Cardiac Emergencies

Question 1

CVP

Answer 1

2-6 mmHg

Question 2

MAP

Answer 2

70-105 mmHg

Question 3

Cardiac Output

Answer 3

4-8 L/min

Question 4

Cardiac Index

Answer 4

2.5-4.0 L/min/m^2

Question 5

Stroke Volume

Answer 5

60-120 mL/beat

Question 6

Stroke Volume Index

Answer 6

30-65 mL/beat/m^2

Question 7

Pulmonary Artery Systolic

Answer 7

15-30 mmHg

Question 8

Pulmonary Artery Diastolic

Answer 8

5-15 mmHg

Question 9

3 Presentations of ACS

Answer 9

Unstable angina, non-ST elevation MI, ST elevation MI

Question 10

Unstable Angina

Answer 10

Results from a sudden plaque rupture, associated with increased risk of cardiac death and MI, EKG changes (ischemia) are usually transient and no biochemical markers are present

Question 11

Coronary Artery Spasm

Answer 11

Most often occurs between 12am and 8 am, may have arrhythmias that can produce unconsciousness, at great risk for sudden death, same risks as with atherosclerotic disease,
tx: nitro and Ca blockers

Question 12

Non-ST Elevation MI

Answer 12

Similar to unstable angina but enough damage done to release biochemical markers, ST depression or T wave changes possible, usually leads to non Q-wave MI

Question 13

ST Elevation MI

Answer 13

EKG changes and biochemical markers present, Q wave develoips when cells are deprived of blood flow, usually leads to Q-wave MI

Question 14

Acute coronary syndrome

Answer 14

represent a spectrum of diseases with underlying coronary plaque ruputure and thrombosis. The severity depends on the degree of occlusion ei UA or NSTEMI is partial occlusion vs STEMI being a full occlusion.

Question 15

Atherosclerosis Phase I: Initiation

Answer 15

Endothelial dysfunction, development of lipid layer, migration of leukocytes
Lipid laden macrophages become foam cells
Endothelial damage cause by HTN, DM, HLD, smoking

Question 16

Atherosclerosis Phase II: Progression

Answer 16

Death of leukocytes and smooth muscle cells produce development of liquid rich core and plaque, remodeling of the vascular wall, lumen size may not change significantly

Question 17

Atherosclerosis Phase III: Plaque Disruption - Stable Plaque

Answer 17

thick fibrous cap with high levels of smooth muscle cells and collagen, small lipid and macrophage core with lower levels of inflammatory cytokines

Question 18

Atherosclerosis Phase III: Plaque Disruption - Unstable Plaque

Answer 18

extensive lipid accumulation, thin weakened fibrous cap and increased inflammatory component - plaque rupture occurs, two thirds of all MI’s caused by lesions with less than 50% stenosis