Cardiac Pumping

1
Cardiac Pumping

• Qiang XIA (??), PhD
• Department of Physiology
• Room C518, Block C, Research Building, School of
  Medicine
• Tel [phone]
• Email xiaqiang_at_zju.edu.cn

2
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.

3
Excitation-Contraction Coupling In Cardiac Muscle
??-????
The mechanism that couples excitation an action
potential in the plasma membrane of the muscle
cell and contraction of heart muscle
4
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
5
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 ???????), the source of about 95 of
the calcium in the cytosol.
Excitation-contraction coupling in cardiac muscle
6
(No Transcript)
7
Cardiac cycle(????)

• The cardiac events that occur from beginning of
  one heartbeat to the beginning of the next are
  called the cardiac cycle

8
What happens in the heart during each cardiac
cycle?

• Pressure(??)
• Volume(??)
• Valves(??)
• Blood flow(??)

9
Systole ventricles contracting Diastole
ventricles relaxed
10
Mechanical Events of the Cardiac Cycle
Click here to play the Mechanical Events of the
Cardiac Cycle Flash Animation
11
Summary of events in the left atrium, left
ventricle, and aorta during the cardiac cycle
12
(No Transcript)
13
Pressure changes in the right heart during a
contraction cycle.
14
Role of atria and ventricles during each cardiac
cycle

• Atria--primer pump(???)
• Ventricles--major source of power

15
Heart Sounds??

• 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

16
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 LISleft intercostal
space ICS--intercostal space LLSB--left lower
sternal border
17
Phonocardiogram(???)
18
Heart valve defects causing turbulent blood flow
and murmurs
19
Acute rheumatic fever
Mitral stenosis -- Accentuated first sound
Mitral stenosis Presystolic murmur
Mitral regurgitation -- systolic murmur
Aortic insufficiency -- Loud systolic ejection
murmur, third sound
20
Evaluation of Heart Pumping

• Stroke volume (SV)(???)
• volume of blood pumped per beat
• SV EDV ESV
• EDV end-diastolic volume(??????)
• ESV end-systolic volume(??????)
• 70ml (6080ml)

21
Stroke volume for evaluating different patients?
heart enlargement
22
2. Ejection fraction (EF)(????) EF(SV/EDV) x
100 5565
23

• 3. Cardiac output (CO)(????) the total volume of
  blood pumped by each ventricle per minute
• COSV x heart rate (HR)
• 5 L/min (4.56.0 L/min)

24
What parameters for comparison of people in
different size?
25

• 4. Cardiac index (CI)(???) cardiac output per
  square meter of body surface area
• 3.0 3.5 L/minm2

26

• 5. Cardiac reserve(????) 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

27
Measurement of Cardiac Function

• Echocardiography

28

• Cardiac angiography

Coronary Angiography from a 56-year-old man
presented with unstable angina and acute
pulmonary edema Rerkpattanapipat P, et al.
Circulation. 1999992965
29
Regulation of heart pumping
30
Regulation of stroke volume

• 1. Preload Frank-Starling mechanism
• Preload(???) of ventricles
• end-diastolic volume (EDV)
• end-diastolic pressure (EDP)

31

• Frank-Starling mechanism
• (Intrinsic regulation or heterometric
  regulation)
• (????,?,????)
• 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

32
Control of stroke volume
Frank-Starling mechanism
To increase the hearts 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.
33

• Ventricular function curve (Frank-Starling curve)

34

• Ventricular function curve (Frank-Starling curve)

35

• Factors affecting preload (EDV)
• (1) Venous return
• Filling time
• Venous return rate
• Compliance
• (2) Residual blood in ventricles after ejection

36
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
  "FrankStarling 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
37
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 FrankStarling 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_(physiolog
ist)
38
Who Discovered the Frank-Starling Mechanism?

• Author Heinz-Gerd Zimmer
• (http//physiologyonline.physiology.org/content/17
  /5/181.full)
• ABSTRACT
• In 1866 at Carl Ludwigs 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.

39
TABLE 1. Comparison of the experimental studies
describing the effect of filling of the heart on
contraction and ejection
Carl Ludwig Otto Frank Ernest H. Starling
Year of publication 1886 (3) 1869 (2) 1895 (4) 1898 (5) 1914 (8,9) 1926 (11)
Performed at Leipzig, Germany Leipzig, Germany Munich, Germany London, England
Animal used Frog Frog Dog
Heart preparation Working, recirculating (3) Closed system pumping into manometer (2) Working heart dependent on preload and afterload Heart-lung preparation
Parameters measured Pressure (2) Pressure and volume Pressure, cardiac output, and heart volume
Aim of study Effect of temperature (3) Vagus stimulation (2) Heart as muscle and reliable pressure recording Application to the mammalian heart
New finding Ejection (3) and contraction amplitude dependent on filling (2) Curves of isovolumetric and isotonic maxima (5) Regulation of heart volume and output by preload and afterload
Effect described (3) recorded (2) quantified and visualized as a graph (5) designated "the law of the heart" (11)
Continued research focusing on the mechanism? No No Yes
40

• 2. Afterload(???)(Usually measured as arterial
  pressure)

41
(No Transcript)
42
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

43

• 3. Myocardial contractility (Inotropic state)
• (?????????)

Homometric regulation (????)
44
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.
45
Sympathetic signals (norepinephrine and
epinephrine) cause a stronger and more rapid
contraction and a more rapid relaxation.
46
(No Transcript)
47

• Factors regulating contractility

48
(No Transcript)
49
Regulation of heart rate

• HR??CO? (CO SV x HR)
• HR??Contractility? (Treppe effect)
• HR?? diastolic filling time ?

• 40180 /min,HR??CO?
• gt180 /min,or lt40/min,CO?

50
(No Transcript)
51
Control of heart rate
52
T, ions, metabolites, other hormones

• To speed up the heart rate
• deliver the sympathetic hormone, epinephrine,
  and/or
• release more sympathetic neurotransmitter
  (norepinephrine), and/or
• reduce release of parasympathetic
  neurotransmitter (acetylcholine).

53
Staircase phenomenon (Treppe effect ,
Force-frequency relationship)
Increase in rate of contraction (heart rate)
causes increase in contractility
54
(No Transcript)
55
To increase SV, increaseend-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.
56
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.

57
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.

58
The End.