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68 Cards in this Set
- Front
- Back
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What is the site of the highest resistance in the cardiovascular system?
What regulates this resistance? |
Arterioles, regulated by the autonomic nervous system.
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What type of receptors are found on the arterioles of the skin, splanchnic, and renal circulations?
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α1-Adrenergic recptors
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Where are the β receptors found in the circulation system? What type of β receptors are they?
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β2-Adrenergic receptors are found on arterioles of skeletal muscle.
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What part of the circulatory system has the largest total cross-sectional and surface area?
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Capillaries
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What part of the circulatory system contains the highest proportion of the blood?
What type of receptors are found here? |
Veins
α1-adrenergic receptors |
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Is velocity of blood flow proportional to Q (blood flow)? A (Cross-sectional area)?
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Velocity is directly proportional to blood flow, inversely proportional to the cross-sectional area at any level of the cardiovascular system.
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Is Cardiac Output (blood flow/Q) proportional to pressure gradient (ΔP)? Resistance?
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Blood flow is directly proportional to ΔP (blood flows from high pressure to low pressure), inversely proportional to the resistance of the blood vessels.
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What is the relationship between Resistance (R) and viscosity of blood, length of blood vessel, and the radius of blood vessels (to the fourth power)?
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Resistance is directly proportional to the viscosity of the blood and length of the vessel, and inversely proportional to the fourth power of the vessel radius.
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How would increasing the hematocrit change the viscosity of the blood, and the resistance?
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Increasing hematocrit will increase viscosity, and will thus increase the resistance and decrease the blood flow.
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What is Reynolds number?
What increases Reynolds number? |
Reynolds number predicts whether blood flow will be laminar or turbulent.
When Reynolds number is increased, there is a greater tendency for turbulence, which causes audible vibrations called bruits. Reynolds number (and therefore turbulence) is increased by: Decreased blood viscosity (e.g. decreased hematocrit, anemia) Increased blood velocity (e.g. narrowing of a vessel) |
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What is the site of the highest resistance in the cardiovascular system?
What regulates this resistance? |
Arterioles, regulated by the autonomic nervous system.
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What type of receptors are found on the arterioles of the skin, splanchnic, and renal circulations?
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α1-Adrenergic recptors
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Where are the β receptors found in the circulation system? What type of β receptors are they?
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β2-Adrenergic receptors are found on arterioles of skeletal muscle.
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What part of the circulatory system has the largest total cross-sectional and surface area?
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Capillaries
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What part of the circulatory system contains the highest proportion of the blood?
What type of receptors are found here? |
Veins
α1-adrenergic receptors |
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Is velocity of blood flow proportional to Q (blood flow)? A (Cross-sectional area)?
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Velocity is directly proportional to blood flow, inversely proportional to the cross-sectional area at any level of the cardiovascular system.
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Is Cardiac Output (blood flow/Q) proportional to pressure gradient (ΔP)? Resistance?
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Blood flow is directly proportional to ΔP (blood flows from high pressure to low pressure), inversely proportional to the resistance of the blood vessels.
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What is the relationship between Resistance (R) and viscosity of blood, length of blood vessel, and the radius of blood vessels (to the fourth power)?
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Resistance is directly proportional to the viscosity of the blood and length of the vessel, and inversely proportional to the fourth power of the vessel radius.
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How would increasing the hematocrit change the viscosity of the blood, and the resistance?
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Increasing hematocrit will increase viscosity, and will thus increase the resistance and decrease the blood flow.
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What is Reynolds number?
What increases Reynolds number? |
Reynolds number predicts whether blood flow will be laminar or turbulent.
When Reynolds number is increased, there is a greater tendency for turbulence, which causes audible vibrations called bruits. Reynolds number (and therefore turbulence) is increased by: Decreased blood viscosity (e.g. decreased hematocrit, anemia) Increased blood velocity (e.g. narrowing of a vessel) |
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What is a chronotropic effect? What is a dromotropic effect?
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Chronotropic effects produce changes in heart rate. Dromotropic effects produce changes in conduction velocity, primarily the AV node.
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How does the parasympathetic system decrease heart rate?
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Parasympathetic innervation causes a negative chronotropic effect (decreases heart rate) by decreasing If, and therefore decreasing the rate of phase 4 depolarization.
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What is the mechanism of the parasympathetic system’s negative dromotropic effect?
