Cardiovascular



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Dr. Vince Scialli

BSC 1086


REV. 7/16/08


CARDIOVASCULAR

SYSTEM

CIRCULATION

LECTURE 4
BLOOD VESSELS ~ OVERVIEW
Blood vessels are the plumbing for the body
Blood vessels are NOT rigid . . . they are dynamic structures
Pulsate
Constrict ~ “vasoconstriction” Relax ~ “vasodilation
Proliferate ~ grow & invade ~ “collateral circulation”
Blood vessels are a closed delivery system
Start at left heart: Aorta > Arteries ~ carry O2 blood
End at right heart: Veins > Vena Cava ~ carry CO2 blood
BLOOD VESSEL TYPES
ARTERIES > Large Arteries > Small Arteries > Arterioles
Carry “oxygenated” blood away from heart ~ high O2
Branch Out ~ from big to small

VEINS < Large Veins < Small Veins < Venules (small to large)
Carry “unoxygenated” blood toward heart ~ high CO2
Merge together from small to big
CAPILLARIES ~ contact tissue through capillary walls
Only one cell layer thick for diffusion ~ endothelium
Exchange O2 & CO2 between blood & tissue ~ O2/CO2

BLOOD VESSEL WALL STRUCTURE
Arteries & Veins ~ Three distinct layers

1. Tunica intima ~ tunica interna ~ inside layer
Lines “lumen” of vessels ~ “opening”
Endothelium ~ simple squamous & elastic tissue
Continuous with endocardium
Veins have flaps or “valves” that prevent back flow

2. Tunica media ~ middle smooth muscle & elastic layer
Thick in arteries Thin in veins
Innervated by Sympathetic NS ONLY
Adrenergic Stimulation > Vasoconstriction BP
Cholinergic Stimulation > Vasodilation BP
Vasa Vasorum ~ blood vessels supplying wall of

other blood vessels
3. Tunica externa ~ outside layer ~ collegen & elastic fibers
Thin in arteries Thick in veins


Capillaries ~ composed of epithelial cells only ~ single layer
Tunica Interna ONLY
CIRCULATORY PATHWAYS

ARTERIES ~ ARTERIAL SYSTEM
Systemic arteries always carry oxygenated blood ~ O2

Pulmonary arteries always carry unoxygenated blood ~ CO2
Arterial walls thicker than veins
Artery walls DO NOT contain valves ~ Veins contain valves
Arteries vasoconstrict ~ Veins collapse
BOTH Arteries & Veins can relax ~ vasodilate

Types of Arteries


  1. ELASTIC ARTERIES ~ AORTA & main branches


Called “Conducting Arteries” . . . Close to heart
Thick Tunica Externa with some elastic fibers

Conduct blood from heart to smaller arteries
Elasticity allows expansion & contraction as blood volumes change
NOT much resistance ~ due to large diameter
DO NOT Vasoconstrict ~ due to thick externa walls
Maintain constant blood flow ~ “conducting”
2. MUSCULAR ARTERIES ~ MOST of arterial system
Called “Distributing” Arteries ~ MOST COMMON
Deliver blood to organs & skeletal muscle
Small Diameter ~ more resistance > greater pressure
Thick tunica media with less elastic tissue
More vasoconstriction than larger elastic arteries
Make up “pressure points”
Can be pressed against bones to stop bleeding



  1. ARTERIOLES ~ smallest arteries


Resistance Vessels ~ increase/decrease resistance
Deliver blood into “capillary beds in tissue
Very small diameter ~ Greatest resistance
DILATION > decreases resistance > increases blood flow into capillaries ----> Lowers Blood Pressure
CONSTRICTION > increases resistance > decreases flow

into Capillaries ----> Increases Blood Pressure

Most important in regulating B.P. & flow to tissues !!!

