CHEST PAIN SCENARIO 3GROUP 10

AinLatifahRafikaNunungAishahAmalinaMiqdadHarry

AndhikaFadliNovaRina

SCENARIOA collapse 60 years old bus driver was brought into casualty complaining of severesustained crushing pain in a band across the chest spreading into arms Previously he had been wellthough he smoked 10 cigarettes a day On examination he was pale with coldsweaty skin His pulse was weakwith occasional extrasystole(ventricular ectopic beats) His arterial blood pressure was 9075 mmHg Heart sound were normal An ECG revealed large Q wave and ST segment elevation He was admitted with a provisional diagnosis of myocardial infarction due to coronary artery thrombosis Plasma analysis showed raised cardiac enzymes( lactic dehydrogenasecreatine phosphokinaseaspartate aminotransferase) He was given O2 and morphine A streptokinase infusion was set up to lyse the coronary thrombus and he was also started on regularlow dose aspirin

KEYWORD

bull Collapsebull Severe sustained crushing pain in band across chest

spreading into armbull Previously been wellbull Palecold sweaty skinbull Pulse weak with occasional extrasystolebull Artery BP 9075bull Large Q wave ST elevationbull Plasma analysis raised cardiac enzymes

QUESTIONbull 1) Why the patient suffered a crushing pain that spread to

the armbull 2) Why occasional extrasystole occur (pathomechanism)bull 3) What is the relationship between smoking and occasional

extrasystolebull 4) Indication for large Q wave and ST elevation What are

the relationship of these findings with chest pain bull 5) Indication for increasing cardiac enzymesbull 6) What are the relationship between myocardial infarction

with the symptoms (why he is having weak pulse)

DIFFERENTIAL DIAGNOSISSIGN AND SYMPTOM

STEMI CAD

Crushing pain at chest spreading to arm yes yes

Occasional extrasystol yes no

Large Q wave and ST elevasi yes no

Hypotension yes yes

Provisional diagnosis MI due to coroner arteri trombosis

yes yes

Enzim CKCKMB LDH increase yes no

httpwwwemedicinehealthcomcogestive_heart_failure

INTRODUCTIONbull STEMI ST segment elevation myocardial infarctionldquo is a type of

heart attack This is determined by an ECG test

bull Myocardial infarctions (heart attacks) occur when a coronay artery suddenly becomes at least partially blocked by a blood clot causing at least some of the heart muscle being supplied by that artery to become infarcted (that is to die) Heart attacks are divided into two types according to their severity

bull A STEMI is the more severe type

httpheartdiseaseaboutcom STEMI - ST Segment Elevation Myocardial Infarction By Richard N Fogoros MD

SCENARIOA collapse 60 years old bus driver was brought into casualty complaining of severesustained crushing pain in a band across the chest spreading into arms Previously he had been wellthough he smoked 10 cigarettes a day On examination he was pale with coldsweaty skin His pulse was weakwith occasional extrasystole(ventricular ectopic beats) His arterial blood pressure was 9075 mmHg Heart sound were normal An ECG revealed large Q wave and ST segment elevation He was admitted with a provisional diagnosis of myocardial infarction due to coronary artery thrombosis Plasma analysis showed raised cardiac enzymes( lactic dehydrogenasecreatine phosphokinaseaspartate aminotransferase) He was given O2 and morphine A streptokinase infusion was set up to lyse the coronary thrombus and he was also started on regularlow dose aspirin

KEYWORD

bull Collapsebull Severe sustained crushing pain in band across chest

spreading into armbull Previously been wellbull Palecold sweaty skinbull Pulse weak with occasional extrasystolebull Artery BP 9075bull Large Q wave ST elevationbull Plasma analysis raised cardiac enzymes

QUESTIONbull 1) Why the patient suffered a crushing pain that spread to

the armbull 2) Why occasional extrasystole occur (pathomechanism)bull 3) What is the relationship between smoking and occasional

extrasystolebull 4) Indication for large Q wave and ST elevation What are

the relationship of these findings with chest pain bull 5) Indication for increasing cardiac enzymesbull 6) What are the relationship between myocardial infarction

with the symptoms (why he is having weak pulse)

DIFFERENTIAL DIAGNOSISSIGN AND SYMPTOM

STEMI CAD

Crushing pain at chest spreading to arm yes yes

Occasional extrasystol yes no

Large Q wave and ST elevasi yes no

Hypotension yes yes

Provisional diagnosis MI due to coroner arteri trombosis

yes yes

Enzim CKCKMB LDH increase yes no

httpwwwemedicinehealthcomcogestive_heart_failure

INTRODUCTIONbull STEMI ST segment elevation myocardial infarctionldquo is a type of

heart attack This is determined by an ECG test

bull Myocardial infarctions (heart attacks) occur when a coronay artery suddenly becomes at least partially blocked by a blood clot causing at least some of the heart muscle being supplied by that artery to become infarcted (that is to die) Heart attacks are divided into two types according to their severity

bull A STEMI is the more severe type

httpheartdiseaseaboutcom STEMI - ST Segment Elevation Myocardial Infarction By Richard N Fogoros MD

KEYWORD

bull Collapsebull Severe sustained crushing pain in band across chest

spreading into armbull Previously been wellbull Palecold sweaty skinbull Pulse weak with occasional extrasystolebull Artery BP 9075bull Large Q wave ST elevationbull Plasma analysis raised cardiac enzymes

QUESTIONbull 1) Why the patient suffered a crushing pain that spread to

the armbull 2) Why occasional extrasystole occur (pathomechanism)bull 3) What is the relationship between smoking and occasional

extrasystolebull 4) Indication for large Q wave and ST elevation What are

the relationship of these findings with chest pain bull 5) Indication for increasing cardiac enzymesbull 6) What are the relationship between myocardial infarction

with the symptoms (why he is having weak pulse)

DIFFERENTIAL DIAGNOSISSIGN AND SYMPTOM

STEMI CAD

Crushing pain at chest spreading to arm yes yes

Occasional extrasystol yes no

Large Q wave and ST elevasi yes no

Hypotension yes yes

Provisional diagnosis MI due to coroner arteri trombosis

yes yes

Enzim CKCKMB LDH increase yes no

httpwwwemedicinehealthcomcogestive_heart_failure

INTRODUCTIONbull STEMI ST segment elevation myocardial infarctionldquo is a type of

heart attack This is determined by an ECG test

bull Myocardial infarctions (heart attacks) occur when a coronay artery suddenly becomes at least partially blocked by a blood clot causing at least some of the heart muscle being supplied by that artery to become infarcted (that is to die) Heart attacks are divided into two types according to their severity

bull A STEMI is the more severe type

httpheartdiseaseaboutcom STEMI - ST Segment Elevation Myocardial Infarction By Richard N Fogoros MD

QUESTIONbull 1) Why the patient suffered a crushing pain that spread to

the armbull 2) Why occasional extrasystole occur (pathomechanism)bull 3) What is the relationship between smoking and occasional

extrasystolebull 4) Indication for large Q wave and ST elevation What are

the relationship of these findings with chest pain bull 5) Indication for increasing cardiac enzymesbull 6) What are the relationship between myocardial infarction

with the symptoms (why he is having weak pulse)

