CARDIOVASCULAR Flashcards by Jonathan Paul Ladera

Cardiac output from the eft side of the hear is the __________

systemic blood flow

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Cardiac output from the right side of the hears is the ________________

pulmonary blood flow

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Direction of blood flow

lungs to the left atrium via the PULMONARY VEIN
left atrium to the left ventricle through the MITRAL VALVE
left ventricle to the aorta through the AORTIC VALVE
from the aorta to the systemic arteries and the systemic tissues
from tissues to the systemic veins and vena cava
vena cava to the Right atrium
RA to the RV through TRICUSPID VALVE
RV to the pulmonary artery though PULMONIC VALVE
pulmonary artery to the lungs for oxygenation

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Deliver oxygenated blood to the tissues

Arteries

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site of highest resistance in the cardiovascular system

arterioles

arteriolar resistance is regulated by the ANS

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________receptors are found on the arterioles of the skin, splanchnic, and renal circulations

alpha 1

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____________ receptors are found on arterioles of skeletal muscle

B2 adrenergic

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have te largest total cross sectional and surface area

Capillaries

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Formed from merged capillaries

Venules

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Under low pressure

contain the highest proporrtion of blood in the cardiovascular system

Veins

(the blood volume is called unstessed volume)

have alpha 1 adrenergic receptors

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Velocity of blood flow can be expressed by this equation

v= Q/A

v = velocity (cm/sec)
Q = blood flow (ml/min)
A = cross sectional area (cm²)

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Velocity is directly proportional to _____________

blood flow

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Velocity is inversely proportion to the ______

cross sectional area

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Blood flow can be expressed by the these equations _______________

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The quation for blood flow (or cardiac output) is analogous to ________

Ohm’s law

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____________ equation gives factors that change the resistance of blood vessels

Poiseuille’s

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Resistance is directly proportional to ____________

viscosity of blood

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Resistance is directly proportional to _____________

length of vessel.

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Resistance is inversely proportional to the _______________

fourth power of the vessel

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____________ resistance is illustrated by the systemic circulation

Parallel

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When an artery is added in parallel, the total resistance ______________

decreases

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___________resistance is illustrated by the arrangement if blood vessels within a given organ

Series

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straight line (streamedlined) flow

Laminar flow

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predicts whether blood flow will be laminar or turbulent

Reynauld’s number

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When reynauld's number is increased, there is a greater tendency for \_\_\_\_\_\_\_\_\_

turbulence

Factors affecting Reynold's number

Decreased viscosity Increased velocity

consequence of the fact that the adjacent layers of blood travel at different velocities within a blood vessel

Shear

velocity of blood is \_\_a\_\_\_ at the wall and \_\_\_b\_\_\_\_ at the center of the vessel

a= zero b= highest

Shear is highest at the \_\_\_\_\_\_\_\_\_\_\_

wall

Decribes the distensibility of blood vessels inversely related to elastance or stiffness

Capacitance

Capacitance is expressed by this equation

Capacitance _________ proportional to volume

Directly

Capacitance \_\_\_\_\_\_proportional to pressure

inversely

Capacitance is much greater for (veins or arteries) ?

Veins

capacitane of the arteries \_\_\_\_\_\_\_\_with age

Decreases

As blood flows through the systemic circulation, pressure _____________ progressively because of the resistance

Decreases

Pressure is highest in the \_\_\_\_a\_\_\_\_\_ and lowest in the \_\_\_\_\_b\_\_\_\_\_\_.

a= aorta b = venae cavae

The largst decrease in pressure occurs across the \_\_\_\_\_\_\_\_

arterioles

Mean pressure in the aorta

100 mmHg

Mean pressure in the arterioles

50 mm Hg

Mean pressurein the capillaries

20 mm Hg

Mean pressure in the vena cava

4 mm Hg

pulsatile pressure not constant during cardiac cycle

Arterial pressure

Highest arterial pressure during a cardic cycle

systolic pressure

Lowest arterial pressure during a cardiac cycle

Diastolic pressure

Difference between the systolic and diastolic pressures

Pulse pressure

The most important determinant of pulse pressure is \_\_\_\_\_\_\_\_\_\_\_\_

Stroke volume * as blood is ejected from the left ventricle into the arterial system, arterial pressure increases because of the relatively low capacitance of the arteries.