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Decreased inward Ca2+ current and increased outward K+ current causes a decreased conduction velocity through the AV node.
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Are mitochondria more numerous in cardiac muscle or in skeletal muscle?
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Cardiac muscle.
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What structure of the myocardial cells are more developed in the ventricles than in the atria? What do they form?
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T tubules, which invaginate the cells at the Z lines and carry action potentials into the cell interior.
T tubules form dyads with the sarcoplasmic reticulum. |
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During excitation-contraction coupling, what does Ca2+ bind to, and what happens after?
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Ca2+ binds to troponin C, and tropomyosin is moved out of the way, removing the inhibition of actin and myosin binding.
Actin and myosin bind, the thick and thin filaments slide past each other, and the myocardial cell contracts. |
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What determines the magnitude of the tension during excitation-contraction coupling?
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The intracellular [Ca2+]
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What is ejection fraction? What is its normal value?
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Ejection fraction = stroke volume/end-diastolic volume
Normally 0.55 (55%) |
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What is inotropism?
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The contractility, or the intrinsic ability of cardiac muscle to develop force at a given muscle length.
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What are some factors that increase contractility?
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1) Increased heart rate: more Ca2+ enters the myocardial cells -> more Ca2+ released from the SR -> greater tension produced
2) Sympathetic stimulation (catecholamines) via β1 receptors: increases inward Ca2+ current during plateau of each action potential; increases the activity of the Ca2+ pump of the SR (by phosphorylation of phospholamban) -> more Ca is accumulated and available for release 3) Cardiac glycosides (digitalis) |
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How do cardiac glycosides (digitalis) work?
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Cardiac glycosides increase the force of contraction by inhibiting Na+, K+-ATPase in the myocardial cell membrane. As a result, the intracellular [Na] increases, diminishing the Na gradient across the cell membrane. Na-Ca exchange (which extrudes Ca from the cell) depends on the size of the Na gradient and thus is diminished, producing an increase in intracellular [Ca].
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What are factors that decrease contractility?
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Parasympathetic stimulation (ACh) via muscarinic receptors decreases the force of contraction in the atria by decreasing the inward Ca-current during the plateau of the cardiac action potential.
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What is preload? What is afterload?
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Preload: End-diastolic volume, which is related to right atrial pressure.
Afterload: Aortic pressure (for the left ventricle) |
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What is the equation for Cardiac Output?
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Cardiac output = stroke volume x heart rate
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What is stroke work? What is the equation?
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Stroke work is the work the heart performs on each beat.
Stroke work = Aortic pressure x stroke volume |
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What increases cardiac oxygen consumption?
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1. Increased afterload
2. Increased size of the heart 3. Increased contractility 4. Increased heart rate |
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How do you measure the pulmonary vein [O2] and pulmonary artery [O2]?
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Pulmonary vein [O2] is measured in a peripheral artery.
Pulmonary artery [O2] is measured in systemic mixed venous blood. |
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What is the a wave on the venous pulse curve?
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The increase in atrial pressure (venous pressure) casued by atrial systole.
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What causes the fourth heart sound?
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Filling of the ventricle by atrial systole.
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What causes the first heart sound?
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Closing of the AV valves (mitral and then tricuspid).
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In which phases of the cardiac cycle does atrial filling occur?
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Atrial filling begins during the rapid ventricular ejection and continues during the reduced ventricular ejection.
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What is the “blip” in the aortic pressure tracing that occurs after closure of the aortic valve?
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Dicrotic notch, or incisura
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What causes the third heart sound?
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Rapid flow of blood from the atria into the ventricles causes the third heart sound.
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What are the two most important mechanisms for regulating arterial pressure?
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Baroreceptor: Fast, neurally mediated
Renin-Angiotensin-Aldosterone: slower, hormonally regulated |
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Where are the baroreceptors located?
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Baroreceptors are stretch receptors located within the walls of the carotid sinus near the bifurcation of the common carotid arteries.
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What is Hering’s nerve? What cranial nerve is it a branch of?
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Hering’s nerve carries information from the baroreceptors of the carotid sinus to the vasomotor center in the brain stem. It is a branch of the glossopharyngeal nerve (CN IX).
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What are the four effects that attempt to increase the arterial pressure to normal (i.e. after acute hemorrhage?)
