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KINE 639 - Dr. Green Section 1 Clinical Physiology I, II, III, IV. Definitions, Concepts, and Hemodynamics. Cardiac Anatomy. Aorta. Superior Vena Cava. Left Pulmonary Artery. Left Atrium. Right Pulmonary Veins. Left Pulmonary Veins. Right CA. Left Anterior Descending CA. Right Atrium.

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KINE 639 - Dr. Green

Section 1

Clinical Physiology I, II, III, IV



Cardiac Anatomy

Aorta

Superior Vena Cava

Left Pulmonary Artery

Left Atrium

Right Pulmonary Veins

Left Pulmonary Veins

Right CA

Left Anterior Descending CA

Right Atrium

Inferior Vena Cava

Left Ventricle

Right Ventricle


Cardiac Anatomy

Aorta

Superior Vena Cava

Left Pulmonary Artery

Aortic Valve

Left Atrium

Right Pulmonary Veins

Left Pulmonary Veins

Right Atrium

Tricuspid Valve

Mitral Valve

Inferior Vena Cava

Left Ventricle

Right Ventricle

Notice that the left ventricle contains more electrically active muscle mass than the right ventricle


Lungs

The Normal Heart and Regional Circulation

Anterior Cutaway View

Pulmonary Semilunar Valve

Aorta

Left Pulmonary Artery

Superior Vena Cava

Left Pulmonary Veins

Left Atrium

Right Pulmonary Artery

Aortic Semilunar

Valve

Bicuspid or Mitral Valve

Right Pulmonary Veins

Tricuspid Valve

Apex

Inferior Vena Cava

Septum


The Normal Heart - Coronary Artery Anatomy

Left Main CA

Layers of the Arterial Wall

Circumflex

Adventitia

Media

Intima

Right CA

Marginal Branch

Left Anterior Descending CA


Left Ventricular Volumes - Definitions

End Diastolic Volume (EDV)

Volume at the end of diastole

(end of ventricular filling). In a

healthy heart this is directly

proportional to venous return

End Systolic Volume (ESV)

Volume at the end of systole

(end of ventricular contraction)

Stroke Volume (SV) = EDV - ESV

Ejection Fraction (EF) = SV

EDV

NOTE: Resting Ejection Fraction (EF) is the best indicator of both heart performance and heart disease prognosis

Left ventricular norm for EF at Rest: approximately 62%

Left Ventricular norms for Max Exercise: approximately 80%


Changes in Left Ventricular Volumes with Exercise of Increasing Intensity

EDV

120

110

100

90

Left Ventricular Volume (ml)

80

70

SV

EDV - ESV = SV

60

50

40

30

20

ESV

10

Rest

300

600 - 750

Peak Exercise

Workload or Power (kg meters / min)


Definitions Increasing Intensity

  • Cardiac Output: (Q) = HR X SV

  • Cardiac Index = Q / body surface area

  • Preload:(EDV) volume of the left ventricle at the end of diastole dependent on venous return & compliance (“stretchability”) of ventricle

  • Afterload:resistance to ventricular emptying during systole or the amount of pressure the left ventricle must generate to squeeze blood into the aorta. In a a healthy heart this is synonymous with Aortic Pressure &Mean Arterial Pressure (MAP)

  • Frank Starling Law of the Heart: the heart will contract with greater force as preload (EDV) is increased r more blood in more blood out

  • Myocardial Contractility: the squeezing contractile force that the heart can develop at a given preload

    • Regulated by:

      • Sympathetic nerve activity (most influential)

      • Catecholamines (epinephrine norepinephrine)

      • Amount of contractile mass

      • Drugs


Starlings Law of the Heart and Contractility Increasing Intensity

Starling’s Law:

The greater the EDV (blood going in the heart), the more blood comes out of the heart

SV

(left ventricular performance)

uContractility

Normal Contractility

SV at Preload X - u contractility

SV at Preload X – Normal cont.