Is the average arterial pressure with respect to time

mean arterial pressure

Left atrial pressure is ________ than venous pressure

lower

Left atrial pressure is estmated by \_\_\_\_\_\_\_\_\_\_\_\_\_\_

Pulmonary wedge pressure

ECG wave

Represents atrial depolarization

P wave * does not include atrial repolarization * buried in the QRS complex

interval from the beginning of the P wave to the beginning of the Q wave (initial depolarization of the ventricle)

PR interval

Depends on conduction velocity through the AV node.

PR interval * if AV nodal conduction decreases, the PR interval increases * decreased by stimulation of the sympathetic * increased by stimulation of parasympathetic

represent depolarization of the ventricles

QRS complex

interval from th beginning of the Q wave to the end of the T wave Representss the entire period of depolarization and repolarization of the ventricles

QT interval

is the segment from the end of S wave to the beginning of the T wave Isoelectric represents the period when the ventricles are deoplarized

ST segment

Represents ventricular repolarization

T wave

the resting membrane potential [cardiac] is determined by \_\_\_\_\_

conductance to potassium and approaches the K equilibrium

Inward current brings positive charge into the cell and \_\_\_\_\_\_the membrane potential

depolarize

Outward current takes positive out of the cell and ________ the membrane potential

hyperpolarizes

Ventricles, atria and the purkinje system have stable resting membrane potentials of about \_\_\_\_\_\_mV.

- 90 mV * This value approaches the K equilibrium potential

Action potentials are of long duration, especially in Purkinje fibers, where they last \_\_\_\_\_\_\_\_\_\_\_\_(msec)

300

the upstoke of the action potential * caused by transient increase in **Na conductance**. this increase results in an inward Na current that depolarizes the membrane

Phase 0

is a brief period of initial repolarization * Initial repolarization is caused by an outward, in part because of the movement of K ions (favored by both chemical and electrical and electrical gradients) out of the cell and in part because of a decrease in sodium conductance

Phase 1

the pateau of the action potential. * caused by transient increase in **calcium conductance,** which results in an inward calcium current, and by an increase in K conductance. * outward and inward currents are approximately equalm so the membrane potential is stable at the plateau level

Phase 2

Repolarization * calcium conductance decreases * K conductance increases * large outward K current - \> hyperpolarizes the membrane

Phase 3

resting membrane potential * period during which inward and outward currents (Ik1) are equal adn the membrane potential potential approaches the K equilibrium potential

Phase 4

Normally the pace maker of the hear has unstable resting membrane potential

Sinoatrial node * Exhibits phase 4 depolarization or automaticiy * The intrinsic rate of phase 4 depolarization (nd heart rate) is fastest in the SA node and slowest n the His-purkinje system

[SA node] upstroke of athe action potential * caused by an increase in calcium conductance * inward calcum current

Phase 0

[SA node] not present in the SA node action potential

Phase 1 and Phase 2

[SA node] repolarization * increase in K conductance. * increase in outward K current that cuases repolarization of the membrane potential

Phase 3

[SA node] * Slow depoalrization * accounts for the pacemaker activity of the SA node (automaticity) * inward Na current call I_f

Phase 4

I_f is turned on by _________ of the membrane potential during the preceding action potential

repolarization

upstoke of the action potential in the AV node is the result of an inward ______ current

Calcium

Reflects the time required for excitation to spread throughout cardiac tissue

Conduction velocity * depends on the **size of the inward current during the upstroke** of the action potential. * The larger the inward curent the higher the conduction velocity

Conduction velocity is fastest in the \_\_\_\_\_\_\_\_\_\_\_

Purkinje system

Conduction velocity is slowest in the \_\_\_\_\_\_\_\_\_

AV nde * allows time for ventricular filling before ventriular contraction.

Is the ability of ardiac cells to initiate action potentials in response to inward, depolarizing current. Reflects the recovery of channels that carry the inward currents of the upstoke of the action potential.

