Hemodynamics #2 Flashcards Preview

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Flashcards in Hemodynamics #2 Deck (22)
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0
Q

Mixed Angina

A

Stable & variant Angina

1
Q

Variant Angina

A

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

2
Q

Nitric Oxide

A
Required for vasodilation, normally released by endothelium. Atherosclerosis makes endothelium dysfunctional, malfunctioning intrinsic nitric oxide production. 
Nitro donor (nitro) quickens release of nitric oxide.
3
Q

Nitro results in venous pooling, decreases which cardiac pressures?

A

Preload and LVEDPs

4
Q

Nitro benefits

A

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

5
Q

Morphine benefits

A
  • Decrease pain = decrease sympathetic tone = decrease workload on heart
  • Histamine release (potent vasodilator)
6
Q

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

A

50

CorrPP = DBP - PCWP

Increase in wedge will decrease CorrPP

7
Q

What pressure pushes blood into the coronary arteries?

A

Diastolic Blood Pressure

8
Q

Beta Blocker Benefit in AMI

A
  • Decreases HR and contractility = decrease workload.
  • increases diastolic filling times.
  • improves ejection fraction & SV
9
Q

Beta blockers used and considerations

A
  • Can be detrimental in acute phase.
  • Tx unnecessary tachycardia. Do not bring down compensatory tachycardia.
  • Treat pain 1st
  • metoprolol & carvedilol (coreg), esmolol
10
Q

Which beta blocker is the only beta blocker administered to CHF

A

carvedilol (coreg)

11
Q

Ca channel blockers & AMI

A

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.
12
Q

3 phases of clot prevention & lysis

A

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

13
Q

Phase 1 examples

A

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)
14
Q

Phase 2 example

A

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
15
Q

Phase 3 example

A

Fibrinolytics

  • activates plasminogen to plasmin
  • normal process to break down clot
  • activates it faster than normal
  • TPA (tissue plasminogen activator), retrovase, streptokinase, TNkase
16
Q

Thrombolytic relative contraindications

A

HTN, recent trauma, pregnancy

17
Q

Thrombolytic Absolute contraindications

A

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

18
Q

Pacing complication: Over Sensing

A

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

19
Q

Pacing complication: Failure to Sense

A

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

20
Q

Other Pacing complications

A

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

21
Q

Pacing verification of electrical and mechanical capture

A

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

Mechanical: heart tones