Acute Coronary Syndromes

EMS Professions
Temple College

1
 The History of Paramedics Begins
with Cardiac Care

✔The original Paramedic idea was based

upon the need for rapid response to,
identification of and emergency care for
victims of:

➨Sudden Cardiac Death (SCD)

➨Acute Myocardial Infarction (AMI)

2
 Ischemic Coronary Syndromes
✔Acute Coronary Syndromes
➨Angina Pectoris
➨Unstable Angina
➨Acute Myocardial Injury
➨Acute Myocardial Infarction
✔ Presentation with suspected ischemia
◆ Non-diagnostic ECG
◆ ST segment depression

◆ ST segment elevation/New BBB

3
 Ischemic Coronary Syndromes

✔Angina Pectoris
➨Acute pain, usually in the chest, resulting from
an increased demand for oxygen and a
decreased ability to provide it
➨Usually due to a partially occluded coronary
artery or vasospasm

4
 Ischemic Coronary Syndromes

✔Angina Pectoris
➨Typical Presentation
◆ Squeezing, Crushing, Heavy, Tight
– Fist to chest = Levine’s sign
◆ Pain/Discomfort may radiate to shoulders,
arms, neck, back, jaw or epigastrium
◆ Usually lasts 3-5 min and rarely exceeds 15 min

◆ Not changed by swallowing, coughing, deep

breathing or positional changes

5
 Ischemic Coronary Syndromes

✔Angina Pectoris
➨Typical Presentation
◆ Anxiety
◆ Diaphoresis or clammy skin

◆ Nausea, vomiting

◆ Shortness of breath

◆ Weakness

◆ Palpitations

◆ Syncope

6
 Ischemic Coronary Syndromes

✔Angina Pectoris
➨Usually Provoked by:
◆ Exercise
◆ Eating

◆ Emotion/Stress

➨Usually Relieved by:

◆ Rest; Removal of provoking factor
◆ Nitroglycerin

7
 Ischemic Coronary Syndromes

✔Stable Angina Pectoris

➨Reasonably Predictable frequency, onset,
duration
➨Relief predictable with rest, nitroglycerin

8
 Ischemic Coronary Syndromes

✔Stable Angina Pectoris

➨Treatment Goals
◆ Reduce myocardial oxygen demand
◆ Improve myocardial oxygen supply

9
 Ischemic Coronary Syndromes
✔Stable Angina Pectoris
➨Treatment
◆ Physical/Psychological rest
◆ Position of comfort, sitting or supine

◆ Oxygen

◆ ECG Monitor

– Assess the underlying rhythm

◆ Nitroglycerin, 0.4 mg SL q 5 min as long as BP
> 90 mm Hg
– Continue until pain relieved or contraindicated
10
 Ischemic Coronary Syndromes

✔Stable Angina Pectoris

➨Transport Considerations
◆ Many persons stay home and treat themselves
◆ Treat first-time angina, unstable angina or

angina requiring more than 3 NTG (>15 min) as

AMI
◆ When in doubt, treat as AMI

11
 Ischemic Coronary Syndromes
✔Stable Angina Pectoris
➨Variant Angina (Prinzmetal’s Angina)
◆ Occurs at rest
◆ Episodes at regular times of day

◆ Results from coronary vasospasms

◆ Treated long term with calcium channel

blockers
◆ May result in abnormal 12 lead ECG changes

that resolve with minimal treatment

12
 Ischemic Coronary Syndromes

✔Unstable Angina
➨Prolonged chest pain/ischemic symptoms or an
atypical presentation of angina without ECG
or laboratory evidence of AMI (Injury)
➨Usually associated with significant or
progressing occlusion of a coronary artery or
severe vasospasm
➨Considered “Pre-infarction Angina”

13
 Ischemic Coronary Syndromes

✔Unstable Angina
➨May have Typical or Atypical Signs &
Symptoms
◆ Atypical Presentation

