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1. CARDIOVASCULAR DISORDERS
GENERIC BSN –BATCH V –SEMESTER IV
PATHOPHYSIOLOGY II
PRESENTED BY –SYED MUHAMMAD HASAN
Presented by -Syed Muhammad Hasan 1

2. KEY HIGHLIGHTS OF THIS CHAPTER
•Reviewing the Anatomy and Physiology of Cardiovascular System.
•Understanding collateral circulation, collateral arteries, conduction
system, myocardial contraction and relaxation.
•Understanding the pathophysiology of atherosclerosis.
•Discussion of the mechanism of Angina and its types with emphasis
on Myocardial infarction.
•Explanation of cardiac performance in light of Frank, Starling and
Laplace's Law i.e. preload, after load and contractility.
Presented by -Syed Muhammad Hasan 2

3. •The cardiovascular system consists of three interrelated components: blood, the
heartand blood vessels. The branch of science concerned with the study of blood,
blood-formingtissues,andthedisordersassociatedwiththemishematology.
•Blood canbe definedas aliquidconnectivetissuethatconsists ofcellssurroundedby
aliquid extracellularmatrixknown asblood plasma.
•Bloodcontributestohomeostasisbytransportingoxygen,carbondioxide,nutrients,
andhormonesto andfromyourbody’scells.
•It also helps regulate body pH and temperature, and provides protection against
diseasethroughphagocytosisand the productionof antibodies.
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THE BASICS OF CARDIOVASCULAR SYSTEM
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4. •The circulatory system can be divided into two parts: pulmonary circulation
and systemic circulation.
•Pulmonary circulation –Moves blood through the lungs and creates a link with
the gas-exchange function of the respiratory system.
•Systemic circulation –Supplies blood to all other tissues of the body.
•The blood present in the heartand pulmonary circulation is sometimes
referred to as the central circulation and that outside the central circulation as
the peripheral circulation.
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PULMONARY AND SYSTEMIC CIRCULATION

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PULMONARY AND
SYSTEMIC
CIRCULATION

6. •The pulmonary circulation consists of the right heart, pulmonary artery (carry
deoxygenated blood) the pulmonary capillaries, and the pulmonary vein
(carry oxygenated blood)
•The systemic circulation consists of the left heart, the aorta and its branches,
the capillariesthat supply the brain and peripheral tissuesand the vena cava.
•The veins from the lower portion of the body merge to form the inferior vena
cava and those from the head and upper extremities merge to form the
superior vena cava, both of which empty into the right heart.
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PULMONARY AND SYSTEMIC CIRCULATION CONSTITUENTS

7. •The pulmonary circulation is the smaller of the two circulations and functions
as a low-pressure system with a mean arterial pressure of approximately12
mm Hg.
•The low pressure of the pulmonary circulation allows blood to move through
the lungs more slowly, which is important for gas exchange.
•In contrast, the systemic circulation which transport blood to distant parts of
the bodyoften against the effects of gravity, functions as a high-pressure
systemwith a mean arterial pressure of 90 to 100 mm Hg.
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DIFFERENCES IN PULMONARY AND SYSTEMIC CIRCULATION

8. •The heart is a four-chambered muscular pump approximately the size of a man’s fist that
beats an average of 70 times/min, 24 hours each day, 365 days each year for a lifetime.
•The heart is located between the lungs in the mediastinal space of the intra-thoracic cavity
in a loose-fitting sac called the pericardium.
•The wall of the heart is composed of an outer epicardium, which lines the pericardial cavity;
the myocardium or muscle layer; and the smoothendocardium, which lines the chambers of
the heart.
•The heart is divided via interatrial septum into a right and left atriums, which serves as a
reservoir for blood coming into the heartand thick-walledright andleft ventricles separated
by interventricular septumwhich pumps blood out of the heart.
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FUNCTIONAL ANATOMY OF HEART

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GROSS ANATOMY OF HEART
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ANATOMICAL
LOCATION AND
LAYERS OF
PERICARDIUM IN
HUMAN HEART

