Chapter 30 - Acute Coronary Syndrome Flashcards
- What can ACS result from?
- What can it lead to?
- Plaque buildup in coronary arteries (Heart)
- The plague can rupture, leading to clot (thrombus) formation and sudden, reduced blood flow (ischemia) to the heart.
What are some risk factors that can lead to plaque build up that causes ACS?
1) Age:
– Men > 45 years
– Women > 55 years (or early hysterectomy)
2) Family history: 1st degree relative with coronary event before 55 years (men) or 65 years (women)
3) Smoking
4) Hypertension
5) Known coronary artery dx
6) Dyslipidemia
7) Diabetes
8) Chronic angina
9) Lack of exercise
10) Excessive alcohol
What are the classic Sx of ACS?
- Chest pain (often described as discomfort, pressure and squeezing) lasting >= 10 minutes
- Severe dyspnea
- Diaphoresis
- Syncope/presyncope
- Palpitations
–The pain can radiate to the arms, back, neck, jaw or epigastric region.
–Females, the elderly and patients with diabetes are less likely to experience the classic symptoms.
–Symptoms can occur at rest, or may be precipitated by minimal exertion, exercise, cold weather, extreme emotions, stress or sexual intercourse.
- Is ACS an emergency?
- How should patients with a prescription for sublingual nitroglycerin take it?
- When should they call 911?
- ACS is a medical emergency.
- 1 dose every 5 min for up to 3 doses to relieve chest pain.
- If the chest pain or discomfort is not improved or is worse 5 minutes after the first dose, call 911 immediately.
What are the types of Acute coronary syndrome?
1) Unstable angina (UA):
- Symptoms: Chest pain
- Cardiac Enzymes: Negative
- ECG Changes: None or transient ischemic changes
- Blockage: Partial blockage
2) Non-ST segment elevation MI (NSTEMI):
- Symptoms: Chest pain
- Cardiac Enzymes: Positive
- ECG Changes: None or transient ischemic changes
- Blockage: Partial blockage
—Are indistinguishable upon presentation
3) ST-segment elevation myocardial infarction (STEMI):
- Symptoms: Chest pain
- Cardiac Enzymes: Positive
- ECG Changes: ST segment elevation
- Blockage: Complete blockage
ACS diagnosis:
- How are the types of ACS differentiated?
- When should they be performed?
The types of ACS are differentiated by:
– ECG changes
– The presence of cardiac enzymes
– The extent of blockage in the affected artery (partial or complete)
When:
- 12-lead ECG: within 10 min at the site of 1st medical contact
- Acute MI (STEMI or NSTEMI) –> URGENT transport to a hospital with percutaneous coronary intervention (PCI)
Cardiac Enzymes:
- Help with diagnosis
- Biochemical markers (enzymes) are released into the blood stream when myocardial cells die.
1- Cardiac troponins I and T (Tnl and TnT):
- Most sensitive and specific biomarkers for ACS.
- Detectable in blood within 2- 12 hrs, and for up to 5 - 14 days, after myocardial necrosis.
- Levels should be obtained at presentation and 3 - 6 hours after symptom onset in all patients with ACS symptoms.
2- Creatine kinase myocardial isoenzyme (CK-MB) and myoglobin
- Less sensitive markers but may still be monitored in clinical practice.
How can NSTE-ACS be treated?
- Medications alone (referred to as medical management)
or - PCI (referred to as an early invasive strategy)
– Coronary revascularization procedure that involves inflating a small balloon inside a coronary artery to widen it and improve blood flow
– Usually, metal mesh, called a stent, is placed into the artery afterward to keep the artery open
- What does a STEMI result from?
- How can STEMI be treated?
-A STEMI results from complete blockage of one or more coronary arteries, and the blocked arteries need to be opened as quickly as possible.
- PCI: preferred approach
- Fibrinolytics: if PCI cannot be done in a reasonable time frame.
- CABG: May also go directly for urgent coronary artery bypass graft (CABG) surgery if there is significant multi- vessel disease within the coronary arteries.
Regardless of the management strategy selected, acute treatment is aimed at:
- Providing immediate relief of ischemia
- Preventing MI expansion
- Death
What is the drug treatment combination to reach these goals?
These work by different mechanisms to reach the goals of acute treatment.
■ Antianginals (morphine, nitrates, beta-blockers):
- Decrease myocardial O2 demand or
- Increase myocardial O2 supply (blood flow) to relieve ischemia.
■ Antiplatelets (aspirin, P2Yl2 inhibitors, glycoprotein lIb/Illa inhibitors):
- Inhibit platelet aggregation to prevent clot formation/ growth.
■ Anticoagulants (UFH, LMWH, bivalirudin):
- Inhibit clotting factors to prevent clot formation/ growth.
