13) Acute coronary syndrome with ST-elevation. Flashcards
what is the clinical prestenation of STEMI
angina duration more than 30!!!!! mins NOW unlike nstemmi
Very severe accompanied by abundant vegetative nervous system symptoms – sweating, nausea, vomiting
UNAFFECTED BY NITROGLYCERIN
specific ECG changes
and lab consolation
what are the ECG changes we see in stemi ?
ecg
we see a ST – elevation:
- ST elevation is equal or > 1 mV in at least two peripheral leads -
ST elevation is > 2 mV in at least two precordial leads
what are the ECG changes in STEMI
acute stage -
infraction or myocardial damage going on
>hyper acute T waves (physiological in high vagal tone , or hyperkalemia )
>ST elevation
intermediate stage -Myocardial necrosis present
> absence of r waves
> ST elevation with T wave inversions (first few days)
> pathological q wave with t wave inversion - week to months
( it is any q wave with duration of more than or equal to 0.04s or more than or an amplitude of equal to 1/4 of preceding r wave, or any q wave seen in lead V1-V3 (seen in hypertrophic cardiomyopathy) )
chronic stage - permanent scarring
>perisirant , broad and deep q waves
> incomplete recovery of R waves
> and permanent t wave inversion can be possible
pathologic Q-waves remain forever
!!!
other than ECG what other modes of diagnosis are used
troponin I (cTnI) troponin T (cTnT) - lasts the longest up to 5-14 days
begin to rise 3 to 4 hours after the onset of chest discomfort, achieve a peak level between 18 and 36 hours,
Elevation of CK-MB
ratio of CK-MB to total CK. The ratio is usually greater than 2.5% in the setting
of myocardial injury
peak time at 12 or more hours
MB2 isoform
if there is ST elevation for more than 2 months what is this a sign for ?
aneurysm
what is the differential diagnosis of ST elevation ?
NEW LEFT BUNDLE BRANCH BLOCK
early depolarisation
pericardtis / myocarditis
takotsubo cardiomyopathy
brugada syndrome
left and right bundle branch block associated with repolarisation abnormalities
hyperkalemia , hypothermia
what is the management of STEMI ?
dual anti platelet therapy
aspirin load 300mg PO
plus an adp inhibitor such as clopidrogel , prasugrel and ticagrelor
(should be continues after 12 months after PCI )
GP 2b and 3a receptor antagonist should be considered in precatherisation setting
ANTICOGULATION also recommenced
we need to do immediate revascularisation and initiation of other therapies should not delay this step in management.
emergency coronary angiography with PCI
ideally less than 90 minutes and should not exceed the 120 minutes given
if PCI cannot be performed under 120 minutes or if PCI is not successful we start with thrombolytic therapy = tPA , reteplase / streptokinase
should be administered in less than 30 minutes of arrival into the hospital , it is contraindicated to administer it 24 hours after the symptoms
PCI should be performed even if the symptoms go away
we can also do a CABG - coronary artery bypass grafting
- indicated only when PCI is unsuccessful
anatomy not suitable
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Mild and moderate heart failure
• Furosemide 20-40 mg i.v. slowly, when no effect – new dosing in 2-4 h
• When the result is not sufficient – Nitroglycerin i.v. infusion with dose titration every 5 min
what further pharmacological therapy can you go to ?
morphine IV or SC
oxygen
beta blockers - within 24 hrs of admission
statins
loop diuretics
ACE or ARB
what are the contraindication of thrombolytic therapy
intracarila bleeding
GI bleeding
hypertension of 180
what are the major complication after myocardial infraction with 0-24 hrs ?
> sudden cardiac death - by cardiac ventricular arrhythmia or unstable hemodynamics
prevent it by ICD - impknatble cardioverter defibrillates device
> arrhythmia
AV block
ventricular tachyaarytmia
systole
> acute left heart failure - pulmonary edema
> cardiogenic shock
what are the complication 3-14 days post infraction ?
papillary muscle rupture - in 2-7 days
lead to mitral regurgitation
rupture of the posteromedial papillary muscle due to occlusion of the posterioir descending artery is very common
New holosystolic, blowing murmur over the 5th ICS on the midclavicular line
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ventricular septal rupture - in 3-5 days
holosystolic murmur is heard
treatment - emergency surgery and revascularisation
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left ventricular free wall rupture - 5-14 days
LV hypertrophy and tissue fibrosis of previous MI decreases the risk - this leads to another complication which is CARDIAC TAMPOADE
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left ventricular pseudo aneurysm
out pouching of the ventricular wall rupture
what are the complications for 2 weeks to months post infraction ?
atrial and ventricular aneurysms
= perisistate st elevation and t wave inversion 3 weeks post MI
- further complication of arrhythmia , rupture and cardiac tamponade and mural thrombus formation leading to thromboembolism - stroke and mesenteric eschemia , and renal infraction
treatment : anticoagulation
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DRESSLER syndrome
pericarditis occurring 2-10 weeks post MI
due to circulating antibodies against cardiac ,muscle cells
leading pleuritic chest pain , dry cough , friction rub can be heard , fever ,
serum troponin levels continue to remain highh
and on ECG diffuse ST elevations
= treatments of NSAID , COLCHINE
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arrhythmia
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congestive heart failure
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rein fraction
dd for troponin increase ?
