Acute Coronary Syndrome (ACS)

• Acute Coronary Syndrome (ACS) includes unstable angina (UA), non-ST segment elevation myocardial infarction (NSTEMI), and ST segment elevation myocardial infarction (STEMI).

Differential Diagnosis of Chest Pain

• Life-threatening causes of chest pain include acute coronary syndrome, aortic dissection, pulmonary embolism, pneumothorax, and expanding aortic aneurysm.
• Other causes of chest pain include pneumonia, pleuritis, pericarditis, costochondritis, cervical disc disease, peptic ulcer disease, gastroesophageal reflux, biliary disease, pancreatitis, and panic attack.

ACS Objectives

• The objectives include definition, pathophysiology, patient presentation, diagnostics, treatment, complications, goals, and reminders.

ACS Definition

• Unstable Angina (UA) presents with ischemic symptoms, including rest angina (usually >20 minutes), new-onset angina that limits physical activity, or increasing angina.
• UA symptoms may occur with or without EKG changes (T wave inversions, ST segment depressions).
• UA does not show elevation of troponin.
• NSTEMI is similar to UA, but troponin is elevated.
• STEMI involves ST-segment elevations of 1 mm (0.1 mV) in 2 anatomically contiguous leads or 2 mm (0.2 mV) in 2 contiguous precordial leads, OR new left bundle branch block, along with presentation consistent with ACS.

Acute Coronary Syndrome

• Stable Angina involves a stable fixed atherosclerotic plaque.
• UA involves plaque disruption and platelet aggregation.
• NSTEMI involves a larger obstruction with occlusion of the lumen.
• STEMI involves complete occlusion of the lumen.
• UA is a partial obstruction.

ACS Pathophysiology

• The most common cause is plaque rupture, involving the rupture of the fibrous cap of an atheromatous plaque and exposure of thrombogenic, necrotic core material rich in red cells.
• Other less common causes include plaque erosion, dynamic obstruction, spontaneous coronary dissection, infection, and progressive mechanical obstruction.

ACS Pathophysiology: Myocardial Tissue Death

• Complete occlusion leads to myocardial tissue death.
• With Left Ventricle involvement, critical mass is reached when 40% of the myocardium is nonfunctional, leading to cardiogenic shock.
• Right Ventricle infarct can cause severe reduced pre-load and hypotension.

Diagnosis of ACS

• Diagnosis requires at least 2 of the following: history (angina or angina equivalent), acute ischemic ECG changes, typical rise and fall of cardiac markers, and absence of another identifiable etiology.

Patient History

• Include assessing chest discomfort (tightness, dullness, heaviness), fatigue, weakness, shortness of breath, activity at onset, and risk factors.

Important History-Related Factors

• The nature of the chest pain is the most important factor.
• The number of traditional risk factors is also very important

Physical Examination

• Vital signs should be assessed.
• Check for skin color/diaphoresis.
• Check the neck and lung sounds.
• Assess heart sounds: friction rub (pericarditis?) or new murmur (MI, acute mitral regurgitation, or VSD).
• Check for lower extremity edema.
• Perform a cursory neuro exam if considering thrombolytics.

ECG in ACS

• ECG is used to look for acute ischemia in the coronary arteries.
• Remember that approximately 50% of ECGs may be initially normal, but then develop ST changes.
• Unstable Angina may have an abnormal or normal EKG.
• N-STEMI may have an abnormal or normal EKG.
• STEMI is defined by ST-segment elevation in contiguous leads (or new LBBB) in the setting of ischemic symptoms.

12-Lead ECG Interpretation

• I is lateral.
• aVR.
• V1 is Septal.
• V4 is anterior.
• II is inferior.
• aVL is lateral.
• V2 is septal.
• V5 is lateral.
• III is inferior.
• aVF is inferior.
• V3 is anterior.
• V6 is lateral.

ECG SITE, FACING, RECIPROCAL

• INFERIOR faces II, III, aVF and is reciprocal to I, aVL.
• HIGH LATERAL faces I, aVL and is reciprocal to II, III, aVF.
• ANTERIOR faces V1, V2, V3, V4 and has no reciprocal.
• POSTERIOR has NONE facing and V1, V2, V3, V4 reciprocal.

ECG Findings

• STEMI has ST Elevation.
• NSTEMI has ST Depression or T Inversion.

Posterior ECG

• Take off leads V5 and V6 and move them to the patient’s back below the left scapula to see ST segment elevations.
• A deep rapid S wave is generated in lead V1 with a New LBBB.

Cardiac Biomarkers/Enzymes

• Troponin I or T (cTnI or cTnT): measured at the time of presentation and every 3-6 hours for 6-12 hours.
• High-sensitivity Troponin (hs-cTn) I or T: measured at the time of presentation and every hour x 1-3 hours.
• Troponin values are utilized to diagnose MI; however, there is a delay in the rise of troponin after an MI.
• It is inappropiate to wait for the results of cardiac biomarkers in patients with Acute ST-elevation MI before sending to cardiac catheterization.
• Examples of False positives: pulmonary embolism, myocarditis, takotsubo cardiomyopathy, chronic kidney disease, rare analytical problem (heterophile antibodies).
• False negative: excessive biotin use
• CK (creatine kinase)MB and myoglobin not commonly used anymore because troponin is much more sensitive and specific.

