8 blood flow and pressure

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BLOOD FLOW AND PRESSURE BLOOD FLOW The volume of blood flowing through the vessels of the body in a given period of time is known as blood flow, measured in ml/minute. Blood flow is increased with a greater pressure difference between regions, and reduced with a higher resistance within the vessel in which it is flowing. Circulation time, usually about 1 minute, is the time taken for a drop of blood to pass through the whole of the pulmonary and systemic circulation, from the right atrium, to the feet, and back up to the right atrium. Total blood flow The volume of blood flowing throughout the entire vascular system, is equivalent to cardiac output (CO), and therefore dependent upon stroke volume (SV), and heart rate (HR). Distribution of blood flow Blood flow to individual tissues varies according to their immediate needs; distribution of blood flow to these different tissues is dependent upon pressure differences between vessels and the surrounding tissue, and resistance within vessels supplying specific tissues. Under normal circumstances, blood flow through vessels runs parallel to the vessel wall and is fairly smooth, or laminar. When the flow of blood becomes high however, it can become disrupted or turbulent. Turbulent flow, usually found at the branches of large arteries, causes higher resistance to blood and ultimately leads to a smaller blood flow. Velocity of blood flow The velocity of blood flow is the speed at which a volume of blood flows through any given tissue. Velocity is slowest where there is extensive branching of blood vessels throughout a tissue, as in capillary networks, and is fastest in single large vessels, such as the aorta. Velocity is inversely proportional to cross-sectional area; as the total cross-sectional area of a whole capillary network is significantly larger than the cross sectional area of a single large blood vessel. Velocity decreases as blood flows from the aorta to the capillaries, and increases again as blood flows back to the heart. Slow movement of blood through capillaries aids the exchange of materials between blood and working tissues. BLOOD PRESSURE Blood hydrostatic pressure (BP) is generated by the pumping action of the heart as the ventricles contract, and results in pressure exerted by blood on the walls of a blood vessel. Cardiac output, blood volume , and vascular resistance are all factors effecting blood pressure. BP is highest in the aorta, the large elastic artery closest to the heart. BP is highest during ventricular contraction/systole, where a maximum systolic blood pressure of about 120 mmHg is reached, and it is lowest during ventricular relaxation/diastole, where it drops to a diastolic blood pressure of about 80 mmHg. Arterial BP decreases with distance from the heart, and BP continues to decrease with the return flow of blood through veins until it reaches the right ventricle, where BP reaches 0 mmHg. © Primal Pictures Ltd. 2010

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Capítulo sobre la presión y el flujo sanguíneo en ingles del libro Anatomy & Physyology (PANREC)

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BLOOD FLOW AND PRESSURE

BLOOD FLOW

The volume of blood flowing through the vessels of the body in a given period of time is known as blood flow,measured in ml/minute.

Blood flow is increased with a greater pressure difference between regions, and reduced with a higherresistance within the vessel in which it is flowing. Circulation time, usually about 1 minute, is the time takenfor a drop of blood to pass through the whole of the pulmonary and systemic circulation, from the right atrium,to the feet, and back up to the right atrium.

Total blood flow

The volume of blood flowing throughout the entire vascular system, is equivalent to cardiac output (CO),and therefore dependent upon stroke volume (SV), and heart rate (HR).

Distribution of blood flow

Blood flow to individual tissues varies according to their immediate needs; distribution of blood flow tothese different tissues is dependent upon pressure differences between vessels and the surrounding tissue,and resistance within vessels supplying specific tissues.

Under normal circumstances, blood flow through vessels runs parallel to the vessel wall and is fairly smooth,or laminar. When the flow of blood becomes high however, i t can become disrupted or turbulent. Turbulentflow, usually found at the branches of large arteries, causes higher resistance to blood and ultimately leadsto a smaller blood flow.