SV at Preload X - d contractility

d Contractility

(heart failure)

The State of Myocardial Contractility determines the amount of blood (SV) that comes out of the heart at a given preload

Preload

(venous return or EDV)

Preload X


Influences on Myocardial Contractility Increasing Intensity

u Contractility related to :

Exercise: - ub sympathetic adrenergic nerve output

Catecholamines:-Epinephrine & Norepinephrine

Excitement or Fear: - Fight or flight mechanism

Drugs:- Digitalis & Sympathomimetics

d Contractility related to:

Loss of contractile mass: - Most likely due to heart attack

Myocardial muscle disease: - Cardiomyopathy

Drugs: - Anesthetics, Barbiturates


Definitions Increasing Intensity

  • Arteriovenous Oxygen Difference (AVO2D) the difference in oxygen content between arterial and venous blood

    • measured in ml% - ml O2 / 100 ml blood

  • Oxygen Consumption (VO2) - the rate at which oxygen can be used in energy production and metabolism

    • “absolute” measures: L O2 / min , ml O2 / min

    • “relative” measures: ml O2 / kg body wt. / min

    • Fick equation: VO2= Q X AVO2D

  • Maximum Oxygen Consumption (VO2max) maximum rate at which a person can take in and utilize oxygen to create usable energy

    • defined as plateau of consumption rate increase

    • often estimated with VO2peak

  • Myocardial Oxygen ConsumptionVO2 of the heart muscle (myocardium)

    • "estimated" by RPP: HR X SBP


  • Definitions Increasing Intensity

    • Systolic Blood Pressure (SBP) pressure measured in brachial artery during systole (ventricular emptying and ventricular contraction period)

    • Diastolic Blood Pressure (DBP) pressure measured in brachial artery during diastole (ventricular filling and ventricular relaxation)

    • Mean Arterial Pressure (MAP) "average" pressure throughout the cardiac cycle against the walls of the proximal systemic arteries (aorta)

      • estimated as: .33(SBP - DBP) + DBP

    • Total Peripheral Resistance (TPR)- the sum of all forces that oppose blood flow

      • Length of vasculature (L)

      • Blood viscosity (V)

      • Vessel radius (r)

    TPR = ( 8 ) ( V ) ( L )

    ( p ) ( r 4 )


    Cardiovascular Hemodynamic Basics Increasing Intensity

    Pressure (MAP) P aorta – P vena cava

    = =

    Resistance (TPR) (8) (V) (L)

    () (r 4)

    Flow (Q)

    = () (Pa – Pv) (r 4)

    (8) (V) (L)

    Flow (Q)

    Normally Resting Q is about 5 - 6 liters / minute

    V = viscosity of fluid (blood) flowing through the pipe

    L = length of pipe (blood vessel)

    r = radius of the pipe (blood vessel)

    Pa = aortic pressure

    Pv = venous pressure


    Respiratory Physiology - Definitions Increasing Intensity

    • Minute Ventilation (VE)– amount of air passing through the lungs in one minute

    • Dyspnea- breathing difficulty

    • Respiratory Exchange Ratio - amount of CO2 expired by the lungs divided by the amount of O2 extracted from the air in the lungs (VCO2 /VO2 ). RER = .7 r 100% fat 0% carb RER = .85 r 50% fat 50% carb RER = 1.0 r 0% fat 100% carb


    Neurophysiology - Definitions Increasing Intensity

    • Afferent - sensory nerves - going toward spinal column

    • Efferent - effector nerves - going away from spinal column

    Motor cortex

    (control of voluntary muscles)

    Central sulcus

    Basil nuclei

    (planning, organizing, coordinating motor movements)

    Sensory cortex

    (Sensation & pain)

    Essential Knowledge of the Areas of the Brain in Green

    Sulcus

    Corpus callosum

    Gyrus

    Choroid Plexus

    Broca’s area

    (motor, speech

    Taste area

    Thalamus

    Parietal lobe

    General interpretive

    area

    Parietal lobe

    Frontal

    lobe

    Pineal gland

    Frontal lobe

    Occipital lobe

    Occipital

    lobe

    Visual

    area

    Reticular

    activation

    system (sleep wake)

    Hypothalamus

    Temporal lobe

    Pituitary gland

    Optic chiasma

    Cerebellum

    (movement

    coordination & balance)

    Lateral sulcus

    Cerebellum

    Pons

    Brainstem (control of HR, BP, and respiration)

    Medulla oblongata

    Auditory

    cortex

    Vestibular

    area

    Temporal lobe

    Fourth Ventricle

    Central canal


    Organization of the Nervous System Increasing Intensity

    Nervous System

    Central Nervous System (CNS)

    Peripheral Nervous System (PNS)

    Spinal Cord

    Brain

    Motor (efferent) Neurons

    Sensor (afferent) Neurons

    Autonomic Nervous System

    Somatic Nervous System

    Voluntary movement

    Output to

    Skeletal muscles

    Involuntary (Reflexes)

    Input from

    Internal receptors

    Output to smooth

    muscles and CVS

    Sympathetic Motor System

    Parasympathetic Motor System

    Relaxing responses

    Neurotransmitter:

    acetylcholine

    Cholinegeric nervous system

    Flight or Fight responses

    Neurotransmitter:

    nonadrenaline

    Adrenergic nervous system


    Adrenergic Receptors & Associated Responses Increasing Intensity

    • a1stimulation:

      • Constriction of blood vessels

        • Vascular smooth muscle activation

      • Constriction of lung bronchioles

      • Constriction of bladder muscles

      • u myocardial cardiac contractility

      • Relaxation of GI tract

    • a2stimulation:

      • u central sympathetic outflow

        • u release of E & NE

        • a1 & b1 receptor activation

      • Constriction of lung bronchioles

    • b1stimulation:

      • u in HR

      • u in myocardial contractility

      • u in Renin secretion

        • u fluid retention

    • b2stimulation:

      • Dilation of lung bronchioles

      • Dilation of blood vessels

    Agonist – body molecule or drug “stimulator”

    Antagonist - body molecule or drug “in-activator”

    a2Agonists

    b1 & b2Agonists

    Agonists in the adrenergic system are primarilyepinephrineandnorepinephrine

    Antagonists are many times associated with drugs known as “blockers” i.e.“b-blocker”or“a-blocker”

    Responses


    Brain Increasing Intensity

    Lungs

    Arteries (Stiff Inflexible “Pipes”)

    Veins (Flexible Compliant “Pipes”)

    Intima

    Intima

    Valve

    Elastin

    Elastin

    Media

    Media

    Liver

    Stomach

    Externa

    Externa

    Pancreas

    Serosa

    Intestines

    Kidneys

    The Systemic Circulation

    Arterioles and Pre-capillary Sphincters

    Skin

    Muscle


    Microcirculatory Anatomy – a Capillary Bed Increasing Intensity

    Arteriole

    Smooth Muscle

    Pre-capillary Sphincters

    (closed in this illustration)

    Anastomosis (Shunt)

    Capillary

    Bed

    Metarteriole

    Capillary in Cardiac Muscle (arrows)

    Venule


    Development of the driving pressure in the human cardiovascular system
    Development of the Driving Pressure in the Human Cardiovascular System

    100

    Arterial

    100

    Pressure

    Normal Resting Pressure Driving the Blood from Left Ventricle to Vena Cava:

    100 - 0 = 100 mmHg

    (mm Hg)

    26

    Mean

    Circulatory

    Filling Pressure

    7

    7

    0

    7

    6

    7

    0

    Central

    0

    Venous

    Pressure

    (mm Hg)

    1

    5

    0

    Normal

    Resting

    Cardiac Output

    Cardiac Output (Q)

    (Liters / min)


    Arterial Pressures in Maroon Cardiovascular System

    The “Closed” Cardiovascular Hemodynamic System

    Venous Pressures in Blue

    LV

    PO2 = 160

    PCO2 = .3

    RV

    LA

    RA

    LUNGS

    AORTA

    (13)

    (100)

    (3)

    (0)

    PO2 = 100

    PCO2 = 40

    9% of blood volume

    (7)

    SYSTEMIC ARTERIES

    Ohms Law: Flow (Q) = upstream pressure – downstream pressure

    resistance

    (92)

    low compliance

    13% of blood volume

    VEINS

    (CAPACITANCE VESSELS)

    (20)

    high compliance

    64% of blood volume

    (40)

    (2)

    CAPILLARYBEDS

    ARTERIOLES

    PO2 = 40 PCO2 = 46

    7% of blood volume

    Systemic Circulation = 100 mmHg – 0 mmHg = 100 ml / sec = 6 liters / min

    Flow (Q) 1 mmHg sec / ml


    Pressure, Flow, and Resistance by Vascular Cross Sectional Area

    Veins

    Vena Cava

    Veins

    Vena Cava

    Capillaries

    Venules

    Capillaries

    Venules

    Arterioles

    Arterioles

    Arteries

    Arteries

    Aorta

    Aorta

    Cross Sectional Area

    100 mmHg

    Flow Velocity

    0 mmHg

    100 mmHg

    Relative Resistance to Flow

    Mean Arterial Pressure

    0 mmHg


    MV is an Atrio-Ventricular Valve (AV) and is bi-cuspid Area

    Aortic valve is a semilunar valve

    The Cardiac Cycle

    Aortic Valve opens

    Aortic Valve closes

    SYSTOLE

    120

    Aortic Pressure (mmHg)

    80

    Left Ventricular Pressure (mmHg)

    MV closes

    MV opens

    Atrial Contraction

    Passive Ventricular Filling

    Left Atrial Pressure (mmHg)

    0

    120

    Left Ventricular Volume (ml)

    0

    0 .2

    Time (sec)

    http://www.youtube.com/watch?v=yGlFBzaTuoI&feature=related

    http://www.youtube.com/watch?v=dYgYcH7R29I&NR=1


    Using Ventricular Pressure Curves as Indices of Contractility & Cardiac Function

    dP/dt = change in pressure per unit of time

    dP/dt

    dP/dt

    Normal

    Heart Failure

    120

    Pressure

    Note elevation in end diastolic pressure indicating the build up of pressure in the heart due to failure

    0

    Time


    Cardiac & Vascular Function Curves Contractility & Cardiac Function

    Cardiac Function Curve

    - illustrates

    Q

    what happens to Q when Pv changes.