DIFFERENTIAL DIAGNOSISSIGN AND SYMPTOM

STEMI CAD

Crushing pain at chest spreading to arm yes yes

Occasional extrasystol yes no

Large Q wave and ST elevasi yes no

Hypotension yes yes

Provisional diagnosis MI due to coroner arteri trombosis

yes yes

Enzim CKCKMB LDH increase yes no

httpwwwemedicinehealthcomcogestive_heart_failure

INTRODUCTIONbull STEMI ST segment elevation myocardial infarctionldquo is a type of

heart attack This is determined by an ECG test

bull Myocardial infarctions (heart attacks) occur when a coronay artery suddenly becomes at least partially blocked by a blood clot causing at least some of the heart muscle being supplied by that artery to become infarcted (that is to die) Heart attacks are divided into two types according to their severity

bull A STEMI is the more severe type

httpheartdiseaseaboutcom STEMI - ST Segment Elevation Myocardial Infarction By Richard N Fogoros MD

DIFFERENTIAL DIAGNOSISSIGN AND SYMPTOM

STEMI CAD

Crushing pain at chest spreading to arm yes yes

Occasional extrasystol yes no

Large Q wave and ST elevasi yes no

Hypotension yes yes

Provisional diagnosis MI due to coroner arteri trombosis

yes yes

Enzim CKCKMB LDH increase yes no

httpwwwemedicinehealthcomcogestive_heart_failure

INTRODUCTIONbull STEMI ST segment elevation myocardial infarctionldquo is a type of

heart attack This is determined by an ECG test

bull Myocardial infarctions (heart attacks) occur when a coronay artery suddenly becomes at least partially blocked by a blood clot causing at least some of the heart muscle being supplied by that artery to become infarcted (that is to die) Heart attacks are divided into two types according to their severity

bull A STEMI is the more severe type

httpheartdiseaseaboutcom STEMI - ST Segment Elevation Myocardial Infarction By Richard N Fogoros MD

INTRODUCTIONbull STEMI ST segment elevation myocardial infarctionldquo is a type of

heart attack This is determined by an ECG test

bull Myocardial infarctions (heart attacks) occur when a coronay artery suddenly becomes at least partially blocked by a blood clot causing at least some of the heart muscle being supplied by that artery to become infarcted (that is to die) Heart attacks are divided into two types according to their severity

bull A STEMI is the more severe type

httpheartdiseaseaboutcom STEMI - ST Segment Elevation Myocardial Infarction By Richard N Fogoros MD

BASIC SCIENCE

EKG

Normal heart

Myocardial InfarctionTwo to three days after an MI the myocytes show that they are irreversibly damaged Theyve lost their nuclei PMNs

(polymorphonuclear leukocytes) are the first inflammatory cells on the scene They will begin to clear away the necrotic tissue Later the macrophages will finish the job These dying myocytes will eventually be replaced with scar tissue

httpwwwkumceduinstructionmedicineanatomyhistowebpathpath01htm

EKG

Normal heart

Myocardial InfarctionTwo to three days after an MI the myocytes show that they are irreversibly damaged Theyve lost their nuclei PMNs

(polymorphonuclear leukocytes) are the first inflammatory cells on the scene They will begin to clear away the necrotic tissue Later the macrophages will finish the job These dying myocytes will eventually be replaced with scar tissue

httpwwwkumceduinstructionmedicineanatomyhistowebpathpath01htm

Normal heart

Myocardial InfarctionTwo to three days after an MI the myocytes show that they are irreversibly damaged Theyve lost their nuclei PMNs

(polymorphonuclear leukocytes) are the first inflammatory cells on the scene They will begin to clear away the necrotic tissue Later the macrophages will finish the job These dying myocytes will eventually be replaced with scar tissue

httpwwwkumceduinstructionmedicineanatomyhistowebpathpath01htm

Myocardial InfarctionTwo to three days after an MI the myocytes show that they are irreversibly damaged Theyve lost their nuclei PMNs

(polymorphonuclear leukocytes) are the first inflammatory cells on the scene They will begin to clear away the necrotic tissue Later the macrophages will finish the job These dying myocytes will eventually be replaced with scar tissue

httpwwwkumceduinstructionmedicineanatomyhistowebpathpath01htm

httpwwwgooglecomimgreshl=enampgl=idampbiw=1366ampbih=624amptbm=ischamptbnid=KajG2QEK1-M4mMampimgrefurl=httpwwwmedicinenetcomheart_attack_pathology_photo_essaypage3htmampdocid=CZHmHLYLNv9ueMampimgurl=httpimagesmedicinenetcomimagesillustrationsmyocardial_infarction_1jpgampw=400amph=308ampei=8_KDUK3PH8nlrAeTzYHwBwampzoom=1ampiact=hcampvpx=398ampvpy=128ampdur=3820amphovh=197amphovw=256amptx=206ampty=150ampsig=116867615274730240580amppage=2amptbnh=151amptbnw=196ampstart=21ampndsp=27ampved=1t429r23s20i206

PATHOPHYSIOLOGY OF

ST-ELEVATION MYOCARDIAL

INFARCTION (STEMI)

myocardial infarction

A myocardial infarction is defined as

Elevated blood levels of cardiac enzymes

(CKMB or Troponin T)

One of the following criteria are met

The patient has typical

complaints

The ECG shows ST elevation or

depression

pathological Q waves develop

on the ECG

bull PATHOPHYSIOLOGY MIA prolonged imbalance between myocardial oxygen supply and demand leads to the death of myocardial tissue Coronary

atherosclerosis is an essential part of the process in most patients

Ischemic heart disease seems to progress through stages of fatty-streak deposition in coronary arteries to development of

fibro-fatty plaque which then increases in size until it causes luminal obstruction

leading to exertional angina

any stages in this process the atherosclerotic lesion may erode

ulcerate fissure or rupture thereby exposing subendothelial

vessel wall substances to the circulating blood

Procoagulant factors (such as tissue factor) reside within the plaque itself

and in the absence of counterbalancing antithrombotic factor (eg heparin tissue-factor-

inhibitor) and fibrinolytic activities (tissues plasminogen activator [t-PA]

and single-chain urokinase-type plasminogen activator) within the endothelial cells of the coronary

artery can cause thrombosis Recent work suggests that inflammation may play a pivotal role in

the genesis of plaque rupture Total thrombotic occlusion occurs most commonly in proximal coronary

arteries its presence has been documented during the first 4 hours

after infarction in more than 85 of the patients with ST segment elevation

(Crawford MH (2009))

This potent procoagulant stimulus results in thrombus development in

this region In general acute MI occurs when this thrombosis

propagates and occludes flow within the artery resulting in ischemia of

cardiomyocytes distal to the obstruction

The ECG leads in which pathologic Q waves appear reflect the anatomical site of an infarction

TABLE 1 Localization of Myocardial Infarction Anatomical Site Leads with Abnormal ECG