Velocity of blood flow

The velocity of blood flow is the speed at which a volume of blood flows through any given tissue. Velocityis slowest where there is extensive branching of blood vessels throughout a tissue, as in capil lary networks,and is fastest in single large vessels, such as the aorta. Velocity is inversely proportional to cross-sectionalarea; as the total cross-sectional area of a whole capil lary network is significantly larger than the crosssectional area of a single large blood vessel.

Velocity decreases as blood flows from the aorta to the capil laries, and increases again as blood flowsback to the heart. Slow movement of blood through capil laries aids the exchange of materials betweenblood and working tissues.

BLOOD PRESSURE

Blood hydrostatic pressure (BP) is generated by the pumping action of the heart as the ventricles contract,and results in pressure exerted by blood on the walls of a blood vessel. Cardiac output, blood volume, andvascular resistance are al l factors effecting blood pressure.

BP is highest in the aorta, the large elastic artery closest to the heart. BP is highest during ventricularcontraction/systole, where a maximum systol ic blood pressure of about 120 mmHg is reached, and it is lowestduring ventricular relaxation/diastole, where it drops to a diastol ic blood pressure of about 80 mmHg.

Arterial BP decreases with distance from the heart, and BP continues to decrease with the return flow of bloodthrough veins unti l i t reaches the right ventricle, where BP reaches 0 mmHg.

© Primal Pictures Ltd. 2010

Bea
Resaltado

Mean arterial pressure (MAP)

Mean arterial pressure (MAP) is the average pressure of blood flowing through all arteries in the body; this isroughly one third of the way between systol ic and diastol ic pressures and is worked out as fol lows:

MAP = diastolic BP + 1/3 (systolic BP – diastolic BP)

It may also be worked out by the fol lowing equation:

MAP = cardiac output (CO) x resistance (R)

MAP wil l therefore rise with cardiac output as long as resistance remains unchanged. As stroke volume andheart rate are both factors influencing cardiac output, increases in these wil l also cause MAP to rise, as longas resistance is kept constant. Total blood volume is another factor influencing MAP. A fal l in total bloodvolume by more than 10% wil l cause a drop in MAP.

Vascular resistance (R)

Lumendiameter

A blood vessel with a smaller lumen diameter has a greater vascular resistance, thus bloodpressure is higher. Vasoconstriction increases resistance, causing BP to rise, and vasodilationdecreases resistance, causing BP to fal l . Vascular resistance is inversely proportional to 1/d4,where d is lumen diameter.

Bloodv iscosity

Blood viscosity refers to the thickness of blood and is determined by the number of red bloodcells per volume of blood plasma. The concentration of circulating plasma proteins also effectsblood viscosity. With a higher blood viscosity there is a greater resistance, thus blood pressure ishigher. A number of factors can cause an increase in blood viscosity, and therefore increaseblood pressure, including a decrease in water intake (dehydration), and increases in red bloodcells, and plasma proteins per volume of plasma.

Bloodv essellength

Longer blood vessels have a greater resistance, as blood has a longer distance to flow. Thereforeincreased blood vessel length causes an increase in blood pressure, such as in hypertension. Agrowth in body size wil l change the length of a vessel, but once the body stops growing, this wil lnot change dramatically and wil l have very l i ttle influence on changes in blood pressure.

Systemic v ascular resistance (SVR)

Systemic vascular resistance (SVR), also referred to as Total peripheral resistance (TPR) is thecombined effect of the vascular resistance of al l systemic vessels.

REGULATION OF BLOOD PRESSURE AND FLOW

Homeostasis of blood pressure is vital for l i fe. As a result, i t is under constant autonomic and hormonalcontrol, as well as being continually mediated by local physical and chemical changes (autoregulation).

Regulation of the heart is mainly control led by the cardiovascular center in the medulla oblongata of thebrain stem; a region that receives input from sensory receptors and higher brain centers.

The cardiovascular center acts by increasing or decreasing both sympathetic (stimulatory) andparasympathetic (inhibitory) innervation of the heart, via the cardiac accelerator nerves and the vagus and,therefore, regulation of the heart rate and the contracti l i ty of the ventricles.

