Emergency Medicine 2: Acute Coronary Syndrome Flashcards
Myocardial ischemia is due to ..
Reduced myocardial blood flow.
This is caused by arterial spasm, disruption of atherosclerotic plaques, and platelet aggregation/thrombus formation
stable angina
Ischemia occurs only when activity increases oxygen demand beyond the supply restrictions of a partially occluded coronary vessel
Unstable angina
The patient now has chest pain at rest or with minimal activity
The pain pattern is increasing in frequency, severity, and duration
Reversible myocardial ischemia without injury develops as a result of plaque rupture and thrombus development
Acute Myocardial Infarction
There is irreversible damage to the myocardium secondary to the ischemia
Myocardium supplied by the LAD
Anterior wall of left ventricle
Most of interventricular septum
Some of lateral wall of left ventricle
Conductions system supplied by LAD
Most of right bundle branch
Anterior fascicle of left bundle branch
Part of posterior fascicle of left bundle branch
Myocardium supplied by Left Circumflex
Left atrium
Most of lateral wall of left ventricle
Posterior wall of left ventricle (in about 15% of population)
Inferior wall of left ventricle (in about 10% of population)
Inferior third of the interventricular septum (in about 10% of population)
Conduction system supplied by the Left Circumflex
SA node (in about 40% of population) AV node (in 10 to 15% of population)
Myocardium supplied by Right Coronary
Right atrium
Right ventricle
Inferior wall of left ventricle (in about 90% of population)
Inferior third of the interventricular septum (in about 90% of population)
Posterior wall of left ventricle (in about 85% of population)
Conduction system supplied by Right Coronary
AV node (in 85 to 90% of population)
SA node (in about 60% of population)
Proximal portion of bundle of His
Part of posterior fascicle of left bundle branch
Risk factors for CAD
> 40 yo
Male or postmenopausal female
Estrogen may be cardio-protective
Hypertension
Cigarette smoking
Hypercholesterolemia
Diabetes
Truncal obesity
Family history
Sedentary lifestyle
*Cocaine
How does cocaine affect the heart
Causes coronary artery vasoconstriction, tachycardia, systemic arterial hypertension, increased myocardial oxygen demand, platelet aggregation, and thrombus formation
Symptoms are often atypical
Can occur after only small amounts of cocaine
Approximately 6% sustain AMI
20 to 60% suffer transient myocardial ischemia
What does routing history determine in regards to chest pain ?
quality, location, radiation, intensity, frequency, associated symptoms, and precipitating factors
Classic angina presentation
is retrosternal left anterior chest/epigastric discomfort consisting of crushing, tightening, squeezing, or pressure
Is prognosis better or worse in atypical patients ? What demographics typically present atypically ?
Worse, due to difficulty in diagnosis.
Women and elderly
Angina (duration)
15-20 mins
Chest pain that lasts for only a few seconds is more likely due to another cause; as is constant, unremitting pain that lasts 12 to 24 hours without EKG changes
What is the response of angina to nitroglycerin ?
Usually improves within 2 to 5 minutes after rest or nitroglycerin
DDx fo Chest pain includes…
Pulmonary embolism (PE) Aortic dissection Pneumothorax Pericarditis Pneumonia Esophagitis/gastritis/cholecystitis Musculoskeletal
What must be done when a patient presents to the ED with chest pain ?
placed on a cardiac monitor, have IV access, oxygen by nasal cannula, vital signs measured immediately, and portable chest x-ray ordered]]
A 12-lead EKG should be performed within 10 minutes of arrival and handed directly to the treating physician for immediate review
what should ED EKG’s be compared with when available ?
Old EKG’s !
Only about 50% of patients with AMI present with diagnostic changes on the initial EKG
What does ST segment elevation suggest ?
suggests acute transmural injury
What does ST depression indicate ?
ST-segment depression suggests subendocardial ischemia (non Q-wave MI)
Reciprocol ST segment changes indicate ?
Reciprocal ST-segment changes predict a larger infarct distribution, increased severity of underlying CAD, more severe pump failure, a higher likelihood of complications, and
Inferior leads
II,III, aVF
Lateral Leads
I, aVL, V5, V6
Septal leads
V1, V2
Anterior Leads
V3, V4
RIght Ventricle Leads
V4 placed on right side of chess
Tachycardia in relation to ACS is may be due to
increased sympathetic tone or decreased left ventricular stroke volume
Bradycardia in relation to ACS may be due to
to inferior wall ischemia
WHat are rales, crackles indicative of on lung ausculation in relation to ACS ?
Congestive Heart Failure.
The presence of jugular venous distention (JVD) or peripheral edema may suggest
RIght Sided heart failure
Reproducible chest pain MAY be indicative of ?
MSK cause
Do not rule out MI because of this though
MONA B (Initiated in all patients with possible ACS
Morphine Oxygen Nitrates Aspirin Beta-Blockers
What may be a benefit of administering O2 ? (this can be seen on EKG*)
Reduces the amount of ST elevation by limiting the amount of ischemic myocardial injury
Dosing rate for 02 ?
