Acute Coronary Syndrome (ACS) Flashcards
ACS continuum
ACS -> 1. unstable angina or 2. acute MI
ECG changes (ST elevation) present -> elevated troponin = STEMI
ECG changes absent (no ST elevation) -> elevated troponin -> NSTEMI (heart damage present)
ECG changes absent -> normal troponin -> unstable angina (no heart damage)
Unstable angina facts
- Often occurs at rest-usually more than 20 minutes duration
- New-onset that markedly limits physical activity
- Increasing angina more frequent, longer in duration, and occurs with less exertion than stable/previous angina
- Poorly relieve by rest or nitroglycerin
- May have associated symptoms
- Unpredictable and is an emergency
- No elevations in serum troponin
Women and atypical angina s/s
Fatigue (most prominent)
SOA
Indigestion
Anxiety
Anginal pain
Precipitated by exertion/stress
Relieved by rest/nitroglycerin
Lasts < 15 minutes
MI pain
Occurs without cause, often in early morning
Relieved only by opioids
Last 20 minutes or longer
Frequently presents with associated symptoms (n/v, diaphoresis, dyspnea, anxiety/fear, dysrhythmias)
MI facts
Process takes time (cells can stand ischemia x 20 minutes before cell death)
Subendocardium layer affected earliest (takes 4-6 hours for entire thickness of heart muscle to necrose)
The location correlates with the involved coronary circulation (i.e., blockage in the left anterior descending coronary artery causes damage to the left ventricle)
MIs are described based on location of damage (anterior, inferior, lateral, septal or posterior)
What does MI Pain feel like?
Severe, immobilizing chest pain not relieved by rest, position changes, or nitrates (hallmark of MI)
Persistent & described as heaviness, pressure, tightness, burning, constriction, and crushing
Women/patients with diabetes mellitus may have different or no symptoms (silent MI)
Complications of MI
- Dysrhythmias (most common complication; most common cause of pre-hospital death; reason patients must be on telemetry)
- Heart failure (occurs from the reduced pumping action of heart; occurs esp. with damage to the left ventricle)
- Cardiogenic shock (low BP/decreased perfusion due to severe left-ventricular failure; if occurs, high mortality rate)
- Papillary muscle dysfunction (consequence: new murmur noted)
- Pericarditis (occurs 2-3 days after acute MI; consequence: new pericardial friction rub)
Pericardial friction rub
High-pitched, scratchy grating sound heard best with the patient sitting and leaning forward and while holding their breath at end of expiration; indicative of pericarditis; caused by friction between the inflamed pericardial surfaces
How can you differentiate between pericardial friction rub (heart) and a pleural friction rub (lungs)?
Have patient hold their breath. If you still hear the rub, it is cardiac.
Diagnostic testing for ACS: EKG
Used to r/o or confirm unstable angina/MI
Look for changes in the QRS complex, ST segment & T wave
STEMI = “ST Elevated Myocardial Infarction” NSTEMI = “Non-ST Elevated Myocardial Infarction”
STEMI – more extensive infarct
NSTEMI or UA = transient thrombosis/incomplete
occlusion
Serial EKGs may be ordered, as ischemia & infarction can change over a matter of a few hours
ST elevation vs. depression in relation to the isoelectric line on an EKG
Normal: ST segment along the isoelectric line
ST elevation: ST segment above the isoelectric line
ST depression: ST segment below the isoelectric line
Ischemia vs infarction
Ischemia: reduced (but not obstructed) blood flow
Infarction: obstructed blood supply causing local tissue death
ST elevation vs depression
ST elevation occurs with infarction (this is permanent)
ST depression occurs with ischemia
Diagnostic testing for ACS: serum cardiac markers
Serum troponin has greater sensitivity & specificity than CK-MB & myoglobin. Troponin increases in 2-3 hrs, returns to baseline in 10-14 days.
STEMI
- ST segment elevation
- QRS usually pathologic (wide)/develops over hours
- T wave peaked, then inverted
- Troponin elevated
- Size of infarct larger
- Poor outcomes
NSTEMI
- ST segment depressed or normal
- QRS normal
- T wave inverted
- Troponin elevated
- Size of infarct smaller
- Better outcomes
Progression of an acute MI
Ischemia (lack of O2 to cardiac tissue represented by ST depression, T wave inversion or both) -> injury -> infarction (death of tissue represented by a pathological Q wave)
ACS initial assessment
Consider diagnosis w/ chest discomfort, SOA or other suggestive symptoms; women, older patients & patients with DM may have atypical presentations.
