CARDIOVASCULAR SYSTEM

CARDIOVASCULAR
SYSTEM
• BLOOD
• HEART
• BLOOD VESSELS
BLOOD
 FLUIDS
BODY FLUIDS
(total H2O vol. = 40L or 60% of BM)

extra¢ fluid intra¢ fluid

(interstitial fluid)
(25L or 40% of BM)
(15L or 20% of BM)

- mobile ¢ of immune system - more proteins than the plasma

- no RBC - supplies O2 & nutrients to ¢
- gets rid of ¢’s waste & CO2

PLASMA:
- fluid part of the blood - platelets (¢ fragments)
- has blood ¢: RBC, WBC

- serous fluid - CSF

- aqueous & vitreous humor - synovial fluid
- gastrointestinal secretions- lymph
 cleans out extra
lymph
¢ fluid of
circulates
has intruders &
in
macrophages returns to the
lymphatic
blood for
vessels
PURIFICATION

What?????

WITHOUT LYMPHATIC SYSTEM, WE WOULD DRAIN OUR BLOOD IN 24 HRS

 ROLES
ensures
transport

regulate the regulate body

fluid volume in temperature by
the body distributing,
BLOOD
absorbing &
ROLES dissipating heat

protection:
coagulation &
[H ] +

transport of ¢ & regulate pH in

fighting infection the tissues
BLOOD COMPOSITION – 5-6L, ≅ 8% of BM
• specialized C.T. : plasma (fluid matrix & formed elements (¢)); the
fibers become evident during coagulation

HEMATOCRIT : % of RBC in total volume of blood; obtained through

centrifugation

55% >1%
WBC 45%
PLASMA
PLATELETS RBC
BLOOD FORMED ELEMENTS
 RBC (or ERYTHROCYTE)
• hematopoiesis: formation of blood ¢
• erythropoiesis: formation of erythrocytes
The production of RBC’s in a healthy human :

MILLIONS/SEC
RBC CYCLE - negative feedback mechanism:
production of RBC is stimulated by ê O2 (blood)
ê
(1) stimulates kidney to produce ERYTHROPOIETIN (hormone)
ê
(2) stimulates red bone marrow of bones to produce RBC

(1)

(2)
HYPOXIA – brought about via:
 HEMOGLOBIN
• essential molecule of RBC, 1/3 of its mass
• transports: CO2 & O2

• parts: globin (protein) + 4 heme groups (molecule containing a Fe 2+ ion)

 HEMOGLOBIN
• heme group + O2 = oxyhemoglobin (bright red)
• globin group + CO2 (picked up from tissues) = carbaminohemoglobin
 HEMOGLOBIN
RBC CYCLE
• FŒTUS: made from stem ¢ : (1) yolk sac (early), (2) liver & spleen
(3-4 mth), (3) bone marrow (7th mth)

• ADULT: made from stem ¢ in red bone marrow of certain long bones
• flat bones (girdle), epiphysis (humerus, femur)

days

to its maturation
 NORMAL HEMOGLOBIN - AMINO ACID SEQUENCE IN THE BETA CHAIN

NORMAL

SICKLE ¢
ANEMIA

GLU=glutamic acid
VAL=valine
RBC CYCLE – in red bone marrow

PHASES

RBC precursor in the

blood
¢ differentiation (at 34% [Hg])

normoblast or
 RBC: ex. ANUCLEATED ADULT CELL
• reticulocyte (mitochondria, endoplasmic reticulum, ribosomes) loses
its nucleus when it goes in the blood – get BICONCAVE shape - RBC
• diameter ≅ 8μm; flexible; passes in the capillaries which ≅ 3μm
• flat shape  the surface/volume ratio for the gaseous exchanges

 weak metabolic activity

 no division CAUSE no nucleus
 have very little organelles
 RBC: ex. ANUCLEATED ADULT CELL

• produces ATP using anaerobic path thus does not consume the O2 it
transports; the LACTATE it produces is released in the blood & is
metabolized by the tissues of the HEART & of the LIVER
• life span: around 120 days; plasmic membrane is used up when
passing in the capillaries; often it bursts in the spleen & the liver
where they are destroyed by specialized macrophages

RBC lifespan: 120 days

RBC RECYCLING 1 MACROPHAGES

MACROPHAGES (liver, spleen, bone 2

marrow) start the recycling of aged or biliverdin
damaged RBC (greenish) 3
4a 4b 4c
* stored in: (yellow)
*
myocytes, macrophages,
liver or spleen
(go to ¢)

5a (go to bone marrow)

