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Cardio Week 4 > ICL 4.4: Clinical Acute Coronary Syndromes > Flashcards

ICL 4.4: Clinical Acute Coronary Syndromes Flashcards

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1
Q

what are the 3 main acute coronary syndromes?

A
  1. STEMI
  2. non-ST-segment elevation MI
  3. unstable angina
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2
Q

what is the pathophysiology of ACS?

A

vulnerable vessel with atherosclerotic plaque –> acute plaque rupture or erosion –> plaque is exposed to the blood stream which creates thrombosis –> thrombosis then blocks the lumen of the vessel

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3
Q

what is stable plaque?

A

atherosclerotic plaque with a fibrous cap = layer of tissue between the lipid core and lumen

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4
Q

what is an unstable plaque?

A

very large lipid core with a thin fibrous cap that often ruptures

when the cap ruptures, the contents of the lipid core are exposed to the blood stream which activates the coagulation cascade and leads to the formation of a thrombus

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5
Q

what is an NSTEMI?

A
  1. chest pain or other ischemic symptoms
  2. abnormal EKG changes (ST depressions or T-wave inversions)
  3. elevated troponin level
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6
Q

what is unstable angina?

A
  1. new or worsening chest pain symptoms
  2. abnormal EKG changes (ST depressions or T-wave inversions)
  3. troponin negative
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7
Q

when someone comes into the ER with chest pain, how do you differentiate between STEMI, NSTEMI and unstable angina? how would you treat each?

A

EKG with ST elevation = STEMI –> immediate cardiac cath lab for stents

positive troponin with other EKG changes = NSTEMI –> cardiac cath lab within 48 hours

negative troponin with normal EKG = unstable angina –> stress test or cardiac cath within 48 hours

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8
Q

why is there ST elevation in a STEMI?

A

with normal perfusion, ST segment is isoelectric compared to the TP interval

a lack of bloodlfow creates a voltage gradient between normal and ischemic tissue which leads to deflection in the normally isoelectric ST segment

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9
Q

ST elevation on an EKG gives you what clinical diagnosis?

A

total occlusion of a coronary artery

STEMI

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10
Q

ST depression or T-wave inversions on EKG gives you what clinical diagnosis?

A

partial occlusion of a coronary artery

unstable angina/NSTEMI

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11
Q

what does time is muscle mean?

A

by 24 hours you have a total infarct of the whole heart

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12
Q

what are biomarkers? give 2 examples and what they entail

A

a measurable substance in an organism whose presence is indicative of some phenomenon such as disease, infection, or environmental exposure

measure something in the blood -> detect a disease process -> make a clinical intervention

ex. BNP level is elevated -> this confirms the presence of CHF -> treat CHF
ex. D-dimer level is elevated -> this indicates there is a risk of Pulmonary Embolism -> a diagnostic study is performed to confirm or refute the possibility of Pulmonary Embolism -> PE is diagnosed -> PE is treated

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13
Q

what is the key biomarker in ACS?

A

Troponin is a commonly utilized biomarker and is very useful for determining if a patient is suffering from an acute coronary syndrome (ACS)

troponin is protein that is normally present within cardiomyocytes but NOT in the circulation

cardiomyocyte Cell death (typically from acute coronary syndrome), results in cell necrosis and spilling of troponin into the blood stream –> troponin is measured from a blood sample

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14
Q

what is the troponin time period post-MI?

A

peaks around 1 day and clears 5-7 days

CKMB has a similar peak but clears a lot earlier; it’s an older biomarker the isn’t used as much

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15
Q

what is the clinic presentation of a STEMI?

A
  1. usually severe, crushing chest pain
  2. diaphoresis
  3. vomiting
  4. left arm pain
  5. jaw pain
  6. looks sick
  7. EKG shows ST segment elevation
  8. can also present with cardiac arrest: typically Vfib cardiac arrest
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16
Q

what is the initial treatment for a STEMI?

