HISTOLOGY

The Circulatory System

dr. Shatha Salah Asaad

Lecturer /Al-kindy College of Medicine
University of Baghdad
Figure 11-2 Copyright © McGraw-Hill Companies
Figure 11–2 Important features of the heart.
As seen in the diagram, the human heart has two atria and two ventricles. The
myocardium of the ventricular walls is thicker than that of the atria.

The valves are basically flaps of connective tissue anchored in the heart’s dense
connective tissue, or cardiac skeleton, concentrated in the regions shown in white.
This fibrous tissue includes the chordae tendineae, cords that extend from the cusps of
both atrioventricular valves and attach to papillary muscles, preventing the valves
from turning inside-out during ventricular contraction. Valves and cords are covered by
the nonthrombogenic endothelium.
Shown in yellow are parts of the cardiac conducting system, which initiates the
electrical impulse for contraction (heartbeat) and spreads it through the ventricular
myocardium.

Both the sinoatrial (SA) node (pacemaker), in the right atrial wall, and the
atrioventricular (AV) node, in the floor of the right atrium, consist of myocardial tissue
that is difficult to distinguish histologically from surrounding cardiac muscle. The AV
node is continuous with specialized bundles of cardiac muscle fibers, the AV bundles
(of His) that run along the interventricular septum to the apex of the heart, where
they branch further as conducting (Purkinje) fibers that extend into myocardium of
the ventricles.
Copyright © McGraw-Hill Companies
Figure 11-3 Copyright © McGraw-Hill Companies
Figure 11–3 Endocardium, myocardium, and fibers of the subendocardial conducting
network.

The endocardium consists of the endothelium, a thin layer of connective tissue with
smooth muscle cells, and a layer of variable thickness lacking smooth muscle called
the subendocardial layer.

(a) Below the endothelium (En) and myoelastic layer, the subendocardial layer (SEn) in
the ventricles contains the conducting (Purkinje) fibers (P) of the heart’s impulse
conducting network. These fibers are cardiac muscle cells joined by
intercalated disks but specialized for impulse conduction rather than contraction. With
glycogen filling much of the cytoplasm and displacing myofibrils to the periphery,
Purkinje fibers typically are more pale staining than contractile cardiac muscle fibers
(M).

(b) In the atria Purkinje fibers (P) are often closer to the endothelium (En) and
intermingle with the contractile fibers within the myocardium (M). Both X200. H&E.

Copyright © McGraw-Hill Companies

Figure 11-4 Copyright © McGraw-Hill Companies
Figure 11–4 Epicardium or visceral pericardium.

The external tunic of the heart, the epicardium, is the site of the
coronary vessels and contains considerable adipose tissue. This section
of atrium shows part of the myocardium (M) and epicardium (Ep).

The epicardium consists of loose connective tissue (CT) containing

autonomic nerves (N) and variable amounts of fat (F). The epicardium is
the visceral layer of the pericardium and is covered by the simple
mesothelium (Mes) that also lines the pericardial space.

The mesothelial cells secrete a lubricant fluid that prevents friction as

the beating heart contacts the parietal pericardium on the other side of
the pericardial cavity. X100. H&E.

Copyright © McGraw-Hill Companies

Figure 11-7 Copyright © McGraw-Hill Companies
Figure 11–7 Tunics of the vascular wall.

Comparison of the three major layers or tunics in the largest artery and
vein. (a) Aorta, (b) vena cava. Simple squamous endothelial cells
(arrows) line the intima (I) that has subendothelial loose connective
tissue and is separated from the media by the internal elastic lamina
(IEL), a sheet of elastin.

The media (M) contains many elastic lamellae and elastic fibers (EF)
alternating with layers of smooth muscle. The media is much thicker in
large arteries than veins, with relatively more elastin. Elastic fibers are
also present in the outer tunica adventitia (A), which is relatively thicker
in large veins.

Vasa vasorum (V) are seen in the adventitia of the aorta. The connective
tissue of the adventitia always merges with the less dense connective
tissue around it. Both X122. Elastic stain.
Copyright © McGraw-Hill Companies
Figure 11-9 Copyright © McGraw-Hill Companies
Figure 11–9 Elastic artery.

The largest arteries contain considerable elastic material and

expand with blood when the heart contracts. A transverse
section through part of a large elastic artery shows a thick
media (M) consisting largely of many well-developed elastic
lamellae.

