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ACLS: Acute Coronary Syndrome (Risk Factors (Smoking, HBP, High blood chol…
ACLS: Acute Coronary Syndrome
STEMI
Definition
Long period of blocked blood supply.
Affects a large area of the heart muscle and causes changes on the ECG as well as in blood levels of chemical markers (CK, troponin, etc)
NSTEMI (NSTE-ACS)
Definition
Chest pain that does not cause ST elevation on an EKG.
Blood levels of chemical markers will show damage to cardiac tissue
The blockage can be partial or temporary, so the extent of cardiac damage is variable.
Unstable Angina
Chest pain that can occur w/ or w/o physical exertion
Rest or medicine may not relieve the pain
Causes
Coronary Artery Dz = most common
Build up of plaque in the arteries with subsequent thrombus causing MI
PathoPhys
Early plaque formation
Significant plaque formation
Plaque rupture and thrombus formation (NSTE-ACS)
STEMI
Resolution/Stable angina
Risk Factors
Smoking
HBP
High blood chol
Diabetes
Physical inactivity
being overweight or obese
FHx of chest pain, heart dz or stroke
Symptoms
Chest pain (angina)
Pain - radiating
Nausea or vomiting
Indigestion
SOB, dyspnea
Sudden heavy
diaphoresis
Lightheadedness, dizziness, fainting
Diagnostics
EKG specific categories
ST-segment depression: Ischemia
ST depression
Dynamic T-wave inversion
Nondiagnostic or normal EKG
low risk ACS
ST-segment elevation: ongoing acute injury
new onset LBBB
ST elevation
Diagnose MI on EKG:
EKG specific categories
T wave peaking followed by T wave inversion (seen in NSTEMI)
Onset of an MI: T waves become Tall & narrow - "peaking"
T waves invert within a few hours
Only indicative of ischemia, not MI
Seen in bundle branch blocks, ventricular hypertrophy w/ repolarization abnormalities
Often occurs in leads "distant" from the site of infarction
ST segment elevation (seen in STEMI)
Reliable sign that a TRUE infarction has occurred
Distinguish it from J-point elevation
T-wave usually remains independent in J-point elevation
Ongoing acute injury
new onset LBBB?
Appearance of new Q waves
Irreversible myocardial cell death has occurred - Diagnostic of MI
Occurs w/i several hours of infarction
ST elevation has usually resolved by the time Q waves have appeared
Q waves are present for life
When an area of the hear dies, it is "electrically silent" and the electrical forces of the myocardium are directed AWAY from the infarcted area. Hence the negative deflection.
Pathologic Q wave
... > 0.04 sec in duration
Depth of Q wave must be at least 1/3 of the height of the R-wave in the same QRS complex
Q waves in aVR are NEVER significant - normally has a deep Q wave
ACLS
Goals of ACLS - ACS
Relief of ischemic chest pain
Prevention of MACE (major adverse cardiovascular events
a. Death
b. Nonfatal MI
c. Need for URGENT postinfarction revascularization
Tx of life-threatening complications of ACS
pVT/VF
Symptomatic bradycardia
Unstable tachycardias
ID of pts with STEMI.
Triage for EARLY reperfusion therapy
Drugs
Reperfusion therapy
Mechanical means
Drugs
Four groups of patients
ID of ischemic chest pain
EMS assessment, care, transport
Advise pt to chew aspirin
Maintain
Administer
oxygen
nitroglycerin
MOA
peripheral arterial & venous dilation
Decrease preload
Administration
1 sublingual nitro tab (or spray) Q 3-5 min?
Contra
RV infarction (ST elevation in V1)
RV is very preload sensitive because infarction limits the contractility of the RV. Relies heavily on the filling pressures to maintain CO & BP
Hypotensive patients (sbp < 90 mmHg)
Marked bradycardia (<50 bpm)
Recent phosphodi
Use Cautiously in:
morphine
Obtain 12-lead
Immediate ED assessment and tx
Classification of pts via ST-segment analysis
First 10 minutes:
Check VS (eval O2 sat)
Establish IV access
Take focused hx
General Treatments