ACS Flashcards
What are the signs and symptoms of acute coronary syndrome?
CV: Palpitations, tachycardia or bradycardia, abnormal BP, weakened/irregular pulse, pericardial friction rub
Pulmonary: Dry cough, SOB, Crackles, JVD, dyspnea, hypoxia
GI: N/V
Neurologic: weakness, cold perspiration, anxiety, restlessness, sense of doom, decreased LOC, unexplained fatigue
Right Coronary artery
- Feeds the RA (SA & AV nodes)
- Feeds RV and inferior LV
If occluded, an inferior wall MI of the LV will occur or a RV MI will occur
Left anterior descending artery (LAD)
- Feeds the anterior wall of LV and the RV
- Feeds the apical wall and anterior 2/3 of septum (Bundle of His)
Occlusion of this artery will cause Anterior wall MI, Septal wall MI (during a bundle block)
Left main coronary artery
Feeds the lateral wall and posterior wall (via the OM)
Occlusion will cause lateral wall MI and/or posterior wall MI
-clot in the left main stops blood flow to the LV, LA, RV
Acute coronary syndrome
Spectrum of acute myocardial ischemia and/or infarction- a continuum with differing severity
Includes:
- Unstable angina (UA)
- Non-ST elevation Myocardial Infarction (NSTEMI)
-ST Elevation Myocardial Infarction (STEMI)
*these three are indistinguishable based on s/s
How is chest pain from ACS different from chronic angina?
New-onset angina or rest angina not relieved by NTG or rest; lasts >20min; occurs while at rest or sleeping
Accelerating angina: more severe, prolonged, or easily provoked (worse than baseline)
*chest pain that lasts more than 15-20min and doesn’t improve is an indicative sign of ACS
ACS clinical presentation in women
Fatigue and sleepiness
Dizzy/faint
Hot, flushed,
Numbness in hands or fingers
Pain may be in high chest, throat/jaw, top of shoulders, left breast, between shoulder blades
How does a coronary artery plaque cause an MI?
When the plaque ruptures, platelets and T cells release creating a thrombus on the pre-existing plaque
Vasoconstriction
- to stop platelets form forming, aspirin is used
What causes a coronary artery plaque to rupture?
Inflammation or infection: arterial narrowing causes plaque destabilization or rupture and thrombus formation
Mechanical obstruction: Progressive atherosclerosis after PCI d/t clot formation
Dynamic obstruction: coronary spasm or vasoconstriction
Secondary: underlying CAD and increased myocardial O2 demand (fever, tachycardia, etc.) or decreased supply (hypotension, hypoxemia, anemia)
Why do some patients wake up with chest pain?
Circadian rhythm!
- physical, mental, and behavioral changes follow roughly a 24-hour cycle
-people are hypercoagulable between 0600-1200
What does Lead I view?
Lateral wall of the LV
What does lead II view?
Inferior wall of the LV
-used most for monitoring heart activity
-RCA is involved with SA node
What does lead III view?
Inferior wall of the LV
-straight up towards the left shoulder
What does lead avL view?
Inferior wall of the LV
What does lead avF view?
Lateral wall of the LV
-circumflex is the artery involved
On what layer of the heart do the coronary arteries sit?
On top of the epicardial surface of the heart; branches will go in deeper.
What is a transmural MI?
Transmural = full thickness MI; takes hours (from onset) to evolve
What are the three zones of injury in a transmural MI?
Zone of ischemia
- cells can be reversed with intervention
Zone of injury
- cells can be saved, but will never return to 100% normal function
Zone of necrosis
-Cells cannot be revived; will be replaced with fibrous tissue
What factors determine which type of ACS occurs?
How much occlusion is produced by the thrombus plaque
How long the occlusion lasts
Upon arriving to the ED with positive ACS signs, how long does the nurse have to obtain an ECG on the patient?
Must obtain an ECG within 10 minutes of presentation to ED
What type of ECG is seen with myocardial ischemia?
T wave inversion and/or ST depression
What type of ECG is seen with myocardial injury?
ST wave elevation
-injury must be full thickness for ST elevation to occur
What type of ECG occurs with myocardial Infarction (necrosis)?