Excitability

Changes in excitability are described by \_\_\_\_\_\_\_\_\_\_\_\_

refractory periods

begins with the upstoke of the action potential and ends after the plateau No action potential can be initiated

Absolute refractory period

Slightly longer than ARP period during which a conducted action potential cannot be elicited

Effective refractory period

is the period immediately after the ARP when repolarization is almost complete Period during which an action potential can be elicited, but more than the usual inward current is required

Relative refractory period

Produces changes in heart rate

Chronotropic effects

Produces changes in conduction velocity, primarily the AV node

Dromotropic

The SA node, atria and AV node have _____________ vagal innervation

pasarympathetic

The neurotransmitter is _________ which acts on the \_\_\_\_\_\_\_receptors in the SA node, AV node, and atria

Acetylcholine Muscarinic receptors

The mechanism of the negative chronotropic effect is \_\_\_\_\_\_\_\_\_\_

Decreased I_f * the inward Na current tht is responsible for phase 4 depolarization in the SA node

Autonomic effects on the heart and Blood Vessels

Mechanism of action of negative dromotropic effect

Decreases inward calcium current and increases outward K current * Decreases conduction velocity through AV node * Increases PR interval

\_\_\_\_\_\_\_\_\_ is the neurotransmitter acting at B1 receptors

Norepinephrine

Mechanism of action of positive chronotropic effects

Increased I_f, the inward sodium current that is responsible for phase 4 depolarization in the SA node ## Footnote Increases heart rate

mechanism of action of positive dromotropic effect

increased inward calcium current * increases conduction velocity through the AV node

Contractlie unit of the myocardial cell

Sarcomere * runs Z line to Z line * Similar to Skeletal muscle

Occur at the ends of the cells maintain cell to cell cohesion

Interacalated discs

Present at the interacalted disks low resistance paths that allow rapid electrical spread of action potential

gap junctions

accont for the observation that the hear behaves as an electrical syncytium

Gap junctions

Continuous with the cell membrane invaginate the cells at the z lines and carry action potentials into the cell interior form dyads with the sarcoplasmic reticulum

T tubules

T tubules are well developed in the \_\_\_\_a\_\_\_\_ but poorly developed in the \_\_\_\_b\_\_\_\_\_

a = ventricle b= atria

small diameter tubules in cross proximity to the contractile elements

Sarcoplasmic reticulum

site of storange and release of calcium for excitation-contraction coupling

Sarcoplasmic reticulum

Steps in excitation-contraction coupling

1. AP spreads from cell membrane to T tubules 2. During the plateau, Ca conductance is increase 3. This ca entry triggers more calcium to be released (ryanodine) 4. Intracellular calcium increases 5. Calcium binds to troponin C and tropomyosin is moced out of the way, removin the inhibition of actin and myosin binding 6. Actin and myosin bind 7. relaxation occurs when calcium is reaccumulated by the SR

Intrinsic ability of the cardiac muscle to develop force at a given muscle length also called inotropism

Contactibility * related to the intracelleular calcium concentration

Contractibility is estimated by the \_\_\_\_\_\_\_

ejection faction normal (o.55 /55%)

Factors that increase contractility

Increased heart rate Sympathetic stmulation via B1 receptors cardiac glycosides

Factors that decrease contractitlity

Parasympathetic atimulation (ACh) via muscarinic receptos * decreases the force of contraction in the atria by decreasing the inward calcium current duint the plateau of the ardiac action potential

Describes the effect of ventricular muscle cell length on the force of contraction Analogous to the relationship in skeletal muscle

Length-tension relationship

End diastolic volume related to right atrial pressure

Preload

for the left ventricle is **aortic pressure.** For the right ventricle, **pulmonary artery pressure**

Afterload * Increases in aortic pressure cause an increase in afterload on the left ventricle * increase in pulmonary artery pressure cause an increase in afterload on the right ventrile

Frank starling relationship and the effect of positive and inotropic agents

Determines the maximum number of cross bridges that can form between actin and myosin

Sarcomere lenght * dtermines the maximum tension or force of contraction

Velocity of contraction ata fixd muscle length is maximal when\_\_\_\_\_

afterload is zero

Describes the increases in SV and cardiac output that occur in response to an increase in venous return or EDV

Frank starling relationship

Increases in EDV cause an _______ in ventricular fier length, which produces an increase in developed tension

Increase

Is the mechanism that matches cardiac output to venous return

Frank staling relationship * The greater the venos return, the greater the cardiac output

Increase in contractily cause an _____ in cardiac output for any level of RA pressure or EDV

Increase

Constrcuted by combining systolic and diastolic pressure curves

Ventricular pressure-volume loops * A single left ventricular cycle of contraction, ejection relaxation, and refililig can e visualized by combining the two curves into a pressure-volume loop

