Cardiac Output, Blood Flow, and Blood Pressure

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Chapter 14
Cardiac Output, Blood Flow, and Blood Pressure
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Cardiac Output (CO)

• Is volume of blood pumped/min by each ventricle
• Stroke volume (SV) blood pumped/beat by each
  ventricle
• CO SV x HR
• Total blood volume is about 5.5L

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Regulation of Cardiac Rate

• Without neuronal influences, SA node will drive
  heart at rate of its spontaneous activity
• Normally Symp Parasymp activity influence HR
  (chronotropic effect)
• Autonomic innervation of SA node is main
  controller of HR
• Symp Parasymp nerve fibers modify rate of
  spontaneous depolarization

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Regulation of Cardiac Rate continued

• NE Epi stimulate opening of pacemaker HCN
  channels
• This depolarizes SA faster, increasing HR
• ACH promotes opening of K channels
• The resultant K outflow counters Na influx,
  slowing depolarization decreasing HR

Fig 14.1
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Regulation of Cardiac Rate continued

• Cardiac control center of medulla coordinates
  activity of autonomic innervation
• Sympathetic endings in atria ventricles can
  stimulate increased strength of contraction

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Stroke Volume

• Is determined by 3 variables
• End diastolic volume (EDV) volume of blood in
  ventricles at end of diastole
• Total peripheral resistance (TPR) impedance to
  blood flow in arteries
• Contractility strength of ventricular
  contraction

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Regulation of Stroke Volume

• EDV is workload (preload) on heart prior to
  contraction
• SV is directly proportional to preload
  contractility
• Strength of contraction varies directly with EDV
• Total peripheral resistance afterload which
  impedes ejection from ventricle
• Ejection fraction is SV/ EDV
• Normally is 60 useful clinical diagnostic tool

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Frank-Starling Law of the Heart

• States that strength of ventricular contraction
  varies directly with EDV
• Is an intrinsic property of myocardium
• As EDV increases, myocardium is stretched more,
  causing greater contraction SV

Fig 14.2
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Frank-Starling Law of the Heart continued

• (a) is state of myocardial sarcomeres just before
  filling
• Actins overlap, actin-myosin interactions are
  reduced contraction would be weak
• In (b, c d) there is increasing interaction of
  actin myosin allowing more force to be
  developed

Fig 14.3
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Extrinsic Control of Contractility

• At any given EDV, contraction depends upon level
  of sympathoadrenal activity
• NE Epi produce an increase in HR contraction
  (positive inotropic effect)
• Due to increased Ca2 in sarcomeres

Fig 14.4
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Fig 14.5
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Venous Return

• Is return of blood to heart via veins
• Controls EDV thus SV CO
• Dependent on
• Blood volume venous pressure
• Vasoconstriction caused by Symp
• Skeletal muscle pumps
• Pressure drop during inhalation

Fig 14.7
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Venous Return continued

• Veins hold most of blood in body (70) are thus
  called capacitance vessels
• Have thin walls stretch easily to accommodate
  more blood without increased pressure (higher
  compliance)
• Have only 0-10 mm Hg pressure

Fig 14.6
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Blood Body Fluid Volumes
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Blood Volume

• Constitutes small fraction of total body fluid
• 2/3 of body H20 is inside cells (intracellular
  compartment)
• 1/3 total body H20 is in extracellular
  compartment
• 80 of this is interstitial fluid 20 is blood
  plasma

Fig 14.8
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Exchange of Fluid between Capillaries Tissues

• Distribution of ECF between blood interstitial
  compartments is in state of dynamic equilibrium
• Movement out of capillaries is driven by
  hydrostatic pressure exerted against capillary
  wall
• Promotes formation of tissue fluid
• Net filtration pressure hydrostatic pressure in
  capillary (17-37 mm Hg) - hydrostatic pressure of
  ECF (1 mm Hg)

Click here to play Fluid Exchange Across The
Walls of Capillaries RealMedia Movie
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Exchange of Fluid between Capillaries Tissues

• Movement also affected by colloid osmotic
  pressure
• osmotic pressure exerted by proteins in fluid
• Difference between osmotic pressures in outside
  of capillaries (oncotic pressure) affects fluid
  movement
• Plasma osmotic pressure 25 mm Hg interstitial
  osmotic pressure 0 mm Hg

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Overall Fluid Movement

• Is determined by net filtration pressure forces
  opposing it (Starling forces)
• Pc Pi (fluid out) - Pi Pp (fluid in)
• Pc Hydrostatic pressure in capillary
• Pi Colloid osmotic pressure of interstitial
  fluid
• Pi Hydrostatic pressure in interstitial fluid
• Pp Colloid osmotic pressure of blood plasma

