Cardiology Flashcards
What is the HEART Score?
What are its elements?
Who can it not be used on?
- A tool used to assess patients presenting with symptoms suggestive of ACS for risk at 6wks of Major Adverse Coronary Events (MACE).
- Each category (below) attracts 0-2 points (low - medium - high)
- History
- ECG
- Age
- Risk factors
- Troponin
- Score 0-3: <1.7%
- Score 4-6: 12-16%
- Score 7-9: 50-65%
- Cannot be used in STEMI, hypotension, life expectancy <1yr or other cause for admission.
What is the TIMI Score?
What are its elements?
Calculates the risk at 14 days in confirmed ACS patients of MACE.
- One point for each:
- Age >65
- >= 3 CAD RFs
- Known CAD (stenosis >=50%)
- Aspirin use in past 7days
- Severe angina (>= 2 episodes in 24h)
- ST changes >= 0.5mm
- Cardiac enzyme elevation
NB >= 3pts = high risk -> early reperfusion
- Risk increments with each point:
- 0-1pt = 5%
- 2pt = 8%
- 3pt = 13%
- 4pt = 20% and so on…
What is the Killip Classification?
What does it predict?
- No signs of CHF
- Crackles, S3, raised JVP
- APO
- Cardiogenic shock
It predicts 30-day mortality:
- 3%
- 9%
- 15%
- 81%
NB: the classification was based on a study from 1960’s - mortalities have changed with improved therapies.
What is the GRACE Score?
What does it predict?
GRACE - Global Registry of Acute Coronary Events
Components of GRACE Score (each component is weighted by the calculator):
- Age
- Heart rate
- SBP
- Creatinine
- Killip Class (CHF classification system)
- Cardiac arrest at presentation
- ST segment elevation
- Elevated cardiac markers
It estimates the risk of 6mth all-cause mortality.
What are the three recommendations of the AHA with regards the mgt of patients with undifferentiated chest pain?
- All patients should undergo an ECG in the first ten minutes of their presentation
- All patients should be risk stratified using an evidence-based Suspected ACS protocol
- All patients should be further stratified using serial troponins in conjunction with the above Suspected ACS protocol.
What 4 conditions make STE more difficult to evaluate?
- LBBB
- RBBB
- LVH
- Paced rhythym
What are pathological Q-waves?
What do they indicate?
Q waves are considered pathological if:
- > 40 ms (1 mm) wide
- > 2 mm deep
- > 25% of depth of QRS complex
- Seen in leads V1-3
Indicate old or current MI.
What are the ECG findings of HOCM?
- LVH
- Deep, “dagger”-like Q-waves in lateral and inferior leads (V4-6 and II, III, aVF
- Can lead to AF, SVTs, VT and sudden death
What is Wellens syndrome?
What does it indicate?
- Deeply inverted or biphasic (up-down) T-waves in V2-3
- Occurs when patient is pain free
- No precordial Q-waves
- Normal R-wave progrssion
- Type A - biphasic T-waves
- Type B - deeply inverted T-waves
- Indicates critical stenosis of LAD w/ extreme risk of extensive ant’r wall MI
Describe the likely pattern of MI in pre-existing or resultant RBBB.
- Q-wave MI + RBBB: RsR’ in V1 and slurred S wave in V6 (RBBB) + pathological Q-waves in ant’r leads + normal ST-T changes (if MI is ant’r) or pathological Q-waves in inf’r leads (if MI is inf’r)
- Non-Q-wave MI: Because of the slurred S-wave in lateral chest leads, the ST segment may be depressed and TWI.
What are the diagnostic criteria of RBBB?
What is incomplete RBBB?
RBBB:
- QRS > 120ms
- RsR’ in V1-3
- Slurred S-wave in lateral leads I, aVL, V5-6
Incomplete RBBB:
- QRS < 120ms
- RsR’ in V1-3
List 7 causes of RBBB.
- RVH/cor pulmonale
- PE
- IHD
- RHD
- Myorcarditis or cardiomyopathy
- Degenerative/infiltrative disease of the conduction system
- Congenital heart disease (eg ASD)
List the ECG changes in posterior MI and the likely site of occlusion.
- Horizontal ST depression in V1-V3
- Tall, broad R waves V1-3
- Upright T-waves
- Dominant R wave in V2 (R:S >1)
- STE >0.5mm in V7-9
- Q-wave formation in V7-9
Posterior MI can be caused by either:
- Occlusion of the (L)Cx, or
- RCA/PDA
Which artery supplies the AV + SA nodes?
The RCA supplies:
- The SA node (60% of the time), and
- The AV node
List the site of occlusion in the following STEs:
- V1-2
- V3-4
- V5-6
- II, II and aVF
- STD in V2 - V3
- LAD
- LAD/Diagonal branch (D1)
- LCx/D1
- RCA/PDA
- Sub-endocardial ischaemia OR Wellens OR reciprocal change from posterior MI (Is there peaked T-waves (Wellens) or R/S ratio > 1 in V2 (Post MI)?
