Acute Coronary Syndromes

1

Acute Coronary Acute Coronary SyndromesSyndromes

EMS ProfessionsEMS Professions

Temple CollegeTemple College

2

The History of Paramedics The History of Paramedics Begins with Cardiac CareBegins with Cardiac Care

The The originaloriginal Paramedic idea was Paramedic idea was based upon the need for rapid based upon the need for rapid response to, identification of and response to, identification of and emergency care for victims of:emergency care for victims of:

Sudden Cardiac Death (SCD)Sudden Cardiac Death (SCD)Acute Myocardial Infarction (AMI)Acute Myocardial Infarction (AMI)

3

Ischemic Coronary Ischemic Coronary SyndromesSyndromes Acute Coronary SyndromesAcute Coronary Syndromes

Angina PectorisAngina PectorisUnstable AnginaUnstable AnginaAcute Myocardial InjuryAcute Myocardial InjuryAcute Myocardial InfarctionAcute Myocardial Infarction

Presentation with suspected ischemia Presentation with suspected ischemia Non-diagnostic ECGNon-diagnostic ECG ST segment depressionST segment depression ST segment elevation/New BBBST segment elevation/New BBB

4

Ischemic Coronary Ischemic Coronary SyndromesSyndromes Angina PectorisAngina Pectoris

Acute pain, usually in the chest, Acute pain, usually in the chest, resulting from an increased demand resulting from an increased demand for oxygen and a decreased ability to for oxygen and a decreased ability to provide itprovide it

Usually due to a partially occluded Usually due to a partially occluded coronary artery or vasospasmcoronary artery or vasospasm

5

Ischemic Coronary Ischemic Coronary SyndromesSyndromes

Angina PectorisAngina PectorisTypical PresentationTypical Presentation

Squeezing, Crushing, Heavy, TightSqueezing, Crushing, Heavy, Tight– Fist to chest = Levine’s signFist to chest = Levine’s sign

Pain/Discomfort may radiate to shoulders, Pain/Discomfort may radiate to shoulders, arms, neck, back, jaw or epigastriumarms, neck, back, jaw or epigastrium

Usually lasts 3-5 min and rarely exceeds Usually lasts 3-5 min and rarely exceeds 15 min15 min

Not changed by swallowing, coughing, Not changed by swallowing, coughing, deep breathing or positional changesdeep breathing or positional changes

6


Angina PectorisAngina PectorisTypical PresentationTypical Presentation

AnxietyAnxiety Diaphoresis or clammy skinDiaphoresis or clammy skin Nausea, vomitingNausea, vomiting Shortness of breathShortness of breath WeaknessWeakness PalpitationsPalpitations SyncopeSyncope

7


Angina PectorisAngina PectorisUsually Provoked by:Usually Provoked by:

ExerciseExercise EatingEating Emotion/StressEmotion/Stress

Usually Relieved by:Usually Relieved by: Rest; Removal of provoking factorRest; Removal of provoking factor NitroglycerinNitroglycerin

8


Stable Angina PectorisStable Angina PectorisReasonably Predictable frequency, Reasonably Predictable frequency,

onset, durationonset, durationRelief predictable with rest, Relief predictable with rest,

nitroglycerinnitroglycerin

9


Stable Angina PectorisStable Angina PectorisTreatment GoalsTreatment Goals

Reduce myocardial oxygen demandReduce myocardial oxygen demand Improve myocardial oxygen supplyImprove myocardial oxygen supply

10

Ischemic Coronary Ischemic Coronary SyndromesSyndromes Stable Angina PectorisStable Angina Pectoris

TreatmentTreatment Physical/Psychological restPhysical/Psychological rest Position of comfort, sitting or supinePosition of comfort, sitting or supine OxygenOxygen ECG MonitorECG Monitor

– Assess the underlying rhythmAssess the underlying rhythm Nitroglycerin, 0.4 mg SL q 5 min as long Nitroglycerin, 0.4 mg SL q 5 min as long

as BP > 90 mm Hgas BP > 90 mm Hg– Continue until pain relieved or contraindicatedContinue until pain relieved or contraindicated

