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Filtration

Secretion

Reabsorption

Circulatory System Circulates

• Nutrients: glucose, amino acids, fatty acids, ketones, etc• Wastes:• Hormones: bound & free

• Gases: CO2 and O2

• Formed Elements: Cells and Cell Fragments– Erythrocytes, Leukocytes, Thrombocytes = Platelets

Other roles of the Cardiovascular System

Thermoregulation

Blood Clotting

Reproduction (ex: penile erection)

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Figure 12.01Blood volume ~ 5 liters

Serum = plasma – clotting factors

Formed elements

Components……

Blood doping & erythropoietin (hormone that stimulates erythrocyte production in bone marrow) to increase hematocrit

Entering and Exiting the blood

Discontinuous capillaries in bone marrow, spleen, & liver permit erythrocytes to enter and exit blood.

Hct = percentage of blood volume occupied by RBCs

Anemia

EPO and “The Scoop on Tissie”

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Fig. 12.02Arteries..away from heart

Veins..return to heart

Regional blood flow determined by arteries and arterioles.

Resting Cardiac Output = 5L/min for each side!

When left heart can’t pump all the blood it receives from pulmonary circuit (due to high aortic pressure and/or damage to left ventricle) blood accumulates in pulmonary circuit. This is congestive heart failure. Symptom: shortness of breath.

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Figure 12.04

CO = 5L/minfor each circuit

Up to 35 L/min in strenuous exercise

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What’s missing?

Microcirculation

Pulmonary circuit

Systemic Circuit

CO = 5 liters/minCO = 5 liters/min

Exchange Vessels

Resistance Vessels

Capacitance vessels

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Recall Portal Systems!Arterial Blood Pressure

Pulmonary circuit

Systemic Circuit

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Pressure gradients makes fluids move. Moving fluids flow, but flow is limited by resistance. Resistance creates pressure.

Arterioles establish Mean Arterial Pressure

F=Q=ΔP/RFlow = Pressure gradient/Resistance

from Ohm’s Law (V=IR)

R = 8Lη/πr4

Q= ΔP πr4

8LηPoiseulle’s equation

Smooth muscles determine radius

Double radius … 16x flow

Half radius….1/16th flow

Radius of arterioles regulates Q to organs

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MAP = CO x TPR

Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance

MAP = (HR x SV) x TPR

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Cardiac Output = Heart Rate X Stroke Volume

What regulatesheart rate?

CO = HR x SV

5L/min = 72 beat/min x 70 ml/beat

The Cardiac Cycle animation

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What regulatesStroke Volume?

Figure 12.07

Bicuspid=Mitral

Tricuspid

Problems with valves:

….Stenosis (narrowing) →Heart Murmurs (turbulent flow past a constriction)

note: origin of neonatal heat murmurs (foramen ovale)

….Prolapse (eversion) allows backflow (also generates murmurs)

SemilunarValves

Heart sounds produced by valve closings

Animation

Heart murmurs ≠ heart sounds

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Figure 12.13

CardiacMyofiber

Plateau phaseCardiac Myofiberaction potential

Long refractory period prevents summation in cardiac myofibers

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Figure 12.11

SA node cells

do not have stable resting membrane potential,

spontaneously produce AP,

are Pacemaker cells

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Figure 12.14

Pacemaker Cells in

Conducting System:

SA Node andBundle of His

Ectopic Pacemaker

Locations other than SA Node

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Cardiac Pacemakeraction potential

These cells set the rhythm & control Heart Rate.

1QQ # 14: Answer one.1. A) Which vessels are classified as exchange

vessels?B) Why are they called exchange vessels?

2. A) What produces a heart sound?B) What produces a heart murmur?

3. With all other factors held constant, how would blood flow be affected by a doubling of the pressure gradient?

4. A) Explain how a heart can continue to beat even if the SA node is not functioning.B) Would this heart rate be faster or slower than the rate produced by the SA node?

Figure 12.22Intrinsic Rate = 100 beat/min

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2 effects of Parasymp:hyperpolarization &slower depolarization

Figure 12.23

Effect of “Beta blockers”

NE EPI ACh

mAChR

Effect of atropine

Beta-adrenergic receptors

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Fibrous connective tissue between atria and ventricles prevents the conduction of action potential. Only route is via AV node, bundle of His, bundle branches, Purkinje fibers, and to ventriclular myofibers.