11. •Epicardium–Externallayercomposedofmesothelium(connective tissue),housesmajor
coronary and cardiac vessels of heart and imparts smooth slippery appearance to heart
surface.
•Myocardium–Middlelayer,responsibleforcontractionofheartwiththehelpofCa+2
mediatedproteinsTroponinandTropomyosinandiscomposedofinvoluntarycardiac
muscles.
•Itmakeups95%ofthetotalheartwallandcontainsabundanceofmitochondriaforhigher
energyneeds.
•Endocardium–Innermost layer, provides smooth surface of chambers of heart and cover
valvesinvolvedin bloodflow.Theliningofthe endocardiumis continuouswith the liningof
thebloodvesselsthatenterandleavetheheart.
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LAYERS OF HEART WALL
11

12. •Themyocardiumhasitsownnetworkofbloodvessels,thecoronarycirculationor cardiaccirculationwhich
allowsoxygentodiffuseintoatriaandventricles tofunctionefficiently.
•TheCoronaryArteriesbranchfromtheascendingaortaincludesLeftCoronaryArtery(LCA)andRight
CoronaryArtery(RCA):
•LeftCoronaryArtery–DividesintoAnterior Interventricular(alsoknownasLeftDescendingArtery–LAD)and
Circumflexbranches.
•LeftDescendingArtery–Suppliesoxygenatedbloodtowallsofbothventricles.
•CircumflexBranches–Suppliesoxygenatedbloodtowallsof theleftventricleandleftatrium.
•Right Coronary Artery –Supply oxygenated blood to right atrium and divides into the Posterior
InterventricularandMarginalBranches.
•PosteriorInterventricular Branch–Supplyoxygenatedbloodtothewallsofbothventricles.
•MarginalBranch–Transportsoxygenatedbloodto thewalloftherightventricle.
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CORONARY ARTERIES
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13. •Afterbloodpassesthroughthecoronaryarteries,itflows into capillariesandthenmovesintocoronaryveins.
•Mostof the deoxygenatedbloodfromthemyocardiumdrainsintoalargevascularsinuscalledthecoronary
sinus which empties into right atrium. The principal veins carrying deoxygenated blood into coronary sinus
include:
•Greater Cardiac Vein –Collects CO2 from regions of heart supplied by the left coronary artery (left and right
ventriclesandleftatrium).
•Middle Cardiac Vein –Collects CO2 from regions of heart supplied by posterior interventricular branch of the
rightcoronaryartery(leftandrightventricles).
•SmallCardiacVein–CollectsCO2fromregionsofheartsuppliedby RCA(the rightatriumandright ventricle).
•Anterior CardiacVein–CollectsCO2 from rightventricleandthendirectlyopensinto rightatrium.
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CORONARY VEINS
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ANTERIOR VIEW
OF CORONARY
ARTERIES AND
CORONARY
VEINS
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15. •Collateral circulation are anastomotic channels potentially offering an important
alternativesourceofblood supply when the original vessel fails to provide sufficient blood
due to occluded blood vessels.
•Timely enlargement of collaterals may even avoid Myocardial Infarction (MI) and deathin
symptomatic patients.
•It may occur via pre-existing vascular redundancy (as in the Circle of Willis in Brain) or via
formation of neovascularization(formation of new branched vessels).
•Collateral circulation in the heart tissue will sometimes bypass the blockage in the main
artery and supply enough oxygenated bloodto enable the cardiac tissue to survive and
recover.
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COLLATERAL CIRCULATION

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BLOOD FLOW THROUGH
THE HEART

18. •The conduction system of the heart consists of cardiac muscle cells and conducting fibers
that are specialized for initiating impulses and conducting them rapidly through the heart.
•Both atria contract together, as do the ventricles, but atrial contraction occurs first providing
the heart its automatic rhythmic beat.
•For the heart to pump efficiently and the systemic and pulmonary circulations to operate in
synchrony, the events in the cardiac cycle must be coordinated.
•The conduction system of heart comprises of five components including Sinoatrial (SA)
Node, Atrioventricular (AV) Node, Bundle of His, Atrioventricular bundle branches and
Purkinje Fibers.
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CONDUCTION SYSTEM OF HEART