11


Stable Angina PectorisStable Angina PectorisTransport ConsiderationsTransport Considerations

Many persons stay home and treat Many persons stay home and treat themselvesthemselves

Treat first-time angina, unstable angina Treat first-time angina, unstable angina or angina requiring more than 3 NTG or angina requiring more than 3 NTG (>15 min) as AMI(>15 min) as AMI

When in doubt, treat as AMIWhen in doubt, treat as AMI

12

Ischemic Coronary Ischemic Coronary SyndromesSyndromes Stable Angina PectorisStable Angina Pectoris

Variant Angina (Prinzmetal’s Angina)Variant Angina (Prinzmetal’s Angina) Occurs at restOccurs at rest Episodes at regular times of dayEpisodes at regular times of day Results from coronary vasospasmsResults from coronary vasospasms Treated long term with calcium channel Treated long term with calcium channel

blockersblockers May result in abnormal 12 lead ECG May result in abnormal 12 lead ECG

changes that resolve with minimal changes that resolve with minimal treatmenttreatment

13

Ischemic Coronary Ischemic Coronary SyndromesSyndromes Unstable AnginaUnstable Angina

Prolonged chest pain/ischemic Prolonged chest pain/ischemic symptoms or an symptoms or an atypicalatypical presentation of angina without ECG or presentation of angina without ECG or laboratory evidence of AMI (Injury)laboratory evidence of AMI (Injury)

Usually associated with significant or Usually associated with significant or progressing occlusion of a coronary progressing occlusion of a coronary artery or severe vasospasmartery or severe vasospasm

Considered “Pre-infarction Angina”Considered “Pre-infarction Angina”

14


May have Typical or Atypical Signs & May have Typical or Atypical Signs & SymptomsSymptoms Atypical PresentationAtypical Presentation

– Increased frequency or duration of Increased frequency or duration of episodesepisodes

– Onset with less exertion than normalOnset with less exertion than normal– Increased severity of symptomsIncreased severity of symptoms– Requires greater number of NTG tablets Requires greater number of NTG tablets

to relieve symptomsto relieve symptoms

15


Treatment same as Angina Treatment same as Angina PLUSPLUS:: IV, NS (no dextrose), TKO IV, NS (no dextrose), TKO

– Some exceptions to restricting fluidSome exceptions to restricting fluid 12 Lead ECG12 Lead ECG

– Assess for RVIAssess for RVI Morphine sulfate, 2 - 4 mg q 5-15 min slow Morphine sulfate, 2 - 4 mg q 5-15 min slow

IV titrated to pain relief and BP > 90IV titrated to pain relief and BP > 90 Aspirin, 160-325 mg POAspirin, 160-325 mg PO

– Chewed & swallowed if possibleChewed & swallowed if possible– Determine if hypersensitive to ASADetermine if hypersensitive to ASA

16


Treatment Treatment Metoprolol, 5 mg slow IV q 5 min to 15 mg Metoprolol, 5 mg slow IV q 5 min to 15 mg

total, prn for total, prn for HR/BP in absence of HR/BP in absence of contraindicationscontraindications

In longer or interfacility transports, consider:In longer or interfacility transports, consider:– Nitroglycerin IV infusion, 10-20 mcg/minNitroglycerin IV infusion, 10-20 mcg/min– HeparinHeparin– GP IIB/IIIA inhibitorsGP IIB/IIIA inhibitors

Thrombolytics Checklist (just in case)Thrombolytics Checklist (just in case) Transport, destination?Transport, destination?