Steps in the ventricular-pressure loops

* isovolumetric contraction * ventricular ejection * isovolumetric relaxation * ventricular filling

Isovolumetric contraction

* Point 1-2 * Cycle begins at the end of diastole at point 1 * The left ventrile is filled with blood from LA (140ml) * End diastolic volume * Ventricular pressure is **low** becausse the ventricular muscle is **relaxed** * **on excitation,** the ventricle contracts and pressure increases. * the mitral valve closes when the LV pressure is greater than the LA pressure * no blood can be ejected from the ventricle

Ventricular ejection

* point 2-3 * Aortic valve open at point 2 whenpressure in the LV exceed pressure in the aorta * Blood is ejected to the aorta * ventricular volume **decreases** * The volume that is ejected = **stroke volume** * width of he pressure volume loop * the volume remaining in theleft ventricle at point 3 is **End systolic volume**

Isovolumetric relaxation

* point 3-4 * at point 3, the ventricle relaxes * When ventricular pressure decreases to less than aortic pressure = aortic valve closes * ventricular volume is constant * isovolumetric

Ventricular filling

* Point 4-1 * once LV pressure decreases to less than aortic pressure * mitral valve opens = filling of the ventricle begins * ventricular volume increases to about 140 ml (EDV)

Changes in ventricular pressure volume loop

simultaneous plots of cardiac output and venous return as a function of right atrial pressure or end diastolic volume

Cardiac and vascular function curves

Depicts the Frank starling relationship for the ventricle Shows the cardiac output is a function of EDV

The cardiac function (cardiac output) curve

Depicts the relationship between the blood flow through the vascular system (or venous return) and right atrial pressure

Vascular function (venous return) curve

the point at which the vascular function curve intersects the x axis equals right atrial pressure when there is "no flow" in the cardiovascular system

Mean systemic pressure

Mean systemic pressure is inreaased by an _______ in boodv volume

Increase

mean systemic pressure is increased by ________ in venous capacitance

decrease

Slope of the venous return curve is determined by \_\_\_\_\_\_\_\_\_\_\_\_\_\_

resistance of the arterioles

A clockwise rotation of the venous return curve indicates a ____________ in total peripheral resistance

decrease

A counterclockwise rotation of the venous return indicates an ______________ in TPR

increase

Effect of a positive inotropic agent on the cardiac function curve, cardiac outpu, and RA pressure

Inceases in blood volume or decrease in venous capacitance _________ the Mean systemic pressure

Increase

Decrease in blood volume or increase in venous capaciance _________ mean systemic pressure

Decrease

Increasing TRP causes a ______ in both cardiac output and venous return

decrease

Decreasing TPR causes an _________ in both cardiac output and venous return

Increase

The volume ejected from the ventricle on each beat

Stroke volume SV = EDV -ESV

Formula for cardiac output

SV x HR

the fraction of the end diastolic volume ejected in each stroke volume Relate to contractility

Ejection fraction EF = SV/EDV

is the work the heart performs on each eat equal to pressure x volume

Stroke work | (aortic pressure x stroke volume)

the primary energy source for stroke work

Fatty acids

Directly related to the amount of tension developed by the ventriles

Cardiac oxygen consumption

Fick Principle fir measuring cardiac output

Preceded by the P wave Contributes to, but is not essential for ventricular filling

Atrial systole

The increase in atrial pressure (venous pressure) caused by the atrial systole is the ______ wave on venous pulse wave

a wave

In ventricular hypertrophy, filling of the ventricle by atrial systole causes the \_\_\_\_\_\_\_

4th heart sound

begins during the QRS complex

Isocolumetric ventricular contraction

ventricular pressure reaches its maximum value during \_\_\_\_\_\_\_\_\_\_

Rapid ventricular ejection

\_\_\_\_\_\_\_\_ wave on venous pulse curve occurs because because of the bulging of tricuspid valve into the RA during right ventricular contraction

C wave

The onset of T wave, which represent repolarization of the ventricles, marks the end of both ventricular contraction and reapid ventricular ejection

Rapid ventricular ejection

Ejection of blood from the ventricles continues, but slower Venricular pressure begins to decrease Aortic pressure also decreases because of the runoff of blood from large arteries into smaller arteries