ARTERY STRUCTURE ABNORMALATIES
Atheriosclerosis ~ thickening & hardening of artery walls
Plaque ~ cholesterol, low density lipoproteins ~ LDL
Coronary Artery Disease ~ Cerebral Strokes ~ Thrombus
Aneurysm ~ bulge ~ thin weakened artery wall
Can be very dangerous if in brain or in large artery
Can result in catastrophic blow out ~ fatal bleeding
Aortic Aneurysm ~ Fatal bleeding
Brain Aneurysm ~ stroke due to hemorrhage
COMMON if associated with high blood pressure

CAPILLARIES
Microscopic in size ~ smallest of all blood vessels
Diameter is slightly larger than diameter of a single RBC
Very thinned wall ~ tunica interna only ~ endothelium only
MOST body tissue has a rich capillary supply

Exceptions: Tendons & Ligaments ~ DON’ T BLEED

Capillaries allow exchange of O2/CO2, nutrients, & hormones between blood & tissue cells thru:

Fenestrations” ~ large pores allow large particle exchange



CAPILLARY BEDS ~ “Capillary Plexus” ~ “Microcirculation”
Network of capillaries ~ controls flow to tissues
Allow blood to flow between arterioles & venules
Artery Vein

O2 CO2

Arteriole Microcirculation Venule

O2 CO2

metarteriole post capillary venule

O2 CO2

Capillary bed

O2/CO2
Thorough fare channel

Mixed Blood
Vasomotion ~ automatic vasoconstriction & vasodilation
Arterioles ~ Most important in regulating flow to tissues

& control of blood pressure
Blood entering capillary beds depends on BODY NEEDS
Dilation of arterioles blood flow into capillaries BP
Constriction of arterioles flow into capillaries BP
Causes pooling in various body parts at different times:
Examples: Blood to digestive organs after a meal
Blood to skeletal muscle after exercise
Exercise after eating > muscle cramps

VENOUS SYSTEM
Systemic veins always carry unoxygenated blood ~ ↑ CO2

Pulmonary veins always carry oxygenated blood ~ ↑ O2
Types of Veins
1. VENULES ~ very small ~ flow into veins
Extremely porous

Fluid & white blood cells move from blood into tissue cells very easily ~ diffusion & pressure
Ascites Edema Inflammation
2. VEINS
Walls thinner but lumen larger than arteries
Tunica externa ~ thick outer wall . . . Very thick near heart
Tunica media ~ thin ~ smooth muscle ~ no constriction
Expandable ~ Veins dilate & hold large volumes of blood
Capacitance Vessels” ~ expandable & can collapse
Blood Reservoirs – contain 65% of body blood volume
Blood pressure is much lower in veins than arteries
Farthest distance from heart ~ no constriction

VENOUS VALVES
In veins of limbs & extremeties . . . not in body cavities
Veins can move blood against gravity ~ valves & muscles
Valves prevent backward flow of blood ~ Prevents pooling
Valve Dysfunction: Vericose Veins & Hemorrhoids
VASCULAR ANASTAMOSIS
Organs receive blood from more than one arterial source
Arterial anastamosis ~ artery to artery merge
By-Pass Surgery ~ coronary artery anastamosis
Venous anastamosis ~ veins to veins

Arterio-venous anastamosis ~ arterioles to venules
Collateral Circulation ~ alternative supply of blood vessels
Maintains blood supply to an area when main supply is cut or blocked by a clot or injury
Part of the Healing process to improve blood supply

Aerobic exercise

Myocardial infarct

Cerebral clot
Occlusion of veins is rare ~ DO NOT become blocked
Tissue death is rare as a result of venous occlusion
PHYSIOLOGY OF CIRCULATION
HEART = PUMP
ARTERIES = CONDUITS O2

ARTERIOLES = RESISTANCE VESSELS
CAPILLARIES = EXCHANGE SITES O2/ CO2

VEINS = CONDUITS & BLOOD RESERVOIRS CO2
FACTORS AFFECTING CIRCULATION
BLOOD FLOW . . . BLOOD PRESSURE . . . RESISTANCE
1. BLOOD FLOW ~ ml/minute
VOLUME OF BLOOD FLOWING THROUGH A VESSEL, ORGAN, or ENTIRE CIRCULATION IN A GIVEN PERIOD
VARIES WIDELY BASED ON ORGAN NEEDS
Skeletal Muscles . . . Digestive Organs
2. BLOOD PRESSURE ~ mmHg
FORCE PER UNIT AREA EXERTED ON THE WALL OF A BLOOD VESSEL BY ITS CONATINED BLOOD
Defined: MEAN SYSTEMIC ARTERIAL PRESSURE IN THE LARGEST ARTERIES ~ NEAR THE HEART
PRESSURE DIFFERENCE PROVIDES THE FORCE THAT KEEPS BLOOD MOVING . . . FROM HIGH PRESSURE TO

