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Cardiology (Acute Coronary Syndrome)
Terms in this set (117)
This constitutes a continuum of acute, potentially life-threatening manifestations of coronary artery disease
Acute coronary syndrome
What is included in acute coronary syndrome in progression?
1) Unstable angina (UA) --> progression/worsening of atherosclerotic plaque
2) Non-ST-elevation MI (NSTEMI)-- (typically) subendocardial infarcts
3) ST-elevation MI (STEMI)--> transmural infarcts
What two diagnosis have the same physiologic process and are essentially treated the same?
Unstable angina and NSTEMI
What do both Unstable angina and NSTEMI mean clinically?
partially occlusive coronary artery thrombus
How is NSTEMI distinguished from Unstable Angina?
By the presence of myocardial necrosis
This acute coronary syndrome is is more clearly distinguished by its electrical findings and biochemical markers
What are the two treatment paths?
1) Unstable Angina & NSTEMI
Unstable angina is defined as angina pectoris (or equivalent) with at least one of three features:
1) Occurring at rest (or with minimal exertion) and usually lasting more than 20 minutes (if not interrupted by nitroglycerin),
2) Being severe and described as frank pain and of new onset (i.e., within 1 month), and
3) Occurring with a crescendo pattern (i.e., more severe, prolonged, or frequent than previously)."
Which patient presentation will I see the most?
1) About 25% with STEMI (400,000)
2) About 75% with UA/NSTEMI (1.5 million)
What causes angina?
The formation of an acute thrombus occurs through "interactions among the atherosclerotic plaque, the coronary endothelium, circulating platelets, and the dynamic vasomotor tone of the vessel wall" (p. 158 Lilly)
- More simply, normal humoral (blood) homeostasis is disturbed
What are ALL patients labled as when they walk into the ER until they are worked up?
What is the "classic" presentation of a patient with STEMI?
Diaphoretic older male performing Levine's sign while stating that it feels like an "elephant is on my chest
What type of patient would a "silent" MI occur in?
All patients get thris drug, but we want to know if they are allergic to it first!
If a patient has an acute coronary syndrome but they are Hypotensive, what do you think of?
Right sided heart failure
If a patient has an acute coronary syndrome, but they have tachycardia, would you slow down their HR?
NO! That may be the only thing keeping them alive
Impaired function despite return of adequate blood flow after an ischemic event
Heart tissue that manifests "CHRONIC" ventricular contractile dysfunction in the face of a persistently reduced blood supply, usually because of multivessel CAD
In addition to recognizing the possibility of an acute coronary syndrome in a given patient presenting with an "anginal syndrome," what are two primary decision points that help to determine the further clinical approach?
(1) Estimating the likelihood of a potential Acute Coronary Syndrome (ACS) due to CAD
(2) Determining the short-term risk for death or non-fatal NSTEMI/STEMI
What is risk stratification?
Stress test or other diagnostic testing performed on a patient after he/she has sustained an STEMI who does not undergo invasive assessment as part of initial management in order to obtain prognostic information prior to, or shortly after, hospital discharge
Virtually all patients presenting with a potential ACS require additional objective means of quantifying the likelihood for clinically significant CAD
How is risk stratification accomplished on most patients?
Non-invasive means (i.e. stress test) usually within 24-48 hours of presentation
Low and intermediate risk patients at presentation who are found to have high risk features on non-invasive testing will usually proceed to
For high risk patients at presentation, risk stratification is usually accomplished by
directly proceeding to an early invasive strategy (i.e. cardiac catheterization with potential PCI
Phase 1: How do we Estimate the likelihood of a potential ACS due to CAD (risk level) ?
A history, a quick PE, and EKG and cardiac markers
What is Phase 2 in the evaulation of potential ACS due to CAD?
