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The A-V valves The Tricuspid valve and the mitral valve
The Semilunar valves The aortic and the pulmonary artery valves
Figure 23-2 Chest areas from which sound from each valve is best heard.
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1st sound=Lub 2nd sound = dub 3rd sound =middle diastole 4th sound= atrial heart sound
Valvular Heart Diseases *Aortic stenosis *Mitral regurgitation *Aortic regurgitation *Mitral stenosis Ref: Guyton &Hall Page 269-272
Figure 9-1 Structure of the heart, and course of blood flow through the heart chambers and heart valves.
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Figure 12-8
The general route of the blood through the body is shown, including passage through the heart (colored box).
Figure 12-2
The heart is the pump that propels the blood through the systemic and pulmonary circuits. Red color indicates blood that is fully oxygenated. Blue color represents blood that is only partially oxygenated.
Figure 14-1 Distribution of blood (in percentage of total blood) in the different parts of the circulatory system.
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Figure 12-3
The distribution of blood in a comfortable, resting person is shown here. Dynamic adjustments in blood delivery allow a person to respond to widely varying circumstances, including emergencies.
Figure 12-61
Dynamic adjustments in blood-flow distribution during exercise result from changes in cardiac output and from changes in regional vasodilation/vasoconstric tion.
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Figure 9-3 Rhythmical action potentials (in millivolts) from a Purkinje fiber and from a ventricular muscle fiber, recorded by means of microelectrodes.
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Figure 9-4 Force of ventricular heart muscle contraction, showing also duration of the refractory period and relative refractory period, plus the effect of premature contraction. Note that premature contractions do not cause wave summation, as occurs in skeletal muscle.
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Figure 12-17
The prolonged refractory period of cardiac muscle prevents tetanus, and allows time for ventricles to fill with blood prior to pumping.
Figure 9-5 Events of the cardiac cycle for left ventricular function, showing changes in left atrial pressure, left ventricular pressure, aortic pressure, ventricular volume, the electrocardiogram, and the phonocardiogram. StudentConsult (on 24 November 2009 06:16 AM) Downloaded from:
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Figure 12-18
Figure 12-19
Pressure and volume changes in the left heart during a contraction cycle.
Figure 12-20
Figure 12-4
Though pressure is higher in the lower tube, the flow rates in the pair of tubes is identical because they both have the same pressure difference (90 mm Hg) between points P1 and P2.
Figure 12-11
The sinoatrial node is the hearts pacemaker because it initiates each wave of excitation with atrial contraction.
The Bundle of His and other parts of the conducting system deliver the excitation to the apex of the heart so that ventricular contraction occurs in an upward sweep.
Figure 12-12
The prolonged plateau of depolarization is due to the slow but prolonged opening of voltage-gated calcium channels PLUS closure of potassium channels.
Figure 12-12
Figure 12-13
Figure 12-14
The relationship between the electrocardiogram (ECG), recorded as the difference between currents at the left and right wrists,
and
an action potential typical of ventricular myocardial cells.
Figure 11-6 Conventional arrangement of electrodes for recording the standard electrocardiographic leads. Einthoven's triangle is superimposed on the chest.
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Figure 11-7 Normal electrocardiograms recorded from the three standard electrocardiographic leads.
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Figure 11-8 Connections of the body with the electrocardiograph for recording chest leads. LA, left arm; RA, right arm.
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Figure 11-9 Normal electrocardiograms recorded from the six standard chest leads.
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Figure 11-10 Normal electrocardiograms recorded from the three augmented unipolar limb leads.
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Figure 12-16
Figure 12-23
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).
Figure 12-26
Sympathetic signals (norepinephrine and epinephrine) cause a stronger and more rapid contraction and a more rapid relaxation.
Figure 12-22
Figure 9-10 Cardiac sympathetic and parasympathetic nerves. (The vagus nerves to the heart are parasympathetic nerves.)
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Figure 9-11 Effect on the cardiac output curve of different degrees of sympathetic or parasympathetic stimulation.
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Figure 12-35
Sympathetic stimulation of alpha-adrenergic receptors causes vasoconstriction to decrease blood flow to that location. Sympathetic stimulation of beta-adrenergic receptors leads to vasodilation to cause an increase in blood flow to that location.