    5

    CARDIAC

    OUTPUT

    (Liters / min)

    operating point for the cardiovascular system

    2

    Pv

    CENTRAL VENOUS PRESSURE (mmHg)

    CARDIAC PRELOAD (mmHg)

    RIGHT ATRIAL PRESSURE (mmHg)


    Cardiac Function Curve Contractility & Cardiac Function- Q is the dependent variable

    (in effect, Q is controlled by venous return & TPR)

    Sympathetic Stimulation

    ( Exercise)

    Normal Curve

    CARDIAC

    u Intrapleural Pressure

    ( Pressure in the chest cavity )

    To maintain same Q, CVP must u

    OUTPUT

    (Liters / min)

    5

    u TPR r u afterload

    Parasympathetic Stimulation

    or

    Heart Failure

    2

    7

    CENTRAL VENOUS PRESSURE (mmHg)

    ( can also be thought of as CARDIAC PRELOAD or RIGHT ATRIAL PRESSURE )


    Cardiac & Vascular Function Curves Contractility & Cardiac Function

    Cardiac Function Curve

    - illustrates

    Q

    what happens to Q when Pv (venous

    5

    return - preload) changes.

    CARDIAC

    OUTPUT

    operating point for the cardiovascular system

    (Liters / min)

    Vascular Function Curve

    - illustrates what

    happens to Pv when Q changes.

    2

    7

    Pv

    CENTRAL VENOUS PRESSURE (mmHg)

    CARDIAC PRELOAD (mmHg)

    RIGHT ATRIAL PRESSURE (mmHg)


    Vascular Function Curve Contractility & Cardiac Function- central venous pressure is dependent variable

    (in effect, CVP and venous return are controlled by Q)

    Sympathetic Stimulation

    Exercise r venoconstriction r u total active vascular volume

    ( Transfusion: u blood Volume )

    CARDIAC

    OUTPUT

    Normal

    Curve

    (Liters / min)

    5

    Decreased Arteriolar Resistance: d TPR

    ( Exercise )

    ( Peripheral Vasodilation )

    Increased Arteriolar Resistance

    ( Peripheral Vasoconstriction)

    (u TPR rd venous return r d CVP)

    2

    7

    CENTRAL VENOUS PRESSURE (mmHg)

    can also be called CARDIAC PRELOAD


    Changes in Cardiac & Vascular Function Curves with Exercise Contractility & Cardiac Function

    • During Exercise, an u in sympathetic output will cause:

    • 1. venoconstriction (VF curve shifted rightward)

    • 2. d TPR r vasodilation (VF curve rotated upward)

      • (caused primarily by vasodilator metabolites)

    • 3. u HR & contractility (cardiac curve shifted upward)

    8 - 13

    CARDIAC

    OUTPUT

    (Liters / min)

    5

    7

    2

    11

    CENTRAL VENOUS PRESSURE (mmHg)

    can also be called CARDIAC PRELOAD


    Changes in Cardiac & Vascular Function Contractility & Cardiac FunctionCurves with Acute Compensated Heart Failure

    CARDIAC

    OUTPUT

    1

    3

    (Liters / min)

    Q = 5 Liters / min

    2

    CENTRAL VENOUS PRESSURE (mmHg)

    can also be called CARDIAC PRELOAD

    1. Normal point of operating system & normal cardiac output

    2 Pump begins to fail r Q falls below normal resting levels

    3. Renin-angiotensin system activated r fluid retained r u MCFP r u Q


    Changes in Cardiac & Vascular Function Contractility & Cardiac FunctionCurves with De-compensated Heart Failure

    CARDIAC

    OUTPUT

    1

    3

    Q = 5 Liters / min

    (Liters / min)

    4

    2

    5

    Cause of peripheral edema

    CENTRAL VENOUS PRESSURE (mmHg)

    can also be called CARDIAC PRELOAD

    • 1. Normal point of operating system & normal cardiac output

    • 2. Pump begins to fail r Q falls below normal resting levels

    • Renin-angiotensin system activated r fluid retained r u MCFP r u Q

    • Pump decline continues and Q falls once again

    • More fluid is retained to try and compensate, but now Q is below a level where normal fluid balances can be maintained r r pattern continues


