ISCHAEMIA

AND
INFARCTION
Presented By- Dr. Ankit Mohapatra
DEPARTMENT OF PUBLIC HEALTH
DENTISTRY
1
 CONTENTS
Ischaemia
Harmful Effects Of Ischaemia
 Causes
General Causes
Local Causes
Arterial Obstruction
Venous Obstruction
Capillary Obstruction
Factors Determining Ischaemia
Subsidiary Factors 2
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 Mechanism
Changes occurring
Symptoms
Treatment
Infarction
Etiology
Pathogenesis
Types of Infarction
Pathologic Changes
 Healing Of An Infarct
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 Infarct of different organs
Pulmonary Infarct
Renal Infarct
Infarct of Spleen
Infarct Of Liver
Cerebral Infarct
Myocardial Infacrt
 Public Health Significance
References
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 ISCHAEMIA
• It is a state, when a tissue or organ has it’s arterial perfusion lowered
relative to its metabolic needs.

OR

Ischemia is defined as a condition of inadequate blood supply to an

area of tissue.

• Ischaemia [ischaem=to check and haim = blood] is inadequate

blood supply to a part of the body, even to the point of complete
deprivation.

• Is simply defined as a condition of inadequate blood supply.

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 HARMFULL EFFECTS OF
ISCHAEMIA
There are three harmful effects of ischemia:

 Hypoxia- Oxygen deprivation. By far the most important factor

for ischemic tissue damage of very active cells. Eg. muscles

 Malnutrition- blood contains glucose and amino acids that

could be metabolised by the amount of oxygen it contain, hence it
is of less importance.

 Failure to remove waste products- ‘accumulation of

metabolites is the most explanatory pain in muscle ischaemia’.
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 CAUSES OF ISCHAEMIA

General Causes -

 May be caused by inadequate cardiac output but not all tissues

are equally affected because of redistribution of avaliable blood.

 Symmterical gangrene of the extremities is an occasional

manifestation.

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 Local causes-
 By far the most important cause of ischaemia is obstruction of
arterial flow.

 Extensive venous and capillary damage also produces

ischaemia.

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 ARTERIAL OBSTRUCTION

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 THROMBOSIS
• Complete obstruction by occlusive thrombosis.
• Most frequentely found in small and medium sized arteries eg:
coronary or cerebral arteries.

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Embolism

•The effects of the embolus

are by the reflex spasm of
the arterial wall and
completed by the rapid
development of thrombus
over the embolus.

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Spasm
•Generalized vaasoconstriction following haemorrhage and
dehydration.

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 Atherosclerosis
 Production of
partial obstruction
in medium-sized
vessels eg:
cerebral, coronary
and renal.

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  Occlusive pressure from outside- caused by tourniquets
and tightly fitting plasters.

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 Effects of arterial obstruction

Effects depend on degree of ischaemia ranging from sudden

death to no damage:

1. Ischaemia is obviated by collateral channels then there is no

effect on tissues supplied by vessels.

2. The collateral channels supply sufficient blood during

inactivity of tissue but sustain normal exercise, there may be
functional disturbances eg:angina pectoris.

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 3. There may be cellular degeneration affecting the parenchyma
eg: fatty changes leading to necrosis. This is a patchy affair,
and leads to atropy accompanied by replacement fibrosis or
in central nervous system gliosis.

4. Both arterial and venous obstruction leads to circumscribed

necrosis of tissue called infarction.

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 VENOUS OBSTRUCTION

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 Mesenteric venous thrombosis- leads to intestinal infarction

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Strangulation of a hernia

obstruction at the neck of the

hernia leads to damage before
the arterial blood flow is
implicated

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Torsion of the testis- leads to haemorrhagic infarction of the organ.

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Cavernous sinus thrombosis- leads to retinal vein thrombosis and
retinal changes resulting in blindness

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  Varicose veins of the legs-venous blood from the deep calf
veins are pumped by contraction of calf muscles through
communicating veins to the superficial veins. These dilate and
become varicose so that their valves become incompetent. The
high venous pressure causes distension of capillaries and
venules of the skin changing its colour to dusky blue.