17

Ischemic Coronary Ischemic Coronary SyndromesSyndromes Acute Myocardial InjuryAcute Myocardial Injury

Presentation of Unstable Angina or Presentation of Unstable Angina or Acute Ischemia with Acute Ischemia with potentialpotential for for myocardium salvage (penumbra)myocardium salvage (penumbra)

Diagnostic evidence of Injury (ECG or Diagnostic evidence of Injury (ECG or elevated Enzymes)elevated Enzymes)

Does not necessarily imply necrosis of Does not necessarily imply necrosis of the myocardiumthe myocardium

Presentation, Signs and Symptoms are Presentation, Signs and Symptoms are the same as Acute MIthe same as Acute MI

18


Acute Myocardial Infarction (AMI)Acute Myocardial Infarction (AMI)Necrosis of myocardial tissue caused by Necrosis of myocardial tissue caused by

a lack of oxygenation and blood flow a lack of oxygenation and blood flow resulting from an occluded coronary resulting from an occluded coronary arteryartery

Often also used to describe acute injury Often also used to describe acute injury when extent of necrosis is unknown but when extent of necrosis is unknown but imminentimminent

Diagnostic evidence of injury is present Diagnostic evidence of injury is present (elevated enzymes and possibly ECG)(elevated enzymes and possibly ECG)

19


Acute Myocardial Infarction Acute Myocardial Infarction (AMI)(AMI)Precipitating FactorsPrecipitating Factors

Coronary thrombosis (most common)Coronary thrombosis (most common) Coronary vasospasmCoronary vasospasm MicroemboliMicroemboli Severe Hypotension/ShockSevere Hypotension/Shock Acute HypoxiaAcute Hypoxia Acute Volume OverloadAcute Volume Overload

20


Acute Myocardial Infarction Acute Myocardial Infarction (AMI)(AMI)Location, size of infarct and severity Location, size of infarct and severity

depends on site of vessel occlusiondepends on site of vessel occlusion majority involve left ventriclemajority involve left ventricle LCALCA

– anterior, septal, lateralanterior, septal, lateral RCARCA

– inferior, right ventricleinferior, right ventricle

21


Acute Myocardial Infarction Acute Myocardial Infarction (AMI)(AMI)Often defined further asOften defined further as

subendocardial: involves only subendocardial: involves only subendocardial musclesubendocardial muscle

transmural: full thickness of ventricular transmural: full thickness of ventricular wall involvedwall involved

22

Anatomy of Plaque Disruption

• Thin, friable fibrous capseparating substantialthrombogenic lipid corefrom blood

• Lumen could be well preserved

Adapted from Libby P. Circulat ion. 1995;91:2844-2850, with permission.

• Thick fibrous capprotecting thrombogeniclipid core from blood

• More luminal narrowing

Lumen Lumen

Shoulder region

Lipid core

Media

“Vulnerable” Plaque “Stable” Plaque

Lipid coreFibrous cap

Evolution of AMIEvolution of AMI

23

Plaque Rupture, Stenosis, and Thrombosis

Adapted from Davies MJ. In: Schlant RC, Alexander RW, eds. The Heart, Arteriesand Veins. 8th ed. 1994:1009-1020, with permission.

Plaque rupture— intraplaque thrombus

Mural thrombus

Occlusivethrombosis

Total chronicocclusion

Healed plaque— increased stenosis

Healed plaque — decreased stenosis

Recanalizedlumen


24

Plaque Rupture and Thrombus Progression

Adapted from Fuster V. N Engl J Med. 1992;326:242-250, with permission.

Lipid-rich

plaque

Plaquedisruptio

n

Thrombus

Lysis and residual thrombus

Disease progression

Completeocclusion

Reocclusion

Partial (labile) occlusion Recurrent pain

Unstableangina

AMI


25

Coronary Artery Without Coronary Artery Without Evidence of PlaqueEvidence of Plaque

Source: University of Utah WebPath

26

Coronary Artery with Coronary Artery with Significant Plaque Formation Significant Plaque Formation

In addition to reduced Lumen size, there is also a calcified portion (right side of photo)


27

Coronary Artery with Coronary Artery with Significant Plaque Formation Significant Plaque Formation


