Total Blood Volume
5.5 L. Each ventricle pumps the equivalent of the total blood volume the equivalent of the total blood volume each minute under resting conditions.
Regulation of Cardiac Rate
Norepinephrine from sympathetic axons and epinephrine from the adrenal medulla also open the HCN channels of the pacemaker cells, inducing a faster rate of diastolic depolarization. Stimulate cAMP to keep the channels open.
ACh from the vagus nerve binds to receptors and opens separate K+ channels. Outward diffusion of K+ counters inward flow of Na+ of HCN channels producing a slower rate of depolarization.
Mechanisms that affect the cardiac rate.
Increase cardiac rate: positive chronotropic effect.
Decrease cardiac rate: negative chronotropic effect
Cardiac Control Center
Center in the medulla oblongata that coordinates the activity of the autonomic innervation of the heart. Affected by higher brain areas and by sensory feedback from baroreceptors in the aorta and carotid arteries. Fall in blood pressure can produce a reflex increase in the heart rate.
Regulation of Stroke Volume (3)
1) End-diastolic volume: the volume of blood in the ventricle at the end of diastole
2) Total Peripheral Resistance: frictional resistance, or impedance to blood flow, in the arteries.
3) Contractility: strength of ventricle contraction
Another term for End-Diastolic Volume. Amount of blood in the ventricles prior to contraction. Workload imposed on the ventricles prior to contraction. An increase in EDV results in an increase in stroke volume.
An impedance to the ejection of blood from the ventricle imposed on the ventricle after contraction has begun. (Caused by total peripheral resistance) The greater the peripheral resistance, the lower the stroke volume.
Contraction strength ejects 70-80 ml of blood out of the total end-diastolic volume of 110-130 ml. 60%
More blood is pumped as the EDV increases so that the fraction remains constant- in order for this to happen, the ventricular contraction strength must increase as the EDV increases.
Frank-Starling Law of the Heart
Relationship between EDV, contraction strength, and stoke volume results from a built in, or intrinsic property of the heart muscle. The strength of ventricular contraction caries directly with the end-diastolic volume.
Intrinsic Control of Contraction Strength (and thus, stroke volume)
Due to the variations in the degree to which the myocardium is stretched by the end-diastolic volume. As the EDV rises within the physiological range, the myocardium is increasingly stretched and contracts more forcefully.
Stretch Increases Strength
Prior to filling w/ blood during diastole, the sarcomere lengths are only about 1.5 μm & actin filaments from each side overlap in the middle of the sarcomeres causing them to contract weakly. Ventricles fill w/ blood & myocardium stretches so that there is only overlap at the edges which increases interactions between actin and myosin. Stretch increases sensitivity to stimulatory effects of Ca²⁺.
How the heart can adjust to rise in total peripheral resistance (Frank-Starling)
1) rise in peripheral resistance causes a decrease in the stroke volume of the vent so that 2) more blood remains in the vent and the end-diastolic volume is greater for the next cycle.
3) vent is stretched to a greater degree in the nect cycle and contracts more strongly to eject more blood.
Extrinsic Control of Contractility
Dependent of the sympathoadrenal system. Norepinephrine and epinephrine produce an increase in contraction strength.
Positive Inotropic Effect
Results from an increase in the amount of Ca²⁺ available to the sarcomeres.
Return of blood to heart via the veins. The rate at which the atria and vents are filled with venous blood depends on the total blood volume and the venous pressure.
Veins have thinner, less muscular walls than the arteries so that a given amount of pressure will cause more expansion in the veins allowing the veins to hold more blood (2/3rds of the blood). Capacitance Vessels
Although the veins contain 70% of the total blood volume, the mean pressure is only 2 mmHg compared to the arterial pressure which is 90-100 mmHg. Results of pressure drop between caps and arteries and veins compliance. Highest is the venules, lowest at venae cavae/ right atrium.
Factors that aid venous return
1. sympathetic nerve activity that stimulates smooth muscle contraction in the venous walls and reduces compliance
2. skeletal muscle pump, which squeezes veins during muscle contraction
3. pressure difference between the thoracic and abdom. cavities which promotes the blood of venous blood back to the heart.
One-third of total body water. 80% of extracellular fluid is contained in tissues as interstitial fluid. 20% as blood plasma.
Distribution of water between the interstitial fluid and blood plasma is determined by a balance between opposing forces acting of the capillaries.