Complexes Coronary Artery Most Often

Responsible Inferior IIIIIaVF RCA

Anteroseptal V1-V2 LAD Anteroapical V3-V4 LAD(distal) Anterolateral V5-V6 I aVL CFX

Posterior V1-V2 (tall R wave not Q wave) RCA

The electrocardiographic differences between these types of MI are summarized as follow

Type of Infarction Pathologic Q waves Acute ST segment Deviation

Q-wave MI Yes ST elevation Non-Q-wave MI No ST depression (and or T

wave inversion)

Angina pectoris- Neck- Shoulder- Arms

ischemic myocardial cells release mediator such as adenosine and

lactate from into local nerve endings

discomfort often refer to other region of the C7 through

dermatome

provocative substances continue to accumulate and active afferent

nerve for longer period

ischemic in acute MI persist and proceed to necrosis

HYPOTENSION

May trigger a dramatic sympathetic nervous system response

Systemic sign of subsequent catecholamine release include diaphoresis (sweating) tachycardia and cool

and clammy skin

cause of vasoconstriction

Systolic Dysfunction

Decrease lungs compliance and stimulates juxtacappilary

receptors

Left ventricle contractility can be

reduced

J receptors effects a reflex that results in rapid shallow

breathing and evokes the subjective feeling of dyspnea

Increase in LV pressure compounded by the ischemia

induced stiffness of the chamber (diastolic dysfunction) is conveyed to the left atrium and pulmonary

veins

Decreasing the stroke volume and causing the diastolic

volume and pressure within the LV to rise

Ischemia affects large amount of myocardium

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of the sarcolemma

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

myocardial infarction

A myocardial infarction is defined as

Elevated blood levels of cardiac enzymes

(CKMB or Troponin T)

One of the following criteria are met

The patient has typical

complaints

The ECG shows ST elevation or

depression

pathological Q waves develop

on the ECG

bull PATHOPHYSIOLOGY MIA prolonged imbalance between myocardial oxygen supply and demand leads to the death of myocardial tissue Coronary

atherosclerosis is an essential part of the process in most patients

Ischemic heart disease seems to progress through stages of fatty-streak deposition in coronary arteries to development of

fibro-fatty plaque which then increases in size until it causes luminal obstruction

leading to exertional angina

any stages in this process the atherosclerotic lesion may erode

ulcerate fissure or rupture thereby exposing subendothelial

vessel wall substances to the circulating blood

Procoagulant factors (such as tissue factor) reside within the plaque itself

and in the absence of counterbalancing antithrombotic factor (eg heparin tissue-factor-

inhibitor) and fibrinolytic activities (tissues plasminogen activator [t-PA]

and single-chain urokinase-type plasminogen activator) within the endothelial cells of the coronary

artery can cause thrombosis Recent work suggests that inflammation may play a pivotal role in

the genesis of plaque rupture Total thrombotic occlusion occurs most commonly in proximal coronary

arteries its presence has been documented during the first 4 hours

after infarction in more than 85 of the patients with ST segment elevation

(Crawford MH (2009))

This potent procoagulant stimulus results in thrombus development in

this region In general acute MI occurs when this thrombosis

propagates and occludes flow within the artery resulting in ischemia of

cardiomyocytes distal to the obstruction

The ECG leads in which pathologic Q waves appear reflect the anatomical site of an infarction

TABLE 1 Localization of Myocardial Infarction Anatomical Site Leads with Abnormal ECG

Complexes Coronary Artery Most Often

Responsible Inferior IIIIIaVF RCA

Anteroseptal V1-V2 LAD Anteroapical V3-V4 LAD(distal) Anterolateral V5-V6 I aVL CFX

Posterior V1-V2 (tall R wave not Q wave) RCA

The electrocardiographic differences between these types of MI are summarized as follow

Type of Infarction Pathologic Q waves Acute ST segment Deviation

Q-wave MI Yes ST elevation Non-Q-wave MI No ST depression (and or T

wave inversion)

Angina pectoris- Neck- Shoulder- Arms

ischemic myocardial cells release mediator such as adenosine and

lactate from into local nerve endings

discomfort often refer to other region of the C7 through

dermatome

provocative substances continue to accumulate and active afferent

nerve for longer period

ischemic in acute MI persist and proceed to necrosis

HYPOTENSION

May trigger a dramatic sympathetic nervous system response

Systemic sign of subsequent catecholamine release include diaphoresis (sweating) tachycardia and cool

and clammy skin

cause of vasoconstriction

Systolic Dysfunction

Decrease lungs compliance and stimulates juxtacappilary

receptors

Left ventricle contractility can be

reduced

J receptors effects a reflex that results in rapid shallow

breathing and evokes the subjective feeling of dyspnea

Increase in LV pressure compounded by the ischemia

induced stiffness of the chamber (diastolic dysfunction) is conveyed to the left atrium and pulmonary

veins

Decreasing the stroke volume and causing the diastolic

volume and pressure within the LV to rise

Ischemia affects large amount of myocardium

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of the sarcolemma

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

bull PATHOPHYSIOLOGY MIA prolonged imbalance between myocardial oxygen supply and demand leads to the death of myocardial tissue Coronary

atherosclerosis is an essential part of the process in most patients

Ischemic heart disease seems to progress through stages of fatty-streak deposition in coronary arteries to development of

fibro-fatty plaque which then increases in size until it causes luminal obstruction

leading to exertional angina

any stages in this process the atherosclerotic lesion may erode

ulcerate fissure or rupture thereby exposing subendothelial

vessel wall substances to the circulating blood

Procoagulant factors (such as tissue factor) reside within the plaque itself

and in the absence of counterbalancing antithrombotic factor (eg heparin tissue-factor-

inhibitor) and fibrinolytic activities (tissues plasminogen activator [t-PA]

and single-chain urokinase-type plasminogen activator) within the endothelial cells of the coronary

artery can cause thrombosis Recent work suggests that inflammation may play a pivotal role in

the genesis of plaque rupture Total thrombotic occlusion occurs most commonly in proximal coronary

arteries its presence has been documented during the first 4 hours

after infarction in more than 85 of the patients with ST segment elevation

(Crawford MH (2009))

This potent procoagulant stimulus results in thrombus development in

this region In general acute MI occurs when this thrombosis

propagates and occludes flow within the artery resulting in ischemia of

cardiomyocytes distal to the obstruction

The ECG leads in which pathologic Q waves appear reflect the anatomical site of an infarction

TABLE 1 Localization of Myocardial Infarction Anatomical Site Leads with Abnormal ECG

Complexes Coronary Artery Most Often

Responsible Inferior IIIIIaVF RCA

Anteroseptal V1-V2 LAD Anteroapical V3-V4 LAD(distal) Anterolateral V5-V6 I aVL CFX

Posterior V1-V2 (tall R wave not Q wave) RCA

The electrocardiographic differences between these types of MI are summarized as follow

Type of Infarction Pathologic Q waves Acute ST segment Deviation

Q-wave MI Yes ST elevation Non-Q-wave MI No ST depression (and or T

wave inversion)