LOW PRESSURE

3. RESISTANCE
OPPOSITION TO BLOOD FLOW due to friction
RESISTANCE -----> FLOW
Causes of Resistance:
1. Blood Viscosity ~ THICKNESS OR STICKINESS
H2O & BLOOD PARTICULATES
PLASMA PROTEIN & LIPIDS

LOW RBC’S ---> LOW VISCOSITY

HIGH RBC’S ---> HIGH VISCOSITY
2. Blood Vessel Length
LONGER VESSELS ---> greater RESISTANCE
FAT REQUIRES MORE & LONGER VESSELS WHICH INCREASES RESISTANCE
3. Blood Vessel Diameter . . . Most Significant Factor
GREATER DIAMETER ----> LESS RESISTANCE

SMALLER DIAMETER ----> MORE RESISTANCE
Vasoconstriction ↑↑↑ . . . Vasodilation ↓↓↓
As radius decreases by ½ ~ resistance increases 16X

4. Turbulance ~ increases resistance

Fatty Plaques ~ atherosclerosis ~ cholesterol

FACTORS AFFECTING BLOOD CIRCULATION
KNOW RELATIONSHIPS: VESSEL DIAMETER
BLOOD FLOW VOLUME
BLOOD FLOW VELOCITY
BLOOD PRESSURE
RESISTANCE ~ most dominant factor

BLOOD PRESSURE ---->  BLOOD FLOW VELOCITY



Vessel Diameter is the greatest resistance factor
RESISTANCE ---->  BLOOD FLOW VOLUME

RESISTANCE ---->  BLOOD PRESSURE



KNOW VASODILATION VASOCONSTRICTION
VESSEL DIAMETER  VESSEL DIAMETER
FLOW VOLUME  FLOW VOLUME
RESISTANCE  RESISTANCE
BLOOD PRESSURE  BLOOD PRESSURE
FLOW VELOCITY  FLOW VELOCITY


CARDIOVASCULAR

SYSTEM

CIRCULATION

LECTURE 5

SYSTEMIC BLOOD PRESSURE ~ Circulatory Pressure
Heart PUMP generates the “circulatory pressure”
Difference in pressure between the base of the AORTA & the entrance to the RIGHT ATRIUM via vena cava
Average Circulatory Pressure ~ 100 mgHg
Depends on: Arterial Pressure ~ 120 mmHg

Capillary Pressure ~ 20 to 40 mmHg

Venous Pressure ~ 0 to 20 mmHg
PRESSURE IS GREATEST CLOSE TO THE PUMP ~ Heart
PRESSURE GRADIENT FLOW FROM HIGH TO LOW
PUMP . . . CREATES FLOW
RESISTANCE . . . CREATES PRESSURE

AORTA ~ 120 mm Hg
ARTERIES ~ 120 mm Hg
ARTERIOLES ~ 60 mm Hg
CAPILLARIES ~ 40 - 20 mm Hg (most critical)
VENULES ~ 20 mm HG
VEINS ~ 10 mm Hg
VENA CAVA ~ 1-5 mm Hg
RIGHT ATRIUM 0

ARTERIAL PRESSURE ~ “BLOOD PRESSURE”
It is what we Actually Measure in determining Blood Pressure
Blood Pressure Dependent on TWO Factors


