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

FOR A RESTING ADULT
CO = 70mL/beat x75beats/min
= 5250 mL/min
= 5.25 L/min

mL/min mL/beat (Beats/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

SYMPATHETIC
NEURONS EXTEND
FROM MEDULLA
OBLANGATA

THE SPINAL CORD
(thoracic region)
HIGHER BRAIN CENTER:
CEREBRAL CORTEX, LYMBIC
SYSTEM, HYPOTHALAMUS
SENSORY RECEPTORS:
PROPRIRECEPTORS,
CHEMORECEPTORS,
BARORECEPTORS.
CARDIAC ACCELERATOR
NERVE EXTENDS TO SA, AV
NODES
TRIGERS NOR-
EPINEPHRINE
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%
SYSTEMIC VEINS AND VENULES 64%
- 13%
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

4
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