Blood Vessels — Comprehensive Study Notes Flashcards

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Capillary Exchange

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The movement of materials between blood and interstitial fluid by diffusion, transcytosis, and bulk flow. It regulates delivery of nutrients and removal of wastes and balances fluid volumes between compartments. Capillary exchange varies by capillary type and tissue demands.

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Diffusion

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The most important method of capillary exchange, where substances move down their concentration gradients. Gases like $O_2$ and $CO_2$, glucose, amino acids, and many hormones cross by diffusion through lipid bilayers, fenestrations, or intercellular clefts. The blood–brain barrier restricts diffusion of many water-soluble substances due to tight junctions.

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Transcytosis

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Passage of materials across endothelium inside tiny vesicles via endocytosis and exocytosis. It transports large, lipid-insoluble molecules such as insulin or maternal antibodies across capillary walls. Transcytosis is important in placental transfer and selective endothelial transport.

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Bulk Flow

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Movement of large amounts of dissolved or suspended material in the same direction in response to pressure differences. It occurs faster than diffusion and is key for regulating relative volumes of blood and interstitial fluid. Bulk flow determines filtration vs reabsorption across capillaries.

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Filtration

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Bulk flow movement of fluid and solutes out of capillaries into interstitial fluid. Filtration is promoted by blood hydrostatic pressure and interstitial fluid osmotic pressure. It predominates at the arteriole end of capillary beds.

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Reabsorption

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Bulk flow movement of fluid from interstitial fluid back into capillaries. Reabsorption is promoted by blood colloid osmotic pressure and interstitial fluid hydrostatic pressure. It predominates at the venule end of capillary beds.

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Blood Hydrostatic Pressure

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The force exerted on vessel walls by blood due to cardiac contraction and blood volume within the vessel. Typical values are about $35\;mmHg$ at the arteriole end and $16\;mmHg$ at the venule end of a capillary. BHP favors filtration from capillaries.

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Interstitial Fluid Osmotic Pressure

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The osmotic “pull” exerted by solutes in the interstitial fluid that draws fluid out of capillaries. For calculations a typical assumed value is $1\;mmHg$. IFOP slightly promotes filtration.

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Blood Colloid Osmotic Pressure

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The osmotic “pull” inside capillaries due mainly to large plasma proteins that cannot leave the vessel. A common value used is $26\;mmHg$. BCOP favors reabsorption of fluid into capillaries.

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Interstitial Fluid Hydrostatic Pressure

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The back pressure exerted by interstitial fluid pushing fluid toward capillaries. Because escaped fluid is rapidly drained away, IFHP is close to zero and often assumed to be $0\;mmHg$. IFHP slightly promotes reabsorption when present.

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Net Filtration Pressure

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The net driving force determining fluid movement across capillaries, given by the formula: $$NFP = (BHP + IFOP) - (BCOP + IFHP).$$ At the arterial end NFP is typically about $+10\;mmHg$ (net filtration) and at the venous end about $8$–$9\;mmHg$ inward (net reabsorption).

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Starling's Law

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A principle stating that the volume of fluid and solutes reabsorbed by capillaries is almost as large as the volume filtered. About $85\%$ of filtered fluid is returned to capillaries while the remainder is collected by lymphatics. This balance helps maintain steady extracellular fluid volumes.

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Lymphatic Drainage

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The lymphatic capillaries collect escaped fluid and plasma proteins from tissues and return them to the circulation. Lymphatics typically reclaim about $3\;L$ of fluid per day. Proper lymphatic function prevents tissue edema.

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Blood Flow

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The volume of blood that flows through a tissue in a given period of time. Flow velocity is inversely related to the total cross-sectional area of the vessels, so blood flows slowest in capillaries to allow exchange. For example, flow in the aorta may be about $40\;cm/s$ versus $0.1\;cm/s$ in capillaries.

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Circulation Time

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The time it takes a drop of blood to travel from the right atrium back to the right atrium through the circulatory system. It reflects overall cardiac output and vascular resistance and varies with activity and physiological state. Shorter times indicate faster circulation.

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Venous Return Factors

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The volume of blood returning to the heart depends on the pressure difference from venules (about $16\;mmHg$) to the right atrium (about $0\;mmHg$) and assisting mechanisms like the respiratory and skeletal muscle pumps. These factors maintain venous flow against gravity. Adequate venous return sustains cardiac output.

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Respiratory Pump

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During inhalation, decreased thoracic pressure and increased abdominal pressure propel blood into thoracic veins and the right atrium. This pressure change enhances venous return. The respiratory pump is especially important during exercise and deep breathing.

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Skeletal Muscle Pump

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Skeletal muscle contractions compress deep veins and, with the help of venous valves, propel blood toward the heart. Muscle pumping is essential for venous return from the lower limbs, especially when upright. Lack of activity reduces venous return and can promote pooling.

