Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
81 Cards in this Set
- Front
- Back
|
What are the main coronary arteries affected by atherosclerosis?
|
Right Coronary Artery, Left Main Artery, Circumflex, Left Anterior Descending
|
|
|
ACS-Plaque Rupture-No-ST Segment Elevations - unstable angina = How do the diagnostics come back?
|
Negative cardiac enzymes (incomplete coronary occlusion: ischemia - no myocyte death)
|
|
|
ACS-Plaque Rupture-No-ST Segment Elevations - NSTEMI = How do the diagnostics come back?
|
Positive cardiac enzymes (incomplete coronary occlusion: infarction - some myocyte death)
|
|
|
ACS-Plaque Rupture-ST-Segment Elevations-STEMI = How do the diagnostics come back?
|
Positive cardiac enzymes (complete coronary occlusion: infarction - myocyte death)
|
|
|
These are factors affecting what?
Sudden changes in intraluminal pressure or tone Bending/twisting of an artery during heart contraction Lipid content of plaque Thickness of the fibrous cap Plaque shape Mechanical injury |
Factors Affecting Plaque Rupture
|
|
|
New onset of CP
Increased severity and frequency Often occurs at rest Due to PLAQUE RUPTURE!!!! Relieved with NTG Still Ischemia not Infarction |
Unstable Angina (Think – Unexpected)
|
|
|
The following set of consequences defines what?
Plaque Rupture Death of the myocardium (Infarction) Due to prolonged ischemia (> 30 minutes) Fibrous scar, irreversible ST-segment Elevation (STEMI) Non-ST-segment Elevations (NSTEMI) |
Definition of Acute Myocardial Infarction
|
|
|
You can't use fibrinolytics with what, due to the increase risk of bleeding?
|
Unstable Angina/NSTEMI: Mural Thrombus (platelets and some fibrin)
|
|
|
You can use fibrinolytics to treat what?
|
STEMI: Occlusive thrombus (platelet, RBC, and Fibrin rich)
|
|
|
A patient presents to the ED with SOB and chest tightness that lasted about 10 minutes. It woke him up out of his sleep. He describes the pain as a 7/10 pressure that radiated from the middle of his chest to his left arm. It was relieved with 2 NTG SL. Just from hearing these symptoms, what is the patient's chest pain most likely caused by?
|
Unstable Angina-Due to the fact that there isn't usually pain relief with sub lingual nitro if it is an MI.
|
|
|
What are the normal values for troponin I, CPK, CPK-MB?
|
Normal Values:
Trop I < 0.05 ng/mL, CPK 5-200 U/L, CPK-MB < 4-5% |
|
|
What are the primary and secondary goals for ACS treatment?
|
Primary Goal
Reduce risk of morbidity/mortality Relieve chest pain Reduce infarct size Prevent or minimize complications Improve quality of life Prevent death BP < 130/80 and HR 55-65 Secondary Goal Prevent adverse events Cost effective therapy |
|
|
This is very sensitive to death of the myocardium?
|
Troponin
|
|
|
This can be increased due to the death of muscle cells. It can be increased due to something such as a heart attack or in someone who has just ran a marathon.
|
CK-MB
|
|
|
A patient comes in with BP 160/94, HR 85 bpm, negative cardiac enzymes, T-wave inversions on EKG consistent with lateral wall ischemia.
What is the diagnosis? |
Unstable Angina
|
|
|
In the ED what are the non-pharmacologic tx's for ACS?
|
EKG
Oxygen Cardiac Enzymes Basic Labs Evaluate for reperfusion therapy Admit to CCU/cardiac monitoring floor |
|
|
In the ED what are the pharmacologic tx's for ACS?
|
Aspirin
Clopidogrel (or Prasugrel – PCI only) Morphine Nitro gtt Heparin or LMWH Beta-blocker Statin Electrolytes |
|
|
What are the details of antiplatelet therapy in treating ACS?
