Cardiovascular System

FAKULTAS FARMASI UAD YOGYAKARTA

CIRCULATORY SYSTEM

BLOOD HEART BLOOD VESSELS

CIRCULATORY SYSTEM
BLOOD VESSELS

The Blood Vessels

The cardiovascular system has three types of blood vessels: Arteries (and arterioles) carry blood away from the heart Capillaries where nutrient and gas exchange occur Veins (and venules) carry blood toward the heart.

Blood vessels

BLOOD VESSELS

ARTERIES

CARRY BLOOD FROM THE HEART ARTERY ARTERIOLES CAPILLARIES SITE OF GAS AND NUTRIENT EXCHANGE RETURN BLOOD TO THE HEART CAPILLARIES VENULES VEINS

CAPILLARIES

VEINS

The Arteries

away from the heart. The largest artery is the aorta. The middle layer of an artery wall consists of smooth muscle that can constrict to regulate blood flow and blood pressure. Arterioles can constrict or dilate, changing blood pressure.

Arteries and arterioles take blood

The Veins

blood to the heart. Veins have much less smooth muscle and connective tissue than arteries. Veins often have valves that prevent the backward flow of blood when closed. Veins carry about 70% of the bodys blood and act as a reservoir during hemorrhage.

Venules drain blood from capillaries, then join to form veins that take

ARTERY AND VEIN WALLS

THREE LAYERS (TUNICS)

TUNICA EXTERNA (OUTERMOST) TUNICA MEDIA TUNICA INTERNA (INNERMOST)

ARTERY AND VEIN WALLS

TUNICA EXTERNA OUTERMOST LAYER LOOSE CONNECTIVE TISSUE

MERGES WITH ADJACENT CONNECTIVE TISSUES

ANCHORS VESSEL PASSAGE FOR NERVES, BLOOD & LYMPH VESSELS

ARTERY AND VEIN WALLS

TUNICA EXTERNA NOURISHMENT

OUTER HALF NOURISHED BY SMALL BLOOD VESSELS (VASA VASORUM) INNER HALF NOURISHED BY DIFFUSION FROM BLOOD IN LUMEN

ARTERY AND VEIN WALLS

TUNICA MEDIA MIDDLE LAYER GENERALLY THE THICKEST LAYER SMOOTH MUSCLE

VASOCONSTRICTION & VASODILATION

COLLAGEN SOMETIMES ELASTIC TISSUE

ARTERY AND VEIN WALLS

TUNICA INTERNA SMOOTH INNER LAYER EXPOSED TO BLOOD SQUAMOUS ENDOTHELIUM (EPI) BASEMENT MEMBRANE FIBROUS TISSUE

ARTERY AND VEIN WALLS

TUNICA INTERNA REPELS BLOOD CELLS (& PLATELETS) SELECTIVELY PERMEABLE BARRIER TO BLOOD SOLUTES SECRETES VASOCONSTRICTORS & VASODILATORS

ARTERIES

MUST WITHSTAND PRESSURE MORE MUSCULAR THAN VEINS ROUND IN CROSS SECTION THREE SIZE CATEGORIES

CONDUCTING (ELASTIC) ARTERIES DISTRIBUTING (MUSCULAR) ARTERIES RESISTANCE (SMALL) ARTERIES

ARTERIES
CONDUCTING (ELASTIC) ARTERIES LARGEST ARTERIES E.G., AORTA, PULMONARY ARTERIES TUNICA MEDIA

NUMEROUS ALTERNATING THIN LAYERS OF

PERFORATED ELASTIC TISSUE SMOOTH MUSCLE, COLLAGEN, AND ELASTIC FIBERS

EXPAND DURING SYSTOLE RECOIL DURING DIASTOLE

MINIMIZES DOWNSTREAM PRESSURE FLUCTUATIONS

ARTERIES
DISTRIBUTING (ELASTIC) ARTERIES SMALLER BRANCHES E.G., BRACHIAL & FEMORAL ARTERIES FURTHER FROM THE HEART 25 40 SMOOTH MUSCLE LAYERS

75% OF WALL THICKNESS

ARTERIES
RESISTANCE (SMALL) ARTERIES MAINLY UNNAMED UP TO 25 SMOOTH MUSCLE LAYERS LITTLE ELASTIC TISSUE SMALLEST ARE ARTERIOLES

1-3 LAYERS OF SMOOTH MUSCLES 40 200 mM DIAMETER

ARTERIES
METARTERIOLES SHORT VESSELS LINKING ARTERIOLES AND CAPILLARIES TUNICA MEDIA DISCONTINUOUS

MUSCLE CELLS FORM PRECAPILLARY SPHINCTER

ENCIRCLES CAPILLARY ENTRANCE REGULATES MOVEMENT OF BLOOD INTO CAPILLARIES

The Capillaries

Capillaries have walls only one cell thick to

allow exchange of gases and nutrients with tissue fluid. Capillary beds are present in all regions of the body but not all capillary beds are open at the same time. Contraction of a sphincter muscle closes off a bed and blood can flow through an arteriovenous shunt that bypasses the capillary bed.

CAPILLARIES

CENTRAL TO CIRCULATORY SYSTEM SITE OF EXCHANGE BETWEEN BLOOD AND TISSUES SMALLEST BLOOD VESSELS ENDOTHELIUM ONLY THIN WALLS (0.2 mM 0.4 mM) 5 9 mM DIAMETER (AVERAGE)

CAPILLARY STRUCTURE

~ BILLION IN BODY HUGE COLLECTIVE SURFACE AREA 6,300 SQUARE METERS (M2) > SIZE OF FOOTBALL FIELD < 80 mM FROM ALMOST ALL CELLS

SOME EXCEPTIONS E.G., TENDONS, LIGAMENTS, ETC.

