ST ELEVATION MI ( CASE STUDY ) and presentation

patient with myocardial infarction

1. LEARNING OUTCOMES
At the end of this lecture , student will be able to :
**Define Coronary artery disease
**Differentiate between types of ( ACS )
**identify last statistic about STEMI
**explain Pathophysiology of ACD
**identify risk factor and causes
**identify most complication of STEMI
**rememmber diagnostic procedure of STEMI
**Explain AHA guideline of STEMI management

2. Introduction:
Cardiovascular disease is the major cause of death in the united state . Coronary artery disease (CAD) is
the most common type of cardiovascular disease and account for the majority of these deaths .
*** THE (CAD) :1- STABLE ANGINA (SA).
2 -ACS .( USA , STEMI ,NSTEMI ) .

The American heart association (AHA) estimate that 1.5 million
Americans have (MI) Annually and about one fourth of these die in
emergency department or before reaching the hospital.

3. Troponin I (–ve) Troponin I (+ve) Troponin I (+ve)Troponin I (–ve) Troponin I (+ve) Troponin I (+ve)

4. Current Landscape
1.5 Million Myocardial Infarctions Annually
400,000 STEMI Patients Annually
American Hospital Association 2007.American Hospital Association 2007.

5. ***ACS
when ischemia is prolonged and not immediately reversible acute
coronary syndrome develops.
*Etiology and pathophysiology:
ACS is associated with deterioration of a stable atherosclerosis plaque in
which the stable plaque rupture exposing the intima to blood and
stimulating platelet aggregation and local vasoconstriction with
thrombus formation . This unstable lesion may be partially occluded by
thrombus ( manifesting as USA or NSTEMI ) or totally occluded
( manifest as STEMI ) .

7. Triggers to Plaque Rupture
Inflammatory
cytokines
Plaque RupturePlaque Rupture
Physical Stress
Vulnerable
Plaque
Emotional
Stress

8. Consequences of
Coronary Thrombosis
Lilly. Pathophysiology of Heart Disease, 4th Ed. Lippincott Williams, 2007. Page 173

9. ACS cont.
2 -myocardial infarction ( MI ) :
Occur as a result of sustained ischemia causing irreversible cardiac cell death
and 90% of all acute MI are secondary to thrombus formation ( when this
thrombus formed it will decrease or halt the perfusion distal to the
occlusion area resulting in necrosis that’s will lead to stop the contractility
function of the necrotic part .
Infarction usually describe based on the location of damage (e.g. anterior ,
inferior , lateral , or posterior wall infarction ) and it can occur in more
than one location (e.g. anterolateral , anteroseptal ) the location of the
infarction correlates with the involved coronary artery.

10. ACUTE CORONARY SYNDROMESACUTE CORONARY SYNDROMES
No ST elevationNo ST elevation ST elevationST elevation
UnstableUnstable
anginaangina
NSTEMINSTEMI STEMISTEMI
Spectrum of CAD
StableStable
anginaangina
Figures reproduced with permission from Davies MJ. Figures reproduced with permission from Davies MJ. HeartHeart. 2000;83:361-366.. 2000;83:361-366.
Rosamond W, et al. American Heart Association Statistics Committee and Stroke Statistics Committee. Rosamond W, et al. American Heart Association Statistics Committee and Stroke Statistics Committee.
Heart Disease and Stroke Statistics 2008 Update [published online ahead of print December 17, 2007]. Heart Disease and Stroke Statistics 2008 Update [published online ahead of print December 17, 2007].
CirculationCirculation. doi:10.1161/CIRCULATIONAHA.107.187998. . doi:10.1161/CIRCULATIONAHA.107.187998.
~0.4 Million~0.4 Million
Discharges Per YearDischarges Per Year
~1 Million~1 Million
Discharges Per YearDischarges Per Year

11. Annual Admissions for Acute
Coronary Syndromes (ACS)
1.6 million1.6 million
Non-ST-Non-ST-
segment segment
elevation elevation
ACSACS
400,000400,000
ST-segment ST-segment
elevation MI elevation MI
(STEMI)(STEMI)
~ 2.0 MM patients admitted~ 2.0 MM patients admitted
to CCU or telemetry annuallyto CCU or telemetry annually

12. Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS)Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS)
Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007;
115:69-171. *Primary and secondary diagnoses. †About 0.57 million NSTEMI 115:69-171. *Primary and secondary diagnoses. †About 0.57 million NSTEMI
and 0.67 million UA.and 0.67 million UA.
Acute Coronary Acute Coronary
Syndromes*Syndromes*
1.57 Million1.57 Million Hospital Admissions - ACSHospital Admissions - ACS
UA/NSTEMIUA/NSTEMI
††
STEMISTEMI
1.24 million1.24 million
Admissions per Admissions per
yearyear
.33 million.33 million
Admissions per Admissions per
yearyear
Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69-171. Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69-171.
*Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.*Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.

13. Chest pain one of the most common symptoms driving patients
to a physician's offices or hospital’s emergency room.
55.3 % of pts were chest pain cardiac origin .
 44.7 % of pts were chest pain non cardiac ( NCCP )
Cardiac chest pain
**************
Stable angina
Unstable angina
Myocardial infarction
aortic dissection
Pericarditis
mitral valve prolapse
Post–stent insertion
Non Cardiac Chest Pain
************
Gastroesophageal reflux
( GERD)
Esophageal spasm
Peptic ulcer
Pulmonary embolism
Pneumonia
Pneumothorax

14. Causes of Acute Coronary Syndromes
Atherosclerosis with superimposed thrombus
Vasculitic syndromes
Coronary emboli (e.g., from endocarditis, artificial valves)
Congenital anomalies of the coronary arteries
Coronary trauma or aneurysm
Severe coronary artery spasm (primary or cocaine-induced)
Increased blood viscosity (e.g., polycythemia vera,
thrombocytosis)
Significantly increased myocardial oxygen demand (e.g.,
aortic stenosis)

15. Risk Factors for CAD
These factors are:
Non modifiable such as
Age , Race , Family history of MI before age of 60
years, Gender ( male > female)
Modifiable such as : elevated serum lipids (cholesterol,
triglycerides). Other factors are high-fat diet, obesity,
physical inactivity, hypertension (SBP > 140 mm Hg or DBP
> 90 mm Hg), cigarette smoking, and chronic kidney
disease. DM… ;
1515

16. smoking
Smoking aggravates the
lining of the arteries and
speeds up the process of
atherosclerosis
Also increase LDL ,
Triglyceride , and
decrease HDL
Nicotine Raises heart
rate and blood pressure
transiently ( addiction)
Active smoking ( M
(25% ), F (20%), Passive
smoking (35% )

17. Physical Inactivity
30 minutes a day at least 3 days a week which can be
split into 15 minute periods of regular, moderate
intensity activity ( e.g. walking, swimming, cycling,
dancing, skipping ..etc )
The most active men and women had risk reductions
of 30-35% for incident CAD
(Sofi F, Capalbo A, Marcucci R, et al. Leisure time but not occupational physical activity significantly affects
cardiovascular risk factors in an adult population. Eur J Clin Invest. 2007 )

18. Central Obesity) ) Obesity
caused by excessive
calorie intake, and
inactivity
can lead to high blood
pressure, raised blood
cholesterol levels, and
diabetes
 BMI is indicator.

19. Research study
**Physical activity, abdominal obesity and the risk of
coronary heart disease: A korean national sample
study
(Kim J, Han B, 2012 )
** Both men and women with large waist
circumference ( WCs) were at increased risk of CHD
compared with those with normal WCs.

20. High Blood Pressure

the force of blood in the
arteries is over 140/90
mmHg
can be lowered with
more activity, weight
loss, low salt diet and
alcohol

21. Diabetes ( Risk equivalent)
 uncontrolled blood sugar encourages the build up
of fatty deposits within the arterial walls
 Glycaemic control is still exceedingly important in
reducing micro-vascular complications and
morbidity (Ali K, Narayan M, Tandon N , Diabetes & coronary
heart disease: Current perspectives 2010)

22. Silent Ischemia
The presence of objective evidence of ischemia
observed on ECG in the absence of chest discomfort .
Diabetic persons at high risk for it due developing of
“ autonomic neuropathy” which decrease their ability
to express chest pain .

