Anatomy and-physiology-of-the-cardiovascular-system-medical-surgical-nursing-ppt

ANATOMY AND PHYSIOLOGY OF THE

CARDIOVASCULAR SYSTEM

LOCATION OF THE HEARTRESTS ON THE DIAPHRAGM NEAR THE MIDLINE OF THE THORACIC CAVITY

PERICARDIUMCONFINES 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

MEDIASTINUMSEROUS: 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 PUMPINGENDOCARDIUM: THIN LAYER OF

ENDOTHELIUM WHICH IS CONTINOUS WITH THE LINING OF THE LARGE BLOOD VESSELS ATTACHED TO THE HEART.

CHAMBERS OF THE HEART

FOUR CHAMBERSTWO AURICLES PRESENTSERIES 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 SYSTEMINHERENT 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

AUTOMATICITYEXCITABILITYCONDUCTIVITYRHYTHMICITYCONTRACTILITYTONICITY

CARDIAC CYCLE

ATRIAL SYSTOLELASTS FOR 0.1 SEC ATRIAL DEPOLARIZATION CAUSES

ATRIAL SYSTOLEIT CONTRIBUTES A FINAL 25mL OF

BLOOD TO EACH VENTRICLEEND OF ATRIAL SYSTOLE IS ALSO

END OF VENTRICULAR DIASTOLEEND-DIASTOLIC VOLUME IS 130 mL

VENTRICULAR SYSTOLELASTS FOR 0.3 SECIT 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 PERIODBOTH 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 SOUNDSPRODUCED 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 VOLUMETHREE FACTORS REGULATE STROKE

VOLUME-PRELOAD-CONTRACTILITY-AFTERLOAD

PRELOADSTRETCH OF CARDIAC MUSCLE

PRIOR TO CONTRACTION.FRANK-STARLING LAWPRELOAD IS PROPOTIONAL TO

END DIASTOLIC VLOUMEIF HR IS MORE THAN 160

BEATS/MIN STROKE VOLUME DECLINES DUE TO SHORT FILLING TIME.

CONTRACTILITYIT 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

AFTERLOADTHE 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 EFFECTPARASYMPATHETIC 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

AGEGENDER PHYSICAL FITNESSBODY 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 ARTERIOLESSYSTEMIC CAPILLARIES – 7%SYSTEMIC VEINS AND VENULES – 64%

- 13%

HEMODYNAMIC AFFECTING BLOOD FLOW

BLOOD PRESSURERESISTANCEVENOUS RETURN

BLOOD PRESSURE

DURING SYSTEMIC CIRCULATION, BLOOD PRESSURE FALLS AS THE DISTANCE FROM THE LEFT VENTRICLE INCREASES

IN ARTERIOLES AND ARTERIES – 35 mm HgIN VENOUS END OF CAPILLARIES– 16mm HgWHEN 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 ONSIZE OF THE LUMEN- R IS INVERSELY PROPOTIONAL TO 1/dBLOOD VISCOSITYTOTAL BLOOD VESSEL LENGTH

4

VENOUS RETURNDEPENDS ONHEART CONTRACTIONPRESSURE IN THE RT ATRIUM

BESIDES THISSKELETAL MUSCLE PUMPRESPIRATORY 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

PROPRIORECEOTORSBARORECEPTORSCHEMORECEPTORS

NEURAL REGULATION 0F BLOOD PRESSURE

BARORECEPTORS CHEMORECEPTORS

BARORECEPTORSPRESSURE SENSITIVE

LOCATED IN THE AORTA, INTERNAL CAROTID AND OTHER LARGE ARTERIES.

2 IMPORTANT BARORECEPTOR REFLEX ARE

- CAROTID SINUS REFLEX

- AORTIC REFLEX

CHEMORECEPTOR REFLEXPRESENT 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 EPINEPHRINEANTIDIURETIC HORMONEATRIAL 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

CHEMICALSSEVERAL 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