UROBILINOGEN 5b1
via blood
5b2

6b
excrete in urine 6a
(urobilin – yellow)
RBC RECYCLING
• newborn : liver does not function well yet thus bilirubin accumulate =>
jaundice; UV rays are used to destroy the bilirubin faster
WBC or LEUKOCYTE; ratio 600:1, RBC:WBC

2 pathway:

role:
immunity
(defence)

WBC lifespan:
a few hrs to
a few days
WBC
granulocytes nucleus cytoplasm-granules % function
(1) neutrophils multilobed acid & basic dyes 40 – 70  phagocytosis

(2) eosinophils bilobed red (acid dyes) 1–4  destroy parasitic

worms
 role with allergies
(foreign proteins,
antigen-antibody
complex)
 role with inflam-
matory response
(inactivates
mediators)

(3) basophils U or S blue-purple (basic 0 – 1 often  role with inflam-

dyes) < 1% matory response
(released hista-
mine)
 heparin (anti-
coagulant)
WBC

agranulocytes nucleus cytoplasm-no % function

granules
(4) lymphocytes spherical pale blue 20 - 45  ¢T– actively battle against
the infected ¢ (virus, tumors)
 ¢B – obtain plasma cells :
produce antibodies relea-sed
in the blood

(5) monocytes U or kidney gray blue 4–8  phagocytosis (transformed in

shaped macrophagocytes in the
tissues)
 helps the lymphocyte (immu-
ne response)
BLOOD GROUPS (ABO & Rh (Rhesus factor))

• RBC have ANTIGENS (AGGLUTINOGENS) on the surface

(protein:genetically determined)

• plasma has ANTIBODIES (AGGLUTININS) (protein)

• ANTIBODIES react to the ANTIGENS that we do NOT have

BLOOD GROUPS (ABO & Rh (Rhesus factor))

compatible
group antigen antibody character
blood

A A b AO, AA A, O

B B a BO, BB B, O

AB A, B no a, no b AB A, B, AB, O

O no A, no B a, b OO O

• blood groups have a genetic origin; receive 1 character from

each parent; incidence of the diverse blood groups vary
between population
BLOOD GROUPS (ABO & Rh (Rhesus factor))
BLOOD GROUPS (ABO & Rh (Rhesus factor))
 AGGLUTINATION
• 2 individuals with non compatible blood group will have an
AGGLUTINATION reaction & the HEMOLYSIS that results
from it
• complex ANTIBODY: ANTIGEN
• perforate the membranes of the RBC
• it opens (lyze) and releases hemoglobin in the blood
• leads to renal problems
 AGGLUTINATION
• example : individual with a blood group A receives
blood from an individual with a blood group B :
• N.B. what is introduced in the body is attacked as
an intruder

• the b (antibody) of A
agglutinates with B
(antigen) of B (major
reaction)
• the a (antibody) of B
agglutinates with A
(antigen) of A (minor
reaction) – diluted

RESULTS:
agglutination + hemolysis
 RHESUS (Rh) BLOOD GROUP

• 8 antigens exists; 3 of them are common (C, D, E)

• if you have it, you are Rh (+) [85%], if you do not
have it, you are Rh (-) [15%] (% for american
population)
 RHESUS (Rh) BLOOD GROUP

difference of Rh blood groups in comparison to the ABO blood groups

normally, the blood does NOT have the antibodies (anti-Rh)

thus an individual Rh (-) that receives from an individual Rh (+), will

produce anti-Rh that stay in the blood; these anti-Rh will react with the
next transfusion & cause blood hemolysis
 RHESUS (Rh) BLOOD GROUP

HEMOLYTIC DISEASE OF THE NEWBORN OR ERYTHROBLASTOSIS FETALIS

Rh+ fœtus & Rh- mother - treat with RhoGAM (prevention)
 PLATELETS
· platelets : cytoplasmic fragments of the megacaryocytes, surrounded by
the plasma membrane, anucleated, has compounds to provoke
coagulation
• formation (red blood marrow) - differentication ¢

N.B. terminology; thrombocyte : ordinarily used only for vertebrates other

than mammals
 PLATELETS
roles :
• clogs the blood leaks by releasing chemical
substances that provoke the formation of a clot

platelets lifespan: 10 days

(following their death, they are phagocytized by macrophages (liver & spleen))
 PROCESS OF HEMOSTASIS
hemostasis (stop of the hemorrhage)
rapid response to a break in a blood vessel

involves 3 steps

VASCULAR SPASMS

PLATELET PLUG FORMATION

COAGULATION
PROCESS OF
HEMOSTASIS
VASCULAR SPASMS (VASOCONSTRICTION)
• contraction of the smooth myocytes at the area of the hemorrhage
permitting ê circulation in the damaged blood vessel for 20-30 min.;