Angina pectoris- Neck- Shoulder- Arms

ischemic myocardial cells release mediator such as adenosine and

lactate from into local nerve endings

discomfort often refer to other region of the C7 through

dermatome

provocative substances continue to accumulate and active afferent

nerve for longer period

ischemic in acute MI persist and proceed to necrosis

HYPOTENSION

May trigger a dramatic sympathetic nervous system response

Systemic sign of subsequent catecholamine release include diaphoresis (sweating) tachycardia and cool

and clammy skin

cause of vasoconstriction

Systolic Dysfunction

Decrease lungs compliance and stimulates juxtacappilary

receptors

Left ventricle contractility can be

reduced

J receptors effects a reflex that results in rapid shallow

breathing and evokes the subjective feeling of dyspnea

Increase in LV pressure compounded by the ischemia

induced stiffness of the chamber (diastolic dysfunction) is conveyed to the left atrium and pulmonary

veins

Decreasing the stroke volume and causing the diastolic

volume and pressure within the LV to rise

Ischemia affects large amount of myocardium

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of the sarcolemma

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

Procoagulant factors (such as tissue factor) reside within the plaque itself

and in the absence of counterbalancing antithrombotic factor (eg heparin tissue-factor-

inhibitor) and fibrinolytic activities (tissues plasminogen activator [t-PA]

and single-chain urokinase-type plasminogen activator) within the endothelial cells of the coronary

artery can cause thrombosis Recent work suggests that inflammation may play a pivotal role in

the genesis of plaque rupture Total thrombotic occlusion occurs most commonly in proximal coronary

arteries its presence has been documented during the first 4 hours

after infarction in more than 85 of the patients with ST segment elevation

(Crawford MH (2009))

This potent procoagulant stimulus results in thrombus development in

this region In general acute MI occurs when this thrombosis

propagates and occludes flow within the artery resulting in ischemia of

cardiomyocytes distal to the obstruction

The ECG leads in which pathologic Q waves appear reflect the anatomical site of an infarction

TABLE 1 Localization of Myocardial Infarction Anatomical Site Leads with Abnormal ECG

Complexes Coronary Artery Most Often

Responsible Inferior IIIIIaVF RCA

Anteroseptal V1-V2 LAD Anteroapical V3-V4 LAD(distal) Anterolateral V5-V6 I aVL CFX

Posterior V1-V2 (tall R wave not Q wave) RCA

The electrocardiographic differences between these types of MI are summarized as follow

Type of Infarction Pathologic Q waves Acute ST segment Deviation

Q-wave MI Yes ST elevation Non-Q-wave MI No ST depression (and or T

wave inversion)

Angina pectoris- Neck- Shoulder- Arms

ischemic myocardial cells release mediator such as adenosine and

lactate from into local nerve endings

discomfort often refer to other region of the C7 through

dermatome

provocative substances continue to accumulate and active afferent

nerve for longer period

ischemic in acute MI persist and proceed to necrosis

HYPOTENSION

May trigger a dramatic sympathetic nervous system response

Systemic sign of subsequent catecholamine release include diaphoresis (sweating) tachycardia and cool

and clammy skin

cause of vasoconstriction

Systolic Dysfunction

Decrease lungs compliance and stimulates juxtacappilary

receptors

Left ventricle contractility can be

reduced

J receptors effects a reflex that results in rapid shallow

breathing and evokes the subjective feeling of dyspnea

Increase in LV pressure compounded by the ischemia

induced stiffness of the chamber (diastolic dysfunction) is conveyed to the left atrium and pulmonary

veins

Decreasing the stroke volume and causing the diastolic

volume and pressure within the LV to rise

Ischemia affects large amount of myocardium

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of the sarcolemma

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

The ECG leads in which pathologic Q waves appear reflect the anatomical site of an infarction

TABLE 1 Localization of Myocardial Infarction Anatomical Site Leads with Abnormal ECG

Complexes Coronary Artery Most Often

Responsible Inferior IIIIIaVF RCA

Anteroseptal V1-V2 LAD Anteroapical V3-V4 LAD(distal) Anterolateral V5-V6 I aVL CFX

Posterior V1-V2 (tall R wave not Q wave) RCA

The electrocardiographic differences between these types of MI are summarized as follow

Type of Infarction Pathologic Q waves Acute ST segment Deviation

Q-wave MI Yes ST elevation Non-Q-wave MI No ST depression (and or T

wave inversion)

Angina pectoris- Neck- Shoulder- Arms

ischemic myocardial cells release mediator such as adenosine and

lactate from into local nerve endings

discomfort often refer to other region of the C7 through

dermatome

provocative substances continue to accumulate and active afferent

nerve for longer period

ischemic in acute MI persist and proceed to necrosis

HYPOTENSION

May trigger a dramatic sympathetic nervous system response

Systemic sign of subsequent catecholamine release include diaphoresis (sweating) tachycardia and cool

and clammy skin

cause of vasoconstriction

Systolic Dysfunction

Decrease lungs compliance and stimulates juxtacappilary

receptors

Left ventricle contractility can be

reduced

J receptors effects a reflex that results in rapid shallow

breathing and evokes the subjective feeling of dyspnea

Increase in LV pressure compounded by the ischemia

induced stiffness of the chamber (diastolic dysfunction) is conveyed to the left atrium and pulmonary

veins

Decreasing the stroke volume and causing the diastolic

volume and pressure within the LV to rise

Ischemia affects large amount of myocardium

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of the sarcolemma

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

Angina pectoris- Neck- Shoulder- Arms

ischemic myocardial cells release mediator such as adenosine and

lactate from into local nerve endings

discomfort often refer to other region of the C7 through

dermatome

provocative substances continue to accumulate and active afferent

nerve for longer period

ischemic in acute MI persist and proceed to necrosis

HYPOTENSION

May trigger a dramatic sympathetic nervous system response

Systemic sign of subsequent catecholamine release include diaphoresis (sweating) tachycardia and cool

and clammy skin

cause of vasoconstriction

Systolic Dysfunction

Decrease lungs compliance and stimulates juxtacappilary

receptors

Left ventricle contractility can be

reduced

J receptors effects a reflex that results in rapid shallow

breathing and evokes the subjective feeling of dyspnea

Increase in LV pressure compounded by the ischemia

induced stiffness of the chamber (diastolic dysfunction) is conveyed to the left atrium and pulmonary

veins

Decreasing the stroke volume and causing the diastolic

volume and pressure within the LV to rise

Ischemia affects large amount of myocardium

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of the sarcolemma

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

HYPOTENSION

May trigger a dramatic sympathetic nervous system response

Systemic sign of subsequent catecholamine release include diaphoresis (sweating) tachycardia and cool

and clammy skin

cause of vasoconstriction

Systolic Dysfunction

Decrease lungs compliance and stimulates juxtacappilary

receptors

Left ventricle contractility can be

reduced

J receptors effects a reflex that results in rapid shallow

breathing and evokes the subjective feeling of dyspnea

Increase in LV pressure compounded by the ischemia

induced stiffness of the chamber (diastolic dysfunction) is conveyed to the left atrium and pulmonary

