24. Acute Coronary Syndrome_ukdw_okt13

8/9/2019 24. Acute Coronary Syndrome_ukdw_okt13

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ACUTE CORONARY

SYNDROME


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What is Acute Coronary Syndrome(ACS) ?

• Acute Coronary Syndrome is when occlusion ofone or more of the coronary arteries occurs,usually following plaque rupture, resulting in

decreased oxygen supply to the heart muscle.• ACS is the largest cause of death in U.S.

• Majority of mortality associated with ST

Elevation Myocardial Infarction (STEMI).


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ACS Types


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Chest Pain

! First symptom of those suffering myocardialischemia.

! Called angina pectoris (angina – “pain”)

!

Feeling of heaviness, pressure! Moderate to severe

! In substernal area

!

Often mistaken for indigestion! May radiate to neck, jaw, left arm/ shoulder


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! Due to :

o

Accumulation of lactic acid in myocytes or

o

Stretching of myocytes

! Three types of angina pectoris:

o Stable, unstable and Prinzmetal


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Stable angina pectoris

! Caused by chronic coronary obstruction

! Recurrent predictable chest pain

! Gradual narrowing and hardening ofvessels so that they cannot dilate in

response to increased demand of physical

exertion or emotional stress

! Lasts approx. 3-5 minutes

! Relieved by rest and nitrates


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Unstable Angina pectoris

! Lasts more than 20 minutes at rest, or

rapid worsening of a pre-existing angina

! May indicate a progression to M.I.


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Prinzmetal angia pectoris

(Variant angina)

!

Caused by abnormal vasospasm of normalvessels (15%) or near atherosclerotic narrowing

(85%)

! Occurs unpredictably and almost exclusively at

rest.

! Often occurs at night during REM sleep

! May result from hyperactivity of sympathetic

nervous system, increased calcium flux inmuscle or impaired production of prostaglandin


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Silent Ischemia

! Totally asymptomatic

! May be due abnormality in innervation

! Or due to lower level of inflammatorycytokines


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Acute Myocardial Infarction


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DEFINITION

"

Acute myocardial infarction (MI) is defined as death ornecrosis of myocardial cells.

" Myocardial infarction occurs when myocardial ischemiaexceeds a critical threshold and overwhelms myocardial

cellular repair mechanisms that are designed to maintainnormal operating function and hemostasis.

" Ischemia at this critical threshold level for an extendedtime period results in irreversible myocardial cell damageor death.


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PREVALENCE

"

In general, MI can occur at any age, but itsincidence rises with age.

" The actual incidence is dependent upon

predisposing risk factors for atherosclerosis" Approximately 50% of all MI's in the US occur in

people younger than 65 years of age.

" However, in the future, as demographics shift

and the mean age of the population increases, alarger percentage of patients presenting with MIwill be older than 65 years


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Risk Factors:

Six primary risk factors have been identified with thedevelopment of atherosclerotic coronary artery disease andMI:

–

hyperlipidemia,

–

diabetes mellitus,

–

hypertension, –

Smoking (Tobacco use),

–

male gender, and

–

family history of atherosclerotic arterial disease.

The presence of any risk factor is associated with doublingthe relative risk of developing atherosclerotic coronaryartery disease.


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Mechanisms of Occlusion:

• Most MIs are caused by a disruption in the vascular

endothelium associated with an unstable

atherosclerotic plaque that stimulates the formation ofan intracoronary thrombus, which results in coronary

artery blood flow occlusion.

• If such an occlusion persists long enough (20 to 40

min), irreversible myocardial cell damage and cell

death will occur.

Pathophysiology


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•

The development of atherosclerotic plaque occurs over a period of years to decades. The initial vascular lesion leadingto the development of atherosclerotic plaque is not knownwith certainty.

•

The two primary characteristics of the clinically symptomatic

atherosclerotic plaque are a fibromuscular cap and anunderlying lipid-rich core.