Strong pressure of blood pulsating into such arteries during

systole expands the arterial wall, reducing the pressure and
allowing strong blood flow to continue during diastole. The
intima (I) of the empty aorta is typically folded, and the dense
irregular connective tissue of the adventitia (A) is thinner
than the media. X200. PT.
Copyright © McGraw-Hill Companies
Figure 11-11 Copyright © McGraw-Hill Companies
Figure 11–11 Muscular artery.

With distance from the heart, arteries gradually have

relatively less elastin and more smooth muscle in their walls.
Most arteries, large enough to have names, are of the
muscular type.

A transverse section through a muscular (medium-caliber)

artery shows a slightly folded intima with only sparse
connective tissue between the endothelial cells (E) and
internal elastic lamina (IEL). Multiple layers of smooth muscle
(SM) in the media (M) are thicker than the elastic lamellae
and fibers with which they intersperse. Vasa vasorum (V) are
seen in the adventitia. X100. H&E.
Copyright © McGraw-Hill Companies
Figure 11-12 Copyright © McGraw-Hill Companies
Figure 11–12 Microvasculature.

Arterioles (A), capillaries (C), and venules (V) comprise the

microvasculature where, in almost every organ, molecular
exchange takes place between blood and the interstitial fluid of
the surrounding tissues.

Lacking media and adventitia tunics and with diameters of only 4-

10 m, capillaries (C) in paraffin sections can be recognized by
nuclei adjacent to small lumens or by highly eosinophilic red blood
cells in the lumen. As described in Figure 5–20, not all interstitial
fluid formed at capillary beds is drained into venules; the excess is
called lymph and collects in thin-walled, irregularly shaped
lymphatic vessels (L), such as those seen in connective tissue and
smooth muscle here. 200X H&E.
Copyright © McGraw-Hill Companies
Figure 11-17 Copyright © McGraw-Hill Companies
Figure 11–17 Types of capillaries.
The vessels between arterioles and venules can be any of three types. (a)
Continuous capillaries, the most common type, have tight, occluding junctions
sealing the intercellular clefts between all the endothelial cells to produce
minimal fluid leakage. All molecules exchanged across the endothelium must
cross the cells by diffusion or transcytosis.

(b) Fenestrated capillaries also have tight junctions, but perforations

(fenestrations) through the endothelial cells allow greater exchange across the
endothelium. The basement membrane is continuous in both these capillary
types. Fenestrated capillaries are found in organs where molecular exchange
with the blood is important, such as endocrine organs, intestinal walls, and
choroid plexus.

(c) Sinusoids, or discontinuous capillaries, usually have a wider diameter than

the other types and have discontinuities between the endothelial cells, large
fenestrations through the cells, and a partial, discontinuous basement
membrane. Sinusoids are found in organs where exchange of macromolecules
and cells occurs readily between tissue and blood, such as in bone marrow,
liver, and spleen. Copyright © McGraw-Hill Companies
Figure 11-22 Copyright © McGraw-Hill Companies
Figure 11–22 Veins.

Veins usually travel as companions to arteries and are classified as small, medium, or
large based on size and development of the tunics.

(a) Micrograph of small vein (V) shows a relatively large lumen compared to the small
muscular artery (A) with its thick media (M) and adventitia (Ad). The wall of a small
vein is very thin, containing only two or three layers of smooth muscle. X200. H&E.

(b) Micrograph of a convergence between two small veins shows valves (arrow). Valves
are thin folds of intima projecting well into the lumen, which act to prevent backflow
of blood. X200. H&E.

(c) Micrograph of a medium vein (MV) shows a thicker wall but still less prominent
than that of the accompanying muscular artery (MA). Both the media and adventitia
are better developed, but the wall is often folded around the relatively large lumen.
X100. H&E.

(d) Micrograph of a medium vein contains blood and shows valve folds (arrows). X200.
Masson trichrome.
Copyright © McGraw-Hill Companies
Copyright © McGraw-Hill Companies
THANK YOU
Basics of ECG
By Dr. : ANAS B. AHMED
 ELECTROCARDIOGRAM
❖The electrocardiogram (ECG) is a representation
of the electrical events of the cardiac cycle.
❖Each event has a distinctive waveform, the study
of waveform can lead to greater insight into a
patient’s cardiac patho physiology.
 ECGs can identify
Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (i.e. hyperkalemia,
hypokalemia)
Drug toxicity (i.e. digoxin and drugs which
prolong the QT interval)
 Recent advances have extended the importance
of the ECG.
⚫ It is a vital test for determining -
1. The presence and severity of acute myocardial ischemia/infarction.
2. Localizing sites of origin and pathways of tachyarrhythmias,
3. Assessing therapeutic options for patients with heart failure,
4. Identifying and evaluating patients with genetic diseases who are prone to
arrhythmias.
 Depolarization

⚫ Contraction of any muscle is associated with

electrical changes called depolarization.

