Unit 2: Myocardial Infarction (MI) Flashcards
Acute Myocardial Infarction
destruction of heart muscle from lack of oxygenated blood supply
-common cause of obstruction = atherosclerosis
Risk Factors for Heart Disease and MI
-cigarette smoking
-high LDLs
-type 2 diabetes
-elevated adrenaline (catecholamines)
-obesity
-inactivity
-hypertension
-male gender
-post menopausal female
-family hx
>can occur at any time
>most dangerous time = early morning hours; may be d/t higher levels of circulating adrenaline at this time
Atherosclerosis
gradual build up of plaque inside the wall of the artery
- rupture of plaque = thrombus formation and obstruction of coronary artery flow = ischemia and death of heart muscle
- heart muscle damaged by inadequate blood supply cannot maintain normal cardiac function = decrease in cardiac output (CO)
- systemic symptoms associated w/ MI = chest pain and poor peripheral perfusion
Stable Angina
episodes of intermittent chest pain present when artery is narrowed 60 to 70%
- associated w/ activity or exercise
- relieved by rest
- not associated w/ damage to heart muscle
- warning sign for potential heart muscle damage
Acute Coronary Syndrome
umbrella term -used when there is concern for myocardial ischemia >unstable angina (UA) >non-ST elevation MI (NSTEMI) >ST elevation MI (STEMI)
Unstable Angina
pain not associated w/ exercise
- not relieved by rest
- may present w/ ECG changes
- no elevation in cardiac markers
- may present w/ nonspecific or transient ST segment depressions or elevations
- emergency = requires immediate tx
Non-ST elevation MI (NSTEMI)
partial occlusion of a major coronary vessel or complete occlusion of a minor coronary vessel
- causes reversible partial thickness heart muscle damage
- ST depressions (0.5 mm at least) or
- T wave inversions (1.0 mm at least)
- w/o q waves in 2 contiguous leads w/ prominent R waves or AR/S ratio > 1
- elevated cardiac markers
ST Elevation MI (STEMI)
complete occlusion of a major coronary vessel
- results in irreversible full thickness heart muscle damage
- ST elevations
- elevated cardiac markers
Clinical Manifestations
-Chest Pain (angina); from obstructed blood flow to the heart muscle
-Angina can be stable or unstable
>Stable (exertional) angina: occurs during activity, has predictable pattern, goes away w/ rest
>Unstable (rest) angina: more serious; can occur at rest w/ no specific pattern, not relieved by change in activity, medical emergency
-angina is a warning sign of impending MI
Symptoms in addition to Chest Pain when there is a complete occlusion of the vessel resulting in an MI and muscle damage
- shoulder and arm pain (more on left)
- jaw and tooth pain
- shoulder blade pain
- upper back pain
- SOB
- nausea and vomiting
- sweating
- generalized fatigue
Things to consider w/ person to person
- symptoms can vary significally from person to person
- women are more likely to have neck, shoulder blade, jaw, and abdominal pain
- diabetes are more likely to have SOB and fatigue
- geriatrics tend to have co-morbidities may mimic angina; may experience dyspnea, syncope, weakness, or confusion
Right MI
right coronary artery/ventricle
- Jugular Vein Distention (JVD)
- Hypotension
- Bradycardia r/t damage to SA node
- Nausea and vomiting
Left MI
left coronary artery/ventricle
-worse prognosis; high risk of sudden death and congestive heart failure
-dyspnea
-tachycardia
-hypertension
>tachycardia and hypertension result from the loss of CO b/c of damage to the left ventricle and subsequent stimulation of sympathetic compensatory mechanisms
-hypotension will quickly evolve
Laboratory Testing
- Creatinine kinase (CK)
- Creatinine Kinase Myocardial Bands (CK-MB)
- Troponin (I and T)
- CMP, CBC, Coagulation, and ABGs
Laboratory Testing: Creatinine Kinase (CK)
general marker of cellular injury
-released from cells in the brain, skeletal muscle, and cardiac tissue after muscle damage has occurred
Laboratory Testing: Creatinine Kinase Myocardial Bands (CK-MB)
0-3 mg/dl
- CK isoenzyme marker specific to cardiac tissue
- when myocardial damage occurs, CK-MB is released from the cells
- can remain elevated for up to 36 hours before returning to normal
- increased levels can be seen at 3 hours after injury
Laboratory Testing: Troponin (T and I)
proteins expressed almost exclusively in the heart; specific marker of cardiac muscle damage
-less than 0.4 mg/ml (<0.4 mg/ml)
-can elevate within 4 hours of injury
-levels can stay elevated for up to 10 days
(b/c it stays elevated longer than CK-MB, it is a valuable marker when attempting to diagnose injury in recent past
-blood test of choice
Laboratory Testing: CMP
complete metabolic profile (CMP)
- electrolytes
- tests of organ system functioning (eg. Renal values: BUN + Creatinine)
Laboratory Testing: CBC
complete blood count (CBC)
-tests hemoglobin, hematocrit, and WBC
Laboratory Tests: Coagulation
- Prothrombin time (PT): 10-13 sec
- Activated Partial Thromboplastin Time (aPTT): 25-35 sec
- INR: <2.0
Diagnostic Tests for MI
Invasive + Noninvasive
- ECG
- Echocardiogram
- Stress testing
- Coronary Angiography
Electrocardiogram (ECG)
-gold standard for diagnosis of MI
-inexpensive, easy to perform, safe, painless
>ST depression = ischemia
>ST elevation = infarction
>Q wave = confirms MI (later on)
Echocardiography
- used to evaluate the ventricular functions (ejection fraction [EF])
- assists in diagnosing an MI by looking at specific areas of heart muscle that are not contracting (wall motion abnormalities)
Stress Testing
- not done during time an MI is evolving
- another way to evaluate heart function
- types: exercise stress test, dobutamine/adenosine test, stress echo, nuclear stress test
- dependent on pts needs and condition
- looks at coronary blood flow
- looks at left ventricular function and wall motion abnormalities