Day 6 Cardiology Flashcards
What causes plaque rupture?
Presentation of ACS?
Signs of ischemia on an EKG?
Thin fibrous cap, lipid content and shape of plaque, mechanical injury, sudden changes in intraluminal pressure and tone, bending/twisting of an artery during heart contractions.
Substernal discomfort, not stabbing pain, not completely relieved by nitroglycerin, brady cardia, hypotension, etc. Atypical in elderly, females, diabetics- dyspnea alone, N&V.
Flattening and inversion of T waves
What does ST depression show on an EKG?
What does ST elevation show on an EKG?
What are signs of necrosis on an EKG?
Injury
STEMI.
Q waves, Significant Q wave= 1 mm(0.4seconds) wide or 1/3 of QRS, not reversible.
What to know about Ck-Mb?
What to know about myoglobin?
What to know about Troponin-I?
Detectable in serum around 3-12 hours. Preferred in infarct, peaks around 24 hours and returns in 48-72 hours.
High sensitive, low specificty early marker of ischemia(1-3 hours), peaks within 6-7 and returns in 24 hours. Can have false positives.
Detectable in serum 3-12 hrs, prolonged elevation 5-10 days and peak at 24., preferred, high sensitivity and specificity.
What are some non thrombotic causes of elevated troponins?
What is NSTEMI?
What is a STEMI?
CHF, pulmonary embolism and hypertension, COPD, chronic renal insufficiency, intracerebral hemorrhage or stroke, pericarditis, cardiotoxic drugs.
Partial block of the coronary artery, ST depression, T wave inversion on EKG, not all patients require immediate reperfusion therapy, intervention may occur as an outpatient.
ST elevation, usually complete block of the artery, damage can go deep into heart muscle, requires immediate management with reperfusion therapy, door to balloon <90 minutes.
What are the main goals of ACS treatment?
Initial therapy for ACS(MONA pneumonic)?
Aspirin therapy for ACS?
Prevent Mortality, Coronary Artery Reperfusion.
Moprhine, Oxygen(may limit MI injury), Nitroglycerin, Aspirin(provides mortality benefit).
160-325 mg. CI’d in true ASA allergy(use clopidogrel), ACTIVE GI bleed.
Nitroglycerin for ACS?
Morphine for ACS?
Use of heparins(UFH and LMWH) for ACS?
No evidence of any difference on mortality rates, CI’d in hypotension and PDE-5.
2-4 mg IV every 5 min as needed. No difference in mortality, use if Nitroglycerin isn’t affected., lowers preload and afterload to lower O2 requirement. No Mortality benefit and CI’d in hypovalemia and hypotension.
Little data to support efficacy, used to prevent recurrent coronary thrombosis.
Advantages of UFH? Disadvantages?
How do you monitor UFH?
Enoxaparin NSTEMI dosing? STEMI?
Inexpensive, short half life, reversible with protamine. Unpredictable response, continuous monitoring, risk of HIT, ineffective against clot bound thrombin, platelets more reactive to other agonists.
monitor aPTT, weight based dosing, keep aPTT 1.5-2 times normal. Bolus 60 units/kg, drip 12 units/kg/hr.
1 mg/kg, CrCl <30, dose q24h. <75y 30 mg IV bolus then 1 mg/kg SubQ every 12 hours(max 100 mg x 2 doses). >75 y: no bolus, .75mg/kg subq every 12 hours.
What DTI do you use in ACS? Dosing of this?
Advantages of bivalrudin? Disadvantages?
Can you use fondaparinux?
Bivalrudin, During PCI dose .75 mg/kg IV bolus, 1.75 mg/kg/h infusion. Prior to PCI: 0.1 mg/kg bolus, 0.25 mg/kg/h( if PCI needed give 0.5 mg/kg bolus then 1.75 mg/kg/h infusion). CrCl< 30: 1 mg/kg/h infusion.
Inhibits soluble and clot bound thrombin, does not activate platelets and very short half life. $$$$.
Yes, but not common. Usually goes Heparin and Bivalrudin–> Enoxaparin–> Fondaparinux.
Clopidogrel BBW?
Clopidogrel indication?
Prasugrel indication? Dose?
Decreased effect with allele defect in CYP2C19 allele.
Reduce the rate of MI and stroke in patients with acute STEMI undergoing medical management.
PCI only. 60 mg loading dose and then 10 mg daily(if less than 60 kg <5 daily), CI’d in patients in history of storke and TIA, patients >75 with caution, BBW for bleeding risk.
Ticagrelor BBW?
Cangrelor dosing?
Guidelines for beta blockers in ACS?
bleeding risk, decreased effectiveness with big aspiring doses(>100), Has A/E of dyspnea.
30 mcg/kg before PCI, 4 mcg/kg/min for 2 hours or length of PCI.
Guidelines recommend PO b-blockers within 24 hrs of MI.
When to use bare metal stents?
When to use drug eluting stents?
When should clopidogrel and ticagrelor should be held before CABG? What about prasugrel?
May require reduced time on DAPT(non compliance and on anticoagulation). Less late restenosis. Plaque and tissue growth can collapse the newly placed stent.
Inhibit the growth of scar tissue within the stent, may also inhibit epithelialization of the stent, reduce the rate of early restenosis, may have higher rates of late restenosis.
5 days, 7 days.
What are STEMI reperfusion strategies?
Are fibrinolytics for STEMI only?
Conservative therapy medical management(NSTEMI or UA)?
Fibrinolytics(door to needle 30 minutes), PCI(door to balloon time to 90 minutes), CABG.
YES, 60% success rate, clot buster.
Oxygen, Aspirin, B-blocker, Nitroglycerin, Enoxaparin or UFH, Clopidogrel or ticagrelor.
TIMI score low risk?
Early invasive strategy medicines?
Medications to reduce mortality?
0-2 low, medical management. 3-4 intermediate, early invasive. 5-7, urgent revascularization.
Aspirin, P2Y12 inhibitor, antithrombin(UFH, enoxaprin, fondaparinux, bivalrudin), Consider GPI(eptifibatide, tirofiban).
Statin, Clopidogrel(prasugrel or ticagrelor), ASA, ACE inhibitor, B-blocker.