⚫ These changes can be detected by electrodes attached

to the surface of the body.
Repolarization
⚫ Phase of recovery/relaxation.

⚫ The dipole moment at any one instant during recovery is less than during
activation.

⚫ Recovery, is a slow process, lasts 100 msec or longer and occurs

simultaneously over extensive portions of the fiber.
 Pacemakers of the Heart
❖ SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute.

❖ AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.

❖ Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.

The Normal Conduction System
MODERN ECG INSTRUMENT
 ECG Leads
Measure the difference in electrical potential
between two points
1. Bipolar Leads: Two different points on the body.

2. Unipolar Leads: One point on the body and a virtual

reference point with zero electrical potential, located in the
center of the heart .
 ECG Leads
The standard ECG has 12 leads:

3 Standard Limb Leads

3 Augmented Limb Leads
6 Precordial Leads
Recording of the ECG
❖ Limb leads are I, II, II.
❖ Each of the leads are bipolar; i.e., it requires two sensors on
the skin to make a lead.
❖ There will be a positive end at one electrode and negative at
the other.
Standard Limb Leads
Standard Limb Leads
Augmented Limb Leads
All Limb Leads
Standard Chest Lead Electrode Placement
Precordial Leads
The ECG Paper
⚫ Horizontally
⚫ One small box - 0.04 s
⚫ One large box - 0.20 s
⚫ Vertically
⚫ One large box - 0.5 mV
NORMAL ECG
NORMAL ECG
RHYTHM
❖ Evaluate the rhythm strip at the bottom of the 12-lead for the following-
Is the rhythm regular or irregular?
Is there a P wave before every QRS complex?
Are there any abnormal beats?
The Heart Rate

1. Rule of 300/1500(Regular
rhythm)
2. 10 Second Rule
 Rule of 300

Count the number of “big boxes” between two

QRS complexes, and divide this into 300.
(smaller boxes with 1500) for regular rhythms.
Rule of 300

(300 / 6) = 50 bpm
 Heart rate?

(300 / ~ 4) = ~ 75 bpm
Heart rate?

(300 / 1.5) = 200 bpm

 10 Second Rule

Count the number of beats present on the ECG during

1o seconds ie (50 big squares).
Multiply them by 6
For irregular rhythms.
 Heart rate?

33 x 6 = 198 bpm
THANK YOU
Baghdad University
Al-Kindy College of Medicine
Clinical Biochemistry Department

Qualitative detection of
cardiac Troponin

Asst.Lecturer. Noor Abdul_Kareem Taher

 Introduction to Troponin
• Troponin is a complex of three regulatory proteins (troponin C, troponin I, and
troponin T) found in skeletal and cardiac muscle.
• Role in cardiac muscle contraction: Troponin regulates the interaction between
actin and myosin, essential for muscle contraction.
• Importance in clinical practice: Troponin tests measure the level of cardiac
specific troponin in the blood, so the Elevation in troponin levels indicate
myocardial injury, making troponin testing crucial for diagnosing acute coronary
syndromes (ACS), including myocardial infarction (MI).
• (creatinine kinase CK-MB, lactate dehydrogenase LDH , Aspartate transaminase
AST) are cardiac enzymes or Cardiac Biomarkers, However, not all of the markers
currently used are enzymes. Such as troponin.
 Cardiac Troponin Isoforms
Troponins are proteins that exist in skeletal and
cardiac muscle that regulate the calcium-
dependent interaction of myosin with actin for
the muscle contractile apparatus.
There are three troponins that work as a
complex:
1- Troponin C: calcium-binding component.
2-cardiac troponin T (cTnT): tropomyosin-binding
component
3- Cardiac troponin I (cTnI): inhibitory
component.
 Troponin Normal Findings:
• Cardiac troponin T: <0.01 ng/mL (no detectable cardiac injury)
• Cardiac troponin I: <0.03 ng/mL (no detectable cardiac injury)
• cTnI concentrations of 0.04-0.5 ng/mL are more significant for myocardial injury
and even higher values (> 0.5 ng/mL) are more indicative of myocardial
infarction.
 Clinical Significance
• Diagnosis of AMI: Troponin elevation is a key criterion for diagnosing
AMI, helping differentiate it from other causes of chest pain.
• This test is performed on patients with chest pain to determine if the
pain is caused by cardiac ischemia. It is a specific indicator of cardiac
muscle injury. It is also helpful in predicting the possibility of future
cardiac events.
• Non-cardiac causes of troponin elevation: Non-cardiac conditions such as renal
failure, sepsis, and pulmonary embolism can also elevate troponin levels,
necessitating careful interpretation.
Myocardial infarction (MI) or heart attack,
occurs when blood flow to a part of the heart
is blocked for a prolonged period, leading to
damage or death of the heart muscle.
symptoms
• Chest Pain or Discomfort
• Pain or Discomfort in Other Areas: including
the arms (especially the left arm), back,
neck, jaw, or stomach.
• Shortness of Breath: which may occur with
or without chest discomfort.
• Nausea or Vomiting
• Sweating
• Fatigue
• Dizziness or Lightheadedness
• Anxiety or Sense of Impending Doom
 Troponin Kinetics - Onset, peak, and duration of elevation: -