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CONDUCTION
SYSTEM OF
HEART

20. •Thecardiac action potentialis a brief change in voltage (membrane potentialacross thecell
membraneofheart cells).
•This is caused by the movement of ions between the inside and outside of the cell,
throughproteinscalledion channelsand differs fromaction potentialsfound in other types
of electrically excitable cells, such as nerves.
•The cardiac action potential is controlled by the autonomic nervous system by arising from a
group of specialized cellsthat have automatic action potential generation capability.
•The mechanism of cardiac action potential varies in SA Node (conductive cells) and atriums
and ventricles(contractile cells) to control the rhythmic contractions of heart.
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CARDIAC ACTION POTENTIAL

21. •Conductive cells contain a series of sodium ion channels that allow aslow influx of sodium
ions that causes the membrane potential to rise from an initial value of −60 mV up to about
–40 mV. The process is called spontaneous (prepotential) depolarization.
•At this point, calcium ion channels open and Ca
2+
enters the cell, further depolarizing it at a
more rapid rate until it reaches a value of approximately +20 mV.
•At this point, the calcium ion channels close and K
+
channels open, allowing outflux of
K
+
and resulting in repolarization.
•When the membrane potential reaches approximately −60 mV, the K
+
channels close and
Na
+
channels open, and the prepotential phase begins again.
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CARDIAC ACTION POTENTIAL IN CONDUCTIVE CELLS OF SA NODE

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CARDIAC ACTION POTENTIAL IN CONDUCTIVE CELLS OF SA NODE

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PHASES OF
CARDIAC
ACTION
POTENTIAL

24. •There are two types of refractory period:
•Absolute Refractory Period –The period of depolarization and
repolarization in which the cardiac cells cannot be stimulated to generate
another action potential. Includes phases 0, 1, 2 and part of 3.
•This condition is referred to as absolute refractory period.
•Relative Refractory Period -When repolarization has returned the
membrane potential to below threshold, the cell is capable of responding to
a greater-than-normal stimulus. Includes phases 3 and 4.
•This condition is referred to as the relative refractory period.
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REFRACTORY PERIOD IN CARDIAC ACTION POTENTIAL

25. •By careful placement of surface electrodes on the body, it is possible to record
the complex, compound electrical signal of the heart. This tracing of the
electrical signal is the electrocardiogram (ECG).
•Careful analysis of the ECG reveals a detailed picture of both normal and
abnormal heart function and is an indispensable clinical diagnostic tool.
•There are five prominent points on the ECG:
•P wave –Represents depolarization of atria.
•QRS complex –Represents depolarization of ventricles.
•T wave –Represents the repolarization of ventricles.
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ELECTROCARDIOGRAM –ECG

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INTERPRETATION OF NORMAL ELECTROCARDIOGRAM

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VARIATIONS IN
ECG DUE TO
PATHOLOGICAL
CONDITIONS

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THE CARDIAC CYCLE
•Asinglecardiaccycleincludesall oftheeventsassociatedwithoneheartbeat.
•Itconsistsofsystoleanddiastoleoftheatriaplussystoleanddiastoleofthe
ventricles.(Systole=Contraction;Diastole=Relaxation).
•The cardiaccycle comprisesofthreephases:
•Atrial Systole.
•Ventricular Systole.
•Relaxationperiod.

