Cardio II Flashcards

(46 cards)

1
Q

With what anatomical location and vessel do leads II, III, and AvF correspond?

A

Inferior wall

RCA

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2
Q

With what anatomical location and vessel do leads V1-V2 correspond?

A

Anteroseptal

LAD

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3
Q

With what anatomical location and vessel do leads V3-V3 correspond?

A

Apical surface

LAD

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4
Q

With what anatomical location and vessel do leads V5-V6 and AvL correspond?

A

Lateral wall

Circumflex artery

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5
Q

At what time post MI does troponin peak?

A

24 hours

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6
Q

For how many days post MI does troponin stay elevated?

A

7-10 days

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7
Q

What happens to ST segment with UA, NSTEMI, STEMI?

A

down, down, up

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8
Q

What happens to troponin levels with UA, NSTEMI, STEMI?

A

no change, up, up

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9
Q

How long after the start of symptoms can you see troponin elevation? CKMB elevation?

A

3-4 hours

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10
Q

Can you tell the difference on EKG between NSTEMI and UA?

A

No

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11
Q

How long after MI does CKMB go back to baseline?

A

48-72 hours?

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12
Q

In people who have Prinzmetal angina, what does EKG look like?

A

ST elevation during spasm that resolves with resolution of therapy?

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13
Q

What is initial therapy of acute coronary syndromes?

A
  1. Reperfusion therapy by cath lab / fibrinolytic therapy (STEMI only)
  2. Antithrombotic drugs [anti platelet (aspirin) and clopidigrel) + anti coagulant therapy (heparin))
  3. Anti-ischemic therapy (beta blockers and nitrates)
  4. Statin therapy + ACE inhibitor
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14
Q

What meds do you give a person post MI on discharge?

A

Antithrombic drugs (ASA + clopidigrel)
Beta blocker
Ace inhibitor
Statin

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15
Q

How do patients having MI die before getting to hospital?

A

ventricular tachycardia or tachyarrhythmia

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16
Q

Why do patients with inferior MIs sometimes have sinus bradycardia + hypotension?

A

Intense parasympathetic activation –> vagal effect (pain + vagal irritation can do this)

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17
Q

Patient with bradycardia in setting of MI should be given what?

A

atropine

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18
Q

Loud systolic murmur in patient two days after MI?

A

Necrosis of a papillary muscle –> MR
Necrosis of intraventricular septum –> VSD
Differentiate by:

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19
Q

Sharp pleuritic chest discomfort and coarse friction sound

20
Q

What is the mechanism of morphine?

A

Analgesic mechanism is not clearly defined; vasodilation occurs via mast cell degranulation and histamine release

21
Q

What is the mechanism of nitroglycerin?

A

Converted to NO –> cGMP –> smooth muscle relaxation –> decreased preload; decreased coronary artery smooth muscle

22
Q

What is the mechanism of aspirin?

A

Inhibits COX1 (+ COX2), thereby inhibiting thromboxane A2 (–> platelet aggregation + activation of new platelets, + vasoconstriction)

23
Q

What should you do if someone comes in with ACS?

24
Q

What is the mechanism of beta blockers?

A

Reduce O2 demand by reducing HR, cardiac contractility, and BP

25
What is the mechanism of heparin?
Activates antithrombin (which normally inhibits thrombin, which normally stimulations platelet aggregation) and inhibits coagulation factor TEN A
26
What is the mechanism of clopidogrel?
Blocks the P2Y12 ADP receptor on platelets, thus preventing platelet aggregation and activation
27
What is the mechanism of GP IIb/IIIa receptor antagonists?
blocks the receptor for fibrinogen to link platelets
28
What is the mechanism of statins?
HMG-CoA reductase inhibitors (blocks production of cholesterol in the liver, which causes up regulation of LDL receptors in the hepatocytes, which causes increased uptake of LDL from blood to liver)
29
What is the mechanism of ACE inhibitors?
Blocks ACE which catalyzes angiotensin I to angiotensin II (vasoconstriction and aldosterone secretion (increased sodium and water retention))
30
What is the mechanism of aldosterone antagonists?
decreased sodium and water retention
31
What is the mechanism of digoxin?
Blocks the sodium-potassium exchange pump, which leads to increased intracellular sodium, which leads to increased intracellular calcium, which leads to increased contractility; also lengthens AV refractory period
32
What is the mechanism of milranone?
Phosphodiesterase 3 inhibitor --> reduced breakdown of cAMP --> enhanced Ca++ entry into the cell and increased force of contraction
33
What is the mechanism of dopamine?
COME BACK LATER
34
What are the two large groupings of heart failure?
``` Systolic dysfunction (ejection problem) Diastolic dysfunction (filling problem) ```
35
What happens to the ventricular action potential when you administer Class I antiarrhythmics?
Block sodium channels; looks like the AP has been tilted to the right 1. Increased (less negative resting potential) 2. Slower upstroke (phase 0) --> negative isotropy 3. Increased refractoriness & AP duration
36
What happens to the ventricular action potential when you administer Class III antiarrhythmics?
Block potassium channel; some tilting of AP but mostly stretching of phases 2, & 3 1. Longer plateau 2. Longer repolarization 3. Increased refractoriness & AP duration
37
What are the major determinants of myocardial oxygen demand?
1. HR 2. Contractility 3. Wall tension = (PxR)/h
38
What are the major determinants of myocardial oxygen supply?
1. Oxygen content (Hg, pO2) | 2. CBF = PP/r
39
What are the main epidemiological risk factors for HD?
1. Smoking 2. Cholesterol 3. Diabetes 4. HTN 5. FH
40
What are the features of unstable plaques?
1. thin fibrous plaque 2. high lipid content 3. high macrophage content
41
What do beta blockers do?
Reduce HR + contractility (and so reduce myocardial oxygen demand)
42
How do nitrates work?
Venodilators --> decreased venous return --> decreased preload --> reduce wall tension --> reduce myocardial oxygen demand; also coronary artery dilators --> increase m. O2 supply
43
How do calcium channels work?
Arterial dilation --> improve supply Venous dilation --> decrease preload --> dec. demand (Verapamil also reduces …) Arterial > Venous
44
Side effects of calcium channels
1. peripheral edema | 2. Constipation;
45
impaired diastolic compliance
S4
46
Side effects of nitrates
Headaches ...