CHAPTER 41 REVIEW OF HEMODYNAMICS

Hemodynamics - study of the movement of blood throughout the circulatory system

as well as the regulatory
mechanisms and driving forces involved

I. OVERVIEW OF CIRCULATORY SYSTEM

Primary Functions: delivery of oxygen, nutrients, hormones, electrolytes,

and other essentials to cells
removal of carbon dioxide, metabolic wastes, and other
detritus from cells
helps fight infection

Divisions: pulmonary circulation – delivers blood to the lungs

systemic circulation – delivers blood to all other tissues

- also known as the greater circulation or peripheral circulation

A. COMPONENTS OF CIRCULATORY SYSTEM

- composed of the
heart – pump that moves blood through the arterial tree
blood vessels - arteries transport blood under high pressure to
tissues
- arterioles are control valves that regulate local blood
flow
- capillaries are the sites for exchange of fluid, oxygen,
carbon dioxide,
nutrients, hormones, wastes, etc.
- venules collect blood from the capillaries
- veins transport blood back to the heart and serve as a
major reservoir for
blood
- arteries are very muscular and do not readily stretch
- large increases in arterial pressure (AP) cause only small increases
in arterial diameter
- veins are less muscular and are 6 – 10 times more distensible
- small increases in venous pressure cause large increases in venous
diameter, producing a
large increase in venous volume

B. DISTRIBUTION OF BLOOD
- adult circulatory system contains about 5 L of blood
9% - pulmonary circulation
7% - heart
84% - systemic circulation

C. WHAT MAKES BLOOD FLOW?

 - blood moves within vessels because the force that drives flow is greater
than the resistance to flow
- force that drives blood flow is the pressure gradient between two points
in a vessel
- resistance to flow is determined by the diameter and length of the
vessel, and by blood viscosity
- the larger the vessel, the smaller the resistance
- when vessels dilate, resistance declines, increasing blood flow
- when vessels contract, resistance rises, decreasing blood flow

D. HOW DOES BLOOD GET BACK TO THE HEART?

- pressure is 120 mm Hg when blood enters the aorta
- pressure is 30 mm Hg when blood enters capillaries
- pressure is only 18 mm Hg when blood leaves capillaries
- pressure drops to negative values in the right atrium (negative atrial
pressure is generated by
expansion of the chest during respiration)

1st – negative pressure in right atrium helps “suck” blood toward the heart
2nd – constriction of smooth muscle in veins increases venous pressure,
helping to drive blood toward
the heart
3 – combination of venous valves and skeletal muscle contraction
rd

constitutes an auxiliary “venous

pump”
- veins are equipped with a system of one-way valves - - when
skeletal muscles contract,
venous blood is squeezed toward the heart – the only direction
permitted by the valves

II. REGULATION OF CARDIAC OUTPUT

A. DETERMINANTS OF CARDIAC OUTPUT

CO = HR x SV CO – cardiac output HR – heart rate SV
– stroke volume

- heart rate for average person is about 70 beats/min

- stroke volume for average person is about 70 ml

1. Heart Rate – controlled primarily by the autonomic nervous system (ANS)

- rate is increased by the sympathetic branch
- rate is decreased by the parasympathetic branch
-parasympathetic impulses reach the heart via the vagus
nerve

2. Stroke Volume – determined largely by:

a. myocardial contractility – the force with which the ventricles
contract
 - contractility is determined primarily by the degree of
cardiac dilation, which is
determined by the amount of venous return
- contractility can be increased by the sympathetic
nervous system
b. cardiac afterload – load against which a muscle exerts its force
(the load a muscle must
overcome in order to contract)
- heart afterload is the arterial pressure that the left
ventricle must overcome to
eject blood
- if afterload increases, stroke volume will rise
- cardiac afterload is determined primarily by the degree
of peripheral
resistance, which is determined by constriction
and dilation of
arterioles
- arterioles constrict, peripheral resistance rises
causing AP (afterload
to rise also
- arterioles dilate, peripheral resistance falls,
causing AP to decline

B. CONTROL OF STROKE VOLUME BY VENOUS RETURN

1. Starling’s Law of the Heart – states that the force of ventricular
contraction is proportional to muscle
fiber length (up to a point) - - as the heart stretches in
response to increased ventricular
filling, actin and myosin are brought into a more optimal
alignment with each other,
allowing them to interact with greater force
- as fiber length (ventricular diameter) increases, contractile force
increases

- when more blood enters the heart, more is pumped out

- healthy heart is able to precisely match its output with the
volume of blood delivered
by the veins
- when venous blood increases, cardiac output increases
- when venous return declines, cardiac output declines to the
same extent
- stroke volume is determined by factors that regulate venous return

2. Factors that Determine Venous Return

- in regard to pharmacology, most important factor is systemic filling
pressure (force that returns
blood to the heart)
 - normal value for filling pressure is 7 mm Hg, which can be raised
by an increase in blood
volume
- filling pressure and venous return can be influenced by:
- vasodilation or by reducing blood volume (lowering)
- blood volume and venous tone altered with drugs (lowering)
- auxiliary muscle pumps
- resistance to flow between peripheral vessels and the right
atrium
- right atrial pressure (elevation of which will impede venous
return)

