Download the vascular system control of the cardiovascular system

FUNCTIONAL ANATOMY
OF THE
CARDIOVASCULAR
SYSTEM
CHAPTER 14
DR. CARLOS ORTIZ
BIO-208
THE HEART
• GROSS ANATOMY
• THE HEART IS A HOLLOW, MUSCULAR ORGAN
APPROXIMATELY THE SIZE OF A FIST.
• IT IS POSITIONED OBLIQUELY IN THE MIDDLE
COMPARTMENT OF THE MEDIASTINUM OF THE CHEST,
JUST BEHIND THE STERNUM.
• APPROXIMATELY TWO THIRDS OF THE HEART LIES TO
THE LEFT OF THE STERNUM’S MIDLINE.
• THE APEX OF THE HEART IS FORMED BY THE TIP OF THE
LEFT VENTRICLE AND LIES JUST ABOVE THE DIAPHRAGM
AT THE LEVEL OF THE FIFTH INTERCOSTAL SPACE.
• THE BASE OF THE HEART IS FORMED BY THE ATRIA.
• THE HEART RESIDES WITHIN A LOOSE, MEMBRANOUS
SAC CALLED THE PARIETAL PERICARDIUM (OUTER
LAYER) AND THE VISCERAL PERICARDIUM OR
EPICARDIUM (INNER LAYER).
• THE PERICARDIAL FLUID SEPARATES THESE TWO
LAYERS.
THE HEART
• GROSS ANATOMY
• THE HEART WALL CONSISTS OF THREE LAYERS 1) THE
OUTER EPICARDIUM 2) THE MIDDLE MYOCARDIUM 3) THE
INNER ENDOCARDIUM.
• THE MYOCARDIUM COMPOSES THE BULK OF THE HEART
AND CONSISTS OF BANDS OF INVOLUNTARY STRIATED
MUSCLE FIBERS. IT IS THE CONTRACTION OF THESES
MUSCLE FIBERS THAT CREATES THE PUMPLIKE ACTION
NEEDED TO MOVE BLOOD THROUGHOUT THE BODY.
• THE ATRIAL CHAMBERS ARE THIN-WALLED “CUPS” OF
MYOCARDIAL TISSUE, SEPARATED BY AN INTERATRIAL
SEPTUM.
• THE TWO LOWER HEART CHAMBERS, OR VENTRICLES,
MAKE UP THE BULK OF THE HEART’S MUSCLE MASS AND
DO MOST OF THE PUMPING THAT CIRCULATES THE
BLOOD. THE MASS OF THE LEFT VENTRICLE IS
APPROXIMATELY TWO THIRDS LARGER THAN THAT OF
THE RIGHT VENTRICLE.
THE HEART
• GROSS ANATOMY
• BECAUSE OF THIS RELATIONSHIP, CONTRACTION OF
THE LEFT VENTRICLE ACTUALLY PULLS IN THE RIGHT
VENTRICULAR WALL, AIDING ITS CONTRACTION.
• THE RIGHT AND LEFT VENTRICLES ARE SEPARATED BY A
MUSCLE WALL CALLED THE INTERVENTRICULAR
SEPTUM.
• THE VALVES OF THE HEART ARE FLAPS OF FIBROUS
TISSUE. THOSE LOCATED BETWEEN THE ATRIA AND
VENTRICLES ARE CALLED AV VALVES. THE VALVE
BETWEEN THE RIGHT ATRIUM AND RIGHT VENTRICLE IS
CALLED THE TRICUSPID VALVE. THE VALVE BETWEEN
THE LEFT ATRIUM AND LEFT VENTRICLE IS CALLED THE
BICUSPID, OR MITRAL VALVE.
• THE AV VALVES CLOSE DURING SYSTOLE, THEREBY
PREVENTING BACKFLOW OF BLOOD INTO THE ATRIA.
CLOSURE OF THESE VALVES PROVIDES A CRITICAL
PERIOD OF ISOVOLUMETRIC CONTRACTION, DURING
WHICH CHAMBER PRESSURES QUICKLY RISE JUST
BEFORE EJECTION OF THE BLOOD.
THE HEART
• GROSS ANATOMY
• COMMON VALVE PROBLEMS INCLUDE REGURGITATION
AND STENOSIS. REGURGITATION IS THE BACKFLOW OF
BLOOD THROUGH AN INCOMPETENT OR DAMAGED
VALVE.
• STENOSIS IS A PATHOLOGICAL NARROWING OR
CONSTRICTION OF A VALVE OUTLET, WHICH CAUSES
INCREASED PRESSURE IN THE AFFECTED CHAMBER AND
VESSELS.
• REGURGITATION AND STENOSIS AFFECT CARDIAC
PERFORMANCE. FOR EXAMPLE, IN MITRAL STENOSIS,
HIGH PRESSURES IN THE LEFT ATRIUM BACK UP INTO
THE PULMONARY CIRCULATION. THIS CAN CAUSE
PULMONARY EDEMA.
