Download Lecture 9 th ​, 10 th week

Department of medical physiology
9th week and 10th week
Semester: winter
Study program: Dental medicine
Lecture: RNDr. Soňa Grešová, PhD.
Department of medical physiology
Faculty of Medicine PJŠU
Cardiovascular system
9th week and 10th week
1. Cardiac cycle
2. Ventricular efficiency, cardiac
output, cardiac work
3. The heart as a pump – its
control mechanism
1. Relationship of the electrocardiogram
to the cardiac cycle
•
•
•
Systole = period of contraction
Diastole = period of relaxation
Phases of the cardiac cycle
1. Atrial Systole
2. Isovolumetric Ventricular Contraction
• Increased pressure in the ventricles
causes the AV valves to close
– Creates the first heart sound
(lub)
3. Ventricular Ejection
• the periods of rapid and slow
ejection of the ventricles
4. Isovolumetric Ventricular Relaxation
• Intraventricular pressure drops
below aortic pressure
– Semilunar valves close =
second heart sound (dup)
5. Filling of the ventricles
• the periods of rapid and slow filling
of the ventricles
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of
medical physiology. Philadelphia, PA: Saunders Elsevier.
1. Relationship of the electrocardiogram
to the cardiac cycle
•
EDV =during diastole, normal filling
of the ventricles increases the
volume of each ventricle to about
110 to 120 milliliters. This volume is
called the end-diastolic
volume.
•
SV= then, as the ventricles empty
during systole, the volume
decreases about 70 milliliters,
which is called the stroke volume
output.
•
ESV = the remaining volume in each
ventricle, about 40 to 50 milliliters,
is called the end-systolic volume.
EDV=
120 ml
SV=
70ml
ESV=
50ml
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of
medical physiology. Philadelphia, PA: Saunders Elsevier.
2. VENTRICULAR EFFICIENCY
• LV does not empty completely during systole
• ESV is around 50 ml
EDV - ESV = SV (stroke volume)
• SV is the amount of blood transferred from LV to the arterial system
during systole
• In healty person SV should be > 60 ml
EF (ejection fraction) = SV / EDV (normally about 55% - 75%)
• EF is an important measurement of cardiac efficiency
• EF is used clinically to assess cardiac status in patients with heart failure
2. CARDIAC OUTPUT
CO (L/min) = HR x SV
•
•
•
•
•
HR is established on the SA node and is controlled by ANS
SV is dependent on,
– LV preload
– LV afterload
– Contractility
Preload: Muscle length before contraction begins
- Preload is related with the volume of blood entering the chamber (EDV)
- Depends from EDV, EDP, Left atrium pressure, Pulmonary veins pressure
Afterload: The load against which a myocyte must shorten
- The principal component of afterload is arterial pressure
- depends from pressure in aorta, total peripheral resistance (TPR)
Contractility: measure of a muscle’s ability to shorten against a afterload
- Contractility equates with the cytoplasmic free Ca concentration
- depends from changes pressure/time, EF
Preload and contractility are directly proporcional with stroke volume
Afterload is inversely proportional with stroke volume
2. Measurement of cardiac output
using the oxygen Fick principle
• 𝐶𝑂 𝐿 ∕ 𝑚𝑖𝑛 = 𝐻𝑅 × 𝑆𝑉
𝐶𝑂 = 72 × 70
𝐶𝑂 = 5040 𝑚𝑙 ∕ 𝑚𝑖𝑛
Fick principle
• 𝐶𝑂 𝐿 ∕ 𝑚𝑖𝑛
=
𝑂2 absorbed per minute by the lungs 𝑚𝑙∕𝑚𝑖𝑛
Arteriovenous 𝑂2 difference 𝑚𝑙 Τ𝐿 𝑜𝑓 𝑏𝑙𝑜𝑜𝑑
𝐶𝑂 𝐿 ∕ 𝑚𝑖𝑛 =
200 𝑚𝑙 ∕ 𝑚𝑖𝑛
40 𝑚𝑙 ∕ 𝐿
𝐶𝑂 = 5 𝐿 ∕ 𝑚𝑖𝑛
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of
medical physiology. Philadelphia, PA: Saunders Elsevier.
2. CARDIAC WORK
Minute Cardiac work = CO x Aortic pressure
• O2 consumption is directly proportional to min. cardiac work
• Heart performs two kinds of work:
I.
II.
Internal work
External work
• Internal work (Aortic pressure = kinetic energy of blood flow):
– Expended in «isovolumic contraction»
– The force necessary to open the aortic and pulmonary valves
– Accounts for ˃ 90% of total cardiac workload
• External work (CO = volume-pressure work) :
– Expended in transferring blood to the arterial system against a
resistance
– Accounts for ˂ 10% of total cardiac workload
Volume – pressure diagram
•
EW= External Work
(CO = volume-pressure work)
•
IW= Internal work
(Aortic pressure = kinetic
energy of blood flow)
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of medical physiology. Philadelphia,
PA: Saunders Elsevier.
3. The heart as a pump – its control
mechanism
3. The heart as a pump –its control mechanism
factors affecting Heart Rate
1. Atrial reflex
- Volumoreceptors (type B in
RA): volume loading conditions
– Bainbridge response prevails (only
HR is affected)
- Atrial baroreceptors (type
A-low pressure receptors)stimulation: vasodilatation,
BP, HR
- Ventricular baroreceptors
(through unmyelinated vagal
nerve fibers) stimulation:
vasodilatation
SY, HR
1.
