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Acute Coronary Syndrome. APS Fleming College. What is an ACS?. A sudden event during which the myocardium suffers from a relative or a complete lack of perfusion Covers the continuum between angina and MI This is reflected in: Signs and symptoms Electrocardiographic changes

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Acute Coronary Syndrome

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Acute coronary syndrome

Acute Coronary Syndrome


Fleming College

What is an acs

What is an ACS?

A sudden event during which the myocardium suffers from a relative or a complete lack of perfusion

Covers the continuum between angina and MI

This is reflected in:

  • Signs and symptoms

  • Electrocardiographic changes

  • Biochemical changes

Symptoms of acs

Symptoms of ACS

  • Pressure

  • Burning (hot)

  • Chest/arms/jaw/back


Sympathetic response

Parasympathetic response

Inflammatory response


  • Sweats

  • Tachycardia

  • Cool, clammy skin

  • Nausea

  • Vomiting

  • Weak

  • Mild fever

  • Dyspnea

  • Asymptomatic

Physical findings

Physical Findings

  • Inspection

    BP- often increase anterior MI

    - often decrease inferior MI

    HR- often increase anterior MI

    - often decrease inferior MI

    RA po - increase in RV MI

Acute coronary syndrome

Stable CAD

Acute Coronary Syndromes

Unstable angina

Non-ST Elevation MI

(Non-Q-wave MI)

ST-Elevation MI

(Q-wave MI)

The continuum of acute coronary syndromes ranges from unstable angina, through non-ST-elevation myocardial infarction (also referred to as “non-Q-wave” myocardial infarction [MI]), to ST-elevation MI (also referred to as “Q-wave” MI).

Platelets acs

Platelets & ACS

  • Platelets become activated by various stimuli

  • Binds to fibrinogen and serves to cross-link and aggregate platelets

  • Platelet plug becomes the centre of a larger thrombus

Triggers to plaque rupture

Triggers to Plaque Rupture



Plaque Rupture





Physical Stress

Extent of myocardial injury

Extent of Myocardial Injury

Determined by:

  • muscle mass perfused by vessel

  • Magnitude/Duration of flow

  • Oxygen demand of affected tissue

  • Adequacy of collaterals

  • Tissue response to ischemia

Preventing acs reducing infarct size

Preventing ACS / Reducing Infarct Size

  • Primary prevention -lifestyle

  • Stabilizing plaque

  • Preventing platelet aggregation

  • Decreasing preload and afterload

  • Decreasing cardiac workload

  • Reperfusion

  • Treating arrhythmia

    Which ones do you as medics do??

Pathophysiology of acs

Pathophysiology of ACS

Myocardial ischemia >>> infarction

  • Plaque formation with narrowing of coronary artery lumen

  • Plaque rupture

  • Thrombus formation with platelet activation and aggregation

  • Ischemia in downstream territory with reversible cell injury

  • Myocardial cell death

Cardiovascular pathology

Cardiovascular Pathology

  • Angina

  • Unstable angina

  • Myocardial Infarction

  • Congestive heart failure

  • Valvular dysfunction

  • Cardiogenic shock

  • Aneurysms

  • Deep vein thrombosis/arterial occlusion

Ischemic chest pain

Ischemic Chest Pain

  • Good history and physical exam

  • 3 & 12/15lead ECG

  • OPQRST to guide history investigation

  • Differential diagnosis

Chapter 27 27.24-27.36



  • Onset - when did it start?

  • Provoked - at rest, exertion, better or worse?

  • Quality - sharp, dull, ache, heaviness?

  • Radiating - to shoulder, back, jaw?

  • Severity - on a scale of 1-10?

  • Time - does it come and go?

Myocardial ischemia

Myocardial Ischemia

  • Blood supply and demand

  • Causes of ischemia

    • HR – too slow or too fast

    • vasospasm (Prinzmetals)

    • coronary artery occlusion

    • narrowing of coronary arteries

    • low blood pressure

    • hypoxemia

Coronary artery disease

Coronary Artery Disease

  • Poor dietary habits

  • Imbalance between good cholesterol (HDL)

    and bad cholesterol (LDL)

  • Atherosclerosis

That s why there are angiograms

That’s why there are angiograms!

