Transcript The Pathophysiology of the Acute MI

Acute Coronary Syndromes
Terry White, RN, EMP-T
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,
> 90 mm Hg
0.4 mg SL q 5 min as long as BP
– Continue until pain relieved or contraindicated
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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
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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
15
– Chewed & swallowed if possible
– Determine if hypersensitive to ASA
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
• Thin, friable fibrous cap
separating substantial
thrombogenic lipid core
from blood
“Stable” Plaque
• Thick fibrous cap
protecting thrombogenic
lipid core 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
occlusion
Recanalized
lumen
Healed plaque
— increased
stenosis
Healed plaque
— decreased stenosis
23
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.
Evolution of AMI
Plaque Rupture and Thrombus Progression
Complete
occlusion
Lysis and residual
thrombus
Disease
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)
26
Source: 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 crosssection
B - Lumen
C - Fissured
Plaque w/o
Cap
D - Acute
thrombus
30
Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas 1997
Plaque and Thrombus Formation
Resulting in Occlusion
31
Source: 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
Normal
myocardium
Normal
myocardium
“At risk”
myocardium,
ischemic but viable
Necrosis starting
subendocardially
6 - 12 h
Normal
myocardium
“At risk”
myocardium,
ischemic but viable
Necrosis extending
towards
subepicardium
Completed infarct
involving whole area
at risk
Ada pte d from Sa ltissi S , Mushahwar S S. Postgrad Med J. 1995;71 :534-54 1, with permission.
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Ischemic Coronary Syndromes
Acute Myocardial Infarction (AMI)
Presentation
 Similar
–
–
–
–
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
34
to Angina but
present atypically with complaints of only
weakness or shortness of breath
 Dysrhythmias
 Sudden Cardiac Death
Ischemic Coronary Syndromes
Acute Myocardial Infarction (AMI)
Presentation
 10-20%
have “silent” MI (no chest pain)
– common in elderly, older women, diabetics
 If
35
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
Enzyme changes
Therapies
Goals for AMI Therapy
Shorten time to reperfusion
Preserve
LV function
Avoid heart failure
or cardiac shock
Limit
Infarct Size
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
Resolve
ST-segment
elevation
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,
–
–
–
–
–
 12
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
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
39
greets all patients”
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
Lead ECG changes
 Chest pain < 20 min or
> 12 hours
 Not oriented, can not
cooperate
 History of stroke or TIA
 Known bleeding
disorder
 Active internal bleeding
in past 2-4 weeks
43
 Surgery or trauma in
past 3 weeks
 Terminal illness
 Jaundice, hepatitis,
kidney failure
 Use of anticoagulants
 Systolic BP < 180 mm
Hg
 Diastolic BP < 110 mm
Hg
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.”
44
Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas, 1997
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/
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