intensive course phase 1 2010a
DESCRIPTION
My lecture notes in pdf during MMed (Emergency Medicine) Phase I Conjoint Board Intensive Course in Universiti Malaya, 22 February 2010TRANSCRIPT
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Intensive Course For Emergency Medicine Phase I
(MMed Professional Exam 2010)
KS Chew
School of Medical Sciences
Universiti Sains Malaysia
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Cardiovascular Physiology Review: Cardiac Output
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• Stroke volume = End diastolic volume – End systolic volume = 135 – 65 = 70 ml
• At rate of 70 beats/min, CO = 70 * 70 = 4900 ml
• Ejection fraction (EF) is the ratio of stroke volume to end-diastolic volume (EDV), expressed as a percentage:
• EF = (SV/EDV) * 100
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Schematic Representation Of The Frog-heart Preparation Used By Otto Frank
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Frank-Starling Law
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Effects On Stroke Volume Of Stimulating The Sympathetic Nerves To The Heart
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The pressure-volume cycle of the human left ventricle. The area bounded by the pressure-volume curve gives the stroke work of the heart. The lower confine of the pressure-volume loop shown by the dotted line is defined by the passive stretch of the relaxed ventricular muscle by the returning blood.
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Increased Preload
Increased Afterload
Increased Contractility
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Vascular Function and Cardiac Function Curve
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Vascular Function and Cardiac Function Curve
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Relationship Between End-diastolic Ventricular Volume and Stroke
Volume
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Pathophysiology of Acute Coronary Syndrome
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Chronology of the interface between the patient and the clinician through the progression of plaque formation and the onset of complications of STEMI.
Management Before STEMI
41 2 3 4 5 6
Onset of STEMI- Prehospital issues- Initial recognition and management in the Emergency Department (ED)- Reperfusion
Hospital Management- Medications- Arrhythmias- Complications- Preparation for discharge
Secondary Prevention/Long-Term Management
Presentation
Working Dx
ECG
Cardiac Biomarker
Final Dx
UA
NQMI QwMI
No ST Elevation
NSTEMI
Ischemic DiscomfortAcute Coronary Syndrome
UnstableAngina
Myocardial Infarction
ST Elevation
Modified from Libby. Circulation 2001;104:365, Hamm et al. The Lancet 2001;358:1533 and Davies. Heart 2000;83:361.
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Pathophysiology of ACS
Fuster V et al NEJM 1992;326:310–318Davies MJ et al Circulation 1990;82(Suppl II):II–38, II–46
Lipid poolLipid pool
MacrophagesMacrophages
Stress, tensile,Stress, tensile,internalinternal
Shear forces,Shear forces,externalexternal
FissureFissure
LargeLargefissurefissure
SmallSmallfissurefissure
Mural thrombusMural thrombus(unstable angina/(unstable angina/non-Q-wave MI)non-Q-wave MI)
Occlusive thrombusOcclusive thrombus(Q-wave MI)(Q-wave MI)
AtheroscleroticAtheroscleroticplaqueplaque
PlaquePlaquedisruptiondisruption
ThrombusThrombus
One example of atherothromboticdisease progression
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Atherothrombosis: a Generalized and Progressive Process
NormalNormalFattyFattystreakstreak
FibrousFibrousplaqueplaque
Athero-Athero-scleroticscleroticplaqueplaque
PlaquePlaquerupture/rupture/fissure &fissure &thrombosisthrombosis MIMI
IschemicIschemicstroke/TIA stroke/TIA
Critical Critical
leg leg ischemiaischemiaClinically silentClinically silent
CardiovascularCardiovasculardeathdeath
Increasing ageIncreasing age
Stable anginaStable anginaIntermittent claudicationIntermittent claudication
UnstableUnstableanginaangina}}ACSACS
ACS, acute coronary syndrome; TIA, transient ischemic attack
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Platelet Inhibition With GP IIb/IIIa Inhibitors
Reproduced with permission from Yeghiazarians Y, Braunstein JB, Askari A, et al. Unstable angina pectoris. N Engl J Med. 2000;342:101-114. Copyright © 2000, Massachusetts Medical Society. All rights reserved.
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Mechanism of Action of Aspirin in Acute Coronary Syndrome
Prostacyclin is produced by endothelial cells and thromboxane A2 by platelets from their common precursor arachidonic acid via the cyclooxygenase pathway.
Thromboxane A2 promotes platelet aggregation and vasoconstriction, whereas prostacyclin inhibits platelet aggregation and promotes vasodilation.
The balance between platelet thromboxane A2 and prostacyclin fosters localized platelet aggregation and consequent clot formation while preventing excessive extension of the clot and maintaining blood flow around it.
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Mechanism of Action of Aspirin in Acute Coronary Syndrome
The thromboxane A2–prostacyclin balance can be shifted toward prostacyclin by administration of low doses of aspirin. Aspirin produces irreversible inhibition of cyclooxygenase.
Although this reduces production of both thromboxane A2 and prostacyclin, endothelial cells produce new cyclooxygenase in a matter of hours whereas platelets cannot manufacture the enzyme, and the level rises only as new platelets enter the circulation. This is a slow process because platelets have a half-life of about 4 days.
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The thrombus in STEMI is RBC & fibrin rich and often called a red clot or red thrombus
Unstable angina and NSTEMI often precedes STEMI (preinfarction angina). During this phase blood flow in the coronary artery becomes sluggish gradually, and therefore the platelets get trapped within the plaque. Hence in NSTEMI, thrombus is predominantly a white thrombus (platelet rich). Often, a central platelet core is seen over which fibrin clot may also be formed.
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Fibrinolytics
• Why is streptokinase not used in treating UA/ NSTEMI?
• All available thrombolytic agents act basically as a fibrinolytic agents, therefore it is difficult to lyse the platelet rich clot.
• There is also a risk of these agents lysing the fibrin cap and exposing underlying platelet core and trigger a fresh thrombus (TIMI IIIb trial)
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STEMI, NSTEMI and UA
• STEMI - occlusive thrombus - ST elevation (and Q waves) - Cardiac Enzyme elevation - Fibrinolytics beneficial
• NSTEMI - non-occlusive thrombus - NO ST/Q - Cardiac Enzyme elevation present - Fibrinolytics not beneficial
• UA - non-occlusive thrombus - NO ST/Q - Cardiac Enzyme elevation absent - Fibrinolytics not beneficial
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Electrophysiological Changes During Cardiac Ischemia
• Ischemia/hypoxia causes an elevation in extracellular K+. This occurs because K+ leaks out through K+ - ATP channels and because of decreased activity of the Na+/K+-ATPase pump
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Pathophysiology of Asthma and COPD
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• A chronic inflammatory disorder of the airways
• Many cells and cellular elements play a role• Characterized by airway hyperresponsiveness
that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing
• Widespread, variable, and often reversible airflow limitation
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YYYYYY
Mast cellMast cell
CD4+ cellCD4+ cell(Th2)(Th2)
EosinophilEosinophil
AllergensAllergens
Ep cellsEp cells
ASTHMAASTHMA
BronchoconstrictionBronchoconstrictionAHRAHR
Alv macrophageAlv macrophageEp cellsEp cells
CD8+ cellCD8+ cell(Tc1)(Tc1)
NeutrophilNeutrophil
Cigarette smokeCigarette smoke
Small airway narrowingSmall airway narrowingAlveolar destructionAlveolar destruction
COPDCOPD
Reversible IrreversibleAirflow LimitationAirflow Limitation
Source: Peter J. Barnes, MD