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 symptomsElectrocardiographic changesBiochemical changes

Symptoms of ACS

Pain

Sympathetic response

Parasympathetic response

Inflammatory response

Other

– PressurePressure– Burning (hot)Burning (hot)– Chest/arms/jaw/backChest/arms/jaw/back

– SweatsSweats– TachycardiaTachycardia– Cool, clammy skinCool, clammy skin

– NauseaNausea– VomitingVomiting– WeakWeak

– Mild feverMild fever

– DyspneaDyspnea– AsymptomaticAsymptomatic

Physical FindingsPhysical 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 Syndromes

Unstable anginaUnstable angina ST-Elevation MIST-Elevation MI(Q-wave MI)(Q-wave MI)

Non-ST Elevation MINon-ST Elevation MI(Non-Q-wave MI)(Non-Q-wave MI)

Stable CADStable CAD

The continuum of acute coronary syndromes ranges from unstable The continuum of acute coronary syndromes ranges from unstable

angina, through non-ST-elevation myocardial infarction (also referred angina, through non-ST-elevation myocardial infarction (also referred

to as to as ““non-Q-wavenon-Q-wave”” myocardial infarction [MI]), to ST-elevation MI myocardial infarction [MI]), to ST-elevation MI

(also referred to as (also referred to as ““Q-waveQ-wave”” MI). MI).

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

Inflammatorycytokines

Plaque RupturePlaque Rupture

Physical Stress

VulnerablePlaque

EmotionalStress

Extent of Myocardial Injury

muscle mass perfused by vessel

Magnitude/Duration of flow

Oxygen demand of affected tissue

Adequacy of collaterals

Tissue response to ischemia

Determined by:Determined by:

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

Myocardial ischemia >>> infarction

1. Plaque formation with narrowing of coronary artery lumen

2. Plaque rupture

3. Thrombus formation with platelet activation and aggregation

4. Ischemia in downstream territory with reversible cell injury

5. Myocardial cell death

Cardiovascular Pathology Angina Unstable angina Myocardial Infarction Congestive heart failure Valvular dysfunction Cardiogenic shock Aneurysms Deep vein thrombosis/arterial occlusion

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

OPQRST

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 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

Poor dietary habits

Imbalance between good cholesterol (HDL)

and bad cholesterol (LDL)

Atherosclerosis

That’s why there are angiograms!

Angina or MI??myocardial ischemia

angina

unstable angina

myocardial infarction

Decreased perfusion

Supply and demand

CP pattern changes orcomplicated

Total occlusion and necrosis

Consequences ofCoronary Thrombosis

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

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.

Angina 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 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 bpmHR and blood pressure parameters…why?

Hemodynamic Parameters

SBP < 100preload reduction - vasodilationdecreased coronary perfusion

HR < 60 bpm or > 160 bpmrate related ischemia?

Ischemic Chest Pain

Nitroglycerin 0.4mg SL, q 5 min. PRNAssess VS after each dosed/c if SBP <100 or SBP drops by 1/3d/c if HR <60 or >160 bpm

ASA 160mg chewable tablets Morphine Sulphate 2mg IV, q 5 min. x 3

PRN

Unstable Angina

Indicates a progression towards serious myocardial disease

5 Indicators of Unstable Anginanew angina pain change in the durationchange in Rx (e.g increased NTG use)onset at rest change in quality (e.g now radiates)

Acute Myocardial Infarction

Definition: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

Killing of myocardial tissue Conventional treatment will only save

ischemic zone Thrombolytics

Ischemic zone

Necrotic zone

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

Change in rate and rhythm

Most often sinus with:No discernible changeHyper-acute T-wavesT wave flattening or inversionST segments up or downQ waves

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

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

Myoglobin is found in cardiac and skeletal muscle

Very sensitive if measured early

Not specific

Not often used

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

Reduce preload and afterloadDilate coronary arteriesAssists coronary perfusion

Disadvantages of Nitrates

Not useful in patients who are reperfused

May cause hypotensionSevere hypotension in patients with RV

dysfunctionMay cause hypotension in inferior MI

30% have RV involvement-check!!!

-blockers

Multi-purpose in the setting of ACS

Anti-arrhythmicAnti-ischemicAnti-hypertensive

-blockers

Decrease myocardial oxygen demand

Decreased heart rate – increases diastoleDecreased myocardial contractilityDecreased MAP

Advantages of -blockers

Reduction in pain Decreased morbidity and mortality Decreased risk of arrhythmia Decreased infarct size Decreased risk of re-infarction

Treatment with a -blocker is a standard of care

ASA

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

Heparins (LMWH) Reperfusion

PCIMechanical (the digger!)Thrombolytic agents

Antiarrhythmic agents

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

Summary

Strategies for reducing morbidity and mortality

Reduce cardiac workload Improve perfusion to cardiac tissueReduce risk of fatal arrhythmiasReduce extension of clot formationReperfuse the ischemic myocardium

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

PCI

Pre-hospital Thrombolysis

Oshawa Land ALS Northern Ornge Bases

Frequent use Southern Ornge Bases

Carry it Positive empirical trends

Pre-hospital Thrombolysis

prolonged transport time

no thrombolysis at the sending facility

Long delays

Indications - Thrombolysis

Ischemic C.P.

Less than 6 hours duration

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

ST segment elevation New onset Left Bundle Branch Block

with S&S? Some acute coronary syndromes

(A.C.S.) do not benefit from thrombolysis

Next

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)