The Anatomy & Physiology of the Circulatory System The circulatory system consists of the blood, the heart, and the vascular system, all of which are essential to the delivery of oxygen to the body. THE BLOOD Blood is made of specialized cells suspended in a liquid substance called plasma. These specialized cells include red blood cells (erythrocytes), white blood cells (leukocytes), and platelets or cell fragments (thrombocytes). Each cell type has a specific function. Erythrocytes Red blood cells, or erythrocytes, make up the majority of all blood cells In healthy adults, there are about 4 to 5 million red blood cells per cubic millimeter of blood. They are produced by the red bone marrow at a rate of about 2 million cells per second. An equal number of worn out RBCs are destroyed by the spleen and liver These cells live for about 120 days and are confined to the bloodstream. A key component of erythrocytes is hemoglobin o Primarily responsible for transporting oxygen and carbon dioxide. Hematocrit The % of RBCs in relation to the total blood volume o Adult male: 45% o Adult female: 42% Leukocytes White blood cells, or leukocytes, protect the body against "invaders" such as bacteria, viruses, parasites, toxins, and tumors. A healthy adult has, on average, between 4,000 and 10,000 leukocytes per cubic millimeter of blood. A count higher than 11,000 cells/cubic millimeter is an indication of infection. Unlike erythrocytes, leukocytes can leave the capillaries to do their work. Leukocytes are grouped into two categories, based on their physical and chemical characteristics. o Granulocytes: These contain membrane-bound cytoplasmic granules that can be stained for observation. Neutrophils Make up 40% to 70% of the white blood cell (WBC) population Phagocytes that destroy bacteria and some fungi Eosinophils Make up 1% to 4% of WBCs Phagocytize antigen-antibody complexes Are increased in allergic conditions (asthma) Basophils Make up 1% or less of the WBC population. Combat allergic reactions o Agranulocytes: These contain a spherical nucleus but no cytoplasmic granules. Lymphocytes Found mostly in lymph tissues T lymphocytes o Attack virus infected cells and tumors B lymphocytes o Produce antibodies Proteins that inactivate antigens Make up 20-25% of the WBC population. Monocytes Make up 4% to 8% of the WBC count. Highly mobile macrophages Increase in chromic infections Also effective against viruses and certain bacterial parasites. Thrombocytes Blood platelets, or thrombocytes, are the smallest elements in the plasma. They prevent blood loss from small vessels by clumping together to begin the clotting process at the site of an injury. Normal platelet count is 250,000 to 500,000 / mm3 Plasma The straw-colored liquid that remains when the cells are removed from the blood. Plasma makes up about 55% of total blood volume About 90% of plasma is made up of water. Serum is the fluid portion of the blood that remains when clotting factors such as fibrinogen are removed. o When blood is drawn for testing, various tubes are used. Some of these tubes contain anticoagulants, while others allow the blood to clot, leaving the serum behind for testing. THE HEART Physical Structure The heart is a hollow, muscular organ that is enclosed in the mediastinum and rests on the top surface of the diaphragm, flanked by the lungs. Its four chambers include two atria (the upper right and upper left portions of the heart) and two ventricles (the lower right and lower left portions). Muscular walls called septa (singular: septum) separate the two atria and the two ventricles. See the graphic below for anterior and posterior views of the heart. Functionally, the heart is actually like two pumps. The right atrium and ventricle act as one to pump unoxygenated blood to the lungs. The left atrium and ventricle pump oxygenated blood through the circulatory system. The ventricles, which are larger and more muscular than the atria, are the key pumping chambers. The Pericardium The heart is enclosed in a sac called the pericardium. The fibrous pericardium, the tough outer layer, functions to: o protect the heart o anchors it to surrounding structures, such as the diaphragm and great vessels o prevent the heart from overfilling The serous pericardium, the inner wall, is composed of two layers: o Parietal layer Lines the inner surface of the fibrous pericardium o Visceral layer Also called the Epicardium o A film of serous fluid between the two layers allows them to glide smoothly against one another This allows the heart to work in a relatively friction-free environment. The Wall of the Heart The heart wall itself is made of three layers. Epicardium o the visceral layer of the pericardium o made of a layer of squamous epithelial cells over connective tissue Myocardium o the thick muscular middle layer forming the bulk of the heart o the part of the heart that actually contracts Endocardium o A glistening white sheet of squamous epithelium that rests on a thin connective tissue layer o Contains small blood vessels and smooth muscle o Located in the inner myocardial surface, it