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Pathology of Cardiovascular System. Dr. S.L. Beh [email protected]. Overview. Review of basics Ischaemic heart diseases Coronary artery occlusions Myocardial infarction Valvular heart diseases Degenerative valvular diseases Rheumatic heart disease Bacterial endocarditis Shock - PowerPoint PPT Presentation

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  • Pathology of Cardiovascular System

    Dr. S.L. [email protected]

  • OverviewReview of basicsIschaemic heart diseasesCoronary artery occlusionsMyocardial infarctionValvular heart diseasesDegenerative valvular diseasesRheumatic heart diseaseBacterial endocarditisShockHypovoleamic shockCardiogenic shockSepticeamic shockAnaphylactic shock

  • ReviewAtherosclerosisEpidemiology of coronary artery diseasePhysiology of the cardiac cycleAnatomy of the myocardiumVascular supply of the myocardium

  • Taken from Colour Atlas of Anatomy Roden, Yokochi and Lutjen-Drecoll

  • Taken from Colour Atlas of Anatomy Roden, Yokochi and Lutjen-Drecoll

  • Taken from Colour Atlas of Anatomy Roden, Yokochi and Lutjen-Drecoll

  • Taken from Colour Atlas of Anatomy Roden, Yokochi and Lutjen-Drecoll

  • Taken from Colour Atlas of Anatomy Roden, Yokochi and Lutjen-Drecoll

  • Anatomy of the myocardiumCardiac muscle cells form a collection of branching and anastamosing striated muscles. They make up 90% of the volume of the myocardium.Unlike skeletal muscles, they contain ten times more mitochondria per muscle cell. This reflects their extreme dependence on aerobic metabolism. They do not need to rest!!

  • Vascular supply of the myocardiumPredominant blood supply is from the coronary arteries, which arises from the aorta and runs along an epicardial route before penetrating the myocardium as intramural arteries. Effectively a one-way street flow and supply.Coronary arterial blood flow to the myocardium occurs during ventricular diastole; when the microcirculation in the myocardium is not compressed by cardiac contraction. The one^way street only flows within a fixed time span.

  • Coronary Angiography

    L = Left main trunkA= Anterior descendingC= CircumflexR= Right coronaryP=Posterior descending

  • Areas of supply (perfusion)The left coronary trunk gives rise to:-Left Anterior Descending (LAD) and the Left Circumflex (LCX)Right Coronary Artery (RCA)

  • Areas of perfusionLeft anterior descending (LAD) supplies most of the apex of the heart, the anterior wall of the left ventricle and the anterior two-thirds of the ventricular septum.Left circumflex branch supplies the lateral wall of the left ventricle.The right coronary artery in 80% of the population supplies the right ventricle, the posterior third of the ventricular septum and the posterior-basal wall of the left ventricle. (Right dominant circulation)

  • Ischaemic Heart DiseasesThis is a generic name for a group of closely related syndromes that result from myocardial ischaemia.In over 90%, this is due to a reduction in coronary blood flow. (Decrease in supply)Other conditions arise as a result of increases in demand e.g. hypertrophy, shock, increase heart rate, etc.

  • Diminished Coronary PerfusionFixed coronary obstructionMore than 90% of patients with IHDOne or more lesions that causes at least 75% reduction of the cross-sectional area of at least one of the major epicardial arteries.

  • Coronary atherosclerosis

  • Coronary atherosclerosis

  • Coronary atherosclerosis

  • Coronary atherosclerosis

  • Taken from Robbins Pathologic Basis of Disease

  • Clinical ManifestationsAngina PectorisMyocardial InfarctionChronic ischaemic heart diseaseProgressive heart failure consequent to previous myocardial infarction.Sudden Cardiac Death

  • Angina PectorisThis is a symptom complex. Symptoms caused by transient myocardial ischaemia that falls short of inducing the cellular necrosis that defines myocardial infarction.Three variants:-Stable anginaPrinzmental anginaUnstable angina

  • Angina PectorisStable Angina Most common form. Chronic stenosing coronary atherosclerosis, reaching a critical level, leaving the heart vulnerable to increased demand.Typically relieved by rest or a vasodilator

  • Prinzmental AnginaUncommon patternOccurs at restDocumented to be due to arterial spasmUnrelated to physical activity, heart rate or blood pressure.Generally responds to vasodilators.