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 CAPILLARY OBSTRUCTION

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Acute leucocytoclastic vasculitis-
Affected vessels with necrosis
having their lumens occlueded by
fibrin and walls infiltered by
neutrophils showing degeneration
with karyorrhexis and clinically the
skin appears as palpable purpura.

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Frost bite-
Harmful effect of excessive cold
on the exposed body parts,
damages small blood vessels
resulting in, arteriolar spasm and
aggravation of ischaemia .

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  Occlusion of fibrin-disseminated intravascular coagulation is
characterized by occlusion of small vessels by deposition of
fibrin mixed with platelets.

 Occlusion of precipitated cryoglobulins- exposure of the

extremities to cold leads to vascular occlusion and
hemorrhages.

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  Occluision of capillaries by red cells-

Exposure of the limbs to to cold leads to haemolysis. Ischaemia

precipitated by cold is a feature of sickle cell disease, in which
chronic leg ulcers are seen. Raynaud’s syndrome may occur due
to vascular obstruction.

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Occlusion by white cells- Due to abnormal clumping of white cells
in chronic myeloid leukaemic condition infarcts may occur. Eg:
spleen

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  Arteriolosclerosis-

The benign and malignant types of arteriolosclerosis can affect

small vessels in many organs; involvement of the retina and
kidney is very serious.

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 FACTORS DETERMINING ISCHAEMIA

 Three crucial factors:

1. Speed of onset- if obstruction is sudden effect is more serious

because of less time for effective collateral circulation.

2. Extent of obstruction- complete obstruction is more serious

than partial eg : partial coronary occlusion due to
atherosclerosis is tolerated while complete obstruction causes
infarction and death.

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 3. Anatomy of collateral circulation – end arteries can have
serious effects as demonstrated by steal syndrome’s eg:
obstruction of the first part of subclavian artery can cause blood
to be diverted down the vertebral artery to the arm, leading to
brain stem ischaemia.

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 SUBSIDIARY FACTORS

1. State of collateral circulation- a collateral circulation is

affected with spasm, atherosclerosis, failing to maintain a
good alternative blood supply.

2. State of oxygenation of blood- it is in respect of arterial

partial oxygen and haemoglobin level.

3. Efficiency of heart

4. Nature of affected tissue- brain and heart are more vulnerable

to ischaemia.
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 MECHANISM : Ischaemia causes damage to tissue
through :

Acuumulation
of waste
products of
Deprivation of
nourishment
metabolism

Anoxia /
deprivation of
oxygen

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 CHANGES

 There are basically two extreme effects of Ischaemia.

 Absence of any damage
 Sudden death

But in between there are four changes that occur

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 Functional Disturbances- Angina pectoris
and intermittent claudication; both
manifested on exertion or activity.

Degeneration atrophy and replacement

fibrosis- Gradual obstruction of blood
supply

Gangrene- sudden or gradual but complete

deprivation of blood supply

Infarction- Sudden and complete

deprivation of blood supply

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 SYMPTOMS OF ISCHAEMIA

 Although pain is common, ischemia may occur without any

symptoms. Generally, symptoms depend on the location of the
ischemia.

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 ISCHEMIA OF THE HEART
Symptoms of cardiac ischemia include:

 Chest pain or pressure, which may radiate to the back, arm,

shoulder, neck, jaw or stomach

 Limitations of physical abilities

 Nausea with or without vomiting

 Palpitations or irregular heart rhythms

 Profuse sweating

 Shortness of breath
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 ISCHEMIA OF THE BRAIN

 Symptoms of ischemia of the brain include:

 Abnormal pupil size or non reactivity to light

 Balance problems, difficulty walking, and falls

 Confusion

 Difficulty with memory, thinking, talking, comprehension,

writing or reading

 Dizziness

 Droopy eyelid
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  Headache

 Loss of muscle coordination

 Loss of vision or changes in vision

 Nausea with or without vomiting

 Numbness or weakness

 Paralysis

 Vision problems (double vision, blurriness, loss of visual field,

sudden blindness)

 Weakness (loss of strength)

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 OTHER TYPES OF ISCHEMIA

Symptoms from ischemia in other parts of the body can include:

 Abdominal discomfort when eating

 Bloody stool (the blood may be red, black, or tarry in texture)

 Diarrhea

 Leg pain with walking or climbing stairs

 Nausea with or without vomiting

 Non-healing sores

 Pain

 Skin changes
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 SYMPTOMS INDICATING A LIFE-
THREATENING CONDITION

 Abnormal pupil size or nonreactivity to light

 Change in level of consciousness or alertness, such as passing

out or unresponsiveness

 Chest pain, chest tightness, chest pressure, palpitations

 Droopy eyelid

 Garbled or slurred speech or inability to speak

 Hallucinations

 Paralysis or inability to move a body part 42

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  Respiratory or breathing problems such as shortness of breath

 Seizure

 Severe abdominal pain or headache

 Sudden change in vision, loss of vision

 Vomiting blood or bloody stool

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 TREATMENT

 Treatment of ischemia begins with seeking regular medical care

throughout your life. Regular medical care allows a health care
professional to provide early screening tests and to promptly
evaluate symptoms and your risks for developing ischemia.

 The goal of treating ischemia is to restore blood flow and

prevent further damage. Surgery may be needed to remove dead
tissue or repair injured areas. Once the initial event is managed,
treatment turns to prevention of future ischemia.

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 Common treatments to reduce ischemia and restore blood flow
include:

 Medications to control pain and dilate blood vessels

 Medications to prevent ongoing clot formation

 Medications to reduce the heart’s workload.

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  Oxygen therapy

 Procedures to expand blood vessels

 Surgery or procedures to remove clots

 Surgery to bypass blocked blood vessels

 Thrombolytic drugs to dissolve clots

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 INFARCTION

Localized area of ischemic necrosis in an organ or tissue

resulting most often from reduction of arterial blood supply
or occasionally its venous drainage

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 ETIOLOGY

•Most Commonly - Infarcts are caused by Interruption in arterial

blood supply, called ischemic necrosis

•Less commonly - Venous obstruction can produce infarcts termed

stagnant hypoxia

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•Generally - Sudden, complete and continuous occlusion by
thrombosis or embolism
•Torsion of a vessel, e.g. in testicular torsion
•Traumatic rupture or vascular compromise by edema, e.g. anterior
compartment syndrome.
• Non occlusive circulatory insufficiency.

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 PATHOGENESIS OF INFARCTION

 Infarction usually leads to circumscribed area of coagulative

necrosis which is subsequently organized into scar tissue.

 Death of cells in an area deprived of blood supply but blood

continues to seep into the devitalized area for a short time.

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THREE POSSIBLE PROCESSESS OF BLOOD TO
SEEP INTO THE DEVITALIZED AREA

BLOOD TRICKELS
OPENING OF IN THROUGH
OCCLUDED VENOUS
PERIPHERAL ARTERY, AS
ANASTOMOTIC OBSTRUSTION IS REFLUX
CHANNELS NOT COMPLETE
INITIALLY.

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  NOTE: At all the events infarcts contain a great deal of blood
and are swollen and red in colour. The red cells entering the
effected area escape through damaged capillaries and lie free
on the dead tissues. Also, a great deal of fibrin derived from
blood lie on the dead tissue.

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 1. DEATH OF CELLS IN AN AREA
DEPRIVED OF BLOOD SUPPLY

2. DEAD TISSUE UNDERGOES

NECROSIS

3. PROGRESSIVE AUTOLYSIS
OF NECROTIC TISSUE AND
HAEMOLYSIS OF RED CELLS.
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4. OUTWARD DIFFUSION OF
TISSUE BREAKDOWN
PRODUCTS AND FREE
HAEMOGLOBIN INGESTED BY
MACROPHAGES

5. INFARCT IS NOW
FIRM AND DULL
YELLOW IN COLOUR
SURROUNDED BY RED ZONE
OF INFLAMMATION

6. FOLLOWED BY SHRINKAGE
OF INFARCT WHICH LATER
BECOMES WHITE
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 After phase of demolition, there is slow
progressive in-growth of granulation tissue from
the periphery and eventually infarct organizes to a
fibrous scar which later undergoes hyaline changes.