• A SET OF SEMILUNAR VALVES SEPARATES THE
VENTRICLE FROM THEIR ARTERIAL OUTFLOW TRACTS.
CONSISTING OF THREE HALF-MOON-SHAPED CUSPS
ATTACHED TO THE ARTERIAL WALL, THESE VALVES
PREVENT BACKFLOW OF BLOOD INTO THE VENTRICLES
DURING DIASTOLE.
THE HEART
• GROSS ANATOMY
• THE PULMONARY VALVE IS AT THE OUTFLOW
TRACT OF THE RIGHT VENTRICLE. DURING
SYSTOLE, BLOOD FLOWS THROUGH THE OPEN
PULMONARY VALVE FROM THE RIGHT
VENTRICLE INTO THE PULMONARY ARTERY.
• THE AORTIC VALVE IS LOCATED AT THE
OUTFLOW TRACT OF THE LEFT VENTRICLE.
DURING SYSTOLE, BLOOD FLOWS THROUGH
THE OPEN AORTIC VALVE FROM THE LEFT
VENTRICLE INTO THE AORTA.
• AS WITH THE AV VALVES, THE SEMILUNAR
VALVES CAN LEAK (REGURGITATION) OR
BECOME OBSTRUCTED (STENOSIS).
THE HEART
• CORONARY CIRCULATION
• LIKE THE LUNG, THE HEART HAS ITS OWN CIRCULATORY
SYSTEM, WHICH IS CALLED CORONARY CIRCULATION.
HOWEVER, UNLIKE THE LUNG, THE HEART HAS A HIGH
METABOLIC RATE, WHICH REQUIRES MORE BLOOD
FLOW PER GRAM OF TISSUE WEIGHT THAN ANY OTHER
ORGAN EXCEPT THE KIDNEY. TO MEET THESE NEEDS,
THE CORONARY CIRCULATION PROVIDES AN EXTENSIVE
NETWORK OF BRANCHES TO ALL MYOCARDIAL TISSUE.
• TWO MAIN CORONARY ARTERIES, A LEFT AND A RIGHT,
ARISE FROM THE ROOT OF THE AORTA.
• THE CORONARY ARTERIES GET THE MAXIMAL PULSE OF
PRESSURE GENERATED BY CONTRACTION OF THE LEFT
VENTRICLE. HOWEVER, ONLY DURING VENTRICULAR
DIASTOLE WILL BLOOD FLOW THROUGH THE CORONARY
ARTERIES.
MINI-CLINI
• HEART RATE AND CORONARY PERFUSION
• WHY MIGHT AN EXTREMELY HIGH HEART RATE
DECREASE BLOOD FLOW THROUGH THE CORONARY
ARTERIES?.
• BLOOD FLOW THROUGH THE CORONARY ARTERIES
OCCURS ONLY DURING VENTRICULAR DIASTOLE.
MYOCARDIAL PERFUSION OCCURS ONLY DURING
DIASTOLE. AS HEART RATE INCREASES, BOTH DIASTOLIC
AND SYSTOLIC TIMES MUST NECESSARILY DECREASE.
AS DIASTOLIC TIME DECREASES, LESS AND LESS TIME IS
AVAILABLE FOR CORONARY ARTERY PERFUSION, UNTIL
FINALLY CORONARY BLOOD FLOW CAN BE
SIGNIFICANTLY REDUCED. NOT ONLY IS CORONARY
ARTERY PERFUSION COMPROMISED WITH SEVERE
TACHYCARDIA, BUT ALSO DECREASED VENTRICULAR
FILLING TIME CAUSES DECREASED STROKE VOLUME
AND DECREASED CARDIAC OUTPUT.
• EXAMPLE,
60 SECONDS /100 BEATS PER MINUTE= 0.6 sec.
60 SECONDS/ 150 BEATS PER MINUTE= 0.4 sec.
CORONARY CIRCULATION
• CORONARY ARTERIES
• THE LEFT CORONARY ARTERY DIVIDES INTO
TWO BRANCHES BETWEEN THE PULMONARY
ARTERY AND THE TIP OF THE LEFT ATRIAL
APPENDAGE. THE ANTERIOR DESCENDING
BRANCH AND THE CIRCUMFLEX BRANCH.
• THE RIGHT CORONARY ARTERY ALSO BEGINS
AT THE AORTA. IT ENDS IN ITS POSTERIOR
DESCENDING BRANCH.
• THE CORONARY VEINS CLOSELY PARALLEL
THE ARTERIES. CORONARY VEINS GATHER
TOGETHER INTO A LARGE VESSEL CALLED THE
CORONARY SINUS. THE CORONARY SINUS
EMPTIES INTO THE RIGHT ATRIUM BETWEEN
THE OPENING OF THE INFERIOR VENA CAVA
AND THE TRICUSPID VALVE.
THE HEART
• CORONARY VEINS
• IN ADDITION TO THESE MAJOR ROUTES FOR RETURN
BLOOD FLOW, SOME CORONARY VENOUS BLOOD
FLOWS BACK INTO THE HEART THROUGH THE
THEBESIAN VEINS. THE THEBESIAN VEINS EMPTY
DIRECTLY INTO ALL THE HEART CHAMBERS.