Determining the short-term risk for death or non-fatal NSTEMI/STEMI
**Approach to a Acute Coronary Syndrome patient Step 1:
Triage-High level, prompt
**Approach to a Acute Coronary Syndrome patient Step 2:
Safety Net - Your initial intervention
- IV access
- O2 (2-4 lpm via nasal canula)
**Approach to a Acute Coronary Syndrome patient Step 3:
Vital Signs with pulse oximetry
**When is aspirin given to a patient?
Upon arrival (Chewed for faster absorption)
If there are no known drug allergies
**How long should it take me to get a patient from the Door to ECG?
< 5 minutes
**How long should it take me to get a patient from the Door to PCI?
< 90 minutes (Early Warning System, EMS Notification, STEMI Alert)
**What drugs should I give when a patient arrives with chest pain?
1) Nitroglycerine SL 0.4mg q 5 minutes
2) Morphine sulfate in 2mg incrememts
Caution or avoid in Right ventricular MI (IWMI) for both drugs
(Remember MONA (Morphine, Oxygen, Nitro, Aspirin)
**When is Nitroglycerine contraindicated?
**Contraindicated with phosphodiasterase inhibitors
**When should Beta Blockers be avoided in the acute MI patient?
Signs of or risk of heart failure
**What labs need to be drawn ASAP when presented with acute coronary syndrome?
Full Cardiac Panel
CBC, CMP, Mag, CA, PT, PTT, INR, Enzymes (CK, CK-MB, Troponin), BNP, D-Dimer, UDS
ABG, Amylase/Lipase, UA w/Cx, Blood Cx), hCG
**What type of imagine is done in acute coronary syndrome?
T or F Up to 40% of ACS patients do NOT have chest pain as chief complaint
Then what is their most common chest complaint?
What is done continuously with an acute coronary syndome when they arrive?
Telemetry (continuous ECG monitoring)
How often is a 12-lead EKG done after admission?
How are serum markers obtained in an acute coronary syndrome patient?
They are usually obtained serially (i.e. every 3-4 hours) with pattern observation
Based upon serum markers, when can we rule out an MI?
A patient with three negative "sets" of cardiac enzymes is often said to have been "ruled out" for MI (at least 12 hours based upon the fact that Im going to do serial enzymes every 3-4 hours )
What are the cardiac markers?
2) CK-MB Isoforms
4) Cardiac Troponin
If a patient has positive MI markers for one acute episode, and then they come back in a couple days later for chest pain you cannot use cardiac markers as a diagnostic tool because the markers will still be elevated from the first MI (they tend to last for approx 7 days). So what the hell should I do?
Invasive method of diagnosis
So let's talk about how we treat the UA/NSTEMI
Remember we said these would both be treated the same.
Acute imbalance of supply vs demand with or without myocardial damage / subendocaridal necrosis
Unstable Angina or
Non-ST Elevation Myocardial Infarction
- This is the first episode of cardiac chest pain or change in pattern of chronic stable angina
- Cardiac chest pain without ST elevation meeting criteria for STEMI
Unstable Angina &
Non-ST Elevation Myocardial Infarction
OK so whats the damn difference between Unstable Angina &
Non-ST Elevation Myocardial Infarction
UA is differentiated from NSTEMI using cardiac enzymes
What are the treatment goals for UA/NSTEMI?
1) Control Symptoms
2) Preserve myocardial function
How do we reach the treatment goals for UA/NSTEMI?
1) Administer analgesia (Morphine, Nitro, Angiolytics)
2) Decrease MVO2 (myocardial demand)
3) Increase coronary flow (Nitro, Aspirin, CCB)
4) Prevent intracoronary thrombosis (Aspirin, Plavix)
5) Prevent long term ischemic event via lifestyle modification
How do we treat Pain / Anxiety in UA/NSTEMI?
What is Anti-ischemic therapy in UA/NSTEMI?
3) Dihydropyridine calcium channel blockers (+/-)
What is "antiplatelet therapy" in UA/NSTEMI?
ASA at least 160mg
What is a drug that can be given to a patient for antiplatelet therapy if there are allergic to Aspirin?
An Adenosine diphosphate inhibitors (antiplatelet)
What is the Adenosine diphosphate inhibitors (antiplatelet) that we use?
What is the initial loading dose of Clopidogrel (Plavix)?
What is the maintenance dose of Clopidogrel (Plavix)?
