Acute coronary syndrome Flashcards

Question

What is the approach to managing a NSTEMI patient?

Answer 1

Secure ABCs and manage symptomatically Calculate TIMI score to prognosticate + whether PCI is EMERGENTLY indicated - Look for high risk features where PCI is EMERGENTLY indicated • Hemodynamic instability or shock • Persistent angina despite medical therapy • New/ persistent mitral regurgitation/new VSD • Ventricular arrhythmia • Severe LV dysfunction or heart failure Otherwise, intermediate-risk and low-risk NSTEMI are indicated for EARLY PCI within 3 days of presentation

Answer 2

``` Medical therapy – i.e. AAABS +/- MON • DAPT • Anticoagulation • ACE-I • BB • Statins • +/- Nitrates, Oxygen, Morphine ``` SERIAL ECG & CARDIAC MARKERS to monitor for STEMI conversion NSTEMI with low / intermediate risk 🡪 early PCI in 3 days’ time Cardiac stress test or other ischemia testing (within 72hours) 🡪 positive results 🡪 early invasive strategy

Answer 3

NSTEMI high risk with features of heart failure etc 🡪 urgent PCI on admission! ABCs & Ix 🡪 NAABS +/ MON 🡪 Coronary angiography 🡪 PCI i.e. exactly the same workflow as per STEMI Note: thrombolysis is NOT administered for UA/NSTEMI

Answer 4

4 main medications: Statins, Aspirin, ACE-I, Beta Blockers General measures - Goals: to reduce myocardial oxygen demand and/or increase oxygen supply - Lifestyle modification (diet, exercise) - Treatment of risk factors: Statins, antihypertensives, etc. 1) Single antiplatelet therapy (first-line therapy) - Aspirin 75mg daily, often taken with omeprazole - Clopidogrel 75mg daily - when ASA absolutely contraindicated (active peptic ulcer disease) 2) β-blockers (first-line therapy: decrease overall mortality) - Increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload) - Cardioselective agents preferred (e.g. metoprolol, atenolol) to avoid peripheral effects (inhibition of vasodilation and bronchodilation via β2 receptors) - Avoid intrinsic sympathomimetics (e.g. acebutolol) which increase demand - Contraindicated in patients with asthma, severe LV dysfunction, bradycardia, coronary artery spasm 3) ACE inhibitors (not used to treat symptomatic angina) - Angina patients tend to have risk factors for CV disease which warrant use of an ACEI (e.g. hypertension, diabetes, proteinuric renal disease, previous MI with LV dysfunction) - Benefit in all patients at high risk for CV disease (concomitant DM, renal dysfunction or LV systolic dysfunction) - Angiotensin II receptor blockers (ARBs) can be used when ACEI contraindicated (e.g. hypersensitivity, angioedema) 4) Nitrates (symptomatic control, no clear impact on survival) - Decrease preload (venous dilatation) and afterload (arteriolar dilatation), and increase coronary perfusion - Maintain daily nitrate-free intervals to prevent tolerance (tachyphylaxis) 5) Calcium channel blockers (CCBs, second-line or combination) - Dihydropyridines e.g. nifedipine, amlodipine 5-10mg - Increase coronary perfusion and decrease demand (HR, contractility) and BP (afterload) - Caution: verapamil/diltiazem combined with β-blockers may cause symptomatic sinus bradycardia or AV block 6) Invasive strategies: Revascularization

Answer 5

MOA - Vasodilator effect on the peripheral veins and arteries with more prominent effects on the veins. - Reduces cardiac oxygen demand by decreasing preload(left ventricular end-diastolic pressure) - Reduce afterload modestly - Dilate coronary arteries and improve collateral flow to ischemic regions Side effects: hypotension, reflex tachycardia Onset of action: Sublingual tablet: 1 to 3 minutes Peak effect: Sublingual tablet: 5 minutes; Duration: Sublingual tablet: At least 25 minutes

Answer 6

MOA - Belongs to a novel chemical class, cyclopentyltriazolopyrimidine - An oral reversibly binding noncompetitive inhibitor of the P2Y12 receptor (adenosine diphosphate (ADP) P2Y12 receptor) on the platelet surface which prevents ADP-mediated activation of the GPIIb/IIIa receptor complex thereby reducing platelet aggregation Side effects: bleeding, shortness of breath Onset of inhibition of platelet aggregation:180 mg loading dose: ~41% within 30 minutes Peak effect: 88% at 2 hours post administration Duration of IPA: 2 to 8 hours