• THUS ANY BLOOD COMING FROM THE THEBESIAN VEINS
WILL MIX WITH ARTERIAL BLOOD COMING FROM THE
LUNGS. THE TOTAL OXYGEN CONTENT (CaO2) FALLS
WHEN VENOUS BLOOD MIXES WITH ARTERIAL BLOOD.
BECAUSE THEBESIAN VEINS BYPASS, OR SHUNT,
AROUND THE PULMONARY CIRCULATION, THIS
PHENOMENON IS CALLED AN ANATOMICAL SHUNT.
• WHEN COMBINED WITH A SIMILAR BYPASS IN THE
BRONCHIAL CIRCULATION THESE NORMAL ANATOMICAL
SHUNTS ACCOUNT FOR APPROXIMATELY 2% TO 3% OF
THE TOTAL CARDIAC OUTPUT.
THE HEART
• CARDIAC CONDUCTION SYSTEM
• MYOCARDIAL TISSUES POSSESS FOUR KEY FUNCTIONS.
• EXCITABILITY, IS THE ABILITY OF CELLS TO RESPOND TO
ELECTRICAL (ELECTROLYTE IMBALANCES), CHEMICAL
(DRUGS), OR MECHANICAL STIMULATION.
• AUTOMATICITY/ INHERENT RHYTHMICITY, UNIQUE
ABILITY OF THE CARDIAC MUSCLE TO INITIATE A
SPONTANEOUS ELECTRICAL IMPULSES. THIS ABILITY IS
HIGHLY DEVELOPED IN SPECIALIZED AREAS CALLED
PACEMAKER OR NODAL TISSUES (SA NODE AND AV
NODE) . AN ELECTRICAL IMPULSE FROM ANY SOURCE
OTHER THAN NORMAL PACEMAKER IS CONSIDERED
ABNORMAL AND REPRESENTS ONE OF THE MANY
CAUSES OF WHAT ARE CALLED CARDIAC ARRHYTHMIAS.
• CONDUCTIVITY, IS THE ABILITY OF MYOCARDIAL TISSUE
TO SPREAD, OR RADIATE, ELECTRICAL IMPULSES. THIS
PROPERTY IS SIMILAR TO THAT OF SMOOTH MUSCLE IN
THAT IT ALLOWS THE MYOCARDIUM TO CONTRACT
WITHOUT DIRECT NEURAL INNERVATION. THE RATE WITH
WHICH ELECTRICAL IMPULSES SPREAD THROUGHOUT
THE MYOCARDIUM IS EXTREMELY VARIABLE.
THE HEART
• CARDIAC CONDUCTION SYSTEM
• CONDUCTIVITY, THESE DIFFERENCES IN
CONDUCTION VELOCITY ARE NEEDED TO
ENSURE SYNCHRONOUS CONTRACTION OF
THE CARDIAC CHAMBERS. ABNORMAL
CONDUCTIVITY CAN AFFECT THE TIMING OF
CHAMBER CONTRACTIONS AND THUS
DECREASE CARDIAC EFFICIENCY.
• CONTRACTILITY, IN RESPONSE TO AN
ELECTRICAL IMPULSE, IS THE PRIMARY
FUNCTION OF THE MYOCARDIUM. THE PERIOD
DURING WHICH THE MYOCARDIUM CANNOT BE
STIMULATED IS CALLED THE REFRACTORY
PERIOD.
THE HEART
• CARDIAC MUSCLE
• UNDERSTANDING OF HOW CARDIAC MUSCLE
CONTRACTS REQUIRES KNOWLEDGE OF THE HEART’S
MICROANATOMY.
• AS SEEN UNDER THE MICROSCOPE, MYOCARDIUM
TISSUE CONSISTS OF AN ARRANGEMENT OF STRIATED,
CYLINDRICALLY SHAPED MUSCLE FIBERS.
• MUSCLE FIBERS CONSISTS OF 1) SARCOLEMMA(CELL
MEMBRANE) 2) INTERCALATED DISKS 3) MYOFIBRILS
4) MYOSIN (THICK FILAMENTS OF PROTEIN) 5) ACTIN
(THIN FILAMENTS OF PROTEIN).
• ACCORDING TO THE SLIDING FILAMENT THEORY,
MYOCARDIAL CELLS CONTRACT WHEN ACTIN AND
MYOSIN COMBINE TO FORM REVERSIBLE BRIDGES.
THESE BRIDGES CAUSE FILAMENTS TO SLIDE OVER ONE
ANOTHER, SHORTENING THE SARCOMERE AND THUS
MUSCLE FIBERS AS A WHOLE.
