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Management of STEMI

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Ryan Tee Heng Seong

on 10 October 2014

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Transcript of Management of STEMI

Management of STEMI
CPG (Clinical Practical Guideline)
Definition of STEMI
New ST elevation at the J point in at least 2 contiguous leads of 2 mm (0.2 mV) in men or
1.5 mm(0.15 mV) in women in leads V2–V3 and/or
1 mm (0.1mV) in other contiguous chest leads or the limb leads

Signs and Symptoms
Radiation to left/right/both shoulder

Exertion pain (pressure-like pain, "angor animi"=perception of dying)

Sweating (Diaphoresis)

Throwing up (Vomiting)
ECG features
Earliest clues for STEMI (without ST elevation)
Hyperacute T wave
Wellen's syndrome
De Winter's T wave

LBBB : Sgarbossa's criteria
RBBB : concordant ST deviation/ excessively discordant ST deviation

avR ST elevation
avR > V1 : LMCA/3VD
(LMCA stenosis is a type of subendocardial ischemia)
avR < V1 : proximal LAD occlusion

Reperfusion therapy
Fibrinolysis (fibrinolysis does NOT equate reperfusion, but it can lead to reperfusion;
we do not know which blood vessels i.e occluded vs non occluded the fibrinolytics will act
Cardiac biomarkers
Support rather than confirm the dx, as they peak later
Cardiac troponin (cTnT and cTnI)

The most useful in troponin
Troponin can be elevated in a lot of conditions
But the key is its dynamism (it rises and falls over 1-2 weeks);
one troponin begets another (a single elevated troponin is useless)
There has been controversy about troponin elevation renal failure; latest literature suggests that if it is elevated, it likely to be significant for future CV events
It's because troponin is not cleared by kidneys !!
In hospital management

Continue what you have done in prehospital management, clopidogrel should be given if not given earlier
Assessment for reperfusion (review for contraindications)
Additional points:

STEMI is a transmural infarction, therefore is also known as Q wave MI

STEMI is caused by complete occlusion of one/more of the coronary artery branches and involves all 3 layers of the heart
Angina-equivalent symptoms
Up to 20-30% of MI are silent, especially in elders, diabetics and women

Angina-equivalent symptoms maybe the only clues that acute ischemia is happening in these patients
Generalized weakness/fatigue
Nausea and vomiting
Posterior STEMI and RV infarction
Always look for evidence of posterior MI/RV infarction in the setting of inferior STEMI
If needed, do a posterior chest leads (V7-9) or right sided precordial leads
Triad of hypotension, clear lung and raised JVP in RV infarction
In RV infarction, nitroglycerin is contraindicated as it may cause cardiogenic shock (low preload due to RV pumping failure); support with IV fluid +/- inotropes
Isolated posterior MI is rare but can happen, look for isolated ST depression in V1-V3
CK washout
Effectiveness of fibrinolysis can be determined in a few ways, and one of them is "CK washout"
CK will be paradoxically elevated after blood flow is restored. Why?
During acute MI, CK leaks out of the cardiac cells into the bloodstream, however due to occlusion, it can only be slowly released to systemic vessels via collaterals, hence the slow peaking time
After reperfusion, now the CK can be released directly into the systemic vessels causing its peaked levels
Criteria for successful reperfusion therapy
Chest pain resolves
ST elevation resolves by 50%
Development of Q waves
Reperfusion arrhythmia
CK washout
Prehospital management
is the traditionally taught prehospital treatment (given in OANM)
300 mg chewable ASA
S/L GTN (repeat every 5 minutes up to 3 tabs)
Morphine (IV morphine 3-5 mg slowly, used together with anti-emetics)
Does morphine work ?
Morphine provides pain relief
But it also reduces preload (vasodilation)
It gives a false sense of security that patient is okay
Also there are studies showing morphine increases mortality in ACS
If possible, avoid morphine !!
Taking GTN after recording the ECG
Giving nitrates before ECG may lead to reperfusion and causes more difficult interpretation

Link for Dr Smith's case

An abstract :
Assessment for reperfusion (onset of MI to presentation)
< 3 hours : Primary PCI/fibrinolytic
3-12 hours : Primary PCI
> 12 hours : medical therapy
Latest ACC/AHA guidelines
In ideal situation:
FMC-device time < 90 mins if primary PCI facility; < 120 mins if needed to be transported from non PCI facility
DIDO time (entering and leaving the non PCI facility) < 30 minutes
Fibrinolytics are given if FMC-device time is expected to be > 120 minutes
Successful fibrinolysis -> angiography within 3-24 hours
Faled fibrinolysis -> rescue PCI is done (cardiogenic shock, c/i of failed fibrinolysis : PCI is done regardless of time delay)
Reperfusion strategies
Time lost = muscle lost
Early presentation (< 3 hours) : primary PCI/fibrinolytics
Late presentation (3-12 hours) : primary PCI is preferred
Very late presentation (>12 hours) : both are not routinely recommended