|
Platelets are an important part of thrombus formation
Aspirin – chew 325 mg ASAP, low or high dose ASA for life* Acute treatment and secondary prevention Decreases morbidity and mortality in the acute setting and secondary prophylaxis |
|
|
Alternative for patients allergic to aspirin
CURE study – 300 mg load, then 75 mg/day with ASA More effective than ASA alone in NSTEMI Decrease in death and MI over 9 months NSTEMI: ASA with this for 1 year Post-stent: 1month – 1year (type of stent) |
Clopidogrel
|
|
|
Genetic variations can cause certain types of patients to not convert plavix to its active form, so this drug can be used as an alternative to compliant patients who may have genetic variations.
|
Prasugrel
|
|
|
New “Clopidogrel-like” antiplatelet agent
Approved for ACS treated with immediate/delayed PCI Useful for clopidogrel “poor responders” or failures Metabolized in liver to active drug (prodrug) Very Potent ADP Inhibitor |
Prasugrel
|
|
|
What are the dosage details of Prasugrel
|
Very fast acting – NOT loaded in ER
Dosing: 60 mg load, 10 mg PO daily |
|
|
What are the cautions with Prasugrel?
|
Not to be used for patients:
w/ History of CVA/TIA w/ Bleeding Going for CABG Weighing < 60 kg Major Adverse Effect – Bleeding Pregnancy Category - B |
|
|
TX for use in ACS
Pain relief Coronary and peripheral venous dilator Coronary artery dilator – increases supply Decreases preload and O2 demand SL at home or in ambulance 5 mcg/min, increase by 5 mcg/min every 5 minutes to 20 mcg/min, then by 10 mcg/min up to a max of 200 mcg/min Monitor – BP, HR |
Nitroglycerin
|
|
|
What is one of the primary complaints with NG if it is given as a drip?
|
Headache
|
|
|
This is often used for analgesia with ACS and is the drug of choice after Nitroglycerin. Quick onset and sedative properties
Blocks sympathetic efferent discharge at the CNS – peripheral venous/arterial dilation |
Morphine
|
|
|
What are the dosing and monitoring parameters with morphine in ACS TX?
|
2-4 mg IV q 5-10 minutes until pain is gone or adverse reaction
Monitor – BP, HR, RR Have naloxone 0.4 mg IVP available ESPECIALLY if patient appears to be going into respiratory failure. |
|
|
This is a class of pain reliever that can be used in ACS that doesn't interfere with plavix.
|
NSAIDS
|
|
|
This binds reversibly to platelets. It blocks the aspirin benefits for the cardiac patient. You have to make sure that the patient isn't taking this close to aspirin.
|
NSAIDS
|
|
|
Increase mortality, reinfarction, and heart failure in proportion to degree of COX-2 selectivity
Discontinue on admission for ACS Do not initiate during acute phase of management |
NSAIDS
|
|
|
Acutely shown to decrease incidence of sudden death
Prevents post/peri-MI arrhythmias May limit infarct size Decreases progression of AMI in patients with USA Long-term: prevents second MI |
Beta Blockers
|
|
|
What are the absolute contraindications for giving beta blockers?
|
Absolute contraindications
HR < 55, SBP < 90, CHF exacerbation Relative – uncontrolled Asthma or COPD Goal HR: 55 – 65 beats/min |
|
|
Attempt to control thrombotic process
Decrease incidence of thromboembolism MOA: Inhibits factors IIa and Xa through ATIII mediated confirmational changes Reversal agent: protamine Usual duration: 48 hours Also – anti-inflammatory |
Heparin
|
|
|
This is effective acutely to decrease progression of AMI and death in patients with ACS.
|
Heparin
|
|
|
What is involved with the dosing of heparin?
|
60 units/kg bolus, then 12 units/kg/hr
Wt based protocol |
|
|
What is involved with the monitoring parameters of heparin?