  1. ELASTICITY OF ARTERIES CLOSE TO HEART


2. VOLUME OF BLOOD FORCED INTO ARTERIES
BLOOD PRESSURE RISES & FALLS WITH EACH BEAT

. . . as measured in arteries nearest the heart
SYSTOLIC PRESSURE
PRESSURE produced in arteries AFTER each

left ventricular contraction

AVERAGE ~ 120 mm Hg
DIASTOLIC PRESSURE
PRESSURE remaining in AORTA & major ARTERIES during DIASTOLE ~ Ventricular filling /heart relaxed
AORTIC SEMI-LUNAR VALVES CLOSED
Prevents back flow into left ventricle
Maintains a lower arterial pressure in diastole
Keeps blood flowing when heart is not pumping
AVERAGE ~ 80 mm Hg
Normal blood pressure = 120/80 = Systolic/Diastolic

PULSE PRESSURE
SYSTOLIC minus DIASTOLIC PRESSURE
AVERAGE ~ 120mm Hg – 80 mm Hg = 40mm Hg

Factors Increasing Pulse Pressure
INCREASED STROKE VOLUME ~ systolic pressure
INCREASED CONTRACTILITY ~  systolic pressure
ATHEROSCLEROSIS ~  resistance

MEAN ARTERIAL PRESSURE ~ “The Real Pressure”
AVERAGE PRESSURE THAT PROPELS BLOOD TO ALL TISSUE DURING CARDIAC CYCLE
Lower than SYSTOLIC but higher than DIASTOLIC
DIASTOLE lasts longer than SYSTOLE ~ 2/3 to 1/3
Know MAP = Diastolic Pressure + 1/3 Pulse Pressure

How

to

Calculate EXAMPLE: Systolic pressure = 120

Diastolic pressure = 80

Pulse Pressure = 40
MAP = 80 + 40/3 = 93 mm Hg
NOTE: BOTH MAP & PULSE PRESSURE DECREASES WITH INCREASING DISTANCE FROM THE HEART ---> systolic pressure

CAPILLARY PRESSURE ~ “Capillary Hydrostatic” Pressure
BEGINNING CAPILLARY BED PRESSURE ~ 40 mm Hg
END CAPILLARY BED PRESSURE ~ 20 mm Hg
LOW CAPILLARY BED PRESSURE is DESIRABLE


Capillary Walls very fragile ~ only one cell layer thick

HIGH PRESSURE ----> RUPTURE
Nose Bleeds ~ mixed O2/CO2 blood


Capillaries very permeable ~ pushes fluid out of capillaries

HIGH PRESSURE ----> EDEMA
EDEMA ~ abnormal accumulation of fluid in tissue
Pulmonary Edema ~ LEFT SIDED FAILURE
Accumulation in lungs
Peripheral Congestion ~ edema/ascites
RIGHT SIDED FAILURE
Accumulation in abdomen & tissue



Arterioles are most critical in regulating blood flow to

tissues & controlling of blood pressure

CAPILLARY BLOOD FLOW
BLOOD FLOW THROUGH CAPILLARY BEDS IS SLOW & INTERMITTENT . . . NOT STEADY
FLOW IS FROM HIGH PRESSURE TO LOW PRESSURE
CAPILLARY EXCHANGE ~ Occurs by DIFFUSION
SOLUTES ~ “Diffuse” ~ HIGH TO LOW SOLUTE CONC.
OXYGEN & CARBON DIOXIDE

NUTRIENTS ~ AA, GLUCOSE, LIPIDS

METABOLIC WASTES

OTHER IONS ~ Na+, Ca+, K+
FLUID Moves ~ HIGH TO LOW PRESSURE
LOW SOLUTE TO HIGH SOLUTE CONC. ~ via OSMOSIS
DEPENDS ON:
HYDROSTATIC PRESSURE
PRESSURE INSIDE Capillary vs. CELL PRESSURE ~ pushes fluid out of capillaries into tissues
COLLOID OSMOTIC PRESSURE ~ Draws in H2O
Solutes carry H2O with them by OSMOSIS

