1) review for the cardiovascular system[1]

Cardiovascular System

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Capillary Beds

Circulatory System & Blood

General & Pulmonary Circulation

Note Pulmonary arteries and veins (the exceptions)

Heart is located in the mediastinum

area from the sternum to the vertebral column and between the lungs

Location of the Heart

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

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

External Heart: Major Vessels of the Heart

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

ChambersBordersSurfacesSulci

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

Infindibulum

Right Ventricle

Tricuspid valve Blood flows through into right ventriclehas three cusps composed of dense CT covered by endocardium

• Forms most of anterior surface of heart• Interventricular septum: partitions ventricles

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 aortajust 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.

Downloaded from: StudentConsult (on 24 November 2009 06:16 AM)© 2005 Elsevier

The heart is the pumpthat propels theblood through the systemic and pulmonary circuits.

Red color indicates blood that isfully oxygenated.

Blue color representsblood that is only partially oxygenated.

Figure 12-2

The distribution of blood in a comfortable, restingperson is shown here.

Dynamic adjustments inblood delivery allow aperson to respond to widely varying circumstances, including emergencies.

Figure 12-3

Dynamic adjustmentsin blood-flow distribution during exercise result from changes in cardiac output and from changes in regionalvasodilation/vasoconstriction.

Figure 12-61

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


Figure 9-3 Rhythmical action potentials (in millivolts) from a Purkinje fiber and from a ventricular muscle fiber, recorded by means of microelectrodes.


The prolonged refractory period of cardiac muscleprevents tetanus, and allows time for ventricles to fill with blood prior to pumping.

Figure 12-17

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.Downloaded from: StudentConsult (on 24 November 2009 06:16 AM)© 2005 Elsevier

Systole:ventricles contracting

Diastole:ventricles relaxed

Figure 12-18

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

Figure 12-19

Pressure changes in the right heart during a contraction cycle.

Figure 12-20

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 12-4

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.

Figure 12-11

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.

Figure 12-12

The prolonged “plateau” of depolarization is due to the slow but prolonged opening of voltage-gated calcium channels PLUSclosure of potassium channels.


Figure 12-12

Opening of potassium channels results in therepolarization phase.


Figure 12-12


Opening of potassium channels results in therepolarization phase.

The prolonged “plateau” of depolarization is due to the slow but prolonged opening of voltage-gated calcium channels PLUSclosure of potassium channels.

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

Figure 12-13

Sodium ions “leaking” in through the F-type [funny] channels PLUScalcium ions moving in throughthe 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 PLUSclosing of calcium channels are responsible for therepolarization phase.

The action potential of anautorhythmic cardiac cell.

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 12-14

Figure 12-16

Control of the Heart by the Sympathetic and Parasympathetic Nerves

SYMPATHETIC STIMULATION(NOREPINEPHRINE & EPINEPHRINE)

Increases HRIncreases Force of Heart Contraction

Increases Cardiac Output

P a r a s y m p a t h e t i c S t i m u l a t i o n

Decreases HRDecreases Strength of Heart Muscle

Pages 112-113, and 121 from Guyton and Hall

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

Figure 12-23

Sympathetic signals (norepinephrine and epinephrine) cause a stronger and more rapid contraction and a more rapid relaxation.

Figure 12-26

Figure 12-22

Figure 9-10 Cardiac sympathetic and parasympathetic nerves. (The vagus nerves to the heart are parasympathetic nerves.)


Figure 9-11 Effect on the cardiac output curve of different degrees of sympathetic or parasympathetic stimulation.


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 12-35

Diversity among signals that influence contraction/relaxationin vascular circular smooth muscle implies a diversity of receptors and transduction mechanisms.

Figure 12-36

Effects of P o t a s s i u m a n d C a l c i u m Ions on Heart Function

Effect of Potassium IonsExcess Potassium causes heart to dilate and HR to slowPotassium decreases the resting membrane potential and result in weak heart contraction

Effect of Calcium ionsExcess calcium causes spastic contractionCalcium 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.Downloaded from: StudentConsult (on 24 November 2009 06:16 AM)

© 2005 Elsevier

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.


Figure 18-2 Sympathetic innervation of the systemic circulation.


Figure 18-3 Areas of the brain that play important roles in the nervous regulation of the circulation. The dashed lines represent inhibitory pathways.


Ref: Chapter 10 in Guyton and 12 in Vander

Rhythmical Excitation of the Heart

Specialized Excitatory and Conductive System of the Heart

S-A nodeA-V node

A-V bundlePurkinjie 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.


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.


Figure 14-2 Normal blood pressures in the different portions of the circulatory system when a person is lying in the horizontal position.

Downloaded from: StudentConsult (on 24 November 2009 07:18 AM)

© 2005 Elsevier

Figure 12-29

In response to the pulsatile contraction of the heart:pulses of pressure move throughout the vasculature, decreasing in amplitude with distance

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

Intercellular clefts assist the exchange.

Capillary walls are a singleendothelial cell in thickness.

Figure 12-37

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 12-38

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 12-40

Absorption: movement of fluid and solutes into the blood.

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

Figure 12-41

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.

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.

Chapter 12:Cardiovascular Physiology (cont.)

The autonomic system dynamically adjusts CO and MAP.

Blood composition and hemostasis are described.

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


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


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


Figure 15-11 Venous valves of the leg.


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