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Chapter 14. Cardiac Output, Blood Flow, and Blood Pressure. 14-1. Chapter 14 Outline Cardiac Output Blood & Body Fluid Volumes Factors Affecting Blood Flow Blood Pressure Hypertension Circulatory Shock. 14-2. Cardiac Output . 14-3. Cardiac Output (CO).

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Chapter 14

Cardiac Output, Blood Flow, and Blood Pressure


Chapter 14 Outline
  • Cardiac Output
  • Blood & Body Fluid Volumes
  • Factors Affecting Blood Flow
  • Blood Pressure
  • Hypertension
  • Circulatory Shock


cardiac output co
Cardiac Output (CO)
  • Is volume of blood pumped/min by each ventricle
  • Heart Rate (HR) = 70 beats/min
  • Stroke volume (SV) = blood pumped/beat by each ventricle
    • Average is 70-80 ml/beat
  • CO = SV x HR
  • Total blood volume is about 5.5L


regulation of cardiac rate
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)
    • Mechanisms that affect HR: chronotropic effect
      • Positive increases; negative decreases
  • Autonomic innervation of SA node is main controller of HR
    • Symp & Parasymp nerve fibers modify rate of spontaneous depolarization


regulation of cardiac rate continued
Regulation of Cardiac Rate continued

Fig 14.1

  • 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, slows depolarization & decreasing HR


regulation of cardiac rate continued7
Regulation of Cardiac Rate continued
  • Vagus nerve:
    • Decrease activity: increases heart rate
    • Increased activity: slows heart
  • Cardiac control center of medulla coordinates activity of autonomic innervation
  • Sympathetic endings in atria & ventricles can stimulate increased strength of contraction


stroke volume
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


regulation of stroke volume
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
    • SV is inversely proportional to TPR
  • Ejection fraction is SV/ EDV (~80ml/130ml=62%)
    • Normally is 60%; useful clinical diagnostic tool


frank starling law of the heart
Frank-Starling Law of the Heart
  • States that strength of ventricular contraction varies directly with EDV
    • Is an intrinsicproperty of myocardium
    • As EDV increases, myocardium is stretched more, causing greater contraction & SV

Fig 14.2


frank starling law of the heart continued
Frank-Starling Law of the Heartcontinued
  • (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


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


extrinsic control of contractility
Extrinsic Control of Contractility
  • Parasympathetic stimulation
    • Negative chronotropic effect
      • Through innervation of the SA node and myocardial cell
    • Slower heart rate means increased EDV
      • Increases SV through Frank-Starling law
venous return
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


venous return continued
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


blood volume
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


exchange of fluid between capillaries tissues
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)


exchange of fluid between capillaries tissues21
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


overall fluid movement
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


  • 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


regulation of blood volume by kidney
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


adh vasopressin
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


  • 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


renin angiotension aldosterone system
Renin-Angiotension-Aldosterone System
  • Decreased BP and flow (low blood volume)
  • Kidney secreted Renin (enzyme)
    • Juxaglomerular apparatus
  • Angiotensin I to AngiotensinII
    • By angiotensin-converting enzyme (ACE)
  • Angio II causes a number of effects all aimed at increasing blood pressure:
      • Vasoconstriction, aldosterone secretion, thirst


angiotensin ii
Angiotensin II
  • Fig 14.12 shows when & how Angio II is produced, & its effects


atrial natriuretic peptide anp
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


vascular resistance to blood flow
Vascular Resistance to Blood Flow
  • Determines how much blood flows through a tissue or organ
    • Vasodilation decreases resistance, increases blood flow
    • Vasoconstriction does opposite


physical laws describing blood flow
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


physical laws describing blood flow35
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()




