CARDIOVASCULAR SYSTEM



REV. 12/22/06 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

3. 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

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 . . . Heart . . . Blood Vessels

LONG TERM CONTROL ~ Hormonal & Renal Mechanisms

AFFECT BLOOD VOLUME & FLUID RETENTION

Involves: Adrenals & Kidney

SHORT TERM CONTROLS of Blood Pressure

“AFFECTS ARE IMMEDIATE & SHORT-ACTING”

CONTROLS PERIPHERAL RESISTANCE by controlling vessel diameter

1. 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 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

HORMONAL CONTROL MECHANISMS ~ Blood Pressure

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

RENAL 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

“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 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 ~

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

................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download