28

Rupture of Atheromatous Rupture of Atheromatous Plaque Results in Thrombus Plaque Results in Thrombus Formation Formation Rupture of “Vulnerable” plaque’s soft Rupture of “Vulnerable” plaque’s soft

lipid core is the initiating event in most lipid core is the initiating event in most acute ischemic coronary eventsacute ischemic coronary events

Occlusion is dependent on clot formation Occlusion is dependent on clot formation and and accompanying fibrinolysis and and accompanying fibrinolysis

A thrombotic occlusion that is relatively A thrombotic occlusion that is relatively persistent (i.e., 2 to 4 hours or longer) persistent (i.e., 2 to 4 hours or longer) may result in acute myocardial infarctionmay result in acute myocardial infarction

29

Rupture of Atheromatous Rupture of Atheromatous Plaque Results in Thrombus Plaque Results in Thrombus FormationFormation Repeated thrombus formations may Repeated thrombus formations may

further decrease the lumen sizefurther decrease the lumen size

Intermittent non-occlusive thrombus Intermittent non-occlusive thrombus formation results in Unstable Anginaformation results in Unstable Angina

Incomplete occlusion may also result in Incomplete occlusion may also result in MI possibly due to coronary artery MI possibly due to coronary artery spasmspasm

30

Coronary Artery With Plaque Coronary Artery With Plaque and Thrombus Formation and Thrombus Formation

A - Coronary Artery cross-section

B - Lumen

C - Fissured Plaque w/o Cap

D - Acute thrombus

Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas 1997

31

Plaque and Thrombus Plaque and Thrombus Formation Resulting in Formation Resulting in OcclusionOcclusion


32

Coronary Artery ThrombusCoronary Artery Thrombus


The external anterior view of the heart shows a dark clot formation in this artery

33

Coronary Artery Occlusion:The Evolution of Infarction

Progression of myocardial necrosis with time since occlusion

Adapted from Saltissi S, Mushahwar SS. Postgrad Med J. 1995;71:534-541, with permission.

4 h30 min 6 - 12 h

Normalmyocardium

“At risk”myocardium, ischemic but viable

Necrosis startingsubendocardially

Normalmyocardium

Completed infarctinvolving whole areaat risk

Normalmyocardium

“At risk”myocardium, ischemic but viable

Necrosis extendingtowardssubepicardium

Evolution of Evolution of Infarction/NecrosisInfarction/Necrosis

34


Acute Myocardial Infarction (AMI)Acute Myocardial Infarction (AMI)PresentationPresentation

Similar to Angina but Similar to Angina but – Last longerLast longer– Not easily relieved with rest or NTGNot easily relieved with rest or NTG– Sx/Sx may be more severe (feeling of impending doom)Sx/Sx may be more severe (feeling of impending doom)– Pain often radiates to arms, neck, jaw, back, epigastriumPain often radiates to arms, neck, jaw, back, epigastrium

Some present atypically with complaints of only Some present atypically with complaints of only weakness or shortness of breathweakness or shortness of breath

DysrhythmiasDysrhythmias Sudden Cardiac DeathSudden Cardiac Death

35

Ischemic Coronary Ischemic Coronary SyndromesSyndromes Acute Myocardial Infarction (AMI)Acute Myocardial Infarction (AMI)

PresentationPresentation 10-20% have “silent” MI (no chest pain)10-20% have “silent” MI (no chest pain)

– common in elderly, older women, diabeticscommon in elderly, older women, diabetics If adding chest pain to the patient’s list of If adding chest pain to the patient’s list of

Sx/Sx completes a clear picture of AMI, then Sx/Sx completes a clear picture of AMI, then the patient is having an AMI!!the patient is having an AMI!!

Vital Signs and monitoring ECG leads DO NOT Vital Signs and monitoring ECG leads DO NOT provide DIAGNOSTIC evidence of AMI!!provide DIAGNOSTIC evidence of AMI!!