A
  1. Aspirin 325 mg x 1 STAT in the ambulance
  2. Heparin 5000 U bolus in the ER
  3. Activate STEMI team: goal is to fix the occluded artery within 90 minutes

door-to-balloon time <90 minutes because time is muscle!

  1. Emergency Percutaneous coronary intervention (PCI)
  2. DAPT: dual antiplatelet therapy after PCI= aspirin plus a P2Y12 antagonist
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17
Q

what is the initial treatment for a NSTEMI?

A

if patient present with chest pain or SOB with ST depressions and/or t wave inversion and elevated troponin levels:

  1. admit to hospital
  2. aspirin and heparin drip
  3. statin and beta blocker
  4. nitroglycerin for chest pain relief
  5. cardiac catheterization within 2-48 hrs as appropriate
  6. DAPT
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18
Q

what happens on the EKG if you don’t treat a STEMI?

A

acute: ST elevation
hours: Q wave appears

days 1-2: T wave inversion and Q wave is deeper

days later: ST normalizes, T wave inverted

weeks: ST and T waves are normal

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19
Q

which leads correlate to the LAD?

A

V1-V6

20
Q

which leads correlate to the RCA?

A

II, III, aVf

21
Q

which leads correlate to the LCX?

A

I and aVf

22
Q

what’s another word for NSTEMI?

A

subendocardial infarction

23
Q

what’s another word for STEMI?

A

transmural infarction

24
Q

what is myocardial ischemia?

A

reduced coronary perfusion resulting in myocardium with inadequate oxygen delivery

25
Q

what is myocardial infarction?

A

death of cardiomyocytes, usually due to acute coronary syndromes

26
Q

what is the pathogenesis of acute coronary syndromes?

A
  1. atherosclerotic plaque issue or rupture: lipid content is released in the blood and it is very thrombogenic = activation of coagulation cascade
  2. platelet adhesion
  3. platelet activation
  4. platelet aggregation
  5. thrombotic occlusion
27
Q

how does the pathogenesis of ACS explain what kinds of drugs we use to treat ACS?

A
  1. plaque rupture -> platelet activation -> antiplatelet agents
  2. plaque rupture -> activation of coagulation cascade - > antithrombotic/anticoagulation agents
  3. large lipid plaques are underlying substrate of ACS -> statin therapy
  4. myocardial infarction –> maladaptive neurohormonal activation (catecholamines and RAAS) -> beta blocker and RAAS inhibitors (ACE-I, ARB, aldosterone antagonist, etc.)
28
Q

how are platelets activated?

A

platelets have alpha granules and dense granules that release ADP, TXA2, thrombin and VWF

29
Q

what are the 3 classes of drugs that can effect platelet activation and prevent ACS?

A
  1. COX/Thromboxane pathway
  2. P2Y12 receptor antagonists (ADP antagonists)
  3. GPIIb/IIIa inhibitors
30
Q

which drugs are COX/Thromboxane pathway?

A

aspirin

31
Q

which drugs are P2Y12 receptor antagonists (ADP antagonists)?

A
  1. clopidogrel
  2. ticagrelor
  3. prasugrel
32
Q

which drugs are GPIIb/IIIa inhibitors?

A
  1. tirofiban
  2. eptifibatide
  3. abciximab
33
Q

which drugs inhibit thrombin?

A
  1. heparin/LMWH = activate antithrombin (III)

2. bivalirudin = direct thrombin inhibitors

34
Q

what is the medical treatment of ACS based on lipids?

A

high intensity statin therapy in all patients with NSTEMI or STEMI

  1. atorvastatin 40-80 mg daily
  2. rosuvastatin 20-40 mg daily

obtain a fasting lipid, preferably within 24 hours

35
Q

what is the medical treatment of ACS based on the RAAS?

