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Flashcards in Acute Coronary Syndrome 2 Deck (23)
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1
Q

Name 3 strategies to reduce myocardial oxygen demand?

A

bed rest and narcotics(does not improve outcomes)
B adrenergic blockers: beneficial effects on post MI (reduces oxygen need, anti arrhythmic properties and inhibit platelet activation
nitrates (potent veno and arterial vasodilators which reduce preload and after load)

2
Q

Name 7 strategies to improve myocardial oxygen supply.

A
supplemental oxygen
nitrates (improve local circulation)
anti platelet therapy 
anticoagulant therapy
early angiography and mechanical revascularization
fibrinolytic therapy
3
Q

Discuss different approaches to anti platelet therapy.

A

aspirin (can be attenuated by adrenaline)
clopidogrel, prasrugrel and ticagrelor (block ADP receptor on platelet
GP IIb/IIIa inhibitors (inhibit of activated glycoprotein IIb/IIIa receptors on platelets)

4
Q

Name two drugs in anticoagulant therapy.

A

anti-thrombin III inhibition (heparin)

direct thrombin and factor Xa inhibition

5
Q

When repercussion can be achieved within 90 min, emergency _____ is better than thrombolytics in terms of medium term survival, culprit artery potency and freedom of complications.

A

percutaneous coronary intervention (PCI)— result is regional MI systems employing rapid helicopter transport of MI patients

6
Q

Name the two most commonly used thrombolytic agents.

A

streptokinase
tissue plasminogen activator (more effective)

greatest benefit if use in first 6hours of onset of chest pain

7
Q

Discuss the major contraindication to thrombolytics.

A

any predispose to internal bleeding such as known intracranial pathology
recent stroke or head trauma
recent major surgery

8
Q

Name 4 strategies that can be used to stabilize an unstable plaque.

A

HMG-CoA reductase inhibitors (statins)
anti-platelet therapy
angiotensin converting enzyme inhib
aggressive management of cardiovascular risk factors with lifestyle changes and medications

9
Q

What is ventricular remodeling?

A

time-dependent, dynamic, and structural alteration in the ventricle resulting from coronary occlusion and myocardial necrosis (occurring in two phases)

10
Q

Describes the process by which larger infarcts are often associated with progressive ventricular dilation.

A

early infarct expansion occurs over days post MI, over weeks, the entire heart enlarges and the infarct things further due to mechanical and neuro-hormonal factors

11
Q

Name the serious complications that can occur post MI.

A

congestive heart failure
life-threatening ventricular arrhythmias
post-MI pericarditis

12
Q

What are common causes of post MI cardiogenic shock?

A

severe left ventricular pump failure
acute formation of a ventricular septal defect
rupture of papillary muscle resulting in severe mitral regurgitation
pericardial tampande from ventricular free wall rupture

13
Q

Discuss the 3 main elements of CHF in the setting got an acute myocardial infarction.

A

increased left ventricular end diastolic pressure, resulting from systolic and diastolic function

activation of sympathetic nervous system, increases arteriolar tone and ventricular after load

infarct related acute mitral regurgitation

14
Q

Does arrhythmia within the first 48 hours following an MI carry prognostic significance? Are they common

A

not long-term prognostic, although ventricular arrhythmias in the subsequent days signify poor prognosis and increase risk of sudden death
telemetry is standard of care for first 48 hrs after MI

15
Q

What can pericardiac chest pain and ECG changes mimic?

A

recurrent myocardial ischmia

16
Q

How should you treat pericariditis, post MI?

A

treat with analgesics, corticosteroids and high dose NSAIDs should be avoid as they impair wound healing and may lead to aneurysm formation and ventricular rupture

NSAIDs may be appropriate with later Dressler’s syndrome

17
Q

List 4 anti-thombins.

A

unfractioned heparin
low molecular weight heparin (Enoxaparin)
direct thrombin inhibitor (bivalirudin)
factor Xa inhibitor (fondaprinux)

18
Q

What are contraction bands? (re MI)

A

wavy fibers seen on histological section that occur through a ca dependent mechanism that causes hyper contraction, lysis of contractile filament and sarcolemmal rupture

19
Q

List histologic features of damaged cardiomyocytes 7d post MI

A

vacuoles within myocytes
mononuclear cell and macrophage infiltration
small vessel proliferation
fibroblast proliferation

20
Q

What are the biggest problems with thrombolytic therapy?

A

failure to open infarct in 40%, contraindications in 40% cases

21
Q

What are time goals in primary PCI and fibronolytic treatments?

A

90 and 30 minutes respectively

22
Q

Name 5 interventions that help improve survival in STEMI.

A

cardiac intensive care
ASA and P2Y12 receptor blocker
beta blocker
statin therapy

23
Q

Antero-apical region is most vulnerable for infarct expansion due to what?

A

thinnest area of myocardium
greatest curvature
greatest deforming forces
site of thrombus due to stasis