Drugs treatment mnemonics for ACS
MONA-GAP-BA
- Morphine
- Oxygen
- Nitrates
- Aspirin
- GPllb/llla antagonists
- Anticoagulants
- P2Y12 inhibitors
- Beta-blockers
- ACE inhibitors
■ NSTE-ACS: MONA-GAP-BA+/- PCI
■ STEMI: MONA-GAP-BA+ PCI or fibrinolytic (PCI preferred)
Drugs treatment mnemonics for ACS
MONA-GAP-BA
Give these immediately (as needed):
- Morphine
- Oxygen
- Nitrates
- Aspirin
Give these next (choice of drug based on plan (CABG or PCI or Medical management)
- GPllb/llla antagonists
- Anticoagulants
- P2Y12 inhibitors
Give within 24 hrs (as needed); Continue as an outpatient
- Beta-blockers
- ACE inhibitors
■ NSTE-ACS: MONA-GAP-BA+/- PCI
■ STEMI: MONA-GAP-BA+ PCI or fibrinolytic (PCI preferred)
Give these immediately (as needed):
MORPHINE
- Clinical Benefit
- Clinical Notes
- SE
Clinical Benefits: Antianginal:
- Produces arterial and venous dilation (decreases preload and afterload)
- Provides pain relief
Clinical Notes:
- Morphine sulfate
- 2-5 mg IV repeated at 5-30 minute intervals PRN
- May be used in patients with ongoing chest discomfort despite NTG therapy
Side effects:
- Hypotension, bradycardia, N/V, sedation and respiratory depression.
Oxygen
- Give immediately (As needed)
- Administer to patients with arterial oxygen saturation < 90% (SaO2 < 90%) or those with respiratory distress.
Nitrates
- Give immediately
- Antianginal:
– Dilate coronary arteries and improve collateral blood flow
– Dec preload and afterload (modestly)
– Reduces chest pain - Sublingual NTG (0.3-0.4 mg) if not already administered.
- Start IV NTG for persistent ischemic pain, hypertension or heart failure.
- Nitrates can reduce blood pressure.
- Do not use IV NTG if:
– SBP < 90 mmHg
– HR < 50 BPM
– If patient is experiencing a right ventricular infarction - PDE-5 inhibitors are contraindicated with NTG.
Aspirin
- Non-enteric-coated, chewable aspirin (162-325 mg) should be given to all patients immediately if no CI are present (do not use extended-release aspirin products).
- A maintenance dose of aspirin 81-162 mg daily should be continued indefinitely.
- If intolerant to aspirin, may use clopidogrel or ticagrelor
List GPllb/llla receptor antagonists drugs
- Abciximab
- Eptifibatide
- Tirofiban
Anticoagulants
- Inhibit clotting factors and can reduce infarct size
- Drugs include LMWHs (enoxaparin, dalteparin), UFH and bivalirudin (preferred for STEMI)
List P2Y12 Inhibitors drugs
- Clopidogrel
- Prasugrel
- Ticagrelor
Beta blockers
Antianginal:
- Dec BP, HR and contractility
- Dec ischemia, reinfarction and arrhythmias;
- Prevent cardiac remodeling;
- INCREASE long-term SURVIVAL
- An oral, low dose beta-blocker (beta-1 selective blocker without intrinsic sympathomimetic activity preferred) should be started within the first 24 hours unless contraindicated (decompensated heart failure, cardiogenic shock, HR< 45 bpm).
- lf the patient has concomitant HFrEF that is stable, choose bisoprolol, metoprolol succinate or carvedilol .
- An IV beta-blocker or an oral long-acting nondihydropyridine calcium channel blocker (verapamil or diltiazem) are alternative options used in some situations.
ACE Inhibitors
- Inhibit angiotensin converting enzyme and block the production of angiotensin II
- Prevent cardiac remodeling
- Dec preload and afterload
- An oral ACE inhibitor should be started within the first 24 hours and continued indefinitely in all patients with LVEF < 40%, those with HTN, DM or stable CKD unless contraindicated (use ARB if ACEi intolerance).
– Use in other patients may be reasonable. - Do not use an IV ACE inhibitor within the first 24 hours due to the risk of hypotension
Medications to Avoid in the Acute Setting
■ NSAIDs (except aspirin), whether nonselective or COX-2-selective, should not be administered during hospitalization due to inc risk of mortality, reinfarction, hypertension, cardiac rupture, renal insufficiency and heart failure.
■ Immediate-release nifedipine should not be used due to inc risk of mortality.
ANTIPLATELET DRUGS: Aspirin
Inhibits platelet aggregation/ clot formation by inhibiting production of thromboxane A2 (TXA2) via irreversible COX1and COX2 inhibition.
ANTIPLATELET DRUGS: P2Yl2 inhibitors moa
- Bind to the adenosine diphosphate (ADP) P2Yl2 receptor on the platelet surface, which prevents ADP- mediated activation of the GPIIb/IIIa receptor complex, thereby reducing platelet aggregation.
ANTIPLATELET DRUGS: GPIIb/IIIa receptor antagonists moa
- Block the platelet glycoprotein IIb/IIIa receptor, which is the binding site for fibrinogen, von Willebrand factor and other ligands, thereby reducing platelet aggregation and further thrombosis.
