Interactive Cases 1 - Cardiology Flashcards
Musculoskeletal causes of CP?
Costochondritis, Tietze’s syndrome
STEMI: V1-4
Anterior MI, Left anterior descending
STEMI: V5-6, I, aVL
Lateral MI, left circumflex artery
STEMI: II, III, aVF
Inferior MI, Right coronary artery
Collapse? what do you ask to determine cause
Before: was there any warning/aura?
During: tongue biting, incontinence, jerky movements
After: confusion
Low volume, slow rising pulse, ESM
AS
Investigation of arrhythmia
ECG for tachy/brady and long QT syndrome, this will predispose to VT
Postural hypotension investigation
BP lying and standing
Classification of long-QT syndrome?
predisposes to VT
Abnormal ventricular repolarisation
Congenital: mutations in K channels (depolarisation problems), FH of sudden death.
Acquired: low K/Mg, drugs.
Draw a line between two R waves. The t wave should finish before the half-way point.
How are the symptoms of hypoglycaemia classified?
Neuroglycopaenic: confusion, drowsy, aggressive, coma
Adrenergic: tachycardia, sweating
May be due to insulinoma if hypo early in the morning, but more commonly due to a DM having taken insulin but not eaten food
45M fever, malaise, IVDrugUser, PSM louder on inspiration, fever 38C, raised JVP, hepatomegaly
tricuspid regurgitation
What are the features of tricuspid regurgitation?
Raised JVP
PSM at the left lower sternal edge louder on inspiration
What are the differential diagnoses of a raised JVP?
- RHF - secondary to LHF (CCF) or pulmonary HTN*
- TR - valve leaflets (IE), RV dilatation (AR)
- Ventricular septal defect (congenital)
- Constrictive pericarditis - fibrosis thickening of pericardium, calcification due to constriction seen on CXR (infection TB, inflammation CTD lupus/sarcoid, malignancy)
A person presents with chest pain. How should they be investigated?
- ECG (STEMI/NSTEMI)
- Troponin; if +ve (=STEMI/NSTEMI) PCI coronary angiography (X ray looks ate coronary arteries), if -ve exercise tolerance test (angina pectoris)
- Echo (ventricular dysfunction)
Gastro causes of CP?
Oesophageal spasm, oesophagitis, gastritis (acid in mouth, Retrosternal pain, alcohol xs is a Rx)
Causes of sudden breathlessness within seconds?
Foreign body obstruction, pneumothorax, PE
What are the cardiac differentials for CP?
IHD especially associated with nausea and sweating, aortic dissection can lead to AR EDM, pericarditis associated with post-viral illness
What are the respiratory differentials for CP?
Pneumonia (cough, sputum, temp), pneumothorax (SOB sudden), PE (haemoptysis, pleuritic CP, sudden SOB, swollen leg)
Symptoms of IHD
CP radiation to jaw, left arm, pressure-like pain, associated symptoms: sweating, nausea
Cardiac History: what do you look out for in PC
1) symptoms
2) associated symptoms
3) DDx/risk factors
1) symptoms - SOCRATES
2) associated symptoms - nausea, sweating, CP, SOB, dizziness, ankle swelling
3) DDx - DM, HTN, cholesterol, BP, FH, previous history of clots
Case - Hx:
60 yo man, chest pain, tight, 4h, nausea and sweating, HTN, DH: amlodipine.
O/E:
temp 37, S1 + S2, BP 120/80 (L), 118/75 (R), clear chest, abdomen SNT
MI
O/E of aorta dissection
difference in BP between arms
collapsing pulse
auscultate ask pt to lean forward, on expiration, left sternal edge hear EARLY DIASTOLIC MURMUR echo with S2 (AR murmur)
What is ACS?
Acute coronary syndrome is a spectrum.
1) MI (STEMI/NSTEMI) (+ve troponin as damage to myocardium)
2) unstable angina (CP at rest due to clot forming and dissolving) (may not be considered ACS as troponin MAY not be elevated)
NB. angina pectoris is pain on exertion (-ve troponin and +ve ETT)
Why is there ST elevation on an ECG?
dead myocardium provides window for electrodes to see spread of depolarization
PC of pericarditis
Pleuritic: worse on breathing in, sharp
Relieved leaning forward
maybe Flu like illness recently
Risk factors: young person with no other risk factors
Tx for STEMI and NSTEMI
Morphine O2 Nitrates Aspirin
STEMI: aspirin, clopidogrel (irreversible platelet aggregation inhibitor) and PCI
NSTEMI: aspirin, clopidogrel, fondaparinux ( ATIII-mediated selective inhibition of Factor Xa, decreased clot formation), thrombolyse (tPA or streptokinase stops clot formation)