30:00
• this is the time needed for other hemostatic mechanisms to come in
action; they are triggered by: lesions to
smooth
myocytes

chemical
nociceptors substances
(inform on the released by
pain) endothelial ¢ &
platelets
VASCULAR SPASMS (VASOCONSTRICTION)
• haemorrhage caused by crushing in comparison to a clean cut are
(+) painful but stops bleeding (+) rapidly
• this step  in efficiency proportionally to the severity of the lesion
 PLATELET PLUG FORMATION
• platelets have granules that contain:
mitochondria

ADP
( platelets
aggregation, Ca2+
ATP) (system of
membranes
lysosome that store)
serotonin
vesicles
(favors
from Golgi thromboxane vasoconstric
that form A2 -tion)
enzymes
(acts upon
ADP &
serotonin)

growth
factors
(PDGF)
PDGF=platelet derived growth factor
 PLATELET PLUG FORMATION
PLATELET ADHESION
as soon as endothelium is damaged & underlying collagen fibers are exposed,
platelet come into CONTACT with them & ADHERE

platelets swell, spread & become more ‘STICKY’ & stick to fibers & platelets

PLATELET – RELEASE RNX
platelets release their GRANULE CONTENTS which react with chemicals
in the blood to amplify the formation of the plug

PLATELET AGGREGATION 
more & more platelets stick together;
adhesion eventually OBSTRUCT the lesion

platelets
 COAGULATION
• formation of the clot is usually done outside
of the blood vessels
• blood thicken with its exposure to air & a gel
forms & separate from serum clot

• this gel is the network of protein fibers

(fibrin) that seals the wound & prevent
bleeding
• this step involves many factors that mutually
activate each other & the mechanisms that
are undertaken are very complex
• most coagulation factors are found in the
plasma & others in the platelets EXCEPT :
thromboplastin => found in the tissues

THIS PROCESS INVOLVES A POSITIVE FEEDBACK MECHANISM

THAT CAN BE DIVIDED IN 3 STEPS:
 COAGULATION
• blood clotting factors (12) – all circulate in the plasma except factor III

PP = plasma protein; HEM = hemophilia, AHEM = antihemophilic; CP=common pathway EP = extrinsic pathway; IP =
intrinsic pathway

# name of factor nature/origin function or pathway

CP; change in fibrin

i fibrinogen PP; liver
(insoluble) (will form clot)

CP; change in thrombin

PP; liver;
ii prothrombin (change fibrinogen to
vit. K essential for its formation
fibrin)

tissue factor (TF), or tissue lipoprotein complex released by

iii active EP
thromboplastin damaged tissues

ion of plasma; comes from food required for

iv calcium ions (Ca2+)
or released by bones coagulation steps

PP; liver; released also by

v proaccelerin, or labile factor EP & IP
platelets

# obsolete; substance identical

vi
to factor V
 COAGULATION
• blood clotting factors (12) – all circulate in the plasma except factor III
PP = plasma protein; HEM = hemophilia, AHEM = antihemophilic; CP=common pathway EP = extrinsic pathway; IP =
intrinsic pathway

# name of factor nature/origin function or pathway

PP; liver; during a process that
vii proconvertin EP & IP
requires vit. K
AHEM factor or globulin made by the liver;
viii IP
thromboplastinogen deficit = HEM A

AHEM B factor or PP; liver; deficit = HEM B;

ix IP
Christmas factor vit. K essential to its formation

Stuart factor, Stuart-Prower PP; liver;

x EP & IP
factor, or thrombokinase vit. K essential to its formation
plasma thromboplastin
xi PP; liver; deficit = HEM C IP
antecedent

IP : activate plasmin (via

contact with glass &
xii Hageman factor PP; liver; proteolytic enzyme
maybe initiates
coagulation in vitro)

cross-links fibrin/
xiii fibrin stabilizing factor (FSF) PP; liver & present in platelets
renders fibrin insoluble
 COAGULATION
(1) pathway to prothrombin activator (2)
• take on 1 pathway or the other :
INTRINSIC PATHWAY (SLOW)
rupture of the vessel’s endothelium EXTRINSIC PATHWAY (A FEW SEC.)
uncovers the underlying collagen fibers TRAUMA TO ¢ causes the release of

platelets stick here

and permit
mobilization of the
factors
TISSUE FACTOR (TF)

Ca2+

XII XIIa VII

XI XIa Ca2+
VIIa
IX IXa
TF/VIIa
release of PF3 by complex
VIII
aggregated
platelets
VIIIa

Ixa/VIIIa complex

X Xa
PF3=platelet factor 3=
Ca2+
negatively charged V
PF3 Va
phosphatidylserine
(from activated
platelets) PROTHROMBIN ACTIVATOR
 COAGULATION
(2) conversion of prothrombin to thrombin by the prothrombin activator:

PROTHROMBIN ACTIVATOR

PROTHROMBIN (II) THROMBIN

 COAGULATION
(3) transformation of fibrinogen (soluble) in fibrin (insoluble)
• fibrin confines the blood ¢ & absorb up to 90% of the thrombin (STOPS the
coagulation thus this is the STOP MECHANISM TO THE POSITIVE
FEEDBACK)

THROMBIN XIII
Ca2+

FIBRINOGEN (I) FIBRIN

XIIIa

stabilization of the fibrin polymers (clot retraction)

healing & fibrinolysis

 CLOT RETRACTION/HEALING
CHEMICALS of the granules +
GROWTH FACTORS derived from the
platelets (PDGF) stimulate these ¢ to rebuild the area :

fibroblasts

proliferation of
the endothelial ¢

PDGF=platelet derived growth factor

 CLOT RETRACTION/HEALING

• gradual contraction of the fibrin strands attached to the ruptured

surfaces of the blood vessel & the contraction of the contractile
proteins (actin/myosin) of the platelets lead to the retraction of the
clot
• PLASMINOGEN that is converted to PLASMIN (called fibrinolysine*)
can inactivate the coagulation factors & digest the clots (takes
several days for the clot to be dissolved completely)
*N.B. essential to remove the clots in blood vessels
 PROCESS OF HEMOSTASIS

• essential factor for coagulation

• necessary for synthesis of : prothrombin &
factors (VII, IX, X) VITAMIN K
• produce by bacterial flora of the large intestine

• anticoagulant produced by WBC

• an analogue of it is produced by the endothelial ¢
HEPARIN (blood vessels) to prevent the formation of a clot
on the inside of blood vessels that they line

N.B. to prevent coagulation

• utilize heparin to coat glass tubes
• add compounds that take out Ca2+ that is essential
for coagulation
 HEART
• in the mediastinum (central cavity of thorax)
• two third of it more to the left (reason: left lung is bilobed whereas the
right lung has three lobes)
 HEART – envelops & tunics
• heart is covered by the PERICARDIUM
• the wall of the heart is made of 3 tunics :

3 tunics

EPICARDIUM MYOCARDIUM ENDOCARDIUM

 HEART – tunics
PERICARDIUM :
• fibrous pericardium (covers the mediastinum) – dense CT
• serous pericardium (serous membrane) : (a) parietal layer, (b)
visceral layer (= epicardium)
• between the layers : pericardial cavity (has the serous fluid)
• the layer are thin & can slide, thus ê the friction of heart in the
mediastinum when it is beating
• very resistant to stretching
• anchors the heart & the b. vessels to the neighbouring structures
 HEART – tunics
MYOCARDIUM
• muscle wall (cardiac myocytes): circular & spiral arrangement
ENDOCARDIUM :
• s.s. epi.
• continuous with endothelium of b. vessels
 HEART – parts
• 4 cavities (chambers): 2 atria (thin) & 2 ventricles (thick)
(N.B. LV thicker: sends blood to all parts)
• separated by CT (electrically isolated = 2 MOTOR UNITS; 1
for atria & 1 for ventricles)
• interatrial septum (btw atria – find FOSSA OVALIS),
interventricular septum (btw ventricles)

*
* *
* foramen ovale in fetus

** *
HEART – vessels
 HEART – valves
• prevent BACKFLOW of the blood (remember :
circulation is unidirectional)
• via the BLOOD PRESSURE, it opens in one
direction & resist in the other direction
• CT covered by the continuous endothelium of the b.
vessels & by the endocardium
 VALVES OF HEART
• R atrioventricular (tricuspid) : 3 cusps; L atrioventricular (bicuspid or
mitral) : 2 cusps
• cuspids are attached by the chordae tendineae & they in turn are
anchored to the papillary muscles emerging from the ventricle wall
• when the valves are closed, the chordae tendineae are tight & the
papillary muscles are contracted

cusp

papillary muscle chordae tendineae (collagen)

 VALVES OF VESSELS
semilunar valves :
• aorta & pulmonary trunk : 3 cusps
• no chordae tendineae nor papillary muscles
large veins of the limbs
• like those aorta & pulmonary trunk; necessary cause blood
pressure in the veins are low & must move against gravity
 HEART – circulation (3)
• blood circuit, unidirectional path
• systemic : heart =>whole body=>heart
• pulmonary : heart =>lungs=>heart
• coronary : heart
• coronary artery originate
from the ascending aorta
HEART – coronary circulation
 HEART – circulation
oxygenated blood of LV
 via semilunar aortic v.