Net Filtration Pressure
Equal to the hydrostatic pressure of the blood in the capillaries minus the hydrostatic pressure of tissue fluid outside the capillaries, which opposes filtration. Hydrostatic pressure against the inner capillary wall is 37 mmHg at arteriolar end and 17 mmHg at the ventricular end.
Colloid Osmotic Pressure
Osmotic pressure exerted by the plasma proteins (proteins are present as a colloidal suspension). Pressure is greater in the plasma than in the interstitial fluid because of the restricted filtration of proteins through the capillary pores.
The difference between the pressure exerted by the proteins in the plasma than the pressure in the capillaries. 25mmHg) Favors the movement of water into the capillaries because water diffuses from a solution of lower pressure to the solution of higher pressure.
Excessive accumulation of interstitial fluid. Normally prevented by balance between capillary filtration and osmitic uptake of water and by lymphatic drainage.
6 Causes of Edema
1) High arterial pressure- increases cap. pressure & causes excessive filtration
2) Venous obstruction- congestive increase in cap pressure
3) Leakage of plasma proteins into interstitial fluid- reduces osmotic flow of water into caps
4) Myxedema- excessive production of glycoproteins in extracellular matrix from hyperthyroidism
5) Decreased plasma protein concentration- liver disease b/c liver makes most plasma protein or kidney disease where plasma proteins are excreted in the urine
6) Obstruction of lymphatic drainage
Regulation of Blood Volume by the Kidneys
Gloleruli produce filtrate that enters system of tubules that modifies and transports filtrate. The precentage of glomeruli filtrate that is reabsorbed (and thus the urine and blood volume) is adjusted according to the action of hormones on the kidneys.
Vasopressin. Produced by neurons of hypothalamus and transported to the posterior pituitary for storage. Release occurs when osmoreceptors in hypothalamus detect increase in plasma osmolality which is the result of plasma becoming more concentrated. Stimulation of osmoreceptors causes thirst and release of ADH. ADH acts on kidneys to retain water.
Blood Volume and ADH
A rise in blood volume can reduce ADH secretion. An increase in blood volume mechanically stimulates stretch receptors in the left atrium, aortic arch, and carotid sinus which can cause an increase in firing of the sensory neurons. ADH is inhibited so that more water is eliminated from the blood by the kidneys.
Steroid hormone secreted by the adrenal cortex that stimulates the reabsorption of salt by the kidneys. "Salt-retaining hormone" Stimulated during salt deprivation, when blood volume and pressure are reduced.
Regulation of Aldosterone
Aldosterone produces an increase in blood volume, but it does not produce a change in blood osmolality. Aldosterone promotes the reabsorption of salt and water in proportionate amounts, whereas ADH promotes only the reabsorption of water.
Enzyme secreted by a group of cells in the kidneys called juztoglomerular apparatus when blood flow and pressure are reduced in the renal artery. Cleaves 10 a.a. called angiotensin I from plasma protein angiotensinogen.
passes through the capillaries of the lungs and two amino acids are removed by angiotensin converting enzyme (ACE) leaving Angiotensin II
Production of this protein is increased during salt deprivation, low blood volume, and low blood pressure. Powerful vasoconstrictor by increasing the total peripheral resistance and arterial blood pressure. Stimulates contraction of smooth muscle layers of the small arteries and arterioles. Stimulates the thirst center in the hypothalamus and the adrenal cortex to secrete aldosterone.
Relationship betweeen kidneys, angiotensin II, and aldosterone. As a result of thirst, the hypothalamus is stimulatedd and more water is traken into the intestine and then the blood. Adrenal cortex is stimulated by angiotensin II to secrete more aldosterone which causes the kidneys to retain more salt and water.
Atrial natriuretic peptide
Hormone that is antagonistic is aldosterone and promotes Na+ and water excretion in the urine in response to a rise in blood volume. Produced by the atria of the heart.
Directly proportional to the length of the vessel and to the viscosity of the blood. Arterioles are the smallest arteries and can become narrower by vasoconstriction to provide the greatest resistance to blood flow.
Regulation of Blood Flow by Sympathetic Nerves
Sympathoadrenal system produces an increase in the cardiac output and in total peripheral resistance by the stimulation of smooth muscle by norepinephrine and epinephrine. This causes vasoconstriction of the arterioles and in skin.