veins

Decreasing the stroke volume and causing the diastolic

volume and pressure within the LV to rise

Ischemia affects large amount of myocardium

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of the sarcolemma

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

Systolic Dysfunction

Decrease lungs compliance and stimulates juxtacappilary

receptors

Left ventricle contractility can be

reduced

J receptors effects a reflex that results in rapid shallow

breathing and evokes the subjective feeling of dyspnea

Increase in LV pressure compounded by the ischemia

induced stiffness of the chamber (diastolic dysfunction) is conveyed to the left atrium and pulmonary

veins

Decreasing the stroke volume and causing the diastolic

volume and pressure within the LV to rise

Ischemia affects large amount of myocardium

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of the sarcolemma

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of the sarcolemma

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

MYOCARDIAL INFARTION

TYPICAL SYMPTOM- Crushing chest pain

more severe and wider than usual angina

SERUM BIOMARKSCreatine kinaseTroponin

ECG initial finding- St elevation- Q Wave

STEMI

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

Left Ventricular Function Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work Four abnormal contraction patterns develop in sequence (1) dyssynchrony that is dissociation in the time course of contraction of adjacent segments(2) hypokinesis reduction in the extent of shortening (3) akinesis cessation of shortening and (4) dyskinesis paradoxical expansion and systolic bulging

Hyperkinesis of the remaining normal myocardium initially accompanies dysfunction of the infarcting segment The early hyperkinesis of the noninfarcted zones likely results from acute compensations including increased activity of the sympathetic nervous system and the Frank-Starling mechanism A portion of this compensatory hyperkinesis is ineffective work because contraction of the noninfarcted segments of myocardium hellip

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

Ventricular Remodelingbull As a consequence of STEMI the changes in left ventricular size shape and

thickness involving both the infarcted and the noninfarcted segments of the ventricle described earlier occur and are collectively referred to as ventricular remodeling which can in turn influence ventricular function and prognosis

bull A combination of changes in left ventricular dilation and hypertrophy of residual noninfarcted myocardium causes remodeling

bull After the size of infarction the two most important factors driving the process of left ventricular dilation are ventricular loading conditions and infarct artery patency

bull Elevated ventricular pressure contributes to increased wall stress and the risk of infarct expansion and a patent infarct artery accelerates myocardial scar formation and increases tissue turgor in the infarct zone reducing the risk of infarct expansion and ventricular dilation

Antman EM Morrow DA McCabe CH et al Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction N Engl J Med 2006 3541477

referencesSLIDE 2 Alpert JS Thygesen K Antman E and Bassand JP Myocardial infarction redefined--a consensus document of The Joint European Society of CardiologyAmerican College of Cardiology Committee for the redefinition of myocardial infarction J Am Coll Cardiol 2000 Sep 36(3) 959-69 pmid10987628bull Book of Pathophysiology of Heart Disease fourth edition editor Leonard SLilly page 179-

184bull ILMU PENYAKIT DALAM Jilid II Edisi V Editor Aru WSudoyo Bambang Setiyohadi

Idrus Alwi page1741-1744

ST elevation MI

ST segment elevation type of acute myocardial infarction require at least 1 mm (01 mV) of ST segment elevation in the limb leads and at least 2 mm elevation in the precordial leads

The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction which include

These elevations must be present in anatomically contiguous leads (I aVL V5 V6 correspond to the lateral wall V1-V2 correspond to the septal wall V3-V4 correspond to the anterior wall II III aVF correspond to the inferior wall)

left ventricular hypertrophy

left bundle branch block

hyperkalemia

early repolarization

ventricular aneurysm

12-lead electrocardiogram showing ST-segment elevation (orange) in I aVL and V1-V5 with reciprocal changes (blue) in the inferior leads indicative of an anterior wall myocardial infarction

An acute STEMI involving the inferior and right ventricular wall Reciprocal changes are seen in the anterior leads

PATHOLOGIC OF Q-WAVEPathologic Q waves

Any Q-wave in leads V2ndashV3 ge 002 s or QS complex in leads V2 and V3

Q-wave ge 003 s and gt 01 mV deep or QS complex in leads I II aVL aVF or V4ndashV6 in

any two leads of a contiguous lead grouping (I aVLV6 V4ndashV6 II III and aVF)

result of absence of electrical activity

previous myocardial infarction

The evolution of an infarct on the ECG ST elevation Q wave formation T wave inversion

normalisation with a persistent Q wave

PATHOMECANISM CHEST PAINhttpemedicinemedscapecomarticle150215-overview2

ProfDrPeter Kabo Bagaimana Menggunakan Obat-obat kardiovasculer secara Rasional

ST segment elevation type of acute myocardial infarction require at least 1 mm (01 mV) of ST segment elevation in the limb leads and at least 2 mm elevation in the precordial leads

The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction which include

These elevations must be present in anatomically contiguous leads (I aVL V5 V6 correspond to the lateral wall V1-V2 correspond to the septal wall V3-V4 correspond to the anterior wall II III aVF correspond to the inferior wall)

left ventricular hypertrophy

left bundle branch block

hyperkalemia

early repolarization

ventricular aneurysm

12-lead electrocardiogram showing ST-segment elevation (orange) in I aVL and V1-V5 with reciprocal changes (blue) in the inferior leads indicative of an anterior wall myocardial infarction

An acute STEMI involving the inferior and right ventricular wall Reciprocal changes are seen in the anterior leads

PATHOLOGIC OF Q-WAVEPathologic Q waves

Any Q-wave in leads V2ndashV3 ge 002 s or QS complex in leads V2 and V3

Q-wave ge 003 s and gt 01 mV deep or QS complex in leads I II aVL aVF or V4ndashV6 in

any two leads of a contiguous lead grouping (I aVLV6 V4ndashV6 II III and aVF)

result of absence of electrical activity

previous myocardial infarction

The evolution of an infarct on the ECG ST elevation Q wave formation T wave inversion

normalisation with a persistent Q wave

PATHOMECANISM CHEST PAINhttpemedicinemedscapecomarticle150215-overview2

ProfDrPeter Kabo Bagaimana Menggunakan Obat-obat kardiovasculer secara Rasional

12-lead electrocardiogram showing ST-segment elevation (orange) in I aVL and V1-V5 with reciprocal changes (blue) in the inferior leads indicative of an anterior wall myocardial infarction

An acute STEMI involving the inferior and right ventricular wall Reciprocal changes are seen in the anterior leads