ORGANIZED INTO CAPILLARY BEDS

CAPILLARY BEDS

UNIT OF CAPILLARY ORGANIZATION 10 100 CAPILLARIES SUPPLIED BY SINGLE METARTERIOLE THOROUGHFARE CHANNEL

ARTERIOLE VENULE

PRECAPILLARY SPHINCTER AT ENTRANCE TO EACH CAPILLARY

OPENED OR CLOSED

Anatomy of a capillary bed

CAPILLARY BEDS

BLOOD VOLUME THERE IS NOT ENOUGH BLOOD TO FILL ALL BLOOD VESSELS SIMULTANEOUSLY ~75% OF THE BODYS CAPILLARIES ARE CLOSED AT ANY GIVEN TIME

TYPES OF CAPILLARIES
TWO TYPES OF CAPILLARIES CONTINUOUS CAPILLARIES FENESTRATED CAPILLARIES

TYPES OF CAPILLARIES
CONTINUOUS CAPILLARIES OCCUR IN MOST TISSUES ENDOTHELIAL CELLS HELD TOGETHER BY TIGHT JUNCTIONS FORM CONTINUOUS TUBE INTERCELLULAR CLEFTS 4 nm WIDE

GLUCOSE, ETC. CAN PASS THROUGH PLASMA PROTEINS, ETC. CANNOT

TYPES OF CAPILLARIES
FENESTRATED CAPILLARIES ALLOW RAPID ABSORPTION / FILTRATION KIDNEYS, SMALL INTESTINE, ETC. RIDDLED WITH HOLES

FENESTRATIONS / FILTRATION PORES 20 100 nm DIAMETER USUALLY COVERED WITH DIAPHRAGM RAPID PASSAGE OF SMALL MOLECULES

CIS dan CES

TYPES OF CAPILLARIES
SINUSOIDS IRREGULAR BLOOD-FILLED SPACES BONE MARROW, SPLEEN, ETC. SOME ARE CONTINUOUS CAPILLARIES SOME ARE FENESTRATED CAPILLARIES

LARGE PORES PROTEINS AND BLOOD CELLS CAN PASS THROUGH ALBUMIN, CLOTTING FACTORS, RBCs, ETC.

CAPILLARY EXCHANGE
CAPILLARIES SITES OF EXCHANGE BETWEEN BLOOD AND SURROUNDING TISSUES ROUTES OF EXCHANGE

PASSAGE THROUGH FENESTRATIONS PASSAGE THROUGH INTERCELLULAR CLEFTS PASAGE THROUGH ENDOTHELIAL CELL CYTOPLASM

CAPILLARY EXCHANGE

MECHANISMS OF EXCHANGE

DIFFUSION TRANSCYTOSIS FILTRATION REABSORPTION

CAPILLARY EXCHANGE
DIFFUSION MOST IMPORTANT MECHANISM MOVEMENT DOWN CONC GRADIENT IMPORTANT FOR

O2, CO2, STEROID HORMONES

THROUGH PLASMA MEMBRANE

GLUCOSE, ELECTROLYTES, ETC.

THROUGH CHANNELS / CLEFTS / FENESTRATIONS

NOT IMPORTANT FOR

PROTEINS, ETC. (TOO BIG)

CAPILLARY EXCHANGE
TRANSCYTOSIS MOVEMENT THROUGH EPITHELIAL CELLS ENDOCYTOSIS, THEN EXOCYTOSIS IMPORTANT FOR

FATTY ACIDS ALBUMIN SOME HORMONES (E.G., INSULIN)

CAPILLARY EXCHANGE
FILTRATION CAPILLARY PRESSURE

~30 mmHg AT ARTERIAL END ~-3 mmHg

TISSUE PRESSURE

FLUID LEAVES AT ARTERIAL END REDUCED, BUT NOT PREVENTED BY ONCOTIC PRESSURE

CAPILLARY EXCHANGE

ONCOTIC PRESSURE

TISSUE FLUID HAS FEWER SOLUTES THAN BLOOD OSMOTIC FORCE PUSHING FLUID INTO CAPILLARIES CANNOT OVERCOME PRESSURE DIFFERENCES AT ARTERIAL END OF CAP. CAN OVERCOME PRESSURE DIFFERENCES AT VENOUS END OF CAPILLARIES

CAPILLARY EXCHANGE
REABSORPTION CAPILLARY PRESSURE

~ 10 mmHg AT VENOUS END ~-3 mmHg

TISSUE PRESSURE

ONCOTIC PRESSURE OVERWHELMS PRESSURE DIFFERENCE FLUID ENTERS AT VENOUS END

CAPILLARY EXCHANGE
FILTRATION AND REABSORPTION FLUID LEAVES CAPILLARY AT ARTERIAL END ~85% OF FLUID REENTERS CAPILLARY AT VENOUS END

CAPILLARIES ARE LARGER AND MORE NUMEROUS AT VENOUS END

~15% REENTERS RETURNED VIA LYMPHATIC SYSTEM

CAPILLARY EXCHANGE
EDEMA EXCESS FLUID IN A TISSUE ACCUMULATION CAUSED BY

INCREASED CAPILLARY FILTRATION REDUCED CAPILLARY REABSORPTION OBSTRUCTED LYMPHATIC DRAINAGE

CAPILLARY EXCHANGE
CAUSES OF EDEMA INCREASED CAPILLARY FILTRATION CAUSES (E.G.)

INCREASED CAPILLARY B.P. INCREASED CAPILLARY PERMEABILITY CONGESTIVE HEART FAILURE POOR VENOUS RETURN INSUFFICIENT MUSCULAR ACTIVITY KIDNEY FAILURE HYPERTENSION

CAPILLARY EXCHANGE
CAUSES OF EDEMA REDUCED CAPILLARY REABSORPTION CAUSES (E.G.)