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 As the dead tissue undergoes necrosis in solid organs,
associated swelling of cells squeeze the blood out of infarct in
this way making it look paler.

Until necrosis is visible the ischaemic area cannot be called

infarct. Hence, human dead body is not possible to distinguish
post-mortem changes from early infarcton

Practically it takes 12-24 hours for a myocardial infarct to be

visible macroscopically recognizable.

But the first microscopic changes of necrosis can be seen only

from 6-12 hours after ischaemic episode
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 Types

• COLOUR

Pale or Anemic

Red or Haemoraghic

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 Presence
Depending or absence
on Age of
- Recent infection
- Bland
or fresh

- Old or
- Septic
healed
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BLAND : when free of bacterial contamination (infarcts of
streptococcus virdians endocarditis behave in a bland way because
organisms in the emboli are rapidly destroyed at the site of infarction)

SEPTIC : when infected (a rapid transition from the stage of

necrosis to one of suppuration resulting in large ragged abscess)

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 PATHOLOGIC CHANGES

•Grossly, infarcts of solid organs -wedge-shaped

• apex -pointing towards occluded artery
wide base - on the surface of the organ.

•Infarcts due to arterial occlusion -pale

venous obstruction - hemorrhagic.
•Most infarcts become pale later as the red cell are lysed but
pulmonary infarcts never become pale due to extensive amount
of blood.
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 •Cerebral infarcts : poorly defined with central softening
(encephalomalacia).

•Recent infarcts : slightly elevated over the surface

• Old infarcts : shrunken , depressed under the surface of the

organ.

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 MICROSCOPICALLY
•The pathognomic cytologic change in all infarcts is coagulative
(ischaemic) necrosis of the affected area of tissue or organ.
•In cerebral infarcts- characteristic liquefactive necrosis.

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 At periphery of an infarct, inflammatory reaction is noted.

Initially neutrophils predominate ,later macrophages and

fibroblasts appear.

Eventually, necrotic area is replaced by fibrous scar tissue, may

show dystrophic calcification.

In cerebral infarcts, the liquefactive necrosis is followed by

gliosis i.e. replacement by microglial cells distended by fatty
material (gitter cells).

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 HEALING OF AN INFARCT

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 •Necrosed tissue is autolysed and much of
Necrosed tissue autolysed material and blood fluid part is
and extravasted absorbed through lymphatics.
blood is • Undigestible red cells, necrotic tissue and
removed. insoluble fibrin are removed through
phagocytosis by macrophages.
 In case of septic infarct both bacterial
products and enzymes of leucocytes are
concerned in liquefaction of dead tissue.

Regeneration of • In organs like brain and heart the

cells and former is not possible.
organization of • so the end result is a scar which
granulation tissue might show deposits of iron and
calcium.
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 INFARCT OF DIFFERENT ORGANS

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 Infarcts of different organs
Location Gross appearance Outcome

1 Myocardial infraction Pale Frequently lethal

2 Pulmonary infraction Hemorrhagic Less commonly fatal

3 Cerebral infraction Hemorrhagic & Pale Fatal if massive

4 Intestinal infraction Hemorrhagic Frequently lethal

5 Renal infraction Pale Not lethal unless

massive & bilateral

6 Infract spleen Pale Not lethal

7 Infract liver Pale Not lethal

8 Infracts of lower extremity Pale Not lethal

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 PULMONARY INFARCTION

•Embolism of the pulmonary arteries

• May occur in patients who have inadequate circulation :
Chronic lung diseases
• Congestive heart failure.

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Page  69
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 GROSS:

PULMONARY INFARCTS :
Wedge-shaped
Base on the pleura,
hemorrhagic, variable in size
lower lobes.

Cut surface : dark purple

Shows blocked vessel near the apex of the infarcted area.

Old organized and healed pulmonary infarcts appear as retracted

fibrous scars. 70
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 MICROSCOPICALLY

• Characteristic histologic feature : coagulative necrosis of the

alveolar walls.

• Initially: infiltration by neutrophils and intense alveolar

capillary congestion hemosiderin, phagocytes and
granulation tissue.