PATHOLOGIC OF Q-WAVEPathologic Q waves

Any Q-wave in leads V2ndashV3 ge 002 s or QS complex in leads V2 and V3

Q-wave ge 003 s and gt 01 mV deep or QS complex in leads I II aVL aVF or V4ndashV6 in

any two leads of a contiguous lead grouping (I aVLV6 V4ndashV6 II III and aVF)

result of absence of electrical activity

previous myocardial infarction

The evolution of an infarct on the ECG ST elevation Q wave formation T wave inversion

normalisation with a persistent Q wave

PATHOMECANISM CHEST PAINhttpemedicinemedscapecomarticle150215-overview2

ProfDrPeter Kabo Bagaimana Menggunakan Obat-obat kardiovasculer secara Rasional

PATHOLOGIC OF Q-WAVEPathologic Q waves

Any Q-wave in leads V2ndashV3 ge 002 s or QS complex in leads V2 and V3

Q-wave ge 003 s and gt 01 mV deep or QS complex in leads I II aVL aVF or V4ndashV6 in

any two leads of a contiguous lead grouping (I aVLV6 V4ndashV6 II III and aVF)

result of absence of electrical activity

previous myocardial infarction

The evolution of an infarct on the ECG ST elevation Q wave formation T wave inversion

normalisation with a persistent Q wave

PATHOMECANISM CHEST PAINhttpemedicinemedscapecomarticle150215-overview2

ProfDrPeter Kabo Bagaimana Menggunakan Obat-obat kardiovasculer secara Rasional

PATHOMECANISM CHEST PAINhttpemedicinemedscapecomarticle150215-overview2

ProfDrPeter Kabo Bagaimana Menggunakan Obat-obat kardiovasculer secara Rasional

AtherosclerosisProduce endothelial derived constricting

factor (EDCF)

Increase tonus artery

coronary

Ischemic myocard

Aerobic glycolysis turn

to anerobic glycolysis

Production of adenosin

Diffuse to extracellular

space

Stimulate A1 receptor in cardiac

afferent nerve ending

Bind with somatic cervico

thoracalis nerve at

ascending pathway in

medulla spinalis

Chest pain

SMOKING KILLS

These effects could potentially trigger

symptoms of ischemia in such smokers

One might also expect that the hemodynamic effects of nicotine would contribute to endothelial damage and accelerate the progression of atherosclerosis

Lipolyis - increased levels of circulating free fatty acids

and glycerol in the blood and the resulting increase in fat

metabolism drives a demand for more oxygen leading to

increased coronary blood flow and myocardial oxygen

uptake

addition to its cardiovascular effects such as elevated heart

rate blood pressure and cardiac output

nicotine has metabolic effects in particular increased lipolysis

Nicotine is a sympathomimetic chemical that promotes the release of catecholamines and other

neurotransmitters

SIGNS AND SYMPTOMS

bullChest pain (pressuretightnessheaviness and might radiate to neck arm)

bullIngestion heartburnbullNausea VomitingbullSweatingbullWeaknessbullDizziness

httpwwwcardiosmartorgManageConditionDefaultaspxid=904 httpwwwncbinlmnihgovpmcarticlesPMC2233977

SMOKING KILLS

These effects could potentially trigger

symptoms of ischemia in such smokers

One might also expect that the hemodynamic effects of nicotine would contribute to endothelial damage and accelerate the progression of atherosclerosis

Lipolyis - increased levels of circulating free fatty acids

and glycerol in the blood and the resulting increase in fat

metabolism drives a demand for more oxygen leading to

increased coronary blood flow and myocardial oxygen

uptake

addition to its cardiovascular effects such as elevated heart

rate blood pressure and cardiac output

nicotine has metabolic effects in particular increased lipolysis

Nicotine is a sympathomimetic chemical that promotes the release of catecholamines and other

neurotransmitters

SIGNS AND SYMPTOMS

bullChest pain (pressuretightnessheaviness and might radiate to neck arm)

bullIngestion heartburnbullNausea VomitingbullSweatingbullWeaknessbullDizziness

httpwwwcardiosmartorgManageConditionDefaultaspxid=904 httpwwwncbinlmnihgovpmcarticlesPMC2233977

These effects could potentially trigger

symptoms of ischemia in such smokers

One might also expect that the hemodynamic effects of nicotine would contribute to endothelial damage and accelerate the progression of atherosclerosis

Lipolyis - increased levels of circulating free fatty acids

and glycerol in the blood and the resulting increase in fat

metabolism drives a demand for more oxygen leading to

increased coronary blood flow and myocardial oxygen

uptake

addition to its cardiovascular effects such as elevated heart

rate blood pressure and cardiac output

nicotine has metabolic effects in particular increased lipolysis

Nicotine is a sympathomimetic chemical that promotes the release of catecholamines and other

neurotransmitters

SIGNS AND SYMPTOMS

bullChest pain (pressuretightnessheaviness and might radiate to neck arm)

bullIngestion heartburnbullNausea VomitingbullSweatingbullWeaknessbullDizziness

httpwwwcardiosmartorgManageConditionDefaultaspxid=904 httpwwwncbinlmnihgovpmcarticlesPMC2233977

SIGNS AND SYMPTOMS

bullChest pain (pressuretightnessheaviness and might radiate to neck arm)

bullIngestion heartburnbullNausea VomitingbullSweatingbullWeaknessbullDizziness

httpwwwcardiosmartorgManageConditionDefaultaspxid=904 httpwwwncbinlmnihgovpmcarticlesPMC2233977

ADDITIONAL EXAMINATION1 Physical examination

Gen appearance Distress Levine signbullHeart rate pulse respirrate variablebullBlood pressure variablebullLow-grade feverbullExamination of jugular venous pulsationsbullPulmonary CracklesbullS4 gallop due to reduced LV compliancebullS3 gallop if LV dysfunction presentbullMurmurs Pericardial friction rubs

2 ECG

The key to rapid diagnosis and risk stratification for the patient with chest painbullTo be obtained within 10 minutes of arrival to Emergency DepartmentbullFor STEMI 1048774ST-segment elevation gt1mm in 2+ contiguous leads OR new left bundle branch block (LBBB)bullLocation of InfarctLeadsInferior MI II III aVFAnterior MI V2-V4Lateral MI I aVL V5-V6

3 Lab studies

Cardiac Biomarkers CK CK-MB cTnbullSerum ChemistriesbullRenal FunctionbullCoagulation StudiesbullComplete Blood Count

TREATMENTAspirin

bullRapidly blocks formation of thromboxaneA2 in platelets by cyclooxygenase inhibitionbull162-325mg chewed (promotes buccalabsorption)bullISIS-2ndash23 reduction in mortality largely additive to the reduction in mortality from streptokinaseOther Adjuvant TherapiesAnalgesicsbullNitratesbullBeta-blockersbullAce InhibitorsbullOxygenbullHeparinbullIV Glycoprotein IIbIIIaInhibitorsbullClopidogrelbullStatins

Thrombolytic TherapybullCommon AgentsbullTNK-tPA30-50mg IV bolusbullReteplase10U x 2 (each over 2 minutes) IVbullAlteplaseup to 100mg in 90mins (based on weight)

bullContraindicationsndashAbsolute Prior intracranial hemorrhage known cerebral vascular lesion malignant intracranial neoplasm ischemic stroke within 3 months suspected aortic dissection active bleeding recent closed head injury or facial trauma within 3monthsndashRelative History of chronic severe HTN severeuncontrolled HTN at presentation (gt180110) history of ischemic stroke gt3 months traumaticprolonged CPR recent internal bleeding (2-4 weeks) pregnancy active peptic ulcer current anticoagulation