    Left Ventricular Pressure Volume Loop Contractility & Cardiac Function

    Aortic Valve Closes

    ESV

    ESP

    Aortic Valve Opens

    120

    Left Ventricular Pressure

    (mmHg)

    SV

    Isovolumic

    contraction

    Mitral Valve Closes

    EDV

    EDP

    6

    Slope of dashed line:

    ventricular contractility

    40

    140

    Mitral Valve Opens

    Ventricular Filling Begins

    Volume (ml)


    Effects of an Increase in Preload on Left Ventricular Pressure Volume Loop

    u Ejection Pressure

    120

    Left Ventricular Pressure

    (mmHg)

    u SV

    u EDV

    u EDP

    6

    40

    140

    Volume (ml)


    Effects of an Increase in Afterload on Left Ventricular Pressure Volume Loop

    u ESV

    u ESP

    120

    Left Ventricular Pressure

    (mmHg)

    d SV

    6

    40

    140

    Volume (ml)



    atrial Systems stretch / pressure receptors located in right & left atria, junction of right atria and vena cava, and junction of left atria and pulmonary veins

    Sites of

    Cardiorespiratory Control


    Cardiorespiratory Control Systems

    • Heart Rate– Neurohormone (neurotransmitter) and CNS (medulla) regulation

    • Parasympathetic vagus control (Neurotransmitter: Acetylcholine)

      • Vagal control is dominant at rest – influence is withdrawn when exercise begins

    • Sympathetic cardioacceleration (Neurotransmitters: EPINEPHRINE & NOREPINEPHRINE)

    • Baroreceptor influences

      • Sympathetic discharge indirectly proportional to firing rate

      • Parasympathetic discharge is directly proportional to firing rate

      • dpressure r dreceptor firing r usympatheticsr u HR r u pressure

      • u pressure r ureceptor firing r uparasympatheticsr d HR r d pressure

    • Atrial Stretch receptors: u receptor stretch ru ANP ruNa+excretionru urine output

      • d receptor stretch ruADHrdNa+excretionrd urine output

  • AtrialNatriureticPeptide released by myocytes in the atria r u urine flow r d BP

  • Aniti-Diuretic-Hormone (vasopressin) released by pituitary r d urine flow r u BP

  • Chemoreceptor influences

    • Main function: protect brain from poor perfusion

    • u O2or d CO2r uparasympathetic discharge r d HR

    • dO2 or u CO2r dpH rpressor area stimulation in medulla r uHR

  • ADH Molecule


    Cardiorespiratory Control Systems

    • Stroke Volume (SV) – regulated by Frank Starling mechanism

      • u venous returnr u EDV r u stroke volume

    • Cardiac Output (Q)– main determinant: body O2 needs

    • Autoregulated by two distinct mechanisms

      • Intrinsic changes in preload, afterload, and SV

        • u afterload r initial d in Q r u EDV (preload) r uSV back to normal

      • Extrinsic hormonal influences

        • Norepinephrine release r u HR and SV


    Cardiorespiratory Control Systems

    • Blood Pressure– influenced by 4 major factors (some interrelated)

    • Total peripheral resistance

      • Baroreceptor (BR) and CNS Influences

        • u BP r u BR firing rate r vasodilation r d BP

        • d BP r d BR firing rate r u sympathetics r u BP

    • Chemoreceptor influences

      • dO2,u CO2, d pH r CNS stim. r vasoconstriction

      • Circulating catecholamine influences

        • E and NE have varying effects on TPR

        • E and NE usually activate areceptors r u TPR

      • Fight or flight response

    • Q

    • Blood Volume

      • Renin – Angiotensin System


    HYPOTENSION Systems

    HYPOVOLEMIA

    Renin - Angiotensin System

    u H2O reabsorbed

    d renal profusion

    u sympathetic tone

    u ADH (vasopressin)

    d stretch in afferent arteriolar JG cells

    d NACL delivery to macula densa cells

    u messangial cell contraction

    uRENIN

    d GFR

    uangiotensin I

    d stretch receptor activation in atria, aorta, and carotid sinuses

    uangiotensin II

    u BLOOD PRESSURE

    via vasoconstriction (angiotensin II is a potent vasoconstrictor)

    u aldosterone

    neg feedback

    u Na+ re-absorption

    (and K+ excretion)