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Fig 14.9
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Edema

• Normally filtration, osmotic reuptake,
  lymphatic drainage maintain proper ECF levels
• Edema is excessive accumulation of ECF resulting
  from
• High blood pressure
• Venous obstruction
• Leakage of plasma proteins into ECF
• Myxedema (excess production of glycoproteins in
  extracellular matrix) from hypothyroidism
• Low plasma protein levels resulting from liver
  disease
• Obstruction of lymphatic drainage

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Regulation of Blood Volume by Kidney

• Urine formation begins with filtration of plasma
  in glomerulus
• Filtrate passes through is modified by nephron
• Volume of urine excreted can be varied by changes
  in reabsorption of filtrate
• Adjusted according to needs of body by action of
  hormones

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ADH (vasopressin)

• ADH released by Post Pit when osmoreceptors
  detect high osmolality
• From excess salt intake or dehydration
• Causes thirst
• Stimulates H20 reabsorption from urine
• ADH release inhibited by low osmolality

Fig 14.11
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Aldosterone

• Is steroid hormone secreted by adrenal cortex
• Helps maintain blood volume pressure through
  reabsorption retention of salt water
• Release stimulated by salt deprivation, low blood
  volume, pressure

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Renin-Angiotension-Aldosterone System

• When there is a salt deficit, low blood volume,
  or pressure, angiotensin II is produced
• Angio II causes a number of effects all aimed at
  increasing blood pressure
• Vasoconstriction, aldosterone secretion, thirst

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Angiotensin II

• Fig 14.12 shows when how Angio II is produced,
  its effects

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Atrial Natriuretic Peptide (ANP)

• Expanded blood volume is detected by stretch
  receptors in left atrium causes release of ANP
• Inhibits aldosterone, promoting salt water
  excretion to lower blood volume
• Promotes vasodilation

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Factors Affecting Blood Flow
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Vascular Resistance to Blood Flow

• Determines how much blood flows through a tissue
  or organ
• Vasodilation decreases resistance, increases
  blood flow
• Vasoconstriction does opposite

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Physical Laws Describing Blood Flow

• Blood flows through vascular system when there is
  pressure difference (DP) at its two ends
• Flow rate is directly proportional to difference
  (DP P1 - P2)

Fig 14.13
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Physical Laws Describing Blood Flow

• Flow rate is inversely proportional to resistance
• Flow DP/R
• Resistance is directly proportional to length of
  vessel (L) viscosity of blood (?)
• Inversely proportional to 4th power of radius
• So diameter of vessel is very important for
  resistance
• Poiseuille's Law describes factors affecting
  blood flow
• Blood flow DPr4(?)
• ?L(8)

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Fig 14.14. Relationship between blood flow,
radius resistance
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Extrinsic Regulation of Blood Flow

• Sympathoadrenal activation causes increased CO
  resistance in periphery viscera
• Blood flow to skeletal muscles is increased
• Because their arterioles dilate in response to
  Epi their Symp fibers release ACh which also
  dilates their arterioles
• Thus blood is shunted away from visceral skin
  to muscles

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Extrinsic Regulation of Blood Flow continued

• Parasympathetic effects are vasodilative
• However, Parasymp only innervates digestive
  tract, genitalia, salivary glands
• Thus Parasymp is not as important as Symp
• Angiotenin II ADH (at high levels) cause
  general vasoconstriction of vascular smooth
  muscle
• Which increases resistance BP

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Paracrine Regulation of Blood Flow

• Endothelium produces several paracrine regulators
  that promote relaxation
• Nitric oxide (NO), bradykinin, prostacyclin
• NO is involved in setting resting tone of
  vessels
• Levels are increased by Parasymp activity
• Vasodilator drugs such as nitroglycerin or Viagra
  act thru NO
• Endothelin 1 is vasoconstrictor produced by
  endothelium

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Intrinsic Regulation of Blood Flow
(Autoregulation)

• Maintains fairly constant blood flow despite BP
  variation
• Myogenic control mechanisms occur in some tissues
  because vascular smooth muscle contracts when
  stretched relaxes when not stretched
• E.g. decreased arterial pressure causes cerebral
  vessels to dilate vice versa

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Intrinsic Regulation of Blood Flow
(Autoregulation) continued

• Metabolic control mechanism matches blood flow to
  local tissue needs
• Low O2 or pH or high CO2, adenosine, or K from
  high metabolism cause vasodilation which
  increases blood flow ( active hyperemia)

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Aerobic Requirements of the Heart