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 RENAL INFARCTION
Renal infarcts are Common
-caused by Thromboemboli
-most commonly originating from heart such as
mural thrombi in the left atrium ,MI,Vegetative
endocarditis

Less commonly
-renal artery atherosclerosis,
-arteritis
-sickle cell anemia.

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 Grossly:
MULTIPLE AND BILATERAL

Characteristically: Wedge shape

Base - under capsule
Apex-pointing towards medulla

Narrow rim of preserved renal tissue is spared

Cut surface in first 2 to 3 days : red and congested

4th day: centre turns pale yellow.

1 week: typically anemic , depressed below

the surface

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 MICROSCOPICALLY
Characteristic:
affected area shows coagulative necrosis of renal
parenchyma i.e. ghosts of renal tubules and glomeruli without
intact nuclei and cytoplasmic content.
The margin of the infarct shows inflammatory reaction – initially
acute but later macrophages and fibrous tissue predominate.

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 INFARCT OF SPLEEN

•Common site for infarcts

•It results from Occlusion of one of the splenic arteries or its
branches.
Most common cause : thromboemboli arising in heart(eg.mural
thrombi in the left atrium
vegetative endocarditis
myocarditis
myocardial infarction)

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 •Less frequently by obstruction of microcirculation (e.g. in
myeloproliferative diseases, sickle cell anemia, arteritis, Hodgkin's
disease, bacterial infections).

•Grossly, splenic infarcts are often multiple.

•Characteristically pale or anemic, wedge-shaped

• base - at the periphery
apex -pointing towards hilum.

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Page  78
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 MICROSCOPICALLY

•Features are similar to those found in anemic infarcts in kidney.

•Coagulative necrosis and inflammatory reaction are seen.

•Later, the necrotic tissues is replaced by shrunken fibrous scar.

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 INFARCT OF LIVER
• Uncommon
• Dual blood supply
•Obstruction of the portal vein is usually secondary to other
diseases : Hepatic cirrhosis,
IV invasion of primary CA of liver,
CA of pancreas
• Generally does not produce ischemic infarction but instead
reduced blood supply to hepatic parenchyma causes non-ischemic
infarct called infarct of Zahn.

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 •Obstruction of the hepatic artery or its branches:
arteritis, arterio-sclerosis, bland or septic emboli.

•Grossly, anemic but sometimes hemorrhagic due to stuffing of

the site by blood from the portal vein.

•Infarcts of Zahn (non-ischemic infarcts) produce sharply defined

red-blue area in liver parenchyma.

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 MICROSCOPICALLY
Infarcts of Zahn
occurring due to reduced portal blood flow result in atrophy of
hepatocytes and dilatation of sinusoids .

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 CEREBRAL INFARCTION

•Local vascular occlusion

•Occasionally,
non-occlusive cause
compression of the cerebral
arteries from outside
and from hypoxic
encephalopathy.

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 •Clinically, the signs and symptoms depend upon the region
infarcted.

•In general, the focal neurologic deficit termed stroke, is present.

•However, significant atherosclerotic cerebrovascular disease may

produce transient ischemic attacks (TIA).

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 ARTERIAL OCCLUSION

•Occlusion of the cerebral arteries by thrombi- common

•Embolic arterial occlusion is commonly derived from the heart

mural thrombosis complicating MI
arterial fibrillation and endocarditis.

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 VENOUS OCCLUSION

• Infrequent phenomenon due to good communications of the

cerebral venous drainage.

•However in cancer, due to increased predisposition to thrombosis,

superior sagittal thrombosis may occur leading to bilateral,
parasagittal, multiple hemorrhagic infarcts.

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 NON-OCCLUSIVE CAUSES

Compression of the cerebral arteries from outside occurs during

herniation

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 PATHOLOGIC CHANGES

• Anemic or hemorrhagic

• Affected area : soft and swollen

blurring of junction between
grey and white matter.

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 •Within 2-3days, the infarct undergoes softening and degeneration.

• Central liquefaction with peripheral firm glial reaction

• thickened leptomeninges, forming a cystic infarct.