THE HEART
• CARDIAC MUSCLE
• IN PRINCIPLE, THE TENSION DEVELOPED DURING
MYOCARDIAL CONTRACTION IS DIRECTLY
PROPORTIONAL TO THE NUMBER OF CROSSBRIDGES
BETWEEN THE ACTIN AND MYOSIN FILAMENTS. IN TURN,
THE NUMBER OF CROSSBRIDGES IS DIRECTLY
PROPORTIONAL TO THE LENGTH OF THE SARCOMERE.
THIS PRINCIPLE UNDERLIES STARLING LAW OF THE
HEART, ALSO KNOWN AS THE FRANK-STARLING LAW,
THE MORE A CARDIAC FIBER IS STRETCHED, THE
GREATER THE TENSION IT GENERATES WHEN
CONTRACTED.
• THE FRANK-STARLING LAW HOLDS TRUE ONLY UP TO A
SARCOMERE LENGTH OF 2.2.um. BEYOND THIS LENGTH,
THE ACTION AND MYOSIN FILAMENTS BECOME
PARTIALLY DISENGAGED, AND FEWER CROSSBRIDGES
CAN BE FORMED. WITH FEWER CROSSBRIDGES, THE
OVERALL TENSION DEVELOPED DURING CONTRACTION
IS LESS. THIS RELATIONSHIP IS OF MAJOR IMPORTANCE
AND WILL BE EXPLORED LATER IN THE DISCUSSION OF
THE HEART AS A PUMP.
THE VASCULAR SYSTEM
• SYSTEMIC VASCULATURE
• CONSISTS OF THREE MAJOR COMPONENTS: 1) THE
ARTERIAL SYSTEM 2) THE CAPILLARY SYSTEM 3)THE
VENOUS SYSTEM. ALTHOUGH ALL THREE COMPONENTS
ARE RESPONSIBLE FOR CIRCULATING BLOOD TO AND
FROM TISSUES AND LUNGS, THESE VARIOUS VESSELS
ARE MORE THAN JUST PASSIVE CONDUITS. IN FACT,
THEY REGULATE NOT ONLY THE AMOUNT OF BLOOD
FLOW PER MINUTE (CARDIAC OUTPUT) BUT ALSO ITS
BODILY DISTRIBUTION.
• THE ARTERIAL SYSTEM, WITH THEIR HIGH ELASTICITY,
THE LARGE ARTERIES HELP TRANSMIT AND MAINTAIN
THE HEAD OF PRESSURE GENERATED BY THE HEART.
TOGETHER THE LARGE ARTERIES ARE CALLED
CONDUCTANCE VESSELS. ARTERIOLES CONTROL
BLOOD FLOW INTO THE CAPILLARIES. ARTERIOLES
PROVIDE THIS CONTROL BY VARYING THEIR FLOW
RESISTANCE. FOR THIS REASON, ARTERIOLES ARE
OFTEN REFERRED TO AS RESISTANCE VESSELS.
THE VASCULAR SYSTEM
• SYSTEMIC VASCULATURE
• THE VAST CAPILLARY SYSTEM, OR MICROCIRCULATION,
MAINTAINS A CONSTANT ENVIRONMENT FOR THE BODY’S
CELLS AND TISSUES BY THE TRANSPORT AND
EXCHANGE OF NUTRIENTS AND WASTE PRODUCTS. FOR
THIS REASON, THE CAPILLARIES ARE COMMONLY
REFERRED TO AS EXCHANGE VESSELS.
• THE VENOUS SYSTEM, BESIDES CONDUCTING BLOOD
BACK TO THE HEART, THESE VESSELS ACT AS A
RESERVOIR FOR THE CIRCULATORY SYSTEM. AT ANY
GIVEN TIME THE VEINS AND VENULES HOLD
APPROXIMATELY THREE FOURTHS OF THE BODY’S
TOTAL BLOOD VOLUME. THE SMALL, EXPANDABLE
VENULES AND VEINS, ARE TERMED CAPACITANCE
VESSELS.
• AS PART OF THE CIRCULATION WITH THE LOWEST
PRESSURE, THE VENOUS SYSTEM MUST OVERCOME
GRAVITY TO RETURN BLOOD TO THE HEART.
THE VASCULAR SYSTEM
• SYSTEMIC VASCULATURE
• THE FOLLOWING FOUR MECHANISMS COMBINE TO AID
VENOUS RETURN TO THE HEART 1) SYMPATHETIC
VENOUS TONE 2) SKELETAL MUSCLE PUMPING, OR
“MILKING” 3)CARDIAC SUCTION 4)THORACIC PRESSURE
DIFFERENCES CAUSED BY RESPIRATORY EFFORTS.
• THORACIC PRESSURE DIFFERENCES IS OFTEN CALLED
THE THORACIC PUMP. THIS AID TO VENOUS RETURN IS
VERY IMPORTANT TO RESPIRATORY THERAPISTS,
BECAUSE ARTIFICIAL VENTILATION WITH POSITIVE
PRESSURE REVERSES NORMAL THORACIC PRESSURE
GRADIENTS. POSITIVE PRESSURE VENTILATION
IMPEDES, RATHER THAN ASSISTS, VENOUS RETURN.
