Transcript Chapter 14

Cardiac Pumping
Qiang XIA (夏强), PhD
Department of Physiology
Room C518, Block C, Research Building, School of Medicine
Tel: 88208252
Email: [email protected]
Case
A 70-year-old man was admitted to the hospital with shortness of breath, severe
fatigue and weakness, abdominal distension, and swelling of ankles. At night he
requires four pillows and often wakes up because of acute air hunger. His history
revealed episodes of angina pectoris and a progressive shortness of breath with
exertion for several years. On examination the chief abnormalities were slight
cyanosis (bluish cast to the skin), distension of the neck veins, rapid respirations
(20/min), rales (crackling sounds) at the lung bases bilaterally, an enlarged heart
with slight tachycardia (110 beats/min) and a diastolic gallop rhythm (sounds like
galloping horse), enlarged liver, excess fluid in the abdomen, and edema at the
ankles and over the lower tibias. His blood pressure was 115/80. The chest x-ray
examination showed an enlarged heart and diffuse density (indicative of fluid in
the lungs) at both lung bases. An electrocardiogram (ECG) showed normal sinus
rhythm, Q waves, and left axis deviation. Treatment included bed rest and
administration of digitalis and a diuretic.
Excitation-Contraction Coupling
In Cardiac Muscle
兴奋-收缩偶联
The mechanism that couples excitation – an
action potential in the plasma membrane of
the muscle cell – and contraction of heart
muscle
Passage of an action
potential along the
transverse tubule opens
nearby voltage-gated
calcium channels, the
“ryanodine receptor,”
located on the
sarcoplasmic
reticulum, and
calcium ions released into the
cytosol bind to troponin.
The calcium-troponin
complex “pulls” tropomyosin
off the myosin-binding site of
actin, thus allowing the
binding of the cross-bridge,
followed by its flexing to
slide the actin filament.
Excitation-contraction coupling in skeletal muscle
Calcium ions regulate the
contraction of cardiac muscle:
the entry of extracellular
calcium ions causes the
release of calcium from the
sarcoplasmic reticulum
(calcium-induced calcium
release [钙诱导的钙释放]), the
source of about 95% of the
calcium in the cytosol.
Excitation-contraction coupling in cardiac muscle
Cardiac cycle（心动周期）
• The cardiac events that occur from beginning of one
heartbeat to the beginning of the next are called the
cardiac cycle
What happens in the heart during
each cardiac cycle?
• Pressure（压力）
• Volume（容积）
• Valves（瓣膜）
• Blood flow（血流）
Systole:
ventricles contracting
Diastole:
ventricles relaxed
Mechanical Events of the Cardiac Cycle
Click here to play the
Mechanical Events
of the Cardiac Cycle
Flash Animation
Summary of events in the left
atrium, left ventricle, and aorta
during the cardiac cycle
Pressure changes in the right heart during a contraction cycle.
Role of atria and ventricles during each
cardiac cycle
• Atria──primer pump（初级泵）
• Ventricles──major source of power
Heart Sounds
心音
• 1st sound
– soft low-pitched lub
– associated with closure of the AV valves
– Marks the onset of systole
• 2nd sound
– louder dup
– associated with closure of the PA and aortic valves
– Occurs at the onset of diastole
Chest surface areas for auscultation of
normal heart sounds
Four traditional value areas
– Aortic space: 2RIS
– Pulmonic valve: 2LIS
– Tricuspid valve: 4ICS LLSB
– Mitral valve: Apex
RIS--right intercostal space
LIS—left intercostal space
ICS--intercostal space
LLSB--left lower sternal border
Phonocardiogram（心音图）
Heart valve defects causing turbulent blood flow and murmurs
Acute rheumatic fever
Mitral stenosis -- Accentuated first sound
Mitral stenosis – Presystolic murmur
Mitral regurgitation -- systolic murmur
Aortic insufficiency -- Loud systolic ejection murmur,
third sound
Evaluation of Heart Pumping
1.
Stroke volume (SV)（搏出量）:
volume of blood pumped per beat
SV = EDV – ESV
EDV: end-diastolic volume（舒张末期容积）
ESV: end-systolic volume（收缩末期容积）
~70ml (60~80ml)
Stroke volume for evaluating
different patients?
heart enlargement
2. Ejection fraction (EF)（射血分数）
EF=(SV/EDV) x 100%
55~65%
3. Cardiac output (CO)（心输出量）: the total volume
of blood pumped by each ventricle per minute
CO=SV x heart rate (HR)
5 L/min (4.5~6.0 L/min)
What parameters for comparison
of people in different size?