Net Filtration Pressure ~ difference between net

(NFP) hydrostatic pressure & net

osmotic pressure
VENOUS BLOOD PRESSURE
NO PULSATION ~ pressure too low ~ from 20 mmHg to 0
BEGINNING VENOUS PRESSURE ~ 20 mm Hg at capillaries
END VENOUS PRESSURE ~ 0 mm Hg at Rt. Atrium
FACTORS AIDING VENOUS RETURN
Small PRESSURE GRADIENT = 20 to NEAR 0 mm Hg
PRESSURE GRADIENT is too small to allow adequate return to heart by itself
GRAVITY will allow some blood to flow from head & neck back to the heart while standing or sitting
Respiratory Pump ~ (pressure/volume relationship)
Breathing action sucks blood upward toward Heart
Inhaling ---> increased abdominal pressure ---> squeezes local veins ---> forcing blood toward heart
Inhaling ---> decreased chest cavity pressure --> thoracic veins to expand ---> speeds blood entry into right atrium
Muscular Pump
Skeletal muscle contraction ---> milking action of blood toward heart & prevents blood pooling
Valves in extremity veins prevent flow back
MAINTAINING BLOOD PRESSURE
PHYSIOLOGIC FACTORS ~ INFLUENCE PRESSURE
 CARDIAC OUTPUT ----> BP
 BLOOD VOLUME ----> BP
 PERIPHERAL RESISTANCE ----> BP

BLOOD = CARDIAC X PERIPHERAL

PRESSURE OUTPUT RESISTANCE

SV Constriction

HR Dilation

Volume Viscosity

Vessel Length


NEURAL . . . HORMONAL . . . RENAL CONTROLS

COMPENSATES for changes in Blood Pressure
SHORT TERM CONTROL ~ Neural & Hormonal Mechanisms
AFFECT PERIPHERAL RESISTANCE ~ VASOMOTOR
Involves: Brain Stem . . . Heart . . . Blood Vessels

LONG TERM CONTROL ~ Hormonal & Renal Mechanisms
AFFECT BLOOD VOLUME & FLUID RETENTION
Involves: Adrenals . . . Kidney . . . Posterior Pituitary

SHORT TERM CONTROLS of Blood Pressure
AFFECTS ARE IMMEDIATE & SHORT-ACTING”
CONTROLS PERIPHERAL RESISTANCE by controlling vessel diameter

NEURAL Mechanisms
Sympathetic NS controls peripheral resistance
ALTERS VESSEL DIAMETER

Constriction ~ INCREASES blood pressure
Dilation ~ LOWERS blood pressure

ALTERS BLOOD FLOW TO MEET TISSUE DEMANDS
Digestion ~ shunts blood from skeletal muscle to digestive organs . . . “cramps”
Exercise ~ shunts blood from digestive organs to skeletal muscle
Skin Vasodilation ~ shunts blood from internal organs to skin to loose body heat
Skin Vasoconstriction ~ shunts blood from skin to internal organs to retain heat
NEURAL & HORMONAL Control Mechanisms
VASOMOTOR CENTER ~ MEDULLA OBLONGATA

Rapid “REFLEX” response to changes in blood pressure
Adrenergic Stimulation ----> Adrenaline Released
Increases heart rate & myocardial contraction
Potent “peripheral” Vasoconstriction
HIGH BRAIN CENTERS ~ Hypothalamus ~ Cerebral Cortex
Blood Pressure changes sensed in Medulla >>> relays stimuli to higher brain centers >>>
Gives us awareness ONLY . . . but NO conscious control
Generalized “fight or flight” sympathetic response
CHEMORECEPTORS ~ chemical detectors
Detect blood & CSF changes in . . . O2, CO2, & H+
LOCATED IN: Aortic Bodies ~ in AORTIC ARCH
Carotid Bodies ~ in NECK ARTERIES

O2, pH, CO2 ---> STIMULATES VASOMOTOR

Reflex Center in Medulla
Increases Heart Rate & Myocardial Contraction & Vasoconstriction
> > > INCREASES BLOOD PRESSURE

BARORECEPTORS ~ detect ARTERIAL pressure changes
LOCATED IN: CAROTID SINUSES

AORTIC SINUSES
An INCREASED Arterial Pressure ----> Triggers Reflex
Stretches receptors ---> impulses to medulla oblongata
----> Sympathetic inhibiton ----> VASODILATION
----> Parasympathetic Stimulation ----> SLOWS HR
Results in ----> LOWER Cardiac Output & LOWER BP
A DECREASED Arterial Pressure ----> Triggers Reflex
Stretches receptors ----> Impulses to medulla oblongata
----> Sympathetic Stimulation ----> Faster HR,
increased myocardial contractility & consriction
Results in ----> HIGHER Cardiac Output & HIGH BP