• Hemorrhagic infarct : red and superficially resembles a hematoma

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 • Initially, eosinophilic neuronal necrosis and
Histolo lipid vacuolization produced by breakdown of
gically
–
myelin.
sequen • Simultaneously infiltrated by neutrophils
tial
change
s

• After the first 2-3days, progressive invasion by

macrophages astrocytic and vascular
proliferation.

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 3. macrophages clear
away the necrotic debris
by phagocytosis followed
by reactive astrocytosis, .

A hemorrhagic infarct has

some phagocytes
containing haemosiderin.

4. after 3-4 months an old

cystic infarct is formed
showing cyst transversed by
small blood vessels and has
peripheral fibrillary gliosis.

Small cavitary infarcts are

called lacunar infarcts and
are commonly found as a
complication of systemic
Page  91 hypertension. 91
 MYOCARDIAL INFARCTION

 Most Important consequence of coronary artery disease

 Patient may die within first few hours of the onset while
remainder suffer from effects of cardiac function
 INCIDENCE : Occurs at all age but more common in elderly.

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 MI Classification

MI

ANATOMIC DIAGNOSTIC

STEMI NSTEMI
TRANSMURAL

SUBENDOCARDIAL

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 Transmural infract & Subendocardial infarct
Feature Transmural infract Subendoca
rdial infarct

1 Definition Full-thickness, solid Inner third to

half, patchy
2 Frequency Most frequent (95%) Less frequent
3 Distribution Specific area of coronary Circumferenti
supply al

4 Pathogenesis > 75% coronary stenosis Hypoperfusio

n of
myocardium
5 Coronary Common Rare
thrombosis
6 Epicarditis
Page  94 Common None 94
 Normal Sinus Rhythm
•Q wave representing septal
depolarisation
•R wave representing
ventricular depolarisation
•S wave representing
depolarisation of the
Purkinje fibres
• P wave, which represents
the depolarization of the
atria
•T wave represents
the repolarization (or
recovery) of the ventricles
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 STEMI

 ST segment elevations

 T wave changes

 Q wave development

 Enzyme elevations

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 NSTEMI

 ST segment depressions

 T wave changes

 No Q wave development

 Mild enzyme elevations

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 ETIOPATHOGENESIS

1. Mechanism of myocardial ischemia

2. Role of platelets
3. Complicated plaques
4. Non – atherosclerotic causes

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 MECHANISM OF
MYOCARDIAL ISCHEMIA
DIMINISHED
CORONARY BLOOD • MYOCARDIAL
FLOW
OXYGEN DEMAND
Coronary artery • Exercise,emotion
disease,shock

HYPERTROPHY OF HEART
W/O SIMULTANEOUS
INCREASE IN CORONARY
BLOOD FLOW
Hypertension,Valvular heart
disease

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 ROLE OF PLATELETS

•Rupture of atherosclerotic plaque exposes : sub endothelial

collagen to platelets which undergo aggregation, activation &
release reaction.

•These events contribute to the build up of the platelet mass

that gives rise to emboli or initiate thrombosis.

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 COMPLICATED PLAQUES
Two complications occur

Superimposed coronary thrombosis – seen in about half of the

cases of acute MI. Infusion of fibrinolysins in the first few hours of
development of acute MI in such cases restores blood flow in the
blocked vessel in majority of cases.

Intramural hemorrhage – is found in about one third of cases of

acute MI. Hemorrhage and thrombosis may occur together in some
cases.
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 NON-ATHEROSCLEROTIC
CAUSES

Coronary vasospasm
Coronary ostial stenosis,
Embolism,
Thrombotic diseases,
Trauma and outside compression.

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 LOCATION OF INFARCTS
• LV
•RV is less susceptible , due to its thin wall, having less
metabolic requirements and is thus adequately nourished
•Atrial infarcts, whenever usually accompany infarct of LV
•LA is relatively protected because it is supplied by oxygenated
blood in the left atrial chamber.

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 REGION OF INFARCTION
Area of obstructed

blood supply by one or more

of three coronary arterial

trunks in descending order:

1.Left anterior descending

coronary artery :40 to 50%

2.Right coronary artery :30 to 40%

3.Left circumflex coronary

artery:15 to 20%
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  3 REGIONS OF MYOCARDIAL INFRACTION.