Figure 12-36
Diversity among signals that influence contraction/relaxation in vascular circular smooth muscle implies a diversity of receptors and transduction mechanisms.
Effects of Function
Ions on Heart
Effect of Potassium Ions Excess Potassium causes heart to dilate and HR to slow Potassium decreases the resting membrane potential and result in weak heart contraction Effect of Calcium ions Excess calcium causes spastic contraction Calcium deficiency causes cardiac flaccidity
Figure 9-12 Constancy of cardiac output up to a pressure level of 160 mm Hg. Only when the arterial pressure rises above this normal limit does the increasing pressure load cause the cardiac output to fall significantly.
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Figure 18-1 Anatomy of sympathetic nervous control of the circulation. Also shown by the red dashed line is a vagus nerve that carries parasympathetic signals to the heart.
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Figure 18-3 Areas of the brain that play important roles in the nervous regulation of the circulation. The dashed lines represent inhibitory pathways.
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Ref: Chapter 10 in Guyton and 12 in Vander Rhythmical Excitation of the Heart Specialized Excitatory and Conductive System of the Heart S-A node A-V node A-V bundle Purkinjie fibers
Figure 12-10
Figure 10-1 Sinus node, and the Purkinje system of the heart, showing also the A-V node, atrial internodal pathways, and ventricular bundle branches.
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Figure 10-2 Rhythmical discharge of a sinus nodal fiber. Also, the sinus nodal action potential is compared with that of a ventricular muscle fiber.
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Figure 10-3 Organization of the A-V node. The numbers represent the interval of time from the origin of the impulse in the sinus node. The values have been extrapolated to human beings. Downloaded from: StudentConsult (on 24 November 2009 06:31 AM)
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Chapter 11
Figure 14-2 Normal blood pressures in the different portions of the circulatory system when a person is lying in the horizontal position.
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In response to the pulsatile contraction of the heart: pulses of pressure move throughout the vasculature, decreasing in amplitude with distance
Figure 12-29
Figure 12-37
The capillary is the primary point exchange between the blood and the interstitial fluid (ISF).
Figure 12-38
Capillaries lack smooth muscle, but contraction/relaxation of circular smooth muscle in upstream metarterioles and precapillary sphincters determine the volume of blood each capillary receives.
Figure 12-39
Six balls in per minute mandates six balls out per minute. Therefore, the velocity of the balls in the smaller tubes is slower.
Figure 12-40
There are many, many capillaries, each with slow-moving blood in it, resulting in adequate time and surface area for exchange between the capillary blood and the ISF.
Figure 12-41
Figure 12-43
Dynamic changes in vasodilation/vasoconstriction in the arterioles regulate downstream pressures and flow rates.
Figure 12-31
Cardiovascular Physiology
CO = HR x SV, as follows. The heart is the pump that moves the blood. Its activity can be expressed as cardiac output (CO) in reference to the amount of blood moved per unit of time.
A small fraction of cardiac muscle cells, called the autorhythmic cells, determine the heart rate (HR). A much larger group, making up 99% of the total cells in
diastolic pressures.
Figure 14-9 A, Demonstration of the effect of vessel diameter on blood flow. B, Concentric rings of blood flowing at different velocities; the farther away from the vessel wall, the faster the flow. Downloaded from: StudentConsult (on 24 November 2009 07:18 AM)
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Figure 12-1
The hematocrit is a rapid assessment of blood composition. It is the percent of the blood volume that is composed of RBCs (red blood cells).
Figure 14-11 Hematocrits in a healthy (normal) person and in patients with anemia and polycythemia.
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Figure 15-7 Auscultatory method for measuring systolic and diastolic arterial pressures.
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Figure 12-32
To estimate systolic and diastolic pressures, pressure is released from an inflatable cuff on the upper arm while listening as blood flow returns to the lower arm.
Figure 12-44
At rest, approx. 60% of the total blood volume is in the veins. Sympathetically mediated venoconstriction can substantially increase venous return to the heart.
Figure 12-45
Venous flow is assisted by the skeletal muscle pump mechanism working in combination with one-way valves.
Figure 12-46
Alterations in venous return alter end-diastolic volume (EDV); increased EDV directly increases stroke volume and cardiac output.
Figure 12-52
Blood loss causes a reduction in MAP, which, if left unchecked, would result in rapid and irreversible damage to the brain and the heart.
The End.