Angina or mi

myocardial ischemia


unstable angina

myocardial infarction

Decreased perfusion

Supply and demand

CP pattern changes or


Total occlusion and necrosis

Angina or MI??

Consequences of coronary thrombosis

Consequences ofCoronary Thrombosis

Lilly. Pathophysiology of Heart Disease, 4th Ed. Lippincott Williams, 2007. Page 173

The importance of history

The Importance of History

  • Someone with angina knows their typical pattern

  • In addition to OPQRST, take an AMPLE history

  • “are you SOB?”

  • Similar pain?

  • MI in past? Is this pain similar?

  • Other cardiac Hx? e.g. CABG, angioplasty ,stress testing, hospitalizations etc.



  • Lasts less than 30 minutes

  • Heaviness, dull, tight or even sharp pain

  • Can radiate but less common

  • Usually on exertion and dissipates with rest

  • Temporary drop in coronary artery blood flow

  • Rule out rate related problems

Angina management

Angina Management

  • Rest/relaxation (Be calm!)

  • O2 therapy

  • IV access ?

  • ASA 160mg chewed & swallowed

  • Vitals

  • Nitroglycerin 0.4mg SL q 5 min. if SBP >100 and

    HR > 60 but less than 160 bpm

    • HR and blood pressure parameters…why?

Hemodynamic parameters

Hemodynamic Parameters

  • SBP < 100

    • preload reduction - vasodilation

    • decreased coronary perfusion

  • HR < 60 bpm or > 160 bpm

    • rate related ischemia?

Acute coronary syndrome

Ischemic Chest Pain

  • Nitroglycerin 0.4mg SL, q 5 min. PRN

    • Assess VS after each dose

    • d/c if SBP <100 or SBP drops by 1/3

    • d/c if HR <60 or >160 bpm

  • ASA 160mg chewable tablets

  • Morphine Sulphate 2mg IV, q 5 min. x 3 PRN

Unstable angina

Unstable Angina

  • Indicates a progression towards serious myocardial disease

  • 5 Indicators of Unstable Angina

    • new angina pain

    • change in the duration

    • change in Rx (e.g increased NTG use)

    • onset at rest

    • change in quality (e.g now radiates)

Acute myocardial infarction

Acute Myocardial Infarction


Necrosis of heart muscle due to absolute or relative lack of blood supply to the myocardium.

The site of infarction is determined by the location of the arterial occlusion.

Myocardial infarction

Myocardial Infarction

  • Killing of myocardial tissue

  • Conventional treatment will only save ischemic zone

  • Thrombolytics

Necrotic zone

Ischemic zone

Presentation of myocardial infarction

Presentation of Myocardial Infarction

  • Varies widely from patient to patient

  • Typical vs. Atypical (e.g.. weakness or SOB)

  • The elderly, alcoholics, and women

  • CP unresolved with rest or NTG

  • 12 Lead shows acute ST elevation, Flipped T waves or Q waves (old)

Electrocardiographic changes

Electrocardiographic Changes

  • Change in rate and rhythm

  • Most often sinus with:

    • No discernible change

    • Hyper-acute T-waves

    • T wave flattening or inversion

    • ST segments up or down

    • Q waves

Acute coronary syndrome

ECG Changes

Biochemical markers of acs

Biochemical Markers of ACS

  • Enzymes which are unique to cardiac myocytes

  • Released into the circulation by dead cells

    • Thus a rise in these indicates that myocardium has suffered damage

Biochemical markers

Biochemical Markers

  • Troponin (remember its role in actin/myosin binding??)