lines the chambers of the heart. The graphic below shows the layers of the pericardium and the heart wall. Blood Supply of the Heart Arterial Supply The heart’s blood supply comes from the aorta by way of the: o Left coronary artery Circumflex artery Anterior interventricular artery Supplies blood to the left atrium and ventricle o Right coronary artery Marginal artery Posterior interventricular artery Supplies the right atrium and ventricle Blockage of these arteries can cause a myocardial infarction (heart attack). Venous Supply The venous system parallels the coronary artery system: Great Cardiac Veins o collects venous blood from the anterior portion of the heart Middle Cardiac Vein o collects venous blood from the posterior portion of the heart Coronary Sinus o Receives blood from the great and middle cardiac veins. Thebesian Vein o Empties into the right and left atria Part of the normal anatomic shunt Figure 5-6 in the text shows the arterial and venous vessels of the heart. Blood Flow Blood flows through the heart in the following stages. Venous blood, which is low in oxygen and high in carbon dioxide, moves through the inferior vena cava and superior vena cava and enters the right atrium. Blood flows through the tricuspid valve into the right ventricle. The ventricles contract. The tricuspid valve, which is located between the right atrium and ventricle, closes to keep blood from flowing backward into the atrium. Blood leaves the right ventricle through the pulmonary semilunar valve and enters the pulmonary trunk. The pulmonary valve closes to prevent blood from flowing back into the right ventricle. Blood enters the lungs via the right and left pulmonary arteries. (Note that these are the only arteries in the body that normally carry unoxygenated blood.) Blood passes through pulmonary arterioles, pulmonary capillaries, and pulmonary venules The blood, which is now high in oxygen and low in carbon dioxide, passes through the four pulmonary veins into the left atrium. (Note that these are the only veins in the body that normally carry oxygenated blood.) Blood flows through the mitral valve into the left ventricle. The mitral, or bicuspid, valve closes, keeping blood from returning to the left atrium when the ventricles contract. The left ventricle pumps blood through the aortic valve and into the ascending aorta where it enters the systemic circulation. The aortic valve closes, keeping blood from flowing back into the left ventricle. THE PULMONARY AND SYSTEMIC VASCULAR SYSTEMS The circulatory system’s vascular network has two major components: Systemic system: begins with the aorta and ends in the right atrium Pulmonary system: begins with the pulmonary trunk and ends in the left atrium Roles and Characteristics of Arteries and Veins Arteries o Strong, elastic vessels that carry blood away from the heart. Arterioles o Called resistance vessels because their size and pressure change with changes in blood flow. o They play a major role in the distribution and regulation of blood pressure. Capillaries o Sites of gas exchange External respiration Gas exchange between the alveoli and pulmonary capillaries Internal respiration Gas exchange between the systemic capillaries and the tissues Venules o Tiny veins arising from the capillaries Veins o Carry blood back to the heart o Called capacitance vessels because they can hold a large amount of blood with very little pressure change. Neural Control of the Vascular System Sympathetic nerve fibers are found in the arteries, arterioles and in the veins. o Nerve fibers to the arterioles are most abundant The vasomotor center in the medulla oblongata controls the number of sympathetic impulses sent to the vascular systems. o Normally, the vasomotor center sends steady sympathetic impulses that result in a moderate state of vessel constriction, called vasomotor tone. o Response to sympathetic impulses: Increased impulses causes vasoconstriction Decreased impulses causes vasodilation o Exception Arterioles of the heart, brain, and skeletal muscle dilate in response to increased sympathetic impulses Increases the blood supply to these areas for “flight or fight” responses. The Baroreceptor Reflex In addition, the brain and the heart regulate arterial blood pressure in response to signals from the arterial baroreceptors. These special pressure receptors are located in the walls of the carotid arteries and the aorta and function as short-term regulators of arterial blood pressure. The graphic below shows the location of the arterial baroreceptors. Baroreceptors regulate arterial blood pressure by initiating reflex adjustments to changes in blood pressure. If arterial pressure decreases, the following occur. o The neural impulses from the baroreceptors decrease. o In response, the brain increases its sympathetic activity which causes increases in: heart rate myocardial force of contraction arterial constriction Increased total peripheral resistance venous constriction Liver, spleen, pancreas, stomach, intestine, kidneys, skin, and skeletal muscle o The contraction force of the heart increases. o