4. Cardiac index (CI)（心指数）
: cardiac output per square
meter of body surface area
3.0~ 3.5 L/min•m2
5. Cardiac reserve（心力储备）: the maximum
percentage that the cardiac output can increase
above the normal level
In the normal young adult the cardiac reserve is 300
to 400 percent
Achieved by an increase in either stroke volume (SV)
or heart rate (HR) or both
Measurement of Cardiac Function
• Echocardiography
• Cardiac angiography
Coronary Angiography from a 56-year-old man
presented with unstable angina and acute
pulmonary edema
Rerkpattanapipat P, et al. Circulation.
1999;99:2965
Regulation of heart pumping
Regulation of stroke volume
1. Preload – Frank-Starling mechanism
Preload（前负荷） of ventricles:
end-diastolic volume (EDV)
end-diastolic pressure (EDP)
Frank-Starling mechanism
(Intrinsic regulation or heterometric regulation)
（内在调节，或，异长调节）
The fundamental principle of cardiac behavior which states
that the force of contraction of the cardiac muscle is
proportional to its initial length
Significance:
Precise regulation of SV
Control of stroke volume
Frank-Starling mechanism
To increase the heart’s stroke volume:
fill it more fully with blood. The increased stretch of the ventricle will
align its actin and myosin in a more optimal pattern of overlap.
Ventricular function curve (Frank-Starling curve)
Ventricular function curve (Frank-Starling curve)
Factors affecting preload (EDV)
• (1) Venous return
• Filling time
• Venous return rate
• Compliance
• (2) Residual blood in ventricles after ejection
Ernest Starling
•
•
•
Ernest Henry Starling (17 April 1866 – 2 May 1927) was an English physiologist. He worked mainly at
University College London, although he also worked for many years in Germany and France. His main
collaborator in London was his brother-in-law, Sir William Maddock Bayliss.
Starling is most famous for developing the "Frank–Starling law of the heart", presented in 1915 and
modified in 1919. He is also known for his involvement along with Bayliss in the Brown Dog affair, a
controversy relating to vivisection. In 1891, when he was 25, Starling married Florence Amelia
Wooldridge, the widow of Leonard Charles Wooldridge, who had been his physiology teacher at Guy's
and died at the age of 32. She was a great support to Starling as a sounding board, secretary, and
manager of his affairs as well as mother of their four children.
Other major contributions to physiology were:
– The Starling equation, describing fluid shifts in the body (1896)
– The discovery of peristalsis, with Bayliss
– The discovery of secretin, the first hormone, with Bayliss (1902) and the introduction of the
concept of hormones (1905)
– The discovery that the distal convoluted tubule of the kidney reabsorbs water and various
electrolytes
– Starling was elected fellow of the Royal Society in 1899.
http://en.wikipedia.org/wiki/Ernest_Starling
Otto Frank
•
•
Otto Frank (June 21, 1865 - November 12, 1944) was a German doctor and an important
figure in the history of cardiac physiology.
Frank's initial research was related to fat absorption. But, in his postdoctoral work
(Habilitationsschrift) Frank investigated the isometric and isotonic contractile behaviour
of the heart and it is this work that he is best known for. Frank's work on this topic
preceded that of Ernest Starling, but both are usually credited with providing the
foundations of what is termed the Frank–Starling law of the heart. This law states that
"Within physiological limits, the force of contraction is directly proportional to the initial
length of the muscle fiber". Frank also undertook important work into the physiological
basis of the arterial pulse waveform and may have coined the term essential hypertension
in 1911. His work on the Windkessel extended the original ideas of Stephen Hales and
provided a sound mathematical framework for this approach. Frank also published on
waves in the arterial system but his attempts to produce a theory that incorporated waves
and the Windkessel are not considered to have been successful. Frank also did work on
the oscillatory characteristics of the auditory apparatus of the ear and the thermodynamics
of muscle. He also worked extensively on developing accurate methods to measure blood
pressure and other physiological phenomena (e.g. Frank's capsule (Frank-Kapsel), optical
Spiegelsphygmograph).
http://en.wikipedia.org/wiki/Otto_Frank_(physiologist)
Who Discovered the FrankStarling Mechanism?
Author: Heinz-Gerd Zimmer
(http://physiologyonline.physiology.org/content/17/5/181.full)
ABSTRACT
• In 1866 at Carl Ludwig’s Physiological Institute at Leipzig,
Elias Cyon described the influence of diastolic filling of the
isolated perfused frog heart on ejection volume. A study
performed at the institute of the effect of filling pressure on
contraction amplitude was published in 1869 by Joseph Coats,
based on a recording made by Henry P. Bowditch.