    Controls Body Fluid Balance and Associated Regulation Mechanisms and Pathways

    u thirst

    (thirst is more strongly regulated by osmotic receptors in the hypothalamus)

    u ECF volume ru BP

    neg feedback

    dRENIN


    Dehydration Systems

    • Dehydration: the loss of body water and associated electrolytes

    • Causes:

      • Gastroenteritis (viral / bacterial infection r vomiting & diarrhea) - most common

      • Diseases: yellow fever, cholera,

      • Excessive alcohol consumption

        • The excess fluid is flushed out by the kidneys: u water usage rdehydration

        • Most liquors have congenerswhich are toxic to body r removal necessary

          • The clearer & better quality your liquor (vodka & gin) the less congeners

            • more distillation cycles r better quality

        • When you drink, head vessels dilate….constriction next morning r headache

        • Congener removal done by liver: d liver glucose r hypoglycemia & lethargy

      • Prolonged exercise without fluid replacement (heat exhaustion & heat stroke risk)

      • Diabetes: hyperglycemia r u glucose excretion r u water loss r dehydration

      • Shock: blood loss due to some hypotensive state caused by injury or disease

        • Gastrointestinal blood loss: bleeding from ulcers or colorectal cancer


    Dehydration Systems

    • Signs & Symptoms of dehydration:

      • Dry mouth, dry swollen tongue, rapid heart rate (possible chest palpitations)

      • Lethargy (sluggishness), confusion

      • Poor skin turgor (a pinch of skin does not spring back into position)

        • Good test for ailing elderly folks

      • Elevated BUN (renal function test): NH4 metabolized in liver & excreted by kidneys

      • Elevated creatinine r d GFR (kidney clearance of waste products)

      • Increased blood viscosity

      • Headache

      • Fluid loss r low blood pressure r dizziness upon standing up

      • A high urinary specific gravity (comparison of density to water: 1 gram / cm 2)

    • Treating Dehydration

      • Sip small amounts of water

      • Drink carbohydrate / electrolyte solutions: Gatorade, Pedialyte, etc.

      • If core body temperature > 104 0 + d BP or u HR r consider IV fluid replacement


    Cardiorespiratory Control Systems

    • Skeletal Muscle Blood Flow – autoregulated – 2mechanisms

    • Mechanism 1: Vasodilator Metabolites

      • Usually overrides adrenergic neurohormone control

      • Mediated by vasodilator metabolite (VDM) buildup & removal

        • Adenosine (ATP by-product), CO2, H+, prostaglandins

        • Exercise Example – (negative feedback control)

          • Muscle exercises r VDM’s released r u vasodilation

          • u vasodilation u blood flow r VDM’s removed r vasoconstriction

    • Mechanism 2: Myogenic response

      • Involves stretch activated Ca++ channels (negative feedback control)

        • u blood flow r vessel stretch r Ca++ channel activation

        • u [Ca++ ] in smooth muscle r vasoconstriction r d flow


    Cardiorespiratory Control Systems

    • Systemic Blood Flow During Exercise:

    • Autonomic influences

    • Sympathetic outflow & circulating catecholamines

      • a activation r vasoconstriction in non - exercising tissue

    • Redistribution of blood flow during maximal exercise

      • - NC in brain blood flow - 500 ml/min u to heart

      • - 11,300 ml/min u to muscle - 400 ml/min u to skin

      • - 500 ml/min d to kidneys - 800 ml/min d to viscera

      • - 200 ml/min d to various other parts of the body


    Cardiorespiratory Control Systems

    • Respiration: Minute Ventilation (VE) = Tidal Volume X Respiratory Rate

    • GenerallyControlled via central chemoreceptors in the medulla-pons respiratory center

    • Peripheral chemoreceptors

      • u blood CO2 content r receptor activation ru VE

      • dblood O2 content r receptor activation ru VE

    • Central chemoreceptors in the medulla respiratory center – Dominant Influence

      • u blood CO2 & lactate r receptor activation ruVE

      • PaCO2 ru HCO3¯ + H+ r H+ activates receptor ru VE

    • Respiratory control during exercise – no consensus but research suggests:

      • Muscle spindle & proprioceptor activation ru VE at early onset of an exercise bout

      • Respiratory centers (medulla) sends afferent signals to expiratory muscles during exercise

      • u venous returnr atrial receptor activation ru VE ??

      • Intrapulmonary receptor activation ru VE ??

      • Peripheral chemoreceptors may play a role in steady state & high intensity exercise VE ??

    • Minute ventilation mechanistic changes during an u in exercise intensity

      • Low exercise intensity: VEu by both u TV and u RR

      • High exercise intensity: VE u by u RR only

    • Notes:

    • O2 cost of breathing during exercise: 4.5% VO2 (low int.) up to 12.5%VO2 (high int.)