Adrenergic Sympathetic Fibers
Release norepinephrine to activate that alpha-adrenic receptors to cause a basal level of vasocontriction throughout the entire body. Digestive system, kidneys, and skin.
Cholinergic Sympathetic Fibers
Release Ach as a neurotransmitter in the arterioles of the skeletal muscles. Causes vasodilation and increased blood flow to the skeletal muscles during fight or flight
Parasympathetic Control of Blood Flow
In arterioles: always cholinergic and promote vasodilation
Blood vessels: limited to the digestive tract, external genitalia, and salivary glands.
Paracrine Regulation of Blood Flow
Molecules produced by one tissue that help to regulate another issue of the same organ. Endothelium of the tunica interna produces a number of paracrine regulators that cause the smooth muscle of the tunica media to relax or contract.
Bradykinin, nitric oxidem and prostaglandin I₂
Produced by the blood vessel endothelium that cause smooth muscle relaxation.
Function of NO
Endothelial arterioles contain endothelial nitric oxide synthase which produces NO from L-arginine. The NO diffuses into smooth muscle cells of the tunica media of arterioles and activates the enzyme guanylate cyclase to convert GTP to cyclic GMP. Lowers Ca²⁺ and leads to relaxation and dilation.
Paracrine regulator stimulates vasoconstriction of arterioles and thus raises the total peripheral resistance.
The ability of some organs to utilize intrinsic mechanisms to maintain a relatively constant blood flow despite wide fluctuations in blood pressure. (Brain and kidneys)
Intrinsic regulation of blood flow
Built in mechanism within individual organs provide a localized regulation of vascular resistance and blood flow. Myogenic or metabolic
Myogenic Control Mechanisms
Changes in systemic arterial pressure are compensated for in the brain and some other organs by response of smooth muscle. Direst responses by vascular smooth muscle. Decrease in arterial pressure causes the cerebral vessels to dilate so that enough blood can be maintained despite decreased pressure. High blood pressure causes cerebral vessels to constrict so that finer vessels are protected from high pressure.
Metabolic Control Mechanisms
Local vasodilation within an organ can occur as a result of the chemical environment. Includes: (1) decreased oxygen concentrations that result from increased metabolic rate, (2) increased carbon dioxide concentrations; (3) decreased tissue pH, and (4) release of K⁺ and paracrine regulators from tissue cells. Organ signals blood vessels that it needs more oxygen.
Constriction allow metabolic products to accumulate, preventing venous drainage of the area. When the constriction is removed and blood flow resumes, the metabolic products that have accumulated and cause vasodilation making the tissue appear red.
Increase in blood flow occurs in skeletal muscles and other organs as a result of increased metabolism. This can wash out the vasodilator metabolites so that blood flow can fall to pre-exercise levels a few minutes after exercise ends.
Regulation of Coronary Blood Flow
Coronary arterioles contain alpha- and beta- adrenergic receptors which promote vasoconstriction and vasodilation. As the metabolism increases (like during exercise), there are increased concentrations of carbon dioxide, K, and released paracrine regulators (NO, adenosine, and prostaglandins) to cause vasodilation.
Regulation of Blood Flow through Skeletal Muscles
Skeletal arterioles have a high vascular resistance at rest because of alpha-adrenergic sympathetic stimulation. Cholinergic fibers (with stimulation of beta-adrenergic receptors by epinephrine) stimulate vasodilation as part of flight or fight response.
Circulation Changes to the Heart and Skeletal Muscles During Exercise
Blood flow to skeletal muscles increases because of 3 simultaneous changes: (1) increased total blood flow (cardiac output), (2)metabolic vasodilation in exercising muscles; and (3) diversion of blood away from the viscera and skin.
Coronary blood flow also increases during exercise.
Blood Flow to the Brain and Skin
Cerbral: regulated by intrinsic mechanisms, relatively constant, and is least tolerant of low rates of blood flow.
Skin: Extrinsic mechanisms, more variation than in any other organ, most tolerant to low rates of blood flow
Held constant at 750 ml per minute- 15% of total cardiac output at rest- because if the brain doesn't have oxygen for even a few seconds, it will lose consciousness. Not influenced by sympathetic nerves unless arterial pressure rises to 200 mmHg which will stimulate vasoconstriction to prevent stroke. Autoregulation by myogenic and metabolic control.
Myogenic Regulation of Cerebral Circulation
When variation in systemic arterial pressure.