CAROTID SINUS REFLEX ~ “ISCHEMIC REFLEX”
Prevents fainting during rapid posture changes
PROTECTS BLOOD SUPPLY TO BRAIN
Stimulates sympathetic nervous system
Lose capability with age ~ causes syncopy ~ fainting

RENAL & HORMONAL REGULATION ~ Long Term Control
KIDNEY RETAINS or EXCRETES H2O IN RESPONSE TO BLOOD PRESSURE CHANGES . . REGULATES BLOOD VOLUME
RENAL Autoregulation
Increased blood volume & pressure increases blood flow to kidney which increases urine formation (Nervousness)
Decreased blood volume or pressure decreases renal blood flow which reduces urine formation
RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM”
DROP BLOOD PRESSURE ----> Kidneys release RENIN
RENIN becomes Angiotensin I in blood
Angiotensin I becomes Angiotensin II
POTENT VASOCONSTRICTOR ~ B P
Angiotensin II ----> Adrenals release of ALDOSTERONE
----> NA+ REABSORPTION & H2O RETENTION

----> INCREASED BLOOD VOLUME & BLOOD PRESSUE
ERYTHROPOIETIN
Large BP drop stimulates release by kidney
EPO stimulates release of RBC’s from bone marrow
INCREASES VOLUME & VISCOSITY OF BLOOD

OTHER HORMONAL CONTROL MECHANISMS
ADRENAL MEDULLA HORMONES ~ catecholamines
INCREASES BLOOD PRESSURE
Norepinephrine ----> VASOCONSTRICTION
Epinephrine ----> INCREASED CARDIAC OUTPUT
----> VASOCONSTRICTION
ANTI-DIURETIC HORMONE ~ ADH ~ “vasopressin”
Secreted By POSTERIOR PITUITARY
INCREASES BLOOD PRESSURE
WATER RETENTION > INCREASED BLOOD VOLUME
CAUSES VASOCONSTRICTION If SEVERE FLUID LOSS OR DROP IN BLOOD PRESSURE
ATRIAL NATRIUETIC PEPTIDE ~ secreted by HEART
LOWERS BLOOD PRESSURE
ANTAGONIZES ALDOSTERONE
INCREASES Na+ EXCRETION IN KIDNEYS
WATER LOSS > DECREASED BLOOD VOLUME
CAUSES VASODILATION
BLOCKS ADH & CATECHOLAMINE RELEASE

TISSUE PERFUSION” ~ BLOOD FLOW THROUGH TISSUES




  1. DELIVERS O2 & NUTRIENTS

  2. REMOVES CO2 AND METABOLIC WASTES

  3. GAS EXCHANGE IN THE LUNGS

  4. URINE FORMATION


Determined by VOLUME & VELOCITY of Blood Flow
VOLUME AT REST EXERCISE

BRAIN 13% 4% HEART 4% 4%

KIDNEYS 20% 3%

ABDOMINAL ORGANS 24% 3%

SKELETAL MUSCLE 20% 71%
VELOCITY
VELOCITY IS INVERSELY PROPORTIONAL TO CROSS SECTIONAL AREA OF THE BLOOD VESSEL
BLOOD FLOWS FASTEST WHERE THE TOTAL CROSS SECTIONAL AREA IS SMALLEST
INDIVIDUAL CAPILLARY HAS SMALL LUMEN BUT TOTAL CROSS SECTION AREA OF CAPILLARY BED IS VERY LARGE
TOTAL CROSS SECTIONAL AREA FLOW SPEED