23. Silent ischemia and diabetes mellitus
The result of study : The prevelance of SMI is 10-20%
in diabetic pt Versus 1-4% in nondiabetic pt.
Exersize treadmill test ( ETT ) and ambulatory
( Holter) monitoring are the most readily aviable and
frequently used tests in identify SMI in clinical
practice
Boras, J., Brkljačić, N., Ljubičić, A., & Ljubić, S. (2010). Silent Boras, J., Brkljačić, N., Ljubičić, A., & Ljubić, S. (2010). Silent
ischemia and diabetes mellitus. ischemia and diabetes mellitus. Diabetologia CroaticaDiabetologia Croatica, , 3939(2).(2).

24. AMI- World Health Organization (WHO)
Definition
 A combination of two of three characteristics:
Typical symptoms (i.e., ischemic-type chest discomfort)
A rise and fall in serum cardiac markers
Typical ECG pattern involving the development of Q waves

25. Number of vessel obstructed
Major determinant of angina outcome
0 vessel 88% survival rate
1 vessel 74% survival rate
2 vessel 59% survival rate
3 vessel 40% survival rate

26. Symptoms
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

27. ECG evolution in Q-wave Myocardial
Infarction
Tall peaked T-waves
ST-segment elevation
Appearance of abnormal Q wave
Decrease of ST-segment elevation with the
beginning of T-wave inversion
Isoelectric ST-segment with symmetrical T-wave
inversion

28. Tall T- Waves
The earliest sign of AMI
Due to subendocardial ischemia
Within minutes or hours after the onset of chest
pain
Transient
Most ECGs fail to show this pattern

29. Complications of MI
Myocardial InfarctionMyocardial Infarction
VentricularVentricular
thrombusthrombus
ContractilityContractility
ElectricalElectrical
instabilityinstability
TissueTissue
necrosisnecrosis
PericardialPericardial
inflammationinflammation
EmbolismEmbolism ArrhythmiasArrhythmias PericarditisPericarditis
PapillaryPapillary
musclemuscle
infarction/infarction/
ischemiaischemia
VentricularVentricular
septalseptal
defectdefect
VentricularVentricular
rupturerupture
MitralMitral
regurgitationregurgitation
CongestiveCongestive
heart failureheart failure
CoronaryCoronary
perfusionperfusion
pressurepressure
IschemiaIschemia HypotensionHypotension
CardiogenicCardiogenic
shockshock
CardiacCardiac
tamponadetamponade

30. Diagnostic studies
In addition to the history of pain , risk factor , and health history, the
primary diagnostic study used to determine if the person has USA or
MI include an ECG, CARDIAC MARkER .
1 -Electrocardiogram finding(ECG):
The ECG is the primary tool to rule out or confirm USA or MI
-But the question is how ? when we talk
about USA or NSTEMI we talk about partially occluded artery so it may
have its reflect on the ECG or may not have but the STEMI which has
the complete occluded artery has its especial reflect on the ECG.

31. Lilly. Pathophysiology of Heart Disease, 4th Ed. Lippincott Williams, 2007. Page 182

32. Diagnostic studies
2 -cardiac markers : it’s a proteins which released from the necrotic
tissue of the heart in large quantities after an MI * Creatinin kinase (ck)
and Tropinin are typically measured to diagnose an MI. (the normal
range 0-9 U/L)
CK levels begin to rise approximately 3-12 hours after an MI and its
return to normal within 2-3 days and the CK is divided into band which
include the MB band ( in which its specific to the heart damage just ) .
Cardiac specific troponin which also increase in the circulation after the
damage to the heart muscle and in the heart there are two subtypes :
A- troponin T (N<0.1 ng/ml ) B- troponin I(N<0.4ng/ml)

34. Time course of the appearance of various markers in the
blood after acute myocardial infarction (AMI)
3434

35. Diagnostic tests/ Lab testsDiagnostic tests/ Lab tests
* * MyoglobinMyoglobin
- - MyoglobinMyoglobin is an oxygen-binding protein found in skeletal is an oxygen-binding protein found in skeletal
and cardiac muscle (thus it is not specific to the heart)and cardiac muscle (thus it is not specific to the heart)
- Onset within 1 to 2 hours of acute MI and peaks within 3 - Onset within 1 to 2 hours of acute MI and peaks within 3
to 15 hours.to 15 hours.