Answer 7

A class of drugs that irreversibly inhibit the binding of ADP to the P2Y12 receptor. Include – Prasugrel (3rd Gen), Clopidogrel (2nd gen), Ticlopidine (1st gen) Ticlopidine can cause – neutropenia (occurs in first 3mths), liver abnormalities and thrombotic thrombocytopenic purpura (TTP), making it less safe than Clopidogrel. Clopidogrel has less major GI bleeding than aspirin. Clopidogrel is a prodrug that requires metabolic activation by hepatic cytochrome P450. (CYP2C19 allele associated with increased rates of ischemic events and stent thrombosis post PCI) Prasugrel-mediated inhibition of platelet aggregation is approx.5-9x more potent than that of Clopidogrel achieving greater platelet inhibition with an onset of action within 1hr BUT has increased bleeding risk and contraindicated in patients with previous stroke, weight less than 60kg and age > 75yrs.

Answer 8

Binds to opioid receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces generalized CNS depression Side effects: Drowsiness, vomiting, constipation, respiratory depression, potential for abuse Onset: Oral (immediate release): ~30 minutes; IV: 5 to 10 minutes Duration for Pain relief: Immediate-release formulations: 4 hours

Answer 9

MOA a) Binds to antithrombin which increases the potency of that plasma protein in the inactivation of clot-forming thrombin. b) Inhibits coagulation factor Xa, slowing thrombin formation and thereby further impeding clot development. - Include: Unfractionated Heparin and Low Molecular weight Heparin. - LMWH preferentially inhibits factor Xa (note Fondaparinux, an alternative factor Xa inhibitor Advantages - greater bioavailability - lower risk of heparin induced thrombocytopenia - easier dosing: does not require monitoring of PTT Disadvantages - slightly delayed onset of action (e.g. 20-30min) rather than instantaneous - longer duration of action, making it more difficult to rapidly stop therapy - less easily inactivated with protamine sulfate - prolonged half life in patients with renal failure, especially with LMWH.

Answer 10

Alteplase, Reteplase, Tenecteplase (Streptokinase) Mechanism: Stimulates the natural fibrinolytic system, transforming inactive precursor plasminogen into the active protease plasmin which then lyses fibrin clots Potential issues: Plasmin can degrade other proteins including fibrinogen and result in bleeding Contraindications: PUD, Bleeding disorders, Recent stroke, Recent surgery

Answer 11

MOA - Class of drugs which inhibit one of the platelet integrin adhesion receptors (GPIIb/IIIa) - Block final platelet activation and cross-linking by fibrinogen and vWF Include – Abciximab, Tirofiban, Eptifibatide (PCI) Significant adverse effects include thrombocytopenia (hence need to monitor platelet counts on FBC) Given IV or intracoronary during PCI

Answer 12

Selective inhibitor of beta1-adrenergic receptors competitively block beta1-receptors, with little or no effect on beta2-receptors at doses ≤20 mg - Cardioinhibitors, by reducing heart rate, contractility, and arterial pressure, reduce the work of the heart and the oxygen demand of the heart. - Relieve a patient of anginal pain that is caused by a reduction in the oxygen supply/demand ratio due to coronary artery disease. - Ability to inhibit subsequent cardiac remodeling. Onset of action: 1 to 2 hours Side Effects: Bradycardia, hypotension, fatigue

Answer 13

MOA - bind to L-type calcium channels located on the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue (sinoatrial and atrioventricular nodes). - CCBs cause vascular smooth muscle relaxation (vasodilation) - Decrease contractility (negative inotropy) - Decrease heart rate (negative chronotropy) - Decrease conduction velocity (negative dromotropy) Dihydropyridines (selective vasodilators, potential reflex increase in HR, myocardial contractility and O2 dd): Amlodipine, Nifidipine, Nicardipine Non dihydropyridines (equipotent for cardiac tissue and vasculature): verapamil, dilitiazem Calcium channel blockers primarily serve as adjunctive therapy in patients with ongoing or recurrent symptoms of ischemia despite optimal therapy with beta blockers (with or without nitrates), in patients who are unable to tolerate adequate doses of one or both of these agents, or in patients with rapid atrial fibrillation when beta blockers are contraindicated. In certain patients they may be harmful - HF - left ventricular dysfunction - atrioventricular block.