Primary PCI

bullPCI = Percutaneous Coronary Intervention

bullPTCA = Percutaneous Transluminal Coronary Angioplasty

bullPOBA = Plain Old Balloon Angioplasty

PROGNOSIS

bullDischarge usually 5 days after admissionbullSmoking CessationbullShort and Long-term survival depend upon resting LV function residual ischemic myocardium and susceptibility to ventricular arrhythmias

THE END

• CHEST PAIN SCENARIO 3 GROUP 10
• SCENARIO
• KEYWORD
• QUESTION
• DIFFERENTIAL DIAGNOSIS
• INTRODUCTION
• BASIC SCIENCE
• EKG
• Normal heart
• Myocardial Infarction Two to three days after an MI the myocyt
• Slide 11
• PATHOPHYSIOLOGY OF ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
• myocardial infarction
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• HYPOTENSION May trigger a dramatic sympathetic nervous system
• Slide 19
• Slide 21
• Left Ventricular Function Systolic Function
• Ventricular Remodeling
• references
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• PATHOLOGIC OF Q-WAVE
• PATHOMECANISM CHEST PAIN
• Slide 31
• SMOKING kills
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• ThE eND

2 ECG

The key to rapid diagnosis and risk stratification for the patient with chest painbullTo be obtained within 10 minutes of arrival to Emergency DepartmentbullFor STEMI 1048774ST-segment elevation gt1mm in 2+ contiguous leads OR new left bundle branch block (LBBB)bullLocation of InfarctLeadsInferior MI II III aVFAnterior MI V2-V4Lateral MI I aVL V5-V6

3 Lab studies

Cardiac Biomarkers CK CK-MB cTnbullSerum ChemistriesbullRenal FunctionbullCoagulation StudiesbullComplete Blood Count

TREATMENTAspirin

bullRapidly blocks formation of thromboxaneA2 in platelets by cyclooxygenase inhibitionbull162-325mg chewed (promotes buccalabsorption)bullISIS-2ndash23 reduction in mortality largely additive to the reduction in mortality from streptokinaseOther Adjuvant TherapiesAnalgesicsbullNitratesbullBeta-blockersbullAce InhibitorsbullOxygenbullHeparinbullIV Glycoprotein IIbIIIaInhibitorsbullClopidogrelbullStatins

Thrombolytic TherapybullCommon AgentsbullTNK-tPA30-50mg IV bolusbullReteplase10U x 2 (each over 2 minutes) IVbullAlteplaseup to 100mg in 90mins (based on weight)

bullContraindicationsndashAbsolute Prior intracranial hemorrhage known cerebral vascular lesion malignant intracranial neoplasm ischemic stroke within 3 months suspected aortic dissection active bleeding recent closed head injury or facial trauma within 3monthsndashRelative History of chronic severe HTN severeuncontrolled HTN at presentation (gt180110) history of ischemic stroke gt3 months traumaticprolonged CPR recent internal bleeding (2-4 weeks) pregnancy active peptic ulcer current anticoagulation

Primary PCI

bullPCI = Percutaneous Coronary Intervention

bullPTCA = Percutaneous Transluminal Coronary Angioplasty

bullPOBA = Plain Old Balloon Angioplasty

PROGNOSIS

bullDischarge usually 5 days after admissionbullSmoking CessationbullShort and Long-term survival depend upon resting LV function residual ischemic myocardium and susceptibility to ventricular arrhythmias

THE END

• CHEST PAIN SCENARIO 3 GROUP 10
• SCENARIO
• KEYWORD
• QUESTION
• DIFFERENTIAL DIAGNOSIS
• INTRODUCTION
• BASIC SCIENCE
• EKG
• Normal heart
• Myocardial Infarction Two to three days after an MI the myocyt
• Slide 11
• PATHOPHYSIOLOGY OF ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
• myocardial infarction
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• HYPOTENSION May trigger a dramatic sympathetic nervous system
• Slide 19
• Slide 21
• Left Ventricular Function Systolic Function
• Ventricular Remodeling
• references
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• PATHOLOGIC OF Q-WAVE
• PATHOMECANISM CHEST PAIN
• Slide 31
• SMOKING kills
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• ThE eND

3 Lab studies

Cardiac Biomarkers CK CK-MB cTnbullSerum ChemistriesbullRenal FunctionbullCoagulation StudiesbullComplete Blood Count

TREATMENTAspirin

bullRapidly blocks formation of thromboxaneA2 in platelets by cyclooxygenase inhibitionbull162-325mg chewed (promotes buccalabsorption)bullISIS-2ndash23 reduction in mortality largely additive to the reduction in mortality from streptokinaseOther Adjuvant TherapiesAnalgesicsbullNitratesbullBeta-blockersbullAce InhibitorsbullOxygenbullHeparinbullIV Glycoprotein IIbIIIaInhibitorsbullClopidogrelbullStatins

Thrombolytic TherapybullCommon AgentsbullTNK-tPA30-50mg IV bolusbullReteplase10U x 2 (each over 2 minutes) IVbullAlteplaseup to 100mg in 90mins (based on weight)

bullContraindicationsndashAbsolute Prior intracranial hemorrhage known cerebral vascular lesion malignant intracranial neoplasm ischemic stroke within 3 months suspected aortic dissection active bleeding recent closed head injury or facial trauma within 3monthsndashRelative History of chronic severe HTN severeuncontrolled HTN at presentation (gt180110) history of ischemic stroke gt3 months traumaticprolonged CPR recent internal bleeding (2-4 weeks) pregnancy active peptic ulcer current anticoagulation

Primary PCI

bullPCI = Percutaneous Coronary Intervention

bullPTCA = Percutaneous Transluminal Coronary Angioplasty

bullPOBA = Plain Old Balloon Angioplasty

PROGNOSIS

bullDischarge usually 5 days after admissionbullSmoking CessationbullShort and Long-term survival depend upon resting LV function residual ischemic myocardium and susceptibility to ventricular arrhythmias

THE END

• CHEST PAIN SCENARIO 3 GROUP 10
• SCENARIO
• KEYWORD
• QUESTION
• DIFFERENTIAL DIAGNOSIS
• INTRODUCTION
• BASIC SCIENCE
• EKG
• Normal heart
• Myocardial Infarction Two to three days after an MI the myocyt
• Slide 11
• PATHOPHYSIOLOGY OF ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
• myocardial infarction
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• HYPOTENSION May trigger a dramatic sympathetic nervous system
• Slide 19
• Slide 21
• Left Ventricular Function Systolic Function
• Ventricular Remodeling
• references
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• PATHOLOGIC OF Q-WAVE
• PATHOMECANISM CHEST PAIN
• Slide 31
• SMOKING kills
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• ThE eND

