Acute Coronary Syndrome presentation and management.pptx
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Jan 14, 2024
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About This Presentation
Cardiology
Size: 555.42 KB
Language: en
Added: Jan 14, 2024
Slides: 25 pages
Slide Content
Acute Coronary Syndrome Dr. Nathan Muluberhan (MD + , Assi. professor of EMCC, HrU School of Medicine Dean & CPD Director of BHE)
Objectives To know and describe different types of ACS To know risk factors, sign and symptoms of patients with ACS To know the ECG manifestation of ACS To the initial stabilization and management of patients with ACS
Acute Coronary Syndrome Acute coronary syndrome (ACS) refers to the constellation of clinical diseases occurring as a result of acute myocardial ischemia. ACS includes a spectrum of clinical presentations ranging from unstable angina (UA) to acute myocardial infarction (AMI). Sudden cardiac death (SCD) is the most extreme form of ACS.
Unstable angina: considered to be an ACS in which there is myocardial ischemia without detectable myocardial necrosis. Characterized by- symptom occurring at rest/with minimal exertion, lasting>10 min; severe & of a new onset; crescendo pattern (i.e. more severe, prolonged, or frequent than previously). Acute Coronary Syndrome
Acute myocardial infarction (AMI): defined by myocardial necrosis with elevation of cardiac biomarkers and is classified by ECG findings as: ST-segment elevation myocardial infarction(STEMI): Chest pain >20 to 30 min occurring at rest (not relieved by nitroglycerin), serologic evidence of myonecrosis , and persistent ST-segment elevation. Non-ST-segment elevation myocardial infarction (NSTEMI): UA with evidence of myocardial necrosis (elevated cardiac biomarkers) Acute Coronary Syndrome
Risk Factors Modifiable Non-Modifiable Increasing age Gender (male) Ethnicity Family History ?Diabetes Smoking Obesity Diet Lack of exercise High serum cholesterol Hypertension
HISTORY AND ASSOCIATED SYMPTOMS C hest discomfort or pain Substernal or in the left chest, with radiation to the arm (either), neck, or jaw. Chest pressure, heaviness, tightness, fullness, or squeezing. Less commonly, patients describe their symptoms as knife-like, sharp, or stabbing Associated symptoms such as nausea, vomiting, diaphoresis, dyspnea, lightheadedness, syncope, and palpitations.
PHYSICAL EXAMINATION The pulse rate may be normal or fast, slow or irregular. Bradycardic ( poor prognostic sign) rhythms are more common with inferior wall myocardial ischemia An S3 is present in 15% to 20% of patients with AMI. The presence of a new systolic murmur is an ominous sign because it may signify papillary muscle dysfunction.
DIAGNOSIS The diagnosis of STEMI depends on the ECG in the setting of symptoms suggestive of MI. The diagnosis NSTEMI depends on abnormal elevation of cardiac biomarkers but may include ECG changes not meeting criteria for STEMI. The diagnosis of unstable angina is based on history because the ECG and cardiac injury biomarkers are nondiagnostic. Early risk assessment for the likelihood of myocardial infarction uses all of these data to aid decision making.
Exercise , stress, and a cold environment classically precipitate angina. Angina typically has a duration of symptoms of <10 minutes, occasionally lasting up to 10 to 20 minutes, and usually improves within 2 to 5 minutes after rest or nitroglycerin. In contrast, AMI is usually accompanied by more prolonged and severe chest discomfort, more prominent associated symptoms. Easy fatigability may be a prominent symptom of ACS, especially in women . HISTORY AND ASSOCIATED SYMPTOMS
Diagnosis The diagnosis of ST-segment elevation myocardial infarction ( STEMI ) depends on the ECG in the setting of symptoms suggestive of myocardial infarction. The diagnosis of non-ST-segment elevation myocardial infarction ( NSTEMI) depends on an abnormal elevation of cardiac biomarkers but may include ECG changes not meeting the criteria for STEMI. The diagnosis of unstable angina is based on history: Angina pain with at least 1 of 3 features: Occurs at rest/with minimal exertion or lasting>10 min, Severe & of a new onset or crescendo pattern (i.e. more severe, prolonged, or frequent than previously).