|
Monitoring
Baseline: aPTT, PT/INR, CBC and Plts aPTT q 6 hours until 2 consecutive aPTT within goal range; then check aPTT q 24 hr Hgb, Hct, GI/GU bleeding, Petechiae, etc. Goal aPTT: 1.5-2 x norm (50-70 sec) AE: Bleeding, Thrombocytopenia |
|
|
1/3 the size of UFH
Mechanism of action similar to heparin (ATIII), except inhibits factor Xa to a greater degree than factor IIa (2-4:1 vs 1:1) |
LMWH
|
|
|
This is a LMWH that is Superior to Heparin for NSTEMI and STEMI
Contraindicated – anuric, HD 1 mg/kg SC QD, CrCl < 30 mL/hr Use in obese unclear No monitoring |
Enoxaparin 1 mg/kg SC BID, 3-5 days
|
|
|
In regards to LMWH vs. UFH, this is preferred in most institutions
No monitoring Easier dosing NSTEMI/STEMI data |
Enoxaparin 1 mg/kg SC BID, 3-5 days
|
|
|
In regards to LMWH vs. UFH, this is contraindicated in the obese and anuric, HD.
|
LMWH
|
|
|
Patients going to for PTCA need to have considerations of half life for UFH and LMWH. What are they?
|
Heparin T1/2 = 1.5 hours
Enoxaparin T1/2 = 5-7 hours |
|
|
Patients on Dialysis and patients (men under 57kg, women under 45kg) shouldn't take what?
|
LMWH
|
|
|
Adjunct therapy to prevent complications in patients undergoing PCI (in stent thrombosis)
Medical management of USA and NSTEMI In combination with ½ dose fibrinolytic therapy in patients with STEMI |
GP IIbIIIa Inhibitors
|
|
|
Patients can come off of this quickly after cath lab procedure, it ian anticoagulant thrombin inhibitor.
|
Bivaliriudin
|
|
|
1. Found only on platelets and their progenitors
2. Fibrinogen and von Willebrand factor binds to these receptors and causes platelet aggregation |
Glycoprotein IIb/IIIa Receptors
|
|
|
Glycoprotein IIb/IIIa Receptor Inhibitors include what three drugs?
|
1. Abciximab (Reopro) – Monoclonal Antibody
2. Eptifibatide (Integrillin) – Peptide 3. Tirofiban (Aggrastat) – Non-peptide |
|
|
What are the MOA's for Abciximab, Eptifibatide and Tirofiban?
|
Mechanism of Action
1. Abciximab – Causes steric hinderances to the receptor, which prevents binding of large molecules (does not bind to the receptor) 2. Eptifibatide/tirofiban – Competitively, reversibly inhibits binding of fibrinogen and von Willebrand (binds) |
|
|
should be used in pts with ongoing ischemia, high risk features, or planned PCI
|
GP IIbIIIa Inhibitors
|
|
|
GP IIbIIIa Inhibitors are high risk in what patients?
|
Prolonged CP (>20 min), angina at rest with ST segment changes
Pulmonary edema New worsening MR murmur, S3 or worsening rales Hypotension, Bradycardia, Tachycardia > 75 years Sustained VT Elevated Troponin |
|
|
STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within ? minutes of first medical contact.
|
90 Minutes
|
|
|
STEMI patients presenting to a hospital without PCI capability and who cannot be transferred to a PCI center for intervention within 90 minutes of first medical contact should be treated with what and in how much time of hospital presentation, unless contraindicated.
|
fibrinolytic therapy within 30 minutes
|
|
|
Reopens occluded artery
Restores blood flow Increases myocardial salvage Preserve LV function Enhance electrical stability Indications: Chest pain > 20 min, <12-24 hours, STE >1 mm in at least 2 leads |
Thrombolytic Therapy
|
|
|
If given within 6 hours of CP and STE, lytics can prevent how many deaths?
|
30 deaths per 1000 patients.
|
|
|
The following are absolute contraindications for what?
