaise, GI features

    Complications: Serious drug interactions, rhabdomyolysis, acute renal failure
  16. What other lipid-lowering therapies are available if statins are not tolerated? What is their MoA? Give 3
    Fibrates: Increase liver FFA uptake and converstion to acetyl-CoA

    Ezetimibe: Reduced absorption of lipids in small intestine

    Resins: Same as ezetimibe
  17. Describe the anatomy of the coronary arteries
    Image Upload
  18. Outline cardiovascular-related factors in the pathogenesis of heart failure
    - Build up of exacerbating factors, especially increased systemic resistance

    - Intrinsic changes, e.g. ventricular hypertrophy and frank-starling mechanism, allow compensation

    - Injury to heart, acute or chronic increase in preload or afterload cause decompensation and dilation of ventricles

    - Loss of systolic output, as sufficient ventricular pressure in systole not able to be maintained
  19. Outline non-cardiovascular related factors in the pathogenesis of heart failure
    • Loss of systolic output causes compensation, relying on frank-starling mechanism
    • Systemic modulation via ANS (carotid sinus receptors - medulla - SA node/peripheral constriction)
    • ADH secretion from carotid/atrial baroreceptor activation
    • RAS system causes vasoconstriction and retention of Na/H20 by aldosterone (juxtaglomerular cells)
  20. What are the causes of an exacerbation of heart failure?
    • Hypertension
    • Environment
    • Anaemia
    • Rheumatic
    • Thyroid
    • Failed medication
    • Arrhythmia
    • Infection/infarction
    • Lung disease
    • Endocrine
    • Diet
  21. Give 5 signs and 5 symptoms of heart failure
    • Symptoms:
    • - Dypnoea
    • - PND
    • - Orthopnoea
    • - Cough
    • - Exercise intolerance

    • Signs:
    • - Crackles
    • - Bilateral effusion
    • - Pitting oedema
    • - Increased JVP
    • - Displaced apex
  22. What are the investigative findings in heart failure?
    • ECG: Axis deviation, evidence of ischaemia/MI (st segment or q wave changes)
    • CXR: Cardiomegaly, effusion, oedema, kerley b-lines [<1cm lines in lung peripheriesl], cuffing
    • Echo: Dilated ventricle/hypertrophy with poor ejection fraction
  23. Briefly outline the classification of arrhythmias
    • Bradyarrhythmias <60bpm
    • Tachyarrhythmias >100bpm

    Tachyarrhythmias: Regular or irregular

    Regular: Narrow or broad QRS
  24. What causes bradycardias? List 5 of them
    Due to failure of impulse formation or impulse conduction from atria to ventricles (AV block)

