ACS Physiology and Pharmacology Flashcards

1
Q

What spectrum do clinical features for ACS fall on?

What is the most important distinguishing feature?

A

Spectrum: From unstable angina to NSTEMI to STEMI
Distinguishing: ST elevation on ECG

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2
Q

What are the clinical features of unstable angina? (4)

A

Sudden increase in frequency, duration, and/or intensity of ischemic episodes
Episodes of angina at rest
New onset of angina episodes
Not relieved by usual doses of nitroglycerin

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3
Q

What are the clinical features for Acute MI:

Characteristic Pain
Sympathetic Effect
Parasympathetic effect
Inflammatory Response
Cardiac Findings
Other
A

C: Severe, persistent, typically substernal
S: Diaphoresis, cool and clammy skin
P: Nausea, vomiting, weakness
I: Mild fever
C: S4 (and S3 if systolic dysfunction) gallop, Dyskinetic bulge (if anterior wall MI), Systolic murmur (if mitral regurgitation or VSD)
O: Pulmonary rales (if heart failure present), JVD (if heart failure or right ventricular MI)

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4
Q

What is the diagnosis of ACS based on?

A

Presenting symptoms
Acute ECG abnormalities
Detection of specific biomarkers of myocardial necrosis

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5
Q

What are the ECG abnormalities of a UA/NSTEMI?

What are ECG abnormalities for a STEMI?

A

UA/NSTEMI
ST segment depression and/or T wave inversions
May be transient and correlate with chest pain for UA or persist for NSTEMI

STEMI
Initial ST elevation, followed by T wave inversion over the course of hours and Q wave development (persists for weeks)

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6
Q

What are the serum markers of infarction?
When do they rise and peak?
Which is more specific?

A

Cardiac troponins - Begin to rise at 3-4 hours, peak 18-36h
Creatine kinase - CK-MB isozyme mainly, begins to rise at 3-8 h, peaks at 24 h, worse specificity

No serum markers for UA

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7
Q

What is the pain distribution of UA versus MI?

A

UA - Crescendo, rest, or new-onset severe angina

NSTEMI - Prolonged crushing chest pain, more severe and wider radiation than usual angina

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8
Q

What is the goal of therapy?

What is the difference for STEMI?

A

Address the intracoronary thrombus, provide anti-ischemic measures, limit myocardial damage and complications
STEMIs have total coronary occlusion and benefit the most from immediate reperfusion therapies

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9
Q

What classes of drugs are used for treatment?

A

Anti-ischemia: Beta blockers, Nitrates, Maybe calcium channel blocker (not much survival aid, mainly for vasospasm)
Pain control (morphine is first choice)
Supplemental O2 as necessary
Antithrombotics
Statin and ACE inhibitor as adjunctive therapy

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10
Q

Management post-MI involves what therapy? (4 drugs)

A

Aspirin
Beta-blocker
Statin
ACE Inhibitor (If LV dysfunction)

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11
Q

What is the most important finding to monitor post-MI?
What is the critical value for this finding?
What prophylactic treatment is used for it?

A

LV Ejection fraction
High risk for sudden cardiac death if <30%
Prophylactic implantation of implantable cardiofibrillator

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