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30. •Cardiacoutput(CO)–Thevolumeofbloodejectedfromtheleftventricle(ortheright
ventricle) intotheaorta(orpulmonarytrunk)eachminute.
•Strokevolume(SV)–Thevolumeofbloodejectedbytheventricleduringeachcontraction.
(70ml/beat)
•Heartrate(HR)–The numberofheartbeatsperminute(75beats/min).
CardiacOutput(CO)=StrokeVolume(SV=70ml)XHeartRate(HR=75)
CardiacOutput=5250ml/minor5.25L/min.
•In atypicalrestingadult male,strokevolumeaverages70mL/beat,and heartrateis
about75 beats/min.Thus,averagecardiac outputis5.25L/minwhich flowsthroughthe
entirepulmonary andsystemiccirculation.
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REGULATION OF CARDIAC PERFORMANCE

31. •It is noteworthy that the ventricles do not eject all the blood they contain in one
beat.
•In a typical example, a ventricle is filled with about 100ml of bloodbut only 60ml is
ejected during contraction. This corresponds to an Ejection fraction of 60%.
•End-Diastolic Volume(EDV)i.e. 100ml can be defined as the blood that entered into
ventricles. End-Systolic Volume(ESV) i.e. 40ml is the blood that remains in the
ventricle after contraction.
•The stroke volume equals EDV minus ESV, and is dependent on 3 factors:
Contractility, Preload and Afterload.
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END DIASTOLIC VOLUME (EDV) & END SYSTOLIC VOLUME (ESV)

32. •Contractility–Refers to the force of the contraction of the heart
muscle. The more forceful the contraction, the more blood it ejects.
•Preload–Related to the end-diastolic volume and by definition, is
the degree of stretch of cardiac myocytes at the end of ventricular
filling.
•According to the Frank-Starling mechanism, the greater the stretch
of actin and myosin filaments in cardiomyocytes, the greater the
force of contraction.
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CONTRACTILITYAND PRELOAD

33. •Afterload is the resistance that the ventricle must overcome to eject blood. It
includes 2 major components: Vascular pressure and Valve damages.
•Vascular Pressure -The pressure in the right ventricle must exceed pulmonary
pressureto open the pulmonary valve. Similarly, the pressure in the left ventricle
must be greater than the systemic pressure for the aortic valve to open.
•In hypertension, higher vascular pressures make it more difficult for the valves to
open, resulting in a reduced amount of ejected blood.
•Valve Damage–As in stenosis, also presents higher resistance and leads to lower
blood output.
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AFTERLOAD

34. •Auscultationor the act of listening to sounds within the body, is usually done with a stethoscope.
The sound of the heartbeat comes primarily from blood turbulence caused by the closing of the
heart valves.
•During each cardiac cycle, there are four heart sounds, but in a normal heart only the first and
second heart sounds(S1 and S2) are loud enough to be heard through a stethoscope.
•S1 sound –Sounded as lubb, louder and much longer. Associated with the closure of AV valves
during ventricular systole.
•S2 sound –Sounded as dubb, quieter and shorter. Associated with the closure of SL valves at the
beginning of ventricular diastole.
•The other two heart sound i.e. S3 is due to blood turbulence during rapid ventricular filling, and S4 is
due to blood turbulence during atrial systole.
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HEART SOUNDS

35. •All blood vessels, except the capillaries, have walls composed of three layers,
composed of endothelial cells called tunicae.
•The outermost layer of a vessel, called the tunica externa or tunica adventitia,
themiddle layer; tunica mediaand the innermost layer is the tunica intima.
•The endothelial layer provides a smooth and slippery inner surface for the
vessel.
•This smooth inner lining, as long as it remains intact, prevents platelet
adherence and blood clotting.
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SYSTEMIC CIRCULATION AND CONTROL OF BLOOD FLOW

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LAYERS OF BLOOD VESSELS AND ORGANIZATION OF A CAPILLARY BED

37. •Lipoproteins are complexes of lipid-protein assembly containing cholesterol, triglycerides,
phospholipidsand proteins called Apoproteins.
•These lipoproteins transport cholesterol and triglyceride to various tissues for energy
utilization, lipid deposition, steroid hormone productionand bile acid formation.
•There are five types of lipoproteins named as:
•Chylomicrons.
•Very Low Density Lipoprotein (VLDL).
•Intermediate Density Lipoprotein (IDL).
•Low Density Lipoprotein (LDL).
•High Density Lipoprotein (HDL).
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LIPOPROTEINS

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CLASSIFICATION OF
LIPOPROTEINS