75 mg daily
What are the IV forms ofr "antiplatelet" drugs that can be given for UA/NSTEMI
GPIIb/IIIa inhibitors (antiplatelet)
When would GPIIb/IIIa inhibitors (antiplatelet) such as Integrelin and Aggrastat be used?
Used for high risk patients and those in whom cardiac catheterization and PCI are planned.
This drug is given for "Anti-thrombotic therapy" in an "inpatient" setting for "STEMI" but the anticoagulation effect stops promptly after the infusion is discontinued
This drug is given for "Anti-thrombotic therapy" for "UA/NSTEMI" and the anticoagulation effect persists for up to 24 hours after the last dose
Low-molecular weight heparin (LMWH
We love this stuff! and guess what, it will be used in 75% of the cases because they are UA/NSTEMI---REMEMBER THIS
T or F. Thrombolytics have no clear survival benefit for patients with UA/NSTEMI
TRUE TRUE TRUE
When are Beta Blockers used in UA/NSTEMI?
Decrease myocardial demand, HR
*Used unless contraindicated
When can Calcium Channel Blockers be used in UA/NSTEMI?
If there is NO HF and preserved LV function
What drug relieves anginal pain?
Do Nitrates have a mortality benefit?
NO! Just increase quality of life
What education/counsleling must all patients get if they have presented with UA/NSTEMI?
Risk Factor modification education
HTN, HLP, Smoking, Obesity
Acute rupture of a atherosclerotic plaque with thrombosis and coronary artery occlusion resulting in myocardial necrosis.
How is a STEMI clinically defined?
1) New ischemic changes on ECG plus
- Ischemic symptoms
- Elevated cardiac enzymes
2) ECG Changes in acute MI
- ST elevation in 2 contiguous leads
- New LBBB (or RBBB)
Lead II, III, aVF
Lead I, V5, V6, aVL
When would you see hyper-acute T waves in a STEMI?
When would you see ST elevation in a STEMI?
When would you see loss of R wave height, development of Q wave, T wave depression in a STEMI?
When would the ST return to baseline in a STEMI?
When would you see normalization of T waves in STEMI?
Days to weeks
What is the general acute "medical management" of a STEMI?
5) Beta Blockers
In the presence of RVH, do not use
What are the initial goals for STEMI?
1) Relieve ischemic pain (nitro, morphine, O2)
2) Assess hemodynamic state and correct abnormalities
- Fluid, Inotropes, Pressors
3) Correct dysrhythmias
4) Antithrombotic therapy
What is the treatment of choice for ALL STEMIs?
Percutaneous Coronary Intervention (PCI)
is our treatment of choice in all STEMI's unless you cannot get access to a cath lab in the appropriate amount of time, then fibrinolytics as your only option becomes the treatment of choice.
if I cannot get a patient to the ER and on the table in 90 minutes. If a patient has a 5 day hx of chest pain, is Percutaneous Coronary Intervention (PCI) my intervention of choice?
PCI trumps Fibrinolytics in nearly all clinical situations involving STEMI but may be limited by immediate availability or transfer time. PCI improves mortality and superior to fibrinolysis if:
1) <90 minutes door to catheterization
2) <12 hours since onset of symptoms
3) Decreased intracranial hemorrhage
4) Decreased recurrent MI
Do not give nitrates for
RV wall or inferior MI / Hypotensive patient (II, III, aVF)
What are the fibrinolytic agents?
1) Recombinant tissue-type plasminogen activator (tPA - Alteplase)
2) Tenecteplase (TnKa)
What is imperative to do if we are going to adminster fibrinolytics?
The use of Fibrinolytics requires careful patient selection and consent
Counsel the patient on bleeding risk
What are the ABSOLUTE contraindications for Thrombolysis in acute MI
1) Active internal bleeding (exculding menses)
2) Suspected aortic dissection
3) Prior hemorrhagic stroke at any time; other stroke within the last 3 months
4) Known intracranial neoplasm or vascular lesion
5) Significant head trauma within the last 3 months
What is the bottom damn line for CABG
No patient goes directly to CABG without a cardiac catheterization first!!!!!