FORTUNATELY, AS LONG AS BLOOD VOLUME, CARDIAC
FUNCTION, AND VASOMOTOR TONE ARE ADEQUATE, PPV
HAS A MINIMAL EFFECT ON VENOUS RETURN.
THE VASCULAR SYSTEM
• SYSTEMIC VASCULATURE
• THE HEART FUNCTIONS AS TWO
SEPARATE PUMPS. THE RIGHT SIDE
PROVIDES PRESSURES TO DRIVE
BLOOD THROUGH THE LOWRESISTANCE, LOW PRESSURE
PULMONARY CIRCULATION.
• THE LEFT SIDE OF THE HEART
GENERATES ENOUGH PRESSURE TO
PROPEL BLOOD THROUGH THE HIGHER
PRESSURE , HIGH RESISTANCE
SYSTEMIC CIRCULATION.
THE VASCULAR SYSTEM
• VASCULAR RESISTANCE
• LIKE THE MOVEMENT OF ANY FLUID THROUGH TUBES,
BLOOD FLOW THROUGH THE VASCULAR SYSTEM IS
OPPOSED BY FRICTIONAL FORCES. THE SUM OF ALL
FRICTIONAL FORCES OPPOSING BLOOD FLOW
THROUGH THE SYSTEMIC CIRCULATION IS CALLED
SYSTEMIC VASCULAR RESISTANCE (SVR). SVR MUST
EQUAL THE DIFFERENCES IN PRESSURE BETWEEN THE
BEGINNING AND THE END OF THE CIRCUIT, DIVIDED BY
THE FLOW.
SVR= MEAN AORTIC PRESSURE-RIGHT ATRIAL PRESSURE
CARDIAC OUTPUT
SVR= 90 MMHG – 4 MM HG = 17.2
5L/min
THE VASCULAR SYSTEM
• VASCULAR RESISTANCE
• THE SUM OF ALL FRICTIONAL FORCES OPPOSING BLOOD
FLOW THROUGH THE PULMONARY CIRCULATION IS CALLED
PULMONARY VASCULAR RESISTANCE (PVR). PVR MUST EQUAL
THE DIFFERENCES IN PRESSURE BETWEEN THE BEGINNING
AND THE END OF THE CIRCUIT, DIVIDED BY THE FLOW.
PVR= MEAN PULMONARY PRESSURE-LEFT ATRIAL PRESSURE
CARDIAC OUTPUT
PVR= 16 MMHG – 8 MM HG = 1.6
5L/min
THE VASCULAR SYSTEM
• DETERMINANTS OF BLOOD PRESSURE
• THE CARDIOVASCULAR SYSTEM MAINTAINS
SUFFICIENT PRESSURE TO PROPEL BLOOD
THROUGHOUT THE BODY. IN FACT, THE
CARDIOVASCULAR SYSTEM’S FIRST PRIORITY
IS TO KEEP PERFUSION PRESSURE NORMAL,
EVEN UNDER CHANGING CONDITIONS.
• MEAN ARTERIAL PRESSURE CAN BE
REGULATED BY THE FOLLOWING: 1) CHANGING
THE VOLUME OF THE CIRCULATING BLOOD
(SHOCK OR BLOOD TRANSFUSION) 2)
CHANGING THE CAPACITY OF THE VASCULAR
SYSTEM (VASOCONSTRICION OR
VASODILATION), 3) CHANGING BOTH.
THE VASCULAR SYSTEM
• DETERMINANTS OF BLOOD PRESSURE
• TO MAINTAIN ADEQUATE PERFUSION
PRESSURES UNDER CHANGING CONDITIONS,
THE CARDIOVASCULAR SYSTEM BALANCES
RELATIVE VOLUME AND RESISTANCE. IN
EXERCISE, THE CIRCULATING BLOOD VOLUME
UNDERGOES A RELATIVE INCREASE.
HOWEVER, BLOOD PRESSURE REMAINS NEAR
NORMAL. THIS IS BECAUSE THE SKELETAL
MUSCLE VASCULAR BEDS DILATE, CAUSING A
LARGE INCREASE IN SYSTEM CAPACITY.
• WHEN BLOOD LOSS OCCURS, AS WITH
HEMORRHAGE , SYSTEM CAPACITY IS
DECREASED BY CONSTRICTING THE VENOUS
VESSELS.
THE VASCULAR SYSTEM
• CONTROL OF THE CARDIOVASCULAR SYSTEM
• THE HEART AND THE VASCULAR SYSTEM
WORK IN COORDINATION IN ORDER TO
MAINTAIN ADEQUATE PERFUSION TO ALL
TISSUES ACCORDING TO THEIR NEEDS.
• THE HEART PLAYS ONLY A SECONDARY ROLE
IN REGULATING BLOOD FLOW. THE
CARDIOVASCULAR SYSTEM REGULATES
BLOOD FLOW MAINLY BY ALTERING THE
CAPACITY OF THE VASCULATURE AND THE
VOLUME OF BLOOD IT HOLDS.