BLOOD ALBUMIN DEFICIENCY

REDUCED ONCOTIC PRESSURE

LIVER DISEASES (LESS ALBUMIN) HYPOPROTEINEMIA (LESS ALBUMIN)

CAPILLARY EXCHANGE
CAUSES OF EDEMA OBSTRUCTED LYMPHATIC DRAINAGE

~15% OF FLUID LOST IS RETURNED VIA LYMPHATIC SYSTEM OBSTRUCTION OR REMOVAL INTERFERES WITH THIS RETURN

VEINS

CAPILLARIES VENULES VEINS RETURN BLOOD TO THE HEART FURTHER FROM THE HEART LOWER BLOOD PRESSURE THAN ARTERIES

AVERAGE 10 mmHg VS. 100 mmHg

NEED NOT WITHSTAND HIGH PRESSURES

VEINS

THINNER WALLS

LESS SMOOTH MUSCLE LESS ELASTIC TISSUE

COLLAPSE WHEN EMPTY EXPAND MORE EASILY PRESSURE NOT HIGH ENOUGH TO RETURN BLOOD TO HEART VENOUS VALVES AND MASSAGING ASSIST RETURN

VEINS
VENULES 15 100 mM DIAMETER PROXIMAL END POROUS

FLUID EXCHANGE WITH TISSUES

GAINS TUNICA MEDIA SMOOTH MUSCLE SPARSE TRIBUTARIES VEINS

VEINS
VENOUS SINUSES ESPECIALLY THIN WALLS LARGE LUMENS NO SMOOTH MUSCLE E.G., CORONARY SINUS OF THE HEART

VENOUS RETURN

FLOW OF BLOOD BACK TO THE HEART MECHANISMS OF VENOUS RETURN

PRESSURE GRADIENT THORACIC (RESPIRATORY) PUMP CARDIAC SUCTION SKELETAL MUSCLE PUMP GRAVITY

VENOUS RETURN
PRESSURE GRADIENT MOST IMPORTANT FORCE IN VENOUS RETURN VENULE PRESSURE ~15 mmHg VENA CAVAE PRESSURE ~ 4.6 mmHg BLOOD FLOW TO THE HEART FAVORED BY DP

VENOUS RETURN
THORACIC (RESPIRATORY) PUMP INFERIOR VENA CAVA SPANS ABDOMINAL AND THORACIC CAVITIES DURING INHALATION

THORACIC PRESSURE DROPS ABDOMINAL PRESSURE INCREASES FLOW OF BLOOD FROM ABDOMINAL TO THORACIC CAVITY PROMOTED

VENOUS RETURN
CARDIAC SUCTION DURING VENTRICULAR SYSTOLE

CHORDAE TENDINEAE PULL AV VALVE CUSPS TOWARD VENTRICLES ATRIAL SPACE SLIGHTLY INCREASED BLOOD DRAWN INTO ATRIA

VENOUS RETURN
SKELETAL MUSCLE PUMP VEINS SURROUNDED AND SQUEEZED BY SKELETAL MUSCLES BLOOD SQUEEZED OUT VALVES

SIMILAR TO SEMILUNAR VALVES INSURE UNIDIRECTIONAL FLOW

VENOUS RETURN
GRAVITY BLOOD IN HEAD AND NECK SIMPLY FLOWS DOWNHILL

VENOUS RETURN
EFFECTS OF EXERCISE INCREASED CARDIAC OUTPUT

INCREASED BLOOD PRESSURE INCREASED FLOW RATE

BLOOD VESSEL DILATION

INCREASED RESPIRATORY RATE

ENHANCED THORACIC PUMP

ENHANCED SKELETAL MUSCLE PUMP

MUSCLE CONTRACTIONS

CIRCULATORY ROUTES

HEART ARTERIES ARTERIOLES METARTERIOLES CAPILLARIES METARTERIOLES VENULES VEINS HEART

CIRCULATORY ROUTES

TYPICAL CIRCULATORY ROUTE

HEART ARTERIES ARTERIOLES CAPILLARIES CAPILLARIES VENULES VEINS HEART

USUALLY PASSES THROUGH SINGLE CAPILLARY BED

EXCEPTIONS?

CIRCULATORY ROUTES
PORTAL SYSTEM BLOOD FLOWS THROUGH TWO CONSECUTIVE CAPILLARY BEDS E.G. KIDNEYS

CIRCULATORY ROUTES
ANASTOMOSIS TWO VESSELS (VEINS OR ARTERIES) MERGE WITH EACH OTHER

ARTERIOVENOUS ANASTOMOSIS ARTERIAL ANASTOMOSIS VENOUS ANASTOMOSIS

CIRCULATORY ROUTES
ARTERIOVENOUS ANASTOMOSIS SHUNT ARTERY VEIN BYPASSES CAPILLARIES E.G. FINGERS, TOES, EARS, ETC. REDUCE HEAT LOSS MORE SUSCEPTIBLE TO FROSTBITE

CIRCULATORY ROUTES
ARTERIAL ANASTOMOSIS TWO ARTERIES MERGE PROVIDE ALTERNATIVE ROUTES OF BLOOD SUPPLY TO A TISSUE E.G. CORONARY CIRCULATION, AROUND JOINTS

CIRCULATORY ROUTES
VENOUS ANASTOMOSIS TWO VEINS MERGE MORE COMMON ALTERNATIVE ROUTS OF DRAINAGE FROM AN ORGAN

Cardiovascular system diagram

The Pulmonary Circuit

The pulmonary circuit begins with the pulmonary trunk from the right ventricle which branches into two pulmonary arteries that take oxygen-poor blood to the lungs. In the lungs, oxygen diffuses into the blood, and carbon dioxide diffuses out of the blood to be expelled by the lungs. Four pulmonary veins return oxygenrich blood to the left atrium.

The Systemic Circuit

The systemic circuit starts with the aorta carrying O2-rich blood from the left ventricle. The aorta branches with an artery going to each specific organ. Generally, an artery divides into arterioles and capillaries which then lead to venules.

The vein that takes blood to the vena cava often has the same name as the artery that delivered blood to the organ. In the adult systemic circuit, arteries carry blood that is relatively high in oxygen and relatively low in carbon dioxide, and veins carry blood that is relatively low in oxygen and relatively high in carbon dioxide. This is the reverse of the pulmonary circuit.