TREATMENTAspirin

bullRapidly blocks formation of thromboxaneA2 in platelets by cyclooxygenase inhibitionbull162-325mg chewed (promotes buccalabsorption)bullISIS-2ndash23 reduction in mortality largely additive to the reduction in mortality from streptokinaseOther Adjuvant TherapiesAnalgesicsbullNitratesbullBeta-blockersbullAce InhibitorsbullOxygenbullHeparinbullIV Glycoprotein IIbIIIaInhibitorsbullClopidogrelbullStatins

Thrombolytic TherapybullCommon AgentsbullTNK-tPA30-50mg IV bolusbullReteplase10U x 2 (each over 2 minutes) IVbullAlteplaseup to 100mg in 90mins (based on weight)

bullContraindicationsndashAbsolute Prior intracranial hemorrhage known cerebral vascular lesion malignant intracranial neoplasm ischemic stroke within 3 months suspected aortic dissection active bleeding recent closed head injury or facial trauma within 3monthsndashRelative History of chronic severe HTN severeuncontrolled HTN at presentation (gt180110) history of ischemic stroke gt3 months traumaticprolonged CPR recent internal bleeding (2-4 weeks) pregnancy active peptic ulcer current anticoagulation

Primary PCI

bullPCI = Percutaneous Coronary Intervention

bullPTCA = Percutaneous Transluminal Coronary Angioplasty

bullPOBA = Plain Old Balloon Angioplasty

PROGNOSIS

bullDischarge usually 5 days after admissionbullSmoking CessationbullShort and Long-term survival depend upon resting LV function residual ischemic myocardium and susceptibility to ventricular arrhythmias

THE END

• CHEST PAIN SCENARIO 3 GROUP 10
• SCENARIO
• KEYWORD
• QUESTION
• DIFFERENTIAL DIAGNOSIS
• INTRODUCTION
• BASIC SCIENCE
• EKG
• Normal heart
• Myocardial Infarction Two to three days after an MI the myocyt
• Slide 11
• PATHOPHYSIOLOGY OF ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
• myocardial infarction
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• HYPOTENSION May trigger a dramatic sympathetic nervous system
• Slide 19
• Slide 21
• Left Ventricular Function Systolic Function
• Ventricular Remodeling
• references
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• PATHOLOGIC OF Q-WAVE
• PATHOMECANISM CHEST PAIN
• Slide 31
• SMOKING kills
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• ThE eND

Thrombolytic TherapybullCommon AgentsbullTNK-tPA30-50mg IV bolusbullReteplase10U x 2 (each over 2 minutes) IVbullAlteplaseup to 100mg in 90mins (based on weight)

bullContraindicationsndashAbsolute Prior intracranial hemorrhage known cerebral vascular lesion malignant intracranial neoplasm ischemic stroke within 3 months suspected aortic dissection active bleeding recent closed head injury or facial trauma within 3monthsndashRelative History of chronic severe HTN severeuncontrolled HTN at presentation (gt180110) history of ischemic stroke gt3 months traumaticprolonged CPR recent internal bleeding (2-4 weeks) pregnancy active peptic ulcer current anticoagulation

Primary PCI

bullPCI = Percutaneous Coronary Intervention

bullPTCA = Percutaneous Transluminal Coronary Angioplasty

bullPOBA = Plain Old Balloon Angioplasty

PROGNOSIS

bullDischarge usually 5 days after admissionbullSmoking CessationbullShort and Long-term survival depend upon resting LV function residual ischemic myocardium and susceptibility to ventricular arrhythmias

THE END

• CHEST PAIN SCENARIO 3 GROUP 10
• SCENARIO
• KEYWORD
• QUESTION
• DIFFERENTIAL DIAGNOSIS
• INTRODUCTION
• BASIC SCIENCE
• EKG
• Normal heart
• Myocardial Infarction Two to three days after an MI the myocyt
• Slide 11
• PATHOPHYSIOLOGY OF ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
• myocardial infarction
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• HYPOTENSION May trigger a dramatic sympathetic nervous system
• Slide 19
• Slide 21
• Left Ventricular Function Systolic Function
• Ventricular Remodeling
• references
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• PATHOLOGIC OF Q-WAVE
• PATHOMECANISM CHEST PAIN
• Slide 31
• SMOKING kills
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• ThE eND

Primary PCI

bullPCI = Percutaneous Coronary Intervention

bullPTCA = Percutaneous Transluminal Coronary Angioplasty

bullPOBA = Plain Old Balloon Angioplasty

PROGNOSIS

bullDischarge usually 5 days after admissionbullSmoking CessationbullShort and Long-term survival depend upon resting LV function residual ischemic myocardium and susceptibility to ventricular arrhythmias

THE END

• CHEST PAIN SCENARIO 3 GROUP 10
• SCENARIO
• KEYWORD
• QUESTION
• DIFFERENTIAL DIAGNOSIS
• INTRODUCTION
• BASIC SCIENCE
• EKG
• Normal heart
• Myocardial Infarction Two to three days after an MI the myocyt
• Slide 11
• PATHOPHYSIOLOGY OF ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
• myocardial infarction
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• HYPOTENSION May trigger a dramatic sympathetic nervous system
• Slide 19
• Slide 21
• Left Ventricular Function Systolic Function
• Ventricular Remodeling
• references
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• PATHOLOGIC OF Q-WAVE
• PATHOMECANISM CHEST PAIN
• Slide 31
• SMOKING kills
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• ThE eND

PROGNOSIS

bullDischarge usually 5 days after admissionbullSmoking CessationbullShort and Long-term survival depend upon resting LV function residual ischemic myocardium and susceptibility to ventricular arrhythmias

THE END

• CHEST PAIN SCENARIO 3 GROUP 10
• SCENARIO
• KEYWORD
• QUESTION
• DIFFERENTIAL DIAGNOSIS
• INTRODUCTION
• BASIC SCIENCE
• EKG
• Normal heart
• Myocardial Infarction Two to three days after an MI the myocyt
• Slide 11
• PATHOPHYSIOLOGY OF ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
• myocardial infarction
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• HYPOTENSION May trigger a dramatic sympathetic nervous system
• Slide 19
• Slide 21
• Left Ventricular Function Systolic Function
• Ventricular Remodeling
• references
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• PATHOLOGIC OF Q-WAVE
• PATHOMECANISM CHEST PAIN
• Slide 31
• SMOKING kills
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• ThE eND

THE END

• CHEST PAIN SCENARIO 3 GROUP 10
• SCENARIO
• KEYWORD
• QUESTION
• DIFFERENTIAL DIAGNOSIS
• INTRODUCTION
• BASIC SCIENCE
• EKG
• Normal heart
• Myocardial Infarction Two to three days after an MI the myocyt
• Slide 11
• PATHOPHYSIOLOGY OF ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
• myocardial infarction
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• HYPOTENSION May trigger a dramatic sympathetic nervous system
• Slide 19
• Slide 21
• Left Ventricular Function Systolic Function
• Ventricular Remodeling
• references
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• PATHOLOGIC OF Q-WAVE
• PATHOMECANISM CHEST PAIN
• Slide 31
• SMOKING kills
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• ThE eND