aorta
(coronary a.=>arterioles=>capillaries=>venules=>cardiac
veins=>coronary sinus=>RA)

brings blood to all of the ¢ of the organism

deoxygenated blood arrive via : the sup. & inf. v. cava in RA

 via right atrioventricular v. (tricuspid)

RV
HEART – circulation
deoxygenated blood of RV
 via semilunar pulmonary v.

pulmonary trunk

R & L pulmonary a.

oxygenated blood in the lung

 via 4 pulmonary v.

oxygenated blood arrive to the LA

 via left atrioventricular v.
LV
HEART CIRCULATION
 HEART – CARDIAC MUSCLE
• striated muscles, ramified, involuntary
• linked between themselves by intercalated discs which
have:
• desmosomes – link ¢ to one another
• gap junctions: permit muscle AP to pass from 1
myocyte to another inside the motor unit
• cardiac myocytes similar to skeletal myocytes; mechanisms
of contraction involving interactions between actin/myosin
are identical
 HEART – CARDIAC MUSCLE

IMPORTANT DIFFERENCES EXIST :

• its functioning mode is principally aerobic thus its
mitochondria are bigger & more abundant
• sarcoplasm more abundant, less SR cause some of
the Ca2+ is from extra¢, has MORE T tubules
N.B. it can use a bit of lactate in the blood & glycogen
accumulated to produce ATP

us in g the
t w or k s
us c le th a to p to
a m s t s
recall : robic path mu t CANNOT
anae t h e h e ar
ER A T E: w o r k in g
RECUP s it is always
stop a
HEART – CARDIAC MUSCLE

dyads
 HEART – CARDIAC MUSCLE
IMPORTANT DIFFERENCES :
• these myocytes are all connected together via
intercalated discs; form 2 networks (units) :
ventricular & atrial; because of this solid
connection, the contraction that is produced acts as
if it came from one single unit (called a functional
syncytium); the units are electrically isolated
through the CT
 HEART – CONDUCTION SYSTEM
• normally, the heart beats at 75 beats/min. in an
autonomic fashion without any nerve impulses
(AUTORHYTHM)

SANS & PANS

the hormones influence
neurons serve to
the frequency of the
accelerate OR
cardiac beats
decelerate the heart

• myocytes stay contracted 10-15 (+) longer than

skeletal myocytes cause the Ca2+ voltage-
dependant channels are also present in the
sarcolemma; these channels are very slow
 HEART – CALCIUM
AP passes along the sarcolemma

voltage-regulated fast Na+ channels open rapidly

causes depolarization of the membrane

get release of Ca2+ from the SR
than, the voltage-dependant slow Ca2+ channels open

leaves the Ca2+ from the extra¢ space to enter

Ca2+ enters for a long time & cause a long contraction

N.B. Ca2+ pumps do not function as rapidly as those of the skeletal myocytes;
the refractory period last longer than that of the contraction; this prevent tetanus
 HEART – CARDIAC STIMULATORS
(AUTORHYTHMIC ¢)

• at birth, around 1% of the cardiac myocytes (autorhythmic ¢) can

generate an AP
• the fastest control for the cardiac rhythm
• threshold is the depolarization necessary to open voltage-dependant
Na+ channels
• autorhythmic ¢ lose the polarization of their membranes slowly up til
they reach the threshold and provoke an AP
 HEART – CARDIAC STIMULATORS
(AUTORHYTHMIC ¢)
autorhythmic ¢ (in the sinoatrial node (SA) of RA)

goes along the network of the atria that contract

AP reaches the atrioventricular node (AV)
(group of specilized fibers) SA

AP goes to the V. (form continuous network) AV
AB

AP goes to the atrioventricular bundle (AB)
 BB
AP reaches the apex via bundle branches (BB)
than ascended toward atria
 SE

thus contraction of the V than of the A

(subendocardial conducting network (SE))
 conduction
a good circulation is obtained :
A empties in the V, and then the V empties
 HEART – ANS
innervates the heart, modifies activities
SANS
cardioacceleratory center
(medulla oblongata) =>
postganglionic neurons (of the
spinal cord - thoracic) => sino-
atrial node, atrioventricular
node, ventricles
release noradrenaline =>
 cardiac frequency
PANS
neurons of the cardioinhibitory
center (medulla oblongata) =>
dorsal vagus nuclei => vagus
nerve (X) => sino-atrial node &
atrioventricular node
release acetylcholine =>
 cardiac frequency
HEART – ANS influence
HEART – ANS influence
HEART – ELECTROCARDIOGRAM (ECG or EKG)
• recording of the electric current during the cardiac cycle
• use electrodes placed at various sites: legs, arms, chest
• 12 leads: the (+) descriptive for the mechanism of cardiac contraction
• 3 waves are distinguishable
• P wave
• QRS complex
• T wave