Major arteries and veins of the systemic circuit

The coronary arteries serve the heart muscle itself; they are the first branch off the aorta. Since the coronary arteries are so small, they are easily clogged, leading to heart disease. The hepatic portal system carries blood rich in nutrients from digestion in the small intestine to the liver, the organ that monitors the composition of the blood.

The Heart
The heart is a cone-shaped, muscular organ located between the lungs behind the sternum. The heart muscle forms the myocardium, with tightly interconnect cells of cardiac muscle tissue. The pericardium is the outer membranous sac with lubricating fluid.

The heart has four chambers: two upper, thin-walled atria, and two lower, thickwalled ventricles. The septum is a wall dividing the right and left sides. Atrioventricular valves occur between the atria and ventricles the tricuspid valve on the right and the bicuspid valve on the left; both valves are reenforced by chordae tendinae attached to muscular projections within the ventricles.

External heart anatomy

Coronary artery circulation

Passage of Blood Through the Heart

Blood follows this sequence through the heart: superior and inferior vena cava right atrium tricuspid valve right ventricle pulmonary semilunar valve pulmonary trunk and arteries to the lungs pulmonary veins leaving the lungs left atrium bicuspid valve left ventricle aortic semilunar valve aorta to the body.

Internal view of the heart

The pumping of the heart sends out blood under pressure to the arteries. Blood pressure is greatest in the aorta; the wall of the left ventricle is thicker than that of the right ventricle and pumps blood to the entire body. Blood pressure then decreases as the cross-sectional area of arteries and then arterioles increases.

Path of blood through the heart

The Heartbeat

Each heartbeat is called a cardiac cycle. When the heart beats, the two atria contract together, then the two ventricles contract; then the whole heart relaxes. Systole is the contraction of heart chambers; diastole is their relaxation. The heart sounds, lub-dup, are due to the closing of the atrioventricular valves, followed by the closing of the semilunar valves.

Intrinsic Control of Heartbeat

The SA (sinoatrial) node, or pacemaker, initiates the heartbeat and causes the atria to contract on average every 0.85 seconds. The AV (atrioventricular) node conveys the stimulus and initiates contraction of the ventricles. The signal for the ventricles to contract travels from the AV node through the atrioventricular bundle to the smaller Purkinje fibers.

Conduction system of the heart

Extrinsic Control of Heartbeat

A cardiac control center in the medulla oblongata speeds up or slows down the heart rate by way of the autonomic nervous system branches: parasympathetic system (slows heart rate) and the sympathetic system (increases heart rate). Hormones epinephrine and norepinephrine from the adrenal medulla also stimulate faster heart rate.

The Heart
The heart is a cone-shaped, muscular organ located between the lungs behind the sternum. The heart muscle forms the myocardium, with tightly interconnect cells of cardiac muscle tissue. The pericardium is the outer membranous sac with lubricating fluid.

The heart has four chambers: two upper, thin-walled atria, and two lower, thickwalled ventricles. The septum is a wall dividing the right and left sides. Atrioventricular valves occur between the atria and ventricles the tricuspid valve on the right and the bicuspid valve on the left; both valves are reenforced by chordae tendinae attached to muscular projections within the ventricles.

External heart anatomy

Coronary artery circulation

Passage of Blood Through the Heart

Blood follows this sequence through the heart: superior and inferior vena cava right atrium tricuspid valve right ventricle pulmonary semilunar valve pulmonary trunk and arteries to the lungs pulmonary veins leaving the lungs left atrium bicuspid valve left ventricle aortic semilunar valve aorta to the body.

Internal view of the heart

The pumping of the heart sends out blood under pressure to the arteries. Blood pressure is greatest in the aorta; the wall of the left ventricle is thicker than that of the right ventricle and pumps blood to the entire body. Blood pressure then decreases as the cross-sectional area of arteries and then arterioles increases.

Path of blood through the heart

The Heartbeat

Each heartbeat is called a cardiac cycle. When the heart beats, the two atria contract together, then the two ventricles contract; then the whole heart relaxes. Systole is the contraction of heart chambers; diastole is their relaxation. The heart sounds, lub-dup, are due to the closing of the atrioventricular valves, followed by the closing of the semilunar valves.

Intrinsic Control of Heartbeat

The SA (sinoatrial) node, or pacemaker, initiates the heartbeat and causes the atria to contract on average every 0.85 seconds. The AV (atrioventricular) node conveys the stimulus and initiates contraction of the ventricles. The signal for the ventricles to contract travels from the AV node through the atrioventricular bundle to the smaller Purkinje fibers.

Conduction system of the heart

Extrinsic Control of Heartbeat

A cardiac control center in the medulla oblongata speeds up or slows down the heart rate by way of the autonomic nervous system branches: parasympathetic system (slows heart rate) and the sympathetic system (increases heart rate). Hormones epinephrine and norepinephrine from the adrenal medulla also stimulate faster heart rate.

HEART VALVES
ATRIOVENTRICULAR (AV) VALVES ATRIUM VENTRICLE VENTRICLE RELAXED

VALVE OPEN ATRIUM VENTRICLE BLOOD FLOW VENTRICLE PRESSURE INCREASES VALVE CLOSES PREVENTS BACK FLOW

VENTRICLE CONTRACTS

HEART VALVES
ATRIOVENTRICULAR (AV) VALVES PAPILLARY MUSCLES

CONTRACT WITH REST OF VENTRICLE PULL ON CHORDAE TENDINEAE CONNECT AV VALVE CUSPS TO PAPILLARY MUSCLES OF REINFORCE AV VALVES PREVENT PROLAPSE

CHORDAE TENDINEAE

HEART VALVES
SEMILUNAR VALVES VENTRICLE ARTERY VENTRICLE RELAXED

PRESSURE HIGHER IN ARTERIES VALVE CLOSED PRESSURE HIGHER IN VENTRICLE VALVES FORCED OPEN BLOOD FLOWS FROM HEART

VENTRICLE CONTRACTS

HEART STRUCTURE
PERICARDIUM DOUBLE-WALLED SAC ENCLOSES HEART CONTAINS PERICARDIAL FLUID (5-30 ML) GREATLY REDUCES FRICTION