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METABOLISM
OF
LIPOPROTEINS

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LIPID PROFILE
ASSESSMENT FOR
HYPERLIPIDEMIA

42. •The term atherosclerosis comes from the Greek words atheros(gruel or paste)
and sclerosis(hardness),denotes the formation of fibro fatty lesions in the
intimal lining of the largeand medium-sized arteries.
•These arteries include such as the aorta and its branches, the coronary
arteries, and the cerebral arteries.
•The major complications of atherosclerosis include ischemic heart disease,
stroke, and peripheral vascular diseaseaccounting for approximately 36.3% of
thedeathsin the United States.
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ATHEROSCLEROSIS

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SITES OF SEVERE
ATHEROSCLEROSIS IN
ORDER OF FREQUENCY

44. •Hypercholesterolemia.
•Increasing age –Aging.
•Family history of premature coronary heart disease –Genetics.
•Alterations in lipoproteins and cholesterol metabolism.
•Estrogen protection –Increased incidence in men as compared to women because of
protective functions of estrogen till menopause.
•Cigarette smoking –Causing oxidative damage and endothelial dysfunction.
•Obesity, Hypertension and Diabetes Mellitus.
•C Reactive Protein –Inciting pro inflammatory effects, activates complement system,
promote platelet activation, thrombus formation and vascular remodeling.
•Infectious agents -Chlamydia pneumoniae, Herpes Virus, Cytomegalovirus
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ATHEROSCLEROSIS –RISK FACTORS

45. •Atherosclerosis is characterized by the development of atheromatous lesions
within the intimal liningof the large and medium-sized arteries that protrude
into and can eventually obstruct blood flow.
•The development of atherosclerotic lesions is a progressive process involving:
•Endothelial cell injury
•Migration of inflammatory cells.
•Smooth muscle cell proliferation and lipid deposition.
•Gradual development of the atheromatous plaque with a lipid core.
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THE MECHANISM OF DEVELOPMENT OF ATHEROSCLEROSIS

46. •The vascular endothelium consists of a single layer of cells with cell-to-cell
attachments, which normally protects the sub endothelial layers from interacting
with blood cells and other blood components.
•Agents which can share the potential for causing endothelial damage with adhesion
of monocytes and platelets include:
•Smoking.
•Elevated low-density lipoprotein (LDL) levels.
•Immune mechanisms.
•Mechanical stress associated with hypertension.
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ENDOTHELIAL CELL INJURY

47. •Early in the development of atherosclerotic lesions, endothelial cells begin to express
selective adhesion molecules which are known as Cell Adhesion Molecules (CAM).
•These molecules are cell surface proteins (cadherins, integrins, selectins, mucins etc.)
that mediate the interaction between cell and the extracellular matrix.
•These proteins bindmonocytesand other inflammatory cells that initiate the
atherosclerotic lesions.
•After monocytes adhere to the endothelium, they migratebetween the endothelial
cells to localize in the intima, transform into macrophages, and engulf lipoproteins,
largely LDL.
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MIGRATON OF INFLAMMATORY CELLS

48. •After the recruitment of monocytes, diapedesisoccurs and they differentiate into
macrophages.
•Activatedmacrophages release toxic oxygen species that oxidize LDL; they then
engulf the oxidized LDL to become foam cells.
•The excess amount of lipids ingested by the macrophages gives the cell a foamy
appearance hence it is named as foam cells.
•The dead endothelial cells, smooth muscle cells and macrophage ingested LDL
molecules begins to form a plaqueat the site of injury.
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SMOOTH MUSCLE CELL PROLIFERATION AND LIPID DEPOSITION

49. •At the site of plaque formation, the smooth muscles continue to divide and forms a
fibrous cap over the atheromatous plaque.
•Continuous exposure to blood flow can cause this plaque to rupture.
•In case of rupturing, deposition of calcium ions occur which promotes the
development of clot and makes the structure of plaque harder.
•Formation of clot (thrombus) into the coronary arteries leads to obstruction of blood
flow which in extreme cases can become an emboluswhich may travel down to
other parts of the body and cause further complications such as ischemic stroke.
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DEVELOPMENT OF ATHEROMATOUS PLAQUE