The arteries and veins constrict. o The final result is increased cardiac output, increased arterial constriction, and a rise in blood pressure. When blood pressure increases, the following occur. o The neural impulses from the baroreceptors increase, which cause the brain to reduce its sympathetic activity which results in decreases in: cardiac output total peripheral resistance o The blood pressure falls. Baroreceptors are short-term regulators of arterial blood pressure: o If factors responsible for altering blood pressure persist for several days, the arterial baroreceptors will be reset and accept the higher pressure as normal Baroreceptors are also found in the large arteries, large veins, pulmonary vessels, and cardiac walls. o Function similarly to the carotid and aortic baroreceptors o Results in increased sensitivity to venous, atrial and ventricular pressures PRESSURE IN THE PULMONARY AND SYSTEMIC VASCULAR SYSTEM Pressure Types Three types of pressure are used to study blood flow. Intravascular o the actual blood pressure in the lumen of any vessel at any point, relative to the barometric pressure Transmural o The difference between the intravascular pressure of a vessel and the pressure surrounding the vessel. Positive transmural pressure exists when the pressure inside the vessel exceeds the pressure outside the vessel. Negative transmural pressure exists when the pressure inside the vessel is less than the pressure surrounding the vessel. Driving o the difference between the pressure at one point in a vessel and the pressure at any other point downstream in the vessel Figure 5-11 in the text gives a schematic illustration of these different pressures. THE CARDIAC CYCLE AND ITS EFFECT ON BLOOD PRESSURE Arterial blood pressure increases and decreases with the phases of the cardiac cycle: Ventricular contraction (systole) o Systolic pressure The maximum pressure generated during ventricular contraction (systole). The normal value is 120 mm Hg for the systemic system. The normal value is 25 mm Hg for the pulmonary system. Ventricular relaxation (diastole) o Diastolic pressure The lowest pressure that remains in the arteries when the ventricles relax (diastole) before the next ventricular contraction. The normal value is 80 mm Hg for the systemic system. The normal value is 8 mm Hg for the pulmonary system. Circulatory System Pressures System Systemic Pulmonary Blood Pressure 120/80 mm Hg 25/8 mm Hg Mean Pressure 100 mm Hg 15 mm Hg Driving Pressure 98 mm Hg 10 mm Hg Driving Pressures for the Circulatory System Pulmonary System o The mean pressure in the pulmonary artery is about 15 mm Hg. o The mean pressure in the left atrium is about 5 mm Hg. o Therefore, the driving pressure through the pulmonary system is 15 - 5 = 10 mm Hg Systemic System o The mean pressure in the aorta is about 100 mm Hg. o The mean pressure in the right atrium is about 2 mm Hg. o Therefore, the driving pressure through the systemic system is 100 - 2 = 98 mm Hg Compared with the pulmonary circulation, the driving pressure in the systemic system is about 10 times greater. Refer to the graphic below for a summary of the diastolic and systolic pressures in the systemic and pulmonary circulation systems. Arterial Pulses In the systemic circulation the arterial walls expand (ventricular contraction) and recoil (ventricular relaxation). This can be felt as a pulse in several systemic arteries: o Temporal o Carotid o Radial o Popliteal o Posterior tibial o Facial o Brachia o Femoral o Dorsal pedal The Blood Volume and its Effect on Blood Pressure Following are some key terms pertaining to blood volume. Stroke volume o the volume of blood ejected from the ventricle during each ventricular contraction o Normal: 40 to 80 mL Cardiac output o The total volume of blood discharged from the ventricles per minute o Formula: Stroke Volume (SV) times heart rate per minute (HR) Example: If HR is 72 bpm and SV is 70 mL then, CO = HR x SV CO = 72 x 70 = 5040 mL/min CO = 5 L/min. o Normal: 4 to 8 L/min. Effect on Blood Pressure Normally, when stroke volume or heart rate increases, blood pressure correspondingly increases. When stroke volume or heart rate decreases, blood pressure decreases. Blood volume varies with age, gender, and body size, but on average, an adult has about 5 L. o 75% in systemic circulation o 15% in the heart o 10% in the pulmonary capillary bed (capacity of 200 mL) THE DISTRIBUTION OF PULMONARY BLOOD FLOW In the upright lung, the blood flow progressively decreases from the base to the apex (or steadily increases from the apex to the base). Distribution of blood flow is a function of gravity, cardiac output, and vascular resistance. Gravity Blood flow in the lung is gravity dependent. Most blood flows to the lower half of the lungs. The intraluminal pressure of the vessels in the lower lung is greater than the pressure in the upper lung (less gravity dependent). Higher pressure causes the vessels to distend and allows more blood flow. The Effects of Gravity and Alveolar Pressure on the Distribution of Pulmonary Blood Flow Zone 1 (least gravity