BP falls: cerebral arteries dilate
BP rises: constrict
CO₂ rises as a result of poor ventilation: dilate
CO₂ falls: contriction
Metobolic Regulation of Cerebral Circulation
Brain regions that are most active (metabolically) receive increased blood flow. Active neurons release many substances that stimulate vasodilation including K, adenosine, and NO. Close association of astrocytes with both veurons and cerebral vessels may also play a role.
Cutaneous Blood Flow
Blood flow through the skin is adjusted to maintain deep-body temperature at about 37 c. Adjusts are made by the degree of constriction or dilation of ordinary arterioles and arteriovenous anastomoses.
Vessels found in the fingertips, palms of the hands, toes, soles of the feet, ears, nose, lips, that shunt blood directly from arterioles to deep venules- bypassing superficial capillary loops.
Innervated by sympathetic nerve fibers.
Polypeptide that stimulates vasodilation secreted by the sweat glands that is stimulated when the body is hot. Increases blood flow to keep the body cool.
The three most important variable affecting blood pressure...
1. Cardiac Rate
2. Stroke Volume
3. Peripheral Resistance
An increase in one of these variable results in an increase in BP
Millimeters of Mercury
Unit it measure BP. Blood pushes on one surface of U shaped column of mercury while the atmosphere pushes on the other.
Stretch receptors located in the aortic arch and in the carotid sinuses. Tonically (constantly) active and produce baseline frequency of action potentials in their sensory neurons. When BP is increased, the walls of the aortic and carotid sinuses stretch and produce in an increased rate of action potentials along their sensory nerve fibers via the vagus and glossopharyngeal to the medulla oblongata.
Vasomotor Control Center
Center in the medulla oblongata that regulates the degree of vasoconstriction/vasodilation and helps to regulate total peripheral resistance.
(1) aortic arch and carotid sinus baroreceptors as the sensors, (2) vasomotor and cardiac control centers as integrating centers, and (3) parasympathetic and sympathetic axons to the heart and blood vessels as effectors.
Fall in BP: increase in sympathetic nerve activity
Rise in BP: decline in sympathetic and rise in parasympathetic
Atrial Stretch Receptors
Receptors activated by increased venous return to the heat and in response, stimulate: (1) reflex tachycardia, (2) inhibit ADH release, resulting in excretion of larger volumes of urine and a lowering of blood volume, (3) promote increased secretion of atrial natriuretic peptide which lowers blood volume by increasing urinary salt and water excretion.
all parts of a fluid move in the same direction, parallel to the axis of the vessel. "Layered" blood- blood in the center of the artery moves faster than blood closer to the arterial wall.
Some parts of the fluid move in different directions, churning and mixing the blood. Causes vibrations of the vessel which may produce sounds.
Sounds of Korotkoff
Sounds heard when the artery begins to open with every systole creating a turbulent flow because of the constriction.
First Korotkoff Sound
When the kuff pressure is equal to the systolic pressure this sound is heard as blood passes in a turbulent flow through the constricted opening of the artery.
Last Korotkoff Sound
Heard when the cuff pressure is equal to the diastolic pressure. The sounds will diminish because the artery remains open and resumes Laminar flow.
Difference between the systolic pressure and diastolic pressure. Reflection of stroke volume
Mean Arterial Pressure
Average arterial pressure during the cardiac cycle. Difference between this pressure and the pressure of the venous system drives blood through the capillary beds of organs.
Diastolic pressure + 1/3 pulse pressure
Primary, Essential Hypertension
Cardiovascular risk increases when a person's systolic bp rises above 115 or diastolic exceeds 75. High salt diet increases plasma osmolality which stimulates ADH secretion which increases water reabsorption by the kidneys- increasing blood volume, blood pressure, and stroke volume. The ability of the kidneys to secrete excess salt decreases with age.
Treatment of Hypertension
Modification of lifestyle. Diuretics increase urine volume and decrease blood volume and pressure. Drugs that block ß₁-adrenergic receptors lowre blood pressure by decreasing cardiac rate. ACE inhibitors.
Circulatory shock due to low blood volume that could be caused by hemorrhage, dehydration, and burn
Dangerously low BP that may result from sepsis, or infection. Endotoxin activates enzyme NO synthase with macrophages.
Rapid fall in BP as a result of allergic reaction, results from widespread histamine release.
Sympathetic tone is decreased, because of upper spinal cord damage or spinal anesthesia.