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Objectives Identify early signs and symptoms of Acute Coronary

Syndrome

Initiate proper protocol for ACS patient

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Purpose of this Education Module:

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Chest Pain Center Accreditation involves the management of chest pain anywhere in the hospital. Intensive Care and Step down Units along with Emergency Department staff care for many patients who have or are at a high risk for heart disease.

Knowledge of ACS pathophysiology and early recognition is key to impacting patient outcomes.

Early recognition reduces the time it takes for patients experiencing symptoms of possible ACS to see a physician thus decreasing the time to treatment which is critical in the early stages when treatment is most effective.

Background Coronary Artery Disease (CAD) = #1 killer of men and

women in U.S. Affects about 12 million Americans

In the US, CAD claims more lives each year than the next 7 leading causes of death combined!

Myocardial Infarction (MI) or “Heart attack” 1.1 million people affected each year

About half present at ED triage not using EMS

460,000 deaths annually from MI

Half of these deaths occur before reaching hospital

Estimated average number of years of life lost due to a heart attack is 14.2

Average delay in presentation about 3 hours from onset on symptoms!

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Acute Coronary Syndrome refers to a state of symptomatic ischemia or infarction resulting from a completely or partially clot-obstructed coronary artery.

ST elevated MI

(Complete occlusion)

Non ST elevation MI

(Partial occlusion)

Cardiac Risk Factors

Non-Modifiable Risk Factors Previous history Family history

1st degree relative (parents, siblings)

Men < 55; Women < 65 Age Gender Socioeconomic Factors

and Ethnicity

9 easily measured and potentially modifiable risk factors account for over 90% of the risk of an initial acute MI

Smoking Hypertension Dyslipidemia Diabetes Obesity Metabolic Syndrome Inactivity Alcohol

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Assessment of Pain

Linking Patient History and Risk factors

Cardiac Biomarkers

ECG Findings

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Assessment of “cardiac pain”

N = Normal (What is the patient’s baseline?)

O = Onset (sudden/gradual?)

P = Precipitation / provoking / palliative factors

Q = Quality or quantity (have patient describe in own words)

R = Radiation and region

S = Severity (pain scale)

T = Time (continuous/intermittent?)

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ACS Symptoms Classic

Symptoms

Stable angina

Unstable angina

MI

Symptom Variations

Women Elderly Diabetics

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Angina

Stable Occurs with physical

exertion or emotional stress

Relieved by rest or sublingual nitroglycerin

Predictable pattern

Predictable = triggered by the same amount of physical or emotional stress and should be easily relieved by rest or sublingual nitroglycerin.

Unstable Occurs with minimal

exertion OR increased dose of

nitroglycerin is required to achieve relief.

Prolonged rest angina is also considered unstable angina.

Angina that increases in severity or is very severe on first presentation

Caused by unstable or ruptured plaque that causes abrupt closure of a coronary artery which may spontaneously reperfuse.

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Characteristics of Angina Sensation of pressure, tightness, heaviness, burning, or squeezing.

• Rarely described as a sharp or stabbing pain.

• Should not worsen with changes in position or respiration.

Location behind the sternum and in the upper back, shoulder, arm, jaw, or epigastric area.

• Not usually located in the middle to lower abdomen and usually does not radiate to the lower extremities.

Associated symptoms (or stand alone symptoms) of dyspnea, nausea, palpitations, or diaphoresis.

Duration typically defined in minutes.

• Not typically defined in seconds or hours.

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CAUTION WHEN ASKING THE PATIENT ABOUT “PAIN”!

May deny pain but may state pressure, fullness or heaviness.

Symptoms in Special Populations ACS in Women Delay presenting with symptoms Attribute symptoms to other

non-cardiac causes Presentation

epigastric discomfort less specific complaints:

dyspnea or fatigue symptoms of discomfort

from nose to navel should be evaluated for presence of heart disease

Older women have higher incidence of complications

ACS in the Elderly Generalized symptoms

Dyspnea, diaphoresis, N&V, and syncope

Confusion Symptoms often attributed to the aging

process such as “activity intolerance” ACS in the Diabetic Patient

Autonomic dysfunction can affect symptoms experienced with angina

Less likely to experience pain.

25% of all patients presenting with ACS are diabetic

Have severe multi-vessel disease

Have higher rates of complications

Have a greater proportion of ulcerated plaques resulting in intracoronary thrombi

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Cardiac Biomarkers

Released into the blood when necrosis occurs as a result of membrane rupture of the myocytes

Used in the evaluation of ACS Myoglobin

Rises the earliest Within 2 hours after damage Very sensitive, not specific

CK (creatine kinase) Enzyme present in the heart, brain, and skeletal muscle Elevations are not specific to myocardial damage.

CK-MB More specific to the heart Helpful in identifying more than minor amounts of myocardial damage Rapidly rises in the presence of myocardial damage.

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Cardiac Biomarkers

Troponin I and T Found only in cardiac muscle Most sensitive indicator of myocardial damage

Capable of diagnosing small amounts of myocardial necrosis not measured by rises in CK-MB levels

Approximately 30% of patients with NSTEMI and normal CKMB levels will test positive

Of equal sensitivity and specificity Troponin remains elevated for a long period (late

presentation) Positive troponin + ECG changes of injury / ischemia =

infarct Non CAD causes of troponin elevation (sepsis,

pulmonary emboli and chronic kidney disease) Troponin I more specific in renal dysfunction

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Cardiac Biomarker Summary

Cardiac

Biomarker

Specificity /

Sensitivity

Rise Peak Duration

Myoglobin Sensitive but

not specific

Within 2 hours 4 to 10 hours < 24 hours

CK-MB

(more specific to

the heart than CK

levels)

Highly specific 4 to 6 hours 18 to 24 hours 2 to 3 days

Troponin I or T Highly specific

and sensitive

4 to 6 hours 18 to 24 hours 10 or more days

ECG Findings A discussion of injury/ischemia ECG findings is

beyond the scope of this module.