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ENDOTHELIAL CELL INJURY AND
MIGRATION OF INFLAMMATORY CELLS

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PROLIFERATION OF SMOOTH MUSCLES, LIPID DEPOSITION
AND FORMATION OF ATHEROMATOUS PLAQUE

52. •The clinical manifestations of atherosclerosis depend on the vessels involved and the extent
of vessel obstruction.
•Atherosclerotic lesions produce their effects through:
•Narrowing of the vessel and production of ischemia.
•Sudden vessel obstruction due to plaque hemorrhage or rupture.
•Thrombosis and formation of emboli resulting from damage to the vessel endothelium.
•Aneurysm formation due to weakening of the vessel wall.
•Although atherosclerosis can affect any organ or tissue, the arteries supplying the heart,
brain, kidneys, lower extremities, and small intestine are most frequently involved.
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ATHEROSCLEROSIS –CLINICAL MANIFESTATIONS

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SUMMARIZING
PROGRESSIVE
DEVELOPMENT OF
ATHEROSCLEROSIS
PLAQUE

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SEQUENCES IN THE
DEVELOPMENT OF
ATHEROSCLEROSIS

55. •The term Coronary Artery Disease (CAD) is characterized by impaired coronary blood
flow mostly due to atherosclerosis.
•It affects not only the coronary arteriesbut arteries in other areas of the body.
•Diseases of the coronary arteries can cause Myocardial Ischemia (Angina),
Myocardial Infarction(Heart Attack), Cardiac Arrhythmias, Conduction Defects,
Heart Failureand Sudden Death.
•Major risk factors for CAD include cigarette smoking, hypertension, elevated LDL and
cholesterol levels, lowHDL cholesterol, Diabetes, Metabolic Syndrome, advancing age,
abdominal obesity and physical inactivity.
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CORONARY ARTERY DISEASE (CAD)

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GLOBAL
BURDEN OF
CARDIOVASCULAR
DISEASES
Source: WHO global health
observatory
https://www.who.int/data/gho

57. •Coronary artery disease is commonly divided into two types of disorders.
•Acute coronary syndrome (ACS) –Represents acute ischemic heart diseases ranging
from unstable angina tomyocardial infarction.
•It results from disruption of an atherosclerotic plaque that did not compromise the
lumen before.
•ChronicIschemic Heart Disease –Characterized by recurrent and transient episodes
of myocardial ischemia and stable angina.
•Result from narrowing of a coronary artery lumen due to atherosclerosisand/or
vasospasm.
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PATHOLOGICAL DIVISION OF CORONARY ARTERY DISEASE

58. •There are two types of atherosclerotic lesions:
•Stable or Fixed Plaque –Obstructs blood flow.
•Unstable or Vulnerable Plaque –Canbe ruptured and cause platelet adhesion and
thrombus formation.
•The fixed or stable plaque is commonly implicated in stable angina while the
unstable plaqueis present in unstable angina which cause myocardial infarction.
•The major disruption factors of unstable plaque is due to various determinants such
as hypertension, emotional stress, physical activity and excessive stimulation of
sympathetic nervous system.
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STABLE AND UNSTABLE PLAQUE

59. •Acute coronary syndrome includes Unstable Angina, Non–ST segment
Elevation MI (NSTEMI), and ST-segment Elevation MI (STEMI).
•NSTEMI –Results from severe coronary artery occlusion and narrowing and
formation of thrombus causing myocardial ischemia.
•STEMI –Complete coronary occlusion leading to myocardial infarction.
•Persons with an ACS are routinely classified as low risk, intermediate riskor
high risk based on history, physical examination, ECG, serum cardiac markers
with primary emphasis on the ECG.
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ACUTE CORONARY SYNDROME (ACS)

