Pathophysiology & Clinical Presentations
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Transcript of Pathophysiology & Clinical Presentations
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Pathophysiology & Pathophysiology & Clinical PresentationsClinical Presentations
Acute Coronary SyndromesAcute Coronary Syndromes
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Ischemic Heart Disease - OverviewIschemic Heart Disease - Overview
Atherosclerosis
Atherothrombosis
Pathophysiology
Clinical Presentations
Silent ischemia
Stable angina Acute Coronary Syndromes
ParametersAnatomy: Atheroma / Atherothrombosis
Subjective: Angina
Objective: EKG T wave ST seg changes
Chemistry: Cardiac serum biomarkers:
CPK, CK-MB, Troponins
Epicardial & Microvascular Spam
Prevalence & severity of stenosis
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Events During AtherogenesisEvents During Atherogenesis
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P x r
2hWall Stress =
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ISCHEMIC CASCADEISCHEMIC CASCADE
Predictable sequence of Predictable sequence of pathophysiologic events post pathophysiologic events post
myocardial supply/demand imbalancemyocardial supply/demand imbalance
•Biochemical metabolic actions
•Flow Maldistribution
•Hypoperfusion
•(Rales)
Angina / SI
• Compliance
• Contractility
• EF
• LVEDP
•(S4)Nuclear
Echo
EKG
TIME FROM ONSET OF ISCHEMIA
± 45 sec.
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Effect of Fixed Stenosis on Myocardial Blood Flow
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Progression of coronary plaque over time Clinical FindingsProgression of coronary plaque over time Clinical Findings
Acute Coronary SyndromesSudden Cardiac Death
Acute silent occlusive process
Angina pectoris
Thrombogenicrisk factors
Atherogenic risk factors
Endothelial dysfunction
20 years 60 yearsAge
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IHD – Clinical SpectrumIHD – Clinical SpectrumChronicChronic
Stable AnginaStable AnginaSilent IschemiaSilent IschemiaMixed AnginaMixed AnginaMicrovascular Angina Microvascular Angina
(Syndrome X)(Syndrome X)Stunned & HibernatingStunned & Hibernating
Acute Acute Unstable AnginaUnstable AnginaAcute Myocardial Acute Myocardial
Infarction (NSTEMI, Infarction (NSTEMI, STEMI)STEMI)
Sudden Cardiac DeathSudden Cardiac DeathPrinzmetal AnginaPrinzmetal Angina
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Clinical Classification of Chest PainClinical Classification of Chest PainTypical angina (defineTypical angina (define))1.1.Substernal chest discomfort with a characteristic Substernal chest discomfort with a characteristic
quality and duration that isquality and duration that is2.2.Provoked by exertion or emotional stress andProvoked by exertion or emotional stress and3.3.Relieved by rest or nitroglycerinRelieved by rest or nitroglycerinAtypical angina ( probable)Atypical angina ( probable) Meets 2 of the above characteristicsMeets 2 of the above characteristicsNoncardiac chest painNoncardiac chest pain Meets one or none of the typical angina Meets one or none of the typical angina
characteristicscharacteristicsDIFFERENTIAL DIAGNOSIS OF CHEST PAINDIFFERENTIAL DIAGNOSIS OF CHEST PAIN1.1.Cardiovascular: Pericarditis, Aortic Valve Disease, Cardiovascular: Pericarditis, Aortic Valve Disease,
Aortic Dissection, Pulmonary Embolism, Mitral Aortic Dissection, Pulmonary Embolism, Mitral Valve ProlapseValve Prolapse
2.2.Gastrointestinal: Esophageal, Biliary, Peptic ulcer, Gastrointestinal: Esophageal, Biliary, Peptic ulcer, PancreatitisPancreatitis
3.3.Pulmonary: Pneumothorax, Pneumonia, PleuritisPulmonary: Pneumothorax, Pneumonia, PleuritisChest Wall: Costochondritis, Rib fracture, Herpes Chest Wall: Costochondritis, Rib fracture, Herpes
zosterzosterPsychological: Anxiety disordersPsychological: Anxiety disorders
ClasClasss
ActivActivity ity evokingevoking
angianginana
LimitLimits to s to normalnormal
activactivityity
II ProlProlonged onged exertionexertion
NoneNone
IIII WalkWalking > 2 ing > 2 blocksblocks
SlighSlightt
IIIIII WalkWalking < 2 ing < 2 blocksblocks
MarkMarkeded
IVIV MiniMinimal or mal or restrest
SeveSeverere
Canadian Cardiovascular Society Classification ( CCSC)
*CHRONIC STABLE ANGINA – 2 TO 10 Min & CCSC I – II*CHRONIC STABLE ANGINA – 2 TO 10 Min & CCSC I – II ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV ACUTE CORONARY SYNDROMES > 15 Min. – Hours & CCSC III - IV
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CAD - Clinical SpectrumCAD - Clinical SpectrumChronic ischemic heart diseaseChronic ischemic heart disease Ischemia precipitated by increased myocardial oxygen demand Ischemia precipitated by increased myocardial oxygen demand in the setting of a fixed, not vulnerable atherosclerotic lesion. It is in the setting of a fixed, not vulnerable atherosclerotic lesion. It is called called Stable AnginaStable Angina when the clinical characteristics (Angina when the clinical characteristics (Angina attacks) do not change in frequency, duration, precipitating attacks) do not change in frequency, duration, precipitating causes, or easy with the angina is relieved, for at least 60 days.causes, or easy with the angina is relieved, for at least 60 days.
