Download 58. Regulation of Cardiac Output

1. Cardiac Physiology
2. Circulatory System Review
Components
Heart
Blood vessels
Blood
3 - 4. Pump = volumes at same time
Pulmonary
Low pressure
Low resistance
Systemic
High pressure
High resistance
Left ventricle
Works harder
More muscular
Thicker wall
http://www.lumen.luc.edu/Lumen/MedEd/medicine/pulmonar/i
mages/hussain1/Scan54.jpg
5 – 6. Heart Wall
Inner layer
Endothelium
Middle layer
Myocardium
Cardiac muscle
Interlacing bundles spiraling around heart
Outer layer
Visceral pericardium
http://www.dkimages.com/discover/previews/740/76722.
JPG
7. Fibrous skeleton
Dense connective tissue
Anatomic and functional separation between
atria and ventricles
Annuli fibrosi
Support heart valves
8 - 9. Cardiac Muscle Tissue
Striated
Sarcomeres
Thick and thin filaments like skeletal muscle
T-tubules
No lateral sacs/triads
Mitochondria
Myoglobin
Intercalcalated discs
Desmosome
Gap junction
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http://www.cytochemistry.net/microanatomy/muscle/mus
cle12.jpg
10. Functional Syncytia
Atria – functional syncytium
Ventricles – functional synctium
Atrial cells do no connect with ventricular cells
Atria and ventricles separated by
nonconducting layer of fibrous connective
tissue
Atrial depolarization and contraction separate
from ventricular depolarization and
contraction
Conduction system provides synchronization
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11. Coordination
Atrial excitation/contraction needs to be
finished before ventricular contraction takes
place
Each chamber must contract as a unit
Each pair of atria should contract
simultaneously
Each pair of ventricles should contract
simultaneously
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12. Electrical Activity
Contractile cells
Autorhythmic cells
Initiate and conduct AP
Don’t “rest”
Pacemaker potential
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13 - 14. Components of Conduction System
Sinoatrial node
Atrioventricular node
Bundle of His (atrioventricular bundle)
Left and right bundle branches
Purkinje fibers
15 - 16. SA Node
Normally functions as pacemaker
Depolarizes spontaneously to threshold
Pacemaker potentials
Membrane voltage
-60mV
gradual depolarization
caused by Na+ influx
Threshold
Voltage-gated Ca2+ channels open
Depolarization
Contraction
Repolarization
Voltage-gated K+ channels open
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17 - 19. Ectopic Pacemakers
Spontaneously active
Slower than SA node
Stimulated to produce APs by SA node
before they spontaneously depolarize to
threshold
If APs from SA node are prevented from
reaching these, they will generate
pacemaker potentials
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20 - 21. Myocardial APs
Myocardial cells
Resting membrane potential = –90 mV
Depolarized to threshold by APs originating in
SA node
Voltage-gated Na+ channels open
Plateau phase
decreases to 15mV
200-300 msec
results from balance between slow Ca2+
influx and K+ efflux
Repolarization
Opening of additional K+ channels
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22 - 27. Electrical Pathway Through heart
From SA node through atrial myocardium
gap junctions
AV node and bundle of His
conduct APs to ventricles
Ventricular septum
Bundle of His divides
right and left bundle branches
Purkinje fibers in walls of ventricles
stimulate contraction of ventricles
28. Speed of Conduction
From SA node
0.8 -1 m/sec
Time delay at AV node
Conduction slows to 0.03– 0.05 m/sec
In Purkinje fibers
5 m/sec
Ventricular contraction begins 0.1–0.2 sec
after contraction of atria
29 - 30. Excitation-Contraction Coupling
Depolarization of myocardial cells opens
voltage-gated Ca2+ channels in sarcolemma
Calcium-induced-calcium-release
Voltage-gated Ca2+ release channels in SR
open
Ca2+ binds to troponin and stimulates
contraction (as in skeletal muscle)
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During repolarization, Ca2+ pumped out of
cell and into SR
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31 – 32. Refractory Period
AP lasts about 250 msec
Refractory period lasts nearly as long as AP
Cannot be stimulated to contract again until
muscles is relaxed
Prevents tetanus
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32 – 33. Electrocardiography
Composite of all APs generated by nodal and
contractile cells
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34 – 35. ECG
Bipolar leads
record voltage between electrodes placed
on wrists and legs (right leg is ground)
Lead I
records between right arm and left arm
Lead II
right arm and left leg
Lead III
left arm and left leg
Unipolar leads
record voltage between a single electrode
placed on body and ground built into ECG
machine
Limb leads
right arm (AVR)
left arm (AVL)
left leg (AVF)
6 chest or precordial leads
37. EKG - Waves
P wave
Depolarization of SA node
QRS complex
Depolarization
ventricles
T wave
Ventricular repolarization
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atria
37. EKG - Intervals
PQ interval (PR)
Start of atrial excitation to
start of ventricular excitation
ST segment
Depolarization of entire ventricular
myocardium
QT interval
Start of ventricular depolarization through
repolarization
38 - 44. EKG and Arrhythmia
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http://www.anaesthesiauk.com/article.aspx?articleid
=100685
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http://www.anaesthesiauk.com/article.aspx?articleid
=100686
http://library.med.utah.edu/kw/ecg/mml/ecg_v_fib.h
tml
45. Mechanical Physiology
Systole
Period of contraction
Diastole
Period of relaxation
Cardiac cycle
Atrial systole + atrial diastole +
ventricular systole + ventricular diastole