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61. •The classic ECG changes that occur with ACS involve T-wave inversion, ST-segment
elevationand development of an abnormal Q wave.
•The repolarization phase of the action potential (T wave and ST segment on the ECG)
is usually the first to be involved during myocardial ischemia and injury.
•As the involved area becomes ischemic, myocardial repolarization is altered, causing
changes in the T wave.
•ST-segment changes occur with ischemic myocardial injurywhile the development
of abnormal Q wave occurs due to myocardial infarction and lack of current
conduction.
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ELECTROCARDIOGRAPHIC CHANGES IN ACS

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ECG CHANGES IN NSTEMI AND STEMI

63. Serum biomarkers for ACS include CardiacSpecific Troponin I (TnI) and Troponin T (TnT), Myoglobin, and
Creatine Kinase MB (CK-MB).
S.NoSerum Biomarkers Description
01 Troponin Primary biomarker tests for the diagnosis of myocardial infarction.
Begins to rise within 3 hours after the onset of myocardial infarction and may remain
elevated for 7 to 10 days after the event.
Advantageous in the late diagnosis of myocardial infarction.
(Normal ranges should be < 0.04 ng/ml).
02Creatine Kinase Intracellular enzymefound in myocardial cells.
Serum levels of CK-MB exceed normal ranges within 4 to 8 hours of myocardial injury
and decline to normal within 2 to 3 days.
(Normal reference values for serum CK–MB range from 5 to 25 IU/L).
03 Myoglobin Oxygen-carrying protein, normally present in cardiac and skeletal muscle. It is released
quickly from infarcted myocardial tissue and becomes elevated within 1 hour after
myocardial cell death, with peak levels reached within 4 to 8 hours.
(Normal reference values 25 to 72 ng/mL).
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SERUM BIOMARKERS IN ACS

64. •Persons having no evidence of serum markers for myocardial damage are
considered to have Unstable Angina.
•Whereas a patient is said to be diagnosed of NSTEMIif a serum marker of
myocardial injury is present.
•The pain associated with UA/NSTEMI can occur at:
•Rest or at minimal exertion usually lasting for 20 minutes.
•Severe and can become more frequent and prolonged to 01 month.
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UNSTABLE ANGINA AND NSTEMI

65. •STEMI also known as heart attack, is characterized by the ischemic death of
myocardial tissueassociated with atherosclerotic disease of the coronary
arteries.
•The area of infarction is determined by the coronary artery that is affected
and by its distribution of blood flow.
•30% to 40% of infarcts affect the right coronary artery.
•40% to 50%affect the left anterior descending artery.
•The remaining 15% to 20%affect the left circumflex artery.
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ST SEGMENT ELEVATION MYOCARDIAL INFARCTION

66. •The infarct depends upon:
•Location, duration and extent of occlusion.
•Amount of heart tissue affected.
•Metabolic needs of the tissue.
•Extent of collateral circulation and cardiac rhythm (blood pressure, heart rate etc.)
•An infarct may involve the endocardium, myocardium, epicardium or a combination
of these.
•Transmural infarcts are caused by obstructions in a single artery. They are the most
common infarcts occurring in the left ventricle and in the Intraventricular septum.
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THE PATHOLOGY OF INFARCTION

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SUBENDOCARDIAL
AND TRANSMURAL
INFARCTION

68. •The biochemical consequence of myocardial infarction is the conversion from aerobic
to anaerobic metabolism with inadequate production of energy to sustain normal
myocardial function.
•As a result, a striking loss of contractile function occurs within 60 secondsof onset.
•Changes in cell structure (glycogen depletion and mitochondrial swelling) develop
within several minuteswhich can be reversedif blood flow is restored.
•The ischemic area ceases to function within a matter of minutes, and irreversible
damage to cells and necrosis occurs in approximately 20 to40 minutes.
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BIOCHEMICAL PATHOGENESIS OF STEMI

