Cardiology - Acute Coronary Syndrome Flashcards
Acute ACS Management
What do you give at SAAS level?
- Aspirin
- O2 if sats <94%
- nitrates
Why don’t we give O2 to everyone with ACS?
AVOID Study:
If sats >94% infarcts are BIGGER and MORE RECURRENT INFARCTS
Cardiac Biomarkers:
Myoglobin
Rise?
Peak?
Normalises?
Rises: 1-2 hours
Peaks: 6-8 hours
Normalises: 1-2 days
Cardiac Biomarkers:
CKMB
Rise?
Peak?
Normalises?
Rises: 2-6 hours
Peaks: 16-20 hours
Normalises: 2-3 days
Cardiac Biomarkers:
CK
Rise?
Peak?
Normalises?
Rises: 4-8 hours
Peaks: 16-24 hours
Normalises: 3-4 days
Cardiac Biomarkers:
Trop T
Rise?
Peak?
Normalises?
Rises: 4-6 hours
Peaks: 12-24 hours
Normalises: 7-10 days
Cardiac Biomarkers:
AST
Rise?
Peak?
Normalises?
Rises: 12-24 hours
Peaks: 36-48hrs
Normalises: 3-4 hours
Cardiac Biomarkers:
LDH
Rise?
Peak?
Normalises?
Rises: 24-48hrs
Peaks: 72hours
Normalises: 8-10 days
Of the cardiac biomarkers what order do they appear?
Myoglobin CKMB CK and Troponin AST LDH
STEMI presents WITHIN 12 hours of symptoms
What management?
PCI within 90 minutes!!
BUT if you can’t, then give fibrinolysis
Given fibrinolysis in a non-PCI hospital. Should we transfer?
Transfer to PCI capable hospital within 24 hours to get either angiography or PCI
Given fibrinolysis in a non-PCI hospital, when would we transfer IMMEDIATELY?
- haemodynamic instability
- <50% ST recovery by 60-90 minutes
What is the PharmacoIntemsive approach to STEMI? What benefits?
In HIGH RISK STEMI within 12 hours of symptoms then give FULL DOSE THROMBOLYSIS followed by PCI within 3-24 hours
Benefits:
- lower infarction rates
- lower recurrent ischaemia
- lower 1yr composite endpoints
BUT more intracranial haemorrhage than just PCI and POTENTIALLY JUST AS EFFECTIVE AS PCI ALONE
How many people don’t reperfuse when given thrombolysis?
30%
Absolute contradictions to thrombolysis?
1) Any previous ICH
2) Known cerebral AVM
3) Ischaemic stroke within past 3 months
4) Active bleeding or bleeding diathesis
5) significant closed head or facial trauma within last 3 months
6) suspected aortic dissection
When should you repeat the ECG after thrombolysis and what should you look for?
At 90 minutes
If there is <=50% ST resolution then NEED IMMEDIATE PCI
Indication for thrombectomy in STEMI?
Do NOT do thrombectomy as NO BENEFIT and INCREASED STROKE
Culprit versus Complete Revascularisation?
Treat culprit at a later date.
DO NOT open a totally occluded artery in 1 or 2 vessel disease if >24 hours post STEMI
When is a CABG superior to PCI?
- 3 vessel disease
- Left Main Disease
- diabetes and >1 vessel disease
Benefits of radial access in STEMI compared to femoral access?
- lower composite MI/death/stroke
- decreased overall MORTALITY
- decreased bleeding
- decreased length of stay
- less painful
Risks of radial access in STEMI compared to femoral access?
- longer
- more contrast
At what sized infarct is there a significantly higher rate of death or heart failure?
Infarct size >17%
Complications post STEMI: What is the impact of arrythmia <24 hours post STEMI
NO IMPACT on PROGNOSIS if ventricular arrythmia in first 24 hours
Complications post STEMI: What is the impact of recurrent ventricular arrythmia >24 hours post STEMI
- Indicate larger infarcts
- Higher short AND long term mortality
Complications post STEMI: Role of lidocaine in arrythmias?
Lidocaine reduces INCIDENCE of VT
BUT not mortality!
AND predisposes to asystole and bradycardia
Complications post STEMI: RV infarct results in what pathophysiological impact? How do you manage initially to avoid shock?
Decreased pulmonary blood flow and LA repair
Results in decreased preload and impaired LV filling
Treatment:
- reperfusion
- aggressive IVT
- Inotropes until RV function improves (usually 2-3 days)
Complications post STEMI: Ventricular Septal Defect
? when do they occur
? signs
? management
HIGH MORTALITY!!
Occur 3-7 days post MI
Signs: new HD compromise and new HOLOSYSTOLIC MURMUR
Treat with vasopressors and intra-aortic balloon pump
Complications post STEMI: Mitral regurgitation
? most common after which type of infarct
? when do they usually occur
More common post INFERIOR-POSTERIOR INFARCTION
If due to papillary muscle rupture then usually 3-7 days post MI
Complications post STEMI: LV Free Wall Rupture
? most common after which type of infarct
? when do they occur
? commonly present with what
HIGH MORTALITY
More common post ANTERIOR MI
Occur 3-7 days post MI
Often present with pericardial tamponade, PEA and death
Complications post STEMI: LV Thrombus
? most common after which type of infarct
? treatment
More common post ANTERIOR MI
Treat with warfarin 3-6 months
What is the use of TIMI score in NSTEMI?
If score 0-2 then use ischaemia guided strategy. Only use invasive if medical fails.
Components of TIMI score in NSTEMI?
- Age >65yrs
- > 3 traditional risk factors
- Known CAD with stenosis >50%
- Aspirin use in past week
- > 2 angina episodes in 24 hours
- ST deviation >0.5mm
- Elevated cardiac biomarkers (CKMB/Troponin)
When is an AICD indicated post ACS?
AICD indicated if LVEF <35% at 40 days post MI
Which CLINICAL factors increase risk of stent thrombosis? (7)
- Age >80yrs
- ACS indication for stent insertion
- Diabetes
- Renal impairment
- Low EF
- Previous brachytherapy
- Previous stent thrombosis
Which ANATOMICAL factors increase risk of stent thrombosis? (6)
- bifurcation stenting
- ostial stenting
- left main stem stenting
- small (<3mm) stent
- long (>18mm) stent
- multiple stents
Which surgeries have an UNACCEPTABLE risk of bleeding?
- intracranial
- spinal
- eye
- TURP
- plastic reconstructive
How long to defer elective non-cardiac surgery post stenting
Post BMS: Defer >6 weeks (ideally 3 months)
Post DES: Defer 12 months
Poor Prognostic Features post ACS
- Age
- Hx of heart failure
- Peripheral vascular disease
- Reduced systolic BP
- Killip Class
- Initial serum Cr
- Initial cardiac biomarker elevation
- Cardiac arrest on admission
- ST segment deviation
Killip Class post ACS
Increased mortality with increased class
Killip 1: No clinical signs of heart failure
Killip 2: Crackles / S3
Killip 3: Frank APO
Killip 4: Cardiogenic shock