• Heart ( brain) must receive adequate blood
  supply at all times
• Heart is most aerobic tissue--each myocardial
  cell is within 10 m of capillary
• Contains lots of mitochondria aerobic enzymes
• During systole coronary, vessels are occluded
• Heart gets around this by having lots of
  myoglobin
• Myoglobin is an 02 storage molecule that releases
  02 to heart during systole

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Regulation of Coronary Blood Flow

• Blood flow to heart is affected by Symp activity
• NE causes vasoconstriction Epi causes
  vasodilation
• Dilation accompanying exercise is due mostly to
  intrinsic regulation

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Circulatory Changes During Exercise

• At beginning of exercise, Symp activity causes
  vasodilation via Epi local ACh release
• Blood flow is shunted from periphery visceral
  to active skeletal muscles
• Blood flow to brain stays same
• As exercise continues, intrinsic regulation is
  major vasodilator
• Symp effects cause SV CO to increase
• HR ejection fraction increases vascular
  resistance

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Fig 14.19
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Fig 14.20
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Cerebral Circulation

• Gets about 15 of total resting CO
• Held constant (750ml/min) over varying conditions
• Because loss of consciousness occurs after few
  secs of interrupted flow
• Is not normally influenced by sympathetic activity

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Cerebral Circulation

• Is regulated almost exclusively by intrinsic
  mechanisms
• When BP increases, cerebral arterioles constrict
  when BP decreases, arterioles dilate (myogenic
  regulation)
• Arterioles dilate constrict in response to
  changes in C02 levels
• Arterioles are very sensitive to increases in
  local neural activity (metabolic regulation)
• Areas of brain with high metabolic activity
  receive most blood

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Cutaneous Blood Flow

• Skin serves as a heat exchanger for
  thermoregulation
• Skin blood flow is adjusted to keep deep-body at
  37oC
• By arterial dilation or constriction activity
  of arteriovenous anastomoses which control blood
  flow through surface capillaries
• Symp activity closes surface beds during cold
  fight-or-flight, opens them in heat exercise

Fig 14.22
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Blood Pressure
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Blood Pressure (BP)

• Arterioles play role in blood distribution
  control of BP
• Blood flow to capillaries BP is controlled by
  aperture of arterioles
• Capillary BP is decreased because they are
  downstream of high resistance arterioles

Fig 14.23
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Blood Pressure (BP)

• Capillary BP is also low because of large total
  cross-sectional area

Fig 14.24
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Blood Pressure (BP)

• Is controlled mainly by HR, SV, peripheral
  resistance
• An increase in any of these can result in
  increased BP
• Sympathoadrenal activity raises BP via arteriole
  vasoconstriction by increased CO
• Kidney plays role in BP by regulating blood
  volume thus stroke volume

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Baroreceptor Reflex

• Is activated by changes in BP
• Which is detected by baroreceptors (stretch
  receptors) located in aortic arch carotid
  sinuses
• Increase in BP causes walls of these regions to
  stretch, increasing frequency of APs
• Baroreceptors send APs to vasomotor cardiac
  control centers in medulla
• Is most sensitive to decrease sudden changes in
  BP

Click here to play Baroreceptor Reflex RealMedia
Movie
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Fig 14.26
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Fig 14.27
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Atrial Stretch Receptors

• Are activated by increased venous return act to
  reduce BP
• Stimulate reflex tachycardia (slow HR)
• Inhibit ADH release promote secretion of ANP

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Measurement of Blood Pressure

• Is via auscultation (to examine by listening)
• No sound is heard during laminar flow (normal,
  quiet, smooth blood flow)
• Korotkoff sounds can be heard when
  sphygmomanometer cuff pressure is greater than
  diastolic but lower than systolic pressure
• Cuff constricts artery creating turbulent flow
  noise as blood passes constriction during systole
  is blocked during diastole
• 1st Korotkoff sound is heard at pressure that
  blood is 1st able to pass thru cuff last occurs
  when can no long hear systole because cuff
  pressure diastolic pressure

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Measurement of Blood Pressure continued

• Blood pressure cuff is inflated above systolic
  pressure, occluding artery
• As cuff pressure is lowered, blood flows only
  when systolic pressure is above cuff pressure,
  producing Korotkoff sounds
• Sounds are heard until cuff pressure equals
  diastolic pressure, causing sounds to disappear

Fig 14.29
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Pulse Pressure

• Pulse pressure (systolic pressure) (diastolic
  pressure)
• Mean arterial pressure (MAP) represents average
  arterial pressure during cardiac cycle
• Has to be approximated because period of diastole
  is longer than period of systole
• MAP diastolic pressure 1/3 pulse pressure

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