Answer 14

MOA - Improvement in the oxygen supply /demand ratio of the myocardium by reversing angiotensin II-induced vasoconstriction and inotropic activity, Improvement in endothelial function - Attenuation of ventricular remodeling and ventricular dilation, which are factors for arrhythmogenesis

Answer 15

Onset of action: 1 hour Peak effect: - Hypotensive: Oral: ~6 hours Side effects: cough, hypotension, elevated potassium and creatinine

Answer 16

Onset of action: Initial changes: 3 to 5 days; Maximal reduction in plasma cholesterol and triglycerides: 2 weeks MOA: results in plaque stabilization, reversal of endothelial dysfunction, inhibition of monocyte recruitment, decreased thrombogenicity, and a reduction in inflammation Side effects: arthralgia, myalgia, GI, increased serum transaminases

Answer 17

MOA - Selective sinus node inhibitor - Inhibits the funny channel (If) receptor in a current-dependent fashion. If current is an inward Na+/K+ current that activates pacemaker cells of the SA node - Slows the heart rate by delaying depolarisation and sinus node activation Ivabradine is a substrate of the CYP450 system and is not an inhibitor of this system. Diltiazem and verapamil, erythromycin and retroviral agents are also metabolised by CYP450 and therefore should not be used with ivabradine. Indicated in chronic stable angina, heart failure Side effects - Blurring of vision - No QT prolongation - No negative inotropic properties - Improvements in exercise tolerance and prevention of exercise-induced ischaemia

Answer 18

MOA - Myocardial cells derive their energy via fatty acid and glucose metabolism. During ischemia the fatty acid pathway predominates. However, this pathway requires more oxygen than the glucose pathway - CPT -1 inhibitor and also acts in inhibition of the enzyme long-chain 3-ketoacyl coenzyme A thiolase (LC 3- KAT) - No significant negative inotropic or vasodilator properties either at rest or during dynamic exercise Side effects - Extrapyramidal and parkinsonian symptoms - Restless leg syndrome. - Use is limited in severe renal impairment.

Answer 19

horizontal ST depression; leads I, II and V4-6; V1; severe left main coronary artery / proximal LAD / severe triple vessel disease early coronary angiography and intervention

Answer 20

* ≥ 1 lead with ≥1 mm of concordant ST elevation -> 5 points * ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression -> 3 points * ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave -> 2 points * Score ≥3 (concordance) was found to be highly specific (95%) for diagnosis of AMI

Answer 21

* ≥ 1 lead with ≥1 mm of concordant ST elevation * ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression * ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave * Score ≥3 (concordance) was found to be highly specific (95%) for diagnosis of AMI

Answer 22

Conventional STEMI: elevation of ST segment at J point De Winter syndrome: J point depression and upsloping ST depression in V1- V6 that continues into tall positive symmetrical T waves often with 1-2mm ST elevation in aVR Posterior STEMI: ST depression in V1-V3 Wellens sign A: Biphasic anterior T waves Wellens sign B: Deeply inverted anterior T waves, not always accompanied by chest pain Hyperacute T waves: tall, often asymmetrical broad based anterior T waves often associated with reciprocral ST depression Sgarboss criterion

Answer 23

Horizontal or down-sloping ≥ 0.5mm at J point in ≥ 2 contiguous leads; ST depression ≥ 1mm; Upsloping ST depression

Acute coronary syndrome Flashcards

(47 cards)