Week 4 Flashcards
(48 cards)
where do afferent fibres run that innervate heart, lungs, great vessels?
Thoracic region
- indistinct quality of pain from cardiac sources – anywhre from epigastrim to jaw
what is radiation of pain caused by with cardiac pain/ischemia
crossing of somatic fibres at the same levels as the efferent fibres from the viscera. which is also why you get shoulder, back and arm pain
what are the 2 types of plaques in CAD? which is worse?
Fibrous plaques - stable - cause stenosis
Lipid plaques - high lipid content with a fibromuscular plauque. Can rupture results in inflammatory cascade, thrombus formation and platelet aggregation
why do we give ASA?
Platelet inhibitor - for life of platelet ~8 days
in ACS platelet aggregation occurs causing further obstruction and ischemia.
- also platelet thrombus are more resistant to fibrinolysis - interesting fact
Why would a 50% lesion still be concerning?
- Can still rupture and whats more important is the event rupture, inflammation, platelet activation and thrombus formation which is badness.
why are traditional RFs for ACS not helpfulin the ED?
Bayesian analysis indicates that they are population phenomenon RFs and do not increase or decrease the likelihood of ACS in the ED
what 3 characteristics make CP less likely ACS? but still possible
- pleuritic
- position
- palpation reproduces
one study found in isolation 15% of those with ACS had reproducible pain on palpation
What artery supplies the SA node?
in 60% of ppl it is supplied by RCA and in 40% the left circumflex
Which artery supplies the AV node?
90% RCA and 10% Left circumflex
whats the difference in timing of development of infarct pericarditis and Dressler’s syndrome?
infarct pericarditis occurs right after so sooner and requires transmural infarction
Dresslers syndrome occurs up to 1 week out (up to several months), is an immune mediated reaction and doesnt require transmural infarction
What is the risk of hemorragic stroke with lytics?
About 1%, sl higher in elderly
what is the ddx STE?
- Normal
- Normal variant
- Benign early repolarization
- Extra cardiac disease
- ICH
- Hyperkalemia
- Hypercalcemia
- Hypothermia – Osborne wave
- Pulmonary embolus
- Iatrogenic
- Post-cardioversion
Heart outside —> in:
- Pericardium: Pericarditis
- Vessels
- STEMI - Thrombus/embolus
- Prinzmetal’s angina – vasospasm
- Aortic dissection into coronary ostia
- Muscle
- LV aneurysm
- LV hypertrophy
- Myocarditis
- Takotsubo’s (most common in post-menopausal F w emotional stress)
- Conduction system
- LBBB
- Paced rhythm
- Brugada
what is the progression of STEMI on ecg? (5 steps)
- hyperacute T waves
- STE
- Loss of R wave Q wave progression
- T wave inversion
- Normalization TW and persistent Q wave
Ddx TWI
ACS ventricular hypertrophy bundle branch block VPR - ventricular paced rhythm myocarditis pericarditis PE pneumothorax Wolff-Parkinson- White syndrome, cerebrovascular accident hypokalemia GI disorders hyperventilation persistent juvenile T wave pattern normal variants
in septal stemi where would you see STE?
V1-V2
If in anterior lateral STEMI, if I, avL involved, which branch off LAD is also likely to be involved?
D1 - diagonal
What is the sn/sp of STE avR for left main dz?
Sn 78%
sp 83%
if V1 >avR then it MAY be p LAD occlusion
As per Rosens, ddx STE aVR?
How to distinguish left main from p. LAD occ?
- left main
- Multivessel disease
- proximal LAD** (may see with DeWinter T waves) or V1>AvR
- RCA occlusion
- Left circumflex
In left main STE greater in avR than V1
What are the STEMI equivalent ecg patterns?
- De Winters TW - acute prox LAD occ
- STE avR
- Scarbossa criteria in presence LBBB
- Posterior MI - STD ant leads
- Wellens syndrome (NOT equivalent but crtiical LAD occl)
New LBBB NO longer
what are the high lateral leadS?
which vessel is culprit?
I, avL
Left circumflex
which vessel occlusion can be occult on ecg?
left circumflex, particularly OM2 (obtuse marginal 2)
what pattern on ecg may you see in left circumflex occlusion?
STE inferior leads but will NOT see III>II (that suggests RV infarct)
may see STE in avL - more subtle though.
List 4 ecg features suggestive of posterior MI
- STD anterior leads
- Upright TW
- tall wide R waves (q waves)
- R:S wave amplitude >1 (dominant R wave in V2)
Tall R-waves in precordial leads are mirror images of posterior q waves
what are ecg patterns suggesting an RV infarct? (list 5)
In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:
- ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle.
- ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.
Other useful tips for spotting right ventricular MI: - ST elevation in V1 > V2.
- ST elevation in V1 + ST depression in V2 (= highly specific for RV MI).
- Isoelectric ST segment in V1 with marked ST depression in V2.
Right ventricular infarction is confirmed by the presence of ST elevation in the right-sided leads (V4R)
