What does the ____ supply?

1. Left anterior descending artery
2. Left circumflex artery
3. Right coronary artery
4. Posterior descending artery
5. Right circumflex

1. Interventricular septum (anterior 2/3rd's), apical portion of anterior papillary muscle, anterior surface of left ventricle
2. Lateral and posterior wall of left ventricle
3. Right ventricle (via acute marginal branches), AV node (via AV nodal artery), SA node (70% of time)
4. Inferior and posterior walls of ventricles
5. SA node (25% of time)

1. 200 ms (1 big box)
2. 60-100 ms (1.5-2.5 little boxes)
3. 400 ms (2 big boxes), although women slightly longer

1. 60,000/(ms between peaks)
2. QT interval
3. Determine if T wave is halfway between the two QRS waves

1. Bundle branch block (>3 boxes
2. Look at V1. If the entire complex is negative and lacks R upstroke, consider left bundle block. If V1 shows a RSR' complex, with large S downstroke, consider right bundle block

What do the following QRS values indicate?

1. Lead I is positive, AVf is positive
2. Lead I is positive, AVf is negative
3. Lead I is negative, AVf is positive
4. Lead I is negative, AVf is negative

1. Normal axis
2. Left axis (left ventricular hypertrophy, inferior wall MI, left anterior fascicular block)
3. Right axis (right ventricular hypertrophy, massive pulmonary edema, left posterior fascicular block)
4. Indeterminate axis

1. ST elevation (acute)
2. Decreased R wave, Q wave begins (hours)
3. T wave inversion, Q wave deeper (day 1-2)
4. ST normalizes, T wave inverted (days)
5. ST and T normalize Q wave persists (weeks)

In electrode closest to the infarct:

• Depressed = transmural MI
• Elevated = nontransmural / non-Q wave MI

• Stage A - risk factors but normal systolic function. 
• Stage B- structural disorders without signs or symptoms of HF
• Stage C- Structural disease with signs of HF now or in the past
• Stage D- End stage

• Diminished EF due loss of myocardial contractility or pressure overload (increased afterload). Can be due to myocyte disfunction/destruction or fibroris. 
• Stiffness of wall due to inability to relax, hypertrophy, fibrosis. Leads to decreased EDV.

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• Class I = sodium channel blockers. CAB (from strongest to weakest)
• Class II = beta adrenergic receptor blockers
• Class III = potassium channel blockers
• Class IV - calcium channel blockers

Atrial flutter, with variable block (variable ventricular response due to AV node "filtering")

Stroke (stagnant blood clots during abnormal heartbeat and is dislodged when heartbeat reverts to normal)

What is the definition of...

1. Accelerated idioventricular rhythm
2. Non-sustained ventricular tachycardia
3. Sustained ventricular tachycardia

1. Rhythm with more than 3 QRS beats in a row, but LESS THAN 100 bpm (usually occurs after reperfusion due to irritation)
2. Same as above, but >100 bpm
3. Same as above, but sustained over 30 second

1. Accelerated idioventricular generated by irritation of heart after reperfusion therapy for MI
2. Electrolyte/catecholamine imbalance.

Wide QRS complex, abnormal (inverted?) T wave, lack of P wave preceding QRS complex.

Note: two normal beats followed by VPD = trigeminy

• First degree = constant P-R interval greater than 200ms (5 little boxes)
• Second degree, Type I = Progressively increased P-R interval followed by dropped beat (Wenkebach)
• Second degree, Type II = Abrupt dropping of QRS (no prolonging). Wide QRS
• Third degree (complete block) = no relationship between P wave and QRS complex. More P wave than QRS 

Class Ia (primarily by definition)

• Atrial fibrillation
• Side effects: Hypotension, agranulocytosis, nausea, vomiting
  • Fast acetylators- NAPA metabolite, a class III drug capable of prolonging QT and causing torsades
  • Slow acetylators- drug-induced lupus

Suppreses ventricular fibrillation/tachycardia due to ischemia (class 1b drug); administered IV (mexilitine is oral form)

Do NOT use it for paroxysmal supraventricular tachycardia since it does not effect atrial beats. Negative inotrope (less useful in heart failure)

Class Ic

1. Supraventricular arrhythmias (atrial fib. and flutter)
2. Contraindicated in patients with abnormal heart structure (e.g. EF markedly reduced); true of ALL class Ic
3. Observe prolonged QRS on stress test 

Class III/beta blocker

• Isomeric mixtures of beta blocker and Class III antiarrhythmetic. Negative inotrope, beneficial in cases of heart-failure. 
• Can exacerbate asthmatic symptoms; only contraindicated in those previously intubated for asthma. Renal failure = contraindication.
• Side effects (all class III): prolong QT leading to torsades.

Class III

• Ventricular and atrial arrhythmias. Used in patients with portable defibrillators to prophylactically prevent VT
• Pulmonary toxicity, thyroid toxicity, corneal deposits, skin coloration
• Increases digoxin levels (causing delayed afterdepolarizations and VPD); increases coumadin level tw fold. 

Fast acting (30 seconds) for supraventricular arrhythmia (suppresses AV node).

Enhanced K+ conductance and inhibition of cAMP induced calcium influx to prevent nodal depolarization. 

Beta blockers primarily, "head and tail are allowed to meet"

Calcium channel blockers can also be used.

• Decrease primary determinants of mycoardial oxygen demand (HR, contractility, conduction velocity)
• HOWEVER, can increase EDV, leading to wall stress (nitrates coadministered). BB's also block reflex tachycardia and increased FOC caused by nitrates
• Vasospastic angina (may worsen condition due to unopposed alpha constriction)

Venodilation decreases preload and workload. Large coronary arteries dilate to increase O2 delivery (w/o coronary steal)

Headaches include postural hypotension. Tolerance frequently occurs with oran and transdermal preps (requires drug holiday)

What is the mechanism of action for

1. Clopidogrel
2. Dipyridamol
3. Aspirin
4. Abciximab
5. Heparin

1. Prevents ADP-mediated activation of platelets
2. Prevents collagen/thrombin/TXA-mediated activation 
3. Inhibits COX-mediated synthesis of TXA2
4. Binds to GPIIb/IIIa site, preventing aggregation
5. Increases activity of antithrombin (reducing II, IX, X, XI), interferes with platelet agg

Early clots -- more rich in fibrin (later clots more rich in platelets). Complete occlusion; best outcome when given 30-90 minutes post-MI.

Activates plasminogen to produce plasmin, which degrades fibrin. Requires fibrin surface to provide binding site. 

ACE inhibitors; decrease BP, enahnace NO production, reduce LVH/dysfunction

Pulmonary side effects (cough)

Angiotensin receptor blockers; block the effect of AngII. 

Used when ACE inhibitors are not well tolerated.