Acute Coronary Syndrome Flashcards
(33 cards)
Coronary Artery Disease
Accounts for most CV deaths in the US
▪ Mostly caused by atherosclerosis
▪ Progressive disease
▪ Risk factors: nonmodifiable, modifiable, contributing modifiable
MI Classification
Affected area of the heart: anterior, lateral, inferior, or
posterior
▪ EKG changes produced: STEMI vs NSTEMI
▪ Time-frame within progression of MI: acute, evolving, old
What’s the culprit for most MIs?
blocked coronary artery
Ischemia, injury, and infarction
imbalance
between myocardial blood supply and oxygen
demand
Unstable angina
Partially occluded by a thrombus, Negative cardiac enzymes
New in onset, or chronic stable angina that increases in frequency, duration, or severity occurs at rest or minimal
exertion pain refractory to NTG
NSTEMI
Partially occluded by a thrombus
Positive cardiac enzymes
STEMI
Totally
occluded by
a thrombus
Positive
cardiac
enzymes
PQRST
Precipitating
events
Quality of pain
Radiation of pain
Severity of pain
Timing
Myocardial
infarction (MI)
Irreversible myocardial cell deathcontractile function of the heart
stops in the necrotic area(s)
▪ Cell death occurs after
approximately 20 minutes of
ischemia
▪ Thrombus formation causes 80-90%
of all acute MIs (other causes?)
▪ Role of collateral circulation
Definition of NSTEMI
“Ischemic ST-segment depression of 0.5 mm (0.5 mV) or
greater -OR- Dynamic T wave inversion with pain or
discomfort / Transient ST elevation of 0.5 mm or greater
for less than 20 minutes.
Definition of STEMI
New ST segment elevation at the J point in at least two
contiguous leads of ≥ 2 mm (0.2 mV) in men or ≥ 1.5
mm (0.15 mV) in women in leads V2-V3 and/or of ≥ 1 mm
(0.1 mV) in other contiguous chest leads or the limb leads
-OR- new or presumed new left bundle branch block.”
Clinical Manifestations of MI: PAIN
severe immobilizing chest pain not relieved by
rest, position change, or nitrate administration
▪
“elephant on my chest”, “pressure”, “tightness”,
“crushing”
▪ Substernal, retrosternal, epigastric; may radiate
to neck, jaw, arms or back
▪ May occur at rest, with exertion, asleep, or awake
Clinical Manifestations of MI
Skin: ashen, clammy, & cool to touch, diaphoretic
▪ Cardiovascular: BP & HR increased at first. Later,
decreased BP with decreased cardiac output. May have
distant heart sounds, S3, S4, or loud holosystolic
murmur
▪ GI: N & V
▪ Fever: low grade within first 24 hrs up to 1 week
Clinical Manifestations of MI- atypical
Women: dizziness, SOB,
unusual tiredness
Patients with diabetes
mellitus: asymptomatic or
atypical (dyspnea), “silent
MI”
Older patient: change in
mental status, dizziness, SOB,
or a arrhythmia
Ignoring signs and symptoms
Half of the patients who die of ACS do so before
reaching the hospital.
▪ Ventricular fibrillation(VF) or pulseless ventricular
tachycardia is precipitating rhythm
▪ VF likely to develop in first 4 hours after onset of
symptoms
Education: seek help early and don’t drive yourself, call
91
ACS Diagnostic Studies -1
12-lead ECG (Obtain within 10 min on arrival to ED)
* Distinguish between unstable angina (UA), non-ST
segment elevation myocardial infarction (NSTEMI), ST
elevation myocardial infarction (STEMI)
* Serial
* If available, will compare to old ECG
ACS Diagnostic Studies (2)
Serum Cardiac Markers
* Cardiac-specific troponin: Troponin T and Troponin I:
serial sampling q6-8 hr x 3 (watch trend)
* CK-MB isoenzyme (if a troponin test is unavailable,
considered an acceptable substitution)
* Myoglobin: one of the first to appear, lacks cardiac
specificity
ACS Diagnostic Studies (3)
Coronary Angiography (cardiac cath)– evaluate patency
of coronary arteries and collateral circulation
- STEMI patients
- high-risk patients with UA or NSTEMI, depending on risk
stratification
Other Measures
* Exercise or pharmacologic stress testing (after 3 negative
troponins)
* echocardiogram
Risk stratification
TIMI Risk Score: estimates mortality with UA, NSTEMI, STEMI
UA/NSTEMI
STEMI
GRACE ACS estimates admission-6month mortality for
patients with ACS
▪ HEART: predicts 6 week risk of major adverse cardiac event
▪ EBP: CRP level and coronary artery calcium scoring to
improve risk classification
Healing Process after MI
Inflammatory process:
Leukocytes, cardiac enzymes released (within 24
hours)
Macrophages (by the fourth day)
Collagen matrix (10-14 days)
Scar tissue (by 6 weeks)
Ventricular remodeling: changes in the infarcted
myocardium causes changes in the unaffected
myocardium
MI Complications - arrhythmias
Arrhythmias
* Present in 80-90% 0f patients
* Most common cause of death in prehospital setting
(get AED!)
* Ischemia, electrolyte imbalance, SNS stimulate can
affect the myocardial cell’s sensitivity to nerve
impulses
MI Complications-III
~ Cardiogenic shock:
shock state resulting from impairment or failure of the
myocardium.
~ anterior MI at greatest risk
May require intra-aortic balloon pump (IABP)
counterpulsation
IV. MI Complications-
Acute Pericarditis
Acute Pericarditis
* occurs 2-3 days after MI
* sharp, stabbing chest pain,
usually comes on quickly
* The pain tends to ease when patient
sits up and leans forward. Lying
down and deep breathing worsens
it.
* Friction rub, fever
Treatment: NSAIDs, ASA, or
corticosteroids
IV. MI Complictions-
Dressler Syndrome
Dressler Syndrome “post
myocardial infarction
syndrome”
▪ develops 4-6 wks. after MI
▪ pericarditis with fever,
pleuritic pain, and effusion
▪ elevated WBC, ESR
▪ elevated ST segments
throughout all 12 leads
Treatment: NSAIDS,
corticosteroids