3. Starling’s Law and Maintenance of Systemic Pulmonary Balance

- because an increase in venous return causes the output of both
ventricles to increase, blood
flow through the systemic and pulmonary circulations is
always in balance, as long as
the heart is healthy
- in the failing heart, Starling’s law breaks down - - force of
contraction no longer
increases in proportion to increased ventricular filling

III. REGULATION OF ARTERIAL PRESSURE

- arterial pressure (AP) is the driving force that moves blood through the
arterial side of the systemic
circulation
- regulated primarily through constriction and dilation of arterioles

AP = PR x CO PR – peripheral resistance CO –
cardiac output

A. OVERVIEW OF CONTROL SYSTEMS

AP is regulated primarily by:
autonomic nervous system (ANS) – acts by:
- responds rapidly (in seconds or minutes) to acute changes in
blood pressure
- provides steady-state control
rennin-angiotensin-aldosterone system (RAAS) – responds more
slowly, taking hours or days to
influence AP
kidneys – responsible for long-term control, and may take days or
weeks to adjust AP
family of natriuretic peptides – come into play primarily under
conditions of volume overload

- these systems differ with regard to time frame of response

B. STEADY-STATE CONTROL BY ANS

 - ANS regulates AP by adjusting Co and peripheral resistance
- sympathetic tone to the heart increases heart rate and
contractility, increasing CO
- parasympathetic tone slows the heart, reducing CO
- constriction of blood vessels is regulated exclusively by the sympathetic
branch of the ANS
- blood vessels have no parasympathetic innervation
- steady-state sympathetic tone provides moderate level of
vasoconstriction
- resistance to blood flow maintains AP

C. RAPID CONTROL BY ANS – BARORECEPTOR REFLEX

- baroreceptor reflex serves to maintain AP at predetermined levels
• baroreceptors in aortic arch and carotid sinus sense AP and relay
information to vasoconstrictor center of the medulla
• when AP changes, vasoconstrictor center compensates by sending
appropriate instructions to arterioles, veins, and the heart
• when AP drops, vasoconstrictor center causes constriction of nearly
all arterioles (increasing peripheral resistance), constriction of veins
(increasing venous return), and acceleration of heart rate (increasing
sympathetic impulses and decreasing parasympathetic impulses to
the heart)
• when AP rises too high, opposite responses occur
- baroreceptor reflex is poised for rapid action – but not sustained action
- when AP falls or rises, reflex acts within seconds to restore the
preset pressure
- when AP remains elevated or lowered, the system resets to the
new pressure within 1 – 2
days, perceiving the new (elevated or lowered) pressure as
“normal” and ceases to
respond

D. RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
- RAAS supports AP by causing:
• constriction of arterioles and veins
• retention of water by the kidneys
- vasoconstriction is mediated by a hormone named angiotensin II
(responses within hours)
- water retention is mediated in part by aldosterone (responses within
days)

E. RENAL RETENTION OF WATER

- when AP remains low for a long time, the kidney responds by retaining
water, causing AP to rise
- water retention is a mechanism for maintaining AP over long periods
(weeks, months, years)
 1st – low AP reduces renal blood flow (RBF), reducing glomerular
filtration rate (GFR)
- less fluid filtered, less urine produced, more water is retained
2nd – low AP activates the RAAS, causing levels of angiotensin II and
aldosterone to rise
- angiotensinn II causes constriction of renal blood vessles,
further decreasing RBF and
GFR
- aldosterone promotes renal retention of sodium, causing
water to be retained

F. POSTURAL HYPOTENSION
- also known as orthostatic hypotension
- a reduction in AP that can occur when we move from a supine or seated
position to an upright position
- the cause of hypotension is pooling of blood in veins, which
decreases venous return,
decreasing CO

Prevention Mechanisms:
• system of auxiliary venous pumps – promote venous return
• baroreceptor reflex can restore AP by constricting veins and
arterioles and increasing heart rate

- as with drugs that reduce AP by dilating arterioles, drugs that reduce AP

by relaxing veins can trigger
the barorecptor reflex, causing reflex tachycardia

G. NATRIURETIC PEPTIDES
- work primarily by reducing blood volume and promoting dilation of
arterioles and veins (both lower AP)

1. Principle Members:
a. atrial natriuretic peptide (ANP) – produced by myocyutes of the atria
- release is triggered by stretching of the atria and ventricles,
occurring because of
increased preload
- reduces blood volume and increasing venous capacitance,
reducing cardiac preload
b. B- or brain natriuretic peptide (BNP) – produced by myocytes of the
ventricles (and to a lesser
extent by cells in the brain, where BNP was discovered)
- release is triggered by stretching of the atria and ventricles,
occurring because of
increased preload
- reduces blood volume and increasing venous capacitance,
reducing cardiac preload
c. C-natriuretic peptide (CNP) – produced by cells of the vascular
endothelium
 - shares some actions of ANP and BNP, but its primary action is
promotion of
vasodilation

1st – ANP and BNP shift fluid from the vasculature to the extravascular
compartment
- underlying mechanism is increased vascular permeability
2nd – they act on the kidney to cause diuresis (loss of water) and
natriuresis (loss of sodium)
3rd – they promote dilation of arterioles and veins, in part by suppressing
sympathetic outflow from the
CNS

ANP and BNP help protect the heart during the early phase of heart failure
by suppressing both the
RAAS and sympathetic outflow, inhibiting proliferation of myocytes.