Download ANPS 020 01-28

ANPS 020 Beneyto-Santonja 01/28/13
Cardiodynamics: The movement and force generated by cardiac contractions
Some basic terms to know:
 End-diastolic volume (EDV): the amount of blood in the ventricle just before contraction
 End-systolic volume (ESV): the amount of blood left in the ventricle after contraction (it doesn’t all
get pumped)
 Stroke volume (SV): the amount pumped out of ventricle during systole
 SV = EDV – ESV
Ejection Fraction  the percentage of EDV represented by SV
 Important clinical measure  weak hearts pump out less
 Example
o Left ventricle volume at end of diastole (EDV): 100 ml
o Left ventricle volume at end of systole (ESV): 40 ml
o Stroke volume (EDV-ESV): 60 ml
o Ejection volume (SV/EDV): 60%
 Typical Ejection Fraction Numbers:
o 50-75%  Heart’s pumping ability is Normal
o 36-49%  Heart’s pumping ability is Below Normal
o 35% and Below  Heart’s pumping ability is low
Cardiodynamics: Measurement of Cardiac Output
 CO = Cardiac Output (mL/min)
o The volume of blood pumped by the left ventricle in one minute
o This determines oxygen available to tissues
o At rest, CO = 5 liters/min and can rise to 30 liters/min during strenuous activity
 CO = HR x SV where HR is heart rate (beats/min) and SV is stroke volume (mL pumped out/beat)
Cardiodynamics: Adjustments to Cardiac Output
 CO = HR x SV
 SV = EDV – ESV
 CO = HR x (EDV – ESV)
 Cardiac output can be adjusted with changes to one or more variables
o Heart rate (speeding up or slowing down)
o End diastolic volume (how much blood fills ventricle between beats)
o End systolic volume (how much ventricle pumps out each beat)
Cardiodynamics
 Sensory input to cardiovascular center from cranial nerves IX and X
o Baroreceptors are sensory receptors monitoring blood pressure
o Chemoreceptors are sensory receptors monitoring arterial oxygen and carbon dioxide
levels
 Cardiac center integrates sensory input and adjusts cardiac activity appropriately  turns UP one
pathway and turns DOWN the other (ie: turns up sympathetic, turns down parasympathetic)
Autonomic Innervation of the Heart
 Note that parasympathetic fibers innervate the SA and AV nodes as well as the atrial muscle
 Sympathetic fibers innervate both nodes, atrial muscle and ventricular muscle
Cardiodynamics: Factors Affecting Heart Rate
 Autonomic innervation is the primary factor affecting heart rate
 Cardiac center of medulla oblongata in the brainstem drives autonomic system:
o Cardioacceleratory center
Controls sympathetic neurons, causes them to release more norepinephrine at
SA node (increases heart rate); norepinephrine binds to Beta-1 adrenergic
receptors on SA node cells
o Cardioinhibitory center
 Controls parasympathetic neurons of vagus nerve, leading to acetylcholine
release at SA node (slows heart rate); Ach binds to muscarinic receptors on SA
node cells
How is the heart rate controlled?
 Autonomic axons adjust heart rate by slowing down or speeding up the rate of spontaneous
depolarization of pacemaker cells

 Middle Image represents cardioinhibitory center working (Parasympathetic)
 Bottom Image represent cardioacceleratory center working (Sympathetic)
Cardiodynamics: Factors Affecting Stroke Volume
1. The End Diastolic Volume (EDV)
a. The amount of blood in ventricle contains at the end of diastole is influenced by several
factors
i. Filling time: duration of ventricular diastole  longer fill time results in larger fill
volume
ii. Venous Return: rate of blood flow during ventricular diastole  factors that
cause more blood to return to heart result in larger fill volume; NOTE:
vasoconstriction is a critical factor affecting venous return
2. The End Systolic Volume (ESV)
a. The amount of blood that remains in the ventricle at the end of ventricular systole is
influenced by 3 factors
i. Preload: Ventricular stretching during diastole  see more notes regarding
preload below
ii. Contractility: Force produced during contraction, at a given preload  see more
notes regarding Contractility below
iii. Afterload: Tension the ventricle produces to open the semilunar valve and eject
blood  see more notes regarding Afterload below
Innervation of the Blood Vessels: Sympathetic (with the exception of erectile tissue)
 Sympathetic fibers are always “talking” to the smooth muscle in the walls of blood vessels… this is
called sympathetic “tone”. This continuous rate of action potential firing leads to continuous
release of transmitter and sustained low level of contraction of the smooth muscle, and thus partial
vasoconstriction of the vessel.
 Increased sympathetic activity increases the degree of constriction to reduce blood flow.
 Decrease sympathetic activity decreases the degree of constriction to increase blood flow.
 Sympathetic Transmitter  Norepinephrine
 Receptor Type  Alpha-1 adrenergic
 Usually, vasodilation of blood vessels occurs because local chemicals in active tissues (ie: skeletal
muscle) trigger the smooth muscle cells to relax, increasing blood flow and providing more oxygen
and nutrients to the tissue.
How does vasoconstriction increase venous return?