HEART STRUCTURE
HEART WALL EPICARDIUM (OUTER)

A.K.A. VISCERAL PERICARDIUM THICKEST LAYER CARDIAC MUSCLE SMOOTH INNER LINING CONTINUOUS WITH BLOOD VESSELS

MYOCARDIUM

ENDOCARDIUM

HEART STRUCTURE
MYOCARDIUM THICKEST; CARDIAC MUSCLE MUSCLE FIBERS CONNECTED BY FIBROUS (PROTEIN) SKELETON

STRUCTURAL SUPPORT SOMETHING TO PULL AGAINST ELECTRICAL NONCONDUCTOR

ALLOWS ATRIA AND VENTRICLES TO CONTRACT SEPARATELY

CARDIAC MUSCLE STRUCTURE

CARDIAC MUSCLE CELLS MYOCYTES / CARDIOCYTES

STRIATED SHORT, THICK (50 100 mM x 10 - 20 mM) BRANCHED SINGLE NUCLEUS LESS DEVELOPED SR (SER) LARGER T-TUBULES (ADMIT Ca++) JOINED VIA INTERCALATED DISKS

CARDIAC MUSCLE STRUCTURE

INTERCALATED DISK FEATURES INTERDIGITATING FOLDS

INCREASED SURFACE AREA CONTACT FASCIA ADHERENS (ACTIN) DESMOSOMES GAP JUNCTIONS ELECTRICALLY STIMULATE NEIGHBORS

MECHANICAL JUNCTIONS

ELECTRICAL JUNCTIONS

CARDIAC METABOLISM

EXCLUSIVELY AEROBIC MYOGLOBIN-RICH (STORED O2) GLYCOGEN-RICH (STORED SUGAR) LARGE MITOCHONDRIA (25% VS 2%) MULTIPLE FUELS USABLE VULNERABLE TO O2 DEFICIENCY NOT PRONE TO FATIGUE

(AEROBIC, NO O2 DEBT, NO FATIGUE)

GBR SISTEM KONDUKSI

Sistem konduksi

MEKANISME POMPA JANTUNG

CARDIAC RHYTHM
HEARTBEAT INVERTEBRATES

TRIGGERED BY NERVOUS SYTEM TRIGGERED BY HEART ITSELF

VERTEBRATES

CARDIAC RHYTHM
CARDIAC MYOCYTES AUTORHYTHMIC

SPONTANEOUS DEPOLARIZATION AT REGULAR INTERVALS

SOME SPECIALIZED TO GENERATE ACTION POTENTIALS

CARDIAC CONDUCTION SYSTEM SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE

CARDIAC RHYTHYM
SINOATRIAL (SA) NODE MYOCYTES IN RIGHT ATRIUM PACEMAKER INITIATES HEARTBEAT DETERMINES HEART RATE FIRING RATE REDUCED BY NERVES 70 80 BEATS PER MINUTE (BPM)

CARDIAC RHYTHYM
SINOATRIAL (SA) NODE CELLS LACK STABLE RESTING MEMBRANE POTENTIAL SPONTANEOUSLY DEPOLARIZE AND REPOLARIZE AT REGULAR INTERVALS (~0.8 SEC) EACH DEPOLARIZATION INITIATES ONE HEARTBEAT GENERATE ACTION POTENTIAL

CARDIAC RHYTHYM
SA ACTION POTENTIAL SPREADS THROUGHOUT ATRIAL MYOCARDIUM ATRIA CONTRACT ~SIMULTANEOUSLY SIGNAL REACHES AV NODE (50MSEC) DELAYED AT AV NODE (100 MSEC) VENTRICLES FILL DURING DELAY

CARDIAC RHYTHYM
ATRIOVENTRICULAR (AV) NODE NEAR RIGHT AV VALVE ELECTRICAL GATEWAY TO VENTRICLES DISTRIBUTES SIGNAL TO VENTRICULAR MYOCARDIUM

AV BUNDLE PURKINJE FIBERS

CARDIAC RHYTHYM

SIGNAL TRAVELS FROM AV THROUGH VENTRICULAR MYOCARDIUM VENTRICULES CONTRACT ~SIMULTANEOUSLY (PAPILLARY MUSCLES CONTRACT FIRST)

CARDIAC RHYTHYM
CARDIAC ACTION POTENTIALS PROLONGED DEPOLARIZATION

200 - 250 MSEC VS. 2 MSEC RESULT OF SLOW Ca++ CHANNELS

SUSTAINED CONTRACTION LONGER REFRACTORY PERIOD

200 MSEC VS. 1 2 MSEC PREVENTS WAVE SUMMATION, TETANUS

SYSTOLE / DIASTOLE

SYSTOLE

CONTRACTION OF A HEART CHAMBER REFERS TO VENTRICLE UNLESS OTHERWISE NOTED PERIOD DURING WHICH A HEART CHAMBER RELAXES AND FILLS WITH BLOOD

DIASTOLE

HUKUM FRANK STARLING

BLOOD FLOW

AMOUNT OF BLOOD FLOWING THROUGH A TISSUE/ORGAN/VESSEL IN A GIVEN TIME

E.G., ML/MIN

SUPPLIES NUTRIENTS AND OXYGEN TO CELLS REMOVES WASTES FROM CELLS

BLOOD FLOW
PERFUSION RATE OF BLOOD FLOW PER GIVEN MASS/VOLUME OF TISSUE

E.G., ML/MIN/G

BLOOD FLOW

MUST KEEP PACE WITH METABOLIC RATE OF CELLS

NECROSIS (TISSUE DEATH)

TOTAL FLOW CONSTANT IN RESTING INDIVIDUAL

EQUAL TO CARDIAC OUTPUT

FLOW TO INDIVIDUAL ORGANS VARIES CONTINUALLY

BLOOD FLOW
HEMODYNAMICS PHYSICAL PRINCIPLES OF BLOOD FLOW BASED UPON

PRESSURE DIFFERENCES (DP)