The vasoconstrictor and vasodilator centers (collectively named the vasomotor center) control blood vessel

diameter by causing constriction or di lation respectively. The cardiovascular center also plays an integral rolein various neural, hormonal, and local negative feedback systems, regulating blood pressure and blood flow toindividual tissues.

AUTONOMIC REGULATION OF BLOOD PRESSURE AND FLOW

The autonomic nervous system (ANS) closely regulates the cardiovascular system through a series ofautonomic reflexes. Sensory receptors throughout the body provide it with the information needed to alterfunctioning of the cardiovascular system. This is essential in ensuring blood supply is adequate according tobody tissue requirements and continually fluctuating external conditions.

Autonomic reflexes are formed in three stages:

Autonomic reflex

1 Sensory receptors are special ized sensory nerve endings located throughout the body that detectvarious changes in the state of the system, and send information via afferent nerves to the brain.

2 The cardiovascular center in the brain processes this information, integrated with information fromvarious other sensory receptors.

3 The reflex occurs as the brain al ters the activity of efferent sympathetic and parasympathetic nervescontrol l ing cardiovascular function, thereby el iciting either a negative or positive response, reversing thechange in state as necessary.

There are three main reflexes to consider:

Baroreceptor reflex

1 Baroreceptors are mechanoreceptors situated in the walls of the carotid sinus and aortic arch. Thesesensory (afferent) nerve endings detect changes in wall stretch resulting from changes in arterial bloodpressure, and form the two most important baroreceptor reflexes that regulate the cardiovascular system.

When a fal l in arterial blood pressure occurs, the arterial walls become less stretched. This decreases thefrequency of impulses traveling from the baroreceptors to the cardiovascular center in the brain, throughefferent fibers in the glossopharyngeal and vagus nerves.

2 In response, the cardiovascular center reduces parasympathetic vagal stimulation to the sinoatrial node.At the same time, sympathetic stimulation, through cardiac accelerator nerves, is increased.

3 The result is that autorhythmic cells increase spontaneous depolarization and the heart rate is raised,with an associated increase in blood pressure.

As with most homeostatic mechanisms, this forms a negative feedback loop, with the response leading toa reduction in stimulus (normal wall stretch leads to the normal frequency of impulses travell ing from thebaroreceptors to the cardiovascular center of the brain).

Proprioreceptor reflex

1 Proprioceptors monitor the position of the l imbs. They detect changes in joint angles, and muscle lengthand tension at the onset of exercise. This information is integrated and sent to the brain through efferentnerves.

2 The cardiovascular center triggers an increase in sympathetic stimulation to the heart.

3 Thus stimulating an increase in the heart rate.

Chemoreceptor reflex

1 Chemoreceptors are sensory receptors situated close to the baroreceptors of the carotid sinus and aorticarch. They are bundled into small structures called carotid and aortic bodies, and they monitor chemicalchanges in the blood. They are stimulated by changes in partial pressures of oxygen and carbon dioxide,and by hydrogen concentration in the blood. Examples of these changes include: hypoxia (low oxygenavailabil i ty), hypercapnia (excess carbon dioxide), and acidosis (elevated hydrogen concentration).When the body experiences a change in the chemical composition of the blood, there is an increase inthe frequency of impulses traveling from the chemoreceptors, via efferent nerves, to the cardiovascularcenter in the brain.

2 In response to this potential ly harmful change, the cardiovascular center increases sympatheticstimulation to the arterioles, veins and heart.

3 As a result, the constriction of arterioles (mainly in skeletal muscle) and a rise in both the heart rate andarterial blood pressure reverses the change in blood composition. The cardiovascular centersimultaneously alters the rate of breathing, further regulating blood composition.

HORMONAL REGULATION OF BLOOD PRESSURE AND FLOW

Various negative feedback systems exist, control l ing the short and long-term homeostasis of blood pressurevia hormones. Heart rate, stroke volume, systemic vascular resistance, and blood volume are all factorsinfluencing mean arterial blood pressure that must be altered in order to keep blood pressure within i tshomeostatic l imits. Blood distribution may also be altered if specific tissues have a higher cellular metabolicdemand at a certain time compared to others.

