ANATOMY AND PHYSIOLOGY

OF THE
CARDIOVASCULAR SYSTEM

LOCATION OF THE HEART

RESTS ON THE DIAPHRAGM
NEAR THE MIDLINE OF THE THORACIC CAVITY

PERICARDIUM

CONFINES HEART TO

THE MEDIASTINUM
ALLOWS SUFFICIENT
FREEDOM OF
MOVEMENT.
CONSISTS OF TWO
PARTS:THE FIBROUS
AND SEROUS.

FIBROUS:THIN INELASTIC, DENSE IRREGULAR

CONNECTIVE TISSUE
---HELPS IN PROTECTION, ANCHORS HEART TO
MEDIASTINUM
SEROUS: THINNER, MORE DELICATE DIVIDED

INTO PARIETAL AND VISCERAL

LAYERS OF THE HEART

WALL

EPICARDIUM: COMPOSED OF MESOTHELIUM

AND DELICATE CONNECTIVE TISSUE (IMPARTS A

SLIPPERY TEXTURE TO THE OUTER SURFACE OF
THE HEART).

MYOCARDIUM:RESPONSIBLE FOR PUMPING

ENDOCARDIUM: THIN LAYER OF

ENDOTHELIUM WHICH IS CONTINOUS WITH

THE LINING OF THE LARGE BLOOD VESSELS
ATTACHED TO THE HEART.

CHAMBERS OF THE HEART

FOUR CHAMBERS
TWO AURICLES PRESENT

SERIES OF GROOVES CALLED SULCI CONTAIN FAT

AND CORONARY BLOOD VESSEL

SULCUS

MYOCARDIAL THICKNESS
AND FUNCTION
ATRIA : THIN

WALLED
VENTRICLES
:THICK WALLED
LT VENTRICLE IS
THICKER THAN THE
RT VENTRICLE.

HEART VALVES AND

CIRCULATION OF BLOOD

ATRIOVENTRICULAR &
SEMILUNAR VALVES

SYSTEMIC AND PULMONARY

CIRCULATION
LEFT SIDE IS A

PUMP TO THE
SYSTEMIC
CIRCULATION.
RIGHT SIDE IS A
PUMP TO THE
PULMONARY
CIRCULATION.

THE CONDUCTION SYSTEM

INHERENT AND RHYTHMICAL

BEAT IS DUE TO
AUTORHYTHMIC FIBERS OF
THE CARDIAC MUSCLE.
THESE FIBERS HAVE 2
IMPORTANT FUNCTION
- ACT AS PACE MAKER
- FORM THE CONDUCTION
SYSTEM

SA NODE WOULD INITITATES ACTION

POTENTIAL ABOUT EVERY 0.6 SEC OR 100

TIMES/MIN
THE ANS ALTERS THE STRENGTH AND
TIMING OF HEART BEATS.

PHYSIOLOGIC
CHARACTERISTICS OF THE
CONDUCTION CELLS
AUTOMATICITY
EXCITABILITY
CONDUCTIVITY
RHYTHMICITY
CONTRACTILITY
TONICITY

CARDIAC CYCLE

ATRIAL SYSTOLE

LASTS FOR 0.1 SEC

ATRIAL DEPOLARIZATION CAUSES

ATRIAL SYSTOLE
IT CONTRIBUTES A FINAL 25mL OF
BLOOD TO EACH VENTRICLE
END OF ATRIAL SYSTOLE IS ALSO
END OF VENTRICULAR DIASTOLE
END-DIASTOLIC VOLUME IS 130 mL

VENTRICULAR SYSTOLE
LASTS FOR 0.3 SEC
IT IS CAUSED BY VENTRICULAR

DEPOLARIZATION
ISOVOLUMETRIC CONTRACTION
LASTS FOR 0.05 SECONDS WHEN
BOTH THE SEMILUNAR AND
ATRIOVENTRICULAR VLAVES ARE
CLOSED.

THE SL VALVES OPEN WHEN

-THE LEFT VENTRICULAR PRESSURES

SURPASSES AORTIC PRESSURE(80 MM OF
MERCURY)
-THE RIGHT VENTRICULAR PRESSURE RISES
ABOVE PULMONARY PRESSURE (20 mmHg)
SL VALVES OPEN FOR 0.25 SEC

THE LEFT VENTRICLE EJECTS ABOUT 70 ML

INTO THE AORTA

THE RIGHT VENTRICLE EJECTS THE SAME
VOLUME INTO THE PULMONARY TRUNK.
END SYSTOLIC VOLUME IS 60mL IN EACH
VENTRICLE .