• Troponin levels rise within hours of myocardial injury, peak within 12-48 hours, and may
remain elevated for several days.
• Understanding troponin kinetics helps optimize the timing of testing for diagnosing AMI and
assessing prognosis.
• Levels of cTnI may remain elevated for 7 to 10 days after myocardial infarction, and cTnT
levels may remain elevated for up to 10 to 14 days. Measurement of these troponins is
preferable to measurement of lactic dehydrogenase (LDH) and its isoenzymes in patients who
seek medical attention more than 24 to 48 hours after the onset of symptoms.
• If, re-infarction is considered, troponins are not helpful because they could be elevated just
from the first ischemic event. Each cardiac monitor has its specific use depending on the time
from onset of chest pain to the time of presentation to the hospital.
 How can troponins be detected
• monoclonal Ab
• ELISA
• monoclonal "sandwich" Ab qualitative testing

• *results from first two are available after about 2 hours. Sandwich technique can be
performed @ bedside in about 20 minutes
• Immunoassay principles: Troponin assays use antibodies to detect and quantify
troponin levels in the blood.
• High-sensitivity troponin assays enable earlier detection of myocardial injury compared
to conventional assays.
• The hs-troponin test may also be positive in people with stable angina and even in
people with no symptoms
What is the Principle of cTnI one step device ? :
chromatographic immunoassay
The cTnI One Step Troponin I Test Device (Whole Blood/Serum/Plasma) is a
qualitative, membrane based immunoassay for the detection of cTnI in whole
blood, serum or plasma. The membrane is pre-coated with capture reagent on
the test line region of the test.
During testing, the whole blood, serum or plasma specimen reacts with the
particle coated with anti cTnI antibodies. The mixture migrates upward on the
membrane chromatographically by capillary action to react with capture reagent
on the membrane and generate a colored line. The presence of this colored line
in the test line region indicates a positive result, while its absence indicates a
negative result.
Procedure:
Allow test device, specimen, and/or controls to reach room
temperature (15- 30°C) prior to testing:
1.Bring the pouch to room temperature before opening it. Remove
the test device from the sealed pouch and use it as soon as possible.
2.Place the test device on a clean and level surface.
3.For Serum or Plasma specimens: Hold the dropper vertically and
transfer 2 drops of serum or plasma (approximately 50 µL) to the
specimen well (S) of the test device, and start the timer.
4.Wait for the colored line(s) to appear. Read results at 10 minutes.
Do not interpret results after 20 minutes.
 Interpreting Troponin Results
POSITIVE:*
`Two distinct colored lines appear. One line should be in the control line region (C) and another
line should be in the test line region (T).
*NOTE:
The intensity of the color in the test line region (T) will vary depending on the concentration of
cTnI present in the specimen. Therefore, any shade of color in the test line region (T) should be
considered positive.

NEGATIVE:
One colored line appears in the control line region (C). No apparent colored line appears in the
test line region (T).
INVALID:
Control line (C) fails to appear. Insufficient specimen volume or incorrect
*NOTE: The cTnI One Step Troponin I Test Device (Whole Blood/Serum/Plasma) cannot detect
less than 0.5 ng/mL of cTnI in specimens.
Case study:
A 66 year old man had experienced central chest pain on exertion for some months ,
but in the afternoon of the day prior to admission he had had a particular sever
episode of the pain, which came on without any exertion and lasted for about an hour.
On examination there were no abnormalities and ECG was normal . The troponin was
clearly detectable (+ve). Comment on these results?
comments:
He has suffered myocardial infarction . He has an elevated troponin plus a typical
history. This is sufficient to diagnose a myocardial infarction by the most recent
definition even in the absence of ECG changes.
Case study:
A 54 year old man , was brought to emergency. He presented with an episode of
severe chest pain at rest, in the context of a 2 week history of exertional chest pain.
His chest pain was described as dull and heavy, associated with shortness of breath.
He had significant cardiac risk factors of hypertension, type 2 diabetes mellitus, and
obesity. His ECG was abnormal. His serum troponin I was elevated at 0.05 µg/L
(normal < 0.03 µg/L) on admission then after several hours it was 9,92 µg/L.
Comments:
This patient had an ischaemic myocardial infarction (MI). His history of chest pain
was typical for myocardial ischaemia. There were ischaemic changes on ECG and a
rise and fall of serum troponin levels.
Thanks for
listening
LAB DIAGNOSIS OF BACTERIAL INFECTIONS
IN CARDIOVASCULAR SYSTEM

