Week 05 - Cardiology

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mewinstanley@googlemail.com
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Week 05 - Cardiology
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2012-01-22 13:01:12
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Cardiology
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Week 5 cardiology
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  1. What is the mnemonic for ECG interpretation?
    The Interpretation of an ECG Does Not Really Recquire A Womans Intuition

    • Date
    • Name
    • Rate → [300/ num of big boxes between ea spike]
    • Rhythm → Sinus/ AF/ VF etc.
    • Axis → Leads I & II, QRS +ve = normal, I+II- = Left axis, I-II+ = right axis [Hand thing]
    • Waves → p waves present? T wave inversion?
    • Intervals → PR [120-200ms] QRS [60-100ms] QT [360-440ms]
  2. Outline the ECG features of the following Bradycardias
    -Sinus Bradycardia
    -Heart Block [1st, 2nd & 3rd degree]
    • Sinus Bradycardia
    • Longer PR, but narrow QRS, still regulated by sinus node
    • <60bpm

    • Heart Block
    • 1 → PR >200ms [delayed conduction thru AVn]
    • 2 → Wenkebach [^PR w each beat until dropped beat] or ^Pr w randomly dropped beats
    • 3 → complete block, no conduction A-V [no correlation between P-QRS]

    *dropped beat = absent QRS
  3. Outline the following Tachycardias
    -Atrial Fibrillation
    -Supraventricular Tachycardia
    -Ventricular Tachycardia
    -Ventricular Fibrillation
    • AF
    • irregular ventricular rhythmn, no P waves [^^clots]
    • Sawtooth ECG? → Atrial Flutter

    • SVT
    • Narrow QRS [rate from atria]
    • Regular Tachy cardia

    • Ventricular Tachycardia
    • Broad QRS [rate from ventricles]
    • regular
    • p wave dissociation

    • Ventricular Fibrillation
    • rapid irregular polymorphic ventricular rhythmn
    • Cause of cardiac arrest
  4. What do each of the waves on an ECG correspond to?
    • P → atrial depolarisation
    • delay to AV node
    • conduction thru bundle branches
    • QRS → ventricular depolarisation
    • Plateau thru repolarisation
    • T → final rapid repolarisation [ventricles]
  5. Which leads give the following views
    -Inferior
    -Anterior
    -Lateral
    • Inferior Leads
    • II III & aVF

    • Anterior Leads
    • V1-6

    • Lateral Leads
    • I aVL & V6
  6. Draw the lipid metabolism
    [diet liver tissues]
  7. Outline the pathogenesis of atheroma
    • Endothelial damage → inflamm/pressure etc
    • LDL into sub-endothelial space → oxidised
    • Macrophages digest → death → foam cells
    • Formation of lipid core

    • Either occlusion of lumen → stable angina
    • or plaque rupture resulting in throbus occlusion → unstable
  8. For statins give
    MoA
    Indications
    A/E
    WWJD?
    • MoA
    • Inhibits HMG-CoA reductase
    • result = dec cholesterol synthesis

    • Indications
    • Cholesterol >5mmol/l in CVD/CVA

    • A/E
    • ^LFTs
    • ^CK [~lethal] myalgia → rhabdomyolysis
    • ~DM

    • WWJD?
    • Advise about muscle pain
  9. What are the risk factors for CVD?
    -Modifiable
    -Non-modifiable
    • Non-Modifiable
    • Age
    • Male
    • FH
    • Asian ethnicity
    • lower social class

    • Modifiable
    • HBP [140/90, for ea ^10mmHg, ^20% CVD risk]
    • Smoking
    • Cholesterol
    • DM
    • Obesity
  10. What is the acute management of an MI
    MONICA

    • Morphine
    • O2
    • Nitrates
    • Interventional cardiology
    • Clopidogrel
    • Aspirin
  11. What is PCI, who gets it?
    • Percutaeneous Coronoray Intervention
    • i.e. put a stent in and get coronary BF back
    • Primary for STEMI pts
    • NSTEMI might get later
  12. What are the signs & symptoms of acute limb ischaemia?
    THE MUTHAFUKIN 6 PS!!!!!!

    • Pain
    • Pallor
    • Parasthesia
    • Power [loss of]
    • Pulseless
    • Perishingly cold
  13. What is Infective endocarditis & where is it most common?
    • IE
    • infection of endocardium
    • damage to cusps of valves [via vegetations]
    • Most common = Mitral
  14. Classify IE and for each give the most likely organisms
    • Native valve Endocarditis
    • Acute → S. Aureus
    • Sub-acute → strep viridans/ Enterococci

    • Prostheitic Valve Endocarditis
    • Coagulase negative staphylococci
    • Also gram negatives

    • IVDU
    • most = staph aureus
    • More common in right side
  15. What are the risk factors for native valve endocarditis?
    • Aortic stenosis
    • due to calcification [normal/congenitally abn valve]
    • Damaged valve from Rheumatic fever [strep pyogenes sOe]
    • Mitral valve prolapse
    • 30% non-identifiable
  16. What are the CF of IE?
    [Acute, subacute & Embolic events]
    • Acute
    • toxic Pc [hypotensive, fever, septic]
    • progressive valve destruction & metastatic infection