•

Plaque erosion may occur due to the actions ofmetalloproteases and the release of other collagenases and

proteases in the plaque, which result in thinning of theoverlying fibromuscular cap.

•

Hemodynamic forces applied to the arterial segment, can leadto a disruption of the endothelium and fissuring or rupture ofthe fibromuscular cap. – a site otherwise known as the plaque's "shoulder region."

Pathophysiology (Cntd.)


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Vulnerable Plaque


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Mechanisms of Myocardial Damage:

"

The severity of an MI is dependent on threefactors:! The level of the occlusion in the coronary artery,

! The length of time of the occlusion

!

The presence or absence of collateral circulation

" The death of myocardial cells first occurs in thearea of myocardium that most distal to the

arterial blood supply—that is, the endocardium.

" As the duration of the occlusion increases, thearea of myocardial cell death enlarges


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Structural, functional changes

"

Decreased contractility" Decreased LV compliance

" Decreased stroke volume

"

Dysrhythmias

" Inflammatory response is severe

" Scarring results –!

Strong, but stiff; can’t contract like healthy cells


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• AcuteMI may have unique presentations in individual patients. Thedegree of symptoms ranges from none at all to sudden cardiac death.An asymptomatic MI is not necessarily less severe than a symptomaticevent; but patients who experience asymptomatic MI's are more likelyto be diabetic.

• Chest pain described as a pressure sensation, fullness, or squeezing inthe midportion of the thorax

•

Radiation of chest pain into the jaw/teeth, shoulder, arm, and/or back• Associated dyspnea or shortness of breath

• Associated epigastric discomfort with or without nausea and vomiting

• Associated diaphoresis or sweating

• Syncope or near-syncope without other cause

•

Impairment of cognitive function without other cause• A MI may occur at any time of the day, but most appear to be clustered

around the early hours of the morning and/or are associated withdemanding physical activity. Approximately 50% of patients have somewarning symptoms (angina pectoris or an anginal equivalent) prior to

the infarct.

SIGNS AND SYMPTOMS


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• The pain of AMI is variable in intensity; in most patients it issevere and in some instances intolerable.

•

The pain is prolonged, usually lasting for more than 30 minutesand frequently for a number of hours.

• Described as constricting, crushing, oppressing, or compressing;often the patient complains of a sensation of a heavy weight or asqueezing in the chest. Although the discomfort is typically

described as a choking, viselike, or heavy pain, it may also becharacterized as a stabbing, knifelike, boring, or burningdiscomfort.

• The pain is usually retrosternal in location, spreading frequently to both sides of the anterior chest, with predilection for the left side.Often the pain radiates down the ulnar aspect of the left arm,

producing a tingling sensation in the left wrist, hand, and fingers.Some patients note only a dull ache or numbness of the wrists inassociation with severe substernal or precordial discomfort. Insome instances, the pain of AMI may begin in the epigastrium andsimulate a variety of abdominal disorders, a fact that often causes to be misdiagnosed as “indigestion

Nature of Pain


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• In other patients the discomfort of AMI radiates to the shoulders,upper extremities, neck, jaw, and interscapular region, again

usually favoring the left side. In patients with preexisting angina pectoris, the pain of infarction usually resembles that of anginawith respect to location. However, it is generally much moresevere, lasts longer, and is not relieved by rest and nitroglycerin.

• In some patients, particularly the elderly, AMI is manifested

clinically not by chest pain but rather by symptoms of leftventricular failure and chest tightness or by marked weakness orfrank syncope. These symptoms may be accompanied bydiaphoresis, nausea, and vomiting.

• The recognition that pain implies ischemia and not infarctionheightens the importance of seeking ways to relieve the ischemia,

for which the pain is a marker. This finding suggests that theclinician should not be complacent about ongoing cardiac painunder any circumstances

Nature of Pain


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• Nausea and vomiting occur in more than 50 percent of patients

with transmural and severe chest pain, presumably owingto activation of the vagal reflex or to stimulation of leftventricular receptors as part of the Bezold-Jarisch reflex.

