Cardiovascular Flashcards
Acute Coronary Syndrome
ACS: Included conditions & Definitions
Acutely compromised myocardial perfusion
1: Unstable angina: ACS without cell death. Big sclerotic plaque but not yet dislodged
2. NSTEMI: Subendocardial cell death
3. STEMI: Transmural cell death
ACS: Risk factors
Non-modifiable:
- sex: male
- age: old
- Hx: FMHx of ACS and other CVS. Hx of DM and previous ACS
Modifiable
- Smoking
- Central obesity
- High LDL and low HDL
- HTN
ACS: Investigations
Blood: Troponin (STEMI & NSTEMI)
ECG: NSTEMI (normal or abnormal), Angina (ST depression/ T wave inversion wtihtou
Coronary arteries: Route and areas of supply
LAD: follows Interventricular groove
- Diagonal branch: lateral wall of LV
- Septal branch: Anterior 2/3 of interventricular septum,
- Terminal bifurcation: Inferior LV, apex of LV
LCx: follows Left AV groove
- Lateral & Posterior wall of LV
RCA: follows right AV groove
- SAN, AVN & Right atrium
- Posterior descending artery: inferior wall of LV, inferior 1/3 of interventricular septum (most common - otherwise ‘dominated’ by LCx)
Posterior MI: ECG interpretation
Changes seen in V1-V3
- horizontal ST depression
- Tall R waves
- Dominant R wave (R/S > 1)
ACS: other causes of troponin rise
Troponin rises within 12hrs of myocardial injury, peaks at 24 hrs and remains elevated for 14 days
Cardiac causes
- Myocarditis
- Pericarditis
Other causes:
- Pulmonary embolism
- Sepsis
- Renal failure
ACS: Other differentials
Aortic dissection: presents with chest pain and ST elevation
- distinguished by abrupt onset, migration to back and tearing sensation
- when ST elevation recorded, usually in inferior region (RCA) as dissection in left main stem is fatal
Acute pericarditis: Chest pain and ST elevation
- Presentation: pain worsens on inspiration and relieves by sitting upright
- ECG changes: Widespread ST elevation and saddle shaped
ACS: Causes
Atherosclerotic plaque
Non-athreroscleotic causes:
- Embolus
- Concentric ventricular hypertrophy: hypertropic cardiomyopathy, HTN, aortic stenosis
- Aortic valve stenosis (decreased blood flow -> Coronary from aorta)
- Vasculitis (eg. Kawasaki syndrome (high suspicious if paeds. ACS)
- Vasospasm (cocaine abuse)
ACS - Immediate management
MONAC
Morphine (IV) - 10mg + Metoclopramide IV
Oxygen: if SpO2 outside 94-98%
Nitrates: Sublingual GTN 92 sprays), if not hypotensive (the PRN)
Aspirin: 300mg PO loading dose then 75mg OD
Clopidpgrel: 300-600mg loading dose then 75mg OD
Plus start: atorvastatin 80mg ON, beta-blocker (eg. bisoprolol 2.5mg OD), ACS-specific LMWH below.
Reperfusion therapy (/ Thrombolysis)
ACS additional management (after MONAC)
Atorvastatin 80mg ON
beta-blocker (eg. atenolol 50mg PO TDS) in absence of HF or BP < 80
ACS-specific LMWH
ACS: Repurfusion therapy (+ indications)
PCI (gold-standard): Any ACS - STEMI, NSTEMI, Unstable angina
indications:
- Evidence of myocardial ischaemia
- Onset within 12 hrs or symptoms persist for up to 24hrs
- ST elevation of > 0.1 mV (1mm) on at least 2 limb leads or > 0.2mV (2mm) on 2 contiguous leads
- New LBBB
- True posterior MI
Thrombolysis: STEMI with ST-elevation in 2 contiguous leads
- >1mm in limb leads or >2mm in chest leads or new LBBB
ACS - Contraindications to reperfusion therapy
PCI: significant co-morbidities (relative contraindication)
Thrombolysis: active internal bleeding, bleeding. disorder, aortic dissection, stoke or surgery/trauma <2 weeks
ACS - Investigations
Bloods - FBC, U&E LFTs, CRP & glucose Troponin, BNP, Magnesium, phosphate and lipids
Imaging: Chest X-ray & ECG
NSTEMI - high risk patients and management
High risk: Raised troponin/ persistent pain/ ST depression/ diabetic
Management for high risk: PCI on semi-elective basis (depends on TIMI/GRACE score)
Aneurysm: Pathology
Abnormal dilation in blood vessels: 1.5x larger than normal vessel dieter ( >3.0cm in aortic & thoracic)
Occurs in areas of high blood pressure: aorta, femoral, iliac, popliteal and cerebral arteries.
Uncommon: veins - pressure on blood vessel walls increase with diameter of vessel lumen (LaPlace’s law)
Aneurysm: Life threatening locations
Abdominal Aortic Aneurysm (AAA): diameter > 3cm or >50% larger than normal
Thoracic AA: less common AAA
Cerebral aneurysm: particularly threatening in Circle of Willis
AAA: Main causes
Atherosclerosis Infection Trauma Arteritis Cystic medial necrosis
Aneurysm: True vs Pseudoaneurysm
True Aneurysm: all layers of vessel wall dilate
- Fusiform: symmetrical wall dilation
- Saccular (berry): asymmetrical ballooning of vessel due to increased BP on one side of vessel wall
Pseudo-aneurysms: small hole in blood vessel wall -> blood leaks out, pools; resembles true aneurysm.
Aneurysm: Causes
Ischaemia:
- Ischaemia of arteries with vasa vasorum: hyaline arterioscelersis leads to decreased smooth muscle in tunica media
- Ischaemia of arteries without vasa vasorum: plaque form atherosclerosis blocks blood vessel walls from receiving O2
Infection:
- Tertiary syphilis
- Mycotic aneurysm
Genetic
- Connective tissue disorders: Marfan’s syndrome, EDS