Clinical diagnosis in absence of 12 Lead ECG Clinical diagnosis in absence of 12 Lead ECG or Enzyme changesor Enzyme changes

36

Goals for AMI Therapy

Shorten time to reperfusion

Preserve LV function

Avoid heart failure or cardiac shock

Limit Infarct Size

ResolveST-segment elevation

REDUCE MORTALITYIMPROVE OUTCOME

Yusuf, et al. Circulation. 1990;82(suppl II):II-117-134.

Schroder R. et al. J Am Coll Cardiol. 1995;26:1657-1664

TherapiesTherapies

37

Ischemic Coronary Ischemic Coronary SyndromesSyndromes Acute Myocardial Infarction Acute Myocardial Infarction

(AMI)(AMI)Treatment GoalsTreatment Goals

Decrease myocardial oxygen demandDecrease myocardial oxygen demand– Remove physical/psychological stressorsRemove physical/psychological stressors– Relieve painRelieve pain– Reduce workload of the heart (BP, HR)Reduce workload of the heart (BP, HR)

Inhibit further clot formationInhibit further clot formation Rapid identification/diagnosisRapid identification/diagnosis Transport for reperfusion therapyTransport for reperfusion therapy

38


Treatment same as Angina Treatment same as Angina PLUSPLUS:: IV, NS, large boreIV, NS, large bore

– TKO with some exceptionsTKO with some exceptions– No dextrose containing solutionsNo dextrose containing solutions– Fluid boluses appropriate in some casesFluid boluses appropriate in some cases– 2nd line if time permits2nd line if time permits– Minimize number of attemptsMinimize number of attempts

12 Lead ECG12 Lead ECG– Diagnostic evidence of AMI presentDiagnostic evidence of AMI present– Assess for RVIAssess for RVI

39


Treatment Treatment Morphine sulfate, 2 - 4 mg q 5-15 min slow IVMorphine sulfate, 2 - 4 mg q 5-15 min slow IV

– Maintain BP > ~ 90 mm HgMaintain BP > ~ 90 mm Hg– Titrated to Pain reliefTitrated to Pain relief– Reduce PVR and workload on the heartReduce PVR and workload on the heart

Aspirin, 160-325 mg POAspirin, 160-325 mg PO– Chewed & swallowed if possibleChewed & swallowed if possible– Determine if hypersensitive to ASADetermine if hypersensitive to ASA

““MONA greets all patients”MONA greets all patients”

40


Acute Myocardial Infarction (AMI)Acute Myocardial Infarction (AMI)TreatmentTreatment

Metoprolol, 5 mg slow IV q 5 min to 15 mg total, Metoprolol, 5 mg slow IV q 5 min to 15 mg total, prn for prn for HR/BP in absence of contraindications HR/BP in absence of contraindications

In longer or interfacility transports, consider:In longer or interfacility transports, consider:– Nitroglycerin IV infusionNitroglycerin IV infusion– HeparinHeparin

Thrombolytics ChecklistThrombolytics Checklist– Exclusions for thrombolysisExclusions for thrombolysis

41


Acute Myocardial Infarction Acute Myocardial Infarction (AMI)(AMI)Treatment Treatment

Transport for reperfusion therapy; Transport for reperfusion therapy; Destination?Destination?

– Thrombolysis vs Coronary Artery CatheterizationThrombolysis vs Coronary Artery Catheterization– For patients with associated pulmonary edema, For patients with associated pulmonary edema,

hypotension or cardiogenic shock, consider hypotension or cardiogenic shock, consider transport to facility with capability of transport to facility with capability of angiography & revascularizationangiography & revascularization

42

Acute Ischemic Syndromes:Diagnostic Considerations

Thrombolytics are not appropriate in all acute ischemicsyndromes

• Not all acute ischemic syndromes are AMIs

• ST-segment elevation suggests thrombic occlusionand need for immediate reperfusion

• No proven benefit of thrombolytic therapy in patientswithout ST-segment elevation

• Patients with ST-segment depression and/or T-waveinversion are currently not candidates for thrombolytictherapy

Considerations for Considerations for FibrinolyticsFibrinolytics

43

Contraindications for Contraindications for FibrinolyticsFibrinolytics Lack of diagnostic 12 Lack of diagnostic 12