• These symptoms occur more commonly in patients withinferior than in those with anterior .

• Occasionally, a patient complains of diarrhea or a violent urgeto evacuate the bowels during the phase of .

• Other symptoms include feelings of profound weakness,dizziness, palpitations, cold perspiration, and a sense ofimpending doom.

• On occasion, symptoms arising from an episode of cerebral

embolism or other systemic arterial embolism are the first signsof AMI.

The aforementioned symptoms may or may not be accompanied by chest pain.

Other symptoms


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•

Population studies suggest that between 20 and 60 percentof nonfatal are unrecognized by the patient and arediscovered only on subsequent routine ECG or postmortemexaminations.

•

Of these unrecognized infarctions, approximately half are

truly silent, with the patients unable to recall anysymptoms whatsoever. The other half of patients with so-called silent infarction can recall an event characterized bysymptoms compatible with infarction whenleading questions are posed after the ECG abnormalities

are discovered.•

Unrecognized or silent infarction occurs more commonlyin patients without antecedent angina pectoris and in

patients with diabetes and hypertension

SILENT


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ECG changes

"

Pronounced, persisting Q waves

" ST elevation

" T wave inversion


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The Three I’s

Ischemia = ST depression or T-wave inversion

Represents lack of oxygen to myocardial tissue

Th Th I’


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The Three I’s

•

Injury = ST elevation -- represents prolongedischemia; significant when > 1 mm above the baselineof the segment in two or more leads


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The Three I’s

•

Infarct = Q wave — represented by firstnegative deflection after P wave; must bepathological to indicate MI


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What part of the heart is affected ?

II, III, aVF =

Inferior Wall

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

I f i W ll MI


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Inferior Wall MI


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Based on the EKG, which vessel in theheart is blocked?

• II, III & aVF = Inferior Wall MI =

Right Coronary Artery

blockage


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Which part of the heart is affected ?

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

•

Leads V1, V2, V3, and V4 =

Anterior Wall MI


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Anterior Wall MI


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•

V1 - V4 = Anterior Wall

(Left Ventricle) =

Left AnteriorDescending Artery

Blockage


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What part of the heart is affected ?

#

I, aVL, V5 and V6

Lateral wall of left ventricle

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6


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Lateral Wall MI


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• I, aVL, V5 + V6 =

Lateral Wall =

Circumflex ArteryBlockage


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THERAPY

"

The goals of therapy in AMI are the expedientrestoration of normal coronary blood flow andthe maximum salvage of functionalmyocardium.

"

These goals can be met by a number ofmedical interventions and adjunctive therapies." The primary obstacles to achieving these goals

are the patient's failure to quickly recognize MIsymptoms and the delay in seeking medicalattention.

" When patients present to a hospital, there are avariety of interventions to achieve treatmentgoals.


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Time is Muscle


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Treatment

"

First 24 hours crucial

" Hospitalization, bed rest

" ECG monitoring for arrhythmias

"

Pain relief (morphine, nitroglycerin)

" Thrombolytics to break down clots

" Administer oxygen

"

Revascularization interventions: by-passgrafts, stents or balloon angioplasty


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General Treatment Measures

"

ASPIRIN

" CONTROL OF CARDIAC PAIN! Analgesics

"

NITRATES

" BETA-ADRENOCEPTOR BLOCKERS

" OXYGEN! Limitation of Infarct Size


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THERAPY (Cntd.)

Antiplatelet Agents: " Aspirin in a dose of at least 160 mg and up to 325mg should be administered immediately onrecognition of MI signs and symptoms and continueddaily indefinitely.