  • Unstable AnginaPattern here is the pain occurs with progressively increasing frequency and tends to be more prolongedAssociated with disruption of the atherosclerotic plaque, with superimposed thrombosis, embolisation or spasm.Predictor of Myocardial Infarction

  • Effects of ischaemia on myocytesOnset of ATP DepletionLoss of contractilityATP reducedto 50% of normalTo 10% of normalIrreversible injuryMicrovascular injurySeconds< 2 minutes

    10 minutes40 minutes20-40 minutes> 1 hour

  • Myocardial InfarctionTransmural InfarctionThe ischaemic necrosis involves the full or nearly the full thickness of the ventricular wall in the distribution of a single coronary artery.Usually associated with chronic coronary atherosclerosis, acute plaque change and superimposed completely obstructive thrombosis.

  • Myocardial InfarctionSubendocardial infarctLimited to the inner one-third or at most one half of the ventricular wallMay extend laterally beyond the perfusion territory of a single coronary arteryIn a majority of cases, there is diffuse stenosing coronary atherosclerosis.

  • Gross changes of myocardial infarctionGross changesNone to occasional mottling (up to 12 hours)Dark mottling (12-24 hours)Central yellow tan with hypereamic border (3-7 days)Gray white scar (2-8 weeks)

  • Varying gross appearance of myocardial infarction

  • Recent and Old Myocardial Infarcts

  • Microscopic changes of myocardial infarctEarly coagulation necrosis and oedema; haemorrhage (4-12 hours)Pyknosis of nucleic, hypereosinophilia, early neutrophilic infiltrate (12-24 hours)Coagulation necrosis, interstitial infiltrate of neutrophils (1-3 days)Dense collagenous scar (> 2 months)

  • Hypereosinophilia

  • Coagulative necrosis

  • Interstitial infiltration of neutrophils

  • Laboratory detection of myocardial infarctionThis is based on the measurement of intracellular macromolecules leaked from the damaged myocytes into the circulationCreatine kinase particularly the MB isoenzymeLactate dehydrogenaseTroponin Troponin 1 and Troponin T

  • Other diagnostic toolsElectrocardiogram Q wavesEchocardiogramRadioisotope studiesMagnetic Resonance Imaging

  • Electrocardiogram (ECG) changes

  • Acute effects of myocardial infarctionContractile dysfunctionArrhythmiasCardiac rupturePericarditisSudden deathInvariably this would be due to a lethal arrhythmia (asystole or ventricular fibrillation)

  • Pathological complications of myocardial infarctionInfarct extensionMural thrombusVentricular aneurysmMyocardial ruptureVentricular free wallSeptalPapillary muscle

  • Infarct extension Diagram from Robbins Pathologic Basis of Disease

  • Ruptured MyocardialInfarct

  • Ruptured Papillary muscle

  • Old myocardial infarct showing evidence of thinning of ventricular wall replaced by fibrous scar

  • Fibrous scarring with compensatory hypertrophy of unaffected ventricular wall

  • Ventricular wall aneurysm

  • Anatomy of Heart ValvesAortic valve Commonly tricuspid semi lunar valves. Can be congenitally bicuspid.Mitral valve Bi-cuspid flaps supported by chordae tendinae attached to papillary musclesPulmonary valves Tricuspid semi lunar valvesTricuspid valves Tri-cuspid flaps supported by chordae tendinae.

  • Aortic Valves

  • Mitral Valves

  • Pulmonary Valves

  • Tricuspid Valves

  • Taken from Colour Atlas of Anatomy Roden, Yokochi and Lutjen-Drecoll

  • Response to injuryMechanical injury superficial fibrous thickening over preserved architecture.Inflammation invariably leads to vascularisation of structure, fibrosis leads to decrease in size/surface area.Degenerative changes distortion and increase in size due to deposits of material such as calcium salts, cholesterol, etc.

  • Effects of valvular diseaseStenosis tightening of the valvular opening resulting in decreased flow of blood through the opening.Incompetence incomplete closure of the valvular opening, allowing backflow of blood through the valvular openingMixed.

  • Effects of valvular diseaseMitral StenosisIncreased atrial volume and pressureAtrial dilatationAtrial thrombusCongestion of lungsPulmonary HypertensionRight Heart FailureSystemic embolisation

  • Common valvular diseasesDegenerativeCalcific aortic stenosisMitral annular calcificationMyxomatous degeneration of mitral valves (mitral valve prolapse)Rheumatic fever and rheumatic heart disease

  • Calcific Aortic StenosisMost frequent of all valvular abnormalitiesCalcification induced by wear and tearOnset in the elderly 50s and 60s in congenital bicuspid individuals70s and 80s in those with previous normal valvesHeaped up calcified masses

  • Aortic Valve Inlet Looking into the left ventricular outletNote the three valvular cusps and the three distinct commissures (arrows)