- The early release of - The early release of myoglobinmyoglobin makes in valuable in makes in valuable in
helping to detect MI.helping to detect MI.

36. Cardiac-Specific Troponins
Regulatory protein that controls interaction
between actin & myosin
3 subunits: TnC, I, T
Unique cardiac troponins I and T exist - absent in
serum of healthy people
Powerful marker of myocyte damage
Rise at 3-4 hours post-MI, peak 18-36 hrs, decline
slowly 10-14 days
Skeletal &Skeletal &
cardiac musclecardiac muscle

37. Creatinine Kinase
Enzyme that converts ADP to ATP
Found in many tissues: heart, brain, skeletal muscle,
kidney, etc.
Can be elevated after injury to any of these tissues
3 isoenzymes:- CK-MM
-CK-MB - CK-BB
In the patient with an MI, the ck-MB2 level rises
resulting in a CK-Mb2 to CK-MB1 ratio greater than
one.

38. CPK-MB
Makes up 1-3% of skeletal CK
Makes up much higher % of cardiac CK
Rises 4-8 hours after MI, peaks by 24 hours
Returns to normal in 48-72 hours

39. serum biomarkers after acute myocardial
infarction table
3939

40. Prognostic value of high sensitivity C reactive protein in
acute ST elevation myocardium infarction in hospitalized
patients.
the comparing also between 1
st
and 3
rd
day of hs-
CRP in acute STEMI who develop worse
outcomes and with patient didn’t develop
outcomes. Among the two groups arrhythmia
was found significantly high in ( high hs-CRP).
The worse outcomes had higher mean value of
the first and the third day hs-CRP in compare
with those who didn’t develop these outcomes .
 Finally, In future we recommend to use hs-
CRP to assess the prognosis of STEMI which is
inexpensive and simple assessment tool.
Basak , S., Akhtaruzzaman, K., Kundu, A., Dey, s.,Uddin, M. Basak , S., Akhtaruzzaman, K., Kundu, A., Dey, s.,Uddin, M. (2012). (2012). Prognostic value of Prognostic value of
high sensitivity C reactive protein in acute ST elevation myocardium infarction in hospitalized high sensitivity C reactive protein in acute ST elevation myocardium infarction in hospitalized
patients. patients. Midicine Today,1(24)Midicine Today,1(24)

41. AMI Diagnosis- ECG
Factors Influencing ECG Interpretation
Clinical observation of the patient
Knowledge of clinical data
Training and experience of interpreter

42. AMI Diagnosis- ECG
Gjorup et al, J Intern Med. 1992; 231: 407-412
16 IM residents read 107 ECGs
Looking for signs indicative of AMI
Disagreement in 70% of the cases

43. AMI Diagnosis- ECG
Willems et al, NEJM. 1991; 325:1767-1773
8 cardiologists interpreted 1220 ECGS
High interobserver agreement -  of 0.67
125 ECGs read twice
Different diagnosis for 10%-23% of ECGs

44. 2004
AHA/ACC GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH
ST-ELEVATION MYOCARDIAL INFARCTION
A REPORT OF THE AMERICAN COLLEGE OF
CARDIOLOGY / AMERICAN HEART
ASSOCIATION TASK FORCE ON PRACTICE
GUIDELINES

45. Patient Education for Early Patient Education for Early
Recognition and Response to STEMIRecognition and Response to STEMI
Patients should understand the advisability Patients should understand the advisability
of calling 199 if symptoms are unimproved of calling 199 if symptoms are unimproved
or worsening after 5 minutes.or worsening after 5 minutes.
Patients should understand their risk of Patients should understand their risk of
STEMI and how to recognize symptoms of STEMI and how to recognize symptoms of
STEMI.STEMI.
IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII
IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII

46. Prehospital 12-lead ECG by ACLS
Prehospital fibrinolysis
Reperfusion “checklist” by ACLS providers that
is relayed with the ECG to a predetermined
medical control facility and/or receiving
hospital
Prehospital IssuesPrehospital Issues
IIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIII
IIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIII

47. Prehospital IssuesPrehospital Issues
Prehospital destination protocols:Prehospital destination protocols:
Patients with STEMI who have contraindications Patients with STEMI who have contraindications
to fibrinolytic therapy should be brought to fibrinolytic therapy should be brought
immediately immediately
(primary-receiving hospital door-to-departure time (primary-receiving hospital door-to-departure time
less than 30 min.) to facilities capable of cardiac less than 30 min.) to facilities capable of cardiac
catheterization and rapid revascularizationcatheterization and rapid revascularization
IIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIII

48. Primary PCIPrimary PCI
STEMI patients presenting to a hospital with PCI STEMI patients presenting to a hospital with PCI
capability should be treated with primary PCI within capability should be treated with primary PCI within
90 min of first medical contact as a systems goal. 90 min of first medical contact as a systems goal.
STEMI patients presenting to a hospital without PCI STEMI patients presenting to a hospital without PCI
capability, and who cannot be transferred to a PCI capability, and who cannot be transferred to a PCI
center and undergo PCI within 90 min of first center and undergo PCI within 90 min of first
medical contact, should be treated with fibrinolytic medical contact, should be treated with fibrinolytic
therapy within 30 min of hospital presentation as a therapy within 30 min of hospital presentation as a
systems goal, unless fibrinolytic therapy is systems goal, unless fibrinolytic therapy is
contraindicated.contraindicated.
IIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIII
IIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIIIIIaIIaIIaIIaIIaIIaIIbIIbIIbIIbIIbIIbIIIIIIIIIIIIIIIIII

49. ReperfusionReperfusion
• Given the current literature, it is not possible to say Given the current literature, it is not possible to say
definitively that a particular reperfusion approach is definitively that a particular reperfusion approach is
superior for all pts, in all clinical settings, at all times of superior for all pts, in all clinical settings, at all times of
day day
• The main point is that some type of reperfusion therapy The main point is that some type of reperfusion therapy
should be selected for all appropriate pts with suspected should be selected for all appropriate pts with suspected
STEMI STEMI
• The appropriate & timely use of some reperfusion The appropriate & timely use of some reperfusion
therapy is likely more important than the choice of therapy is likely more important than the choice of
therapytherapy

50. Criteria for Thrombolysis
ST elevation (greater than 1 mm in two or more
contiguous leads), time to therapy 12 hours or less, age
less than 75 years .
Bundle branch block (obscuring ST-segment analysis)
and history suggesting acute MI .

51. Fibrinolysis vs. angioplasty
Meta-analyses
8.5
7.3 7.2
22
2.0
7.2
4.9
2.8
6.8
1.0
0
5
10
15
20
25
Death Death SHOCK
excl.
ReinfarctionRecurrent
ischemia
Stroke
P
e
r
c
e
n
t

(
%
)
Lysis PCI
4-6 weeks4-6 weeks
Ellen C Keeley, Judith A Boura, Cindy L Grines. Lancet 2003; 361:13–20.Ellen C Keeley, Judith A Boura, Cindy L Grines. Lancet 2003; 361:13–20.
P=0.0002P=0.0002 P=0.0003P=0.0003 P<0.0001P<0.0001
P<0.0001P<0.0001
P=0.0004P=0.0004

52. STEMI Chain of Survival

53. Symptoms Symptoms to to balloon inflation balloon inflation
(minutes)(minutes)
O
n
e
-
y
e
a
r

m
o
r
t
a
l
i
t
y
,

O
n
e
-
y
e
a
r

m
o
r
t
a
l
i
t
y
,

%%
6 RCTs of Primary PCI by Zwolle Group 6 RCTs of Primary PCI by Zwolle Group
1994 1994 – – 20012001
N = 1791N = 1791
RR = 1.08 [1.01 RR = 1.08 [1.01 – – 1.16] for each 30 1.16] for each 30
min delaymin delay
((PP = 0.04) = 0.04)
PP < <
0.00010.0001
1212
1010
88
66
44
22
00
00 6060 120120 180180 240240 300300
360360
Symptom Onset to Balloon Time and Symptom Onset to Balloon Time and
Mortality in Primary PCI for STEMIMortality in Primary PCI for STEMI
DeLuca et al. Circulation 2004;109:1223.DeLuca et al. Circulation 2004;109:1223.