    • Sub-Acute
    • Mild toxicity
    • Pc Months → weeks
    • rarely metastatic

    • Embolic Events
    • Splinter haemorrhages [fingernails]
    • Janeway lesions → painless microabscess in palms & soles
    • Small emboli → petechiae, haematuria
    • Large Emboli → CVA, renal infarction
  17. What are the long term effects of IE?
    [untreated]
    • Oslers nodes → painful palpable lesions [hands & feet]
    • Immunological reaction [splenomegaly, nephritis, clubbing]
    • Valve destruction → abscess formation
  18. When should you think IE?
    Fever + Murmur = IE

    • All Pts w S.Aureus Bacteraemia
    • IVDU w +ve B/C
    • Prosthetic valve Pt w +B/C
  19. Outline the Dx of IE
    [Duke Criteria]
    • 3 sets of B/C before antibiotics
    • Echo
    • Transthoracic/ Trans oesophageal [^^sensitivity]

    Duke Criteria [2major/1maj, 2minor]

    • Major
    • Typical org in 2 separate B/C
    • +ve echo/valve regurg

    • Minor
    • predisposition
    • fever >38
    • vascular phenomena [septic emboli]
    • Immunological phenomena [Oslers nodes]
    • +ve B/C
  20. What are the typical orgs in IE?
    • Gram +ve
    • Streptococci → viridans/ enterococci
    • Staphylococci → Aureus [MSSA/MRSA] also coagulase negative staph

    • Gram -ve
    • HACEK organisms [Haemophilus, aggregatibacter, cardiobacterium hominis, eikenella corrdens, kingella]
  21. Outline Tx for IE?
    • Medical
    • Antibiotic therapy, bactericidal for 4-6wks
    • e.g. streptococci → ben pen + gentamicin

    • Surgical
    • if → heart failure/abscess/embolism
  22. Define Heart Failure
    • failure of heart to pump blood at a sufficient rate to meet metabolic req of tissues
    • abnormalities of cardiac function
    • characteristic haemodynamic changes & neurohumeral activation
  23. What are the causes of HF?
    • CAD [MI]
    • HBP
    • Idiopathic
    • Toxins
    • Outside UK → valve disease, congenital deformations
  24. Outline the pathology of Heart Failure
    [Look at 2nd year notes, draw diagram]
  25. What are the 4 types of Heart failure?
    • Systolic HF
    • Younger
    • >m:f
    • Coronary aetiology

    • Congestive [Chronic]
    • Present for a period of time, may have been acute/become acute

    • Diasolic HF
    • Older
    • female
    • hypertensive aetiology

    • Acute [Decompensated]
    • admitted to hospital
    • worsening chronic/new onset
  26. What are the signs & symptoms of Heart failure?
    • Symptoms
    • dyspnoea [orthopnoea & PND] & cough
    • Ankle swelling → pitting oedema
    • Fatigue/Tiredness

    • Signs
    • Peripheral pitting oedema
    • ^JVP
    • Third heart sound
    • Displaced apex beat [cardiomegaly]
    • Basal crackles [Pulmonary oedema]
    • Pleural effusion
  27. What are the classifications of HF?
    New york heart association

    • 1 → no symptoms/limitations
    • 2 → mild symptoms/limitations
    • 3 → [moderate] marked limitation due to symptoms, comfortable at rest
    • 4 → severe limitations, symptoms at rest
  28. How would you investigate HF?
    • ECG → LVH/previous MI
    • Echo → chamber size, systolic & diastolic function
    • Natriuretic peptides → BNP & ANP
    • Bloods → usual U&E, FBC & LFTs
    • CXR → rule out pulmonary [cardiomegaly]
  29. Outline the Treatment of HF
    • Diuretics
    • Not disease modifying, but ^QoL

    • Block RAAS
    • ACEi/ARB
    • Aldosterone inhibitors [Spirinolactone RALES study]

    • Block sympathetic NS
    • Beta-blockers

    All Pts should get ACEi + Beta-blocker
  30. What are Kerly B lines?
    • Kerley B
    • Thickening of interlobular septa
    • due to fluid leak into septa
    • Seen → bases, perpendicular to pleural surface & costophrenic angles
    • transiet/raid development? → interstitial pulmonary oedema
  31. Compare interstitial & alveolar oedema
    • Interstitial Oedema
    • Kerley B lines
    • Peribronchial cuffing → bronchial walls visible
    • hazy contour of lung BV

    • Alveolar Oedema
    • fluid in alveolar space → airspace opacity
    • bilateral butterfly distribution
    • central perihilar shadoing that fades to periphery
  32. What is a pleural effusion?
    What are the types & common causes?
    Pleural Effusion = fluid in pleural cavity

    • Transudate
    • plasma ultrafiltrate due to hydrostatic & oncotic imbalance in chest
    • e.g. LVF, Cirrhosis, Nephrotic syndrome

    • Exudate
    • Pleural/lung inflammation w impaired lymphatic drainage
    • Elevated protein content
    • e.g. PTE, bacterial infection, Bronchial Ca
  33. What are the CXR findings of Pleural Effusion?
    Visible on PA >175ml of fluid

    • homogenous lower zone opacity w curvilinear upper border
    • large? → obscure heart border & displace mediastinum airways & diaphragm

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