  • Calcific Aortic Stenosis (3 cusps)

  • Calcific Bicuspid Aortic Valve

  • Mitral Annular calcificationDegenerative calcific deposits in the ring of the mitral valve.Generally does not affect valvular function, but can lead to mitral regurgitationSource of thrombi and emboli, also prone to infective endocarditisMost common in women over 60

  • Calcification of Mitral Valve RingDiagram from Robbins Pathologic Basis of Disease

  • Mitral Valve ProlapseMyxomatous degeneration of valve.Characteristically ballooning of the valvular cusps with the affected leaflets thickened and rubbery.Basis for the change unknown but believed to be due to developmental anomaly of connective tissue.Association with Marfans syndrome (a syndrome whereby there is a mutation in the gene encoding fibrillin)

  • Mitral Valve Inlet Viewed from the left atrium.Note bicuspid valve leaflets.Slight tenting of the valve leaflets suggestive of early mitral valve prolapse.

  • Mitral Valve ProlapseNotice tenting of valve leaflet(arrow)

  • Rheumatic feverOnce the most common cause of valvular heart disease in Hong Kong.It is an acute immunologically mediated , multi-system inflammatory disease that occurs a few weeks after an episode of Group A (-hemolytic) streptococcal pharyngitis.

  • Diagram from Robbins Pathologic Basis of Disease

  • Rheumatic ValvulitisDiagram from Robbins Pathologic Basis of Disease

  • Acute Rheumatic Carditis Aschoff BodyDiagram from Robbins Pathologic Basis of Disease

  • Chronic Rheumatic Valvular Heart DiseaseMost important consequence of rheumatic feverInflammatory deformity of valvesAlmost always involve the mitral valveInvolvement of aortic or other valves also common

  • Characteristics of rheumatic valvular diseaseAcute phaseFoci of fibrinoid degeneration surrounded by lympocytes Aschoff bodiesMost distinctive within the heart, but widely disseminated.Pancarditis PericarditisMyocarditisVerrucae vegetations (1-2 mm)

  • Chronic Rheumatic Disease of Aortic ValveDiagram from Robbins Pathologic Basis of Disease

  • Characteristics of rheumatic valvular diseaseChronicLeaflet thickeningCommissure fusionShortening, thickening and fusion of chordae tendinae

  • Chronic Rheumatic Disease of Mitral ValveVascularisation)Diagram from Robbins Pathologic Basis of Disease

  • Infective EndocarditisColonisation or invasion of heart valves by microbiologic agent.Formation of friable vegetations (composed of thrombotic debris and organisms.Leads to destruction of underlying cardiac tissue.Source of infective embolisation

  • Infective endocarditisMost common sites involve the left heart valvesTricuspid valves typically involved in intravenous drug abusersDevelopment of infective endocarditis preventable in patients with valvular diseases by provision of antibiotic cover for any surgical or dental procedures.

  • Bacteria EndocarditisDiagram from Robbins Pathologic Basis of Disease

  • The elements of circulationAn effective pump(The heart)(Normal blood vessels)A clear channelAn effective return(No peripheral pooling)

  • The elements of circulationBlood Pressure/Heart RateIntact and unblocked blood vesselsEffective venous and lymphatic return

  • The economics of circulation

  • Distribution of blood volume in the circulatory system

  • Body Fluid CompartmentsBlood volume contains both extracellular fluid (plasma) and intracellular fluid (fluid in RBC). Average blood volume is about 8% of body weight, approximately 5L (60% plasma 40% RBC)

  • What is shock?A state of generalised hypoperfusion of all cells and tissues due to reduction in blood volume or cardiac output or redistribution of blood resulting in an inadequate effective circulating volumeA systemic (whole body) event resulting from failure of the circulatory systemIt is at first reversible, but if protracted leads to irreversible injury and death.

  • Causes of shockHypovoleamiaCardiogenic (pump failure)Anaphylactic (peripheral pooling) (return failure)Septic (Septiceamic) Complex reasons

  • Hypovoleamic shockHaemorrhageExternal (Chop wounds, Gastro-intestinal bleeding, etc)Internal (Hemoperitoneum due to ruptured aortic aneurysm, ruptured ectopic pregnancy, etc.Fluid lossDehydration (low intake or excessive loss)

  • External loss

  • Internal Bleeding

  • Effect of volume loss onCardiac Output and Arterial PressureTaken from Guyton & Hall Human Physiology and Mechanisms of Disease

