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 SYMPATHETIC NEURONS EXTEND FROM MEDULLA OBLANGATA THE SPINAL CORD (thoracic region)
CARDIAC ACCELERATOR NERVE EXTENDS TO SA, AV NODES TRIGERS NOREPINEPHRINE HIGHER BRAIN CENTER: CEREBRAL CORTEX, LYMBIC SYSTEM, HYPOTHALAMUS SENSORY RECEPTORS: PROPRIRECEPTORS, CHEMORECEPTORS, BARORECEPTORS.

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

INCREASES STROKE VOLUME

PARASYMPATHETIC NERVE REACHES THE HEART VIA LEFT VAGUS (x) NERVES

PARASYMPATHETIC EFFECT
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

 PRESSURE SENSITIVE

BARORECEPTORS

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