12-lead EKG within 10 minutes of arrival (repeat every 10-15 mins if non-diagnostic, but suspicion remains)
STEMI EKG
STEMI = ST segment elevation in two anatomically contiguous leads
NSTEMI or unstable angina EKG
NSTEMI or UA = ST depressions or deep T wave inversions without Q waves or possibly no EKG changes
ACS initial interventions
Assess/stabilize ABCs
Position patient upright to support oxygenation
Administer oxygen (NC initially)
Obtain V.S., including O² sat
Attach cardiac monitor (continuous telemetry)
Monitoring for dysrhythmias & ST changes
Establish IV access
More ACS initial interventions
Give ASA 325 (chew/swallow)
Assess pain using PQRST
For pain:
- Give 3 SL NTG (0.4 mg) one at a time, spaced 5 minutes apart for persistent chest pain (monitor BP)
- Give morphine sulfate (2-4 mg IVP q 5-15 mins) for unacceptable, persistent discomfort
Obtain baseline lab work (cardiac markers, electrolytes esp. K, Ca, and Mg, H&H; possibly coags)
Monitor heart (murmur, gallop or rubs?) & lung sounds (crackles may be heard with left HF from left ventricle infarction)
What may patients need instead of nitroglycerin if their BP is too low?
Morphine; morphine eases the workload on the heart (decreases preload and afterload) and also decreases anxiety
What is nitroglycerin?
A potent coronary vasodilator
PQRST assessment of angina
Precipitating events
(What precipitated?)
Quality of pain
(Feel like? Ache? Squeeze? etc)
Radiation of pain
(Where is the pain?)
Severity of pain
(1-10 scale)
Timing
(When did it begin?)
Three reperfusion strategies for a blockage
- Emergent percutaneous coronary intervention (PCI)-for STEMI or NSTEMI
- Thrombolytic (fibrinolytic) therapy-for STEMI
- Coronary artery bypass graft (CABG)-for patients with DM, 3 or more-vessel disease, or when blockage unreachable by catheter
Percutaneous Coronary Intervention (PCI)
First-line of treatment for patients with confirmed MI
Goal: open within 90 minutes of ED arrival
First must perform a cardiac cath to locate blockage(s), assess the severity of blockage(s), determine the presence of collateral circulation (compensatory/alternate circulation around a blockage), and evaluate left ventricular function
Which location for heart cath is required to assess the coronary arteries?
LEFT heart cath
Percutaneous coronary intervention (aka angioplasty or balloon procedure) steps
LEFT cardiac cath –> blockage located –> deflated balloon catheter placed at the occlusion site in the coronary artery –> balloon inflated –> plaque flattened –> patency of coronary artery reestablished
PCI: advantages
Alternative to surgical intervention
Performed with local anesthesia rather than general anesthesia
Patient is ambulatory shortly after procedure
Length of hospital stay = 1-3 days (4-6 days with CABG)
Can return to work sooner
Currently, more PCIs are performed than CABGs.
PCI: Nursing Care
Similar to cardiac cath; monitor closely for manifestations of myocardial ischemia, such as chest pain/EKG changes, dysrhythmias or hemodynamic instability
Patient typically on dual antiplatelet therapy (ASA & heparin, for instance)
Vascular sheath removal usually 4-6 hours after procedure (manual pressure x 20 minutes esp. if arterial puncture); check site & distal circulation.
Thrombolytic therapy
AKA clot blusters
Fibrinolytics used to dissolve thrombi in coronary arteries- restores myocardial blood flow
May be administered during cardiac catheterization
Most effective when administered within 6 hours of coronary event
Goal: start within 30 minutes of ED admission
Important: Monitor for BLEEDING post-administration
Examples of fibrinolytics/clot busters
Tissue Plasminogen Activator (t-PA)
Reteplase (Retavase)
Thrombolytic therapy contraindications
History of intracranial hemorrhage
Recent abdominal surgery or stroke
Any active bleeding (excluding menses)
Reasons for coronary artery bypass graft (CABG)
Elective vs emergency
CABG procedure
Graft anastomosed distal and proximal to blockage to bypass it
CABG grafts options
May involve grafts using the internal mammary artery or a harvested saphenous vein
CABG complications
Stroke
Myocardial infarction
Infection (sternal wound, vein harvest sites)
Dysrhythmias
Pleural effusion
Pericardial effusion
Cardiac tamponade (fluid accumulation in the pericardium)
Renal failure
ACS ongoing care
Continuous monitoring with telemetry
Rest & comfort-activity restrictions
Help examine source of anxiety & address
For anxiety teach at patient’s level-not from pre-packaged program
Help deal with emotional and behavioral reactions
Patient teaching – timing is important; start where the patient “is”
Teaching regarding resumption of sexual activity
ACS going home
Refer to “Cardiac Rehabilitation” program in community:
Physiologic
Psychological
Mental
Spiritual
Economic
Vocational
