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Copyright © 2010 Pearson Education, Inc.

Blood Tests

Copyright © 2010 Pearson Education, Inc.

Diagnostic Blood Tests

• Hematocrit

• Blood glucose tests

• Microscopic examination reveals variations in size and shape of RBCs, indications of anemias

• Differential WBC count

• Prothrombin time and platelet counts assess hemostasis

• SMAC, a blood chemistry profile

• Complete blood count (CBC)

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Regulation of Blood Pressure and Heart Rate

Autoregulation (meaning that the tissue or organ regulates blood pressure and flow locally)

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Autoregulation

• Automatic adjustment of blood flow to each tissue in proportion to its requirements at any given point in time

• Is controlled intrinsically by modifying the diameter of local arterioles feeding the capillaries

• Is independent of MAP, which is controlled as needed to maintain constant pressure

• Two types of autoregulation

1.Metabolic

2.Myogenic

Copyright © 2010 Pearson Education, Inc. Figure 19.15

Metaboliccontrols

pH Sympathetic

Receptors

ReceptorsEpinephrine,norepinephrine

Angiotensin II

Antidiuretichormone (ADH)

Atrialnatriureticpeptide (ANP)

Dilates

Constricts

Prostaglandins

Adenosine

Nitric oxide

Endothelins

Stretch

O2

CO2

K+

Amounts of:

Amounts of:

Nerves

Hormones

Myogeniccontrols

Intrinsic mechanisms(autoregulation)

• Distribute blood flow to individual organs and tissues as needed

Extrinsic mechanisms

• Maintain mean arterial pressure (MAP)• Redistribute blood during exercise and thermoregulation

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Long-Term Autoregulation

• Angiogenesis

• Occurs when short-term autoregulation cannot meet tissue nutrient requirements

• The number of vessels to a region increases and existing vessels enlarge

• Common in the heart when a coronary vessel is occluded, or throughout the body in people in high-altitude areas

Copyright © 2010 Pearson Education, Inc.

Copyright © 2010 Pearson Education, Inc.

Reminder: repeated from previous set of slide, purpose of blood is -

• Diffusion of

• O2 and nutrients from the blood to tissues

• CO2 and metabolic wastes from tissues to the blood

• Lipid-soluble molecules diffuse directly through endothelial membranes

• Water-soluble solutes pass through clefts and fenestrations

• Larger molecules, such as proteins, are actively transported in pinocytotic vesicles or caveolae

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Fluid Movements: Bulk Flow

• Extremely important in determining relative fluid volumes in the blood and interstitial space

• Direction and amount of fluid flow depends on two opposing forces: hydrostatic and colloid osmotic pressures

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Hydrostatic Pressures

• Capillary hydrostatic pressure (HPc) (capillary blood pressure)

• Tends to force fluids through the capillary walls

• Is greater at the arterial end (35 mm Hg) of a bed than at the venule end (17 mm Hg)

• Interstitial fluid hydrostatic pressure (HPif)

• Usually assumed to be zero because of lymphatic vessels

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Colloid Osmotic Pressures

• Capillary colloid osmotic pressure (oncotic pressure) (OPc)

• Created by nondiffusible plasma proteins, which draw water toward themselves

• ~26 mm Hg

• Interstitial fluid osmotic pressure (OPif)

• Low (~1 mm Hg) due to low protein content

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Net Filtration Pressure (NFP)

• NFP—comprises all the forces acting on a capillary bed

• NFP = (HPc—HPif)—(OPc—OPif)

• At the arterial end of a bed, hydrostatic forces dominate

• At the venous end, osmotic forces dominate

• Excess fluid is returned to the blood via the lymphatic system

Copyright © 2010 Pearson Education, Inc. Figure 19.17

HP = hydrostatic pressure• Due to fluid pressing against a wall• “Pushes”• In capillary (HPc) • Pushes fluid out of capillary • 35 mm Hg at arterial end and 17 mm Hg at venous end of capillary in this example• In interstitial fluid (HPif) • Pushes fluid into capillary • 0 mm Hg in this example

OP = osmotic pressure• Due to presence of nondiffusible solutes (e.g., plasma proteins)• “Sucks”• In capillary (OPc) • Pulls fluid into capillary • 26 mm Hg in this example• In interstitial fluid (OPif) • Pulls fluid out of capillary • 1 mm Hg in this example

Arteriole

Capillary

Interstitial fluid

Net HP—Net OP(35—0)—(26—1)

Net HP—Net OP(17—0)—(26—1)

Venule

NFP (net filtration pressure)is 10 mm Hg; fluid moves out

NFP is ~8 mm Hg;fluid moves in

NetHP35mm

NetOP25mm

NetHP17mm

NetOP25mm

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Circulatory Shock

• Any condition in which

• Blood vessels are inadequately filled

• Blood cannot circulate normally

• Results in inadequate blood flow to meet tissue needs

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Circulatory Shock

• Hypovolemic shock: results from large-scale blood loss

• Vascular shock: results from extreme vasodilation and decreased peripheral resistance

• Cardiogenic shock results when an inefficient heart cannot sustain adequate circulation