AORTA 250 cm sq FASTEST

ARTERIES 500 cm sq FAST

ARTERIOLES 3000 cm sq SLOW

* * * CAPILLARIES 4500 cm sq SLOWEST

VENULES 3000 cm sq SLOW

VEINS 500 cm sq FAST
* * * SLOW CAPILLARY FLOW ALLOWS ADEQUATE TIME

FOR EXCHANGES TO BE MADE

CIRCULATORY IMBALANCES ~ (May Not be Covered in Lecture)
HYPOTENSION ~ LOW BLOOD PRESSURE
SYSTOLIC PRESSURE DROPS BELOW < 100 mm Hg
ACUTE HYPOTENSION ~ MOST common
DUE TO: DROP IN BLOOD VOLUME & PRESSURE
-----> CIRCULATORY SHOCK ~ SYSTEM SHUTDOWN
Hypovolemic ~ large volume loss ~ Hemorrhage

Anaphylaxis ~ system vasodilation ~ Histamine

Cardiogenic ~ heart failure ~ inadequate circulation

Vascular ~ damaged vessels, dilation, aneurisms

Septic ~ bacterial toxins
IMMEDIATE THERAPY: IV FLUIDS TO REPLACE VOLUME ~ TRANSFUSIONS
CHRONIC HYPOTENSION
DUE TO: “THIN” BLOOD ~ LOW VISCOSITY

POOR NUTRITION & ANEMIA

LOW PROTEIN ~ low hemoglobin
ORTHOSTATIC HYPOTENSION ~ OLD AGE
Loss of Carotid Sinus SYMPATHETIC RESPONSE
LOW BLOOD PRESSURE & DIZZINESS
FAINTING WHEN STAND UP . . . BLOOD POOLS
HYPERTENSION ~ HIGH BLOOD PRESSURE
SYSTOLIC PRESSURE > 140 mm Hg (BORDERLINE)
DIASTOLIC PRESSURE > 90 mm Hg (now > 85)
NORMAL INCREASES: FEVER

EXERCISE & EXCITEMENT

EMOTIONAL UPSET
CHRONIC HYPERTENSION ~ MOST COMMON
High Stress for Years > INCREASE VESSEL RESISTANCE
SLOWLY STRAINS HEART & DAMAGES VESSELS

“SILENT KILLER”

HEART FAILURE

RENAL FAILURE

ATHEROSCLEROSIS

STROKE
Causes: DIET ~ NA+, FAT, CHOLESTEROL
OBESITY ~ LONGER VESSEL LENGTH
AGE ~ > 40
STRESS & SMOKING ~ NICOTINE is a

vasoconstrictor
PRIMARY HYPERTENSION ~ NO SPECIFIC CAUSE IN 90%
RACE ~ BLACKS > WHITE
HEREDITARY ~ FAMILIES

AGING EFFECTS ON CARDIOVASCULAR SYSTEM

HEART CHANGES
REDUCTION IN MAXIMUM CARDIAC OUTPUT
CHANGES IN CONDUCTION CAPABILITIES
REDUCTION IN ELASTACITY OF FIBROUS SKELETON
PROGRESSIVE ATHEROSCLEROSIS
RESTRICTS CORONARY CIRCULATION ~ ↑ Resistance
DAMAGED CARDIAC CELLS REPLACED BY SCAR TISSUE

VESSEL CHANGES
WALLS LOOSE ELASTICITY
LESS TOLERANT TO SUDDEN PRESSURE CHANGES
MORE PRONE TO ANEURYSM FORMATION
CALCIUM DEPOSITS ON WEAKENED VESSEL WALLS
INCREASED RISK OF STROKE OR INFARCTION
PRONE TO THROMBI FORMATION ~ ATHEROSCLEROSIS

The remaining material will not be covered in lecture ~ Reference

Only
TISSUE PERFUSION
AUTO REGULATION
Constant Dilation/Constriction of Capillaries regulates local blood flow
Due to CHANGES in DIAMETERS of ARTERIOLES FEEDING CAPILLARY BEDS
METABOLIC CONTROLS
RESPONSE TO NUTRIENTS, O2 & CO2
VASODILATION OF ARTERIOLES ----> INCREASES PERFUSION
VASOCONSTRICTION ----> DECREASES PERFUSION
MYOGENIC CONTROLS
LOW PERFUSION ----> DEATH OF TISSUE ~ Necrosis
High PERFUSION ----> RUPTURED VESSELS ~ nose bleeds
REACTIVE HYPEREMIA ~ Local Redness & Swelling
DRAMATIC INCREASE IN BLOOD FLOW INTO TISSUE AFTER BLOCKAGE OR INJURY
ANGIOGENESIS ~ COLLATERAL CIRCULATION
NEW ARTERIOLES DEVELOP ~ COLLATERAL