– Increased frequency or duration of episodes

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

14
 Ischemic Coronary Syndromes
✔Unstable Angina
➨Treatment same as Angina PLUS:
◆ IV, NS (no dextrose), TKO
– Some exceptions to restricting fluid
◆ 12 Lead ECG
– Assess for RVI
◆ Morphine sulfate, 2 - 4 mg q 5-15 min slow IV
titrated to pain relief and BP > 90
◆ Aspirin, 160-325 mg PO

– Chewed & swallowed if possible

– Determine if hypersensitive to ASA
15
 Ischemic Coronary Syndromes
✔Unstable Angina
➨Treatment
◆ Metoprolol, 5 mg slow IV q 5 min to 15 mg total,
prn for  HR/BP in absence of contraindications
◆ In longer or interfacility transports, consider:

– Nitroglycerin IV infusion, 10-20 mcg/min

– Heparin
– GP IIB/IIIA inhibitors
◆ Thrombolytics Checklist (just in case)
◆ Transport, destination?

16
 Ischemic Coronary Syndromes

✔Acute Myocardial Injury

➨Presentation of Unstable Angina or Acute
Ischemia with potential for myocardium
salvage (penumbra)
➨Diagnostic evidence of Injury (ECG or
elevated Enzymes)
◆ Does not necessarily imply necrosis of the
myocardium
◆ Presentation, Signs and Symptoms are the same

as Acute MI
17
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Necrosis of myocardial tissue caused by a lack
of oxygenation and blood flow resulting from
an occluded coronary artery
➨Often also used to describe acute injury when
extent of necrosis is unknown but imminent
➨Diagnostic evidence of injury is present
(elevated enzymes and possibly ECG)

18
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Precipitating Factors
◆ Coronary thrombosis (most common)
◆ Coronary vasospasm

◆ Microemboli

◆ Severe Hypotension/Shock

◆ Acute Hypoxia

◆ Acute Volume Overload

19
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Location, size of infarct and severity
depends on site of vessel occlusion
◆ majority involve left ventricle
◆ LCA

– anterior, septal, lateral

◆ RCA
– inferior, right ventricle

20
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Often defined further as
◆ subendocardial: involves only subendocardial
muscle
◆ transmural: full thickness of ventricular wall

involved

21
 Evolution of AMI

Anatomy of Plaque Disruption

Shoulder region
Lipid core
Media
Lumen Lumen

Lipid core
Fibrous cap

“Vulnerable” Plaque “Stable” Plaque

• Thin, friable fibrous cap • Thick fibrous cap

separating substantial protecting thrombogenic
thrombogenic lipid core lipid core from blood
from blood
• More luminal narrowing
• Lumen could be well preserved

Ada pte d from Libby P . Circulat ion. 1995;9 1:2844- 2850, w ith permission.
22
 Evolution of AMI

Plaque Rupture, Stenosis, and Thrombosis

Plaque rupture
— intraplaque thrombus
Mural
thrombus

Occlusive
thrombosis

Total chronic Recanalized Healed plaque

occlusion lumen — increased
stenosis

Healed plaque
— decreased stenosis

Ada pte d from Davies MJ . In: Schla nt RC, Alexander RW, eds. The Heart, Arteries
and Ve ins. 8th ed. 1994:1 009-102 0, with permission.
23
 Evolution of AMI

Plaque Rupture and Thrombus Progression

Complete Lysis and residual Disease
occlusion thrombus progression
AMI

Lipid- Plaque
rich disruptio
plaque n

Reocclusion

Unstable
angina

Thrombus
Partial (labile) occ lusion Recurrent pain

Ada pte d from Fus ter V. N Engl J Med. 199 2;326:2 42-250, with perm iss ion.