Dr. Sumayah Ibraheem

 LEARNING OBJECTIVES

Study lab Diagnosis

biochemical tests and other tests.
 PRINCIPLES OF DIAGNOSTIC MEDICAL
MICROBIOLOGY

Lab diagnosis of bacterial infections is useful for

the following purpose: –
1- Identification:- causative bacterial agent.
2 – Treatment:- perfect antimicrobial therapy.
Steps of diagnosis :
1- Specimen collection :
▪ Direct detection :
▪ – Microscopy:- Gram stain, Acid fast stain, Albert stain,
histopathological staining, dark ground, phase-contrast and
fluorescence microscopy .
Culture – Culture media – Culture methods – Colony
morphology, smear and motility testing.

Detection of antigen from the agent by immunologic assay (latex

agglutination, enzyme immunoassay [EIA], etc) or by
fluorescein-labeled (or peroxidase-labeled) antibody stains.

biochemical tests .

Molecular methods.

Specimen collection depends upon the type of underlying

infections.
 MICROSCOPIC CHARACTERISTICS OF
STAPHYLOCOCCI

All staphylococci appear gram-positive cocci occur most

commonly in grape-like clusters, and also appear singly ,in
pairs & in short chain .
Non motile
do not form spores
aerobic or faccultative anaerobe.
Colony 1-2 mm in diameter ,raised ,concave ,opaque with
smooth surface & entir margin.
Colonies appear colored or pigmented as following:-
Staph.aureus :golden-yellow colonies
Staph .epidermides :white colonies
Staph. saprophyticus : white colonies
 BIOCHEMICAL PROPERTIES :

1. Catalase positive
2. oxidase negative
3. Ferment glucose ,lactose, maltose , sucrose and
mannitol with production of acid but no gas.
Grams staining of Staphylococcus aureus
(grape-like clusters of G+ve cocci)
 LAB DIAGNOSIS
1-Specimen :
a) Pus (from cases of abscess, osteomyelitis ,otitis media ,wound
infection)
b) Urine (from cases of Urinary tract infection)
c) Blood (from cases of septicemia)
e) sputum (in case of lower .R.T.I)
2)Microscopic investigation:
Gram –stained smear showing: Gram-positive cocci ,grape-like
clusters .
 3)CULTURE:
▪ On Blood agar:
Staph.aureus : Beta Haemolysis (due to hemolysin enzyme)
Staph.epidermidis : No hemolysis
(beta--hemolysis appear as clear zone around the colonies)
▪ On Mannitol salt agar (Selective &differential medium)
contain Mannitol +7.5% Nacl +phenol red (indicator) +agar :
only Staphylococci can grow on this medium while the other
bacteria inhibited (this is due to the resistant of it to high salt
concentration in the medium).
▪ The color of the medium is red in alkaline pH (before
fermentation & become yellow in color in acidic pH (after
fermentation).
Growth on Mannitol -Salt agar differentiates
S. aureus from other
catalase positive gram positive cocci like s.
epidermidis. S. aureus grows
as shown here on an agar medium containing
7.5% NaCl which inhibits
the growth of many other organisms. S.
aureus also can ferment mannitol into acid
detected here by the change in pH indicator
from red to yellow.
 Biochemical tests

