ACUTE CORONARY SYNDROME

1. Dr.Mullapudi Rama Krishna

2. Acute coronary syndrome (ACS) refers to any
group of symptoms attributed to obstruction of
the coronary arteries. The most common
symptom prompting diagnosis of ACS is chest
pain, often radiating to the left arm or angle of the
jaw, pressure-like in character, and associated
with nausea and sweating. Acute coronary
syndrome usually occurs as a result of one of three
problems: ST elevation myocardial
infarction (30%), non ST elevation myocardial
infarction (25%), or unstable angina (38%).

4. Thrombosis on the damaged atherosclerotic plaque
Increase of requirement for oxygen (physical actyvity
or psyhoemotional stress) or decrease in delivery
(spasm of CA, embolism of CA, anemia, hypotonia,
hypertonia etc.)
After stenting, Coronary bypass surgery.

5. ACS occurs when an atherosclerotic plaque slowly
builds up in the inner lining of a coronary artery
and then suddenly ruptures, causing catastrophic
thrombus formation, totally or no totally
occluding the artery and preventing blood flow
downstream.

6. it is a necrosis of cardiac muscle, caused by serious
discrepancy between requirement of a myocardium
and oxygen delivery for a coronary artery.
It happens when blood stops flowing properly to part
of the heart and the heart muscle is injured due to not
receiving enough oxygen. Usually this is because one
of the coronary arteries that supplies blood to the
heart develops a blockage due to an unstable
buildup of white blood cells, cholesterol and fat. The
event is called "acute" if it is sudden and serious

7. A myocardial infarction occurs when an
atherosclerotic plaque slowly builds up in the
inner lining of a coronary artery and then
suddenly ruptures, causing catastrophic thrombus
formation, totally occluding the artery and
preventing blood flow downstream.

8. 1. Q-wave MI
2. Non Q-wave MI.

9. 1. Primary MI. it is new necrosis of myocardium.
Before no any myocardial scarring in ECG.
2. Spreading of MI. It is new necrosis place of
myocardium (MI) in 72 hours after MI.
3. Recurrent of MI. It is new necrosis place of
myocardium (MI) from 72 hours till 2 month after
MI.
4. Repeated of MI. It is new necrosis place of
myocardium (MI) after more than 2 month.

10. Stage of MI.
1. Peracute MI. It is time of MI from begin till 2 hours.
2. Acute MI. It is time of MI from 2 hours till 7 days.
3. Subacute of MI. It is time of MI from 7 days till 28
days.
4. Postinfarction period. It is time of MI after 29 days (1
month).

11. Localization of MI:
1. I, aVL – high lateral wall of LV
2. V1-V2 – anterior part of IVS
3. V3-V4 – anterior wall of LV
4. II, III, aVF – inferior wall of LV
5. V7-V9 – posterior wall of LV
6. RV3-RV4 – Right Ventricle

12. Clinical finding
The onset of symptoms in MI is usually gradual, over
several minutes, and rarely instantaneous.
 Chest pain is often described as a sensation of
tightness, pressure, or squeezing.
Chest pain due to ischemia. Pain radiates most often
to the left arm, but may also radiate to the lower jaw,
neck, right arm, back, and epigastrium.
 Levine's sign, in which the patient localizes the chest
pain by clenching their fist over the sternum, has
classically been thought to be predictive of cardiac
chest pain.

13. dyspnea occurs when the damage to the heart
limits the output of the left ventricle, causing left
ventricular failure and consequent pulmonary
edema.
diaphoresis (an excessive form of sweating),
weakness, light-headedness, nausea, vomiting, and
palpitations.
Women and older patients report atypical
symptoms. Women also report more numerous
symptoms compared with men.
 The most common symptoms of MI in women
include dyspnea and fatigue. In women, chest
pain may be less predictive of coronary ischemia
than in men.