What prevents the AP from being conducted from ventricles back to atria?S 7

1st Heart Sound = Closure of Atrioventricular (AV) valves at beginning of Ventricular Systole

2nd Heart Sound = Closure of Semilunar valves at beginning of Ventricular Diastole

S 8 “Sis-toe-lee”

“die-ass-toe-lee”

Figure 12.20Systolic

Diastolic

Ejection Fraction = SV/EDV

Atrial Fibrillation

Ventricular Fibrillation & Defibrillation

Stroke Volume

Animation

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Events are same for Cardiac Cycle for Right Side of Heart; only difference is lower systolic pressures in right atrium and right ventricle.

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CO = HR x SV

5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat

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So far, we’ve dealt with the factors that control Cardiac Output by changing heart rate.

+ sympathetic- parasympathetic

2

1

3

Figure 12.20

Stroke Volume

Animation

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Frank-Starling Law of the Heart

FS LoH = SV is proportional to EDV

Ventricular Function Curve

Does not depend on hormones or nerves

Assures that the heart adjusts its output based on VENOUS RETURN

Ways to enhance Venous Return:1) muscle contractions2) “respiratory pump”3) venoconstriction

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↑VR→ ↑EDV → ↑SV

Fig. 09.21

Low EDV

High EDV

Length-tension “curve” for Cardiac muscle

Overinflation of ventricles leads to less effective pumping

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Overinflation of ventricles results in reduction in stroke volume

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Treatments?…..diuretics

Contractility

NE from Symp postganglionics & EPI from Adrenal medulla

Note: cardiac myofibers NOT innervated by parasympathetic division

Increase Ejection Fraction

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3 Effects of SympatheticStimulation

1: Increase rate of contraction2: Increase peak tension3: Decrease twitch duration

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Why should the contraction be shorter?

Afterload is analogous to trying to pump more air into a tire that is already fully inflated (heart contracting to overcome diastolic pressure.)

High blood pressure increases the workload of the heart….. Cardiac hypertrophy….increase chance of irregular conduction of AP through heart

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Hypertrophic cardiomyopathy

Summary: Control of Stroke Volume

• End diastolic volume (preload)

• Contractility (strength of ventricular contraction due to adrenergic stimulation)

• Pressure in arteries that must be overcome = Afterload

FS LoH

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CO = HR x SV

5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat

S 11 Factors that control Cardiac Output by changing heart rate and stroke volume.

+ sympathetic- parasympathetic

EDV (FSLoH)

contractility

Afterload (MAP)

Fig. 12.28Even persons with heart transplants can adjust CO in the absence of innervation of heart.

Summary of Factors that Regulate Cardiac OutputS 12

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Heart is pump that generates pressure gradient.

Blood flows through vessels, which have resistance.

Arterioles have greatest resistance and create “backpressure” in the arteries and aorta.

Mean Arterial Pressure = diastolic +1/3(systolic – diastolic) = 70 + 1/3(120-70) = 70 + 17

= 87 mm Hg

CO = HR x SV

5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat

S 11 Factors that control Cardiac Output by changing heart rate and stroke volume.

+ sympathetic- parasympathetic

EDV (FSLoH)

contractility

Afterload (MAP)

Properties of Blood Vessels

• Arteries

• Arterioles

• Capillaries

• Venules

• Veins

Elastic, low compliance, large diameter, low resistance vessels

Variable Resistance vessels

Exchange

Capacitance vessels, high compliance, low pressure, valves for unidirectional flow

All vessels and heart chambers lined with ENDOTHELIAL cells (simple squamous)

Wall = simple squamous endothelium

No smooth muscle; cannot change diameter

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Fig. 12.29Aorta Brachial or Femoral artery

Pusatile flow

Damage to artery vs vein

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Fig. 12.39b

Analogy: river width and flow

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Fig. 12.30

Elastic recoil of stretched arterial walls during ventricular systole maintains arterial pressure during diastole as blood drains into arterioles.

Point of Confusion: Smooth muscles in arterial walls DO NOT rhythmically contract, do not pump!

