Presentation on theme: "The heart circulates blood to every tissue and organ, sustaining all bodily strength."— Presentation transcript:
The heart circulates blood to every tissue and organ, sustaining all bodily strength
Functions of the Circulatory System Transportation: –Respiratory: Transport 0 2 and C0 2. –Nutritive: Carry absorbed digestion products to liver and to tissues. –Excretory: Carry metabolic wastes to kidneys to be excreted.
Functions of the Circulatory System (continued) Regulation: –Hormonal: Carry hormones to target tissues to produce their effects. –Temperature: Divert blood to cool or warm the body. –Protection: Blood clotting. –Immune: Leukocytes, cytokines and complement act against pathogens.
Components of Circulatory System Components of Cardiovascular system (CV): –Heart: Pumping action creates pressure head needed to push blood through vessels. –Blood vessels: Permits blood flow from heart to cells and back to the heart. –Arteries, arterioles, capillaries, venules, veins. Lymphatic System: –Lymphatic vessels transport interstitial fluid. Lymph nodes cleanse lymph prior to return in venous blood.
Composition of Blood Composition of blood Plasma: –Straw-colored liquid. Consists of H 2 0 and dissolved solutes. –Ions, metabolites, hormones, antibodies. »Na + is the major solute of the plasma. Plasma proteins: –Constitute 7-9% of plasma. Albumin: –Accounts for 60-80% of plasma proteins. –Provides the colloid osmotic pressure needed to draw H 2 0 from interstitial fluid to capillaries. »Maintains blood pressure.
Composition of blood: Plasma proteins (continued): –Globulins: globulin: –Transport lipids and fat soluble vitamins. globulin: –Transport lipids and fat soluble vitamins. globulin: –Antibodies that function in immunity. Fibrinogen: –Constitutes 4% of plasma proteins. –Important clotting factor. Converted into fibrin during the clotting process. Composition of the Blood (continued)
Composition of blood Serum: –Fluid from clotted blood. Does not contain fibrinogen. Plasma volume: –Number of regulatory mechanisms in the body maintain homeostasis of plasma volume. Osmoreceptors. ADH. Renin-angiotensin-aldosterone system. Composition of the Blood (continued)
Erythrocytes –Flattened biconcave discs. –Provide increased surface area through which gas can diffuse. –Lack nuclei and mitochondria. Half-life ~ 120 days. –Each RBC contains 280 million hemoglobin with 4 heme chains (contain iron). –Removed from circulation by phagocytic cells in liver, spleen, and bone marrow.
Leukocytes Leukocytes: –Contain nuclei and mitochondria. –Move in amoeboid fashion. Can squeeze through capillary walls (diapedesis). –Almost invisible, so named after their staining properties. Granular leukocytes: –Help detoxify foreign substances. »Release heparin. Agranular leukocytes: –Phagocytic. »Produce antibodies.
Platelets (thrombocytes) –Smallest of formed elements. Are fragments of megakaryocytes. Lack nuclei. –Capable of amoeboid movement. –Important in blood clotting: Constitute most of the mass of the clot. Release serotonin to vasoconstrict and reduce blood flow to area. –Secrete growth factors: Maintain the integrity of blood vessel wall. –Survive 5-9 days.
Hematopoiesis Hematopoiesus –Undifferentiated cells gradually differentiate to become stem cells, that form blood cells. –Occurs in myeloid tissue (bone marrow of long bones) and lymphoid tissue. –2 types of hematopoiesis: Erythropoiesis: –Formation of RBCs. Leukopoiesis: –Formation of WBCs.
Figure 23.14 The circulatory plan in gill-breathing fish (Part 2)
Figure 23.22 Circulation through the body of a crayfish or lobster (Part 1)
Figure 23.18 Blood flow in heart ventricles and systemic and pulmonary arteries of crocodilians
Pulmonary and Systemic Circulations Pulmonary circulation: –Path of blood from right ventricle through the lungs and back to the heart. Systemic circulation: –Oxygen-rich blood pumped to all organ systems to supply nutrients. Rate of blood flow through systemic circulation = flow rate through pulmonary circulation.
Figure 23.10 The circulatory plan in mammals and birds (Part 1)
Figure 23.10 The circulatory plan in mammals and birds (Part 2)
Figure 23.14 The circulatory plan in gill-breathing fish (Part 1)
Figure 23.15 The circulatory plans of some air-breathing fish (Part 1)
Figure 23.15 The circulatory plans of some air-breathing fish (Part 2)
Figure 23.16 The branchial vascular arches of a lungfish
Figure 23.19 The circulatory plan of squids and octopuses (Part 1)
Figure 23.22 Circulation through the body of a crayfish or lobster (Part 2)
Box 23.3 Blood flow through the tissues of an insect is principally through lacunae and sinuses
Conducting Tissues of the Heart Contracting tissues of the heart: –APs spread through myocardial cells through gap junctions. –Impulses cannot spread to ventricles directly because of fibrous tissue. –Conduction pathway: SA node. AV node. Bundle of His. Purkinje fibers. –Stimulation of Purkinje fibers cause both ventricles to contract simultaneously.