Treatment Goals

• To prevent extension, remove obstruction, and preserve function.
• Time is muscle.
• Save cardiac muscle.
• Saving muscle saves heart function.
• Remember critical mass of 40% or greater.
• Watch for Cardiogenic Shock.

ECG - Left Ventricular Aneurysm

• Persistent ST segment elevation occurring 6 weeks after a known transmural MI may mimic an acute ST segment elevation MI.

ACS Treatment: Initial Interventions

• Assess and stabilize airway, breathing, and circulation.
• Provide oxygen only if O2 saturation is below 90% in patients with respiratory distress or heart failure, or those with high-risk features for hypoxia; hyperoxia can have vasoconstrictor effects on coronary arteries.
• Attach cardiac and oxygen saturation monitors.
• Establish IV access.
• Treat sustained ventricular arrhythmia rapidly according to ACLS protocols.
• Monitor vital signs.
• Perform a focused history and examination, including looking for signs of hemodynamic compromise and left heart failure and neurologic function, especially if fibrinolytic therapy is considered.
• Obtain labs, including cardiac biomarkers (x3), CBC, CMP, PT/INR, PTT.
• Get a portable CXR.

ACS Treatment: Initial Medications

• Aspirin
• Nitroglycerin
• Beta Blockers
• Morphine
• Statin

Aspirin Administration

• Give 162 to 325 mg of non-enteric coated Aspirin, chewed and swallowed.
• If oral administration isn't feasible, give as a rectal suppository
• Aspirin reduces the synthesis of prostaglandins/thromboxane.
• Prostaglandins play a key role in promoting inflammation.
• Thromboxane is central to platelet activation.
  • Contraindications: Aspirin allergy and Aortic Dissection

Nitroglycerin Administration

• Give three sublingual nitroglycerin tablets (0.4 mg), one at a time spaced five minutes apart, or one aerosol spray under the tongue every five minutes for three doses if the patient has persistent chest discomfort, hypertension, or signs of heart failure.
• Add IV nitroglycerin for persistent symptoms.
• Nitroglycerin causes vasodilation of coronary arteries, which may increase oxygen delivery.
• Aids in better blood pressure control during ACS.
• Nitroglycerin usage may relieve edema in the lungs.
  • Contraindications: Hemodynamic compromise (e.g., right ventricular infarction) and use of phosphodiesterase inhibitors (e.g., for erectile dysfunction).

Beta Blocker Administration

• Give a beta blocker (e.g., metoprolol 25 mg orally).
• If hypertensive, may initiate beta blocker IV instead (e.g., metoprolol 5 mg intravenously every 5 minutes times three doses as tolerated).
• Beta Blockers are antiarrhythmic, decreasing systemic arterial pressure.
• Decreases myocardial contractility, increases filling time, increasing time for coronary blood flow.
• Decreases 02 consumption by the heart.
  • Contraindications: Decompensated heart failure, hemodynamic compromise, bradycardia, severe reactive airway disease and cocaine use.

Morphine Sulfate Administration

• Give 2 to 4 mg slow IV push every 5 to 15 minutes ONLY for persistent discomfort or anxiety; this may increase mortality.
  • Morphine delays clopidogrel resorption and may decrease afterload via venodilation.

Statin Administration

• Start 80 mg of atorvastatin as early as possible, and preferably before PCI, in patients not on statin.
  • Statins decrease inflammation and may have a protective effect beyond just LDL lowering in ACS.

STEMI Management

• Immediate reperfusion therapy is needed
  • Cardiac catheterization (angioplasty/percutaneous intervention) is most common.
    • Goal for cath lab: door to balloon 90 minutes.
• Do not wait for the troponin results, go straight to the cath lab if there are ST segment elevations on EKG in contiguous leads.

Stent Placement (Figure 1, Figure 2)

• A wire-mesh tube, or stent, when premounted on a balloon catheter, is ready for deployment either in an artery that has just been cleared with angioplasty or in a native artery with an atherosclerotic lesion. Stents are available in many designs and sizes.
• Stents are deployed in conjunction with balloon angioplasty.
  • They are premounted onto the deflated balloon taken to the insertion point with a guide wire.
  • The balloon is inflated, expanding the stent.
  • The balloon is deflated and withdrawn, leaving the stent in place.