Heart beat
46 - 47. Summary
Blood flows from region of higher pressure
to region of lower pressure
Pressure changes due to alternating
contraction and relaxation of myocardium
Pressure changes control opening and
closing of valves
48. Early Ventricular Diastole EKG –
Atria
AV valves
SL valves
Ventricular volume
Ventricular pressure
49. Late Ventricular Diastole EKG –
Atria
AV valves
SL valves
Ventricular volume
Ventricular pressure
50. End of Ventricular Diastole
Ventricle at maximum volume
End-diastolic volume (EDV)
~135m
51. Ventricular Excitation
EKG – QRS complex
Onset of ventricular systole
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Increased ventricular contraction
of AV valves
closing
52. Isovolumetric Contraction
EKG –
Atria in
AV valves
SL valves
Ventricular volume
Ventricular pressure
53. Ventricular Ejection - Fig. 9-16, pg. 256
EKG –
Atria in
AV valves
SL valves
Ventricular volume
Ventricular pressure
54. End of Ventricular Systole
End-systolic volume
Amount of blood remaining in ventricle
at end of systole (ESV)
~65ml
Stroke volume
Amount of blood pumped out of each
ventricle during each contraction (SV)
SV = EDV - ESV
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55. Isovolumetric Relaxation - Fig. 9-16, pg. 256
EKG –
Atria in
AV valves
SL valves
Ventricular volume
Ventricular pressure
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56. Summary
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57. Cardiac Output
Cardiac output (CO)
CO = HR x SV
~5 liters/minute
Cardiac reserve
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58. Regulation of Cardiac Output
Heart rate (HR)
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Stroke volume (SV)
59. Regulation of Stroke Volume
Stroke volume is difference between EDV
and end systolic volume (ESV)
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SV = EDV -ESV
Typically ~60% of blood in ventricle is
pumped out when ventricle contracts
Factors affecting SV
Preload
Contractility
Afterload
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60. Preload
Degree of stretch of heart muscle
Resting cardiac muscles cells are less than
optimum length
Increased venous return
Increased ED
Increased SV
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61. Frank-Starling Law
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62. Contractility
Strength of contraction given any EDV
Increased contractility leads to increased
ejection fraction
Due to increased Ca2+
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63. Afterload
Back pressure exerted by arterial blood
80mmHg/8mmHg
Not usually a major determinant of stroke
volume
64 - 66. Control of Stroke Volume
Intrinsic control
Venous return
Increased return results in increased SV
Extrinsic control
Degree of sympathetic stimulation
Increased epinephrine and
norepinephrine results in increased
calcium influx and greater cross-bridge
cycling
Shifts Starling curve to left
Also enhances venous return
67. Heart Rate
Intrinsic rate set by SA node
Autonomic influences
Parasympathetic
Atrium
SA node
AV node
Sparse in ventricles
Sympathetic
All of the above + rich innervation of
the ventricles
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68 - 70. ANS Influence on Heart Rate
Parasympathetic
Decrease rate of depolarization of SA
Increases AV delay
Little effect of ventricular contraction
Sympathetic
Increase rate of depolarization of SA
Decrease AV delay
Speed transmission of AP through
conduction pathway
Increased contractile strength
71 - 72. Heart Failure
Inability of cardiac output to meet demands
for oxygen/nutrient delivery and removal of
wastes
Decrease in contractility
http://www.colorado.edu/intphys/Class/IPHY3430200/image/figure0926.jpg
73. Compensatory Mechanisms
Sympathetic stimulation
Increased salt and water retention by the
kidneys
Decompensated heart failure
Cardiac muscle cells stretched
Congestive heart failure
Backup of blood in venous system
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74. Heart Failure
Causes
Damage to heart muscle
Prolonged pumping against elevated BP
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75. Coronary Artery Disease (CAD)
Coronary Circulation
Endothelium impermeable
Myocardium too thick for diffusion
Receives blood during diastole
Blood flow adjusted to match heart’s
requirements
CAD
Pathology in coronary arteries
Insufficient flow in times of need
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76 - 77. Atherosclerosis
Localized plaques
Atheromas
reduce blood flow in an artery
Site of blood clot formation
Plaques begin at sites of damage to
endothelium
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E.g. from hypertension, smoking, high
cholesterol, or diabetes
78 - 79. Cholesterol/Lipoproteins
High blood cholesterol increases risk of
atherosclerosis
LDLs and HDLs
Transport lipids including cholesterol
Myocardial ischemia/myocardial infarction
Vascular spasm
Cold, exertion, anxiety
Atherosclerotic plaques
Thromoboembolism
80 - 82. Ischemic Heart Disease
Commonly due to atherosclerosis in
coronary arteries
Ischemia
Insufficient blood supply to tissue
Causes increased lactic acid from
anaerobic metabolism
Accompanied by angina pectoris (chest
pain)
S-T segment changes in ECG
Myocardial infarction (MI) is a heart attack
Usually caused by occlusion of a
coronary artery
Death of heart muscle
Diagnosis
high levels of
creatine phosphokinase
(CPK)
lactate dehydrogenase (LDH)
Presence of plasma troponin from
damaged muscle
Scar tissue
83. Thrombosis
Embolism
Thromboembolism
http://myhealth.ucsd.edu/library/healthguide/enus/images/media/medical/hw/n5551339.jpg
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