Prior Intracranial Hemorrhage Structural Cerebrovascular Lesion Malignant Intracranial Neoplasm Ischemic stroke with 3 months Suspected aortic dissection Active bleeding Significant closed head or facial trauma with in 3 months |
Thrombolytic Therapy
|
|
|
What do does the TIMI flow scale mean?
|
Grade Definition
0 No perfusion 1 Penetration of occlusion without perfusion 2 Partial perfusion (rate is slow) 3 Complete perfusion (clearance is prompt) |
|
|
What are the major risk with thrombolytics, 3 of them?
|
bleeding (20-50%), serious hemorrhage (1-2%),
Hemorrhagic stroke (0.5%) |
|
|
What are the details of the thrombolytics?
|
1. r-tPA 2.TNK-tPA 3. Reteplase
T ½ 1. 4-8 min 2. 20-24 min 3.15 min 90 min TIMI 3 flow rate 1.50-60 2.50-60 3.50-60 Doses 1. 100mg/90min: 15 mg IV bolus, then 0.75 mg/kg for 30 min (don’t exceed 50 mg), then 0.5 mg/kg over next 60 min (don’t exceed 35 mg) 2. < 60 kg – 30 mg 60-70 kg – 35 mg 70-80 kg – 40 mg 80-90 kg – 45 mg > 90 kg – 50 mg (As a 5 min bolus) 3. 2 x 10 IU boluses 30 minutes apart |
|
|
What are the adjuncts to thrombolysis?
|
Heparin or LMWH
Full dose IV heparin or enoxaparin for 48 hours Longer infusions/use depends on risk of systemic thromboembolism Aspirin/clopidogrel ASA 160 – 325 mg/day No role for clopidogrel (unless allergice to ASA) Role of IIb/IIIa inhibitors Prasugrel not studied |
|
|
PCI of a totally occluded infarct artery greater than 24 hours after STEMI is not recommended in
|
asymptomatic patients with one- or two-vessel disease if they are hemodynamically stable and do not have evidence of severe ischemia.
|
|
|
Acute thrombosis is avoided through what therapies?
|
Aspirin
Clopidogrel Prasugrel (alternative) Heparin (prior to cath) GP IIb/IIIa Inhibitors Direct Thrombin Inhibitors (alternative) - Bivalirudin |
|
|
Rationale: Decreases in-stent restenosis by slowing incorporation of the stent into the endothelial lining
Sirolimus Paclitaxel Decreases restenosis from roughly 30% to 0-8% |
Drug-Eluting Stents
|
|
|
What is the dosage of Aspirin and DES for antiplatelet therapy?
|
BMS: High Dose (162-325 mg) for 1 month, then low dose (75-162 mg) for life
DES: High Dose for 3-6 months, then low dose for life |
|
|
What is the dosage of Clopidogrel and DES for antiplatelet therapy?
|
New dosing: 150 mg PO daily x 1 week, THEN
BMS: 75 mg PO daily for at least 1 month, prefer 1 year DES: 75 mg PO daily for at least 1year, probably longer |
|
|
What is the dosage of pasugrel and DES for antiplatelet therapy?
|
Prasugrel (Alternative): 60 mg PO load
BMS or DES: 10 mg PO daily for same duration as clopidogrel |
|
|
These can be a result of what?
Retroperitoneal bleed Acute renal failure Contrast Induced Nephropathy (CIN) Acidosis caused by contrast |
Cath lab procedure
|
|
|
How do you avoid acute renal failure after a cath lab procedure?
|
DC Metformin (48 hrs prior and post)
Fluid resuscitation N-acetylcystine Dose: 600 mg PO BID prior to cath and 600 mg PO BID post cath Sodium Bicarbinate Dose: 150 meq in 1 L D5w; infused 3 mL/kg over 1 hour prior to cath and 1 mL/kg/hr for 6 hours post cath |
|
|
In the 48 hour window after revascularization this on EKG is a good sign?
|
Non Sustained V-Tach
|
|
|
ACS complications include?
|
Left Ventricular Damage
Cardiogenic Shock Arrhythmias Ventricular tachyarrhythmias Cellular changes in electrophysiologic characteristics of ischemic myocardial cells LIFE THREATENING!!!!! Vfib most common No reduction in mortality with antiarrythmic prophylaxis |
|
|
Treatment with Amiodarone for Post MI Arrhythmia
|
150 mg IV bolus (over 10 minutes)
1 mg/min for 6 hours 0.5 mg/min for maintenance 150 mg boluses for breakthrough Lidocaine second option |
|
|
If a patient has ACS and doesn't receive a stent what is the TX plan?