" Other antiplatelet agents—including clopidogrel,ticlopidine, and dipyridamole-have not been shownin any large-scale trial to be superior to aspirin in MI.These other antiplatelet agents (specificallyclopidogrel) may be useful for patients who have atrue allergy to aspirin and for patients with knownresistance to aspirin's effects.11-13


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THERAPY (Cntd.)

"

Supplemental Oxygen:!

There are no published studies demonstrating that oxygentherapy reduces mortality or morbidity of a MI.

" Nitrates:

" Beta-blockers:!

Beta-blocker therapy is recommended within 12 hours of MIsymptoms and is continued indefinitely.

! Treatment with a beta-blocker reduces MI mortality—presumably by decreasing the incidence of arrhythmogenicdeath.

!

Beta blockade decreases the rate and force of myocardialcontraction and decreases overall myocardial oxygendemand. In the setting of reduced oxygen supply in MI, thereduction in oxygen demand provided by beta blockademinimizes myocardial injury and death.


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Heparin:

Unfractionated Heparin: " Intravenous unfractionated heparin is recommended in

patients with a MI who undergo percutaneousrevascularization or fibrinolytic therapy with alteplase.

" Intravenous unfractionated heparin is also recommendedin patients with a MI who receive fibrinolytic therapy witha non-selective fibrinolytic agent (urokinase,streptokinase, anistreplase) and are at increased risk for

systemic emboli (prior embolic event, large or anteriorwall infarction, known left ventricular thrombus, or atrialfibrillation).4


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Low-molecular-weight Heparin

(LMWH)

" LMWH can be administered to MI patients not treatedwith fibrinolytic therapy that have no contra-indicationto heparin.4

"

The LMWH class of drugs includes several agents thathave distinctly different anticoagulant effects.

" These effects can be characterized by a given agent'sratio of activity against factors Xa and IIa.

" LMWHs have been proven to be effective in treatingacute coronary syndromes that are characterized byunstable angina and non-Q-wave MI.

" Their fixed doses are easy to administer, andlaboratory testing to measure their therapeutic effect is

not necessary.


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Fibrinolytics:

" Fibrinolytic therapy is indicated for patients with apresentation compatible with MI and ST segmentelevation greater than 0.1 mV in 2 contiguous EKGleads, or new onset of a bundle branch block, who

present less than 12 hours but not more than 24 hoursafter symptom onset.4

" Restoration of coronary blood flow in MI can also beaccomplished pharmacologically with the use of afibrinolytic agent.As a class, the plasminogen activators

have been shown to restore coronary blood flow in 50%to 80% of MI patients.

" The successful use of fibrinolytic agents provides adefinite survival benefit that is maintained for years

" A fibrinolytic is most effective when the "door-to-needle"

time is 30 minutes or less


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• Percutaneous coronary intervention is an

alternative therapy to fibrinolysis if performed

by a skilled operator supported by experienced

personnel performed in a well-equipped

catheterization laboratory.

Percutaneous Coronary

Intervention:


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•

The performance standard for primary percutaneousintervention as a MI therapy is a "door-to-balloon" time of 90minutes (± 30 minutes).4 Restoration of coronary blood flowin a MI can be accomplished mechanically by percutaneouscoronary intervention (PCI). Mechanical revascularization byPCI is used as a primary therapy in many well-equippedmedical centers and as an alternative to fibrinolysis whenfibrinolysis is not clearly indicated or contraindicated. PCI cansuccessfully restore coronary blood flow in 90% to 95% of a

MI patients•

PCI provides a definite survival advantage over fibrinolysis forMI patients who are in cardiogenic shock

Percutaneous Coronary

Intervention:


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• Grade 0 = complete occlusion of the infarct-relatedartery.

• Grade 1 = some penetration of the contrast material

beyond the point of obstruction but without perfusionof the distal coronary bed.

• Grade 2 = perfusion of the entire infarct vessel intothe distal bed but with delayed flow compared with a

normal artery.• Grade 3 = full perfusion of the infarct vessel with

normal flow

TIMI grading system:


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