24
 Coronary Artery Without Evidence
of Plaque

25 Source: University of Utah WebPath

 Coronary Artery with Significant
Plaque Formation
In addition
to reduced
Lumen size,
there is also
a calcified
portion
(right side
of photo)

26Source: University of Utah WebPath

 Coronary Artery with Significant
Plaque Formation

27 Source: University of Utah WebPath

 Rupture of Atheromatous Plaque
Results in Thrombus Formation

✔ Rupture of “Vulnerable” plaque’s soft lipid

core is the initiating event in most acute
ischemic coronary events

✔ Occlusion is dependent on clot formation and

and accompanying fibrinolysis

✔ A thrombotic occlusion that is relatively

persistent (i.e., 2 to 4 hours or longer) may
result in acute myocardial infarction
28
 Rupture of Atheromatous Plaque
Results in Thrombus Formation
✔ Repeated thrombus formations may further
decrease the lumen size

✔ Intermittent non-occlusive thrombus

formation results in Unstable Angina

✔ Incomplete occlusion may also result in MI

possibly due to coronary artery spasm

29
 Coronary Artery With Plaque and
Thrombus Formation
A - Coronary
Artery cross-
section

B - Lumen

C - Fissured
Plaque w/o
Cap

D - Acute
thrombus

30Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas 1997
 Plaque and Thrombus Formation
Resulting in Occlusion

31Source: University of Utah WebPath

 Coronary Artery Thrombus

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

32 Source: University of Utah WebPath

 Evolution of Infarction/Necrosis

Coronary Artery Occlusion:

The Evolution of Infarction
Progression of myocardial necrosis with time since occlusion

30 min 4h 6 - 12 h

Normal Normal Normal

myocardium myocardium myocardium

“At risk” “At risk”

myocardium, myocardium,
ischemic but viable ischemic but viable

Necrosis starting Necrosis extending Completed infarct

subendocardially towards involving whole area
subepicardium at risk

Ada pte d from Sa ltissi S , Mushahwar S S. Postgrad Med J. 1995;71 :534-54 1, with permission.

33
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Presentation
◆ Similar to Angina but
– Last longer
– Not easily relieved with rest or NTG
– Sx/Sx may be more severe (feeling of impending doom)
– Pain often radiates to arms, neck, jaw, back, epigastrium
◆ Some present atypically with complaints of only
weakness or shortness of breath
◆ Dysrhythmias

◆ Sudden Cardiac Death

34
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Presentation
◆ 10-20% have “silent” MI (no chest pain)
– common in elderly, older women, diabetics
◆ If adding chest pain to the patient’s list of
Sx/Sx completes a clear picture of AMI, then
the patient is having an AMI!!
◆ Vital Signs and monitoring ECG leads DO NOT

provide DIAGNOSTIC evidence of AMI!!

◆ Clinical diagnosis in absence of 12 Lead ECG or

35
Enzyme changes
 Therapies

Goals for AMI Therapy

Shorten time to reperfusion

Preserve Avoid heart failure Limit Resolve

LV function or cardiac shock Infarct Size ST-segment
elevation

REDUCE MORTALITY
IMPROVE OUTCOME

Yusuf, et al. Circulation. 199 0;82(suppl II):II-11 7-134.

36 Schroder R. e t al. J Am Coll Cardiol. 1995;2 6:1657- 1664
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Treatment Goals
◆ Decrease myocardial oxygen demand
– Remove physical/psychological stressors
– Relieve pain
– Reduce workload of the heart (BP, HR)
◆ Inhibit further clot formation
◆ Rapid identification/diagnosis