RELAXATION PERIOD
BOTH ATRIA AND VENTRICLES

ARE RELAXED .IT LASTS FOR

0.4 SEC.
WHEN HEART BEATS FASTER
THE RELAXATION TIME
SHORTENS.
VENTRICULAR
REPOLARIZATION CAUSES
VENTRICULAR DAISTOLE.

HEART SOUNDS
PRODUCED FROM BLOOD

TURBULENCE CAUSED BY
CLOSING OF HEART VALVES
S1 ATRIOVENTRICULAR
VALVE CLOSURE
S2 SEMILUNAR VALVE
CLOSURE
S3 RAPID VENTRICULAR
FILLING
S4 ATRIAL SYSTOLE

CARDIAC OUTPUT
CO = SV X HR
mL/min

mL/beat

(Beats/min)

FOR A RESTING ADULT

CO = 70mL/beat x75beats/min
= 5250 mL/min
= 5.25 L/min

REGULATION OF STROKE
VOLUME
THREE FACTORS REGULATE STROKE

VOLUME
-PRELOAD
-CONTRACTILITY
-AFTERLOAD

PRELOAD
STRETCH OF CARDIAC MUSCLE

PRIOR TO CONTRACTION.
FRANK-STARLING LAW
PRELOAD IS PROPOTIONAL TO
END DIASTOLIC VLOUME
IF HR IS MORE THAN 160
BEATS/MIN STROKE VOLUME
DECLINES DUE TO SHORT
FILLING TIME.

CONTRACTILITY

IT IS THE STRENGTH OF

CONTRACTION AT ANY GIVEN

PRELOAD.
POSITIVE AND NEGATIVE
IONOTROPICS.
STIMULATION OF SYMPATHETIC
DIVISION OF ANS LEADS TO
POSITVE IONOTROPIC EFFECT
INHIBITION OF SYMPATHETIC
DIVISION OF ANS LEADS TO
NEGATIVE IONOTROPIC EFFECT

AFTERLOAD
THE PRESSURE THAT MUST BE OVERCOME

BEFORE A SEMILUNAR VALVE CAN OPEN IS

TERMED THE AFTERLOAD.
INCREASE IN AFTERLOAD CAUSE DECREASE
IN STROKE VOLUME
HTN AND AHTEROSCLEROSIS INCREASES
THE AFTERLOAD.

REGUALTION OF HEART
RATE
SA NODE INITIATES 100

BEATS/MIN IF LEFT TO
ITSELF.
TISSUE REQUIRE
DIFFERENT VOLUME OF
BLOOD FLOW UNDER
DIFFERENT
CONDITIONS(EX: EXERCISE)
ANS AND HORMONES OF
ADRENAL MEDULLA ARE
IMPORTANT IN REGULATING
THE HEART RATE.

AUTONOMIC REGULATION
OF HEART RATE
INPUT TO
CARDIOVASCULAR
CENTRE

HIGHER BRAIN CENTER:

CEREBRAL CORTEX, LYMBIC
SYSTEM, HYPOTHALAMUS
SENSORY RECEPTORS:

SYMPATHETIC
NEURONS EXTEND
FROM MEDULLA
OBLANGATA

PROPRIRECEPTORS,
CHEMORECEPTORS,
BARORECEPTORS.

THE SPINAL CORD

(thoracic region)
CARDIAC ACCELERATOR
NERVE EXTENDS TO SA,
AV NODES

TRIGERS NOREPINEPHRINE

NOR-EPINEPHRINE
HAS 2 EFFECTS
-IN SA NODE, SPEEDS THE RATE OF SPONTANEOUS
DEPOLARIZATION
-IN AV NODE,INCREASES CONTRACTILITY
INCREASES STROKE VOLUME

PARASYMPATHETIC
EFFECT
PARASYMPATHETIC NERVE REACHES THE HEART VIA
LEFT VAGUS (x) NERVES
THEY RELAESE ACETYL CHOLINE, WHICH
DECREASES THE HEART RATE
AT REST PARASYMPATHETIC STIMULATION
PREDOMINATES

CHEMICAL REGULATION OF
HEART RATE
HORMONES: EPINEPHRINE AND

NOREPINEPHRINE, THROID HROMONE ALSO

INCREASES HEART RATE
CATIONS: ELEVATED K+ AND Na+
DECREASES HEART RATE, MODERATE
INCREASE IN INTERSTITIAL Ca+ LEVELS
SPEEDS HEART RATE.