2. The heart as a pump –its control mechanism
factors affecting Heart Rate
2. Autonomic innervation
– Parasympathetic stimulation - a
negative chronotropic factor
•
Supplied by vagus nerve, decreases
heart rate, acetylcholine is secreted and
hyperpolarizes the heart
– Sympathetic stimulation - a positive
chronotropic factor
•
•
•
•
•
Supplied by cardiac nerves.
Innervate the SA and AV nodes, and the
atrial and ventricular myocardium.
Increases heart rate and force of
contraction.
Epinephrine and norepinephrine
released.
Increased heart beat causes increased
cardiac output. Increased force of
contraction causes a lower end-systolic
volume; heart empties to a greater
extent. Limitations: heart has to have
time to fill.
2.
Key Properties of Myocardial
Cells
• Automaticity (Chronotropic effect)
– Can produce electrical activity without
outside nerve stimulation
• Conductivity (Dromotropic effect)
– Ability to transmit an electrical stimulus
from cell to cell throughout myocardium
• Excitability (Batmotropic effect)
– Ability to respond to an electrical
stimulus
• Contractility (Inotropic effect)
– Ability of myocardial cells to contract when
stimulated by an electrical impulse
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and Hall textbook of
medical physiology. Philadelphia, PA: Saunders Elsevier.
3. The heart as a pump –its control mechanism
factors affecting Heart Rate
3. Hormones
– Epinephrine and
norepinephrine from the
adrenal medulla
• Occurs in response to increased
physical activity, emotional
excitement, stress
• increase heart rate
– Glucagon
• Increases heart rate and force
of contraction
– Thyroid hormones
• Increases heart rate and force
of contraction
3.
3. The heart as a pump –its control mechanism
Intrinsic factors affecting Stroke Volume
Frank-Starling Law of the Heart
1. Preload, or degree of stretch, of cardiac
muscle cells before they contract is the critical
factor controlling stroke volume; EDV leads
to stretch of myocard.
–
–
–
•
Slow heartbeat and exercise increase venous
return (VR) to the heart, increasing SV
–
–
–
•
preload  stretch of muscle  force
of contraction  SV
Unlike skeletal fibers, cardiac fibers
contract MORE FORCEFULLY when
stretched thus ejecting MORE BLOOD
(SV)
If SV is increased, then ESV is decreased!!
VR changes in response to blood volume,
skeletal muscle activity, alterations in
cardiac output
VR  EDV and in VR   in EDV
Any  in EDV   in SV
Blood loss and extremely rapid heartbeat
decrease SV
1.
3. The heart as a pump –its control mechanism
Extrinsic Factors Influencing Stroke Volume
2. Contractility is the increase in
contractile strength, independent of
stretch and EDV
• Referred to as extrinsic since the
influencing factor is from some
external source
• Increase in contractility comes
from:
– Increased sympathetic stimuli
– Certain hormones
– Ca2+ and some drugs
• Agents/factors that decrease
contractility include:
– Increased extracellular K+
– Calcium channel blockers
2.
3. The heart as a pump –its control mechanism
Extrinsic Factors Influencing Stroke Volume
2 a) Effects of Autonomic innervation on
Contractility
• Sympathetic stimulation
– Release norepinephrine from symp.
postganglionic fiber
– Also, EP and NE from adrenal medulla
– Have positive ionotropic effect
– Ventricles contract more forcefully,
increasing SV, increasing ejection
fraction and decreasing ESV
• Parasympathetic stimulation via
Vagus Nerve -CNX
– Releases ACh
– Has a negative inotropic effect
•
Hyperpolarization and inhibition
– Force of contractions is reduced,
ejection fraction decreased
2 a)
3. The heart as a pump –its control mechanism
Extrinsic Factors Influencing Stroke Volume
2 b) Effects of Hormones on
Contractility
• Epi, NE, and Thyroxine all have
positive ionotropic effects and
thus contractility
• Digitalis elevates intracellular
Ca++ concentrations by
interfering with its removal
from sarcoplasm of cardiac
cells
• Beta-blockers (propanolol,
timolol) block beta-receptors
and prevent sympathetic
stimulation of heart (neg.
chronotropic effect)
2 b)
3. The heart as a pump –its control mechanism
Extrinsic Factors Influencing Stroke Volume
3. Afterload
– back pressure exerted by
blood in the large arteries
leaving the heart (or the
load against which a
myocyte must shorten)
- the principal component
of afterload is arterial
pressure
- depends from pressure in
aorta, total peripheral
resistance (TPR)
3.
3. The heart as a pump –its control mechanism
Extrinsic Factors Influencing Stroke Volume
Effect of Potassium and Calcium
Ions on Heart Function
- the high potassium
concentration in the
extracellular fluids decreases
the resting membrane potential
in the cardiac muscle fibers
- An excess of calcium ions
causes effects almost exactly
opposite to those of potassium
ions, causing the heart to go
toward spastic contraction
Copyright: Hall, J. E., & Guyton, A. C. (2006). Guyton and
Hall textbook of medical physiology. Philadelphia, PA:
Saunders Elsevier.
3. The heart as a pump –its control mechanism
Extrinsic Factors Influencing Stroke Volume
Effect of Temperature on
Heart Function
- the heat increases the permeability of
the cardiac muscle membrane to ions
that control heart rate, resulting in
acceleration of the self- excitation
process
- Contractile strength of the heart often
is enhanced temporarily by a moderate
increase in temperature, as occurs
during body exercise, but prolonged
elevation of temperature exhausts the
metabolic systems of the heart and
eventually causes weakness