--Silent Ischemia, -Mixed Angina -Syndome X -Silent Ischemia, -Mixed Angina -Syndome X -Stunning & Hibernating.Stunning & Hibernating.Acute Coronary Syndromes (ACS)Acute Coronary Syndromes (ACS) Ischemia or infarction are caused from a primary reduction in Ischemia or infarction are caused from a primary reduction in coronary flow, precipitated by plaque disruption and subsequent coronary flow, precipitated by plaque disruption and subsequent thrombus formation:thrombus formation:
Unstable Angina, NSTEMI, STEMIUnstable Angina, NSTEMI, STEMI Prinzmetal AnginaPrinzmetal Angina
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Stable Plaque Vulnerable Plaque
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UA NSTEMI STEMI
+ S. Markers
Plaque DisruptionPlaque Disruption
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Distinguishing Features of Acute Coronary Syndromes
STEMISTEMINSTEMINSTEMI
Positive (+)Positive (+)Positive (+)Positive (+)Negative (-)Negative (-)Cardiac Cardiac Serum Serum BiomarkersBiomarkers
ST elevation ST elevation ( and Q waves ( and Q waves later)later)
ST depression ST depression and/pr T Wave and/pr T Wave inversioninversion
Dynamic, transiet < 24 hours
T-wave inversion and/or ST seg
depression
EKC initial EKC initial findingsfindings
Prolonged ( > 30 min ) Prolonged ( > 30 min ) crushing, strangling crushing, strangling
chest pain more severe chest pain more severe and wider radiation than and wider radiation than
usual anginausual angina
•Rest anginaRest angina - Rest or nocturnal - Rest or nocturnal Angina ≥ 20 minutes occurring Angina ≥ 20 minutes occurring within a week of presentation.within a week of presentation.•New onset anginaNew onset angina - ( < 2 months ) - ( < 2 months ) exertional angina progressing to exertional angina progressing to CCSA IIICCSA III•Crescendo anginaCrescendo angina - < 2 moths - < 2 moths acceleration of previously stable acceleration of previously stable angina to at least CCSA III.angina to at least CCSA III.•Within 30 day post MI, PCI or Within 30 day post MI, PCI or CABGCABG
Anginal Anginal PresentationPresentationss
Myocardial InfarctionMyocardial InfarctionUnstable AnginaUnstable Angina
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Acute Coronary Syndromes Acute Coronary Syndromes Coronary AtherothrombosisCoronary Atherothrombosis
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-RCA, 1yr. Before of the acute MI (B)
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Acute MITypical rise and gradual fall (troponin) or more rapid rise and fall of CK-MB, markers of myocardial necrosis, with at least one of the following:
•Ischemic symptoms
•EKG changes indicative of ischemia (ST-seg elevation or depression)
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T-wave ∆
ST-seg ∆
Path. Q waves
Zone of ischemia
Zone of injury
Zone of necrosis
Lateral AnteriorSeptal
Inferior
T Wave – ST seg. changes
>0.03 seconds
>1/3 the total of QRS
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2020
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“ Time is muscle”
Myocardial Infarction is a true emergency in cardiac care.
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If the clinical picture is consistent with acute STEMI (including True Posterior MI) or new left bundle branch block (LBBB) is present in EKG, select and implement reperfusion therapy, Fibrinolysis or PCI as quickly as possible within 12 hours of symptoms onset to obtain and sustain optimal flow in the infarct-related artery (IRA). Do not wait for serum cardiac biomarkers result before implementing reperfusion strategy !
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ACS Treatment ACS Treatment
RevascularizationRevascularizationMechanical: PCI, CABGMechanical: PCI, CABGPharmacologic: ThrombolyticsPharmacologic: Thrombolytics
Stabilization of Vulnerable Plaque AspirinStabilization of Vulnerable Plaque AspirinAntithromboticsAntithromboticsBeta-BlockersBeta-BlockersACE-InhibitorsACE-InhibitorsLipid-Lowering Agents (+stantins)Lipid-Lowering Agents (+stantins)AntioxidantsAntioxidantsAggressive Risk Factors ModificationsAggressive Risk Factors Modifications
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Complications of Ml
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COMPLICATIONS OF INFARCTION
Ventricular Septal RupturePapillary Muscle Rupture
Ventricular Free Wall Rupture
Left Ventricular Thrombus