• Catalase test :
1. differentiate Staphylococci from
Streptococci.
2. Done by mixing some isolated colonies of
the bacteria in a drop of physiological saline
or water ,then add 3% H2O2 to the mixture.
3. Notice production of air bubbles(in positive
result) this mean the catalase is +ve. ( in
Staphylococcus)
Catalase test
 Coagulase test
This test is used to detect the ability of Staph.aureus to
coagulate blood plasma (convert Fibrinogen
Fibrin). This test is done by two methods:
• 1-Slide method :Combine some colonies in saline or
water . Add 0.5 ml of plasma &notice the bacterial
aggregation or clumping within 10-15 sec. If this test
negative do the second method
• 2-Tube method: Is performed by inoculating 0.5 ml
of 1:10 dilution of coagulated rabbit plasma with
loopful of the suspected colony. After mixing,
incubate the tube at 35-37 Degree Celsius. Examine
for clotting after 1 hours. If no clotting has occurred,
examine at 30 minutes intervals for up to 6 hours.
Slide Coagulase test:
The most important distinction among staphylococci is whether they produce
or not the enzyme coagulase. S. aureus is the most common pathogen among
the catalase positive gram positive cocci and is differentiated from other
staphylococci by the coagulase test. Here the bacterial cells have been
suspended in a drop of rabbit plasma. Coagulase bound to the cell wall acts on
fibrinogen and causes the clumping of the bacteria (right). Coagulase is an
important virulence factor of S. aureus
 oxidase test
• The oxidase test is a biochemical reaction THAT used to
determine if an organism possesses the cytochrome c oxidase
enzyme.
• PROCEDURES:
• 1. Soak a small piece of filter paper in 1% Kovács oxidase
reagent and let dry.
• 2. Use a loop and pick a well-isolated colony from a fresh (18-
to 24- hour culture) bacterial plate and rub onto treated filter
paper (please see Comments and Tips section for notes on
recommended media and loops).
• 3. Observe for color changes.
4. Microorganisms are oxidase positive when the color changes to
dark purple within 5 to 10 seconds. Microorganisms are delayed
oxidase positive when the color changes to purple within 60 to 90
seconds. Microorganisms are oxidase negative if the color does not
change or it takes longer than 2 minutes.
STREPTOCOCCI
Human Streptococcal Pathogens • S. Pyogenes • S.
Viridans • S. Pneumoniae • S. Faecalis.
General Characteristics of Streptococci •
Gram-positive spherical/ovoid cocci arranged in long
chains; commonly in pairs.
• Non-spore-forming, non motile.
• Can form capsules
• Facultative anaerobes
• Most parasitic forms are fastidious and require enriched
media.
• Small, non pigmented colonies. • Sensitive to drying,
heat, and disinfectants
STREPTOCOCCUS VIRIDANS
STEPS OF BACTERIOLOGIAL DIAGNOSIS

blood
API test
4- BACILLARY ANGIOMATOSIS
BARTONELLA
The Gimenez staining technique uses
biological stains to detect and identify bacterial
infections in tissue samples. Although largely superseded
by techniques like Giemsa staining,
the Gimenez technique may be valuable for detecting
certain slow-growing or fastidious bacteria.
 Pathology lab
cardiovascular system
Assistant professor Dr. Alaa Qasim Yahya
Hypertrophic cardiomyopathy in 53 y/o female.
Gross
• Classically, there is
disproportionate
thickening of the
ventricular septum
relative to the left
ventricle free wall
(so-called
asymmetric septal
hypertrophy)
Hypertrophic cardiomyopathy.
Microscopic
This myocardium shows
myofiber disarray in
hypertrophic
cardiomyopathy. In the left
panel with
H&E stain and in the right
panel with trichrome stain
are sections of myocardium
showing these irregular
myofibers with surrounding
collagen.
Dilated cardiomyopathy (DCM).
Gross
• The image shows ventricular
dilation of the heart and a
thrombus at the apex of the
left ventricle.
• characterized by progressive
cardiac dilation and contractile
(systolic) dysfunction, usually
with concurrent hypertrophy
• The causes of DCM are many
and include genetic (30% to
50% of cases), toxic (e.g.
alcohol, chemotherapeutic
agent doxorubicin), metabolic
(e.g. iron overload in hereditary
hemochromatosis), and
infectious agents.
Stable atheromatous plaque
• Atheroma has intra- and
extracellular lipid deposits
(foam cells and cholesterol
crystals) and a thick
fibrous cap.
• Major Risk Factors for
Atherosclerosis:
Coronary artery with plaque rupture in a
70 y/o male
• The contents of the
atheroma fill the lumen of
the coronary artery. Such
events usually lead to the
formation of
superimposed thrombus
at the site of plaque
damage causing partial or
complete blockage of the
involved artery. This is
usually followed by one of
the acute coronary
syndromes such as
unstable angina, acute
myocardial infarction, or
sudden death.
Left anterior descending (LAD) coronary artery with
plaque rupture and superimposed thrombosis.

