Acs Anaes

Acute coronary
Syndrome
Prepared by: B.Ananth Sai Roop Sagar
Group no:5/103
 Acute coronary syndrome (ACS): the suspicion or
confirmed presence of acute myocardial ischemia
 Acute coronary syndrome may be further classified
into the following categories:
Acute  NSTE-ACS: acute coronary syndrome manifesting
coronary without ST-elevations on ECG
 NSTEMI: positive myocardial injury biomarkers
syndrome  Unstable angina: absence of detectable myocardial
injury biomarkers
 STE-ACS: acute coronary syndrome manifesting with
ST-elevations on ECG
 Unstable angina (UA):
 Acute myocardial ischemia that is not severe enough to cause detectable
quantities of myocardial injury biomarkers or ST-segment elevations On ECG
 Angina at rest/with minimal exertion and is usually not relieved by rest or
nitroglycerin
 New-onset angina
 Severe, persistent, and/or worsening angina (crescendo angina)
 Autonomic symptoms may be present: diaphoresis, syncope, palpitations,
nausea, and/or vomiting
NSTE-ACS  Partial occlusion of coronary vessel → decreased blood supply → ischemic

symptoms (also at rest)
Cardiac ttroponin :Not elevated
ECG findings: No ST elevations
Treatment: Invasive management depends on risk stratification (e.g., TIMI
score)
Anticoagulants, antiplatelet therapy (e.g., aspirin, ADP receptor inhibitors)
Statins
Antihypertensive therapy (beta blockers, ACEIs)
Pain management (opioids, nitrates)
 Non-ST-segment elevation myocardial infarction (NSTEMI)
 Acute myocardial ischemia that is severe enough to cause detectable quantities
of myocardial injury biomarkers but without ST-segment elevations on ECG
 Angina at rest/with minimal exertion and is usually not relieved by rest or
nitroglycerin
 Autonomic symptoms may be present: diaphoresis, syncope, palpitations,
nausea, and/or vomiting
 Classically due to partial occlusion of a coronary artery
NSTE- ACS  Affects the inner layer of the heart (subendocardial infarction)
 Cardiac troponin: Elevated
 ECG findings: No ST elevations
 Normal or nonspecific (e.g., ST depression, loss of R wave, or T-wave inversion)
 Treatment : Invasive management depends on risk stratification (e.g., TIMI
score)
 Anticoagulants, antiplatelet therapy (e.g., aspirin, ADP receptor inhibitors)
 Statins
 Antihypertensive therapy (beta blockers, ACEIs)
 Pain management (opioids, nitrates)
 ST-segment elevation myocardial infarction (STEMI)
 Acute myocardial ischemia that is severe enough to cause ST-
segment elevations on ECG
 Angina at rest/with minimal exertion and is usually not relieved by
rest or nitroglycerin
 Autonomic symptoms may be present: diaphoresis, syncope,
STE-ACS palpitations, nausea, and/or vomiting
 Classically due to complete occlusion of a coronary artery
 Affects the full thickness of the myocardium (transmural
infarction)
 Cardiac troponin : Usually elevated
 ST elevations (in two contiguous leads) or new left bundle branch
block with strong clinical suspicion of myocardial ischemia
 Treatment: Immediate revascularization
 Adjunctive medical therapy similar to NSTE-ACS
Classic presentation :
Acute retrosternal chest pain
Typical: dull, squeezing pressure and/or tightness
Commonly radiates to left chest, arm, shoulder, neck, jaw, and/or
epigastrium
Precipitated by exertion or stress
Symptom relief after administration of nitrates is not a diagnostic criterion
for cardiac ischemia.
Clinical  The peak time of occurrence is usually in the morning.
 Dyspnea (especially with exertion)
features  Pallor
 Nausea, vomiting
 Diaphoresis, anxiety
 Dizziness, lightheadedness, syncope
 Other findings
 Tachycardia, arrhythmias
 Symptoms of CHF (e.g., orthopnea, pulmonary edema) or cardiogenic
shock (e.g., hypotension, tachycardia, cold extremities)
 New heart murmur on auscultation (e.g., new S4)
Atypical presentations: more likely in elderly, diabetic
individuals, and women
Stabbing, sharp chest pain
No or minimal chest pain
”Silent MI” without chest pain is more common in
patients with diabetes, as a result of polyneuropathy.
 Autonomic symptoms (e.g., nausea, diaphoresis)
 More common in inferior wall infarction
 Epigastric pain
 Bradycardia
 Clinical triad in right ventricular infarction:
hypotension, elevated jugular venous pressure, clear
lung fields
 ECG: should be performed immediately once ACS is suspected or
considered as differential diagnosis
 ST-elevations present: immediate revascularization therapy, preferably
PCI
 No ST-elevations present (i.e., NSTE-ACS): management strategy is
guided by ECG findings, troponin levels, clinical features, and risk factors
 Cardiac troponin levels: Measure as soon as possible and repeat after 1–
6 hours.
 Consider bedside TTE if the diagnosis is unclear.
Diagnostics 12-lead ECG