    Acute Responses to Aerobic Exercise Systems

    • Oxygen Consumption (VO2)

      • u VO2 in direct proportion to u workload (power requirement of exercise)

      • Expressed in both relative and absolute terms

        • Relative: ml O2/kg/min Absolute: ml/min or L/min

        • Average VO2max for 40 year old male 37 ml/kg/min

      • Oxygen consumption linked to caloric expenditure (1 liter of O2 consumed = 5 kcal)

    • Heart Rate

      • u up to 3 times resting value at peak exercise (mainly due to dtime spent in diastole)

    180

    160

    140

    100

    Heart

    Rate

    • HR – VO2 relationship is linear until about 90% VO2max

    1.0 2.0 3.0

    Oxygen Uptake (L / min)

    50 150 250

    Workloads (Watts)


    Acute Responses to Aerobic Exercise Systems

    • Stroke Volume

      • u up to 1.5 resting value at peak exercise

        • Increase levels off at 40% - 50% VO2 max??

      • u in venous return r u EDV (Starling mechanism)

      • d ESV eluding to an u in myocardial contractility

      • u ejection fraction rest: 58% max exercise: 83%

    • Cardiac Output (Q)

      • u up to 4 times resting value at peak exercise (u is rapid at onset, then levels off)

      • u Q r u venous return

        • Venous return mediated by and related to:

          • Sympathetic venoconstriction

          • Muscle pump

          • u inspiration r d thoracic pressure

            • Blood flows to an area of reduced pressure

          • u inspiration r u abdominal pressure

            • Contraction of abdominal muscles r squeezing of abdominal veins

    ??

    120

    110

    70

    120

    110

    70

    Stroke

    Volume

    (ml/beat)

    Recent Findings

    All Older Studies

    25% 50% 75% 100%

    25% 50% 75%

    Percentage of VO2 max

    Percentage of VO2 max


    • Arteriovenous oxygen difference Systems

      • Difference in [O2] between arterial and mixed venous blood

      • Illustrated by the oxyhemoglobin desaturation curve

      • u approximately 3 fold from rest to max exercise

      • At rest, about 25% of arterial O2 is extracted

      • At peak exercise about 75% - 85% of arterial O2 is extracted

    • Blood Pressures and Resistance to Flow

      • SBP: u - failure to u signifies heart failure

      • DBP: slight u or slight d or NC

      • MAP: slight u

      • TPR: d - mainly due to vasodilation in exercising muscle

    • Coronary (Myocardial) Blood Flow

      • 4.5% of Q goes to myocardium at rest and at peak exercise

        • This increase is due to u MAP and CA vasodilation

    • Blood Flow to the Skin

      • u as exercise duration u to allow for heat dissipation

      • d at max exercise to meet exercising muscle demands

      • u during exercise recovery, again for heat dissipation

    Acute Responses to Aerobic Exercise


    Acute Responses to Aerobic Exercise Systems

    • Minute Ventilation

      • Resting average: 6 Liters/min

      • Peak exercise average: 175 Liters/min (29 fold increase from rest to max)

      • Respiratory rate: resting 12-18 peak exercise: 45-60

      • Tidal volume: resting .5 liters peak exercise: 2.25 Liters

    • Plasma Volume

      • Blood plasma u in the interstitium of exercising muscle

      • Fluid shift results in a 5% d in plasma volume

        • This is termed “Hemoconcentration”

      • Blood viscosity increases


    Acute Responses to Aerobic Exercise Systems

    • Immune system

      • During moderate / vigorous exercise, the following changes occur in immune activity

        • Transient u in the re-circulation of neutrophils, NKC’s, and immunoglobulins

          • More pathogens detected and killed

        • Transient din stress hormones (cortisol) and inflammatory mediators (cytokines)

          • Cortisol and cytokines suppress the immune system

      • Immune function returns to normal in a few hours, but exercise improves “surveillance”

      • 25% - 50% reduction in sick days with upper respiratory infections (colds, flu, etc.)

