Body System1 Cardiovascular System

Prepared by Dr.Mustafa Al-Shehabat

Capillary Beds

Circulatory System & Blood

General & Pulmonary Circulation

Note Pulmonary arteries and veins (the exceptions)

Location of the Heart

 Heart is located in the mediastinum  area from the sternum to the vertebral column and between the lungs

Heart Anatomy

Fig.20.02b

Pericardial Layers of the Heart

Heart Wall
 Epicardium visceral layer of the serous pericardium  Myocardium cardiac muscle layer  Endocardium endothelial layer of the inner myocardial surface

External Heart: Major Vessels of the Heart

Vessels returning blood to the heart include:  Right and left pulmonary veins  Superior and inferior venae cavae

Vessels conveying blood away from the heart include:  Aorta  Right and left pulmonary arteries

Atria of the Heart

   Atria are the receiving chambers of the heart Blood enters right atria from superior and inferior venae cavae and coronary sinus Blood enters left atria from pulmonary veins

Ventricles of the Heart

   Ventricles are the discharging chambers of the heart Right ventricle pumps blood into the pulmonary trunk Left ventricle pumps blood into the aorta

Chambers Borders Surfaces Sulci

Heart Valves
One Way Direction

Atrioventricular Valves

A-V valves open and allow blood to flow from atria into ventricles when ventricular pressure is lower than atrial pressure occurs when ventricles are relaxed, chordae tendineae are slack and papillary muscles are relaxed

A-V valves close preventing backflow of

blood into atria occurs when ventricles contract, pushing valve cusps closed, chordae tendinae are pulled taut and papillary muscles contract to pull cords and prevent cusps from everting

Fig. 20.06a,b

Semilunar Valves

SL valves open with ventricular contraction allow blood to flow into pulmonary trunk and aorta SL valves close with ventricular relaxation prevents blood from returning to ventricles, blood fills valve cusps, tightly closing the SL valves Aortic Sinuses

Nodule of semiluar valve

Right Atrium Receives All Venous Blood (front and behind). Interatrial septum partitions the atria musculi pectinati (pectinate muscles)

Crista Terminalis

Right Ventricle Forms most of anterior surface of heart Interventricular septum: partitions ventricles

Infindibulum

Tricuspid valve Blood flows through into right ventricle has three cusps composed of dense CT covered by endocardium Pulmonary semilunar valve: blood flows into pulmonary trunk

Left Ventricle Forms the apex of heart Bicuspid (Mitral) valve: blood passes through into left ventricle has two cusps Chordae tendineae anchor bicuspid valve to papillary muscles (also has trabeculae carneae like right ventricle) Aortic semilunar valve: blood passes through valve into the ascending aorta just above valve are the openings to the coronary arteries

Interventricular septum

Cardiac cycle

Pathway of Blood Through the Heart and Lungs

Heart Sounds
Sounds of heartbeat are from turbulence in blood flow caused by valve closure
first heart sound (lubb) is created with the closing of the atrioventricular valves second heart sound (dupp) is created with the closing of semilunar valves

The A-V valves The Tricuspid valve and the mitral valve

The Semilunar valves The aortic and the pulmonary artery valves

Figure 9-1 Structure of the heart, and course of blood flow through the heart chambers and heart valves.
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Figure 12-2

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 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.

Figure 9-2 "Syncytial," interconnecting nature of cardiac muscle fibers.

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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 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:
2005 Elsevier

Figure 12-18

Systole: ventricles contracting

Diastole: ventricles relaxed

Figure 12-19

Pressure and volume changes in the left heart during a contraction cycle.

Figure 12-20

Pressure changes in the right heart during a contraction cycle.

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 heart s 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.

The action potential of a myocardial pumping cell.

The rapid opening of voltage-gated sodium channels is responsible for the rapid depolarization phase.

Figure 12-12

The action potential of a myocardial pumping cell.

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

The action potential of a myocardial pumping cell.

Opening of potassium channels results in the repolarization phase. Figure 12-12

The action potential of a myocardial pumping cell.

The rapid opening of voltage-gated sodium channels is responsible for the rapid depolarization phase. The prolonged plateau of depolarization is due to the slow but prolonged opening of voltage-gated calcium channels PLUS closure of potassium channels.

Opening of potassium channels results in the repolarization phase. Figure 12-12

Figure 12-13

The action potential of an autorhythmic cardiac cell.

Sodium ions leaking in through the F-type [funny] channels PLUS calcium ions moving in through the T [calcium] channels cause a threshold graded depolarization. The rapid opening of voltage-gated calcium channels is responsible for the rapid depolarization phase. Reopening of potassium channels PLUS closing of calcium channels are responsible for the repolarization phase.

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 12-16

Control of the Heart by the Sympathetic and Parasympathetic Nerves

Increases HR Increases Force of Heart Contraction Increases Cardiac Output

Decreases HR Decreases Strength of Heart Muscle

Pages 112-113, and 121 from Guyton and Hall

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 18-2 Sympathetic innervation of the systemic circulation.

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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 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

Capillary walls are a single endothelial cell in thickness.

The capillary is the primary point exchange between the blood and the interstitial fluid (ISF). Intercellular clefts assist the exchange.

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 12-40

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

Filtration: movement of fluid and solutes out of the blood.

Absorption: movement of fluid and solutes into the blood.

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.

Chapter 12: Cardiovascular Physiology (cont.)

Mean arterial pressure, which drives the blood, is the sum of the diastolic pressure plus one-third of the difference between the systolic and diastolic pressures.

The autonomic system dynamically adjusts CO and MAP.

Blood composition and hemostasis are described.

Figure 14-3 Interrelationships among pressure, resistance, and blood flow.

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Figure 14-10 Vascular resistances: A, in series and B, in parallel.

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Figure 14-12 Effect of hematocrit on blood viscosity. (Water viscosity = 1.)

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Figure 15-11 Venous valves of the leg.

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Figure 15-7 Auscultatory method for measuring systolic and diastolic arterial pressures.
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