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Blood Pressure

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The force exerted by blood on the walls of a vessel, generated mainly by ventricular contraction. Typical systemic arterial pressure is given as $120/80\;mmHg$ (systolic/diastolic). Blood pressure decreases steadily with distance from the left ventricle.

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Pressure Gradient in Circulation

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Arterial pressure falls progressively through the systemic circuit: about $35\;mmHg$ entering capillaries and about $0\;mmHg$ entering the right atrium. This gradient drives blood flow back to the heart. Loss of gradient impairs tissue perfusion and venous return.

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Factors Affecting Blood Pressure

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Blood pressure is influenced primarily by cardiac output, blood volume, and arterial elasticity. Changes in any of these factors alter arterial pressure: increased cardiac output or volume raises BP, while decreased arterial elasticity (stiffer arteries) also raises systolic pressure. Long-term control involves vascular resistance and renal regulation.

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Cardiac Output

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The product of heart rate and stroke volume, determining the volume of blood pumped per minute. Higher heart rate or stronger contractions increase cardiac output and therefore tend to raise blood pressure. Cardiac output is a major short-term regulator of arterial pressure.

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Blood Volume

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The total amount of blood in the circulatory system; changes affect venous return and arterial pressure. A loss greater than about $10\%$ of blood volume typically causes a drop in blood pressure, while water retention increases pressure. Kidneys and hormones regulate blood volume long-term.

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Vascular Resistance

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Opposition to blood flow due to friction between blood and vessel walls, often called peripheral resistance. Resistance depends on vessel radius, blood viscosity, and vessel length. Moment-to-moment BP regulation is largely achieved by changing vessel diameter, especially in arterioles.

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Vessel Radius

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The average radius of vessels has a large effect on resistance because smaller diameters dramatically increase resistance. Arterioles are the primary regulators of peripheral resistance and thus control blood pressure by constricting or dilating. Small changes in radius produce large changes in flow.

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Blood Viscosity

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The thickness of blood determined largely by the ratio of red blood cells to plasma volume. Increased viscosity, from dehydration or polycythemia, raises vascular resistance and blood pressure. Viscosity changes are slower to adjust than vessel diameter changes.

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Vessel Length

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Longer blood vessels increase resistance because blood experiences friction over a greater distance. Body fat increases total vessel length; an estimated additional $200$ miles of vessels per pound of fat raises resistance and can contribute to hypertension. Vessel length is a relatively fixed long-term factor.

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Systemic Vascular Resistance

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Also called total peripheral resistance, it represents the sum of resistances offered by all systemic blood vessels. Most of this resistance arises in arterioles, capillaries, and venules because of their small diameters. SVR is a key determinant of arterial blood pressure.

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Cardiovascular Center

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A group of neurons in the medulla oblongata that regulate heart rate, contractility, and blood vessel diameter. The CV center integrates inputs from higher brain centers, proprioceptors, baroreceptors, and chemoreceptors to adjust autonomic output. Its outputs travel via sympathetic and parasympathetic fibers to effectors.

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Baroreceptors

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Stretch-sensitive receptors that monitor blood pressure in major arteries, responding to changes in vessel wall tension. They provide rapid feedback to the CV center to maintain stable arterial pressure. Major baroreceptor sites include the carotid sinus and aortic arch.

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Carotid Sinus Reflex

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A baroreceptor reflex originating in swellings of the internal carotid artery wall that helps maintain stable cerebral perfusion. Signals travel via the glossopharyngeal nerve to the CV center to adjust heart rate and vessel tone. It is particularly important for protecting brain blood flow.

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Aortic Reflex

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A baroreceptor reflex from receptors in the wall of the ascending aorta that helps maintain systemic arterial pressure. It signals via the vagus nerve to the CV center to modulate cardiac and vascular responses. The aortic reflex coordinates general systemic blood pressure control.

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Parasympathetic Output

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Autonomic signals, primarily via the vagus nerve, that decrease heart rate and reduce cardiac output. Parasympathetic activity predominates at rest to conserve energy and lower blood pressure. Its effects on contractility and vessels are limited compared to sympathetic output.

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Sympathetic Output

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Autonomic signals that increase heart rate and contractility via cardioaccelerator nerves and stimulate vasoconstriction via vasomotor nerves. Continuous sympathetic tone produces vasomotor tone, a baseline vasoconstriction. Sympathetic activation raises blood pressure and redirects blood flow to active tissues.

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Vasomotor Tone

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A moderate, tonic state of smooth muscle contraction in blood vessel walls maintained by continuous sympathetic activity. Vasomotor tone sustains baseline vascular resistance and blood pressure. Reflex changes in sympathetic firing rapidly alter vessel diameter.