• This 68 y/o male

with history of
ischemic heart
disease died
suddenly. The lumen
of the LAD coronary
artery was nearly
completely blocked
over a 1.0 cm
segment.
Healed myocardial infarction of the posterior
and lateral walls in a 70 y/o male
• There is biventricular
concentric myocardial
hypertrophy. There is
also scarring of the
posterior papillary
muscle. The patient had
history of hypertensive
cardiomyopathy..
Transmural infarction is sometimes complicated
by myocardial rupture.
• The most common form is the
rupture of the free left
ventricular wall as shown in
this image. There was 300 ml
blood in the pericardial space
(tamponade). The patient was
a 67 y/o female with
biventricular concentric
myocardial hypertrophy and
severe coronary artery disease.
Rupture of the interventricular
septum is less common. The
least common form of
myocardial rupture following
acute myocardial infarction is
the rupture of papillary
muscles.
Rupture of the papillary muscle is the least common form of myocardial rupture
following an acute myocardial infarction (MI). It results in severe acute mitral
regurtitation. The image shows rupture of posterior papillary muscle in the left
ventricle following postero-septal myocardial infarction in a 64 y/o male. The patient
had atherosclerotic occlusion of the right coronary artery.
• Acute myocardial infarction in a
43 y/o male. There is biventricular
hypertrophy and a mural
thrombus at the apex. There was
history of obesity, smoking and
type II diabetes. The patient died
suddenly. There was severe
atherosclerosis-induced
narrowing of the major coronary
vessels. Following a myocardial
infarction (MI), the contractility of
the affected muscle is abnormal
and often leads to circulatory
stasis. The damaged
endocardium, in the presence of
stasis, creates a thrombogenic
surface and easily leads to the
formation of a mural thrombus.
The thrombus can embolize and
cause further problems
downstream.
A mural thrombus
First few hours of myocardial infarction
• Irreversible myocyte damage
occurs within 20 to 40 minutes of
severe ischemia. The affected
area undergoes coagulative
necrosis following by typical
inflammatory response and
repair. The changes of coagulative
necrosis become evident in the
first 6 to 12 hrs. after infarct.
Wavy fibers (as shown in this
image) are seen at the periphery
of the infarct. These are non-
contractile necrotic cardiac fibers
that are stretched and
compressed by the systolic tugs of
viable fibers nearby.
In 12 to 72 hours after myocardial infarction, there is
infiltration of neutrophils with progressive coagulative
necrosis of myocytes. Dead myocytes become
hypereosinophilic with loss of nuclei
Between 3 and 7 days, The necrotic myocytes
have been largely phagocytized and replaced
by granulation tissue consisting of loose
collagen and abundant capillaries.
A healed myocardial infarct (more than 6 weeks)
showing dense collagenous scar tissue between viable
myocytes. Once the infarct has completely healed, it is
impossible to determine its age from morphologic
features.
 The myocardial inflammatory lesions—Aschoff
bodies—are pathognomonic for acute rheumatic fever
• collections of
lymphocytes
(primarily T cells),
scattered plasma
cells, and plump
activated
macrophages called
Anitschkow cells
with abundant
cytoplasm and
central nuclei with
chromatin
condensed to form a
slender, wavy ribbon
(so-called caterpillar
cells).
• occasionally
punctuating zones of
fibrinoid necrosis.
Chronic rheumatic heart disease
• Classically, the mitral
valves exhibit leaflet
thickening,
commissural fusion
and shortening, and
thickening and fusion
of the chordae
tendineae
• Fibrous bridging
across the valvular
commissures and
calcification create
“fishmouth” or
“buttonhole”
stenoses
Infective endocarditis
shown here the aortic valve with
irregular reddish tan vegetations
overlie valve cusps that are being
destroyed.

acute bacterial infective endocarditis

can lead to serious valvular
destruction . Also, Portions of the
vegetation can break off and become
septic emboli that travel to other
organs, leading to foci of infarction or
infection.
Capillary hemangioma
Cavernous hemangioma
Intravenous fluid therapy

PHARMACOLOGY
Fluid management
Fluid management is crucial in inpatient medical settings,
For instance, a patient with severe burns will encounter more substantial fluid losses than a
relatively healthy patient placed on nothing by mouth (NPO) before a procedure.
patient admitted for dehydration due to severe diarrhea may require different fluid solutions
than a patient with hypovolemic shock due to a significant upper gastrointestinal bleed
 Types of fluid therapy
Tow types of fluid tharpy ; crystalloid and colloid
Crystalloid solutions :
1. normal saline.
2. half-normal saline.
3. Hypertonic saline
4. lactated Ringer solution.
Colloid solutions :
1. albumin solutions
2. hyperoncotic starch
3. Dextran
4. gelatin.
 Normal saline (0.9% Saline)