Reperfusion Therapy for Patients with STEMI

• For a STEMI patient who is a candidate for reperfusion who presents initially at a PCI-capable hospital: send to cath lab for primary PCI, with FMC-device time ≤ 90 min.
• For a STEMI patient who is a candidate for reperfusion who presents initially at a non-PCI-capable hospital: transfer for primary PCI, with FMC-device time as soon as possible and ≤ 120 min; if unable to meet this time, administer a fibrinolytic agent within 30 min of arrival when anticipated FMC-device time is > 120min.
• Urgent transfer for PCI is needed for patients with evidence of failed reperfusion or reocclusion.
• Transfer for angiography and revascularization within 3-24 hours for other patients as part of an invasive strategy.
• Angiography and revascularization should not be performed within the first 2 to 3 hours after administration of fibrinolytic therapy.
• Patients with cardiogenic shock or severe heart failure initially seen at a non-PCI-capable hospital should be transferred for cardiac catheterization and revascularization ASAP, irrespective of time delay from MI onset.

NSTEMI and Unstable Angina Management

• Telemetry
• Aspirin
• Other antiplatelet agents (IIb/IIIA inhibitors, Adenosine diphosphate receptor antagonists)
• Beta blocker
• Nitrates
• Heparin (UFH or LMWH)
• Statin
• Cardiac catheterization for sicker patients

Other Medications in ACS

• Heparin
• IIb/IIIA inhibitors
• Adenosine diphosphate receptor antagonists

Heparin

• Heparin prevents clot enlargement by reducing the formation of fibrin clots via inhibiting thrombin.
• Thrombin converts soluble fibrinogen to insoluble fibrin.
• Heparin onset of activity is immediate and can be reversed if needed with protamine but not LMWH.
• Heparin is administered via bolus and continuous infusion.

GP IIb/IIIA Inhibitors

• Inhibits the binding of fibrinogen to GP IIB/IIIA receptor sites on platelets (the final step in platelet aggregation).
• Occupies these sites on the platelets.
• Receptor antagonists.

Adenosine Diphosphate (ADP) Receptor Antagonists

• Examples include Ticagrelor/Brilinta or prasugrel/Effient or clopidogrel/Plavix.
• Prevents ADP-induced "fibrinogen binding" to GP IIB/IIIA receptor sites on platelets.
• Platelet receptor inhibitors.

Treatment of Acute Coronary Syndrome (ACS)

• Initial treatment involves distinguishing between STEMI and UA/NSTEMI, where the treatment depends on the diagnosis.
• STEMI treatment: antiplatelet, anti-ischemic, or anticoagulant therapy plus thrombolytics, PCI, or CABG
• UA/NSTEMI treatment: antiplatelet, anti-ischemic, or anticoagulant therapy followed by PCI or CABG.
• Long-term medical management is applied to both STEMI and UA/NSTEMI.

Long Term Medical Management

• Dual antiplatelet therapy for at least 12 months (Aspirin + ADP inhibitor)
• Statin
• ACE-I or ARB
• Beta Blocker

Invasive Treatment Options

• CABG is considered if the patient has multiple vessel involvement (3), failed PTCA, or a large left main lesion.

ACS Treatment Reminder

• Re-evaluate the patient as often as necessary.
• Repeat EKG.
• The pain returned or is getting worse.
• Treat the patient and not just the paper.
• Expedite care/National Standard.
• Aim for a 90 minute goal from entry to the emergency room to the opening of the balloon in the cath lab.

MI Complications

• Arrhythmias (75-95%)
• Congestive heart failure (60%)
• Right ventricular infarction (30-40% of inferior MI's)
• Pericarditis (6-20%)
• Left ventricular aneurysm (5-30%)
• Cardiogenic shock (10%).
• 40% Critical Mass of LV
• Reinfarction (5%)
• Ventricular septum perforation
• Acute mitral regurgitation

Arrhythmias in MI

• Most people who die during an MI die from Ventricular Fibrillation.
  • Early defibrillation is crucial.

Right Ventricular (RV) Infarct

• RV infarct has 8x higher mortality versus Inferior MI
• ECG findings of acute inferior and right ventricular myocardial infarction: shows Q waves and prominent doming ST segment elevation in leads II, III, and aVF, which are characteristic of an acute inferior myocardial infarction, plus ST elevation in the right precordial leads V4R, V5R, and V6R.

Right-Sided EKG

• Modified precordial lead V4R Placement
• If a patient has a hypotensive inferior MI, obtain an RT sided EKG.
  • The left sided leads are V4, V5, and V6.
  • The right sided leads are V4R, V5R and V6R.
  • ST elevation = RV infarct.
    • The patient needs no pre-load and must have INCREASED volume to the left Ventricle.
    • Treatment requires bolus of IV fluids.
      • Do not give nitroglycerin to these patients.

EKG Pericarditis

• Do not confuse with AMI.
• Post-MI pericarditis may develop two to four days after an acute infarction and results from a reaction between the pericardium and the damaged adjacent myocardium.
• Dressler's syndrome is a post-MI phenomenon in which pericarditis develops weeks to months after an acute infarction; this syndrome is thought to reflects a late autoimmune reaction mediated by antibodies to circulating myocardial antigen.
  • This is treated with NSAID/Aspirin

Cardiogenic Shock

• Loss of 40% of critical LV mass
• Cardiac output is reduced PCWP is increased CVP/RAP is increased Blood Pressure is low Systemic Vascular Resistance is increased </existing_notes>