Conduction of Impulse Conduction of impulse –APs from SA node spread quickly at rate of 0.8 - 1.0 m/sec. –Time delay occurs as impulses pass through AV node. Slow conduction of 0.03 – 0.05 m/sec. –Impulse conduction increases as spread to Purkinje fibers at a velocity of 5.0 m/sec. Ventricular contraction begins 0.1–0.2 sec. after contraction of the atria.
Refractory Periods Refractory periods: Heart contracts as syncytium. Contraction lasts almost 300 msec. Refractory periods last almost as long as contraction. Myocardial muscle cannot be stimulated to contract again until it has relaxed. –Summation cannot occur.
Excitation-Contraction Coupling in Heart Muscle Excitation-contraction coupling in heart muscle –Depolarization of myocardial cell stimulates opening of VG Ca 2+ channels in sarcolema. Ca 2+ diffuses down gradient into cell. –Stimulates opening of Ca 2+ -release channels in SR. Ca 2+ binds to troponin and stimulates contraction (same mechanisms as in skeletal muscle). –During repolarization Ca 2+ actively transported out of the cell via a Na + -Ca 2+ - exchanger.
Electrocardiogram (ECG/EKG) EKG (ECG) The body is a good conductor of electricity. –Tissue fluids have a high [ions] that move in response to potential differences. Electrocardiogram: –Measure of the electrical activity of the heart per unit time. Potential differences generated by heart are conducted to body surface where they can be recorded on electrodes on the skin. Does NOT measure the flow of blood through the heart.
ECG Leads ECG leads Bipolar leads: –Record voltage between electrodes placed on wrists and legs. –Right leg is ground. Unipolar leads: –Voltage is recorded between a single “exploratory electrode” placed on body and an electrode built into the electrocardiograph. –Placed on right arm, left arm, left leg, and chest. Allow to view the changing pattern of electrical activity from different perspectives.
Figure 23.4 The conducting system and the process of conduction in the mammalian heart (Part 1)
Figure 23.4 The conducting system and the process of conduction in the mammalian heart (Part 2)
Figure 23.4 The conducting system and the process of conduction in the mammalian heart (Part 3)
Figure 23.2 The heart as a pump: The dynamics of the left side of the human heart
Figure 23.2 The heart as a pump: The dynamics of the left side of the human heart (Part 1)
Cardiac Cycle (continued) Step 1: Isovolumetric contraction: –QRS just occurred. –Contraction of the ventricle causes ventricular pressure to rise above atrial pressure. AV valves close. –Ventricular pressure is less than aortic pressure. Semilunar valves are closed. –Volume of blood in ventricle is EDV. Step 2: Ejection: –Contraction of the ventricle causes ventricular pressure to rise above aortic pressure. Semilunar valves open. –Ventricular pressure is greater than atrial pressure. AV valves are closed. –Volume of blood ejected: SV.
Cardiac Cycle (continued) Step 3: T wave occurs: –Ventricular pressure drops below aortic pressure. Step 4: Isovolumetric relaxation: –Back pressure causes semilunar valves to close. AV valves are still closed. –Volume of blood in the ventricle: ESV. Step 5: Rapid filling of ventricles: –Ventricular pressure decreases below atrial pressure. AV valves open. –Rapid ventricular filling occurs.
Figure 23.2 The heart as a pump: The dynamics of the left side of the human heart (Part 2)
Figure 23.3 Four systems evolved by animals to supply O 2 to the myocardium (Part 1)
Figure 23.3 Four systems evolved by animals to supply O 2 to the myocardium (Part 2)
Figure 23.7 Fluid-column effects on blood pressure in the arterial vascular system
Figure 23.8 Total fluid energy: The true driving force for blood flow
Cardiac Output (CO) Cardiac output is determined by venous return and neural and hormonal controls Resting heart rate is controlled by the cardioinhibitory center via the vagus nerves –Stroke volume is controlled by venous return (end diastolic volume, or EDV) Under stress, the cardioacceleratory center increases heart rate and stroke volume –The end systolic volume (ESV) decreases and MAP increases
Controls of Blood Pressure Short-term controls: –Are mediated by the nervous system and bloodborne chemicals –Counteract moment-to-moment fluctuations in blood pressure by altering peripheral resistance Long-term controls regulate blood volume
Short-Term Mechanisms: Neural Controls Neural controls of peripheral resistance: –Alter blood distribution in response to demands –Maintain MAP by altering blood vessel diameter Neural controls operate via reflex arcs involving: –Baroreceptors –Vasomotor centers and vasomotor fibers –Vascular smooth muscle
Short-Term Mechanisms: Vasomotor Center Vasomotor center – a cluster of sympathetic neurons in the medulla that oversees changes in blood vessel diameter –Maintains blood vessel tone by innervating smooth muscles of blood vessels, especially arterioles Cardiovascular center – vasomotor center plus the cardiac centers that integrate blood pressure control by altering cardiac output and blood vessel diameter
Short-Term Mechanisms: Vasomotor Activity Sympathetic activity causes: –Vasoconstriction and a rise in BP if increased –BP to decline to basal levels if decreased Vasomotor activity is modified by: –Baroreceptors (pressure-sensitive), chemoreceptors (O 2, CO 2, and H + sensitive), higher brain centers, bloodborne chemicals, and hormones
Short-Term Mechanisms: Baroreceptor-Initiated Reflexes Increased blood pressure stimulates the cardioinhibitory center to: –Increase vessel diameter –Decrease heart rate, cardiac output, peripheral resistance, and blood pressure
Short-Term Mechanisms: Baroreceptor-Initiated Reflexes Declining blood pressure stimulates the cardioacceleratory center to: –Increase cardiac output and peripheral resistance Low blood pressure also stimulates the vasomotor center to constrict blood vessels
Regulation by ADH Released by posterior pituitary when osmoreceptors detect an increase in plasma osmolality. Dehydration or excess salt intake: –Produces sensation of thirst. –Stimulates H 2 0 reabsorption from urine.