Fig 14.14. Relationship

between blood flow,

radius & resistance


extrinsic regulation of blood flow
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


extrinsic regulation of blood flow continued
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
  • Angiotensin II & ADH (at high levels) cause general vasoconstriction of vascular smooth muscle
    • Which increases resistance & BP


paracrine regulation of blood flow
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


intrinsic regulation of blood flow autoregulation
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


intrinsic regulation of blood flow autoregulation continued
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)


aerobic requirements of the heart
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


regulation of coronary blood flow
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


regulation of blood flow through skeletal muscles
Regulation of Blood Flow Through Skeletal Muscles
  • At rest, flow through skeletal muscles is low because of tonic sympathetic activity
  • Flow through muscles is decreased during contraction because vessels are constricted


circulatory changes during exercise
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


cerebral circulation
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


cerebral circulation49
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


cutaneous blood flow
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


blood pressure bp
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


blood pressure bp54
Blood Pressure (BP)
  • Capillary BP is also low because of large total cross-sectional area

Fig 14.24


blood pressure bp55
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


baroreceptor reflex
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 & cardiaccontrol centers in medulla
  • Is most sensitive to decrease & sudden changes in BP


atrial stretch receptors
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


measurement of blood pressure
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


measurement of blood pressure continued
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


pulse pressure
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


  • Is blood pressure in excess of normal range for age & gender (> 140/90 mmHg)
  • Afflicts about 20 % of adults
  • Primary or essentialhypertension is caused by complex & poorly understood processes
  • Secondary hypertension is caused by known disease processes


essential hypertension
Essential Hypertension
  • Constitutes most of hypertensives
  • Increase in peripheral resistance is universal
  • CO & HR are elevated in many
  • Secretion of renin, Angio II, & aldosterone is variable
  • Sustained high stress (which increases Symp activity) & high salt intake act synergistically in development of hypertension
  • Prolonged high BP causes thickening of arterial walls, resulting in atherosclerosis
  • Kidneys appear to be unable to properly excrete Na+ and H20


dangers of hypertension
Dangers of Hypertension
  • Patients are often asymptomatic until substantial vascular damage occurs
    • Contributes to atherosclerosis
    • Increases workload of the heart leading to ventricular hypertrophy & congestive heart failure
    • Often damages cerebral blood vessels leading to stroke
    • These are why it is called the "silent killer"


treatment of hypertension
Treatment of Hypertension
  • Often includes lifestyle changes such as cessation of smoking, moderation in alcohol intake, weight reduction, exercise, reduced Na+ intake, increased K+ intake
  • Drug treatments include diuretics to reduce fluid volume, beta-blockers to decrease HR, calcium blockers, ACE inhibitors to inhibit formation of Angio II, & Angio II-receptor blockers


circulatory shock70
Circulatory Shock
  • Occurs when there is inadequate blood flow to, &/or O2 usage by, tissues
    • Cardiovascular system undergoes compensatory changes
    • Sometimes shock becomes irreversible & death ensues


hypovolemic shock
Hypovolemic Shock
  • Is circulatory shock caused by low blood volume
    • E.g. from hemorrhage, dehydration, or burns
    • Characterized by decreased CO & BP
  • Compensatory responses include sympathoadrenal activation via baroreceptor reflex
    • Results in low BP, rapid pulse, cold clammy skin, low urine output


septic shock
Septic Shock
  • Refers to dangerously low blood pressure resulting from sepsis (infection)
  • Mortality rate is high (50-70%)
  • Often occurs as a result of endotoxin release from bacteria
    • Endotoxin induces NO production causing vasodilation & resultant low BP
    • Effective treatment includes drugs that inhibit production of NO


other causes of circulatory shock
Other Causes of Circulatory Shock
  • Severe allergic reaction can cause a rapid fall in BP called anaphylactic shock
    • Due to generalized release of histamine causing vasodilation
  • Rapid fall in BP called neurogenicshock can result from decrease in Symp tone following spinal cord damage or anesthesia
  • Cardiogenicshock is common following cardiac failure resulting from infarction that causes significant myocardial loss


congestive heart failure
Congestive Heart Failure
  • Occurs when CO is insufficient to maintain blood flow required by body
  • Caused by MI (most common), congenital defects, hypertension, aortic valve stenosis, disturbances in electrolyte levels
  • Compensatory responses are similar to those of hypovolemic shock
  • Treated with digitalis, vasodilators, & diuretics