The Heart: Cardiac Output
 Cardiac output (CO)
• Amount of blood pumped by each side of the heart
in one minute
• The average resting CO for an adult is 3-5
liters pumped per minute
• Entire volume passes through body ~ once per
minute
• CO = (heart rate (beats/min) x stroke volume
(Liters/beat)
o At rest: CO (ml/min) =
HR (75 beats/min)  SV (70 ml/beat)
= 5.25 L/min
o
Maximal CO is 4–5 times resting CO in nonathletic
people
o
Maximal CO may reach 35 L/min in trained athletes
 Stroke volume = Volume of
blood pumped by each
ventricle in one contraction
Regulation of Blood Pressure
 The main factors influencing blood pressure:
• Cardiac output (CO) = Stroke volume x heart rate
• Peripheral resistance (PR)
Blood pressure = CO x PR
• Blood volume (BV)
Three Types of Blood Pressure Control
• Autoregulatory mechanisms
• Metabolic O2 & myogenic control cause vasodilation
• Neural mechanisms
• Motor centers, chemo- & baroreceptors influence CO
• Hormonal mechanisms
• Many hormones increase PR through vasoconstriction or
through osmoregulation to increase BV
Regulation of Blood Pressure
 The main factors influencing blood pressure:
• Cardiac output (CO)
• Peripheral resistance (PR)
Blood pressure = CO x PR
• Blood volume (BV)
Three Types of Blood Pressure Control
• Autoregulatory mechanisms
• Metabolic O2 & myogenic control cause vasodilation
• Neural mechanisms
• Motor centers, chemo- & baroreceptors influence CO
• Hormonal mechanisms
• Many hormones increase PR through vasoconstriction or
through osmoregulation to increase BV
Autoregulatory (Intrinsic) Mechanisms
Autoregulation occurs at the local level, in capillary beds of organs and tissues
(acidosis)
High O2, high pH, high nutrients,
low CO2 cause precapillary
sphincters to close
Low O2, high CO2,
low pH, low
nutrients cause
precapillary
sphincters to open
(from locally high BP)
Regulation of Blood Pressure
 The main factors influencing blood pressure:
• Cardiac output (CO)
• Peripheral resistance (PR)
Blood pressure = CO x PR
• Blood volume (BV)
Three Types of Blood Pressure Control
• Autoregulatory mechanisms
• Metabolic O2 & myogenic control cause vasodilation
• Neural mechanisms
• Motor centers, baro- & chemoreceptors influence CO
• Hormonal mechanisms
• Many hormones increase PR through vasoconstriction or
through osmoregulation to increase BV
Neural Control of Blood Pressure
 A short-term control mechanism
 Controls peripheral resistance in two ways
• Vasodilation/constriction
• Altering blood distribution
 Brain regulation in the medulla oblongata
• Vasomotor center: maintains arteriole tone and
receive baro- and chemoreceptor inputs
• Cardiac centers: Acceleratory and inhibitory
via sympathetic and parasympathetic divisions
• VC + CC = Cardiovascular center
Cardiac Centers Increase or Decrease Heart Rate
BP activates cardiac centers in medulla
Parasympathetic
activity
Sympathetic activity
Heart rate (HR)
Cardiac output (CO = SV x HR
Figure 19.8
Baroreceptor-Initiated Reflexes

Baroreceptors (Pressure sensors)
•
Location: carotid sinuses, aortic arch, walls of
large neck and thorax arteries
•
Increased blood pressure:
1. Stimulates baroreceptors to increase input to the
vasomotor center which then:
2. Inhibits the vasomotor center, causing arteriole
dilation and venodilation
3. Stimulates the cardioinhibitory center, or
parasympathetic (vagus) nerve impulses to turn
down heart rate
Effects of Baroreceptor Sensing on Cardiovascular Center
3 Impulses from baroreceptors
stimulate cardioinhibitory center
(and inhibit cardioacceleratory
center) and inhibit vasomotor
center.
4a Sympathetic
impulses to heart
cause HR,
contractility, and
CO.
2 Baroreceptors
in carotid sinuses
and aortic arch
are stimulated.
Vasodilation
4b Rate of
vasomotor impulses
allows vasodilation,
causing R
BP too high
1 Stimulus:
Blood pressure
(arterial blood
pressure rises above
normal range).
Homeostasis: Blood pressure in normal range
5
CO and R
return blood
pressure to
homeostatic range.
1 Stimulus:
5
CO and R
return blood pressure
to homeostatic range.
Blood pressure
(arterial blood
pressure falls below
normal range).
BP too low
4b Vasomotor
fibers stimulate
vasoconstriction,
causing R
Vasoconstriction
2 Baroreceptors
in carotid sinuses
and aortic arch
are inhibited.
4a Sympathetic
impulses to heart
cause HR,
contractility, and
CO.
3 Impulses from baroreceptors stimulate
cardioacceleratory center (and inhibit cardioinhibitory
center) and stimulate vasomotor center.
Figure 19.9
Chemoreceptor-Initiated Reflexes
 Chemoreceptors (Chemical sensors)
• Location: carotid sinus, aortic arch, large neck
arteries
• Respond to rise in CO2, drop in pH or O2
o Increase blood pressure via the vasomotor center
and the cardioacceleratory center
o Are more important in the regulation of respiratory
rate, which also controls blood pH and O2/CO2
levels
Regulation of Blood Pressure
 The main factors influencing blood pressure:
• Cardiac output (CO)
• Peripheral resistance (PR)
Blood pressure = CO x PR
• Blood volume (BV)
Three Types of Blood Pressure Control
• Autoregulatory mechanisms
• Metabolic O2 & myogenic control cause vasodilation
• Neural mechanisms
• Motor centers, baro- & chemoreceptors influence CO
• Hormonal mechanisms
• Many hormones increase PR through vasoconstriction or
through osmoregulation to increase BV
Hormonal Mechanism of BP Control
 Norepinephrine (NE) and epinephrine (Epi)
cause generalized vasoconstriction and increase
cardiac output
BP
 Atrial natriuretic peptide (ANP) causes blood
volume and blood pressure to decline, causes
generalized vasodilation
BP
 Antidiuretic hormone (ADH-vasopressin)
causes intense vasoconstriction in cases of
extremely low BP
BP
 Erythropoietin (EPO) from kidneys increases
RBC production, blood pressure (banned in Olympics)
BP
 Angiotensin II, generated by kidney release of
renin, causes vasoconstriction
BP
Kidney Specific Hormonal Mechanisms