A number of different hormones are involved in the regulation of blood pressure, acting directly on the heart,vascular smooth muscle cells or kidney tubule cells.

Renin-angiotensin-aldosterone (RAA) system

In response to a fal l in blood volume or decreased blood flow, juxtaglomerular cells of the kidneys secretethe enzyme renin in to the bloodstream. This enzyme is involved in the production of angiotensin II fromangiotensiogen. The active hormone angiotensin II causes vasoconstriction, increasing systemic vascularresistance and BP.

Aldosterone

The active hormone angiotensin II also stimulates the secretion of aldosterone and antidiuretic hormone(ADH), which increase water reabsorption by the kidneys, increasing total blood volume and increasing BP.As with most homeostatic mechanisms, this forms a negative feedback loop, with the response leading to areduction in stimulus.

Epinephrine and norepinephrine

During stress, in response to sympathetic stimulation, the adrenal medulla releases epinephrine andnorepinephrine into the bloodstream. Both hormones increase heart rate and contracti l i ty, thus increasingblood pressure. As with most homeostatic mechanisms, this forms a negative feedback loop, with theresponse leading to a reduction in stimulus. In addition, they cause generalized vasoconstriction, except inskeletal muscle where they cause vasodilation, increasing blood flow to muscles during exercise.

Antidiuretic hormone (ADH)

In response to dehydration or low blood volume, the cardiovascular center increases sympatheticstimulation to the hypothalamus, causing it to synthesize antidiuretic hormone, also known as vassopressin,which is then released from the posterior pituitary into the blood stream. ADH causes water retention bycollecting ducts in the kidneys, which in turn increases BP. As with most homeostatic mechanisms, this formsa negative feedback loop, with the response leading to a reduction in stimulus.

Atrial natriuretic peptide (ANP)

When released from atrial cells, atrial natriuretic peptide (ANP) causes vasodilation, which decreases BP. Aswith most homeostatic mechanisms, this forms a negative feedback loop, with the response leading to areduction in stimulus. It also reduces total blood volume by promoting the loss of salt and water in the urine.

Erythropoietin

In response to low levels of oxygen in the blood, as seen at alti tude, the kidneys release erythropoietin. Thisglycoprotein hormone stimulates the bone marrow to produce more red blood cells, which increases theoxygen-carrying capacity of the blood.

SHOCK AND HOMEOSTASIS

When the cardiovascular system fai ls to supply enough oxygen and nutrients to tissues in order to meetcellular metabolic needs, the body goes into a state of shock. Without adequate supplies of oxygen, cells areforced to produce energy (ATP) anaerobically, causing the accumulation of lactic acid, which is potential lydamaging to cells and organs.

The fol lowing signs and symptoms are characteristic of shock:

Decrease in blood pressure

Drop in systolic blood pressure to below 90 mmHg may cause faintness.

Increased heart rate

Increased heart rate (HR) compensating for the decrease in cardiac output (CO), leads to a rapid but weakpulse.

Sympathetic stimulation increases levels of epinephrine and norepinephrine in the blood, which leads to arise in resting heart rate.

Sw eating and sickness

Sympathetic stimulation induces vasoconstriction and sweating, causing the skin to become cool, pale, andclammy; vasoconstriction of vessels supplying to the digestive organs may lead to a feeling of sickness.

Reduced urination, thirst, and dehydration

Increased levels of aldosterone and antidiuretic hormone in the blood causes reduced urination. Loss ofextracellular fluid leads to thirst and dehydration.

Acidosis

Lactic acid build-up causes acidosis (low blood pH).

Mental confusion

Lack of oxygen supply to the brain may cause mental confusion.

There are four types of shock:

Hypov olemic shock

Hypovolemic shock is the most common form of shock, resulting from sudden blood loss. Lost body fluidsmust be replaced to overcome hypovolemic shock.