|
NO STENT
ASA 75-325 mg PO Daily for life Clopidogrel 75 mg PO Daily USA/NSTEMI: min 1 month, prefer 1 year STEMI: min 14 days, 1 year reasonable |
|
|
If you receive a bare metal stent, what is the TX plan?
|
BARE METAL STENT
ASA 162-325 mg PO Daily for 1 month, then 75-162 mg PO Daily Clopidogrel 150 mg PO daily for 1 week, then 75 mg PO Daily for at least 1 month, prefer 1 year Prasugrel (alternative) 10 mg PO Daily for same duration |
|
|
If you receive a drug eluding stent what is the TX plan?
|
DRUG ELUTING STENT
ASA 162-325 mg PO Daily for 3-6, then 75-162 mg PO Daily for life Clopidogrel 150 mg PO Daily x 1 week, then 75 mg PO Daily for at least 1 year, maybe longer Prasugrel (alterative) 10 mg PO Daily for same duration |
|
|
What is the PPI plavix controversy?
|
Potential: Coadministration of omeprazole and clopidogrel increase the risk of REINFARCTION!!!!
|
|
|
Which patients on dual antiplatelet therapy should receive a acid suppression therapy?
|
Patients with a history of or have an active GI bleed or ulcer;
Patients currently on anticoagulant therapy (heparin, LMWH, and/or warfarin); Patients with multiple risk factors for GI bleeding including: age >60 years, corticosteroid/NSAID use, or history of GERD. |
|
|
If a PPI is necessary for a patient with ACS, which is safest?
|
Pantoprazole does not seem to have the same interaction.
AVOID OMEPRAZOLE!! H2 antagonists may work for prevention (weaker). Basically… Not everyone needs acid suppression. If someone does require it… Famotidine 20 mg PO BID Pantoprazole 40 mg PO Daily |
|
|
How are beta blockers and NTG used in acute therapy of ACS?
|
Beta-blocker
Titrate to HR and BP goals (sample dosing) Atenolol 100 mg PO Daily Metoprolol 100 mg PO BID NTG SL PRN CP Long acting NTG Does not decrease mortality Continue in pts with continued angina Decreases hospital admissions |
|
|
Decreases LV remodeling (CHF)
Administer within 4-6 wks post MI to improve mortality and decrease development of CHF HOPE trial Chronic administration in all CAD and high risk patients (Ramipril) Titrate to BP goal (sample dosing) Lisinopril 5 mg QD titrate to 10 mg QD Ramipril 5 mg QD titrate to 10 mg QD ARB good alternative if intolerant |
ACEI
|
|
|
These should be drawn within 24 hours of the onset of ACS
Artificially low lipids (up to 40%) Can remain low for up to 3 months TREAT LDL AGRESSIVELY |
Lipids
|
|
|
Not shown to improve outcomes during ACS
May be useful in patients with resistant CP on max BB and NTG therapy (max other therapies first) Diltiazem 30 mg Q6h or Diltiazem CD PO Daily (max 360-480mg QD) Amlodipine 5-10 mg QD DO NOT USE SHORT ACTING NIFEDIPINE! |
Calcium Channel Blockers
|
|
|
Selective aldosterone antagonist
EPHESIS Trial Improved Survival Post-MI with LVD (EF 40%) and signs of CHF Dose: 25 mg QD for 4 weeks, then titrate to 50 mg QD Contraindications: K > 5.5 mEq/L, CrCl < 30 mL/min, CYP 3A4 inhibitors, K supplements, K sparing diuretics |
Eplerenone
|
|
|
All ACS Patients should go home on…
|
ASA
Beta-blocker ACE I (or ARB) Statin NTG SL Clopidogrel (or Prasugrel for PCI only) Maybe a long acting NTG, CCB, Eplerenone, Niaspan Avoid Omeprazole |