◆ Transport for reperfusion therapy

37
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Treatment same as Angina PLUS:
◆ IV, NS, large bore
– TKO with some exceptions
– No dextrose containing solutions
– Fluid boluses appropriate in some cases
– 2nd line if time permits
– Minimize number of attempts
◆ 12 Lead ECG
– Diagnostic evidence of AMI present
– Assess for RVI
38
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Treatment
◆ Morphine sulfate, 2 - 4 mg q 5-15 min slow IV
– Maintain BP > ~ 90 mm Hg
– Titrated to Pain relief
– Reduce PVR and workload on the heart
◆ Aspirin, 160-325 mg PO
– Chewed & swallowed if possible
– Determine if hypersensitive to ASA
◆ “MONA greets all patients”
39
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Treatment
◆ Metoprolol, 5 mg slow IV q 5 min to 15 mg total,
prn for  HR/BP in absence of contraindications
◆ In longer or interfacility transports, consider:

– Nitroglycerin IV infusion
– Heparin
◆ Thrombolytics Checklist
– Exclusions for thrombolysis

40
 Ischemic Coronary Syndromes

✔Acute Myocardial Infarction (AMI)

➨Treatment
◆ Transport for reperfusion therapy; Destination?
– Thrombolysis vs Coronary Artery Catheterization
– For patients with associated pulmonary edema,
hypotension or cardiogenic shock, consider transport to
facility with capability of angiography &
revascularization

41
 Considerations for Fibrinolytics
Acute Ischemic Syndromes:
Diagnostic Considerations
Thrombolytics are not appropriate in all acute ischemic
syndromes
• Not all acute ischemic syndromes are AMIs
• ST-segment elevation suggests thrombic occlusion
and need for immediate reperfusion
• No proven benefit of thrombolytic therapy in patients
without ST-segment elevation
• Patients with ST-segment depression and/or T-wave
inversion are currently not candidates for thrombolytic
therapy

42
 Contraindications for
Fibrinolytics
✔ Lack of diagnostic 12 ✔ Surgery or trauma in
Lead ECG changes past 3 weeks
✔ Chest pain < 20 min or ✔ Terminal illness
> 12 hours ✔ Jaundice, hepatitis,
✔ Not oriented, can not kidney failure
cooperate ✔ Use of anticoagulants
✔ History of stroke or TIA ✔ Systolic BP < 180 mm
✔ Known bleeding Hg
disorder ✔ Diastolic BP < 110 mm
✔ Active internal bleeding Hg
in past 2-4 weeks
43
 Ischemic Coronary Syndromes

“Ischemic and injured tissue have reduced blood flow

but may be salvaged. The area of the Penumbra may be
viable for several hours after onset of occlusion.”
Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas, 1997
44
 Ischemic Coronary Syndromes
✔Sudden Cardiac Death (SCD or SCA)
➨Sudden, unexpected biologic death presumably
resulting from cardiovascular disease
➨Most common rhythm of SCA is Ventricular
Fibrillation
➨May be primary or secondary VF
➨Chain of Survival is the greatest determinant of
outcome
➨Treatment based on ECG rhythm & arrest events
45
 Time is Muscle!!!

46
 References and Resources

✔ Advanced Cardiac Life Support, Edited by R O Cummins, MD, American Heart

Association, Dallas, 1997
✔ “Emergency Cardiovascular Care Library” (CD-ROM), American Heart
Association and ProEducation International, Dallas, 1997
✔ Eisenberg, M S, Life in the Balance: Emergency Medicine and the Quest to
Reverse Sudden Death, Oxford University Press, New York, 1997
✔ “A Definition of Advanced Types of Atherosclerotic Lesions and a Histological
Classification of Atherosclerosis”, A Report From the Committee on Vascular
Lesions of the Council on Arteriosclerosis, American Heart Association, 1995
✔ “Coronary Artery Calcification: Pathophysiology, Epidemiology, Imaging
Methods, and Clinical Implications”, A Statement for Health Professionals From
the American Heart Association, 1995
✔ Cardiovascular Disease Statistics, American Heart Association, Dallas, 1997
✔ “Diagnosis and Therapy of Acute Myocardial Infarction: Today’s Look at
Tomorrow’s Therapies and Outcomes”, DuPont Pharma, 1997
✔ University of Utah WebPath, http://medstat.med.utah.edu/webpath/
47