• IN ESSENCE, THE CARDIOVASCULAR SYSTEM
TELLS THE HEART HOW MUCH BLOOD IT
NEEDS, RATHER THAN THE HEART DICTATING
WHAT VOLUME THE VASCULAR SYSTEM WILL
RECEIVE.
THE VASCULAR SYSTEM
• CONTROL OF THE CARDIOVASCULAR
SYSTEM
• TWO MECHANISMS REGULATE BLOOD
FLOW IN THE CARDIOVASCULAR
SYSTEM:
• LOCAL OR INTRINSIC CONTROL,
OPERATES INDEPENDENTLY WITHOUT
CENTRAL NERVOUS CONTROL. ALTERS
PERFUSION UNDER NORMAL
CONDITIONS.
• CENTRAL OR EXTRINSIC CONTROL,
INVOLVES BOTH THE CNS AND THE
CIRCULATING HUMORAL AGENTS.
MAINTAINS BASAL LEVEL OF VASCULAR
TONE.
THE VASCULAR SYSTEM
• CONTROL OF THE CARDIOVASCULAR SYSTEM
• A BASAL LEVEL OF VASCULAR MUSCLE TONE IS
NORMALLY MAINTAINED THROUGHOUT THE
VASCULAR SYSTEM AT ALL TIMES. IT MUST BE
PRESENT TO ALLOW EFFECTIVE REGULATION.
• LOCAL VASCULAR TONE IS MAINTAINED BY THE
SMOOTH MUSCLE OF THE PRECAPILLARY
SPHINCTERS OF THE MICROCIRCULATION.
• CENTRAL VASCULAR TONE IS MAINTAINED BY
THE CNS INNERVATION OR CIRCULATION
HORMONES. IT AFFECTS MAINLY THE HIGHRESISTANCE ARTERIOLES AND CAPACITANCE
VEINS.
THE VASCULAR SYSTEM
•
•
•
•
CONTROL OF THE CARDIOVASCULAR SYSTEM
LOCAL CONTROL.
INVOLVES BOTH MYOGENIC AND METABOLIC CONTROL.
MYOGENIC- IT IS THE RELATION BETWEEN VASCULAR
SMOOTH MUSCLE TONE AND PERFUSING PRESSURE.
*INCREASED PERFUSING PRESSURE, INCREASE IN
VASCULAR TONE AND VICE VERSA.
• METABOLIC-INVOLVES THE RELATIONSHIP BETWEEN
VASCULAR SMOOTH MUSCLE TONE AND THE LEVEL OF
LOCAL CELLULAR METABOLITES.( HIGH CO2,HIGH LACTIC
ACID, LOW pH, LOW PO2, HISTAMINES, ETC.) ALL CAUSE
RELAXATION OF THE SMOOTH MUSCLE, THEREBY
INCREASING FLOW TO THE AFFECTED AREA.
• THE INFLUENCE OF BOTH MECHANISMS VARIES IN
DIFFERENT ORGAN SYSTEMS ( BRAIN BEING THE MOST
SENSITIVE TO CHANGES IN CO2 AND pH)
THE VASCULAR SYSTEM
• CONTROL OF THE CARDIOVASCULAR SYSTEM
• CENTRAL CONTROL.
• INVOLVES MAINLY THE SYMPATHETIC DIVISION
OF THE ANS.
• THE BRAIN, SKELETAL MUSCLES AND SKIN ARE
REGULATED BY CENTRAL CONTROL.
• SMOOTH MUSCLE CONTRACTION AND
INCREASED FLOW RESISTANCE ARE MAINLY
CAUSED BY ADRENERGIC STIMULATION AND
THE RELEASE OF NOREPINEPHRINE.
• SMOOTH MUSCLE RELAXATION AND VESSEL
DILATION OCCUR AS A RESULT OF
STIMULATION OF EITHER CHOLINERGIC OR
SPECIALIZED ADRENERGIC BETA-RECEPTORS.
THE VASCULAR SYSTEM
• REGULATION OF CARDIAC OUTPUT
• THE HEART, LIKE THE VASCULAR SYSTEM IS REGULATED
BY BOTH INTRINSIC AND EXTRINSIC FACTORS. THESE
MECHANISMS ACT TOGETHER, ALONG WITH VASCULAR
CONTROL, TO ENSURE THAT THE HEART’S OUTPUT
MATCHES THE DIFFERENT NEEDS OF THE TISSUES.
•
CO = HR X SV
• REGARDLESS OF THE INDIVIDUAL’S STATE OF HEALTH
OR DISEASE, A CHANGE OF CO MUST INVOLVE A
CHANGE IN STROKE VOLUME, RATE OR BOTH.
• STROKE VOLUME IS AFFECTED MAINLY BY INTRINSIC
CONTROL OF THREE FACTORS: 1- PRELOAD
• 2- AFTERLOAD 3- CONTRACTILITY
• RATE IS AFFECTED PRIMARILY BY EXTRINSIC OR
CENTRAL, CONTROL MECHANISMS.
