Hospital Course of Treatment for ACS Flashcards
Define Coronary Artery Disease (CAD)
- Inadequate supply of blood and oxygen to a specific part(s) of the myocardium, usually due to coronary plaque
- Imbalance between myocardial oxygen supply and demand
pathophysiology of CAD
Disruption of myocardial oxygen supply and demand within coronary anatomy
cardinal signs/symptoms of CAD
- ECG changes
- Presence of biomarkers
- Angina pectoris (chest pain)
- Others: Diaphoresis, Syncope, Hypotension, Hypertension, Tachycardia, Bradycardia, Pain radiating to left arm, Nausea, Vomiting, Dyspnea upon exertion, Dyspnea at rest, Atypical Symptoms
ECG changes
- Blood supply to cardiac conduction system mostly supplied by coronary arteries to the SA node, AV node, and Bundle of His so if there is a blockage there, ECG will be abnormal
- ST segment changes, T-wave inversions, Q-waves (indicative of pervious MI in the past), bundle brand blocks
Biomarkers
- Troponin: Most specific, Troponin INT is specific -> only found in myocardium
- Myoglobin
- Creatine Kinase (CK)-MB
Angina pectoris (chest pain)
- Ischemic manifestation
- Substernal chest discomfort with a characteristic quality and duration, that can be provoked by exertion or emotional stress
- Things to think about: quality of chest pain, location, duration, precipitating factors, relieving factors
pathophysiologic manifestations of CAD
- Coronary artery with unstable plaque that resulted in formation of partial occlusive thrombus can lead to ischemia or infarction
- Coronary artery with unstable plaque that resulted in formation of TOTAL occlusive thrombus can lead to infarction
- All about plaque stability and degree of thrombus occlusion!!!
- Thrombus Occlusion
Thrombus Occlusion
- Partial Occlusion of Coronary Artery -> unstable angina (UA) or NSTEMI
▪ UA: unstable plaque causing ischemia
▪ NSTEMI: unstable plaque causing infarction - Total Occlusion of Coronary Artery -> STEMI
▪ Unstable plaque causing infarction
▪ Requires immediate intervention to clear plaque from coronary artery
assessment for CAD
- Risk factors
- Ischemic chest pain
- Stress testing
- Electrical conduction abnormalities in the ECG
- Biomarkers (as a rule OUT)
- Cardiac catheterization
Stress testing
- causing ischemia to help diagnose CAD
- if pt cannot reach peak heart rate (220-age) and is experiencing chest pain and ECG changes = CAD
- can also be done via pharmacologic intervention: dobutamine injected -> vasodilates and steal oxygen from the vessels
How does electrical conduction abnormalities in the ECG relate to ischemia?
when pts experience ischemic symptoms, it will show in the ECG
CSA
chronic stable angina
SIHD
stable ischemic heart disease
CSA or SIHD
- Stable coronary plaque
- Angina precipitated by exertion or emotional stress and relieved by rest
- Do not have biomarkers
- Transient ST-segment changes that develop during symptomatic episodes that resolves when the patient becomes asymptomatic
UA
- unstable angina
- Unstable coronary plaque
- Angina can precipitate by exertion or emotional stress or at rest, and is NOT relieved by rest
- Do not have biomarkers
- ST-segment changes that may develop during symptomatic episodes that do not resolve
AMI
- acute myocardial infarction
- Unstable coronary plaque
- Angina can precipitate by exertion or emotional stress or at rest and is NOT relieved by rest
- Presence of biomarkers
- ST-segment changes that do not resolve when the patient becomes asymptomatic or that develop at rest
empiric treatment of agents used to restore balance of myocardial oxygen supply and demand for patients who are hospitalized for ACS
MONA-B
- Morphine
- Oxygen
- Nitroglycerin
- Aspirin
- Beta blocker
Morphine
- Decrease pain (when pts feel pain, they put more work on their heart) -> decrease work of breathing -> decrease HR -> decrease myocardial oxygen demand
- Also increase in venodilation
- Administration: 2-4mg IV; Titrate by 2-8 mg q. 5-15 min
- NO EFFECT ON MORTALITY
morphine adverse effects
- Hypotension
- Nausea/vomiting
- Respiratory depression
Oxygen
- Only get oxygen if your O2 saturation (SaO2) is < 90%
- Increase myocardial oxygen supply
- NO EFFECT ON MORTALITY
- Administer only for the first 6 hours
Nitroglycerin
- decrease myocardial oxygen demand (reduce preload; reduce afterload at higher doses)
- 0.4 mg PO SL q. 5 minutes x 3 doses maximum
- Assess for IV nitroglycerin (5-10 mcg/min then 5-20 mcg/min until symptoms are relieved)
- NO EFFECT ON MORTALITY
Nitroglycerin contraindications
- have a SBP ≤ 90 mmHg or SBP drop 30 mmHg below baseline
- have a HR < 50 bpm
- have a suspected RV infarct
- have taken sildenafil or vardenafil within the past 24 hours or taken tadalafil within the pat 48 hours
Aspirin
- If have not received ASA in ambulance or at home, administer 325mg non-enteric coated tablet (ask them to chew)
- Produces a rapid anti-thrombotic effect via immediate and neartotal inhibition of thromboxane A2 production
- DECREASES MORTALITY
Beta blocker
- Decrease heart rate = decreased myocardial demand = heart remains in diastole longer = increase in myocardial perfusion
- Reduces magnitude of infarction and associated complications
- Reduces life-threatening ventricular tachyarrhythmias
- DECREASES MORTALITY
oral beta blockers is recommended within 24 hours to patients who do not present with what?