A

RAAS antagonists aka ACE inhibitors and ARBs

  1. ACE-I = lisinopril
  2. ARB = losartan, candesartan, valsartan for those intolerance to ACEI
  3. Aldosterone blockade (spironolactone or eplerenone) post MI if Ejection Fraction (EF) < 40%

limitation of aldosterone antagonist is that it can raise potassium, contraindicated if significant renal disease (Cr>2.0) or hyperkalemia (K>5.0)

36
Q

what is the medical treatment of ACS via anti platelet therapy?

A

dual antiplatelet therapy (DAPT): aspirin plus a p2y12 receptor antagonist (clopidogrel, prasugrel, or ticagrelor)

aspirin 162-365mg should be given at presentation and 81 mg daily continued

P2y12 inhibitor for 1 year after STEMI and NSTEMI –> Ticagrelor favored over clopidogrel

37
Q

how is anticoagulation treatment used to treat ACS?

A

anticoagulation is usually done with IV heparin from the time of presentation to catheterization

anticoagulant therapy (e.g. heparin) is stopped after PCI

Dual Antiplatelet therapies (e.g. Aspirin and Clopidogrel) are continued after PCI

38
Q

what are the other major causes of chest pain and should be in the differential?

A
  1. acute PE
  2. pericarditis
  3. costochondritis
  4. musculoskeletal chest pain
  5. aortic dissection
  6. GERD esophageal spasm
39
Q

what is an acute PE?

A

one of the “great masqueraders” due to varying presentation

very common to be misdiagnosed in urgent care with asthma or pneumonia; if lucky, patients present to ER after not getting better

diagnostic algorithms and risk scores are used to calculate the risk of it actually being a PE: Wells score, Revised Geneva Score, sPESI score

40
Q

what is the clinical presentation of acute PE?

A
  1. chest apin
  2. SOB at rest or with exertion
  3. fatigue/limited functional capacity
  4. lightheadedness
  5. pre-syncope
  6. cough
41
Q

which biomarker suggests acute PE?

A

D-dimer - high sensitivity, low specificity

D-dimer is a biomarker, representing turnover of thrombus –> D-dimer is elevated in cases of venous thromboembolism (DVT and PE)

if d-dimer positive, then a diagnostic study is needed like CTA chest PE protocol

if d-dimer is negative, PE is effectively ruled out

42
Q

how do you treat a PE?

A

heparin anticoagulation or LMWH like lovenox

then transition to oral anticoagulants like coumadin or apixaban, dabigatran, rivaroxaban, edoxaban (DOACs)

for high risk presentation like hypotension, shock or cardiac arrest advanced therapies may be required = IVC filter, surgical embolectomy, catheter directed thrombolysis

43
Q

what is the clinical presentation of acute pericarditis? how do you treat it?

A
  1. pleuritic chest pain = sharp, worse with deep inspiration
  2. difficulty breathing due to sharp pain with deeper breaths
  3. positional pain, better with leaning forward

often viral cause, treat with NSAIDs and/or colchicine

44
Q

what are the EKG changes seen in acute pericarditis?

A
  1. diffuse ST elevations
  2. PR segment depression in lead II
  3. PR segment elevation in lead aVR

STEMI only has regional ST elevations with reciprocal ST depressions; acute pericarditis has diffuse ST elevations in every single lead

45
Q

Patient’s with NSTEMI or STEMI treated with PCI are also treated with dual anti-platelet therapy (DAPT), consisting of two oral anti-platelet drugs. Which of the following is not an example of DAPT.

A) aspirin and clopidogrel

B) aspirin and prasugrel

C) aspirin and tirofiban

D) aspirin and ticagrelor

A

C) aspirin and tirofiban

tirogiban is a GPIIb/IIa inhibitor

46
Q

what is the medical treatment for STEMI after PCI?

A
  1. Aspirin 81 mg daily
  2. P2Y12 antagonist: Clopidogrel or Ticagrelor or Prasugrel (DAPT)
  3. atorvastatin or rosuvastatin high intensity statin therapy
  4. metoprolol
  5. lisinopril
  6. smoking cessation counseling and therapy
  7. medical therapy for hypertension and diabetes as needed

Cardio Week 4 (16 decks)

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