Stenosis of the left anterior descending coronary is the most

common (40-50%).

 Region of infarction in the anterior part of the left ventricle

including the apex and the anterior two-thirds of the
interventricular septum.

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107
 Stenosis of the right coronary artery is the next
most frequent (30-40%) .

 It involves the posterior part of the left ventricle

and the posterior one-third of the interventricular
septum.

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 Stenosis of the left circumflex coronary artery is
seen least frequently (15-20%).

 Its area of involvement is the lateral wall of the

left ventricle.

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 MICROSCOPICALLY

The changes are similar in both transmural and subendocardial

infracts.

There is ischemic coagulative necrosis of the myocardium

which eventually heals by fibrosis.

However, sequential microscopic changes are observed.

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 Treatment Options

 The immediate goal for any acute MI is to restore normal

coronary blood flow to vessels and salvage myocardium.

 There are a variety of medical and medicinal therapies to treat

an MI.

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 GENERAL TREATMENT

MONA
 Morphine
 Oxygen
 Nitroglycerin
 Aspirin

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 FIBRINOLYTIC THERAPY

 Indicated for patients with STEMI.

 Should be given within 12 hours of symptom onset.

 Fibrinolytics will break down clots found within the vessles

 Contraindications: post op surgical patients, history of

hemorrhagic stroke, ulcer disease, pregnancy, etc.

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 CARDIAC CATHETERIZATION

 A diagnostic angiography which includes angioplasty and

possible stenting.

 Performed by an interventional cardiologist with a cardiac

surgeon on stand by.

 Percutaneous procedure through the femoral or brachial artery.

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  Upon arrival to the cath lab all actue MI patients will receive:

– A bolus dose of plavix

– IV Integrelin

– Heparin dose either subcu or IV drip

– Angiomax : a DTI may be substituted for heparin and

integrelin.

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 CORONARY ARTERY BYPASS
GRAFT
 Surgical treatment where saphenous vein is harvested from the
lower leg and used to bypass the occluded vessels.

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 LONG TERM CARE

 Smoking Cessation and lifestyle modifications.

 Aspirin, Beta Blockers and Clopidogrel will be indefinite.

 Lipid lowering medication along with diet modifications.

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 PUBLIC HEALTH SIGNIFICANCE

 Occupational heavy lifting- It was found that people with

high amount of physical activity and those who endorse in
heavy weight lifting during their day to day physical activity
were at a high risk of IHD.

Petersen CB, Eriksen L, Tolstrup JS, Søgaard K, Grønbæk M, Holtermann A.

Occupational heavy lifting and risk of ischemic heart disease and all-cause
mortality. BMC public health. 2012 Dec 11;12(1):1070.

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 CORONARY OBSTRUCTIVE PULMONARY
DISEASE

 COPD, or chronic obstructive pulmonary (PULL-mun-ary)

disease, is a progressive disease that makes it hard to breathe.

 Most people who have COPD smoke or used to smoke.

 Long-term exposure to other lung irritants also is a risk factor

for COPD leading to IHD. Examples of other lung irritants
include secondhand smoke, air pollution, and chemical fumes
and dust from the environment or workplace.

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  There is a high risk of ischaemic heart disease caused by
exposure to environmental tobacco smoke or second hand
smoking.

 Breathing other people's smoke is an important and avoidable

cause of ischaemic heart disease, increasing a person's risk by a
quarter.

Law M R, Morris J K, Wald N J. Environmental tobacco smoke exposure and

ischaemic heart disease: an evaluation of the evidence BMJ 1997;315 :973

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 REFERENCES
1. Robbins and Cotran - Pathologic basis of diseases.
8th edition.
2. Harsh Mohan – Text book of pathology. 3rd edition.
3. Mc Gee, Isaacson and Wright – Oxford text book of
Pathology. Principles of Pathology volume 1.
4. Anderson’s Pathology – 10th edition
5. Y.M. Bhende’s - General Pathology, 5th edition
6. Edward Sheffild - Pathology in Dentistry 1st edition122
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 REFERENCES

7. http://www.virtualmedstudent.com
8. http://www.emsa.ca.gov
9. http://nstemi.org
10.https://en.wikipedia.org

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