    • - Sinus bradycardia
    • - AV-block escape rhythm
    • - Hypothyroidism
    • - Infarction
    • - Drugs; B-Blockers, CCBs, digitalis
  25. Describe the use of troponin measurement in suspected MI
    • Protein not detectable in normal people (high specificity)
    • Also highly sensitive
    • Troponin levels can take 9-12 hours to raise, so should be checked on admission AND 12 hours later
  26. Give 5 medications used in the prevention of MI
    • Aspirin
    • Lipid lowering therapy (Statin)
    • B-Blockers
    • CCBs
    • Isosorbide mononitrate (symptomatic)
  27. What ECG leads are:
    - Inferior
    - Lateral
    - Anterior
    • II, III and aVF (Bottom left)
    • I, aVL
    • V3, 4 initially and others if infarction large. Lower leads = anteroseptal, higher means anterolateral
  28. Give 5 ECG features that might be seen in acute MI
    • Hyperacute T wave
    • ST segment elevation
    • Q waves
    • New BBB
    • VF/VT
  29. Give 5 short term or long term complications of MI
    • Heart failure
    • Myocardial rupture
    • Bundle branch block
    • Arrhythmias
    • VSD
  30. Outline the pathophysiology of mitral stenosis and the resulting clinical features
    • Almost always due to rheumatic fever (foreigners or elderly)
    • Left atrial pressure/volume increases and hypertrophy occurs to maintain flow through valve
    • Pulmonary venous pressure increases, causing pulmonary artery hypertension
    • Right ventricle hypertrophy, dilatation and failure
    • Stenosed valve means mid-diastolic murmur as ventricle refills
  31. Give 5 signs of mitral stenosis
    • Malar flush
    • Weak pulse
    • AF
    • Increased JVP (RHF)
  32. Outline the pathophysiology of mitral regurgitation and the resulting features
    • Hypertensive or systemic disease causes valve damage
    • Compliance of L.A. causes regurgitating blood to increase pressure
    • Pulmonary venous pressure rises and oedema occurs
    • Ventricular systole pushes blood into atrium causing pan-systolic murmur
  33. Outline the pathophysiology of aortic stenosis and its resulting features
    • Increased resistance leads to left ventricular hypertrophy and ischaemia
    • Exercise intolerance, arrhythmia and angina occur in moderate stenosis
    • Increased pressure causes ejection systolic murmur
  34. Outline the pathophysiology of aortic regurgitation and its resulting features
    • Reflux of blood means reduction in cardiac ouput, meaning ventricular hypertrophy occurs
    • Diastolic run off causes reduction in diastolic BP and reduced coronary perfusion
    • Systolic pressure increases to improve perfusion
    • "Hyperdynamic" circulation, i.e. difference in sys/dia greater
  35. Give 5 signs of aortic regurgitation
    • Early diastolic AND ejection systolic
    • Collapsing pulse
    • Pistol shot femorals
    • Capillary pulsation
    • Head nodding
  36. Outline the pathophysiology of tricuspid stenosis
    • Don't bother with this condition
    • Caused by rhematic fever and associated with other valve disease typically
    • Features of right heart failure
  37. Outline the pathophysiology of tricuspid regurgitation and its resulting features
    • Don't bother with this condition
    • Can be functional due to right ventricle dilation or rheumatic fever
    • "Blowing" pan systolic murmur
  38. Outline the pathophysiology of pulmonary stenosis and its resulting features
    • Increase in right ventricle pressure causes hypertrophy and dilation
    • Systemic features of heart failure occur; JVP, ascites, oedema
    • Ejection systolic murmur
  39. Outline the pathophysiology of pulmonary regurgitation and its resulting features
    • Occurs due to pulmonary hypertension
    • Diastolic murmur
  40. Outline the management of acute heart failure
    • Fuck My NOPP
    • Frusemide
    • Morphine
    • Nitrates
    • Oxygen
    • Positive pressure airway ventilation
  41. What is a ventricular assist device and when is it used?
    • Implanted device which takes blood from the ventricle and pumps it into the corresponding great vessel
    • Can be extra or intracorporeal
    • Complications include TE, bleeding, infection and malfunction
  42. Outline the pathophysiology of AF
    • Any condition resulting in injury or distension of atria
    • Fibrillation of atria, which conducts to AV node but is physiologically slowed
    • Ventricles beat quickly but inefficienctly
    • Loss of CO and blood stasis causes thrombosis
  43. What factors aid in deciding between rate or rhythm control in AF?
    • Rate:
    • - Patient age >65
    • - Known IHD
    • - AF duration >1yr
    • - Anti-arrhythmics contraindicated

    • Rhythm control:
    • - Young symptomatic patients
    • - Correctable aetiology
  44. How is the stroke risk of AF patients stratified?
    • High risk: Previous TE event, >75 with disease or evidence of impaired LV function Warfarin
    • Moderate: >65 or <75 with HBP/DM W/A
    • Low: Anyone else Aspirin
  45. Give 5 patient factors which indicate careful monitoring is required when warfarin prescribed
    • Over 75
    • Concurrent antiplatelet therapy
    • NSAIDs
    • Uncontrolled hypertension
    • History of bleeds; e.g peptic ulcer, cerebral
  46. What stratergies are used to induce cardioversion and when are they indicated?
    • Electrical alone: When little risk of failure
    • Sotalol/amiodarone: 4 weeks, then electrical cardioversion
    • Drugs: Rhythm control alone
  47. When are anticoagulants required before/after cardioversion and for how long?
    • Before
    • - If onset <48 hours then heparin
    • - If >48 then 3 weeks of anticoagulation before