      • Opposite effect occurs with prolonged heavy exercise

        • Example: after marathon, immune function d 2 - 6 fold depending on time of year


    Oxygen Debt and Deficit Systems

    Note upward “Drift” in VO2

    Oxygen Deficit

    Oxygen Debt

    (EPEOC)

    “Steady State”

    VO2

    VO2

    Untrained or people with

    certain cardiorespiratory

    diseases will have larger

    DEFICITS andDEBTS

    Rest

    EXERCISE TIME

    AT CONSTANT WORKLOAD

    Termination of bout

    Onset of bout

    • Oxygen Deficit due to:

      • Delay in time for aerobic ATP production to supply energy

    • Oxygen Debt due to:

      • Resynthesis of high energy phoshosphates (CP, ATP)

      • Replace oxygen stores

      • Lactate conversion to glucose (gluconeogenesis)

      • u HR, respiration, catecholamines, body temperature


    OBLA Systems

    Respiratory Compensation

    (hyperventilation)

    “Desaturation” in

    CHF & COPD patients

    “Desaturation” in

    Elite Athletes

    No Change in

    VE

    VCO2

    Ventilatory and Metabolic Changes During Exercise

    Increasing workload



    • Resting Systems

    • NC NC

    • VO2= HR x SV x AVO2diff

    • due to: due to:

    • u time in diastole u preload

    • d afterload (small)

    • u ventricle size

    • u blood volume

    • Submax Workload (measured at same pre-training workload)

    • NCNC

    • VO2= HR x SV x AVO2diff

    • note: a slight d in afterload (mentioned above)

    • accompanied by a d in HR translates into a reduction

    • myocardial VO2at rest or at any submaximal workload

    • Max Workload (measured at peak exercise)

    • NC

    • VO2= HR x SV x AVO2diff

    • some studies show

    • a slight decrease

    Effects of Exercise Training on the Components of the Fick Relationship


    Training Adaptations Systems

    • Mean Arterial Pressure

      • Small d at rest or during exercise

    • Systolic and Diastolic Blood Pressure

      • Small d(6 – 10 mmHg) at rest

      • Larger d(10 – 12 mmHg)at submaximal workload

        • Exercise: first line of therapy for borderline hypertensives

        • Some studies report a mean d of about 9 mmHg

    • Total Peripheral Resistance and Afterload

      • u capillarization (more parallel circuits) r d Transit time for blood

      • d TPR r d Afterload

    • Respiratory Variables

      • Respiratory Rate

        • Rest: NC

        • Submax exercise: d slightly

          • Air remains in lungs longer

          • More O2 extracted (about 2%)

        • Max exercise: u u VEduring submax & max exercise

      • Tidal Volume

        • Rest: NC dVE / VO2during submax exercise

        • Submax exercise: uu significantly

        • Max exercise: u

      • Anaerobic Threshold or OBLA or Ventilatory Threshold

        • Occurs at a higher percentage of VO2 max

        • Pre-training: 50% VO2max Post-training: 80% VO2max


    • Mitochondria Systems

      • u number, size and membrane surface area

    • Aerobic Enzymes in Exercising Muscle

      • u Krebs cycle enzymes (succinate dehydrogenase)

      • ub oxidation enzymes (carnitine acyltransferase)

      • u electron transport enzymes (cytochrome oxydase)

    • Fatty Acid & Glycogen Utilization

      • u utilization of boxidative pathways to produce ATP

      • Called the “glycogen sparring effect”

      • d RER for any given submaximal workload

      • u muscle glycogen stores (with high carbohydrate diet)

    • No Appreciable Change in Resting Metabolic Rate

      • Exception: training induced u in lean muscle mass

    • d Platelet Aggregation

    • u Fibrinolytic Activity

    • d Circulating Catecholamines

      • u vagal tone r d risk of arrhythmia

    • u Resistance to Pathological Events

      • Smallerinfarct size and quicker recovery

      • Less of a d in ventricular function during ischemia

    Training Adaptations

    Death from all causes increases significantly when VO2max falls below

    7.9 METS (27.65 ml/kg/min)

    Kodama’s Meta Analysis, JAMA, 301, 19, 2009.


    "Average" Values for Sedentary and Trained Individuals Systems

    Heart Rate

    ( beats / minute )


    "Average" Values for Sedentary and Trained Individuals Systems

    Stroke Volume

    ( ml / beat )


    "Average" Values for Sedentary and Trained Individuals Systems

    Cardiac Output

    ( liters / minute)



    "Average" Values for Sedentary and Trained Individuals Systems

    Oxygen Consumption

    ( liters / minute)


    "Average" Values for Sedentary and Trained Individuals Systems

    Oxygen Consumption

    ( ml / kg / minute)


    "Average" Values for Sedentary and Trained Individuals Systems

    Systolic Blood Pressure

    ( mm Hg)


    "Average" Values for Sedentary and Trained Individuals Systems

    Diastolic Blood Pressure

    ( mm Hg)


    "Average" Values for Sedentary and Trained Individuals Systems

    Minute Ventilation

    ( liters / minute)


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