Cardiac Alterations

Question 1

Stable Angina

Answer 1

occurs w/ exertion, relieved by rest or Nitroglycerin
pain usually less than 5 mins
typically PREDICTABLE!!

results from “fixed lesions” of more than 75% of the CA lumen

demand from exertion blood and oxygen supply

Question 2

Variant Angina/Prinzmetal’s Angina

Answer 2

not predictable
caused by coronary vasospasm
not r/t physical activity
often occurs at night

cause of spasm is unknown

Question 3

Acute Coronary Syndrome (ACS)

Answer 3

unstable angina, STEMI, NSTEMI

imbalance between myocardial oxygen supply and demand

Question 4

STEMI

Answer 4

ST segment elevated MI
occlusive thrombus
cardiac enzyme elevation
fibrinolytics beneficial
entire thickness (transmural) of cardiac muscle is necrotic/infarcted

classic MI

Question 5

NSTEMI

Answer 5

non-ST segment elevation MI

Question 6

Unstable Angina (UA)

Answer 6

non-occlusive thrombus, no ST segment elevation, NO cardiac enzyme elevation
NO fibrinolytics, not beneficial

Decreased flow, tissue not completely dead

Question 7

Unstable Angina Characteristics

Answer 7

CHANGE in previously established pattern of angina

severe angina that persists for more than 5 mins, worsens in intensity, not relieved by one nitro is a medical emergency

can signal atherosclerotic plaque instability/thrombus formation
CAN lead to an MI

Question 8

Myocardial Infarction

Answer 8

irreversible myocardial necrosis secondary to a decrease/total interruption of blood flow to a specific area of myocardium

causes of acute reduction of O2 to the myocardium: plaque rupture, new CA thrombosis, CA spasm

Question 9

Clinical presentation of Acute MI

Answer 9

tachycardia, ectopy (PVCs), badycardia, normo/hypotensive, tachypneic, diminished heart sounds, may have gallop, systolic murmur, crackles, pulmonary edema, air hunger, orthopnea, decreased CO, decreases urine output, decreased peripheral pulses, decreased capillary refill, restlessness, confusion, anxiety, agitation, denial –> big

Question 10

ASA/Plavix

Answer 10

antiplatelet

Question 11

Nitrates

Answer 11

dilates coronary arteries to perfuse better and control pain

Question 12

morphine

Answer 12

pain control

Question 13

beta blockers

Answer 13

lowers BP and Hr

Question 14

Heparin, LMQH, GP IIb/IIIA (ReoPro/Integrillin)

Answer 14

anticoagulants (don’t break up clot)

prevent clot from getting bigger

Question 15

ACE inhibitors

Answer 15

lowers BP

Question 16

Inotropes (dobutamine, dopamine, milrinone)

Answer 16

increases contractility (not really used)

Question 17

CK - MB and Troponins

Answer 17

initial elevation of CK-MB and Troponin I and Triponin T occurs 3-6hrs after acute myocardial damage

Troponin I only found in cardiac muscle, highly specific for myocardial damage, more so than CK-MB

Troponin T also elevated 3-12 hrs after injury. Peaks in 12-48hrs

Question 18

Tenecteplase (TNKase)

Answer 18

fibrinolytic therapy

an enzyme used as a thrombolytic drug

a newer fibrinolytic with longer plasma half-life and greater specificity for fibrin than alteplase, achieves rapid thrombolysis in patents with acute MI

systemic -> worry about bleeding everywhere else

Question 19

nursing measures for TNKase

Answer 19

identifying candidates - IV, labs, VS

observing for signs of reperfusion

providing patient education