FUNCTIONAL ANATOMY OF THE

CARDIOVASCULAR SYSTEM

CHAPTER 14DR. 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 LOW-RESISTANCE, 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 HIGH-RESISTANCE 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 INCREASED PERFUSING PRESSURE, INCREASE IN

VASCULAR TONE AND VICE VERSA.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. 2- LOCATED 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.