EKG = K german for kardio

 HEART – ELECTROCARDIOGRAM (ECG or EKG)
12 leads: 3 bipolar (I, II, III), 3 unipolar (aVR, aVF, aVL), 6 unipolar precordial (V1-V6)

DI
aVR aVL

DI Einthoven triangle:
DI: btw right & left arm
DII: btw right arm & left leg DII DIII
DIII: btw left arm & left leg

aVF

aVR: on right arm

aVL: on left arm
aVF: on left leg

DII
DIII

aVL aVF
aVR

aVR: augmented vector right

aVL: augmented vector left
aVF: augmented vector foot
HEART – ELECTROCARDIOGRAM (ECG or EKG)
12 leads: 3 bipolar (I, II, III), 3 unipolar (aVR, aVF, aVL), 6 unipolar precordial (V1-V6)

V1 V2
V3
V4 V5 V6

V1 : 4th right intercostal space, right side of sternum

V2 : 4th left intercostal space, left side of sternum
V3 : mid way btw V2 & V4
V4 : 5th left intercostal space, on the left midclavicular line
V5 : same horizontal as V4, anterior axillary line
V6 : same horizontal as V4, midaxillary line
HEART – ELECTROCARDIOGRAM (ECG or EKG)
P wave (0.08 s):
• atrial depolarization that goes from the sino-atrial node and
throughout the atria
• 0,1 sec. after the beginning of P wave, the atria contracts
HEART – ELECTROCARDIOGRAM (ECG or EKG)
P-R interval (0.16 s)
• delay btw the start of the atrial contractions & the start of ventricular
contractions
• mesures the time necessary for the AP to go throughout the
atrioventricular node, atrioventricular bundle & the rest of the
conduction system
HEART – ELECTROCARDIOGRAM (ECG or EKG)
QRS complex (0.08 s) :
• ventricular depolarization that goes throughout the ventricles
• the ventricles start to contract at the beginning of the QRS complex
HEART – ELECTROCARDIOGRAM (ECG or EKG)
S-T segment :
- the end of the S wave & the start of the T wave
- period where the fibers of the ventricles are depolarized
Q-T interval (0.38 s):
- period from ventricular depolarization up to ventricular repolarization
HEART – ELECTROCARDIOGRAM (ECG or EKG)
T wave (0.16 s):
• ventricular repolarization; produced immediately before the
ventricular fibers relaxation
N.B. it is possible to perceive the repolarization of the atria but it is
ordinarily INVISIBLE because of the superimposed QRS complex
ECG: P QRS T wave

sinus rhythm

junctional rhythm
1. SA node non functional
2. P waves absents
3. AV node paces heart at 40-60 beats/min.

2nd degree heart block

1. P waves not going to AV nodes
2. more P than QRS waves
3. ratio: 2 P for each QRS wave

ventricular fibrillation
1. irregular, chaotic
 HEART – CARDIAC CYCLE
• arterial pressure varies with which ventricle is contracting or relaxing
(2 ventricles expulse the same volume of blood by contraction)
• pressure in the left & right ventricles & atria are not the same:
 RV = weaker pressure = thinner wall

SYSTOLE = PHASE OF CONTRACTION

DIASTOLE = PHASE OF RELAXATION

 HEART – CARDIAC CYCLE
• have systole & diastole for both : (a) atrial & (b) ventricular
• 75 beats/ min. or cardiac cycle = 0.8 sec.

