Unit 2 - Cardiovascular System Part 2 Flashcards
myocardial infarction
occurs when there is a complete interruption in blood/O2 delivery to the heart muscle from a blockage in an artery
-result is necrosis (tissue death)
acute MI (AMI)
- typically result of significant CAD that culminates in a complete blockage
- ischemia often a precipitating factor
- often fatal - 30%
transmural
full thickness MI affecting all 3 layers of the heart
nontransmural
partial thickness MI involving sub endocardial layer
most common sites of coronary artery occlusion
- left anterior descending artery (LAD)
- left circumflex artery (LCX)
- right coronary artery (RCA)
STEMI
“ST Elevation Myocardial Infarction”. Typically “transmural” infarctions
~70% of AMI’s are STEMI
non-STEMI
MI that does not demonstrate ST segment elevation on the EKG – Typically “subendocardial” infarctions
pathogenesis
The rupture of a vulnerable atherosclerotic plaque with subsequent thrombus formation, appears to be most common cause of AMI.
“soft” plaques are more likely to rupture than “hard”
diagnosis of MI
- similar to angina but more profound/severe
- chest pain, jaw/neck/shoulder discomfort, dyspnea, overwhelming fatigue
- **may also include nausea and diaphoresis
EKG changes
“injury” pattern is often noted
hallmark characteristic is ST segment elevation (indicator of tissue damage)
Serum enzyme levels
elevations in:
- troponin
- CPK-MB
- LDH “flipped ratio”
- AST
- myoglobin
major complications of MI
Dysrhythmias Heart Failure (HF) Sudden Death Syndrome Mural thrombus / CVA Ventricular aneurysm Ventricular rupture with tamponade
dysrhythmias
Multiple PVC’s - indicates myocardial irritability
Ventricular Tachycardia
Ventricular Fibrillation
requires immediate treatment - medication or defibrillation
heart failure
heart is unable to pump enough blood through the body
causes: decrease myocardial capacity, intrinsic muscle disease, increased BP, valvular disease
sudden death syndrome
death occurring within 1 hour of the onset of cardiac symptoms
in adolescents/young adults under 30, “hypertrophic cardiomyopathy” is most common cause
mural thrombus/CVA
blood clot on endocardial wall
if the thrombus breaks loose, it can travel to the brain causing a CVA/stroke
ventricular aneurysm
when necrosis occurs during MI, the tissue is vulnerable during the healing stage and may develop an abnormal ballooning
ventricular rupture with tamponade
heart becomes compressed and can no longer contract and relax normally
medical and surgical management of MI
- treat symptoms (rest, O2, meds)
- limit damage (meds, surgery)
- secondary prevention (lifestyle changes, rehab)
sternal precautions
No lifting, pulling, pushing (10# limit) for 6 wks
Log roll technique in/out bed
No driving (4-8 wks)
ROM exercises – neck, shoulders, torso (“caution with sternectomy”)
Scar mobilization when incision is healed
Be conservative if: osteoporosis, diabetes, advanced age
Phase I of cardiac rehab
= Inpatient phase: (typically 3-7 days) - review sternal precautions, initiate physical activity and provide home exercise/activity guidelines. Refer to comprehensive out-patient cardiac rehabilitation program!!
Note: monitor vital signs pre, during, and post exercise. Be aware of contraindications to exercise in the cardiac patient.
Phase II of cardiac rehab
Acute outpatient: (may last up to 12 weeks) comprehensive program including individually prescribed and monitored exercise, and individual and group educational sessions aimed at reducing risk factors and secondary events.
Phase III of cardiac rehab
Follows phase II: (may last 6 months or more) a continuation of phase II but patients no longer receive continuous telemetry monitoring during exercise and are more independent.