THE VASCULAR SYSTEM
• REGULATION OF CARDIAC OUTPUT
• STROKE VOLUME IS THE VOLUME OF
BLOOD EJECTED BY THE LEFT
VENTRICLE DURING EACH
CONTRACTION, OR SYSTOLE.
• THE HEART DOES NOT EJECT ALL THE
BLOOD IT CONTAINS DURING SYSTOLE.
INSTEAD, A SMALL VOLUME, CALLED
THE END-SYSTOLIC VOLUME (ESV),
REMAINS BEHIND IN THE VENTRICLE.
• DURING RESTING PHASE, OR DIASTOLE,
THE VENTRICLES FILL BACK UP TO A
VOLUME CALLED THE END-DIASTOLIC
VOLUME (EDV).
THE VASCULAR SYSTEM
• REGULATION OF CARDIAC OUTPUT
• STROKE VOLUME
• THE HEART ABILITY TO CHANGE STROKE
VOLUME SOLELY ACCORDING TO THE EDV IS
AN INTRINSIC REGULATORY MECHANISM
BASED ON THE FRANK-STARLING LAW.
BECAUSE THE EDV CORRESPONDS TO THE
INITIAL STRETCH, OR TENSION, PLACED ON
THE VENTRICLE, THE GREATER THE EDV( UP
TO A POINT) THE GREATER THE TENSION
DEVELOPED ON CONTRACTION AND VISE
VERSA.
• IN CLINICAL PRACTICE, THIS INITIAL
VENTRICULAR STRETCH IS CALLED PRELOAD,
WHILE THE TENSION OF CONTRACTION IS
EQUIVALENT TO STROKE VOLUME.
THE VASCULAR SYSTEM
• REGULATION OF CARDIAC OUTPUT
• STROKE VOLUME
• ANOTHER MAJOR FACTOR AFFECTING
STROKE VOLUME IS THE FORCE
AGAINST WHICH THE HEART MUST
PUMP, THIS IS CALLED AFTERLOAD. IN
CLINICAL PRACTICE, LEFT VENTRICULAR
AFTERLOAD EQUALS THE SVR. IN
OTHER WORDS THE GREATER THE
RESISTANCE TO BLOOD FLOW, THE
GREATER THE AFTERLOAD.
• NORMALLY, HOWEVER THE HEART
MUSCLE RESPONDS TO INCREASED
AFTERLOAD BY ALTERING ITS
CONTRACTILITY.
RULE OF THUMB
• INCREASES IN PRELOAD RESULT IN
INCREASED STROKE VOLUME IN
THE HEALTHY HEART.
• INCREASES IN AFTERLOAD CAN
DECREASE STROKE VOLUME,
ESPECIALLY IN THE FAILING HEART.
THE VASCULAR SYSTEM
• REGULATION OF CARDIAC OUTPUT
• CONTRACTILITY
• REPRESENTS THE AMOUNT OF SYSTOLIC FORCE
EXERTED BY THE HEART MUSCLE AT ANY GIVEN
PRELOAD.
• AT A GIVEN PRELOAD (EDV), AN INCREASE IN
CONTRACTILITY RESULTS IN A HIGHER EF, A LOWER ESV,
AND THUS A HIGHER STROKE VOLUME.
• HIGHER STROKE VOLUMES FOR A GIVEN PRELOAD
INDICATE A STATE OF INCREASED CONTRACTILITY,
OFTEN REFERRED TO AS POSITIVE
INOTROPISM.(SYMPATHETIC STIMULATION)
• LOWER STROKE VOLUMES FOR A GIVEN PRELOAD
INDICATE DECREASED CONTRACTILITY, REFERRED TO
AS NEGATIVE INOTROPISM.(PARASYMAPATHETIC
STIMULATION)
THE VASCULAR SYSTEM
• REGULATION OF CARDIAC OUTPUT
• CHANGES IN HEART RATE
• FACTORS AFFECTING HEART RATE ARE MAINLY
OF CENTRAL ORIGIN.
• CARDIAC OUTPUT RISES AND FALLS WITH LIKE
CHANGES IN HEART RATE. HOWEVER THIS
RELATIONSHIP IS MAINTAINED ONLY UP TO
APPROXIMATELY 160 TO 180 BEATS/min IN A
HEALTHY HEART. AT HIGHER HEART RATES,
THERE IS NOT ENOUGH TIME FOR THE
VENTRICLES TO FILL COMPLETELY. THIS
CAUSES DROP IN EDV, A DECREASE IN STROKE
VOLUME, AND A FALL IN CARDIAC OUTPUT.
• RULE OF THUMB- INCREASE HEART RATE WILL
INCREASE CO IN HEALTHY HEART UP TO A
RATE OF 160-180 BEATS/min.
The Vascular system
• CARDIOVASCULAR CONTROL MECHANISMS
• CARDIOVASCULAR CONTROL IS ACHIEVED BY
INTEGRATING LOCAL AND CENTRAL
REGULATORY MECHANISMS THAT AFFECT
BOTH THE HEART AND THE VASCULATURE.