54. 5454
Barriers to Timely Reperfusion
The patient
Time to transport
Decision process on arrival
Time to implement treatment
strategy

55. Media campaignMedia campaign
Patient education Patient education
Methods of Methods of
Speeding Speeding
Time to Time to
ReperfusionReperfusion
Greater use of Greater use of
9-1-19-1-1
Prehospital RxPrehospital Rx
MI protocolMI protocol
Critical pathwayCritical pathway
Quality Quality
improvement improvement
programprogram


Bolus lytics Bolus lytics
Dedicated Dedicated
PCI teamPCI team
55 minmin<< 30 min 30 min
Prehospital Prehospital
ECGECG
PatientPatientTransporTranspor
tt
ECGECG ReperfusionReperfusion
Reperfusion goalsReperfusion goals
TimesTimes
Door to Door to needleneedle < 30 minutes< 30 minutes
11
stst
medical contact to medical contact to balloon < balloon <
90 minutes90 minutes (including transfers) (including transfers)
< 10 min< 10 min

56. Treatment of AcuteTreatment of Acute
Coronary Syndromes:Coronary Syndromes:
STE MISTE MI

57. Treatment of Acute Coronary Treatment of Acute Coronary
SyndromesSyndromes
ST-Elevation
(STEMI)
Emergent PCI available
within 90 min?
Fibrinolytic
Therapy
(e.g., tPA)
Primary PCI
No Yes

58. Cardiac biomarkers & reperfusion
5858
-Management of ST-elevation myocardial infarction
(STEMI) is to open the coronary artery obstructed by a
thrombus
&re -perfuse the injured area as rapidly as possible
-Individuals who have recent onset of chest pain ( within
12
hrs) are candidates for reperfusion therapies including-:
*Fibrinolytic agent
Cardiac catheterization) *balloon angioplasty,
atherectomy, or stent placement)

59. ManagementManagement
* Fibrinolytic therapy* Fibrinolytic therapy
- Lyse coronary thrombi by converting plasminogen to - Lyse coronary thrombi by converting plasminogen to
plasmin which degrade fibrin and fibrinogen.plasmin which degrade fibrin and fibrinogen.
- The goal is administration of the thrombolytic drug (if - The goal is administration of the thrombolytic drug (if
indicated) indicated) within 30 within 30 minutes of the patient's arrival to the minutes of the patient's arrival to the
emergency department.emergency department.
- Thrombolytic therapy provides maximal benefit if given - Thrombolytic therapy provides maximal benefit if given
within the within the first 3 hours first 3 hours after the onset of symptoms. after the onset of symptoms.
- Significant benefit still occurs if therapy is given up - Significant benefit still occurs if therapy is given up to 12 to 12
hours after onset of symptoms.hours after onset of symptoms.
- Minimal benefit if thrombolytic are given more than 12 hours - Minimal benefit if thrombolytic are given more than 12 hours
after the onset of symptoms.after the onset of symptoms.

60. ManagementManagement
* The patient is closely monitored during and after the infusion * The patient is closely monitored during and after the infusion
of a thrombolytic agent.of a thrombolytic agent.
- - The nurse The nurse assesses the patient for resolution of assesses the patient for resolution of chest pain chest pain , ,
normalization of elevated ST segments, development of normalization of elevated ST segments, development of
reperfusion reperfusion dysrhythmiasdysrhythmias ( accelerated idioventricular rhythm, ( accelerated idioventricular rhythm,
ventricular tachycardia, and AV heart block) any ventricular tachycardia, and AV heart block) any allergic allergic
reactionsreactions, evidence of bleeding , and the onset of , evidence of bleeding , and the onset of hypotensionhypotension..

- The nurse monitor the development of complications such as - The nurse monitor the development of complications such as
reocclusion of the coronary artery reocclusion of the coronary artery (chest pain, ST segment (chest pain, ST segment
elevation, and hemodynamic instability), bleeding (urine elevation, and hemodynamic instability), bleeding (urine
and stool for blood or altered levels of consciousness due to and stool for blood or altered levels of consciousness due to
intracranial bleeding). intracranial bleeding).