- Signs of heart failure
- Evidence of low output state
- Increased risk for cardiogenic shock
Beta blocker contraindications
- Prolonged PR interval on ECG (> 240 ms)
- 2nd or 3rd degree AV block
- Active asthma or reactive airway disease – relative CI; if you’re treating the asthma or COPD, you CAN use beta blockers
if pt has contraindications to beta blockers, what can you do?
If pt does NOT have heart failure with reduced ejection fraction or an AV node block, can administer non-DHP CCB for the angina relief but do not affect mortality
time to elevation and peak for cTnI (Cardiac Troponin I)
- > 1.5 ng/mL
- Time to initial elevation: 3-12 hours; seen more after 6 hours
- Mean time to peak elevations: 24 hours
- Time to return to normal range: 5-10 days
time to elevation and peak for cTnT (Cardiac Troponin T)
- > 0.1 ng/mL
- Time to initial elevation: 3-12 hours; seen more after 6 hours
- Mean time to peak elevations: 12-48 hours
- Time to return to normal range: 5-14 days
What intervals should you measure troponin levels?
Measure within 6 hours, remeasure every 6-8 hours until levels have peaked (2-3 times)
Reperfusion Strategy goal
- Occlusion of infarcted artery can occur from 6-12 hours while affected myocardial zone is undergoing necrosis
- Restore perfusion to coronary vasculature by attenuating thrombus burden
What are the reperfusion strategies?
- Pharmacologic (Fibrinolysis)
- Percutaneous Coronary Intervention (PCI)
Percutaneous Coronary Intervention (PCI)
- Using a stent or balloon to open up artery
- performed in the cardiac catheterization lab
- associated with the best outcomes because have less risk of bleeding but is more invasive
- two types: Drug-Eluting Stent (DES), Bare Metal Stent (BMS)
role of high-intensity statin therapy in the treatment of ACS
- Reduces rate of recurrent MI, CAD mortality, revascularization, and stroke
- Decrease in anginal symptoms (?)
- Lowering of LDL-C
- Decrease in ischemic symptoms
- Pleiotropic effects
- Plaque stabilization
- Regression of atheroma
- Reduced inflammation
When should high-intensity statins be used?
High-intensity statin therapy should be initiated or continued in all patients with ACS and no contraindications to its use
pharmacogenomic considerations with the use of clopidogrel
- Needs to be activated by CYP2C19
- Avoid PPI’s; they will inhibit CYP2C19 -> Nexium and Prilosec; Can use H2 blockers -> Dexlansoprazole, lansoprazole and pantoprazole
- P-glycoprotein can kick it out
- People also have polymorphism of CYP2C19
P2Y12 receptor antagonists
- Ticlopidine (Ticlid®)
- Clopidogrel (Plavix®)
- Prasugrel (Effient®)
- Ticagrelor (Brilinta®)
- Cangrelor (Kengreal®)
Ticlopidine doses
250 mg PO twice daily
Clopidogrel doses
- LD: 300-600 mg
- MD: 75 mg once daily
Prasugrel doses
- LD: 60 mg
- MD: 10 mg once daily
Ticagrelor doses
- LD: 180 mg
- MD: 90 mg twice daily
Cangrelor doses
30 mcg/kg IV bolus prior to PCI followed immediately by an infusion of 4 mcg/kg/minute continued for at least 2 hours or for the duration of the PCI
pearls for Ticlopidine
- Black box warning: Hematologic Toxicity
- Avoid in patients with thienopyridine
pearls for Clopidogrel
- Bleeding
- Avoid in patients with thienopyridine hypersensitivity
- CI: active bleeding
pearls for Prasugrel
- Only to be used in UA/NSTEMI or STEMI patients managed with PCI
- CI in pts with history of stroke and active bleeding
- Should not be used in pts ≥ 75 years of age or < 60 kg due to increased risk of bleeding -> Has better outcomes but comes with increased risk of bleeding
- Avoid in patients with thienopyridine hypersensitivity
pearls for Ticagrelor
- Greater platelet inhibition compared to prasugrel
- greater, and more consistent platelet inhibition than clopidogrel -> better outcomes but comes with increased risk of bleeding (not as much as effient)
- Maintenance doses of ASA > 100 mg reduces the effectiveness of ticagrelor
- AE: bleeding, dyspnea, increased uric acid, CV events (Ventricular pauses, Bradycardia)
- CI: history or HPI of intracranial hemorrhage, active bleeding
- Drug-drug interaction with morphine: decreases the rate and extent of absorption
pearls for Cangrelor
- First IV; reversible; half life of 3-6 min
- Platelets returns to normal function within an hour
- Avoid in pts receiving GP IIb/IIIa receptor antagonists, prasugrel or clopidogrel
Which medications should you avoid that has a thienopyridine allergy?
