ACS Flashcards
ACS Algorithm?
- Recognize symptoms suggestive of ischemia or infarction
- EMS assessment and care and hospital preparation:
- Monitor and support ABCs. Be prepared to provide CPR and defibrillation.
- Administer ASA (chew 160-325 mg non-enteric-coated ASA, unless allergy or recent/history of GI bleeding, or if already taken that day; can use rectal suppository 300 mg if N/V, active PUD, other upper GI tract disease) + O2, nitroglycerin, and morphine if needed
- Obtain 12-lead EKG. If STEMI, notify receiving hospital (include time of onset and first medical contact)
- Notified hospital should mobilize resources to respond to STEMI
- If considering prehospital fibrinolysis, use fibrinolytic checklist - Concurrent ED assessment (<10 minutes)
- Vitals, evaluate O2; if <90%, start O2 at 4 L/min, titrate
- Establish IV access
- Brief, targeted H&P
- Review/complete fibrinolytic checklist; check contraindications
- Obtain initial cardiac marker levels, lytes, and coags
- Obtain portable CXR (<30 minutes)
- Give ASA if not given by EMS, nitroglycerin sublingual or spray (1 dose every 3-5 minutes up to 3 doses, ensure no contraindications such as severe bradycardia, tachycardia, hypotension, PDE inhibitor use in the past 24-48 hours), morphine IV if discomfort not relieved by nitroglycerin (use w/caution if unstable angina) - EKG interpretation
A - if ST elevation or new/presumed new LBBB, strong suspicion for STEMI -> start adjunctive therapies as indicated, but do not delay reperfusion
B - if ST depression or dynamic T-wave inversion, strong suspicion for ischemia/high-risk non-ST elevation ACS, and patient is high-risk or has troponin elevation, consider early invasive strategy if refractory ischemic chest discomfort, recurrent/persistent ST deviation, VTach, hemodynamic instability, signs of heart failure; start adjunctive therapy as indicated
C - normal or nondiagnostic changes in ST segment or T wave, low-intermediate risk ACS -> consider admission to ED chest pain unit or appropriate bed for further monitoring, possible intervention - For STEMI - if time from onset of symptoms is 12 hours of less, proceed w/reperfusion - door-to-balloon inflation goal of 90 minutes or door-to-needle goal of 3.0 minutes. If >12 hours, proceed to 4B
How can you identify a RV infarction on EKG? Clinically?
Often present as inferior wall STEMIs
Confirm with R-sided 12-lead EKG
Hypotension, clear lungs, elevated JVP
Adjunctive treatments in ACS?
Unfractionated or LMWH Bivalirudin P2Y12 inhibitors IV nitroglycerin Beta-blockers Glycoprotein IIb/IIIa inhibitors
True or false - elevated cardiac markers are required to proceed with fibrinolytics or angioplasty/stenting in STEMI patients.
False - not required
Symptoms suggestive of ischemic chest discomfort
Most common - retrosternal chest discomfort/pressure/tightness
Uncomfortable pressure, fullness, squeezing, or pain in the center of the chest last several minutes
Chest discomfort spreading to the shoulders, neck, one or both arms, or jaw
Chest discomfort spreading into the back or between the shoulder blades
Chest discomfort with light-headedness, dizziness, fainting, sweating, N/V
Unexplained sudden dyspnea +/- chest discomfort
What lethal mimics should always be considered when suspecting ACS?
Aortic dissection, acute PE, acute pericardial effusion w/tamponade, and tension pneumothorax
Why is O2 beneficial in ACS?
High inspired-oxygen tension will tend to maximize arterial oxygen saturation and, in turn, arterial oxygen content. This helps support O2 delivery (CO x arterial O2 content) when CO is limited. This short-term oxygen therapy does not produce toxicity. However, its usefulness in normoxic patients has not been established
When should O2 be administered by EMS in the setting of suspected ACS? What should it be titrated to?
If the patient is dyspneic, hypoxemic, has obvious signs of heart failure, has O2 <90%, or unknown O2 saturation
O2 90+%
MOA ASA?
Immediate and near-total inhibition of thromboxane A2 production by inhibition of platelet cyclooxgenase (COX-1) - useful because platelets are on of the principal and earliest participants in thrombus formation. This rapid inhibition also reduces coronary reocclusion and other recurrent events independently and after fibrinolytics
MOA nitroglycerin?
Reduces ischemic chest discomfort + beneficial hemodynamic effects (reduction in LV and RV preload through peripheral arterial and venous dilation)
When is nitroglycerin contraindicated?
Hemodynamic instability (SBP <90 or no lower than 30 below baseline if known, HR <50 or >100)
Use cautiously or not at all in patients with inadequate preload, including - inferior wall MI and RV infarction, recent PDE inhibitor use (sildenafil or vardenafil w/in 24 hours, tadalafil w/in 48 hours)
When to suspect/confirm RV infarction?
Suspect if inferior STEMI, confirm w/R-sided EKG or clinical findings
When should morphine be used with caution in NSTE-ACS?
Associated w/increased mortality
MOA of morphine?
Produces CNS analgesia, which reduces the adverse effects of neurohumoral activation, catecholamine release, and heightened myocardial O2 demand
Produces venodilation (reduces LV preload and O2 requirements)
Decreases SVR, reducing LV afterload
Helps redistribute blood volume in patients w/acute pulmonary edema
True or false - pain relief w/nitroglycerin is diagnostic of ACS
False - chest pain of various kinds can respond to nitroglycerin