MIs

Question 1

STEMI=

Answer 1

st segment of ECG elevated myocardial infarction

• large vessel FULLY occluded (proximal occlusion)
• massive MI

Question 2

NSTEMI=

Answer 2

no st segment elevation myocardial infarction

-branch fully occluded or partially occluded (distal occlusion)

Question 3

MI=

Answer 3

myocardial infarction, end stage of coronary artery disease

Question 4

etiology of MI?

Answer 4

most cases atheroclerosis (plaque)

• thrombus
• unexplained vasospasm
• severed vessel, hemmorhage

Question 5

pathophysiology of MI?

Answer 5

-atherosclerosis (vessel cannot dilate because too damaged or in max dilation)—-> complicated lesion—>
ischemia—> cardiac hypoxia—> anaerobic metabolism (glucose breaks down pyruvate and produces lactic acid)—> metabolic acidosis
arrhythmias—> CO decreased, inability to pump—> infarction (local death of tissues)

Question 6

determining extent of MI?

Answer 6

1. proximal or distal occlusion= proximal: larger area of heart, distal: smaller
2. degree of occlusion= partial or complete
3. duration of MI= longer, more damage
4. metabolic status of heart= what the person was doing when they had an MI
5. HR, BP, rhythm of heart
6. collateral circulation (if collateral vessels ALREADY exist, extent of MI is less because other vessels there to perfuse, must ALREADY be present!

Question 7

types of MI? (2)

Answer 7

1. transmural infarction

2. subendocardial infarction

Question 8

transmural infarction?

Answer 8

ST elevation
ENTIRE ventricular wall (endocardium–> epicardium)
result of PROXIMAL occlusion= STEMI

Question 9

subendocardial infarction?

Answer 9

ST depression
INNER part of ventricular wall (1/2-1/3 of thickness)
result of DISTAL occlusion or partial proximal
NSTEMI

Question 10

manifestations of MI?

Answer 10

-mostly result of atherosclerosis, MI comes on suddenly
ACUTE CRUSHING pain
-ANXIETY and stress makes MI worse
-TACHYCARDIA 
-NAUSEA AND VOMITING

Question 11

why does nausea and vomiting follow severe pain?

Answer 11

pain receptors in brain are very close to N/V center in brain, so when pain is severe, this center is always activated

Question 12

diagnosis of an MI?

Answer 12

-ECG tracing: ST segment elevated= STEMI vs NSTEMI
T inversion (should be upwards, if down= MI)
loss of R wave (ventricles not pumping)
abnormal Q waves
-ANGIOGRAM: catheter inserted through central line releases dye which flows to point of obstruction
-SERUM MARKERS

Question 13

serum markers that diagnose an MI?

Answer 13

• heart cells die and release proteins into blood, more protein= more dead cells= worse MI.
• TROPONIN I and T= proteins in cardiac muscle, released first
• MYOGLOBIN= indicates muscle cell death
• CREATINE KINASE (enzyme in varying tissues)

Question 14

creatine kinase of heart?

Answer 14

CKMB

Question 15

CKMM?

Answer 15

skeletal muscle

Question 16

CKBB?

Answer 16

brain

Question 17

treatment of an MI?

Answer 17

must be ASAP
-pharmacology: thrombolytics, anticoagulants, antiarrthymias, morphine PRN, O2 (temporary) for ischemia
ONCE patient stabilized: IV diuretic (decrease BV and workload) and INOTROPE- positive or negative

Question 18

if damage is too far gone for MI, drugs will not have an effect so?

Answer 18

TREATMENT limited to SURGERY

• revascularization!
• angioplasty: surgical repair or unblocking of a vessel (often a stent, balloon angioplasty)
• BYPASS: surgically created pathway that goes around blocked vessel that causes ischemia