Week 05 - Cardiology
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. What would you like to do?
What is the mnemonic for ECG interpretation?
The Interpretation of an ECG D
ecquire A W
- 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]
Outline the ECG features of the following Bradycardias
-Heart Block [1st, 2nd & 3rd degree]
- Sinus Bradycardia
- Longer PR, but narrow QRS, still regulated by sinus node
- 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
Outline the following Tachycardias
- irregular ventricular rhythmn, no P waves [^^clots]
- Sawtooth ECG? → Atrial Flutter
- Narrow QRS [rate from atria]
- Regular Tachy cardia
- Ventricular Tachycardia
- Broad QRS [rate from ventricles]
- p wave dissociation
- Ventricular Fibrillation
- rapid irregular polymorphic ventricular rhythmn
- Cause of cardiac arrest
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]
Which leads give the following views
- Inferior Leads
- II III & aVF
Draw the lipid metabolism
[diet liver tissues]
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
For statins give
- Inhibits HMG-CoA reductase
- result = dec cholesterol synthesis
- Cholesterol >5mmol/l in CVD/CVA
- ^CK [~lethal] myalgia → rhabdomyolysis
- Advise about muscle pain
What are the risk factors for CVD?
- Asian ethnicity
- lower social class
- HBP [140/90, for ea ^10mmHg, ^20% CVD risk]
What is the acute management of an MI
- Interventional cardiology
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
What are the signs & symptoms of acute limb ischaemia?
THE MUTHAFUKIN 6 PS!!!!!!
- Power [loss of]
- Perishingly cold
What is Infective endocarditis & where is it most common?
- infection of endocardium
- damage to cusps of valves [via vegetations]
- Most common = Mitral
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
- most = staph aureus
- More common in right side
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
What are the CF of IE?
[Acute, subacute & Embolic events]
- toxic Pc [hypotensive, fever, septic]
- progressive valve destruction & metastatic infection
- 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
What are the long term effects of IE?
- Oslers nodes → painful palpable lesions [hands & feet]
- Immunological reaction [splenomegaly, nephritis, clubbing]
- Valve destruction → abscess formation
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
Outline the Dx of IE
- 3 sets of B/C before antibiotics
- Transthoracic/ Trans oesophageal [^^sensitivity]
- Typical org in 2 separate B/C
- +ve echo/valve regurg
- fever >38
- vascular phenomena [septic emboli]
- Immunological phenomena [Oslers nodes]
- +ve B/C
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]
Outline Tx for IE?
- Antibiotic therapy, bactericidal for 4-6wks
- e.g. streptococci → ben pen + gentamicin
- if → heart failure/abscess/embolism
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
What are the causes of HF?
- CAD [MI]
- Outside UK → valve disease, congenital deformations
Outline the pathology of Heart Failure
[Look at 2nd year notes, draw diagram]
What are the 4 types of Heart failure?
- Systolic HF
- Coronary aetiology
- Congestive [Chronic]
- Present for a period of time, may have been acute/become acute
- Diasolic HF
- hypertensive aetiology
- Acute [Decompensated]
- admitted to hospital
- worsening chronic/new onset
What are the signs & symptoms of Heart failure?
- dyspnoea [orthopnoea & PND] & cough
- Ankle swelling → pitting oedema
- Peripheral pitting oedema
- Third heart sound
- Displaced apex beat [cardiomegaly]
- Basal crackles [Pulmonary oedema]
- Pleural effusion
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
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]
Outline the Treatment of HF
- Not disease modifying, but ^QoL
- Block RAAS
- Aldosterone inhibitors [Spirinolactone RALES study]
All Pts should get ACEi + Beta-blocker
- Block sympathetic NS
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
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
What is a pleural effusion?
What are the types & common causes?
Pleural Effusion = fluid in pleural cavity
- plasma ultrafiltrate due to hydrostatic & oncotic imbalance in chest
- e.g. LVF, Cirrhosis, Nephrotic syndrome
- Pleural/lung inflammation w impaired lymphatic drainage
- Elevated protein content
- e.g. PTE, bacterial infection, Bronchial Ca
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
What would you like to do?
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