• THE GOAL IS TO ENSURE THAT ALL TISSUES
RECEIVE SUFFICIENT BLOOD FLOW TO MEET
THEIR METABOLIC NEEDS.
• UNDER NORMAL RESTING CONDITIONS, THE
LOCAL REGULATION OF THE HEART AND THE
VASCULATURE ACHIEVES THE GOAL OF
SUFFICIENT BLOOD FLOW TO TISSUES.
• UNDER ABNORMAL CONDITIONS (EXERCISE OR
MASSIVE BLEEDING) CENTRAL MECHANISMS
TAKE OVER PRIMARY CONTROL.
THE VASCULAR SYSTEM
• CARDIOVASCULAR CONTROL CENTERS
• AREAS IN THE MEDULLA RECEIVE INPUT FORM HIGHER
BRAIN CENTERS, PERIPHERAL PRESSURE, AND
CHEMICAL RECEPTORS.
• STIMULATION OF THE VASOCONSTRICTOR AREA WITHIN
THE MEDULLA INCREASES OUTPUT TO ADRENERGIC
RECEPTORS IN THE VASCULAR SMOOTH MUSCLE,
CAUSING VASOCONSTRICTION AND INCREASED
VASCULAR RESISTANCE. A VASODEPRESSOR AREA
WORKS MAINLY BY INHIBITING THE VASOCONSTRICTOR
CENTER.
• STIMULATION OF THE CARDIOACCELERATOR AREA
INCREASES HEART RATE BY INCREASING SYMPATHETIC
DISCHARGE TO THE HEART’S SA AND AV NODES.
• STIMULATION OF THE CARDIOINHIBITORY AREA
DECREASES THE HEART RATE BY INCREASING VAGAL
(PARASYMPATHETIC) STIMULATION TO THE HEART.
THE VASCULAR SYSTEM
• CARDIOVASCULAR CONTROL CENTERS
• HIGHER BRAIN CENTERS ALSO INFLUENCE THE
CARDIOVASCULAR SYSTEM, BOTH DIRECTLY AND
THROUGH THE MEDULLA.
• THE CARDIOVASCULAR CENTERS ALSO ARE AFFECTED
BY LOCAL CHEMICAL CHANGES IN THE SURROUNDING
BLOOD AND CEREBRAL SPINAL FLUID. FOR EXAMPLE,
DECREASED LEVELS OF CARBON DIOXIDE TEND TO
INHIBIT THE MEDULLARY CENTERS. GENERAL INHIBITION
OF THESE CENTERS CAUSES A DECREASE IN VASCULAR
TONE AND THUS A FALL IN BLOOD PRESSURE.
A LOCAL DECREASE IN PO2 HAS THE OPPOSITE EFFECT.
MILD HYPOXIA IN THIS AREA TENDS TO ELEVATE BOTH
HEART RATE AND BLOOD PRESSURE.
THE VASCULAR SYSTEM
• PERIPHERAL RECEPTORS
• THERE ARE TWO TYPES OF PERIPHERAL
CARDIOVASCULAR RECEPTORS: (BARORECEPTORS AND
CHEMORECEPTORS)
• BARORECEPTORS- RESPOND TO PRESSURE CHANGES.
THE CARDIOVASCULAR SYSTEM HAS TWO DIFFERENT
SETS: 1- LOCATED IN THE AORTIC ARCH AND CAROTID
SINUSES. THESE RECEPTORS MONITOR ARTERIAL
PRESSURES GENERATED BY THE LEFT VENTRICLE. 2LOCATED IN THE WALLS OF THE ATRIA AND THE LARGE
THORACIC AND PULMONARY VEINS. THESE LOW
PRESSURE SENSORS RESPOND MAINLY TO CHANGES IN
VASCULAR VOLUMES.
• TOGETHER WITH THE CARDIOVASCULAR REGULATORY
CENTERS, THESE RECEPTORS FORM A NEGATIVE
FEEDBACK LOOP. IN A NEGATIVE FEEDBACK LOOP,
STIMULATION OF A RECEPTOR CAUSES AN OPPOSITE
RESPONSE BY THE EFFECTOR.
THE VASCULAR SYSTEM
• PERIPHERAL RECEPTORS
• CHEMORECEPTORS- RESPOND TO CHANGES
IN BLOOD CHEMISTRY. THESE ARE SMALL,
HIGHLY VASCULARIZED TISSUES LOCATED
NEAR THE HIGH-PRESSURE SENSORS IN THE
AORTIC ARCH AND CAROTID SINUS. THEY ARE
STRONGLY STIMULATED BY DECREASED
OXYGEN TENSIONS, ALTHOUGH LOW PH OR
HIGH LEVELS OF CARBON DIOXIDE ALSO CAN
INCREASE THEIR DISCHARGE RATE. THE
MAJOR CARDIOVASCULAR EFFECTS OF
CHEMORECEPTOR STIMULATION ARE
VASOCONSTRICTION AND INCREASED HEART
RATE.