1"Silent MIs" (without chest pain) are more likely to occur in which patient population? Why?
diabetics because of polyneuropathy
2Atypical MI presentation is more likely in ?
elderly, diabetic and women
3If the patient is having an inferior wall infarction how will they likely present?
epigastric pain
bradycardia
hypotension, elevated jugular venous pressure, clear lung fields
4What is the first intervention after patients experience a stemi?
revascularization should occur as soon as possible
5Low dose ASA causes what?
inhibits platelet aggregation
6Intermediate dose ASA causes what?
antipyretic and analgesic effect
7High dose ASA has what effect?
anti-inflammatory
8What is MONA and what is it used to treat?
Morphine
Oxygen
Nitroglycerin
Aspirin
acute medical treatment in ACS
9When would you consider oxygen therapy as a supportive measure for a patient with an ACS?
cyanosis
severe dyspnea
SP02 less than 90%
10When would you consider intravenous fluids as a supportive measure for a patient with an ACS?
inferior MI causing RV dysfunction
11How do IV fluids help with RV dysfunction?
increases preload which optimizes left and right ventricular filling and reduces hemodynamic instability
12When would you consider LOOP diuretic as a supportive measure for a patient with an ACS?
consider for patients with pulmonary edema or acute HF
13What causes unstable angina
rupture of a stable plaque
14Whats the different between unstable angina and NSTEMI?
NSTEMI biomarkers are present
15ACS
the suspicion or confirmed presence of acute myocardial ischemia
16NSTE-ACS
ACS manifesting without ST elevations on ECG
17STE-ACS
acute coronary syndrome manifesting with ST elevations on ECG
18Type 1 MI
MI caused by atherothrombotic coronary artery disease
19Type 2 MI
MI caused by mismatch between oxygen supply and demand
20T/F STEMI manifests with more severe symptoms than NSTEMI
false
21MOA for fibrinolytics
initiates local fibrinolysis by binding fibrin in a thrombus and converts entrapped plasminogen to plasmin
22What are fibrinolytics indicated for?
acute ischemic stroke (presenting within 3-4.5 hours of symptom onset)
ST-elevation MI
documented massive PE
23What are the absolute contraindications for fibrinolytics?
any prior hemorrhagic stroke
ischemic stroke within 3 months
intracranial neoplasm or arteriovenous malformation
active internal bleeding
aortic dissection
considerable facial trauma or closed head trauma in past 3 months
intracranial or intraspinal surgery within 2 mo
severe uncontrolled HTN
24Who should be treated with antiplatelet agents?
patients with STEMI and NSTE-ACS
25MOA for aspirin?
ASA covalently attaches and acetyl group to COX --> irreversible COX-1 inhibition causes inhibition of thromboxane synthesis in platelets which inhibits platelet aggregation
26What is the established first line therapy in ACS and why?
aspirin because it reduces the incident of recurrent MI and death
27GI adverse effects of ASA?
dyspepsia, gastric ulceration, hemorrhage, perf
28Coag and bleeding adverse effects of ASA?
increase bleeding time
29Ear adverse effects of ASA?
tinnitus
30What are the renal adverse effects of ASA?
acute kidney injury and acute interstitial nephritis with long term use of ASA
31Alteplase, Reteplase and Tenecteplase are which type of drugs?
fibrinolytics
32What are some examples of P2Y12 inhibitors?
clopidogrel
prasugrel
ticagrelor
ticlopidine
cangrelor
33P2Y12 inhibitors MOA
inhibition of P2Y12 receptors on platelets which decreases Gp IIb/IIIa receptors on platelets which inhibits platelet aggregation
34Irreversible inhibitors of the P2Y12 receptors
clopidogrel, prasugrel, ticlopidine
35Reversible inhibition of P2Y12 receptors
ticagrelor
36When is P2Y12 inhibitors usually used?
with ASA
for:
-STEMI, unstable angina or NSTEMI
-secondary prevention of cardiac events in patients post PCI and or stenting
-before PCI
-alternative to ASA if there is an intolerance
37Ticagrelor is used for?
ACS-PCI, ACS, prior MI, CAD
38Clopidogrel is used for?
ACS-PCI, ACS and prior MI
39Prasugrel is only used for?
ACS-PCI
40When should you avoid prasugrel?
in patients with active pathological bleeding or a history of TIA or CVA
41When should you avoid ticagrelor?
in patients with active pathological bleeding or hx of ICH
42What are the main 3 drugs that fall under the glycoprotein IIb/IIIa inhibitor?
abciximab
eptifibatide
tirofiban
43MOA for glycoprotein llb/llla inhibitors?
bind to and block glycoprotein IIb/IIIa receptors on the surface of activated platelets which causes prevention of platelets binding to fibrinogen leading to inhibition of platelet aggregation and thrombus formation
44When are glycoprotein llb/llla inhibitors indicated?
for prevention of thrombotic complications in high risk patients with unstable angina/NSTEMI that are planned for a PCI within 24 hours
45Contraindication for glycoprotein llb/llla inhibitors?
recent bleeding, severe HTN, aortic dissection, thrombocytopenia
46Contraindications of nitrates
systolic blood pressure less than 90
use of PDE 5 inhibitor in the previous 24 hours
suspected RV infarction h
47Indications for opioids?
severe pain despite antianginal medicaction
48CI for opioids?
lethargy, hypotension, bradycardia, known hypersensitivity
49Indication for ACE/ARB?
consider within 24 hours in stable patients with STEMI, LVEF less than or equal to 40%, HF, HTN, DM
50Aldosterone antagonist is considered in patients who are already receiving an ACE inhibitor and beta blocker with:
LVEF less than or equal to 40%, heart failure, diabetes mellitus
51Indications for a high intensity statin?
all STEMI/NSTEMI patients (cholesterol baseline doesnt matter)
52What are the acute coronary syndromes?
unstable angina, NSTEMI, STEMI
53What drugs should be initiated if a patient has moderate to severe left ventricular HF
(beta blockers) carvedilol, bisoprolol, metoprolol SUCCINATE with gradual titration
54How should nitroglycerin be taken?
under tongue- let dissolve
55What is the MOA of nitroglycerin?
forms free radical nitric oxide
inhibits coronary vasoconstriction causing an increase in coronary perfusion
vasodilation decreases preload
modest decrease in afterload
because of the decrease in PL/AL myocardial oxygen demand decreases
56MOA of isosorbide?
relaxes vascular smooth muscle, dilation of peripheral arteries and veins, venodilation reduces LV end diastolic pressure and pulmonary capillary wedge pressure (preload)
Arteriodilation reduces systemic vascular resistance, systolic arterial pressure and mean arterial pressure (afterload)
57What is your priority in patients with stable angina?
control angina symptoms
primary prevention
58What is your priority in patients with unstable angina?
prevent total occulsion
control CP and other symptoms
59What is your priority with patients who are experiencing NSTEMI?
prevent total occlusion
limit infarct size
control CP
60What is your priority in patients with a STEMI?
restore patency of infarcted artery
prevent complications such as arrhythmias or death
61Symptoms of an atypical presentation
no/minimal chest pain
autonomic symptoms
62Common s/s of an inferior wall infarction?
epigastric pain
bradycardia