Chemicals that Decrease Blood Pressure Atrial natriuretic peptide (ANP) – causes blood volume and pressure to decline Nitric oxide (NO) – is a brief but potent vasodilator Inflammatory chemicals – histamine, prostacyclin, and kinins are potent vasodilators Alcohol – causes BP to drop by inhibiting ADH
Long-Term Mechanisms: Renal Regulation Long-term mechanisms control BP by altering blood volume Baroreceptors adapt to chronic high or low BP –Increased BP stimulates the kidneys to eliminate water, thus reducing BP –Decreased BP stimulates the kidneys to increase blood volume and BP
Kidney Action and Blood Pressure Kidneys act directly and indirectly to maintain long-term blood pressure –Direct renal mechanism alters blood volume –Indirect renal mechanism involves the renin- angiotensin mechanism
Kidney Action and Blood Pressure –Declining BP causes the release of renin, which triggers the release of angiotensin II –Angiotensin II is a potent vasoconstrictor that stimulates aldosterone secretion –Aldosterone enhances renal reabsorption and stimulates ADH release
Renin-Angiotension-Aldosterone System (continued)
Diving physiology part 1 The oxygen store of divers –Adjustment of circulatory function CNS and heart dependent on aerobic catabolism for ATP production Skeletal muscle tolerant of O 2 deprivation Blood flow to skin, gut, kidneys is curtailed by vasoconstriction Oxygen deprived tissue will turn to anaerobic catabolism –Lactic acid accumulates
Diving physiology part 2 The amount of O 2 stored in blood depends on: –O 2 carrying capacity of the blood –Volume of blood –Degree of saturation of blood with O 2 at the time of submergence
Diving physiology Thoracic cavity and lungs-- compressible High myoglobin concentrations –In skeletal muscle –Large myoglobin-bound O2 stores –O2 remains bound to the myoglobin until the O 2 partial pressure in the muscles falls to a low level
Circulatory adjustment during dives Bradycardia –Drop in cardiac output –Weddell seals show an 86% drop in cardiac work and an 85% reduction in blood flow to their ventricular heart muscle Regional vasoconstriction –Becomes a “heart-lung-brain” machine –Large concentration of rbcs in their blood when they are diving –Rbcs stored in their spleen- release during dive
Metabolism during dives 3 factors determine the limits of endurance of the O 2 –dependent tissues –Magnitude of O2 store available –Rate of use of the O2 store –Extent to which P02 can fall before impairing the function of O 2 -dependent tissues MR during dive is the most important factor in determining metabolic limits on dive duration –low MR, slow O 2 depletion, and slow lactic acid accumulation
The aerobic dive limit Prolong dive has major behavioral consequences –Requires time for ridding body of lactic acid –Must stay at the water’s surface where it can breathe –Lactic acid burdens of successive dives Additive Example- a seal that accumulates 80 ml lactic acid/ 100 ml of blood has to remain at the surface over an hour to return its lactic acid to resting level
Decompression sickness (DS) Caused by N 2 absorption from a compressed-air source –Start of dive– tissue contains a [N2] DS occur after a long deep dive and then surfaces suddenly –PN 2 pressure falls in the lungs to its ordinary value –N2-charged blood and other tissues start to lose N2 in the lung air –Bubbles of blood may form within the blood and tissues
Decompression sickness (DS) 2 Breath-hold dives must be repeated many times to cause DS in humans Marine animals avoid DS during deep dives by alveolar collapse –Special features of lungs and thorax Keep pulmonary N 2 within lungs Avoid build up in blood and tissues Lung air moves to conducting airways