Normal saline has a higher concentration of chloride

ions (154 mmol/L) than in human serum (98 to 106
mmol/L).
With the administration of large volumes of normal
saline, hyperchloremia occurs.
Half normal saline
Half-normal saline (0.45% NaCl), often with "D5" (5% dextrose), contains 77 mEq/L of Na and Cl
and 50 g/L dextrose.
Hypotonic solutions are typically utilized when treating hypernatremia.
Hypertonic saline 3%
Hypertonic saline is used in treating hyponatremia and cerebral edema. Rapid correction of
hyponatremia via hypertonic saline greatly increases risk of central pontine myelinolysis (CPM).
Due to hypertonicity, administration may result in phlebitis and tissue necrosis
3% NaCl has 513 mEq/L of Na and Cl.
5% NaCl has 856 mEq/L of Na and Cl.
Ringer lactate
type crystalloid fluid further classified as a
balanced or buffered solution used for fluid
replacement.
The contents of Ringer's lactate include sodium,
chloride, potassium, calcium, and lactate in the
form of sodium lactate, mixed into a solution
Ringer's lactate is largely used in aggressive
volume resuscitation from blood loss or burn
injuries, sepsis and acute pancreatitis
Dextran
Type of colloid fluid
glucose polymer mixture that has a plasma half-life 2h
it is associated with anaphylactic reactions & profound coagulopathy.
Albumin
Albumin is a naturally occurring plasma protein,
sterilized by ultrafiltration: 5% albumin is
isotonic; 20% albumin is hypertonic.
Indications for use of albumin as a volume
expander are very limited.
Others
Blood, platelets, FFP (fresh Frozen Plasma) & cryoprecipitate.
 Which is the best solution?
• in hypovolemia Crystalloid solutions are typically preferred as the first-line treatment, whereas colloid
solutions are not the recommended initial option.
• if the patient not respond to crystalloid or if the patient had a shock due to hypoalbuminemia colloid
solutions, such as albumin, may be considered.
•it is essential to avoid hypertonic starch solutions in patients with hypovolemia due to the potential risk of
acute kidney injury.
Indications of fluid therapy
Dehydrations due to diarrhea or vomiting of any cause
Burn
Distributive shock
Certain toxicities
Kidney failure
Hypoglycemia
Hypoalbuminemia
Pre. or post. operative measures
Which fluid should be considered in
practice?
The choice of IV fluid depends on the type of body fluid lost and any associated electrolyte or acid-
base abnormalities. The most commonly used fluids in the medical settings are:
Sodium chloride (0.9%) or normal saline, with or without potassium

Sodium chloride (0.9%) or normal saline, with or without potassium

Lactated Ringer solution

Dextrose (5%) in sodium chloride (0.9%), with or without potassium

Dextrose (5%) in sodium chloride (0.45%), with or without potassium

Which fluid should be considered in
practice?
Hypotonic solutions are typically utilized when treating hypernatremia.
isotonic and hypertonic solutions are chosen to manage cases of hyponatremia..
Patients with hypokalemia may require potassium supplementation.
bicarbonate may be beneficial in cases of severe acidosis.
Solutions containing dextrose for patients experiencing hypoglycemia and alcohol or fasting
ketoacidosis, as well as for those with hyperkalemia but no hyperglycemia when administered
with insulin.
Patients with severe hypovolemia or hypovolemic shock may achieve better outcomes with
lactated Ringer solution
Which fluid should be considered in
practice?
Normal saline contains a higher chloride concentration compared to plasma, rendering it
hyperchloremic.
Complications of fluid therapy
1. Electrolyte Derangements
Hyponatremia The risks associated with hyponatremia encompass the possibility of cerebral
edema, carrying the potential for severe neurological complications, including seizures.
Hypernatremia
Hyperkalemia
2. Volume Overload
patients should be regularly monitored for peripheral edema, pulmonary edema, or
hepatomegaly signs
3. Metabolic Acidosis
4. air embolism
5. thrombophlebitis
Contraindications
Patients who are fluid-overloaded should not receive crystalloid fluids.
Hypertonic saline is contraindicated in all clinical settings except in patients with severe
hyponatremia and neurologic sequelae. Rapid correction of hyponatremia may cause central
pontine myelinolysis, a devastating neurologic condition.
Hypotonic solutions are also contraindicated in patients with or at risk of developing cerebral
edema.

Ringer's lactate solution contains calcium ions. Calcium can induce coagulation of the blood
products in the IV tubing and therefore inhibit their effective delivery. In patients who require a
blood transfusion, blood products should utilize a separate IV setup.