- Clopidogrel
- Prasugrel
- Ticlopidine
Describe the role of antiplatelet therapy (ASA, P2Y12 receptor antagonists, and GP IIb/IIIa receptor antagonists in the treatment of ACS.
- ASA: 81mg now; prevents TxA2
- P2Y12 receptor antagonists: for ADP inhibition
- GP IIb/IIIa receptor antagonists: temporarily inactivate platelet cascade by promoting crosslinking of fibrinogen
Risk Factors for Bleeding
- Age ≥ 65 years
- Body weight < 60 kg
- Recent trauma/surgery (ex. CABG)
- Anemia
- Uncontrolled HTN
- Recent or recurrent GI bleeding
- Active Peptic Ulcer Disease (PUD)
- Moderate-severe renal impairment
- Severe hepatic impairment
- Concomitant drugs that increase risk of bleeding
What are the GP IIb/IIIa receptor antagonists?
- Abiciximab
- Eptifibatide
- Tirofiban
- more often used IN the cathlab, not so much after the procedure in the cathlab
- Mostly administered in setting of no pretreatment with ASA/P2Y12 inhibitor
- “Bail-out” therapy
Why should you always treat chest pain seriously?
because it could be a sign of:
- Aortic Dissection
- Aortic Aneurysm
- Peptic Ulcer Disease (PUD)
- Gastroesophageal Reflux Disease (GERD)
- Pericarditis
- Pulmonary Embolism (PE)
- Panic Disorder (“Panic Attack”)
What is an acronym for the assessment of CAD in the ER?
“The Three Ds”
- Door
- Data
- Decision
How soon should you revascularize the coronary vasculature?
as soon as possible
What is ischemic time?
the time it takes for the pt to get to the hospital until treatment
When should you perform an ECG?
- within 10 min of ED arrival
- one every 15-30 min for first hour (ECG changes are only captured 30% of the time) if pt is symptomatic and initial ECG is not diagnostic
Anticoagulation Therapy to Support Reperfusion
- Unfractionated Heparin (UF)
- Low Molecular Weight Heparin (LMWH): Enoxaparin, Dalteparin
- Direct Thrombin Inhibitors (DTIs): Bivalirudin, Argatroban
- Factor Xa Inhibitor: Fondaparinux
Bare Metal Stent (BMS)
- risk of repeat revascularization and restenosis
- lower bleed risk
- used over DES when issues with adherence arises, high risk bleeding with dual DAPT, surgery is about to happen
Drug Eluting Stent (DES)
- Anti-proliferative agents coated on the stent to decrease restenosis
- increased risk of bleeding
- delayed healing
What are the drugs used in drug eluting stents?
- Sirolimus
- Everolimus
- Zatarolimus
- Paclitaxel
What should be done after a drug eluting stent?
patient should be on P2Y12 receptor antagonists for at least 12 months
Management/Inpatient Pharmacotherapy
- MONA-B (administered in the ED)
- MONA-BAAS (administered in catheterization lab and/or cardiac intensive care unit)
What are the anti-platelet therapies?
- ASA
- ADP inhibition: clopidogrel, prasugrel, ticagrelor, cangrelor
- GP IIb/IIIa Receptor Antagonists: Abciximab, Eptifibatide, Tirofiban
What is the purpose of AAS in MONA-BAAS?
- have to keep artery open
- temporarily inactivate platelet cascade
- temporarily keep artery potent and keep thrombogenic material from moving downstream