Q wave
What is unstable angina?
Flow is restricted enough to produce symptomatic ischemia, but no cell injury
-occurs when a plaque is disrupted and a thrombus forms, but it is non-occlusive
Pt will have same symptoms as someone with an MI
-t wave inversion and/or ST depression
-cardiac markers will be normal
What is an NSTEMI?
Non-ST Elevation MI: ischemia with non-transmural cell death
Ischemia is severe enough to cause non-transmural necrosis
-occurs when the thrombus is non-occlusive or only transiently occlusive, but plot aggregates and portions of the disrupted plaque microembolize downstream
-T wave inversion and/or ST depression
-cardiac markers will be elevated (only thing that differentiates unstable angina from NSTEMI)
What is a STEMI?
ST Segment Elevation MI: Transmural cell necrosis
-occurs when a thrombus on a disrupted atherosclerotic plaque is totally occlusive and persistent
ST elevation= indication of COMPLETE coronary occlusion producing transmural injury
-cardiac markers are elevated
What are the cardiac serum biomarkers and when is each elevated?
Troponin I: Rises 4-6hours after event, peaks at 10-24hours and returns to normal after 4 days
Troponin T: Rises 4-6hours after event, peaks at 10-24hours, returns to normal after 10 days
CK-MB: Rises within 4 hours, peaks at 18-24hours, and returns to normal in 2-3 days
What are the main therapeutic goals for treating ACS?
- Increase coronary blood supply & restore blood flow
— Antiplatelet therapy
—anticoagulant therapy
— Anti-ischemic therapy: Nitrates
— for STEMI: revascularize via PCI or fibrinolytics - Decrease Myocardial O2 demand by decreasing workload
—BB, pain relief, nitrates
Want to increase O2 supply and decrease demand
What is the order of actions to treat a patient presenting with unstable angina or NSTEMI?
- 12 lead ECG
- Initiate anti-ischemic treatment
—O2, NTG to vasodilate, Morphine sulfate for symptoms not relieved by NTG - Antiplatelet treatment (need aspirin and one other)
—aspirin continued indefinitely
—P2Y inhibitor (clopidogrel or ticagrelor >12 months) or GP IIb/IIIa inhibitor if high risk or PCI - Anticoagulants
—Unfractionated heparin, enoxaparin, bivalirudin, fondarparinux
NO NSAIDS FOR LIFE
What is the protocol for treating a STEMI patient?
*TOTAL ISCHEMIC TIME WITHIN 120 MIN
- Initial anti-ischemic treatment
—O2, NTG, MS
2.Reperfusion treatment: PCI** (within 90-120min) or Fibrinolytics
- Immediate Antiplatelet treatment
—ASA (continued indefinitely), P2Y, GP IIb/IIIa inhibitor (if PCI) - Anticoagulant treatment
—heparin or alternative
continuous treatment: BB within 24 hours continued indefinitely, ACEI within 24 hours, Statin continued indefinitely
Percutaneous coronary intervention (PCI) in STEMI
Angioplasty with stent within 12hrs of symptom onset
-preferred method unless there’s too much time delay (must be within 120 minutes)j
—FMC (first medical contact) to device= 90min or less. ***
When is fibrinolytic therapy used in STEMI patients?
Only used if PCI is not available or cannot perform PCI in time
**door to drug time: <30 min
What are complications of AMI?
ALL dysrhythmias- especially ventricular
Recurrent ischemia- must monitor for ST or T wave changes
—>50% of patients don’t have chest pain as a s/s
Anterior wall:
- mobitz type II & 3rd AV block
- LV dysfunction/HF
- Cardiogenic chok
What are inferior wall complications associated with AMI?
Inferior wall:
- bradycardia
- 1st degree & Mobitz type I AV block
-Hypotension
- RV dysfunction
- Psuedoaneurysm
What are the mechanical complications associated with MI?
- emergency mitral valve replacement
-psuedoanuerysm
-Free wall rupture
-Ventricular septal defect
Patient/family education if they have early signs of MI
Take 1 NTG, if not improved or worsens within 5 min, call 911 and chew one non-enteric coasted ASA
