Medicine Notes Cardiology Notes
Complete set of notes on Cardiology. COvering all the main conditions with pathophysiology, presenting symptoms, investigation and management. Includes relevant pharmacology. Clear headings and concise bullet points, including table summaries. ...
The following is a more accessible plain text extract of the PDF sample above, taken from our Cardiology Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:
Acute Coronary Syndrome
ACS = term covers
Unstable angina
NSTEMI
STEMI
Risk factors
Non-modifiable | Modifiable |
---|---|
|
|
Pathogenesis
Myocardial ischaemia occurs when there is an imbalance between the supply of O2 + myocardial demand for it
Coronary blood flow to a particular region of the heart may be reduced by
Mechanical obstruction e.g atheroma, thrombosis, spasm, embolus
Decreased flow of oxygenated blood e.g anaemia, hypotension
Increased myocardial demand for O2 may be caused by
Increased cardiac output e.g thyrotoxicosis
Myocardial hypertrophy
Myocardial ischaemia most commonly occurs from obstructive CAD in the form of coronary atherosclerosis
Process of atherosclerosis
Endothelial injury
Result of mechanical stresses e.g hypertension
Biochemical abnormalities e.g raised LDL, DM
Immunological factos e.g free radicles from smoking
Genetic alteration
Accumulation of lipids and macrophages leads to foam cells
Form the fatty streak
Cytokine release causes further accumulation of macrophages
+ SMC migration and proliferation
= Plaque
Plaque becomes unstable
Rupture
Thrombosis
Obstruction
Diagnosis
Need to have two or more of the following
Typical history
ECG changes
Raised cardiac enzymes
Clinical features
Symptoms
Acute central chest pain >20mins
Associated N+V, sweating, SOB, palpatations
Pain can radiate to jaw, left arm
NB β in elderly/diabetics may be no symptoms (silent infarct) therefore suspect with varied presentations, e.g syncope, pulm. Oedema, acute confusion etc
Signs
Distress
Anxiety
Pallor
Sweating
Investigations
ECG
STEMI
Immediately
Hyperacute peaked T waves
Mins-hours
ST elevation +/- T wave inversion
Days
STs fall, Q waves develop
Months
Pathological βold infarctβ Q waves
>1 little square wide
>2mm depth
NSTEMI + Unstable angina
May be
ST depression
T wave inversion
Non-specific changes
Normal
Localising STEMI
Anteroseptal = V1-V4 (LAD)
Inferior = II, III, aVF (RCA)
Anterolateral = I, aVL, V5, V6 (circumflex)
Posterior = tall R + ST depression in V1-2 (RCA, circumflex) Difficult to see
CXR
Signs of HF
Rule out any differentials
Bloods
FBC, U+E, hyperglycaemia, TFTs, lipids (LDH) raised cardiac enzymes (trops, ck-mb, LDH)
Management
Pre-hospital
300mg aspirin chewed
GTN sublingual spray (unless hypotensive)
Analgesia + antiemetic e.g 5-10mg morphine...
Buy the full version of these notes or essay plans and more in our Cardiology Notes.
Complete set of notes on Cardiology. COvering all the main conditions with pathophysiology, presenting symptoms, investigation and management. Includes relevant pharmacology. Clear headings and concise bullet points, including table summaries. ...
Ask questions π Get answers π It's simple ποΈπποΈ
Our AI is educated by the highest scoring students across all subjects and schools. Join hundreds of your peers today.
Get Started