Lead ECG changesLead ECG changes Chest pain < 20 min or Chest pain < 20 min or

> 12 hours> 12 hours Not oriented, can not Not oriented, can not

cooperatecooperate History of stroke or TIAHistory of stroke or TIA Known bleeding Known bleeding

disorderdisorder Active internal bleeding Active internal bleeding

in past 2-4 weeksin past 2-4 weeks

Surgery or trauma in Surgery or trauma in past 3 weekspast 3 weeks

Terminal illnessTerminal illness Jaundice, hepatitis, Jaundice, hepatitis,

kidney failurekidney failure Use of anticoagulantsUse of anticoagulants Systolic BP < 180 Systolic BP < 180

mm Hgmm Hg Diastolic BP < 110 Diastolic BP < 110

mm Hgmm Hg

44


““Ischemic and injured tissue have reduced blood flow Ischemic and injured tissue have reduced blood flow but but maymay be salvaged. The area of the Penumbra may be salvaged. The area of the Penumbra may be viable for several hours after onset of occlusion.”be viable for several hours after onset of occlusion.”Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas, 1997Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas, 1997

45


Sudden Cardiac Death (SCD or SCA)Sudden Cardiac Death (SCD or SCA)Sudden, unexpected biologic death presumably Sudden, unexpected biologic death presumably

resulting from cardiovascular diseaseresulting from cardiovascular diseaseMost common rhythm of SCA is Ventricular Most common rhythm of SCA is Ventricular

FibrillationFibrillationMay be primary or secondary VFMay be primary or secondary VFChain of Survival is the greatest determinant of Chain of Survival is the greatest determinant of

outcomeoutcomeTreatment based on ECG rhythm & arrest Treatment based on ECG rhythm & arrest

eventsevents

46

Time is Time is Muscle!!!Muscle!!!

47

References and ResourcesReferences and Resources

Advanced Cardiac Life SupportAdvanced Cardiac Life Support, Edited by R O Cummins, MD, American , Edited by R O Cummins, MD, American Heart Association, Dallas, 1997Heart Association, Dallas, 1997

““Emergency Cardiovascular Care Library” (CD-ROM), American Heart Emergency Cardiovascular Care Library” (CD-ROM), American Heart Association and ProEducation International, Dallas, 1997Association and ProEducation International, Dallas, 1997

Eisenberg, M S, Eisenberg, M S, Life in the Balance: Emergency Medicine and the Quest to Life in the Balance: Emergency Medicine and the Quest to Reverse Sudden DeathReverse Sudden Death, Oxford University Press, New York, 1997, Oxford University Press, New York, 1997

““A Definition of Advanced Types of Atherosclerotic Lesions and a A Definition of Advanced Types of Atherosclerotic Lesions and a Histological Classification of Atherosclerosis”, A Report From the Histological Classification of Atherosclerosis”, A Report From the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association, 1995Heart Association, 1995

““Coronary Artery Calcification: Pathophysiology, Epidemiology, Imaging Coronary Artery Calcification: Pathophysiology, Epidemiology, Imaging Methods, and Clinical Implications”, A Statement for Health Professionals Methods, and Clinical Implications”, A Statement for Health Professionals From the American Heart Association, 1995From the American Heart Association, 1995

Cardiovascular Disease Statistics, American Heart Association, Dallas, 1997Cardiovascular Disease Statistics, American Heart Association, Dallas, 1997 ““Diagnosis and Therapy of Acute Myocardial Infarction: Today’s Look at Diagnosis and Therapy of Acute Myocardial Infarction: Today’s Look at

Tomorrow’s Therapies and Outcomes”, DuPont Pharma, 1997Tomorrow’s Therapies and Outcomes”, DuPont Pharma, 1997 University of Utah WebPath, http://medstat.med.utah.edu/webpath/University of Utah WebPath, http://medstat.med.utah.edu/webpath/

Acute Coronary Syndromes

Documents

Transcript of Acute Coronary Syndromes