Physiology: Cardiac output, blood flow, and blood pressure

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

Cardiac Output, Blood

Flow, and Blood

Pressure

Physiology

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Cardiac Output

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

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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)

• 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

• NE & Epi stimulate

decreasing HR

Fig 14.1

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

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

• States that strength

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

• At any given EDV,

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

Fig 14.5

• Skeletal muscle pumps

• Pressure drop during

inhalation

Venous Return continued

• Veins hold most of

Fig 14.8

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 & 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

• 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

Fig 14.9

• 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

• 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 released by Post Pit

reabsorption from urine

• ADH release inhibited by

low osmolality

• 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

• 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

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

• Determines how much blood flows through a tissue or organ

• Vasodilation decreases resistance, increases blood flow

• Vasoconstriction does opposite

Physical Laws Describing Blood Flow

• Blood flows through

vascular system when

Physical Laws Describing Blood Flow

• Flow rate is inversely proportional to resistance

• 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 = DPr 4 ()

L(8)

Fig 14.14 Relationship

between blood flow,

radius & resistance

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

• 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

• 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)

• 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

• 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

• 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

• 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

• 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

• 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

Fig 14.19

Fig 14.20

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

Fig 14.21

Cutaneous Blood Flow

• Skin serves as a heat

which control blood flow

through surface capillaries

• Symp activity closes surface beds during cold & fight-or- flight, & opens them in heat &

exercise

• Capillary BP is decreased because they are

downstream of high resistance arterioles

Fig 14.23

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

• Baroreceptors send APs to vasomotor & cardiac control centers in medulla

• Is most sensitive to decrease & sudden changes in BP

Fig 14.26

Fig 14.27

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

• 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

• 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

Hypertension

Hypertension

• Is blood pressure in excess of normal range for age &

gender (> 140/90 mmHg)

• Afflicts about 20 % of adults

• Primary or essential hypertension is caused by complex & poorly understood processes

• Secondary hypertension is caused by known disease

processes

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

• 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

• 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 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

• 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

• 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

• 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 neurogenic shock can result from

decrease in Symp tone following spinal cord damage or

anesthesia

• Cardiogenic shock is common following cardiac failure

resulting from infarction that causes significant myocardial loss

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