Key tips

Mark chart copy as “pain free” or “with pain” on top of ECG

ECG Critical Values at Aultman include the following and require physician notification

• Acute MI

• Bradycardia <45 beats

• Ventricular Tachycardia

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STAT ECG Indications

Chest pain or severe epigastric pain, non traumatic in origin, with components typical of myocardial ischemia or MI: Central/substernal compression or crushing chest pain

Pressure, tightness, heaviness, cramping, burning, aching sensation

Unexplained indigestion, belching, epigastric pain

Radiating pain in neck, jaw, shoulders, back, or 1 or both arms

Associated dyspnea

Associated nausea/vomiting

Associated diaphoresis

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If non diagnostic:

Repeat every 15 to 30 minutes

Use ST segment monitoring

Consider right-sided/posterior ECG

SCREEN for ACS if … > 30 years old with any of the following: Chest discomfort of any kind

“Heartburn”, indigestion, or epigastric pain

Complaints of “heart racing” (HR >150 or irregular and >120)

Complaints of “heart too slow” (HR < 50 and symptomatic)

Syncopal episode or severe weakness in patients > 45 years old

Difficulty breathing (no obvious non cardiac cause)

</= 30 with any of the above PLUS: Prior Cardiac disease

Family history of early heart disease

Diabetes mellitus

Severe Obesity

Recent cocaine use

Remember: Women and diabetic patients are more likely to present with atypical symptoms

Elderly patients may have symptoms such as generalized weakness, altered mental status, shortness of breath, or syncope, as their only sign of acute heart attack.

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When in doubt, do the ECG!

< 25% of ACS patients Complete occlusion of a vessel by a thrombus

Fibrin stable clot (red clot)

Classified more specifically by the portion of the left ventricle suffering injury.

Mortality is greatest within the first 24 to 48 hours of symptom onset

TREATMENT FOCUS = REPERFUSION

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Acute MI Symptoms

Symptoms occur spontaneously and are not relieved by rest or nitroglycerin

Chest pressure or discomfort may be accompanied by nausea, vomiting, or diaphoresis

Patient may have hemodynamic instability or cardiac arrest from ventricular fibrillation

Acute MI patients have positive biomarkers and are classified as STEMI or NSTEMI based on ECG presentation

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STEMI Management

Reperfusion is number one treatment strategy

Primary Coronary Intervention (PCI) preferred treatment strategy if within 90 minutes

Goal: 90 minutes from 1st medical contact

Fibrinolytics within 30 minutes of hospital

presentation (or 30 minutes from EMS to fibrinolytics)

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Facilitated PCI with full dose fibrinolytics is not recommended.

Rescue PCI may be done after failed fibrinolytics

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Reperfusion Therapy

Primary PCI Fibrinolytic Therapy

Primary PCI has clear outcome advantage in those > 65 years: Mortality Stroke Intracranial Hemorrhage

Reperfusion has proven benefit up to age 85.

The Winner!

Medical Management of STEMI

ASA Clopidogrel (with or without reperfusion)

Oxygen NTG MS D/C NSAIDS Beta-blockers (within 24 hours)

ACE Inhibitors (within 24 hours with impaired EF, HTN, diabetes or chronic kidney disease)

Anticoagulants (related to reperfusion strategy)

Intravenous insulin may be indicated in first 24 to 48 hours after STEMI to tightly control blood sugars.

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Reperfusion is primary management strategy.

Treatment of NSTEMI / UA: New Guidelines

ASA Oxygen (1st 6 hours) NTG

IV in first 48 hours for persistent ischemia, HTN, HF Should not interfere with mortality reducing beta

blockers or ace inhibitors

MS (if NTG unsuccessful and other anti ischemic drugs on board )

Beta Blockers (within 24 hours)

Start PO when hemodynamically stable May use IV if hypertensive

ACE Inhibitors (within 24 hours)

In select patients – pulmonary congestion or LVEF < 40%) – may also be used in other patients

DC – NSAIDS

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Medical Supportive Therapy: Similar to STEMI

Complications of MI

Hemodynamic Alterations Ventricular Arrhythmias Atrial Arrhythmias Pericarditis Ventricular Aneurysms Mechanical Complications

Myocardial Rupture (free wall or VSD) Papillary Muscle Rupture

Long Term: Ventricular Remodeling

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New addition to all admission power plans

In order to improve our patient care for an In house STEMI patient a communication order will be added to each admission power plan. This order is pre-checked and states

“Stat ECG will be obtained in the setting of a Rapid Response for suspected heart attack signs or symptoms”

This will allow the rapid response team to immediately obtain an ECG allowing quicker diagnosis and “STEMI alert” will be called if ECG is diagnostic for STEMI.

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Information that needs charted with In House STEMI patient

Onset of symptoms EKG time Notification of physician Time STEMI called Departed from floor ( to either Heart Cath lab or CCU) It is important to accurately chart the times the above occurs. Use

IP phone or computer for atomic time. Atomic time is a synchronized time and is very important when

tracking quality data. This patient may be in three different locations during this quality data collection and each area using this atomic time will allow accurate data collection.

This data will be tracked and used as quality data to improve our care for the In house STEMI patient.

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Summary

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Remember, time is muscle!

Save hearts and lives by knowing the signs/symptoms of ACS

Activate the rapid response team and notify the physician

Obtain an EKG