    • After
    • - 4 weeks of anticoagulation unless >48hr onset
    • - Further anticoagulation if appropriate
  48. Outline the drugs used in rhythm control of AF, from first choice onwards
    • Standard beta blocker
    • Class 1c (flecanide) or sotalol if SHD present
    • Amiodarone if SHD present or other drugs fail
    • If rhythm control fails, move to rate control or refer for other methods
  49. What medications are used in the rate control of AF?
    • Thromboprophylaxis first
    • Beta blocker/rate limiting CCB
    • Add digoxin if further control required
    • Refer to specialist for amiodarone/other if still required
  50. Outline the pathophysiology of atrial flutter
    • Rapid but regular atrial depolarisation >300bpm
    • Caused by a re-entrant rhythm, i.e. 'loop'
    • AV node blocks to a ratio of 2:1 (or 3:1) so pulse is 150bpm
  51. What ECG features are seen in atrial flutter?
    • "Sawtooth" in inferior leads
    • Valsalva/massage or adenosine can reduce ventricular beats and reveal P-waves
  52. Give 3 ECG features seen in VT
    • Ventricular rate >100bpm
    • Monomorphic or polymorphic (life threatening)
    • Broad complex
  53. Give 8 causes of cardiac arrest
    • Hypovolemia
    • Hyperkalaemia
    • Hypothermia
    • Hydrogen ions
    • Thromboembolism
    • Tension pneumothorax
    • Tamponade
    • Tablets
  54. Outline the NYHA scoring system
    • New York Heart Association
    • 1: No symptoms or limitation
    • 2: Mild
    • 3: Marked limitation but comfortable at rest
    • 4: Severe limitations even at rest
  55. Give 5 causes of sinus bradycardia
    • Physiological
    • Hypothermia
    • Hypothyroidism
    • Drugs
    • Sick sinus syndrome
  56. Describe the ECG findings in each type of AV block
    • 1st degree: PR interval >200ms
    • 2nd type 1: Elongating PR interval until QRS drops
    • 2nd type 2: PR interval normal but QRS dropped. Can become 3rd
    • 3rd degree: No relation between P and QRS (complete). Bradycardia
  57. Give 5 signs of heart block seen on chest x-ray
    • Cardiomegaly
    • Bat-wing mediastinal opacification
    • Bilateral pleural effusions/CPh angle blunting
    • Kerley B lines
    • Bronchoalveolar cuffing
  58. Give 3 methods of managing chronic heart failure
    • Lifestyle: Elevate head at night and secondary prevention
    • Symptom management: Domiciliary O2
    • Pharmacological: RAAS, IsMN, diuretics, bBs
  59. Give 5 underlying causes of hypertension
    • Essential (likely atherosclerosis)
    • Renal disease (e.g. ADPKD, failure)
    • Cushing's
    • Phaeo
    • Pregnancy
  60. List the steps of drugs in hypertension management
    • ACE inhibitors/ARBs (skip step if <55 or black)
    • + calcium channel blocker
    • + Thiazide
    • + increase diuretic, alpha or beta blockers
  61. Give 4 features typical of pericarditis
    • Sudden "sharp" pain
    • Pain relieved when leaning forward
    • Friction rub
    • Excessive sweating
  62. Give 4 signs on examination found in PVD
    • Pallor
    • Absent pulses
    • Cold
    • Low ankle:brachial pressure index
  63. How might suspected peripheral vascular disease be investigated?
    • US doppler to find atherosclerosis
    • X-ray angiogram
    • CT angiogram
  64. Outline the acute management of critical limb ischaemia
    • Exam and doppler US to assess ischaemia
    • WHO ladder analgesia
    • Surgical referral for revascularisation with angioplasty/stenting
    • If revascularisation contra-indicated, amputation required
  65. What management options are available for PVD
    • Supervised exercise
    • Medical: Antiplatelet therapy, thrombolysis
    • Surgical: Angioplasty/stenting/bypass/graft when severe
    • If above not effective, naftidofuryl oxalate
  66. Give 5 features suggesting AAA rupture
    • Extreme general abdominal pain
    • Hypotension
    • Tachycardia
    • Flank bruising
    • Abdominal mass/rigid
  67. Give 5 risk factors for abdominal aortic aneurysm
    • Male
    • Increasing age
    • Atherosclerosis
    • Connective tissue disorders
    • Trauma/surgery
  68. Outline the screening programme for AAA
    • Men >65
    • 10 minute US
    • Conservative management if <5.5cm
  69. Outline the management options for AAA
    • Lifestyle: Smoking
    • Medication: HTN and dyslipidemia
    • Surgical: Endovascular stent
  70. What is the prognosis for a ruptured aortic aneurysm?
    • 1 in 3 fail to survive trip to hospital
    • Emergency repair mortality 80%
    • Compare with 5% mortality for elective repair
  71. Give 3 management options for varicose veins
    • Conservative: Compression stockings, NSAIDs, dry skin
    • Stripping: Removal of saphenous vein
    • Ablation: Endovascular laser causes contraction
  72. Give 5 risk factors for varicose veins
    • Female
    • Increasing age
    • Pregnancy
    • Obesity
    • Family history
  73. Give 4 features of an arterial ulcer
    • 'Punched out' appearance
    • Intensely painful
    • Distal limb/digits
    • Underlying fascia visible
Card Set:
A: Finals: Cardiology
2014-02-10 15:27:41
Heart block anatomy

Heart blocka antomy
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