Reuced Ventricular ejection

Cardiac cycle

\_\_\_\_\_wave on venous pulse curve represents blood flow into the RA (rising phase of wave) and from RA into RV

V wave

Repolarization of the ventricles (end of T wave) The AV valves remain closed during most of this phase

Isoviumetric ventricular relaxation

The blip in the aortic pressure tracing occurs after closure of the aortic valve and is called the\_\_\_\_\_\_\_

dicrotic notch or incisura

When ventricular pressure, becomes less than atrial pressure, the mital valcve opens

Rapid ventricular filling

Rapid flow of blood from the atria into the ventricles causes the \_\_\_\_\_\_\_\_\_

third heart sounds

The longest phase of the cardiac cycle ventricular filling continues, but at a slower rate The time required for diastasis and ventricular filling depends on heart rate

Reduced ventricular filling (diastasis)

The most important mechanisms for regulating arterial pressure a fast, neurally mediated \_\_\_\_\_\_\_a\_\_\_\_\_ and a slower, hormonally regulated \_\_\_\_\_\_\_\_\_\_b\_\_\_\_\_\_\_mechanism

a = baroreceptor b = renin-angiotensin aldosterone mechanism

Includes fast, neural mechanisms negative feedback system that is responsible for the minute to minute regulation of arterial blood pressure

baroreceptor reflex

\_\_\_\_\_\_are stretch receptors located within the walls of the carotid sines near the bifurcation of the common carotid arteries

baroreceptors

Steps in the baroreceptor reflex

1. A decrease in arterial pressure decreases stretch on the walls of the carotid sinus 2. Decreased stretch decreases the firing rate of the carotid sinus nerve. [Herring's nerve, cranial nerve], which carries information to the vasomotor center in the brain stem 3. The set point for mean arterial pressure is the vasomotor center is about 100 mmHg. 4. The responses of the vasomotor center to a decrease in mean arterial bp are coordinated to increase the arterial pressure back * Decreased parasympathetic (vagal) outflow to the heart * Increased sympathetic outflow

Four effects that increase the arterial pressure back to normal

* Increase heart rate * decreased parasympathetic tone * increased sympathetic tone * Increase contractility and stroke volume * increased sympathetic tone to the heart * Increase vasoconstriction of arterioles * increased sympathetic outflow * Increase vasoconstriction of veins * increased sympathetic outflow

Renin angiotensin aldosterone system

enzyme that catalyze the conversion of the angiotensinogen to angiotensin I in plasma

Renin

catalyzes the conversion of angiotensin I to angiotensin II, primarily in the lungs

Angiotensin converting enzyme

Four effects of angiotensin II

* Stimulates the synthesis and secretion of aldosterone by the adrenal cortex * Increases Na-H exchange * It increases thirst and therefore water intake * causes vasoconstriction of the arterioles, thereby increasing TPR and arterial pressure

When the brain is ischemic, the partial pressure of ___________ in brain tissue increases

carbon dioxide

Chemoreceptors in the vasomotor center and respond by __________ sympathetic outflow to the heart and blood vessels

Increasing

example of the response to cerebral ischemia. Increases in intracranial pressure cause compression of the cerebral blood vessels, leading to cerebral ischemia and increased cerebral PCO2

Cushing reaction

Are located near the bifurcation of the common carotid arteries and along the aortic arch. have very high rates of Oxygen consumption and are very sensitive to decrease in the partial pressure of oxygen

Chemoreceptors in the carotid and aortic bodies

\_\_\_\_\_in PO2 activate vasomotor centers that produce vasoconstriciton, an increase in TPR and an increase in arterial pressure

Decrease

involved in the regulation of blood pressure in response to hemorrhage, but not in minute to minute regulation of normal blood pressure

Vasopressin (ADH)

Vasopressin is a potent vasoconstrictior that increases TPR by activating ___________ on the arterioles

V1 receptors

Vasopressin increases water reabsorption by the renal distal tubule and collecting ducts by activating \_\_\_\_\_\_\_\_\_\_\_\_\_receptors

released from the atria in response to an increase in blood volume and atrial pressure causes relaxation of vascular smooth muscle causes increased excretion of sodium and water by the kidney which reduces blood volume and attemps to bring arterial pressure down to normal

Atrial natriuretic peptide (ANP)