4L /min
What does Aspirin inhibit ?
Thromboxane A2 production and Platelet cycle-oxygenase –> inhibition of coronary artery re-occlusion
Normally, nitrates are given sublingually 0.4 mg, which can be repeated X 2 at 5 minute . What can you do if patient is not pain free after admin in traditional manner ?
Infusion of nitrates at 10 mcg/minute
At what BP would you not administer Nitro ?
systolic blood pressure is < 90 mm Hg
Also do not give in severe bradycardia or RV infarction
With what other meds should nitro be avoided ?
Viagara (within 24 hrs) or other PDEF inhibitors (anything that would increase vasodilation)
Would you give Morphine in a right sided heart disease (infarction) ?
No, it is a venodilator and will decrease right sided preload. (will also decrease after load)
What co-morbidities would you avoid use of morphine with ?
hypersensitivity, hypotension, or respiratory depression
In which patients should you exercise caution with when administering Beta Blockers ?
Patients with LV failure or severe COPD/asthma
LV failure requires high inotropic effect to move blood
COPD and asthma may be worsened due to unspecific B2 blockade.
What is the EKG criteria needed to be a candidate for reperfusion therapy ?
ST-segment elevation > 1 mm in two or more contiguous EKG leads or a new LBBB
Unstable angina, especially in patients with recurrent ischemia, depressed LV function, widespread EKG changes, or prior MI
Indications for fibrinolytic therapy
Chest pain suggesting AMI
ST-segment elevation > 1 mm in two or more contiguous EKG leads or a new LBBB
Time to therapy < 12 hours
Age < 75 years
Absolute Contraindications to fibrinolytic therapy
Previous hemorrhagic stroke Other stroke within one year Active internal bleeding (excluding menses) Suspected aortic dissection Arteriovenous malformation Cerebral malignancy
Cautionary co-morbidities when using fibrinolytic therapy include :
Severe uncontrolled hypertension (BP >180/110)
Current use of anticoagulants (INR > 2.5)
Known bleeding disorder
Recent trauma or major surgery within 2 - 4 weeks
Recent internal bleeding within 2 - 4 weeks
Pregnancy
What is the goal time for getting a patient catheterized for PCI ?
Door to balloon intervention time < 90mins
What patients will receive the most benefit from Percutaneous Coronary Intervention ?
Patients in cardiogenic shock
For patients with contraindications to fibrinolytic therapy
Unfractionated Heparin directly inhibits which molecule ?
thrombin
Why is UFH used as an adjunct therapy to fibrinolytic and PCI therapies ?
To inhibit re-occlusion
In unstable angina with ST depression, UFH can be given with what other drug as treatment ?
Aspirin
What must be monitored with UFH ?
aPTT
Is LMWH useful in Non Q-wave MI ?
Yes !
Also, useful in angina
Like UFH, LWMH inhibits thrombin. What does not need to be done in with LWMH that is needed with use of UFH ?
Monitoring via aPPT.
How is LWMH administered ?
Sub Q (1mg/kg BID)
Like LWMH, Glycoprotein IIB/IIIA inhibitors are useful in
Non-Q wave MI and unstable Angina
Can you use GP IIB/IIIA inhibitors in conjunction with ASA and heparin ?
YES ! This is actually a very good regimen.
Contraindications for GP IIA/IIIB inhibitors
Active internal bleeding or bleeding disorder in the past 30 days
History of intracranial hemorrhage, neoplasm, arteriovenous malformation, aneurysm, or stroke within 30 days
Major surgical procedure or trauma within one month
Aortic dissection, pericarditis, or severe hypertension
Platelet count < 150,000
When does Myoglobin double in the blood ? Peaks ? Is it a good marker
2x in 2 hours, peaks in 4 hours
Not really
When does CK-MB peak in the blood ?
within 24 hrs
What conditions other than MI can present with elevated CK-MB ?
elevated levels are also seen in patients with skeletal muscle disease, acute muscle exertion, chronic renal failure, and cocaine use
Is Troponin I found in skeletal muscle ?
No, it is not. Unlike with CK-MB
Describe the chronology of Troponin I elevation, peak and prolongation
Elevation 6 hours post MI, peak at 12 hrs post MI and remain elevated 7-10 days
What makes Troponin I the main marker tested for ?
It is the most specific and can be tested at bedside !
The only disadvantage for this marker is that due to it prolonged elevation it is difficult to test for re-infarction
Who gets put into a Cardiac Care Unit ?
Positive myocardial infarction S/P fibrinolytic therapy or PCI Ongoing ischemia Unstable angina Unstable vital signs *High-dose antianginal medication
Which patients will often be put into a step-down unit ?
Prior history of CAD
CHF
Recurrent chest pain in the ED
New EKG changes
Telemetry floors are appropriate for which patients ?
patients with very low risk of adverse events and no EKG changes