Indicated for every patient with suspected ACS (best initial test)
Findings:
ECG changes in STEMI
ECG changes in NSTEMI/unstable angina
Repeat every 15–30 minutes in the first hour (especially if the first ECG is
inconclusive or symptoms recur or change in quality)
 Compare with previous ECGs (if available).–6
 Significant ST elevation in two contiguous leads
 Classical timeline of ECG changes in STEMI:
 Acute stage: myocardial damage ongoing
 Hyperacute T waves (peaked T wave)
 ST elevations in two contiguous leads with reciprocal ST
ECG depressions
changes in Intermediate stage: myocardial necrosis present
STEMI Absence of R wave

T-wave inversions
Pathological Q waves
Duration ≥ 0.04 seconds
Amplitude ≥ ¼ of the R wave or ≥ 0.1 mV
Any Q wave in leads V1–3
Chronic stage: permanent scarring
Persistent, broad, and deep Q waves
Often incomplete recovery of R waves
 Permanent T-wave inversion is possible.
 Immediate revascularization
 Emergency coronary angiography with PCI
 Indication: preferred method of revascularization
 in patients suspected of having STEMI
 Procedure: balloon dilatation with stent implantation
 First medical contact (FMC) to PCI time
 Ideally ≤ 90 minutes.
 Should not exceed 120 minutes
Indications (in STEMI and STEMI equivalents, if all of the
following apply):
PCI cannot be performed ≤ 120 minutes after FMC.
Symptom onset
≤ 12 hours
Fibrinolytic  OR 12–24 hours with clinical signs of ongoing ischemia
(PCI is even more preferable in this context)
therapy in Timing: within < 30 minutes of patient arrival at the
STEMI hospital
Regimens (one of the following)
Tenecteplase
Alteplase
Reteplase
Streptokinase
 Coronary artery bypass grafting:
 Antiplatelet therapy and anticoagulation in
STEMI:
 Dual antiplatelet therapy: Aspirin
 AND one of the following ADP receptor inhibitors
 Prasugrel
 Ticagrelor
 Clopidogrel
 Anticoagulation: Unfractionated heparin
 OR Bivalirudin
 Glycoprotein Iib/IIIa inhibitor (GPI): Abciximab
 Eptifibatide
 Tirofiban
No ST elevations present
ECG Nonspecific signs of ischemia may be present,

including:
changes in ST depression, especially if horizontal or downsloping
NSTEMI/UA Transient ST deviations
T-wave inversions

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Acs Anaes

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Acute coronary

NSTE-ACS  Partial occlusion of coronary vessel → decreased blood supply → ischemic

Diagnostics 12-lead ECG

STEMI Absence of R wave

ECG Nonspecific signs of ischemia may be present,

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