INCREASED PRESSURE DIFFERENCE INCREASED FLOW INCREASED RESISTANCE DECREASED FLOW

RESISTANCE (R)

BLOOD PRESSURE

EASILY MEASURED SYSTOLIC PRESSURE

PEAK PRESSURE DURING SYSTOLE PRESSURE DURING DIASTOLE SYSTOLIC MINUS DIASTOLIC MEASURE OF STRESS ON ARTERIES

DIASTOLIC PRESSURE

PULSE PRESSURE

BLOOD PRESSURE
MEAN ARTERIAL PRESSURE (MAP) AVERAGE OF CONTINUOUS READINGS ESTIMATE

DIASTOLIC + 1/3 PULSE PRESSURE

AFFECTED BY GRAVITY

~62 mmHg IN HEAD ~180 mmHg IN ANKLES

BLOOD PRESSURE

HYPERTENSION

CHRONIC RESTING BP > 140/90

CHRONIC, NOT TRANSIENT

CAN WEAKEN SMALL ARTERIES ANEURYSMS CHRONIC LOW RESTING BP RESULT OF ANEMIA, BLOOD LOSS, DEHYDRATION, ETC.

HYPOTENSION

BLOOD PRESSURE
ANEURYSM WEAK POINT IN BLOOD VESSEL PULSATES, MAY RUPTURE

PAIN, DEATH
CONGENITAL WEAKNESS TRAUMA INFECTIONS (E.G., SYPHILIS) ATHEROSCLEROSIS AND HYPERTENSION

RESULT FROM

BLOOD PRESSURE

ARTERIES DISTEND AND RECOIL

ABSORB SOME OF THE FORCE OF THE EJECTED BLOOD REDUCE PRESSURE FLUCTUATIONS MAINTAIN STEADY BLOOD FLOW CONTINUOUS, YET PULSATILE
AORTA 120 CM/SEC SYSTOLE AORTA 40 CM/SEC DIASTOLE

DOWNSTREAM B.P. & PRESSURE FLUCTUATIONS REDUCED

BLOOD PRESSURE
EFFECTS OF AGING INCREASE IN BLOOD PRESSURE ARTERIES LESS DISTENDIBLE ATHEROSCLEROSIS STIFFENS ARTERIES

RESISTANCE
PERIPHERAL RESISTANCE RESISTANCE BLOOD ENCOUNTERS IN THE VESSELS RESULTS FROM FRICTION AGAINST VESSEL WALLS PROPORTIONAL TO THREE VARIABLES

BLOOD VISCOSITY VESSEL LENGTH VESSEL RADIUS

RESISTANCE
VARIABLES AFFECTING RESISTANCE BLOOD VISCOSITY

MAINLY DUE TO ERYTHROCYTES AND PLASMA PROTEINS INCR VISCOSITY INCR RESISTANCE

RESISTANCE
VARIABLES AFFECTING RESISTANCE VESSEL LENGTH

FRICTION IS CUMULATIVE INCR LENGTH INCR RESISTANCE

RESISTANCE
VARIABLES AFFECTING RESISTANCE VESSEL RADIUS

INNATE RADIUS DIFFERENCES ALTERATIONS POSSIBLE

VASOCONSTRICTION (NARROWING) VASODILATION (WIDENING)

INCREASED FRICTION NEAR VESSEL WALL DECR RADIUS INCR RESISTANCE

RESISTANCE
LAMINAR FLOW BLOOD TRAVELS IN SHEETS FASTER NEAR CENTER OF VESSEL

LESS FRICTION

SLOWER NEAR VESSEL WALLS

MORE FRICTION

SIMILAR TO WATER FLOW IN RIVERS

RESISTANCE
LAMINAR FLOW LARGER VESSELS

GREATER FRACTION OF BLOOD IN CENTER GREATER FRACTION OF BLOOD NEAR VESSEL WALLS

SMALLER VESSELS

RESISTANCE = CONSTANT / RADIUS4 FLOW RATE = CONSTANT * RADIUS4

REGULATION OF BLOOD SUPPLY

VASOCONSTRICTION WIDESPREAD VASOCONSTRICTION

RESULTS IN INCREASE IN BP RESULTS IN INCREASED PERFUSION INCREASES RESISTANCE IN AREA REDIRECTS BLOOD FROM ONE ORGAN TO ANOTHER

LOCALIZED VASOCONSTRICTION

REGULATION OF BLOOD SUPPLY

LOCAL CONTROL AUTOREGULATION REACTIVE HYPEREMIA VASOACTIVE CHEMICALS ANGIOGENESIS

REGULATION OF BLOOD SUPPLY

LOCAL CONTROL AUTOREGULATION

INADEQUATE BLOOD FLOW BUILDUP OF WASTE PRODUCTS VASODILATION STIMULATED INCREASED BLOOD FLOW

REGULATION OF BLOOD SUPPLY

LOCAL CONTROL REACTIVE HYPEREMIA

BLOOD SUPPLY CUT OFF, THEN RESTORED INCREASED BEYOND NORMAL LEVEL OF FLOW E.G., AFTER COMING IN FROM COLD POSSIBLY DUE TO BUILDUP OF WASTE PRODUCTS

REGULATION OF BLOOD SUPPLY

LOCAL CONTROL VASOACTIVE CHEMICALS

RELEASED BY PLATELETS, ENDOTHELIAL CELLS, ETC. E.G., HISTAMINE

STIMULATES VASODILATION STIMULATES VASOCONSTRICTION

E.G., PROSTACYCLIN

REGULATION OF BLOOD SUPPLY

LOCAL CONTROL ANGIOGENESIS

GROWTH OF NEW BLOOD VESSELS LONG-TERM CHANGE E.G. REGROWTH OF UTERINE LINING FOLLOWING MENSTRUATION E.G., MUSCLES OF ATHLETES E.G., ARTERIAL BYPASSES AROUND CORONARY OBSTRUCTIONS