14. At least 14 of all MI are silent, without chest pain or
other symptoms. These cases can be discovered later
on ECG, using blood enzyme tests or at autopsy
without a prior history of related complaints.
 A silent course is more common in the elderly, in
patients with diabetes mellitus and after heart
transplantation, probably because the donor heart is
not fully innervated by the nervous system of the
recipient.

15. Increasing of cardio-specific enzymes – Troponin.
ECG: Acute changes segment ST, acute left bundle-
branch block.
ECG: Pathological Q.
Echocardiography: akinesia, hypokinesia.
Autopsy of myocardium (thrombus, necrosis).

16. New elevation of ST at 2 or more leads ≥ 0,15 - 0,2 mV
at V2-V3, and ≥ 0,1 mV at other leads.
In ECG Q wave MI – pathological Q and inversion T.
In ECG non Q wave MI – complex QRS is normal, no
pathological Q, but it is inversion T.

17. New regional wall motion abnormalities on an
echocardiogram are also suggestive of a myocardial
infarction.
Akinesia, hypokinesia, postinfarction cardiosclerosis,
aneurysm of myocardium, intracardiac thrumbus,
systolic or diastolic dysfunction of myocardium,
ejection fraction, pulmonary hypertension,
hypertrophy of LV, LA ect.

20. Analysis of blood.
Increase ESR (erithrocyte sedimantation rate).
Increase temperature of body.
Increase leucocytes.
Enzymes blood.
Enzymes Activity peak Lasting
Myoglobin 4-8 hours 0,5-1 day
Troponin I 10-24 hours 5-10 days
Troponin T 10-24 hours 5-14 days
Creatine kinase-MB 10-24 hours 2-4 days
Creatine kinase 7-10 hours 2-5 days

21. Unstable angina is a condition more serious than
stable angina and less serious than an actual heart
attack.
Stable angina is chest pain from a temporary
decrease in oxygen to the heart that is caused by
exertion and goes away with rest.
A heart attack is a prolonged decrease in oxygen
to the heart that results in permanent damage to
the heart

22. As a result, unstable angina symptoms occur
suddenly, often in an unexpected or unpredictable
fashion.
The symptoms may be new, prolonged, more
severe, or occur with little or no exertion.
Unstable angina may also be less responsive to
nitroglycerin medication than stable angina.
 Unstable angina is a medical emergency .

23. 1. Primary unstable angina. it is heart attack during 1
month after first heart attack of stable angina.
2. Progressive unstable angina. Sudden increase of
frequency, heavy, lasting of heart attack time to
simple physical activity. Decrease effective of
nitroclycerin.
3. Early postinfarction angina. It is heart attack during
48 hours after AMI. Postoperative angina. It is
during 1 month after operative treatment (stenting,
coronary bypass surgery).

24. 1. Clinical finding. Same MI.
2. ECG critaria: no ST elevation, depression ST
segment, invertion T.

25. Laboratory: same, but NO troponin I, T, Creatine
kinase-MB.

26. Pre-hospital treatment ACS (first aid)
Hospatal treatment ACS.
1. Treatment of Q wave MI.
2. Treatment of non Q wave MI and Unstable angina are
same.

27. Nitroglicerin 0,5 mg sublingua or Izoket sprey 2 dose
sublingua (it is important to control blood pressure).
Aspirin 165-325 mg chew.
Clopidogrel 75 mg 4 tabs. (300 mg).
Morphini 4-8 mg i/v.
Beta-blockers (atenolol 25-50 mg, bisoprolol 2,5-10
mg)
Trombolysis (alteplaza, streptokinasa). If in ECG ST
elevation.
Heparin 5000-7500 U p/c, 4000 U i/v. (if didn’t give
Trombolysis).

28. Streptokinaza 1,5 mln U i/v during 30-60 min.
Alteplaza 100 mg i/v during 90 min
Tenektoplaza 50 mg during 5-10 sec.
Indications to use Trombolysis.
1. Elevation ST segment ≥ 0,1 mV at 2 or more leads
2. Acute left bundle-branch block with MI clinic.
3. Chest pain ≤ 12 hours.
4. Age ≤ 75 years old.