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1) Increased heart rate: resulting from decreased parasympathetic and increased sympathetic tone to the SA node of the heart
2) Increased contractility and stroke volume 3) Increased vasocontriction of arterioles 4) Increased vasocontriction of veins Note: All effects result from increased sympathetic tone |
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How can you test the baroreceptor mechanism?
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Valsalva maneuver. Expiring against a closed glottis causes an increase in intrathoracic pressure, which decreases venous return -> decreased cardiac output and arterial pressure (Pa).
If the baroreceptor is intact, the decrease in Pa is sensed and leads to an increase in sympathetic outflow to the heart and blood vessels. In the test, an increase in heart rate would be noted. |
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What causes the secretion of renin? What secretes renin?
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A decrease in renal perfusion pressure causes the juxtaglomerular cells of the afferent arteriole to secrete renin.
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What happens during cerebral ischemia?
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Partial pressure of CO2 (PCO2) in brain tissue increases -> Chemoreceptors in the vasomotor center respond by increasing sympathetic outflow to the heart and blood vessels -> constriction of arterioles causes intense peripheral vasoconstriction and increased TPR.
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Besides baroreceptors and chemoreceptors, what else regulates arterial blood pressure? What are they in response to? What is their mechanism?
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Vasopressin: released from posterior pituitary in response to hemorrhage; is a potent vasoconstrictor that increases TPR by activating V1 receptors on arterioles; increases water reabsorption by the renal distal tubule and collecting ducts by activating V2 receptors.
Atrial natriuretic peptide (ANP): released from atria in response to increase in blood volume and atrial pressure; causes relaxation of vascular smooth muscle, dilation of arterioles, and decreased TPR; causes increased excretion of Na and water by the kidney; inhibits renin secretion. |
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What is blood flow through the capillaries regulated by?
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Contraction and relaxation of the arterioles and the precapillary sphincters (smooth muscle bands at the arteriole-capillary junctions).
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When does edema occur?
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Edema occurs when the volume of interstitial fluid exceeds the capacity of the lymphatics to return it to the circulation. This can be caused by excess filtration or blocked lymphatics.
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What effect does Histamine have on the blood flow?
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Histamine causes arteriolar dilation and venous constriction. The combined effects cause increased Pc and increased filtration out of the capillaries, resulting in local edema. Histamine is released in response to tissue trauma.
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What effect does Bradykinin have on the blood flow?
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Bradykinin causes arteriolar dilation and venous constriction, and produces increased filtration out of the capillaries (similar to histamine). It also causes local edema.
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What effect does Serotonin (5-hydroxytryptamine) have on the blood flow?
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Serotonin causes arteriolar constriction and is released in response to blood vessel damage to help prevent blood loss. Serotonin has also been implicated in the vascular spasms of migraine headaches.
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What effect do Prostaglandins have on the blood flow?
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Prostacyclin (PGI2) is a vasodilator in several vascular beds.
E-series prostaglandins are vasodilators F-series prostaglandins are vasoconstrictors Thromboxane A2 is a vasoconstrictor |
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What is the difference between active and reactive hyperemia?
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Active hyperemia is an increased blood flow that is proportional to its increased metabolic activity (i.e. skeletal muscles)
Reactive hyperemia is an increase in blood flow to an organ that occurs after a period of occlusion of flow. The longer the period of occlusion is, the greater the increase in blood flow is above preocclusion levels. |
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W1. hat special circulations are controlled almost entirely by local metabolic factors? What are those vasoactive metabolites/metabolic factors?
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Coronary circulation: Hypoxia, Adenosine
Cerebral circulation: CO2, H+ Muscle (during exercise): Lactate, K+, Adenosine Pulmonary: Hypoxia vasoconstricts |
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What special circulations are controlled almost entirely by sympathetic control?
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Muscle (at rest): α1 receptor causes vasoconstriction; β2 receptor causes vasodilation.
Skin (temperature regulation) |
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What are the changes that occur when an individual moves from a supine position to a standing position?
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1) When a person stands, a significant amount of blood pools in the lower extremities because of the high compliance of the veins.
2) Pc in the legs increases and fluid is filtered into the interstitium. If net filtration exceeds the ability of the lymphatics to return it to circulation, edema occurs. 3) Blood volume and venous return decrease, resulting in both stroke volume and cardiac output decreasing 4) Arterial pressure decreases because of the reduction of cardiac output. If cerebral blood pressure is low enough, fainting may occur 5) Compensatory mechanisms attempt to increase blood pressure to normal. Carotid sinus baroreceptors decrease firing -> increased sympathetic outflow |
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What is orthostatic hypotension?