CIRCULATION

EG. CORONARY ~ Heart Attacks
HIGH ALTITUDE CONDITIONS

UNIQUE TISSUE PERFUSION ~ (Not Covered in Lecture- Reference Only)
SKELETAL MUSCLE
EXTREMELY VARIABLE WITH MUSCLE ACTIVITY
HYPEREMIA: FLOW INCREASES DIRECTLY WITH METABOLIC ACTIVITY AND O2 REQUIREMENT
CHOLINERGIC RECEPTORS ----> STIMULATE VASODILATION
BLOOD FLOW CAN INCREASE 10X DURING EXERCISE
BLOOD DIVERTED FROM SKIN & DIGESTIVE ORGANS

BRAIN
TOTAL BLOOD FLOW TO BRAIN REMAINS CONSTANT

750 ml/min
BRAIN NEURONS TOTALLY INTOLLERANT OF ISCHEMIA
CEREBRAL EDEMA > DEATH
BRAIN IS MOST METABOLIC ACTIVE ORGAN IN BODY
BRAIN IS LEAST ABLE TO STORE ESSENTIAL NUTRIENTS
GLUCOSE
VERY RESPONSIVE TO CO2 INCREASE & H+ DECREASE
VERY SENSITIVE TO CHANGES IN ARTERIAL PRESSURE

FAINTING OR “SYNCOPE” IF MAP < 60 mm Hg
CEREBRAL EDEMA IF MAP > 160 mm Hg
Transient Ischemic Attacks ~ TIA’s
Cerebro-vascular Accident ~ CVA ~ stroke

UNIQUE TISSUE PERFUSION ~ (Not Covered in Lecture ~ Reference Only)
SKIN
BLOOD FLOW THROUGH THE SKIN


  1. SUPPLIES NUTRIENTS TO CELLS

  2. BODY TEMPERATURE REGULATION

  3. BLOOD RESERVOIR


WHEN BODY TEMPERATURE INCREASES >

SYMPATHETIC STIMULATION IS INHIBITED > VASODILATION OF SKIN VESSELS
WHEN BODY TEMPERATURE DECREASES >

SYMPATHETIC STIMULATION > VASOCONSTRICTION

OF SKIN VESSELS

LUNGS
PULMONARY CIRCULATION VERY SHORT
LOW PRESSURE SYSTEM ~ SYSTOLIC = 24 mm Hg
DIASTOLIC = 8 mm Hg
ARTERIAL VESSELS STRUCTURED LIKE VEINS
THINNER WALLS – LARGER LUMEN
AUTOREGULATION IS OPPOSITE SYSTEMIC CIRCULATION
LOW BLOOD O2 > VASOCONSTRICTION TO ALLOW MORE O2 TO MOVE INTO BLOOD
HIGH BLOOD O2 > VASODILATION TO ALLOW O2 TO MOVE OUT OF BLOOD



UNIQUE TISSUE PERFUSION ~ (Not Covered in Lecture ~ Reference Only)

HEART
WHEN VENTRICLES CONTRACT, CORONARY VESSELS BECOME COMPRESSED ----> BLOOD FLOW THROUGH THE MYOCARDIUM STOPS
BLOOD FLOW TO THE MYOCARDIUM OCCURS WHEN THE HEART IS IN DIASTOLE OR RELAXED
ABNORMALLY FAST HEARTBEAT REDUCES THE ABILITY OF THE MYOCARDIUM TO RECEIVE ADEQUATE O2
CARDIAC CELLS USE 65% OF O2 CARRIED TO IT COMPARED TO 25% FOR NON-CARDIAC CELLS
25% of Cardiac Cell is Mitochondria
2% of Skeletal Muscle cell is Mitochondria



Blood Vessels & Circulation ~ Chapter 21~3/28/2017


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