29. Contraindication to use Trombolysis.
Hemorrage stroke.
Brain trauma
Stratify aneurism of aorta.
Bleeding
High blood pressure ≥ 180/100.

30. NG i/v infusion 1,0 ml with physiol. Sol. 100,0 ml
(under control BP, HR)
Heparin 7500 U p/c – 2 days, 5000 U – 2 days, 2500 U
– 2 days.
Aspirin 75-150 mg/day
Clopidogrel 75 mg/day
Statin: Atorvastatin 20-40 mg/day, Rosuvastatin 5-20
mg/day
Beta-blockers: Bisoprolol 2,5-10 mg/day, Carvediolol
6,25-12,5 mg/day.

31. ACE inhibitors: Captorpil 25-50 mg/day, Lisinopril
2,5-10 mg/day (under control BP).
Calcium channel blockers: Amlodipin 2,5-10 mg/day.

32. NG i/v infusion 1,0 ml with physiol. Sol. 100,0 ml
(under control BP, HR)
Heparin 7500 U p/c – 2 days, 5000 U – 2 days, 2500 U
– 2 days.
Aspirin 75-150 mg/day
Clopidogrel 75 mg/day
Statin: Atorvastatin 20-40 mg/day, Rosuvastatin 5-20
mg/day
Beta-blockers: Bisoprolol 2,5-10 mg/day, Carvediolol
6,25-12,5 mg/day.
Calcium channel blockers: Amlodipin 2,5-10 mg/day.
ACE inhibitors: if it is Heart filure.

35. Is fluid accumulation in the air spaces and
parenchima of the lungs. It leads to impaired gas
exchange and may cause respiratory failure.
Pathogenesis of PE
Fastly decrease of systolic function of LV =>
hypotension in the small circle of blood
circulation (pulmonary vessels) => Increase of
hydrostatic pressure in the lung vessels 25-30 mm
Hg – it is intersticial pulmonary edema =>
increase of hydrostatic pressure in the lung vessels
≥ 30 mm Hg – it is alveolar pulmonary edema.

38. Fast progressive breathlessness
Dry cough
Acrocyanosis
Increase of HR
Tachypnoe >30-32 p/m
Orthopnoe
Bubble breathe
Foamy phlegm

39. 1. NG 1,0 + phys.sol. 100,0 i/v infusion
2. ACE inhibitors: captopril 25-50 mg chew
3. Furosemide 40-80 mg i/v
4. Morphini 1% - 1-2 ml i/v
5. Vertical position of patient

40. It is extreme stage of acute LV heart failure
syndrome of “low ejection fraction”.
Pathogenesis of cardiogenic shock.
Fast decrease of systolic function of LV => decrease
EF, BP => hypoperfusion of issue.

41. Systolic BP ≤ 90 mm Hg.
Oliguria
Cold skin
Acrocyanosis
Echocardiography: low EF.

42. If systolic BP < 70 mm Hg – Noradrenaline.
If systolic BP > 70 mm Hg < 90 mm Hg – Dophamine.
When BP is normal:
Diuretics
ACE inh.
Beta blockers.

43. Chaotic irregular rhytm. Complex QRS and T are
absent.

44. CPU
Defibrillation (200, 300, 360 Dj)
Ventilation of the lungs
Adrenalin 1 mg i/v every 3-5 min
Amiodaron 300 mg i/v

46. If Ventricle tachicardia and heart failure (EF < 40%):
Novocainamide, Amiodarone.
If there is no HF: Novocainamide, Amiodarone,
sotalol.
Basis treatment of MI.

47.  it is extreme decrease systolic function of LV.
Acute heart failure is generally defined as inability of
the heart to supply sufficient blood flow to meet the
body's needs.
Classification of AHF
1. Killip I. No rattles in the lungs.
2. Killip II. Rattles more than 50% area of the lungs.
3. Killip III. Rattles more than 50% area and pulmonary
edema.
4. Killip IV. Cardiogenic shock.