Atherosclerosis

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Stretching elastic connective tissue

Recoil of elastic connective tissue

Arteries and Arterial PressureMean Arterial Pressure

ArterioleArterioles have two main functions: 1) regulate flow to tissues and organs and 2) responsible for Total Peripheral Resistance which influences Blood Pressure.

MAP = CO x TPR

Poiseulle’s Equation

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Fig. 12.50

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Heart

Arteries

Arterioles

Kid

neys

Gut

Sk.

Mus

cle

Ski

n

CN

S

Totol Peripheral Resistance

MeanArterial

Pressure

CardiacOutput

Alpha receptors more common

except in skeletal muscle arterioles which have more

B2 receptors

Receptors for other ligands

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Fig. 12.36

Metabolic autoregulation, flow autoregulation, myogenic autoregulation

No parasympathetic innervation of arterioles!Importance of sympathetic “tone.”

Metabolic vasodilators

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Figure 12.02

Capillaries = 5% of Blood Volume

Veins = 60% of Blood Volume

Arteries = 10% of Blood Volume

Arterioles = Resistance vessels

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Figure 12.38Capillaries: Continuous, discontinuous, and fenestrated capillaries:Ex: brain liver endocrine glands

Generate vasodilators and vasoconstrictors

Arterioles:1) Extrinsic control by hormones and nerves2) Intrinsic (local) control by …..a) metabolic autoregulation, …..b) flow autoregulation, and …..c) myogenic autoregulation.

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1QQ # 15 Answer one.1. Describe metabolic autoregulation and

list four substances that are classified as metabolic vasodilators.

2. What is the main difference between flow autoregulation and metabolic autoregulation?

3. Explain why the pressure in a major artery doesn’t fall to 0 during ventricular diastole.

Capillary exchange by: Diffusion, vesicle transport, bulk flow, mediated transport

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Fig. 12.40

Diffusion is the most important mode of

exchange of nutrients

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Figure 12.41

Crystalloids

Colloids

Bulk Flow

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= colloids (impermeable proteins)

Cell Membrane: selectively permeable

Capillaries: highly permeable except to proteins

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Figure 12.42

Main difference in the Pulmonary circuit?

Net filtration = 4L/day

Bulk Flow through aqueous channels and intracellular clefts

Regulated by arterioles

Starling Forces

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Fig. 12.43

Pc

Pc

Pc

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Who Cares?Aunt Esther

Cancer of the liver;Failure of hepatocytes to produce plasma colloids

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Figure 12.41

Crystalloids

Colloids

Bulk Flow

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Figure 12.47

Liver &Bone Marrow

& Spleen

Fate of 4 L/d excess filtrate

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Mode of propulsion?

Figure 12.44Veins are

Capacitance vessels(high compliance)

with valves for unidirectional flow

Arteries are low compliance,

so any increase in volume increases

pressure.

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Fig. 12.53

MAP = CO x TPR

Negative feedback control:stimulus, receptors, afferent pathway(s), integrator, efferent pathway(s), effector(s)response(s)

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+ other baroreceptors

Fig. 12.54

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What happens to the set point for MAP during exercise?

MAP = CO x TPR

Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance

MAP = (HR x SV) x TPR

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Test 3 Hemorrhage DiagramOn one page, create a well-organized diagram for the following.

Beginning with a loss of about 1 liter of blood from a vein, diagram the early events associated with hemorrhage and the negative feedback responses to hemorrhage in a well-organized diagram. Write legibly! Completeness, accuracy, and detail, together with the proper sequence earn maximal points.

The following abbreviations can be used: ACE, AI, AII, Aldo (aldosterone), JGA, mAChR, Hct, Q, SV, EF (ejection fraction), RBC, HR, EDV, ACh, ANH, ADH, CO, TPR, EPO, VR, MAP, EPI, NE, SAN (SA Node), aAdR , bAdR, Symp (sympathetic), Parasymp (parasympathetic), PV (plasma volume), r (radius), Pc, fAP (frequency of action potentials.) Any other abbreviations must be defined. "If in doubt, write it out!" Use single headed arrows (→) to indicate sequential relationships and doubled-stemmed arrows to indicate increases or decreases.

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