Streptokinase: NOT fibrin specific, widely used; but is antigenic and cannot be used 5 days after the first administration
Alteplase (rTPA) : fibrin specific and better reperfusion than streptokinase
Second generation rTPA : tenecteplase, reteplase
The biggest concern : intracranial hemorrhage
A new found side effect : angioedema (How?)
Fibrin specific vs fibrin non specific
Streptokinase is fibrin-non specific
It forms a complex with plasminogen and releases plasmin
It does not bind preferentially to clot-specific fibrin, it binds equally to both circulating and non-circulating plasminogen causing fibrinogenolysis (fibrinogen is circulating clotting factor)

Fibrin specific agents bind specifically to clot-associated fibrin
They do not deplete fibrinogen, so is associated with higher incidence of post-fibrinolytic reocclusion
Heparin needs to be given for 48 hours
Meta analysis showed that all fibrinolytic drugs appear to be of similar efficacy in reducing mortality
Alteplase is associated with higher incidence of stroke (because fibrinogen is not depleted and clots can be formed again)
SK is associated with less intracranial bleeding compared to rTPA (a bit weird considering that SK depletes fibrinogen as well, could be related to greater amount of FDP released after tPA induces a systemic lytic state)

Types of PCI
Primary PCI : muscle saving (<12 hours)

Facilitated PCI : PCI after fibrinolysis; basically offers no additional benefits and causes more bleeding

Late/Rescue PCI ; life saving (>12 hours), indications for rescue PCI include cardiogenic shock, contraindicated/failed fibrinolysis

Delayed PCI (>72 hours after fibrinolysis): controversial
Contraindications to tPA
urgery history within 3 months
ead trauma within 3 months
ntracranial hemorrhage
latelets < 100,000/mm3, PT > 15s
> 185/110
evel of glucose < 50 or > 400 mg/dL
nticoagulation use
urgery recently

Can catogerise into 3 groups:
Any head trauma, bleeding, surgery
Factors that increase bleeding (low platelets, high PT/aPTT, too high BP)
Others: glucose < 50/>400
After reperfusion........

These drugs give mortality benefits :
ACS BAS (Aspirin, Clopidogrel, Statins, BB, ACEi, Spironolactone); ARB may not have the same benefits as ACEi
Spironolactone is given in symptomatic HF (class II and above) patients with intact renal function
The lower the HR, the better is cardiac function:
BBs should be given early in all post-MI patients (hemodynamically stable after 48 hours)
; cardioselective BBs should be given (atenolol, metoprolol, carvedilol, bisoprolol)
COPD is NOT a contraindication for BBs
if patient can tolerate the side effects (cardioselective drugs are less likely to precipitate airway bronchospasm)
Nitrates do NOT decrease mortality in post-MI patients; however
hydralazine+isosorbide dinitrate
in those that could not tolerate ACEi/ARB therapy may confer benefits
Anticoagulations (UFH, LMWH, Fondaparinux) are indicated for 48 hours in post-fibrin specific fibrinolytic agent
(maybe as well in non fibrin specific agent). Other indications : post-infarct angina, prothrombotic conditions eg
poor EF, LVA and AF
(warfarin needs to be added later)
ardiogenic shock (Killip class)
upture of papillary muscles
ericardial tamponade
ressler syndrome
Causes acute mitral regurgitation associated with cardiogenic shock and pulmonary edema ( early and soft systolic murmur !!)
Stigmata of previous MI in ECG
QS/Q waves
Loss of precordial r wave progression
Persistent ST elevation of LVA
T wave inversion (reperfusion T wave)
Tall R in avR (reflects Q waves in limb leads) (Goldberger's sign)
In the presence of LBBB, Chapman's sign and Cabrera's sign
Fragmented QRS pattern in inferior and midprecordial leads
El-Sheriff's sign
Early post-MI pericarditis vs Dressler syndrome
Early pericarditis : < 1 week
Dressler syndrome : > 1 week

May lead to shock if effusion becomes tamponade

Studies have shown the efficacy of colcichine in Dressler syndrome; other drugs include aspirin and corticosteroids
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