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Renin-Angiotensin-Aldosterone System

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A hormonal cascade where kidney-released renin converts liver-derived angiotensinogen ultimately into angiotensin II. Angiotensin II causes systemic vasoconstriction and stimulates adrenal release of aldosterone, which increases $Na^+$ and $H_2O$ retention by the kidneys. The net effect is increased blood volume and blood pressure.

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ACE Inhibitors

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Drugs that inhibit angiotensin-converting enzyme (ACE), reducing production of angiotensin II and lowering blood pressure. They commonly end in \-pril, such as lisinopril and benazepril. ACE inhibitors are used to treat hypertension and heart failure.

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ARBs

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Angiotensin receptor blockers (ARBs) are drugs that prevent angiotensin II from binding its receptors, reducing vasoconstriction and aldosterone effects. An example is losartan. ARBs are an alternative to ACE inhibitors for hypertension management.

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Aldosterone Antagonists

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Drugs that block aldosterone receptors, reducing $Na^+$ and water retention and thereby lowering blood volume and pressure. An example is spironolactone. These agents are used in resistant hypertension and some heart failure cases.

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Epinephrine and Norepinephrine

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Adrenal catecholamines that increase heart rate and contractility and alter vascular tone. They cause vasoconstriction in skin and abdominal organs while producing vasodilation in cardiac and skeletal muscle vessels. Their overall effect is an increase in blood pressure and redistribution of blood flow during stress.

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ADH

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Antidiuretic hormone promotes vasoconstriction and increases water retention by the kidneys, which elevates blood volume and arterial pressure. ADH release is triggered by hypotension or high plasma osmolarity. It acts alongside other systems to conserve fluid during volume loss.

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ANP

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Atrial natriuretic peptide is released by atrial cardiomyocytes in response to stretch and lowers blood pressure. ANP causes vasodilation and promotes loss of salt and water in the urine, decreasing blood volume. It opposes the actions of RAAS.

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Shock

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A pathophysiological condition in which cardiac output cannot deliver sufficient oxygen and nutrients to meet cellular needs, leading to tissue hypoperfusion. Shock may progress through stages and can be life-threatening without prompt treatment. It has multiple causes and variants.

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Stages of Shock

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Three progressive stages are recognized: nonprogressive (compensated) where negative feedback can restore homeostasis, progressive (decompensated) where tissue damage begins but recovery is possible, and irreversible where cellular injury is too severe and survival is unlikely despite therapy. Early recognition and intervention improve outcomes.

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Hypovolemic Shock

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Shock caused by decreased blood volume from hemorrhage or excessive fluid loss such as vomiting, diarrhea, sweating, or burns. Reduced preload leads to diminished cardiac output and tissue perfusion. Treatment focuses on restoring circulating volume and stopping ongoing losses.

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Cardiogenic Shock

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Shock resulting from failure of the heart to pump effectively, caused by myocardial infarction, severe valve dysfunction, or arrhythmias. Cardiac output falls dramatically and organs become hypoperfused; mortality is high with many cases being fatal. Supportive measures and correcting the underlying cardiac problem are critical.

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Vascular Shock

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Shock due to inappropriate vasodilation and increased vascular capacity such that normal blood volume cannot fill the circulatory system. Subtypes include neurogenic, anaphylactic, and septic shock, each with distinct triggers but a common problem of reduced venous return. Treatment targets the underlying cause and restores vascular tone.

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Neurogenic Shock

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A form of vascular shock caused by sudden loss of vasomotor tone leading to widespread vasodilation and venous pooling. It can occur after spinal anesthesia, spinal cord injury, or severe brain damage. The result is reduced venous return and hypotension without initial blood loss.

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Anaphylactic Shock

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A severe allergic reaction in which massive histamine release from basophils and mast cells causes profound vasodilation and increased vascular permeability. This reduces venous return and can rapidly lead to life-threatening hypotension and airway compromise. Immediate epinephrine and supportive care are essential.

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Septic Shock

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A life-threatening condition resulting from widespread bacterial infection and toxin release, causing vasodilation, increased permeability, and tissue damage. It is a common cause of in-hospital mortality and often requires intensive care for hemodynamic support and infection control. Early recognition and antibiotics improve outcomes.

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Obstructive Shock

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Shock due to mechanical blockage of blood flow in a portion of the circulatory system, such as by a pulmonary embolus or cardiac tamponade. The blockage causes backup of blood, increased upstream pressure, and leakage of plasma and proteins into tissues, reducing effective circulating volume. Treating the obstruction is the primary intervention.

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Signs of Shock

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Common signs include rapid resting heart rate (tachycardia), weak rapid pulse, hypotension, clammy cool pale skin, sweating, altered mental state, decreased urine output, thirst, metabolic acidosis, and nausea. These findings reflect inadequate tissue perfusion and compensatory responses. Early detection and correction of the underlying cause are vital.