Hemodynamics #2

Question 0

Mixed Angina

Answer 0

Stable & variant Angina

Question 1

Variant Angina

Answer 1

Spontaneous CP on rest or early morning, coronary spasm , can lead to infarction

Question 2

Nitric Oxide

Answer 2

Required for vasodilation, normally released by endothelium. Atherosclerosis makes endothelium dysfunctional, malfunctioning intrinsic nitric oxide production. 
Nitro donor (nitro) quickens release of nitric oxide.

Question 3

Nitro results in venous pooling, decreases which cardiac pressures?

Answer 3

Preload and LVEDPs

Question 4

Nitro benefits

Answer 4

Decreased workload on ventricle, decreased ventricular wall tension, does not effect sympathetic tone other than decreasing myocardial O2 demand = decreased pain = decreased sympathetic tone.

Question 5

Morphine benefits

Answer 5

• Decrease pain = decrease sympathetic tone = decrease workload on heart
• Histamine release (potent vasodilator)

Question 6

CorrPP needs to be at least what to perfuse whole heart…

Answer 6

50

CorrPP = DBP - PCWP

Increase in wedge will decrease CorrPP

Question 7

What pressure pushes blood into the coronary arteries?

Answer 7

Diastolic Blood Pressure

Question 8

Beta Blocker Benefit in AMI

Answer 8

• Decreases HR and contractility = decrease workload.
• increases diastolic filling times.
• improves ejection fraction & SV

Question 9

Beta blockers used and considerations

Answer 9

• Can be detrimental in acute phase.
• Tx unnecessary tachycardia. Do not bring down compensatory tachycardia.
• Treat pain 1st
• metoprolol & carvedilol (coreg), esmolol

Question 10

Which beta blocker is the only beta blocker administered to CHF

Answer 10

carvedilol (coreg)

Question 11

Ca channel blockers & AMI

Answer 11

Hydralazine

• dilates coronary arteries/collateral vessels
• at cost of decreasing myocardial contraction & conduction.
• Detrimental if heart is not beating fast enough or putting out enough volume.

Question 12

3 phases of clot prevention & lysis

Answer 12

1- stops clots from forming
2- stop formed clots in their tracks
3- breaks down existing clots

Question 13

Phase 1 examples

Answer 13

ASA

• inhibit platelet aggregation
• indefinitely poisons platelets by preventing release of thromboxane A2 (platelet interaction)

Glycoprotein IIb/IIIa inhibitors

• prevents common pathway by preventing plately interaction w/ other platelets.
• integelin, abciximab(RePro), tirofiban (aggrastat)

Question 14

Phase 2 example

Answer 14

Heparin

• Prevent clot from further clotting & clumping
• prevents conversion of fibrinogen to fibrin
• prevents net from forming and stabilizing clot
• prevents formation of future clots

Question 15

Phase 3 example

Answer 15

Fibrinolytics

• activates plasminogen to plasmin
• normal process to break down clot
• activates it faster than normal
• TPA (tissue plasminogen activator), retrovase, streptokinase, TNkase

Question 16

Thrombolytic relative contraindications

Answer 16

HTN, recent trauma, pregnancy

Question 17

Thrombolytic Absolute contraindications

Answer 17

Active internal bleeding, suspected aortic dissection, known intracranial neoplasm, pH hemorrhagic CVA, any CVA in past year.

Question 18

Pacing complication: Over Sensing

Answer 18

Sensing activity that is not there, false or not productive and not pacing as a result

Question 19

Pacing complication: Failure to Sense

Answer 19

Failure to pick up low amplitude QRS complexes and pacing over them. Potential for R on T

Question 20

Other Pacing complications

Answer 20

Failure to capture (electrolyte disorder), myocardial penetration or perforation (tamponade/Becks triad)
-treatment (early) force fluids (late) pericardial centesis.

Question 21

Pacing verification of electrical and mechanical capture

Answer 21

Electrical: t-wave of opposite polarity following wide bizarre complex

Mechanical: heart tones