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Fainting or lightheadedness on standing, may occur in individuals whose baroreceptor reflex mechanism is impaired (e.g. individuals treated with sympatholytic agents)
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What are the changes that occur with exercise?
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A) The central command (anticipation of exercise)
-sympathetic outflow to the heart and blood vessels is increased, parasympathetic outflow is decreased -> heart rate and contractility increased -cardiac output is increased -venous return is increased -arteriolar resistance in skin, splanchnic regions, kidneys, and inactive muscles is increased B) Increased metabolic activity of skeletal muscle -vasodilator metabolites (lactate, K+, adenosine) accumulate because of increased metabolism of muscle -these metabolites cause arteriolar dilation in the active skeletal muscle, increasing muscle blood flow (active hyperemia) -as a result of increased blood flow, O2 delivery is increased -vasodilation accounts for the overall decrease in TPR that occurs with exercise. |
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What are the compensatory responses to acute blood loss?
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1) A decrease in blood volume produces a decrease in mean systemic pressure -> decreased cardiac output and arterial pressure
2) Carotid sinus baroreceptors detect decreased arterial pressure -> increased sympathetic outflow to heart and blood vessels and decreased parasympathetic outflow to the heart -> increased heart rate, increased contractility, increased TPR (arteriolar constriction, except in coronary and cerebral vessels) 3) Chemoreceptors in the carotid and aortic bodies sense hypoxia -> increase sympathetic outflow 4) Cerebral ischemia (If present) causes an increase in PCO2 -> increases sympathetic outflow 5) Arteriolar vasoconstriction causes a decrease in Pc -> capillary absorption is favored 6) Adrenal medulla releases epinephrine and NE 7) Renin-angiotensin-aldosterone system is activated 8) ADH is released when atrial receptors detect decreased blood volume. |
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What are the changes that occur when an individual moves from a supine position to a standing position?
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1) When a person stands, a significant amount of blood pools in the lower extremities because of the high compliance of the veins.
2) Pc in the legs increases and fluid is filtered into the interstitium. If net filtration exceeds the ability of the lymphatics to return it to circulation, edema occurs. 3) Blood volume and venous return decrease, resulting in both stroke volume and cardiac output decreasing 4) Arterial pressure decreases because of the reduction of cardiac output. If cerebral blood pressure is low enough, fainting may occur 5) Compensatory mechanisms attempt to increase blood pressure to normal. Carotid sinus baroreceptors decrease firing -> increased sympathetic outflow |
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What is orthostatic hypotension?
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Fainting or lightheadedness on standing, may occur in individuals whose baroreceptor reflex mechanism is impaired (e.g. individuals treated with sympatholytic agents)
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What are the changes that occur with exercise?
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A) The central command (anticipation of exercise)
-sympathetic outflow to the heart and blood vessels is increased, parasympathetic outflow is decreased -> heart rate and contractility increased -cardiac output is increased -venous return is increased -arteriolar resistance in skin, splanchnic regions, kidneys, and inactive muscles is increased B) Increased metabolic activity of skeletal muscle -vasodilator metabolites (lactate, K+, adenosine) accumulate because of increased metabolism of muscle -these metabolites cause arteriolar dilation in the active skeletal muscle, increasing muscle blood flow (active hyperemia) -as a result of increased blood flow, O2 delivery is increased -vasodilation accounts for the overall decrease in TPR that occurs with exercise. |
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What are the compensatory responses to acute blood loss?
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1) A decrease in blood volume produces a decrease in mean systemic pressure -> decreased cardiac output and arterial pressure
2) Carotid sinus baroreceptors detect decreased arterial pressure -> increased sympathetic outflow to heart and blood vessels and decreased parasympathetic outflow to the heart -> increased heart rate, increased contractility, increased TPR (arteriolar constriction, except in coronary and cerebral vessels) 3) Chemoreceptors in the carotid and aortic bodies sense hypoxia -> increase sympathetic outflow 4) Cerebral ischemia (If present) causes an increase in PCO2 -> increases sympathetic outflow 5) Arteriolar vasoconstriction causes a decrease in Pc -> capillary absorption is favored 6) Adrenal medulla releases epinephrine and NE 7) Renin-angiotensin-aldosterone system is activated 8) ADH is released when atrial receptors detect decreased blood volume. |