OTHER FACTORS IN HEART

RATE REGULATION
AGE
GENDER PHYSICAL FITNESS
BODY TEMPERATURE

STRUCTURE
AND
FUNCTIONS OF BLOOD
VESSELS

BODY CONTAINS THREE KINDS OF

CAPILLARIES
CONTINUOUS- LUNG, SMMOTH MUSCLE,

CONNECTIVE TISSUES

FENESTRATED- KIDNEY, SMALL

INTESTINE,BRAIN

SINUSOIDS- LIVER RED BONE MARROW, SPLEEN

AND ENDOCRINE GLANDS

BLOOD DISTRIBUTION IN THE

CARDIOVASCULAR SYSTEM
PULMONARY VESSELS - 9%
HEART 7%
SYSTEMIC ARTERIES

AND ARTERIOLES
SYSTEMIC CAPILLARIES 7%
- 13%
SYSTEMIC VEINS AND VENULES 64%

HEMODYNAMIC AFFECTING
BLOOD FLOW
BLOOD PRESSURE
RESISTANCE
VENOUS RETURN

BLOOD PRESSURE
DURING SYSTEMIC CIRCULATION, BLOOD PRESSURE

FALLS AS THE DISTANCE FROM THE LEFT

VENTRICLE INCREASES
IN ARTERIOLES AND ARTERIES 35 mm Hg
IN VENOUS END OF CAPILLARIES 16mm Hg
WHEN BLOOD FLOW IN RT.VENTRICLE -0 mmHg

MAP = DIASTOLIC PRESSURE +

1/3 (SYS PRESSURE DIASTOLIC

PRESSURE)

VASCULAR RESISTANCE
IT IS THE OPPOSTION TO BLOOD FLOW
DUE TO FRICTION BETWEEN BLOOD
AND THE WALLS OF BLOOD VESSELS.

VASCULAR RESISTANCE
DEPENDS ON
SIZE OF THE LUMEN-

R IS INVERSELY PROPOTIONAL TO 1/d

BLOOD VISCOSITY
TOTAL BLOOD VESSEL LENGTH

VENOUS RETURN
DEPENDS ON
HEART CONTRACTION
PRESSURE IN THE RT ATRIUM
BESIDES THIS
SKELETAL MUSCLE PUMP
RESPIRATORY PUMP

VELOCITY OF BLOOD
FLOW
VELOCITY IS INVERSELY PROPOTIONAL

TO CROSS SECTIONAL AREA.

VELOCITY DECREASES AS IT PROCEEDS
FROM ARTERIES,
ARTERIOLES,CAPILLAREIS
VELOCITY INCREASES AS IT PROCEEDS
FROM VENULES, VEINS.
THIS ALLOWS EXCHANGE OF MATERIALS
IN THE CAPILLARIES.

CONTROL OF BLOOD
PRESSURE AND
BLOOD FLOW

ROLE OF CARDIOVASCULAR
CENTRE
PROPRIORECEOTORS
BARORECEPTORS
CHEMORECEPTORS

NEURAL REGULATION 0F
BLOOD PRESSURE
BARORECEPTORS
CHEMORECEPTORS

BARORECEPTORS

PRESSURE SENSITIVE

LOCATED IN THE
AORTA, INTERNAL
CAROTID AND OTHER
LARGE ARTERIES.
2 IMPORTANT
BARORECEPTOR
REFLEX ARE
- CAROTID SINUS
REFLEX
- AORTIC REFLEX

CHEMORECEPTOR REFLEX
PRESENT CLOSE TO THE
- BARORECEPTORS OF CAROTID SINUS AND
ARCH OF AORTA
- THEY ARE CALLED CAROTID BODIES AND
AORTIC BODIES.

HORMONAL REGULATION
OF BLOOD PRESSURE
RENIN ANGIOTENSIN-ALDOSTERONE

MECHANISM
EPINEPHRINE AND NOR EPINEPHRINE
ANTIDIURETIC HORMONE
ATRIAL NATRIURETIC PEPTIDE

AUTOREGULATION OF
BLOOD PRESSURE
ABILTY OF TISSUE TO

AUTOMATICALLY ADJUST ITS

BLOOD FLOW TO MATCH ITS
METABLOIC DEMAND IS CALLED
AUTOREGULATION. MAINLY
DURING EXERCISE.

TWO TYPE OF STIMULI CAUSES

AUTOREGULATORY CHANGESHSICALY
- PHYSICAL CHANGE
- VASODILATING AND VASOCONSTRICTING
CHEMICALS

PHYSICAL CHANGES
WARMING AND COOLING CAUSES

VASODILATION AND VASOCONSTRICTION.

SMOOTH MUSCLE IN ARTERIOLE EXHIBIT
MYOGENIC RESPONSE

VASODILATING AND
VASOCONSTRICTING
CHEMICALS

SEVERAL CELLS RELEASE A WIDE VARIETY

OF CHEMICALS THAT ALTER THE BLOOD

VESSEL DIAMETER
VASODILATORS - K+, H+, LASCTIC ACID
AND ADENOSINE AND MAINLY NO
VASOCONSTRICTORS THROMBAXANE A2 ,
SEROTONIN AND ENDOTHELINS