 Vasoconstriction mobilizes blood in capacitance vessels
 Some clinical treatments are used to improve venous return  Compression cuffs/stockings
Preload
 Preload is the degree of ventricular stretching during diastole
o Directly proportional to EDV: more blood in ventricle = more stretch
o Stretch affects the ability of muscle cells to produce tension
 The Frank-Starling Principle
o As EDV increases, stroke volume increases
o Translation  the heart pumped whatever it gets. The more blood in the ventricle, the
greater the stretch on the ventricle wall and the stronger the contraction)
 There are physical limits to ventricular expansion:
o Myocardial connective tissue in and around the heart cells
o The cardiac (fibrous) skeleton – the connective tissue framework of the heart
o The pericardial sac outside the heart
Contractility
 Contractility  how hard the ventricle contracts is affected by factors that adjust calcium levels in
the muscle cells
 Autonomic activity
o Sympathetic stimulation causes the ventricles to contract with more force, pumping out
more blood (Increasing ejection fraction and thus decreasing ESV)
 NE released by postganglionic fibers of cardiac nerves
 Epinephrine and NE released by the adrenal gland into the blood
 Contractile cells have Beta-1 adrenergic receptors
o Parasympathetic system does not innervate ventricles so has no significant effect on
contractility
 Hormones
o Many hormones affect heart contraction (epinephrine, norepinephrine, thyroid hormone)
o Pharmaceutical drugs mimic hormone actions
 Some drugs stimulate or block beta receptors to increase or decrease
sympathetic effect (beta blockers are a commonly used class of drugs to reduce
heart work in cardiac patients)
 Some drugs alter levels of calcium ions (e.g., calcium channel blockers)
Afterload
 Afterload  the aortic pressure that must be overcome in order for the ventricle to eject blood – is
affected by any factor that restricts arterial blood flow
 Any factor that increases peripheral resistant affects afterload (valve stenosis, high blood pressure,
atherosclerosis, etc.)
 As afterload increases, stroke volume increases stroke volume, and therefore ESV increases
Review: Main Factors Affecting Cardiac Output
 CO = HR x SV
 CO = HR x (EDV – ESV)
1. Heart Rate Control Factors
a. Autonomic Nervous System
b. Circulating Hormones
2. Stroke Volume Control Factors
a. EDV (End Diastolic Volume)
i. Filling time; rate of venous return
b. ESV (End Systolic Volume)
i. Preload
ii. Contractility
iii. Afterload
The Circulatory System: Regulating Blood Flow
 Organs must receive a steady of oxygen and
nutrients in order to survive. Maintaining a
steady flow of blood to the organs is the job of
the cardiovascular system.
 Both the heart and the blood vessel are
capable of change in order to adjust the flow
of blood
 There are only 5 liters of blood in the body,
and it is constantly being redistributed
between different organ systems
Blood Flow to Organs as a percentage of Cardiac
Output  See Image to the right
What drives movement of blood through the circulatory
system?  See image below
Pressure and Resistance
 Blood flow to tissues = Difference in blood pressure between heart and capillaries
 Peripheral Resistance
o Blood flows from a region of high pressure to one of lower pressure; the greater the
pressure difference driving the movement, the greater the flow
o The heart generates pressure to overcome resistance P (the pressure difference) across
the systemic circuit is about 100 mm Hg
o The greater the peripheral resistance the lower the flow
Blood Pressure  The pressure exerted by blood onto the vessel wall
 Blood pressure (BP): Usually refers specifically to arterial pressure (measured in mm Hg); typically
120/80
 Venous pressure: pressure in the venous system
 Capillary hydrostatic pressure: pressure within the capillary beds
3 Sources Contribute to Peripheral Resistance
1. Vascular Resistance
a. Due to friction between blood and the vessel wall
b. Dependent on vessel length (constant) and diameter (adjustable)
2. Viscosity
a. Resistance caused by molecules and suspended materials in a liquid
b. Whole blood viscosity is about 4 times that of water
3. Turbulence
a. Swirling action that disturbs smooth flow
Pressures in the Cardiovascular System
 Systolic pressure  Peak arterial pressure during ventricular systole
 Diastolic pressure  Minimum arterial pressure during diastole
 Pulse pressure  Difference between systolic pressure and diastolic pressure
 Mean arterial pressure (MAP) = Diastolic pressure + 1/3 pulse pressure
 Normal = 120/80; Normal MAP ~ 93
o Hypertension: Abnormally high blood pressure (greater than 140/90)
o Hypotension: Abnormally low blood pressure
Changes in Pressure and Resistance in the Circuit
 Although capillaries have the smallest diameter, there are so many of them that the cross-sectional
area increases at that point of the circulation, causing a drop in pressure and a decrease in flow
velocity.
 These features enhance exchange in the capillary beds
Pressure in a pulsatile in larger arteries
 Pulse pressure creates the “throbbing” feeling in an artery
 During systole, the heart forces blood into the vessels and exerting great pressure on the vessel
walls
 During diastole, the heart is not pushing blood, but the recoil of the walls of the elastic arteries
continues to push blood and exert pressure
Venous Pressure and Venous Return
 Determines the amount of blood arriving at right atrium each minute
 Low effective pressure in venous system
 There is more blood on venous side of circulation: capacitance vessels
 Low venous resistance is assisted by
o Muscular compression of peripheral veins:
 Compression of skeletal muscles pushes blood toward heart
The respiratory pump: thoracic cavity action – inhaling decreases thoracic pressure, increasing
return to heart; exhaling raises thoracic pressure, decreasing return to heart