REGULATION OF BLOOD SUPPLY

NEURAL CONTROL VASOMOTOR CENTER OF MEDULLA OBLONGATA NERVE FIBERS

CAN STIMULATE VASOCONSTRICTION IN MOST BLOOD VESSELS CAN STIMULATE VASODILATION IN CARDIAC AND SKELETAL MUSCLE

REGULATION OF BLOOD SUPPLY

NEURAL CONTROL THREE AUTONOMIC REFLEXES

BAROREFEXES CHEMOREFLEXES MEDULLARY ISCHEMIC REFLEXES

Guyenet Nature Reviews Neuroscience 7, 335346 (May 2006) | doi:10.1038/nrn1902

REGULATION OF BLOOD SUPPLY

NEURAL CONTROL BAROREFLEXES

RESPONSE TO D IN BLOOD PRESSURE D DETECTED BY BARORECEPTORS

PRESENT IN AORTIC ARCH AND IN OTHER ARTERIES ABOVE HEART NEGATIVE FEEDBACK RESPONSE

REGULATION OF BLOOD SUPPLY

NEURAL CONTROL CHEMOREFLEXES

RESPONSE TO D IN BLOOD CHEMISTRY

ESPECIALLY pH, [O2], [CO2]

D DETECTED BY CHEMORECEPTORS
PRESENT IN AORTIC ARCH AND IN OTHER ARTERIES ABOVE HEART ADJUST RESPIRATION STIMULATE VASOCONSTRICTION

INCREASE BP INCREASE PERFUSION

REGULATION OF BLOOD SUPPLY

NEURAL CONTROL MEDULLARY ISCHEMIC REFLEX

RESPONSE TO INADEQUATE PERFUSION IN BRAINSTEM INCREASE HEART RATE & CONTRACTION FORCE INDUCE WIDESPREAD VASOCONSTRICTION

INCREASE BP INCREASE PERFUSION

REGULATION OF BLOOD SUPPLY

HORMONAL CONTROL ANGIOTENSIN II

VASOCONSTRICTIVE HORMONE

INCREASE BP INCREASE PERFUSION CONVERSION STIMULATED BY RENIN KIDNEYS PRODUCE RENIN IN RESPONSE TO LOW BP CONVERSION STIMULATED BY ACE (ENZYME) ACE PRESENT IN LUNGS ACE INHIBITORS TREAT HYPERTENSION

ANGIOTENSINOGEN ANGIOTENSIN I

ANGIOTENSIN I ANGIOTENSIN II

MEKANISME ACE inhibitor

ACE dan AT II
Perubahan angiotensinogen ke AT I & AT II

ANGIOTENSIN II

1. 2. 3.

4.

Angiotensonogen dari hati dirubah oleh renin menjadi angiotensin I (ATI). AT I oleh chimase dirubah menjadi AT II ATII memiliki efek: Meningkatkan aktivitas jantung Meningkatkan tahanan perifer Memacu sekresi ADH dan aldosteron Merangsang pusat haus

REGULATION OF BLOOD SUPPLY

HORMONAL CONTROL EPINEPHRINE / NOREPINEPHRINE

VASOACTIVE HORMONES

BIND TO a-ADRENERGIC RECEPTORS ON SMOOTH MUSCLE OF MOST BLOOD VESSELS

VASOCONSTRICTION INCREASE BP INCREASE PERFUSION

BIND TO b-ADRENERGIC RECEPTORS ON BLOOD VESSELS OF SKELETAL MUSCLE AND CORONARY BLOOD VESSELS

VASODILATION INCREASED BLOOD FLOW TO HEART & MUSCLES

The Electrocardiogram
An electrocardiogram (ECG) is a recording of the electrical changes that occur in the myocardium during a cardiac cycle. Atrial depolarization creates the P wave, ventricle depolarization creates the QRS wave, and repolarization of the ventricles produces the T wave.

Electrocardiogram

The Vascular Pathways

1)

2)

3)

The cardiovascular system includes two circuits: Pulmonary circuit which circulates blood through the lungs, and Systemic circuit which circulates blood to the rest of the body. Both circuits are vital to homeostasis.

Blood Flow
The beating of the heart is necessary to homeostasis because it creates pressure that propels blood in arteries and the arterioles. Arterioles lead to the capillaries where nutrient and gas exchange with tissue fluid takes place.

Blood Flow in Arteries

Blood pressure due to the pumping of

the heart accounts for the flow of blood in the arteries. Systolic pressure is high when the heart expels the blood. Diastolic pressure occurs when the heart ventricles are relaxing. Both pressures decrease with distance from the left ventricle because blood enters more and more arterioles and arteries.

Cross-sectional area as it relates to blood pressure and velocity

Blood Flow in Capillaries

Blood moves slowly in capillaries because there are more capillaries than arterioles. This allows time for substances to be exchanged between the blood and tissues.

Blood Flow in Veins

1)
2)

3)

Venous blood flow is dependent upon: skeletal muscle contraction, presence of valves in veins, and respiratory movements. Compression of veins causes blood to move forward past a valve that then prevents it from returning backward.

Changes in thoracic and abdominal pressure that occur with breathing also assist in the return of blood. Varicose veins develop when the valves of veins become weak. Hemorrhoids (piles) are due to varicose veins in the rectum. Phlebitis is inflammation of a vein and can lead to a blood clot and possible death if the clot is dislodged and is carried to a pulmonary vessel.

Blood

Blood separates into two main parts: plasma and formed elements. Plasma accounts for 55% and formed elements 45% of blood volume. Plasma contains mostly water (9092%) and plasma proteins (78%), but it also contains nutrients and wastes. Albumin is a large plasma protein that transports bilirubin; globulins are plasma proteins that transport lipoproteins.