61. ManagementManagement
* Absolute contraindications to fibrinolytic therapy* Absolute contraindications to fibrinolytic therapy
- Previous hemorrhagic stroke at any time; other strokes or - Previous hemorrhagic stroke at any time; other strokes or
cerebrovascular events within 1 year. cerebrovascular events within 1 year.
- Known intracranial neoplasm - Known intracranial neoplasm
- Active intracranial bleeding (does not include menses)- Active intracranial bleeding (does not include menses)
- Suspected aortic dissection- Suspected aortic dissection
* Relative contraindication to fibrinolytic therapy* Relative contraindication to fibrinolytic therapy
- Sever uncontrolled hypertension on presentation (blood - Sever uncontrolled hypertension on presentation (blood
pressure>180/110mmHg) current use of anticoagulants in pressure>180/110mmHg) current use of anticoagulants in
therapeutic does (international normalized ratio therapeutic does (international normalized ratio
{INR}>=2:3);Known bleeding {INR}>=2:3);Known bleeding
- Recent trauma (within 2_4weeks ),including head trauma or - Recent trauma (within 2_4weeks ),including head trauma or
traumatic prolonged (>10monutes )cardiopulmonary traumatic prolonged (>10monutes )cardiopulmonary
resuscitation(CPR) or major surgery (< 3 weeks) resuscitation(CPR) or major surgery (< 3 weeks)

62. Nitrates
Reduce ischemia (not mortality)
Venodilation: R heart return
Coronary vasodilation
Usually given SL then IV
Reduce pain/ischemia
Relieve pain
Reduce pulmonary congestion in heart failure

63. Beta Blockers
Sympathetic drive; HR & BP
O
2 demand
Shear stress
Sudden death, death, recurrent MI

64. ß- Blockers
 Risk arrhythmia, reinfarction, rupture, death
Give IV, then orally unless contraindication exists
(asthma, hypotension, significant bradycardia)

65. Non Dihydropyridine
Calcium Channel Blockers
 Heart rate
Vasodilate
Relieve ischemia, not mortality
Don’t give in patients with sx/signs
of heart failure

66. Aspirin
Reduces mortality & reinfarction
Give immediately on
presentation and daily thereafter
If aspirin allergy, use clopidogrel

67. Heparin
Give 1-2 days IV after PCI or lysis with tPA, rPA, or
TNK-tPA… NOT SK
Also if:
Atrial fibrillation
LV thrombus
New anterior MI with large wall motion change
All others: SQ heparin while at bed rest to prevent
DVT

68. ACE - Inhibitors
Limit adverse LV remodeling
 Heart failure/death
 MI
Benefit additive ASA, BB
Esp. benefit anterior MI and/or LV
dysfunction

69. Statins
Reduce reinfarction, death
More benefit when started early
Give if LDL cholesterol is > 100

70. Additional Rx: STE MI
Maintain vessel patency
Restore balance between 0
2 supply
and demand
Relieve chest pain
Prevent complications

71. Management Management
Percutaneous transluminal coronary angioplasty (PTCA)Percutaneous transluminal coronary angioplasty (PTCA)
-PTCA is an invasive procedure in which the infarct related PTCA is an invasive procedure in which the infarct related
coronary artery is dilated with a balloon catheter and possibly coronary artery is dilated with a balloon catheter and possibly
stent placement after balloon dilatation .stent placement after balloon dilatation .
- PTCA is used for patient - PTCA is used for patient present within 24hr present within 24hr of the onset of of the onset of
symptoms, with persistent ischemia symptoms, for patients symptoms, with persistent ischemia symptoms, for patients
ineligible for thrombolytic therapy. ineligible for thrombolytic therapy.
- Complication include retroperitoneal or vascular - Complication include retroperitoneal or vascular
hemorrhagehemorrhage, ,
early acute reocclusion, and late restenosis. early acute reocclusion, and late restenosis.
  

72. ANY QUESTIONS..…

73. References:
Andrews, J. (1982). Teaching assistants: A handbook of
teaching ideas. San Diego, CA: University of California,
San Diego, TA Development Program.

Arreola, R.(1998). Writing learning objectives.A teaching
resource document from the office of the vice chancellor
for planning and academic support, University of
Tennessee, Memphis
Bloom, B.S., Englehatt, M D., Furst, EJ., Hill, W.H and
Krathwole D.R (1956). Taxonomy of educational objectives:
Handbook, Cognitive domain. New York: Wiley