69. •Multiple dynamic structural changes maintain cardiac function in persons with STEMI.
•The infarcted and non-infarcted areas of the ventricle undergo progressive changes in size,
shape, and thickness, comprising early wall thinning, healing, hypertrophy, and dilation,
collectively termed Ventricular Remodeling.
•As the infarcted area becomes thin and dilated, the muscle in the surrounding, non-infarcted
area becomes thicker as it undergoes adaptive hypertrophy so it can take over the work of
the muscle in the infarcted zone.
•However, the adaptive effect of remodeling may be overwhelmed by aneurysm formation or
depression of myocardial function, causing further impairment of ventricular function.
Presented by -Syed Muhammad Hasan 69
VENTRICULAR REMODELING IN STEMI

70. Presented by -Syed Muhammad Hasan 70

71. Presented by -Syed Muhammad Hasan 71

72. •STEMI may occur as an abrupt-onset event or as a progression from UA/NSTEMI with
painas the significant symptom.
•The pain typically is severe and crushing, often described as constrictingand
suffocatingwhich radiates to the left arm, neck or jaw, although it may be
experienced in other areas of the chest.
•Unlike that of angina, the pain associated with STEMI is more prolonged and not
relieved by rest or nitroglycerin, and narcoticsfrequently are required.
•Other manifestations include epigastric distress, nausea, vomiting, fatigue,
weakness andpale cool skin.
Presented by -Syed Muhammad Hasan 72
CLINICAL PRESENTATION OF STEMI

73. Presented by -Syed Muhammad Hasan 73
LOCATION OF PAIN AND COMPLICATIONS DURING STEMI

74. •The specific diagnosis of STEMI often is difficult to make at the time of complication,
the immediate management of UA/NSTEMI and STEMI is generally the same.
•For any person presenting with symptoms of ACS, certain regimens should be
adopted and presented in the most urgent manner:
•Institution, monitoring and interpretation of ECG (ST segment elevation,
Prolongation of Q wave and inversion of T wave).
•The typical ECG changes may not be present immediately but arrhythmiasmay be
observed which may act as a clinical indicator for STEMI.
Presented by -Syed Muhammad Hasan 74
MANAGEMENT OF ACS

75. Commonly indicated treatment regimens include Nitroglycerin, administration of oxygen, aspirin, nitrates, analgesics,
antiplatelet, anticoagulant therapy, beta blockers and ACE inhibitors.
S.NoTreatment regimens Mechanism of Action
01 Nitroglycerin Administered sublingually andis used due to its vasodilation effectfor reliefof ongoing ischemic pain,
controlling hypertension and pulmonary congestion. It is also indicatedto limit infarct size and is most
effective if given within 4 hours of onset.
02 Analgesics Morphine(preferredchoice) usually given IV. Used in case of unrelieved pain symptoms from other drugs.
03Oxygen AdministrationArterial oxygen levels may fall precipitously after STEMI, and oxygen administration helps to maintain the
oxygen content of the blood.
04 Beta blockers Antagonists that block β-receptormediated functions of the sympathetic nervous system and thus decrease
myocardial oxygen demand by reducing heart rate,cardiac contractilityand systemic arterial blood pressure.
(Metoprolol)
05 Antiplatelets drugsAspirinis the preferred antiplatelet agent for preventing platelet aggregation by inhibiting synthesis of the
prostaglandin thromboxane A2.
06 Anticoagulants The use of anticoagulants in patients with STEMI is to prevent formation of fibrin clots.
07 ACE inhibitors Interferes with Renin Angiotensin Pathway and causes vasodilationreducing heart work load.75
TREATMENT REGIMENS OF ACS
Presented by -Syed Muhammad Hasan

76. Presented by -Syed Muhammad Hasan 76
ANGIOPLASTY
INVASIVE
TREATMENT OF
ACUTE CORONARY
SYNDROME

77. Presented by -Syed Muhammad Hasan 77
CORONARY ARTERY
BYPASS GRAFTING
INVASIVE TREATMENT
OF ACUTE CORONARY
SYNDROME

78. PORTH’S PATHOPHYSIOLOGY
CONCEPT OF ALTERED HEALTH STATES –8
TH
EDITION
Presented by -Syed Muhammad Hasan 78
REFERENCES