Coronary Artery Disease Flashcards

0
Q

What are the inferior, anterior, and lateral leads and which blood vessels supply those areas?

A

II, III, aVF - supplied by RCA
V1-V4 - supplied by LAD
I, aVL, V5-V6 - supplied by circumflex

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1
Q

What can a new LBBB in a patient presenting with chest pain be suspicious for?

A

STEMI

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2
Q

Of the acute coronary syndromes, which are more common?

A

NSTEMI and unstable angina more common than STEMI

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3
Q

Where is a plaque particularly vulnerable to rupture?

A

The shoulder

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4
Q

When during the day is acute MI most likely to occur?

A

Between 6am and noon

Peak incidence in first three hours after awakening

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5
Q

What’s the main goal of treatment for patients presenting with a STEMI?

A

Achieve reperfusion within 120 minutes - optimally within 60

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6
Q

What are the options for reperfusion in a STEMI?

A

PCI - primary coronary intervention - door to balloon time of less than 90 minutes
Thrombolytic therapy - door to needle time within 30 minutes

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7
Q

What are absolute contraindications to thrombolytic therapy?

A

Active internal bleeding
Recent (<1 mo) GI bleeding
Recent serious trauma, including prolonged CPR

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8
Q

What are relative contraindications to thrombolytic therapy?

A
Severe hypertension (s>200, d>110)
Recent minor trauma
Hemostatic defect
Severe hepatic or renal disease
Diabetic hemorrhagic retinopathy
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9
Q

What are 3 major factors to consider when crossing between PCI and thrombolytic therapy?

A

Availability of PCI capable lab that can achieve door to balloon of 90 minutes - if not, thrombolytic, then transfer later
Bleeding risk or contraindications for thrombolytic - use PCI
experience of operator doing PCI

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10
Q

What are acute medications commonly given after MI?

A
Aspirin
Other antiplatelet agents (clopidogrel)
Heparin
Nitrates
Beta blockers - but can precipitate cardiogenic shock in tachycardia, heart failures or large infarctions - don't use
ACE inhibitors - if normal creatinine and not hypotension
Statins 
Admin of oxygen
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11
Q

Which two drugs have been proven in long term studies to reduce mortality following MIs?

A

Beta blockers

Captopril (ACE inhibitor)

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12
Q

What is the pathophysiology of NSTEMI or unstable angina?

A

Periodic platelet plugging and platelet mediated coronary arterial vasoconstriction occur after which portions of plug break off and are swept away, partially restoring perfusion

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13
Q

What is the medical therapy for NSTEMI and unstable angina?

A

Reperfusion with thrombolytics not beneficial
Emergent coronary intervention not required
Invasive management reduces morbidity but not mortality and is warranted if: older than 65, marked ST and T alterations, enzyme evidence of myocyte necrosis –> angiography followed by revascularization (catheter based or surgical)
Also indicated if patient has spontaneous or inducible ischemia despite adequate medical therapy

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14
Q

In addition to coronary revascularization, what does therapy of unstable angina or NSTEMI center on?

A
Platelet inhibition (clopidogrel, aspirin)
Thrombin inhibition (LMWH)
Control of oxygen demands (beta blocker)
Prevention of vasoconstriction (nitroglycerin)
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15
Q

What cocktail are patients who have been diagnosed with NSTEMI or unstable angina given when discharged from the hospital?

A
Aspirin
Clopidogrel
Beta blocker
ACE inhibitor 
Statin
16
Q

What 3 factors determine long term prognosis following acute MI?

A

Patient age
Residual left systolic function
Extent and severity of underlying coronary artery disease

17
Q

What irregular ventricular rates are common after an acute MI and how are they treated?

A

Ventricular premature beats common 2-3 days post MI - don’t require therapy but monitor in case turns into VT or VF
Prophylactic therapy with antiarrhythmics not used
VT/VF within 24 hrs after acute MI not associated with adverse prognosis

18
Q

Other than ventricular rates, what other abnormality is commonly seen after an acute MI and how is it treated?

A

AV block of some degree
First degree usually with inferior MI - require no therapy, almost always transient, lasting no more than 24-48 hrs, but watch for development of more serious blocks
Type I second degree - inferior - usually transient 2-3 days, no therapy unless ventricular rate too slow, then give atropine
Type II second degree - anterior - often permanent, pacemaker
Third degree - inferior - transient within a few days, no pacemaker
Third degree - anterior - infarct of BBs, permanent pacemaker

19
Q

What are the kilip classes of left ventricular heart failure following an acute MI?

A
I - none
II - mild
III - substantial
IV - cardiogenic shock
Mortality increases as you go up in class
20
Q

What are the clinical manifestations of cardiogenic shock?

A

Hypotension and hypo perfusion of critical organs
Elevated LV filling pressures
Cardiac index depressed
Pulmonary congestion

21
Q

What are the risk factors for cardiogenic shock?

A
Severe coronary atherosclerosis (usually in LAD)
Prior MI
increased age
Female gender
Diabetes 
STEMI
anterior infarct
22
Q

What is the treatment of cardiogenic shock?

A

Agents to support BP and augment ventricular function
Intraaortic balloon pump
PCI or bypass surgery

23
Q

What are the 3 main MECHANICAL complications of acute MI?

A

Ventricular septal rupture (ant or inf infarct, 1-5 post MI)
Papillary muscle rupture –> mitral regurgitation (inf infarct, usually posterior leaflet because only LAD, ant has LAD and circumflex, 1-5 days post MI)
Free wall rupture (can lead to SCD, ant or inf infarct)

24
What are the various manifestations of an acute ventricular septal rupture?
Pulmonary congestion with or without hypotension Systolic murmur with or without thrill at left sternal border Increase in oxygenated blood in RV
25
What is the treatment for an acute VSD?
Diuretics and inotropes Vasodilator to reduce shunting Emergency cath to confirm, visualize, and define anatomy Surgical closure and possible bypass grafting
26
What are the various manifestations of an acute papillary muscle rupture?
Pulmonary congestion with or without hypotension | Mitral regurgitation and holo systolic murmur with no thrill
27
What is the management of an acute MR?
Diuretics and inotropes Vasodilator to reduce regurgitation Emergent cath to confirm and define anatomy Immediate surgery (MVR and any bypass grafting appropriate)
28
What are the clinical manifestations of a free wall rupture?
NO pulmonary congestion | NO murmur
29
What is the treatment for free wall rupture?
Emergent pericardiocentesis and surgery
30
How does RV infarction occur as a complication of inf MI?
RCA supplies both
31
What are the various manifestations of right ventricular infarction?
Hypotension Elevated neck veins No pulmonary congestion No murmur
32
What is the treatment of RV infarction?
``` Preload reduction Rapid reperfusion of RCA Positive inotropic agents Frequently covers over time Most imp prognostic factor is degree of associated LV dysfunction ```
33
When is PCI not better than thrombolytics therapy?
Stable angina | It is a chronic disease