My Cardiology

  1. Outline the approach to interpreting an ECG
    • "An ECG does Not Really Require A Woman's Input"
    • Name
    • Rate
    • Rhythm
    • Axis
    • Waves
    • Intervals
  2. What are the common ECG findings in an acute MI?
    • ST segment elevation (>80ms)
    • Prominent, symmetrical, pointed T waves
  3. How is heart axis determined on an ECG?
    • Examine lead I and II
    • If the QRS complex of both are mostly positive = normal axis
    • If I-QRS positive and II-QRS negative, then posterior deviation
    • If opposite; I-negative, II positive then anterior deviation
  4. What are the ECG findings of 1st and 3rd degree heart block?
    • 1st degree: Prolonged PR interval (>0.2 secs); delayed conduction from atria-ventricles
    • 3rd: No relation between P and QRS; complete block of conduction
  5. How are the waves of an ECG examined?
    • P: One per QRS, no bifidity [except v1]
    • ST: Elevation?
    • T: Inversion in V3-6 or I/II?
  6. How is the heart rate measured and rhythm determined using an ECG?
    • 300 divided by the number of large boxes between each R spike. (0.6-1.2 seconds)
    • Mark a strip of paper at every R spike; abnormal/repetitive pattern?
  7. What are the important intervals to note when examining an ECG?
    • PR: 1/2 - 1 full large box
    • QRS: 1/2 a large box
    • QT: 2 large boxes in II
  8. What is the relation between cholesterol levels and CVD risk?
    • High total cholesterol: CVD risk
    • High LDL:HDL ratio: CVD risk
    • High total triglyceride: Diabetes risk
  9. 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
  10. What are the normal plasma concentrations of total cholesterol, HDLs and TAGs?
    • Cholesterol: <5mmol/L
    • Triglyceride: <2-3mmol/L
    • HDL: >1mmol/L
  11. Outline the pathogenesis of atheroma
    • LDL enters sub-endothelial space
    • Macrophages oxidise and consume the LDL
    • Toxic products are released, causing CAM expression and monocyte infiltration
    • Macrophages saturate and apoptose = LDL deposition
    • Thickness of endothelium related to stable/unstable plaque due to collagen exposure
  12. What are the roles of HDLs in preventing atheroma?
    • Removes cholesterol from muscle/fat for bile acid conversion
    • Inhibit monocyte adhesion
    • Antioxidant, preventing LDL oxidation
  13. What are some risk factors for CHD?
    • Smoking
    • Increasing age
    • Hypertension
    • Lipid ratio
    • Gender
  14. Outline the mechanism of action of statins
    • Inhibit HMG-CoA reductase; prevent cholesterol production from acetyl CoA
    • To maintain bile acid production, cholesterol removed from tissue by increased HDL ratio
  15. Why would a patient on statins need their plasma CK monitored?
    • Muscle pain a common adverse effect, related to myopathy and rhabdomyolysis
    • If it occurs, monitoring required due to CK release; risk of renal impairement
  16. What is ezetimibe used for?
    Prevents cholesterol absorption in the brush border of the small intestine
  17. Describe the course of the coronary arteries
    Image Upload 1
  18. What are the common acute coronary syndromes?
    • Stemi
    • Non-stemi
    • Unstable angina: Angina caused by atherosclerotic plaque disruption and so thombosis/embolism. Acute, severe, wave-like pain at rest
  19. What are the recommendations for reperfusion after MI?
    • Treated <90 minutes after diagnosis if possible
    • Primary PCI; angioplasty, where stent inflated and plaque 'crushed' against walls
    • Thrombolysis given until PCI available
    • Abciximab; Ig which antagonises platelet activation
  20. Briefly outline the pathogenesis of heart failure
    • Failure of the heart to pump blood sufficiently to supply tissue's demands
    • Characterised by typical haemodynamic changes, e.g. systemic vasoconstriction and neuro-humoral activation
    • Causes include MI, hypertension, valve disease
  21. What are the common clinical featuers of heart failure?
    • Breathlessness, crackles, orthopnoea, PND, cough
    • Effort intolerance, muscle fatigue
    • Fluid retention and oedema
    • Elevated JVP and displaced apex beat
  22. What investigations are performed in suspected HF?
    • ECG
    • CXR/Ct angio
    • Echo
    • Biochemistry; U+Es, cr, urea, LFTs, urate
    • Exercise test
  23. What pharmacological interventions are used in HF?
    • O2
    • ACE/ARB and beta blockers the cornerstone of acute therapy
    • Diuretics
    • IV nitrates
    • Many treatments depend on cause; kidney failure/LV remodelling can make HF refractory
  24. What is cardiac resynchronization therapy?
    • Pacemaker controlled right and left ventricle
    • Used in patients with ventricular fibrillation in severe HF
    • Only really used in patients with LBBB
  25. Define infective endocarditis
    • Infection of the endocardium (inner heart lining)
    • Results in valve damage
  26. In what order are the valves most frequently damage in IE?
    • Mitral
    • Aortic
    • Tricuspid
    • Pulmonary (very rare)
  27. What are some of the acute clinical features of IE?
    • Sepsis; hypotension, tachycardia
    • Valve destruction
    • Metastatic infection
  28. What clinical features suggest IE?
    • Fever and heart murmur
    • Left sided: embolism = splinter haemorrhage, petichae, renal infarction
    • Right sided: septic pulmonary emboli
  29. What circumstances should instigate investiation for IE?
    • Established Staph Aureus infection
    • IVDU with positive blood culture
    • Prosthetic valve patient with positive blood culture
    • Sepsis of unknown origin
  30. What investigations are performed to diagnose IE?
    • CXR: Multiple focal infiltrates and calficiations
    • ECG: Ischaemia, conduction delay or arrhythmia
    • Blood cultures: Take 3 before antibiotics; bacteraemia
    • Echo: transthoracic/oesophageal
    • CMRI and CTA
  31. How many of the duke criteria must be met to establish IE?
    • Two major criteria
    • One major, three minor
    • Five minor
  32. 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
  33. What are the minor criteria in the Duke diagnosis of IE?
    • Predisposing factor, e.g. IVDU, cardiac lesion
    • Fever (>38)
    • Evidence of embolism
    • Immunological problems
    • Positive blood culture with inconsistent organism
    • Serological evidence of consistent organism infection
  34. What are the common causes of IE in:
    - The general populace
    - IVDUs
    - PVE
    • Strep Viridance (or enterococci)
    • Staph Aureus
    • Coagulase negative staph
  35. What is rheumatic fever, and how does it cause IE?
    • Strep pyogenes infection
    • Bacteria or exotoxin have 'molecular mimicry'
    • Antibodies cause autoimmunity against cardiac valves and kidneys
    • Stenosis and regurgitation occur
  36. Outline the antibiotics used in IE
    • Before cultures: Benzylpenicillin and gentamicin
    • Strep: Benzyl and gentamicin
    • Entero: Amoxicillin and vanco/gentamicin
    • S.A: Flucloxacillin
    • MRSA: Vancomycin and rifampicin
    • CONS: Vancomycin+/gentamicin+/rifampicin
  37. What are some important complications of acute MI
    • Congestive heart failure
    • Myocardial rupture
    • Arrhythmia
  38. Describe the long term care of patients after an MI
    • Lifestyle changes: diet, alcohol/smoking, physical activity, weight
    • Cardiac rehabilitation: Educational/exercise/supportive role
    • Drug therapy: ACE, aspirin, B1 and statin
Card Set
My Cardiology
ECG, cardiology, lipids, MI