Copyright © 2010 Pearson Education, Inc. Figure 19.18

Signs and symptoms

Acute bleeding (or other events that causeblood volume loss) leads to:

1. Inadequate tissue perfusion resulting in O2 and nutrients to cells2. Anaerobic metabolism by cells, so lactic acid accumulates3. Movement of interstitial fluid into blood, so tissues dehydrate

Initial stimulus

Result

Physiological response

Chemoreceptors activated(by in blood pH)

Baroreceptor firing reduced(by blood volume and pressure)

Hypothalamus activated(by pH and blood pressure)

Major effect Minor effect

Brain

Activation ofrespiratory centers

Cardioacceleratory andvasomotor centers activated

Sympathetic nervoussystem activated

ADHreleased

Neuronsdepressed

by pH

Intense vasoconstriction(only heart and brain spared)

Heart rate Centralnervous system

depressed

Adrenalcortex

Kidney

Renin released

Renal blood flow

Aldosteronereleased

Kidneys retainsalt and water

Angiotensin IIproduced in blood

Waterretention

Urine outputRate anddepth of

breathing

Tachycardia,weak, thready

pulse

Skin becomescold, clammy,and cyanotic

Thirst Restlessness(early sign)

Coma(late sign)

CO2 blownoff; bloodpH rises

Blood pressure maintained;if fluid volume continues to

decrease, BP ultimatelydrops. BP is a late sign.

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Maintaining Blood Pressure

• The main factors influencing blood pressure:

• Cardiac output (CO)

• Peripheral resistance (PR)

• Blood volume

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Maintaining Blood Pressure

• F = P/PR and CO = P/PR

• Blood pressure = CO x PR (and CO depends on blood volume)

• Blood pressure varies directly with CO, PR, and blood volume

• Changes in one variable are quickly compensated for by changes in the other variables

Copyright © 2010 Pearson Education, Inc.

Cardiac Output (CO)

• Determined by venous return and neural and hormonal controls

• Resting heart rate is maintained by the cardioinhibitory center via the parasympathetic vagus nerves

• Stroke volume is controlled by venous return (EDV)

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Cardiac Output (CO)

• During stress, the cardioacceleratory center increases heart rate and stroke volume via sympathetic stimulation

• ESV decreases and MAP increases

Copyright © 2010 Pearson Education, Inc. Figure 19.8

Venous return

Exercise

Contractility of cardiac muscle

Sympathetic activity Parasympathetic activity

Epinephrine in blood

EDV ESV

Stroke volume (SV) Heart rate (HR)

Cardiac output (CO = SV x HR

Activity of respiratory pump(ventral body cavity pressure)

Activity of muscular pump(skeletal muscles)

Sympathetic venoconstriction

BP activates cardiac centers in medulla

Initial stimulus

Result

Physiological response

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Control of Blood Pressure

• Short-term neural and hormonal controls

• Counteract fluctuations in blood pressure by altering peripheral resistance

• Long-term renal regulation

• Counteracts fluctuations in blood pressure by altering blood volume

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Short-Term Mechanisms: Neural Controls

• Neural controls of peripheral resistance

• Maintain MAP by altering blood vessel diameter

• Alter blood distribution in response to specific demands

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Short-Term Mechanisms: Neural Controls

• Neural controls operate via reflex arcs that involve

• Baroreceptors

• Vasomotor centers and vasomotor fibers

• Vascular smooth muscle

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The Vasomotor Center

• A cluster of sympathetic neurons in the medulla that oversee changes in blood vessel diameter

• Part of the cardiovascular center, along with the cardiac centers

• Maintains vasomotor tone (moderate constriction of arterioles)

• Receives inputs from baroreceptors, chemoreceptors, and higher brain centers

Copyright © 2010 Pearson Education, Inc.

Short-Term Mechanisms: Baroreceptor-Initiated Reflexes

• Baroreceptors are located in

• Carotid sinuses

• Aortic arch

• Walls of large arteries of the neck and thorax

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Short-Term Mechanisms: Baroreceptor-Initiated Reflexes

• Increased blood pressure stimulates baroreceptors to increase input to the vasomotor center

• Inhibits the vasomotor center, causing arteriole dilation and venodilation

• Stimulates the cardioinhibitory center

Copyright © 2010 Pearson Education, Inc. Figure 19.9

Baroreceptors in carotid sinusesand aortic archare stimulated.

Baroreceptorsin carotid sinusesand aortic archare inhibited.

Impulses from baroreceptorsstimulate cardioinhibitory center(and inhibit cardioacceleratorycenter) and inhibit vasomotorcenter.

Impulses from baroreceptors stimulatecardioacceleratory center (and inhibit cardioinhibitorycenter) and stimulate vasomotor center.

CO and Rreturn bloodpressure tohomeostatic range.

CO and Rreturn blood pressureto homeostatic range.

Rate ofvasomotor impulsesallows vasodilation,causing R

Vasomotorfibers stimulatevasoconstriction,causing R

Sympatheticimpulses to heartcause HR, contractility, and CO.

Sympatheticimpulses to heartcause HR, contractility, and CO.