CONTRACTION RELAXATION

atrial systole 0.1 s atrial diastole 0.3 s

ventricular ventricular
0.3 s 0.1 s
systole diastole
 HEART – CARDIAC CYCLE
(A) isovolumetric relaxation : early diastole
• short phase following the T wave
• ventricles relaxes, ê in ventricular pressure
• blood of aorta & pulmonary trunk backflow towards the
ventricles closing their semilunar valves
• dicrotic notch: brief  in aortic pressure when the valve
close, the blood backflows & bounce between the cusps
• ventricles are entirely closed : 4 valves are closed
 HEART – CARDIAC CYCLE
(B) phase of ventricular filling: mid to late diastole
· low pressure in atria & ventricles ; than, it  in atria
· circulating blood passively flow in atria & via open AV valves flow to
ventricles
· aortic & pulmonary valves are closed during the relaxation period
· ventricles fill up at around 70% & cusps of AV valves begin to close
· depolarization (systole) of atria (P wave) thus contraction & blood is
compressed
· pressure in atria  & residual blood (30% left over) is ejected into the
ventricles
 HEART – CARDIAC CYCLE
(C) ventricular systole  :
· atria relaxes (atrial diastole) & ventricles depolarize (systole) (QRS
complex)
· pressure in ventricles  which closes the AV valves
· phase of isovolumetric contraction: during a fraction of a sec., all is
closed (ventricles), the blood volume is constant
· pressure in ventricles continue to  until it exceeds the pressure of
the large arteries of ventricles
· aortic & pulmonary valves open; the blood is expulsed: ventricular
ejection phase: here, the pressure normally reaches 120 mmHg in
the aorta
SV=stroke vol.
=blood ejected from
ventricle; EDV &
ESV are end of
diastole & end of
systole vol.
respectively
 HEART – SOUNDS
• principally produced by the closure of valves
• 4 distinct sound are heard; normally have the 2 following sound :
• 1st lub is loud & long; closure of AV valves; start of ventricular systole
• 2nd dup is sharp & short; closure of aortic & pulmonary valves : start of
ventricular diastole
• there is a refractory period = PAUSE after the last sound
N.B. left AV valve closes before the right AV valve; aortic valve closes
before pulmonary valve;
• THUS fundamental rhythm is : lub-dup, pause lub-dup, pause, etc…
HEART – SOUNDS
 BLOOD VESSELS
• arteries & veins are made of 3 tunics :
 BLOOD VESSELS - TUNICS
TUNICA INTERNA
• s.s. epi. (endothelium)
• basal membrane
• internal elastic lamina

TUNICA MEDIA
• smooth myocytes, elastics fibers
• vasomotor neurofibers of ANS
(vasoconstriction, vasodilation)
• generally thickest layer (arteries)

TUNICA EXTERNA
• collagen fibers, neurofibres & lymphatics vessels
• bigger b. vessels have VASA VASORUM (own vessels)
• btw external & medial tunics, can have external elastic lamina
• generally thickest layer (veins)
 BLOOD VESSELS - ARTERIAL

ARTERY
• thick wall, small lumen
• high pressure & varies with if the
heart contracts or not;
• moves blood away from the
heart
• elastics arteries (bigger, close to
the heart), muscular arteries
(brings the blood to the viscera)
ARTERIOLE
• smallest of the arteries
 BLOOD VESSELS - VENOUS
VEIN
thin wall, large lumen, valve
low & continuous pressure
bring blood back to the heart
VENULE
• smallest of the vein
VENOUS SINUS
• reservoir that can be expanded
according to the quantity &
pressure of the blood
• no smooth muscle
BLOOD VESSELS - CAPILLARY
CAPILLARY
• thinnest vessels (ENDOTHELIUM)
• exchanges: nutrients, gas, waste with ¢ of organism
• exchanges almost done SOLELY here in the
cardiovascular system
large vein elastic artery

medium vein muscular artery

veinule arteriole

fenestrated capillary continuous capillary

BLOOD VESSELS - QUANTITIES
BLOOD VESSELS - CAPILLARIES

3 types of capillaries based

on structure

CONTINUOU FENESTRATE
SINUSOID
S D
BLOOD VESSELS - CONTINUOUS
• abundant (skin, muscles), (+) common)
• endothelial ¢ form an uninterrupted covering
• cytoplasm with pinocytotic vesicles (active process)
• tight junctions
• intercellular clefts: permit the passage of small
molecules
BLOOD VESSELS - FENESTRATED
• kidney, small intestine (important absorption)
• pores (fenestrations): covered by delicate membrane
(diaphragm) OR not covered
• cytoplasm with pinocytotic vesicles
• superior permeability
 BLOOD VESSELS - SINUSOIDAL
• liver, red blood marrow, lymphoid tissue, spleen, adrenal
medulla
• large irregular lumen, basal lamina absent or discontinued
• tight junctions (-) numerous, blood flows slowly; lack
pinocytotic vesicles
• large intercellular cleft allows big molecules to pass (ex.
protein
BLOOD VESSELS
TRANSPORT
diffusion
• direct diffusion
• diffusion via intercellular cleft
• diffusion via fenestration (pore)
 
transcytosis
• substances in vesicles are
transferred from plasma to intra¢
fluid or vice-versa : by
endocytosis (internal) &
exocytosis (external)
• filtration: large quantity of fluid is
expulsed from plasma at the
arterial end of capillaries to the
inter¢ fluid; it returns in the blood
at venous end of the capillaries;
due to many different pressures
 CIRCULATION
N.B.: capillary bed is an area where the nutrients/waste exchanges
occur & includes : metarterioles, true capillaries & thoroughfare channels