Baroreceptors quickly adapt to chronic high or
low BP

Long-term mechanisms step in to control BP by
altering blood volume

Kidneys act directly and indirectly to regulate
arterial blood pressure
1. Direct renal mechanism- elimination or
retention of salts and water based on BP and BV
2. Indirect renal (renin-angiotensin) mechanism
Renin-Angiotensin Pathway: Indirect Mechanism


The renin-angiotensin mechanism
•
 Arterial blood pressure  release of renin
•
Renin production of angiotensin II
Ways that Angiotensin II increases BP
1. It is a potent direct vasoconstrictor
BP
2. Angiotensin II  aldosterone secretion

Aldosterone  renal reabsorption of Na+ and  urine
formation, increasing blood volume
BV
3. Angiotensin II stimulates ADH release, saving water
and Na+ and increasing blood volume
BV
4. It reduces blood flow through the kidneys, reducing
urine output
BV
Renin-Angiotensin II Mechanism of Blood Pressure Increase
Arterial pressure
Indirect renal
mechanism (hormonal)
Direct renal
mechanism
Baroreceptors
Sympathetic stimulation
promotes renin release
Reduction of
blood flow
Kidney
Renin release
Angiotensin-converting
enzyme (ACE) inhibitors
are drugs that block
angiotensin II production.
ACEs are used to treat
hypertenion and congestive
heart failure.
catalyzes cascade,
resulting in formation of
Angiotensin II
Filtration
ADH release
by posterior
pituitary
Aldosterone
secretion by
adrenal cortex
Water
reabsorption
by kidneys
Sodium
reabsorption
by kidneys
Blood volume
Vasoconstriction
( diameter of blood vessels)
Initial stimulus
Physiological response
Result
Arterial pressure
Figure 19.10
Summary of Mechanisms Controlling Blood Pressure
Activity of
muscular
pump and
respiratory
pump
Release
of ANP
Fluid loss from
hemorrhage,
excessive
sweating
Crisis stressors: Bloodborne
Dehydration,
exercise, trauma, chemicals:
high hematocrit
body
epinephrine,
temperature
NE, ADH,
angiotensin II;
ANP release
Conservation
of Na+ and
water by kidney
Blood volume
Blood pressure
Blood pH, O2,
CO2
Blood
volume
Baroreceptors
Chemoreceptors
Venous
return
Stroke
volume
Body size
Caused by
EPO release
Activation of vasomotor and cardiac
acceleration centers in brain stem
Heart
rate
Cardiac output
Diameter of
blood vessels
Blood
viscosity
Blood vessel
length
Peripheral resistance
Initial stimulus
Physiological response
Result
Mean systemic arterial blood pressure
Figure 19.11
Blood Pressure: Effects of Factors
Blood Pressure = Cardiac Output x Peripheral Resistance
BP = CO x PR

Neural factors
•



Renal factors
•
Regulation by altering blood volume:
salt and water retention
•
Renin – hormonal control
Temperature
•
Heat has a vasodilating effect
•
Cold has a vasoconstricting effect
Chemicals
•

Autonomic nervous system
adjustments (sympathetic division):
vasoconstriction
Various substances can cause
increases or decreases
Diet
•
High salt causes elevated BP
Comparison of Blood Pressures
Blood pressure results when flow is opposed by resistance
Disease causing blood
pressure change
Arteriosclerosis:
Hardening of the artery
walls and decrease of
elasticity, restricting flow
and increasing blood
pressure.
Atherosclerosis: A specific
type of arterosclerosis
where arteries are clogged
by an accumulation of
plaques: cholesterol
particles (lipoproteins), fat,
calcium, cellular waste and
other substances.
Capillary Exchange: Mechanisms
 Direct diffusion across
plasma membranes
 Endocytosis or
exocytosis
 Some capillaries have
gaps (intercellular
clefts)
• Plasma membrane
not joined by tight
junctions
 Fenestrations of some
capillaries
• Fenestrations =
pores
Blood and Osmotic Pressure Drive Transport
• Blood pressure is higher than osmotic pressure at the arterial end of the capillary
bed; net flow inwards
• Osmotic pressure is higher than blood pressure at the venous end; net flow
inwards
Therefore, fluid moves out of capillaries at the afferent end and into capillaries
(reabsorption) at the efferent end