Composition of blood

The Red Blood Cells

Red blood cells (erythrocytes or RBCs) are made in the red bone marrow of the skull,

ribs, vertebrae, and the ends of long bones. Normally there are 4 to 6 million RBCs per mm3 of whole blood. Red blood cells contain the pigment hemoglobin for oxygen transport; hemogobin contains heme, a complex ironcontaining group that transports oxygen in the blood.

Physiology of red blood cells

The air pollutant carbon monoxide combines more readily with hemoglobin than does oxygen, resulting in oxygen deprivation and possible death. Red blood cells lack a nucleus and have a 120 day life span. When worn out, the red blood cells are dismantled in the liver and spleen.

Iron is reused by the red bone marrow where stem cells continually produce more red blood cells; the remainder of the heme portion undergoes chemical degradation and is excreted as bile pigments into the bile. Lack of enough hemoglobin results in anemia. The kidneys produce the hormone erythropoietin to increase blood cell production when oxygen levels are low.

The White Blood Cells

White blood cells (leukocytes) have nuclei,

are fewer in number than RBCs, with 5,000 10,000 cells per mm3, and defend against disease. Leukocytes are divided into granular and agranular based on appearance. Granular leukocytes (neutrophils, eosinophils, and basophils) contain enzymes and proteins that defend the body against microbes.

The aganular leukocytes (monocytes and lymphocytes) have a spherical or kidneyshaped nucleus. Monocytes can differentiate into macrophages that phagocytize microbes and stimulate other cells to defend the body. Lymphocytes are involved in immunity. An excessive number of white blood cells may indicate an infection or leukemia; HIV infection drastically reduces the number of lymphocytes.

Macrophage engulfing bacteria

The Platelets and Blood Clotting

Red bone marrow produces large cells called megakaryocytes that fragment into platelets at a rate of 200 billion per day; blood contains 150,000300,000 platelets per mm3. Twelve clotting factors in the blood help platelets form blood clots.

Blood Clotting

Injured tissues release a clotting factor called prothrombin activator, which converts prothrombin into thrombin. Thrombin, in turn, acts as an enzyme and converts fibrinogen into insoluble threads of fibrin. These conversions require the presence of calcium ions (Ca2+). Trapped red blood cells make a clot appear red.

Blood clotting

Hemophilia

Hemophilia is an inherited clotting disorder

due to a deficiency in a clotting factor. Bumps and falls cause bleeding in the joints; cartilage degeneration and resorption of bone can follow. The most frequent cause of death is bleeding into the brain with accompanying neurological damage.

Bone Marrow Stem Cells

A stem cell is capable of dividing into new cells that differentiate into particular cell types. Bone marrow is multipotent, able to continually give rise to particular types of blood cells. The skin and brain also have stem cells, and mesenchymal stem cells give rise to connective tissues including heart muscle.

Blood cell formation in red bone marrow

Capillary Exchange

At the arteriole end of a capillary, water moves out of the blood due to the force of blood pressure. At the venule end, water moves into the blood due to osmotic pressure of the blood. Substances that leave the blood contribute to tissue fluid, the fluid between the bodys cells.

In the midsection of the capillary, nutrients diffuse out and wastes diffuse into the blood. Since plasma proteins are too large to readily pass out of the capillary, tissue fluid tends to contain all components of plasma except it has lesser amounts of protein. Excess tissue fluid is returned to the blood stream as lymph in lymphatic vessels.

Capillary exchange

Cardiovascular Disorders

Cardiovascular disease (CVD) is the

leading cause of death in Western countries. Modern research efforts have improved diagnosis, treatment, and prevention. Major cardiovascular disorders include atherosclerosis, stroke, heart attack, aneurysm, and hypertension.

Atherosclerosis

cholesterol, under the inner lining of arteries. The plaque can cause a thrombus (blood clot) to form. The thrombus can dislodge as an embolus and lead to thromboembolism.

Atherosclerosis is due to a build-up of fatty material (plaque), mainly

Stroke, Heart Attack, and Aneurysm

A cerebrovascular accident, or stroke, results when an embolus lodges in a cerebral blood vessel or a cerebral blood vessel bursts; a portion of the brain dies due to lack of oxygen. A myocardial infarction, or heart attack, occurs when a portion of heart muscle dies due to lack of oxygen.

Partial blockage of a coronary artery causes angina pectoris, or chest pain. An aneurysm is a ballooning of a blood vessel, usually in the abdominal aorta or arteries leading to the brain. Death results if the aneurysm is in a large vessel and the vessel bursts. Atherosclerosis and hypertension weaken blood vessels over time, increasing the risk of aneurysm.

Coronary Bypass Operations

A coronary bypass operation involves removing a segment of another blood vessel and replacing a clogged coronary artery. It may be possible to replace this surgery with gene therapy that stimulates new blood vessels to grow where the heart needs more blood flow.

Coronary bypass operation

Clearing Clogged Arteries

Angioplasty uses a long tube threaded

through an arm or leg vessel to the point where the coronary artery is blocked; inflating the tube forces the vessel open. Small metal stents are expanded inside the artery to keep it open. Stents are coated with heparin to prevent blood clotting and with chemicals to prevent arterial closing.

Angioplasty

Dissolving Blood Clots

Medical treatments for dissolving blood clots include use of t-PA (tissue plasminogen activator) that converts plasminogen into plasmin, an enzyme that dissolves blood clots, but can cause brain bleeding. Aspirin reduces the stickiness of platelets and reduces clot formation and lowers the risk of heart attack.

Heart Transplants and Artificial Hearts

Heart transplants are routinely

performed but immunosuppressive drugs must be taken thereafter. There is a shortage of human organ donors. Work is currently underway to improve self-contained artificial hearts, and muscle cell transplants may someday be useful.

Hypertension

About 20% of Americans suffer from hypertension (high blood pressure). Hypertension is present when systolic pressure is 140 or greater or diastolic pressure is 100 or greater; diastolic pressure is emphasized when medical treatment is considered. A genetic predisposition for hypertension occurs in those who have a gene that codes for angiotensinogen, a powerful vasoconstrictor.