Commoncauses:

Acute hemorrage, loss of body fluids through excessive sweating, diarrhea, or vomiting, andextensive burns. It is also common in patients with diabetes mell i tus, when an excessive volumeof fluid is lost in the urine.

Cardiogenic shock

Cardiogenic shock is less common, resulting from damage to the heart, causing it to fai l to pump efficiently.

Commoncauses:

Myocardial infarction (heart attack), poor blood supply to the heart (ischemia), abnormalelectrical activity of the heart (arrhythmia), damaged heart valves, impaired contracti l i ty andexcessive preload or afterload.

Vascular shock

Vascular shock results from poor circulation due to extreme vasodilation. The rapid drop in vascularresistance due to vasodilation causes a drop in mean arterial blood pressure and hence slows down the flowof blood to body tissues.

Commoncauses:

Severe al lergic reactions, where histamines released cause vasodilation (also referred to asanaphalactic shock); damage to the cardiovascular center through head trauma (also referred toas neurogenic shock); septicemia, where bacterial toxins cause vasodilation (also referred to asseptic shock) and heat stroke, where prolonged exposure to extreme heat causes vasodilation(also referred to as transient vascular shock).

Obstructiv e shock

Obstructive shock results from a blockage stopping the flow of blood through a portion of the circulatorysystem.

Commoncauses:

A common cause of obstructive shock is pulmonary embolism, a blood clot obstructing a vesselin the lungs.

HOMEOSTATIC RESPONSE TO SHOCK

Shock is overcome by a homeostatic response in the form of negative feedback systems that work to returnmean arterial blood pressure and cardiac output to within normal l imits. If shock prevails and this homeostaticresponse fai ls to maintain sufficient blood flow to tissues, cells start to die and l i fe may be threatened.

There are four main negative feedback systems involved in the homeostatic response to shock:

Renin-angiotensin-aldosterone system

Baroreceptors in the kidneys detect a reduction in blood flow and in response, stimulate juxtaglomerularcells of the kidneys to secrete renin into the blood.

Once in the blood, renin and angiotensin converting enzyme (ACE) produce angiotensin II from theirsubstrates. Angiotensin II induces vasoconstriction, which increases systemic vascular resistance, helping toraise blood pressure. Angiotensin II also stimulates secretion of the hormone aldosterone from the adrenalcortex.

Aldosterone acts on the kidney tubules to increase sodium and water reabsorption, which in turn increasesblood volume, again, helping to raise blood pressure.

Antidiuretic hormone (ADH)

Baroreceptors in the arch of the aorta and the carotid sinus detect a decrease in blood pressure and signalto the pituitary gland to release more ADH into the blood. ADH induces vasoconstriction, which increasessystemic vascular resistance helping to raise blood pressure. ADH also acts on the kidney tubules to increasewater reabsorption, conserving blood volume.

Sympathetic stimulation

Baroreceptors in the arch of the aorta and the carotid sinus detect a decrease in blood pressure and signalto the cardiovascular center in the brain to el icit sympathetic responses throughout the body. They functionto:

1 Induce vasoconstriction of vessels in the skin and abdominal viscera, which increases systemic vascularresistance and venous return, helping to raise blood pressure.

2 Increase heart rate and contracti l i ty, helping to return cardiac output to normal.

3 Trigger the adrenal medulla to secrete more epinephrine and norepinephrine into the blood, hormonesthat induce vasoconstriction, raise heart rate and increase contracti l i ty, helping to raise blood pressureand return cardiac output to normal.

Local v asodilation

Chemicals that act locally to induce vasodilation, including potassium ions (K+), hydrogen ions (H+),lactic acid, nitric oxide, and adenosine, are released from cells during shock.

Local vasodilation increases blood flow to these cells, helping to restore oxygen levels to normal. Excessivelocal vasodilation may have adverse effects, where systemic vascular resistance decreases, causing bloodpressure to drop.