Stimulus: Blood pressure(arterial bloodpressure falls belownormal range).

Stimulus: Blood pressure(arterial bloodpressure rises abovenormal range).

3

2

1

5

4a

4b

Homeostasis: Blood pressure in normal range

4b

3

2

1

5

4a

Copyright © 2010 Pearson Education, Inc. Figure 19.9 step 5

Baroreceptorsin carotid sinusesand aortic archare inhibited.

Impulses from baroreceptorsstimulate cardioacceleratory center(and inhibit cardioinhibitory center)and stimulate vasomotor center.

CO and Rreturn bloodpressure tohomeostaticrange.

Vasomotorfibers stimulatevasoconstriction,causing R

Sympatheticimpulses to heartcause HR, contractility, and CO.

Stimulus: Blood pressure(arterial bloodpressure fallsbelow normalrange).

2

3

1

4b

4a

5

Homeostasis: Blood pressure in normal range

Copyright © 2010 Pearson Education, Inc.

Short-Term Mechanisms: Baroreceptor-Initiated Reflexes

• Baroreceptors taking part in the carotid sinus reflex protect the blood supply to the brain

• Baroreceptors taking part in the aortic reflex help maintain adequate blood pressure in the systemic circuit

Copyright © 2010 Pearson Education, Inc.

Short-Term Mechanisms: Chemoreceptor-Initiated Reflexes

• Chemoreceptors are located in the

• Carotid sinus

• Aortic arch

• Large arteries of the neck

Copyright © 2010 Pearson Education, Inc.

Short-Term Mechanisms: Chemoreceptor-Initiated Reflexes

• Chemoreceptors respond to rise in CO2, drop in pH or O2

• Increase blood pressure via the vasomotor center and the cardioacceleratory center

• Are more important in the regulation of respiratory rate (Chapter 22)

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Influence of Higher Brain Centers

• Reflexes that regulate BP are integrated in the medulla

• Higher brain centers (cortex and hypothalamus) can modify BP via relays to medullary centers

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Short-Term Mechanisms: Hormonal Controls

• Adrenal medulla hormones norepinephrine (NE) and epinephrine cause generalized vasoconstriction and increase cardiac output

• Angiotensin II, generated by kidney release of renin, causes vasoconstriction

Copyright © 2010 Pearson Education, Inc.

Short-Term Mechanisms: Hormonal Controls

• Atrial natriuretic peptide causes blood volume and blood pressure to decline, causes generalized vasodilation

• Antidiuretic hormone (ADH)(vasopressin) causes intense vasoconstriction in cases of extremely low BP

Copyright © 2010 Pearson Education, Inc.

Long-Term Mechanisms: Renal Regulation

• Baroreceptors quickly adapt to chronic high or low BP

• Long-term mechanisms step in to control BP by altering blood volume

• Kidneys act directly and indirectly to regulate arterial blood pressure

1. Direct renal mechanism

2. Indirect renal (renin-angiotensin) mechanism

Copyright © 2010 Pearson Education, Inc.

Direct Renal Mechanism

• Alters blood volume independently of hormones

• Increased BP or blood volume causes the kidneys to eliminate more urine, thus reducing BP

• Decreased BP or blood volume causes the kidneys to conserve water, and BP rises

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Indirect Mechanism

• The renin-angiotensin mechanism

• Arterial blood pressure release of renin

• Renin production of angiotensin II

• Angiotensin II is a potent vasoconstrictor

• Angiotensin II aldosterone secretion

• Aldosterone renal reabsorption of Na+ and urine formation

• Angiotensin II stimulates ADH release

Copyright © 2010 Pearson Education, Inc. Figure 19.10

Arterial pressure

Baroreceptors

Indirect renalmechanism (hormonal)

Direct renalmechanism

Sympathetic stimulationpromotes renin release

Kidney

Renin release

catalyzes cascade,resulting in formation of

ADH releaseby posterior

pituitary

Aldosteronesecretion by

adrenal cortex

Waterreabsorptionby kidneys

Blood volume

Filtration

Arterial pressure

Angiotensin II

Vasoconstriction( diameter of blood vessels)

Sodiumreabsorptionby kidneys

Initial stimulus

Physiological response

Result

Copyright © 2010 Pearson Education, Inc. Figure 19.11

Activity ofmuscularpump andrespiratory

pump

Releaseof ANP

Fluid loss fromhemorrhage,

excessivesweating

Crisis stressors:exercise, trauma,

bodytemperature

Bloodbornechemicals:

epinephrine,NE, ADH,

angiotensin II; ANP release

Body size

Conservationof Na+ and

water by kidney

Blood volumeBlood pressure

Blood pH, O2, CO2

Dehydration,high hematocrit

Bloodvolume

Baroreceptors Chemoreceptors

Venousreturn

Activation of vasomotor and cardiacacceleration centers in brain stem

Heartrate

Strokevolume

Diameter ofblood vessels

Cardiac output

Initial stimulus

Result

Physiological response

Mean systemic arterial blood pressure

Bloodviscosity

Peripheral resistance

Blood vessellength