Ok Ok Ok.....Here it is pimp...... the difference in treatment of UA/NSTEMI vs STEMI
Ev-Erebody Gets the following
1) Anti-ischemic medication
- Beta Blockers
- +/- CCB
2) General Measures
- Pain control
3) Additional therapies
- ACE inhibitor
UA/NSTEMI takes the "antithromotic approach"?Remeber LMWH (For high risk patients use GP IIb/IIIa inhibitor and proceed with cardiac catheter)
STEMI takes the "reperfusion approach"
Choose the reperfusion method
Primary PCI (with GP IIb/IIIa inhibitor)
- Fibrinolytic drug
What is the long term management and secondary prevention of a STEMI with "Ant-iplatelet"?
1) Aspirin 81mg QD
2) Consider Clopidrogel 75mg QD
What is the long term management and secondary prevention of a STEMI with "Anti-Coagulation"?
Warfarin (target INR 2.0-3.0)
- Large anterior wall MI
- LV Aneurysm
- LV Thrombus
What is the long term management and secondary prevention of a STEMI with "ACE-I"?
1) Decreases mortality
2) Asymptomatic patients even with EF > 40%
3) All CHF
4) Reduced EF (<40%)
5) Anterior wall MI
6) ARB in patients who can not tolerate ACE I
What is the long term management and secondary prevention of a STEMI with "Beta-Blockers"?
1) Within 24 hours
2) Remember contraindications
What is the long term management and secondary prevention of a STEMI with "CCB"?
What is the long term management and secondary prevention of a STEMI with "Aldosterone Antagonists"?
For Heart failure
What is the long term management and secondary prevention of a STEMI with "Nitrates"?
1) No mortality benefit
2) Symptom relief
What is the long term management and secondary prevention of a STEMI with "Statins"?
1) Risk stratification
2) Regardless of lipid levels
3) **High dose atorvastatin
What is the long term management and secondary prevention of a STEMI with "NSAIDs"?
What is the long term management and secondary prevention of a STEMI with "Echo"?
ECHO prior to discharge to assess LV function
- Prognostic indicator
Low likelihood & low risk =
Intermediate likelihood & low risk =
outpatient evaluation versus inpatient admission with telemetry (i.e. 24-hour chest pain unit)
Intermediate likelihood & intermediate risk =
inpatient admission with telemetry
Intermediate or high likelihood & high risk
Cardiac care unit (CCU)
I don't give a damn whats going on. If my patient has the following, he is getting admitted
1) Continuous chest pain
2) Positive serum markers
3) Significant, new ST segment abnormalities
4) New, deep T-wave inversions ("Wellens" T-waves)
5) Significant hemodynamic abnormalities, especially hypotension
6) "High risk" stress test results (+/-)
What clincal finding is the MOST useful prognostic indicator?
Resting Left Ventricular Ejection Fraction
I counseled patients on a bunch of things post discharge, but what will I tell them all
Smoking cessation advice or counseling if they smoke**
After I diagnose STEMI and OMI (oxygen, monitor, IV) and MONA have been given what must I do next?
With reperfusion therapy, the best way to reperfuse is
If PCI is not available within 90 minutes, what should I do?
Transfer to a PCI facility (if I can get them there in 90 min)
If thrombolysis is unsucessful then what?
Consider transfer for resuce PCI
If thrombolysis is sucessful then what?
1) Maximize medications
2) Risk Stratification
3) Risk factor modification
What are the four "post discharge complication" categories?
1. Heart Failure (common post discharge)
2. Cardiogenic Shock (most common cause of acute MI-related-in-hospital deaths)
4. Mechanical Complications
This is a post discharge complication that is defined as an Inflammatory process that can occur 1-7 days later
How do we treat the post discharge pericarditis?
Tx with ASA
** - remember NSAIDS increase mortality
This is a post discharge complication that is defined as an autoimmune process that can occur 2-8 weeks later
How is Dressler's Syndrome treated?
Tx with ASA
** - remember NSAIDS increase mortality
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