  • CPK (Creatine Phosphokinase)

    • Specifically one isoenzyme -MB band

  • LDH (Lactose dehydrogenase)

  • AST

    Hospital staff will draw blood for these tests early but do NOT generally help in the decision making

Cardiac markers

Cardiac Markers

  • Myoglobin is found in cardiac and skeletal muscle

  • Very sensitive if measured early

  • Not specific

  • Not often used

Use of nitrates in acs

Use of Nitrates in ACS

  • Nitrates, typically nitroglycerin

  • Nitrous Oxide acts as a smooth muscle relaxant leading to vasodilatation

  • Transdermally, sublingually and/or parenterally

Benefits of nitrates

Benefits of Nitrates

  • Reduce preload and afterload

  • Dilate coronary arteries

  • Assists coronary perfusion

Disadvantages of nitrates

Disadvantages of Nitrates

  • Not useful in patients who are reperfused

  • May cause hypotension

  • Severe hypotension in patients with RV dysfunction

  • May cause hypotension in inferior MI

    • 30% have RV involvement-check!!!

B blockers


Multi-purpose in the setting of ACS

  • Anti-arrhythmic

  • Anti-ischemic

  • Anti-hypertensive

B blockers1


Decrease myocardial oxygen demand

  • Decreased heart rate – increases diastole

  • Decreased myocardial contractility

  • Decreased MAP

Advantages of b blockers

Advantages of b-blockers

  • Reduction in pain

  • Decreased morbidity and mortality

  • Decreased risk of arrhythmia

  • Decreased infarct size

  • Decreased risk of re-infarction

    Treatment with a b-blocker is a standard of care

Acute coronary syndrome


  • Anti-inflammatory

    • prevents the formation of arachidonic acid

  • A pathway that can be blocked to prevent platelet aggregation

  • Does not block all platelet activators

Other treatment modalities in acs

Other Treatment Modalities in ACS

  • Heparins (LMWH)

  • Reperfusion

    • PCI

    • Mechanical (the digger!)

    • Thrombolytic agents

  • Antiarrhythmic agents

Focus of acs

Focus of ACS

  • Common reason for transport

  • Much can be done during transfer

  • Reduce risk of morbidity and mortality

    The first step = recognizing the ACS

    • Signs and symptoms

    • ECG changes

    • Biochemical changes



Strategies for reducing morbidity and mortality

  • Reduce cardiac workload

  • Improve perfusion to cardiac tissue

  • Reduce risk of fatal arrhythmias

  • Reduce extension of clot formation

  • Reperfuse the ischemic myocardium

Myocardial infarction1

Myocardial Infarction

  • ASA (2 x 80 mg) P.O.

  • O2 therapy

  • IV access

  • NTG via SL, transdermal, and/or IV

  • Morphine (ACP)

  • Heparin and/or Beta blockers (Hosp)

  • 12/15 Lead ECG as soon as possible

  • Angioplasty (hosp)

  • Thrombolytics if PCI not available or contraindicated

Acute coronary syndrome


Time sensitive

Pre hospital thrombolysis

Pre-hospital Thrombolysis

  • Oshawa Land ALS

  • Northern Ornge Bases

    • Frequent use

  • Southern Ornge Bases

    • Carry it

  • Positive empirical trends

Pre hospital thrombolysis1

Pre-hospital Thrombolysis

  • prolonged transport time

  • no thrombolysis at the sending facility

  • Long delays

Indications thrombolysis

Indications - Thrombolysis

  • Ischemic C.P.

  • Less than 6 hours duration

Ischemic chest pain1

Ischemic Chest Pain?

O - at rest or with exertion

P – better or worse

Q - heaviness, tightening, sharp, weakness etc

R - neck, jaw and/or left arm

S - varies

T - consistent, does NOT come & go

12 lead ecg criteria

12 Lead ECG Criteria

  • ST segment elevation

  • New onset Left Bundle Branch Block with S&S?

  • Some acute coronary syndromes (A.C.S.) do not benefit from thrombolysis

Acute coronary syndrome


  • We will be looking at 12 leads specifically

  • Look at the hand powerpoint (12lead)

  • Read the sample handouts

  • Read your text 12 lead ECG (big book)

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