  • Stages of hypovoleamic shockAsymptomatic (< 10%) Early stage (15-25% loss) Compensated hypotensionProgressive/Advance Stage Results when no therapeutic intervention is given for the early stage, compensatory mechanisms become harmful. Autoregulation mechanisms breakdown.Irreversible shockIrreversible hypoxic injury to vital organs

  • Compensated hypotensionHypotension (low volume or low cardiac output)Sympathetico-adrenal stimulation (fight or fright)Release of catecholamines resulting in peripheral vasoconstriction maintain BPActivation of renin-angiotensin-aldosterone system and increased anti-diuretic hormone releaseFluid retention by kidneys, further vasoconstrictionImpaired renal perfusion and perfusion to other organs with every effort made to maintain perfusion to brain and heart (auto-regulation)

  • Taken from Guyton & Hall Human Physiology and Mechanisms of Disease

  • Splenic Infarct

  • Infarct of kidneyReplaced by scarred tissue

  • Haemorrhagic infarct of lung

  • Cardiogenic shockFailure of myocardial pump.Intrinsic due to myocardial damageExtrinsic Due to external pressure e.g. cardiac tamponadeDue to obstructed flow e.g. thrombosis

  • Compensated heart failureHere the situation is one of a compromised cardiac pump which has been compensated by an increase in right atrial pressure ( increased blood volume caused by retention of fluid ). Thus cardiac output is maintained.It may not be noticed as it would have developed gradually over time. However any strain on the heart, eg sudden increase in exercise would tip the balance and lead to a decompensated heart failure.

  • Decompensated heart failureThe pump is so damaged that no amount of fluid retention can maintain the cardiac output. This failure also means that the renal function cannot return to normal, thus fluid continues to be retained and the person gets more and more oedematous with eventual death. In short, failure of the pump to pump enough blood to the kidneys.

  • Anaphylactic shockUsually due to prior sensitisationExposure to specific antigensMediated by histamines, complements and prostaglandinsVasodilatation of micro-circulation associated with pooling and fluid extravasation

  • Septic shockCommonly due to gram-negative endotoxin producing bacteria. May also accompany gram-ve bacteria.Predisposing factors include:-Debilitating diseasesComplications of instrumentation and treatmentBurns

  • Septic shockPathogenesis include:-Inflammatory reaction vasodilatation mediated by histamines and complementsDisseminated intravascular coagulopathy activation of clotting factors and platelets together with consumption of clotting factors Endothelial damage extensive due to endotoxinsRelease of interleukin-1 and TNF-alpha (Tumor necrosis factor alpha) from macrophages

  • Possible mechanisms of septic shockTaken from Guyton & Hall Human Physiology and Mechanisms of Disease

  • Pathological changesHypoxic injury to vital organs infarctionNecrosis of tissuesLysis of cells

    The extent of pathological changes is dependent on the duration of decompensation before death.In acute deaths, often no significant findings are found.

  • Pathological changesBrainHypoxic and ischaemic damageInitially found at boundary zonesMay also be associated with marked cerebral oedema.

  • Pathological changesHeartFocal myocardial necrosisSubendocardial infarction (vulnerable region of blood supply)

    If there is pre-existing coronary artery diseases, may also lead to acute transmural myocardial infarction

  • Pathological changesIn cardiogenic shockDue to previous ischaemic heart diseases the ventricular chambers may well be dilated and distended. The walls are often thin and may be replaced by non-elastic fibrous scarsIn intrinsic myocardial diseases leading to pump failure, the myocardium may be unusually thickened and rigid.

  • Pathological changesLungsDiffuse alveolar damage (adult respiratory distress syndrome)Damage to Type 1 pneumocytes and to endothelial cells oedema as well as hyaline membrane due to decreased surfactant productionHaemorrhages, fibrosis, atelectasis and infection

  • Pathological changesKidneysAcute tubular necrosis often associated with remarkably well preserved glomeruli

  • Pathophysiology ofAcute Tubular NecrosisTaken from Guyton & Hall Human Physiology and Mechanisms of Disease

  • Acute Tubular Necrosis,

  • Pathological changesGastrointestinal tractMucosal ischaemia, haemorrhage, necrosis, gangreneLiverCentrilobular necrosis, fatty degenerationAdrenal glandsFocal necrosisDiffuse haemorrhagic destruction

  • Pump Failure Cardiogenic ShockVessel injuryPhysical injuries such as wounds, ruptures of aneurysms, etc (Hypovoleamic)Toxins , infection and immune-complexes (DIC, Anaphylaxis, Septiceamic)Peripheral PoolingHypoalbumineamia, Ascites, Renal failure,(Hypovoleamic)Septiceamic, Anaphylaxis(Capillary pooling)