Cardiac causes Myocarditis Decompensated congestive heart failure Pulmonary embolism Cardiac arrhythmia Takotsubo cardiomyopathy
Noncardiac causes
Renal failure
Stroke
what is the choice of strategy according to the onset of time ?
pain in 5 minutes
in less than half an hour ambulance
why do we prefer pic to thrombolysis?
PCI the cranial hemorrhages are twice less frequent
complications of pci ?
Acute thrombosis
• Restenosis
• Multiple stenting (full metal jacket)
Major haemorrhages
contrast dye nephropathy
how do we combat restenosis ?
correct selection – optimal result”:
• Avoiding multiple stenting
• Pursuit stent edges to step on at least 2 mm in the healthy section of the affected vessel
– Using drug eluting stents
after dehospitalization
Continue the aggressive secondary medical prevention of CHD including:
– Dual antiplatelet therapy – ASA+clopidogrel – Statins
– β-blockers
Treatment of complicated ACS with ST-elevation
Severe heart failure or shock
О2-therapy
Follow-up of blood gasses analysis
Monitoring of PP with Swan-Ganz catheter in a.pulmonalis – target mean PP < 20 mmHg
In absence of hypotension – Nitroglycerin i.v. infusion – initial dose 0,25 μg/kg/min until SBP drops down no less than 90 mmHg
• In hypotension – inotropic agents:
– In reduced kidney perfusion Dopamine 2,5-5,0 μg/kg/min
– In prevailing pulmonary congestion Dobutamine in initial dose 2,5 μg/kg/min with dose increase every 5-10 min to maximal dose 10,0 μg/kg/min or until adverse reactions occur
Treatment of complicated ACS with ST-elevation
With ventricular tachycardia
Lidocaine 1 mg/kg slowly i.v
Amiodarone 5 mg/kg for 1 h
Treatment of complicated ACS with ST-elevation
With atrial fibrillation
Amiodarone 5 mg/kg for 1 h
β-blockers
Treatment of complicated ACS with ST-elevation
AV block
AV block I degree – monitoring
ІІ degree Wenckebach type and hemodynamically significant bradicardia
• Atropine 0,5 mg i.v
no effect – temporary electrocardiostimulation
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ІІ degree type Mobitz II and III degree AV block in combination with HR bellow 40/min or hypotension or heart failure
• Temporary electrocardiostimulation
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In presence of newly-diagnosed bundle branch block in anterior myocardial infarction with acs stemi
preventive pacing electrode situated in RV because of the great risk of developing complete AV block
Treatment of complicated ACS with ST-elevation
Hypertension crisis?
Nitroglycerin i.v. infusion – initial dose 0,25 μg/kg/
Furosemide 20-40 mg i.v. slowly
Treatment of complicated ACS with ST-elevation
Pericarditis epistenocardica
NSAID
• Termination of anticoagulant treatment
Problems with PCI • Acute thrombosis how do we combat that?
Combination:
Heparin or GP IIb/IIIa blocker 24-36 h
ASA 325 mg, followed by 100-150 mg/d maintenance dose
Clopidogrel 600 mg loading dose followed by 75-150 mg/d maintenance dose
how can we figure out the localisation of the myocardial infract on ECG ?
first primary ischemic changes = ST elevation
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V1-V6 - extensive anterior
proximal left anterior descending artery - LAD
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V1-V2 = anteroseptal infraction - LAD
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V3-V4 =
anteropical infraction - distal
LAD
reciprocal changes (eg st depression in 2,3, avF )
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V5 , V6 (plus or minus 1 and AVL )
lateral
proximal left circumflex
(reciprocal 2 ,3 , avF )
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V1- V4 = anteroseptal but apical
LAD
(reciprocal , 2,3,AVF)
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1 or AVL (without V1 to V6)
high lateral lateral infraction
proximal left circumflex / RCA
(reciprocal 2,3,avF )
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2,3,AVF
inferior infraction
Right coronary artery
reciprocal v2-v3
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V3-V6 , 1 and avL
anterolateral
LAD
reciprocal = 2,3,avf
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2,3, avF , V5-V6
infeolateral
proximal left circumflex artery
reciprocal v2-v3
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ST elevation in V1 higher than in V2
then V3R - V6R
2,3, AVF
right ventricular
RIGHT CORONARY ARTERY