dependent area) o PA>Pa>Pv o Alveolar deadspace Normally does not occur because pressure is usually sufficient to raise the blood to the top of the lungs May occur in abnormal conditions such as: Hemorrhage Dehydration Positive pressure ventilation Zone 2 o Pa>PA>Pv o pulmonary capillaries are perfused the effective driving pressure steadily increases down through this zone o some limitation to venous flow Zone 3 o Pa>Pv>PA o Blood flow throughout this region is constant Figure 5-11 in the text gives a schematic illustration of these relationships. Determinants of Cardiac Output Cardiac output is the product of the stroke volume and the heart rate. Stroke volume is determined by the following: o Ventricular preload The degree to which the myocardial fiber is stretched prior to contraction (end diastole). Normally, the more a myocardial fiber is stretched, the more strongly it contracts, allowing the heart to convert increased venous return into increased stroke volume. However, in disease states, if the heart is enlarged, sometimes the ventricular fibers are overstretched, resulting in decreased output. The figure below illustrates the Frank-Starling curve, which describes the relationship between myocardial stretch and cardiac output. o Ventricular afterload The force against which the ventricles must work to pump the blood. The arterial systolic blood pressure best reflects the ventricular afterload. As BP increases, resistance increases Ventricular afterload is determined by: The volume and viscosity of the blood ejected The peripheral vascular resistance The total cross-sectional space into which the blood is ejected Afterload reduction Decreasing peripheral vascular resistance will increase the stroke volume o Myocardial Contractility The force generated by the myocardium when the ventricular muscle fibers shorten. When the contractility of the heart increases, cardiac output increases. o Positive inotropism When the contractility decreases, cardiac output decreases. o Negative inotropism Vascular Resistance In general, when vascular resistance increases, blood pressure increases (in turn increasing the ventricular afterload). Resistance is calculated by dividing blood pressure by cardiac output. o R = BP / CO Active and passive mechanisms in the pulmonary system change vascular resistance. These mechanisms are discussed below. Active Mechanisms Affecting Vascular Resistance Abnormal blood gases: The pulmonary vascular system constricts or increases resistance in response to: o Hypoxia Causes pulmonary vascular constriction which shunts blood to ventilated areas of the lung Sequence leading to right heart failure (cor pulmonale) Increased pulmonary vascular resistance (PVR) Elevated right ventricular pressure Right ventricular strain Right ventricular hypertrophy Right heart failure o Hypercapnia an acute increase PCO2 in the capillary blood increased H+ concentration increased vasoconstriction increased PVR o Acidemia a decreased pH that develops in response to either metabolic or respiratory causes pulmonary vasoconstriction due to metabolic or respiratory acidosis Pharmacologic Stimulation o Pulmonary vessels constrict in response to: Epinephrine Norepinephrine Dobutamine Dopamine Phenylephrine o Pulmonary vessels relax in response to: Oxygen Isoproterenol Aminophylline Calcium-channel blocking agents Pathologic Conditions o The following conditions can cause increases in pulmonary vascular resistance. Vessel blockage or obstruction Vessel wall disease Vessel destruction Vessel compression Passive Mechanisms Affecting Vascular Resistance Pulmonary Arterial Pressure Changes o As pulmonary arterial pressure increases, pulmonary vascular resistance decreases This occurs through: Recruitment o Opening of vessels that previously closed Distention o Stretching or widening of vessels that were open but not to full capacity This increases the cross-sectional area of the vascular system, decreasing PVR Left Atrial Pressure Changes o The pulmonary vascular resistance decreases as the left atrial pressure increases (assuming the lung volume and pulmonary arterial pressure remain constant). Lung Volume Changes o Decreased Lung Volumes (Expiration) At low lung volumes the extra-alveolar vessels narrow and vascular resistance increases the alveolar vessels dilate and vascular resistance decreases o Increased Lung Volumes (Inspiration) At high lung volumes the extra-alveolar vessels dilate and vascular resistance decreases the alveolar vessels narrow and vascular resistance increases o PVR is lowest at FRC and increases in response to increased and decreased lung volumes. Blood Volume Changes o As blood volume increases, the pulmonary vascular resistance tends to decrease. Recruitment and distention of pulmonary vessels Blood Viscosity Changes o As blood viscosity increases, the pulmonary vascular resistance increases. o Influences on the viscosity of the blood Hematocrit Integrity of the red blood cells The composition of the plasma See Table 5-4 in the text for a summary of the effects of active and passive mechanisms on vascular resistance.