ECG ECG: done at presentation; repeat at 6–12 h& with any change in symptoms UA/NSTEMI= ST depression/transient elevation or deep T inversion (>=0.3mV) STEMI=New ST elevation in 2 contiguous leads >= 0.2 mV in men or 0.15 mV in women in leads V2-3 and/or 0.1mV in other leads OR new LBBB N.B the ECG must also be analyzed for rate, rhythm,etc (look for arrhythmias)
Cardiac Biomarkers Serial testing at presentation & 6–12 h after symptom onset. Cardiac troponins ( T&I) rise 20 -50 Xs Upper normal limit/UNL/ in acute MI; rise 4-8 hr after injury; may remain elevated for 7-10 days; more Specific & Sensitive than CK-MB Creatine kinase (CK )-rises in 4–8 hr ; normalize by 48–72 h; lacks specificity
Other investigation Echocardiography : may show new wall motion abnormality RBS, electrolytes, OFTs, lipid profiles CXR : to look for pulmonary edema; R/o other DDx (PTE, pneumonia, Pneumothorax...) Coronary angiography if indicated
Management Should focus on stabilizing the patient's condition, relieving ischemic pain, and providing antithrombotic therapy to reduce myocardial damage and prevent further ischemia. The goal is early revascularization.
1) General measures: Continuous ECG monitoring for arrhythmia & ST changes V/S: Q 2 hr until stable, then Q 4hr & as needed O2 (2-4 lit/min) if SaO2<90% Bed rest, Sedation, VTE(venous thrombo -embolism) prophylaxis NPO except for sips of water until stable; IV fluid – e.g. For inferior MI Glycemic control-goal is RBS of 140-180mg/dl(if > 180mg/ dl,give regular Insulin-1-2IU for each 50mg/dl increase above 180mg/dl, by measuring RBS Q 6hrs) Treat comorbidities like DM (for both types-standing doses of lente /NPH
2) Medications: Aspirin(ASA): loading:162–325 mg chewed, then 75–162 mg/d plus Clopidogre l : loading: 300mg Po, then 75 mg/d for at least 1 yr (but ASA lifelong) Nitroglycerin (NTG): sublingual 0.4 mg Q 5 min as needed or persistent chest pain *IV NTG for persistent ischemia .C/I= low BP, sildenafil use Morphine sulphate sulfate : 2–5 mg IV, may be repeated Q 5–30 min as needed to relieve Symptoms (can also use morphine syrup, pethidine or tramadol)
Metoprolol: 25–50 mg PO q 6 h* (If HTN, ongoing pain, tachycardia: give IV over 1–2 min by 5mgincrements. If not available- use atenolol, propranolol/carvedilol. C/I- CHF, bradycardia. UFH: Bolus 60–70 U/kg (max. 50000 IU) IV then infusion of 12–15 U/kg/ h (initial Maximum 1000 U/h) titrated to aPTT 50–70 s * If no per fuser, 12,500U SC BID is possible; OR LMWH (Enoxaparin):1 mg/kg SC Q 12 h(if GFR< 30,1mg/kg once daily) Statins: atorvastatin 80mg PO/d is preferred. Others options are pravastatin/ Simvastatin/ lovastatin 40mg Po/day ACEIs : start low dose eg . Enalapril / lisinopril 2.5 to 5mg po /d OR captopril 6.25-12.5mg TID; then escalate gradually to clinically effective dose.
Invasive therapy in ACS : for a high risk patients who present early, referral to a better set up is recommended (If the patient can afford) Time since onset of symptoms- 90 min for PCI / 12 hours for fibrinolysis Determine if fibrinolysis candidate- Meets criteria with no contraindications Determine if PCI candidate- Based on availability and time to balloon treatment STEMI: Fibrinolysis Vs PCI/CABG Unstable angina /NSTEMI: PCI/ CABG; but fibrinolysis is not indicated.