TABLE 1. Comparison of the experimental studies describing the effect of filling of the
heart on contraction and ejection
Year of publication
Carl Ludwig
1886 (3); 1869 (2)
Otto Frank
1895 (4); 1898 (5)
Ernest H. Starling
1914 (8,9); 1926 (11)
Performed at
Leipzig, Germany
Leipzig, Germany;
Munich, Germany
London, England
Animal used
Frog
Frog
Dog
Working, recirculating
(3); Closed system
Working heart dependent
Heart-lung preparation
pumping into manometer on preload and afterload
(2)
Heart preparation
Pressure and volume
Pressure, cardiac output,
and heart volume
Parameters measured
Pressure (2)
Aim of study
Heart as muscle and
Effect of temperature (3);
reliable pressure
Vagus stimulation (2)
recording
New finding
Ejection (3) and
contraction amplitude
dependent on filling (2)
Regulation of heart
Curves of isovolumetric
volume and output by
and isotonic maxima (5)
preload and afterload
Effect
described (3); recorded
(2)
quantified and visualized designated "the law of the
as a graph (5)
heart" (11)
Continued research
focusing on the
mechanism?
No
No
Application to the
mammalian heart
Yes
2. Afterload（后负荷）(Usually measured as arterial
pressure)
Congestive heart failure (CHF)
 Afterload has very little effect on the normal ventricle
 However, as systolic failure develops even small increases in
afterload have significant effects on compromised ventricular
systolic function
 Conversely, small reductions in afterload in a failing ventricle can
have significant beneficial effects on impaired contractility
3. Myocardial contractility (Inotropic state)
（心肌收缩性[变力状态]）
Homometric regulation
（等长调节）
To further increase the stroke volume:
fill it more fully with blood
AND
deliver sympathetic signals (norepinephrine and epinephrine);
it will also relax more rapidly, allowing more time to refill.
Sympathetic signals (norepinephrine and epinephrine) cause a
stronger and more rapid contraction and a more rapid relaxation.
Factors regulating contractility
Regulation of heart rate
• HRCO (CO = SV x HR)
• HRContractility (Treppe effect)
• HR diastolic filling time 


40~180 /min，HRCO
>180 /min，or <40/min，CO
Control of heart rate
To speed up the heart rate:
T, ions,
metabolites,
other
hormones
• deliver the sympathetic hormone, epinephrine, and/or
• release more sympathetic neurotransmitter (norepinephrine), and/or
• reduce release of parasympathetic neurotransmitter (acetylcholine).
Staircase phenomenon (Treppe effect , Forcefrequency relationship)
Increase in rate of
contraction (heart
rate) causes
increase in
contractility
To increase SV, increase:
end-diastolic volume,
norepinephrine delivery from
sympathetic
neurons, and
epinephrine
delivery
from the
adrenal
medulla.
To increase HR, increase:
norepinephrine delivery from
sympathetic neurons, and
epinephrine
delivery from
adrenal medulla
(reduce
parasympathetic).
It is not possible, under normal circumstances, to increase one
but not the other of these determinants of cardiac output.
Case
A 70-year-old man was admitted to the hospital with shortness of breath, severe
fatigue and weakness, abdominal distension, and swelling of ankles. At night he
requires four pillows and often wakes up because of acute air hunger. His history
revealed episodes of angina pectoris and a progressive shortness of breath with
exertion for several years. On examination the chief abnormalities were slight
cyanosis (bluish cast to the skin), distension of the neck veins, rapid respirations
(20/min), rales (crackling sounds) at the lung bases bilaterally, an enlarged heart
with slight tachycardia (110 beats/min) and a diastolic gallop rhythm (sounds like
galloping horse), enlarged liver, excess fluid in the abdomen, and edema at the
ankles and over the lower tibias. His blood pressure was 115/80. The chest x-ray
examination showed an enlarged heart and diffuse density (indicative of fluid in
the lungs) at both lung bases. An electrocardiogram (ECG) showed normal sinus
rhythm, Q waves, and left axis deviation. Treatment included bed rest and
administration of digitalis and a diuretic.
Questions
1. Would you expect cardiac output and stroke volume to be
normal, high, or low? Why?
2. What do the distension of the neck veins and enlargement of
the liver indicate? What is the mechanism?
3. Is the efficiency of the heart altered? If so, why?
4. What do you expect to find on measurement of ejection fraction
and residual volume? Explain.
……
The End.