2
6 3
5 4
 BLOOD VESSELS

• blood does not always

pass in each capillaries
• at the entry into the
capillaries, each one is
individually regulated
for its flow by the
precapillary sphincters
 BLOOD VESSELS
• lymph takes its origin at the level of the capillary beds
BLOOD VESSELS - PRESSURE
VENTRICULAR SYSTOLE :
• walls of elastic arteries (principal, systemic) distend
• the heart pushes on one side and the capillaries resist on the other
BLOOD VESSELS - PRESSURE
VENTRICULAR DIASTOLE (SEMILUNAR VALVES CLOSED)
• wall of elastics arteries take back their shape & push the blood in the
capillaries thus the blood continually advance in the capillaries
BLOOD VESSELS - PRESSURE
· flow of blood in b. vessels follows gradient of pressure (high to low)
· caused by the contraction of the veins : slow to compress the blood
· arterial pressure (young adult) :

·  blood flow = blood pressure if resistance does not change

(OPPOSITE also applies)
· pressure of the arterioles offer the maximum resistance to the flow;
here we obtain a  in blood pressure; plays a key role in the
regulation of blood pressure by modifying the resistance by
VASOCONSTRICTION (can act upon the local or systemic
circulation)
N.B. vasoconstriction & vasodilation is largely controlled by the
vasomotor centre of the medulla oblongata
BLOOD VESSELS - PRESSURE
· pressure in the veins is very low ex. vena cava ≅ 0 mmHg
· this weak rate can’t permit adequate venous return thus there is:

2 PUMP SYSTEMS

RESPIRATORY MUSCULAR
BLOOD VESSELS - PRESSURE
respiratory pump
• blood is drawn toward the heart during inspiration
• here, compression of the abdominal cavity crush the large veins
• valve prevent backflow & thus the blood moves towards the heart
· pressure of the thoracic cage
· dilation of the thoracic veins
·  entry of blood in RA direction
of blood

volume 
pressure

diaphragm
lowers when
contracting
BLOOD VESSELS - PRESSURE
muscular pump 
· (+) important
· contraction & relaxation: skeletal muscles surround the deep veins
thus with their activity push blood toward the heart from one valve to
another
 BLOOD VESSELS - PRESSURE
baroreceptor reflexes 
· maintain blood pressure homeostasis

CO=cardiac output
R=total peripheral resistance
 FLUID FLOW
NET FILTRATION PRESSURE (NFP) 
· determine direction of fluid mv’t; 2 kinds:
FLUID FLOW
FLUID FLOW
 FLUID FLOW
PRESSURE

HPc   capillary hydrostatic pressure

 pressure exerted by the blood on the wall of the capillary
(outward mv’t)

 varies from 35mmHg (arterial end) to 17mmHg (venous

end)

HPif   interstitial fluid hydrostatic pressure

 opposes the HPc (inward mv’t)
 around 0 mmHg everywhere, ordinarily (reason : lymphatic
vein constantly drain)
 FLUID FLOW
PRESSURE
OPc   capillary colloid osmotic pressure

 due to the presence of plasma protein (ex. albumen); they

attract H2O & favor osmosis
 around 26 mmHg (does not change cause its the proteins that
cause it, do not leave)
OPif  interstitial fluid osmotic pressure

 due to the presence of inter¢ proteins (very small quantity)

 varie between 0.1 & 5mmHg; generally 1 mmHg

NFP   net filtration pressure NFP= (HPc - HPif) – (OPc - OPif)

 difference between arterial end (fluid exit) & the venous end
(entry or reabsorption) is the non reabsorbed fluid that will follow
along the lymphatic capillaries
FLUID FLOW-RESULT
 TERMINOLOGY
ANEMIA
• capacity of blood to transport insufficient quantity O 2
for the production of ¢ energy (ATP)
• cause : bleeding, destructive mechanism for RBC,
incapacity of the red bone marrow
 
POLYCYTHEMIA
• excess RBC;  viscosity of blood &  circulation
• different types: primary (gene mutation occurs),
secondary (underlying conditions: ex. tissue
hypoxia, kidney disease, hormone-related
medications etc.)
 TERMINOLOGY

LEUKEMIA
• group of cancerous state of WBC
 
HEMOPHILIA
• hereditary bleeding disorders
• different kinds, missing different factors
 
SEPTICEMIA
• state of severe infection caused by bacteria (or their
toxins) in the blood
 TERMINOLOGY

ANGINA PECTORIS
· pain caused by  for a moment of irrigation of myocardium
· cause : stress, partial obstruction
· temporary lack of O2 which weakens the myocardium ¢
BUT does not destroy them!
 TERMINOLOGY

MYOCARDIAL INFARCTION (HEART ATTACK OR CORONARY)

· obstruction or prolonged spasm causing non contractile scar tissue

ARTERIOSCLEROSIS
· thickening of the arterial walls by lipid deposits (plaques)