Atrial natriuretic peptide inhibits _________ secretin

renin

At the junction of the arterioles and capillaries is asmooth muscle band called the \_\_\_\_\_\_\_\_\_\_

Precapillary sphincter

true capillaries do not have smooth muscle; they consist of a single layer of _______________ surrounded by a basement membrane

Enothelial cells

In the liver and intestine, theclefts are exceptionally wide and allow passage of protein. These capilalries called

sinusoids

large water soluble substances can cross by \_\_\_\_\_\_\_\_\_\_\_

pinocytosis

The starling equation

Fluid flow

when Jv is positive, there is net fluid movement out of the capillary (filtration) when Jv is negative, there is net fluid movement into the capilalry (absorption)

\_\_\_\_\_\_\_is the filtration coefficient the hydraulic conductance (water permeability) of the capillary wall

K_f

determined by arterial and venous pressures and resistances

capillary hydrostatic pressure * an increase in Pc favors filtration out of the capillary * an increase in either arterial or venous pressure produces an increase in Pc; increases in venous pressure have a greater effect on Pc * Higher at the arteriolar end of the capilalry than at the venous end (except in glomerular capilalries, where it is nearly constant)

Interstitial fluid hydrostatic pressure

opposes filtration normally close to 0 mm Hg

Factors that increase filtration

* Increase in capilalry hydrostatic pressure * caused byincreased arterial pressure, increased venous pressure, arteriolar dilation and venous constriction * decrease interstitial hydrostatic pressure * increase capillary oncotic pressure * caused by decreased protein concentration in the blood * increase in interstitial oncotic pressure * inadequate lymphatic function

Excess filtered fluid is returned to the circulation via the \_\_\_\_\_\_\_\_\_\_\_

lymph

\_\_\_\_\_\_\_\_\_\_permits interstitial fluid to enter, but notleave, the lymph vessels. flow through larger lymphatic vessels is also unidirectional

one-way flap valves

oCcurs when the volume of interstital fluid exceeds the capacity of the lymphathics to return it to the circulation can be caused by excess filtration or bloccked lymphatics

Edema

causes both arteriolar dilation and venous constriction, which together produces a large increase in Pc and local edema

Histamine

produced in the endothelial cells causes local relaxation of vascular smooth muscle

Nitric oxide

Causes and examples of edema

The mechanism of action

activation of guanylate cyclase and production of cyclic guanosine monophosphate (cGMP)

Blood flow to an organ remains constant over a wide range of perfusion pressures

Autoregulation * Organs that exhibit autoregulation are the * heart * brain * kidney * if perfusion pressure to the heart is suddenly decreased, compensatory vasodilation of the arterioles will occur to maintain a cconstant flow

Summary of control of special circulations

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 the peocclusion levels

Reactive hyperemia

Mechanism tat explain local control of blood flow

Myogenic hypotheis Metabolic hypothesis

Explains autoregulation but not active or reactive hyepremia based on the observaton that vascular smooth muscle contracts when it is stretched

Myogenic hypotheis

based on the observation that te tissue supply of oxygen is matched to the tissue demand of oxygen. vasodilator metabolites are produced as a result of metabolic activity in tissue.

metabolic hypothesis * Vasodilators" * CO2 * H * K * lactate * adenosine

Increae in sympathetic tone cause\_\_\_\_\_\_\_\_\_\_

vasoconstriction

causes arteeriolar dilaion and venous constriction produces increaed filtraion out of the capilalries and causes local edema

Bradykinin

causes arteriolar constriction and is released in response to blood vessel damae to help prevent blood loss implicaed in the vascular spasms of migraine headaches

Serotonin

E series prostaglandings are \_\_\_\_\_\_\_\_\_\_\_

vasodialtors

F series prostaglandins are \_\_\_\_\_\_\_\_

vasoconstrictors

Thromboxane A2 is a \_\_\_\_\_\_\_\_

vasoconstrictor

Coronary circulation is controlled almost entirely by\_\_\_\_\_\_\_\_\_\_\_\_

local metabolic factors * exhibits autoregulation * exhibits active and reactive hyperemia

The most important metabolic factors are \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

hypoxia and adenosine

Cerebral circultion is almost entirely controlled by \_\_\_\_\_\_\_\_\_\_\_

local metabolic factors * Exhibits autoregulation * exhibits active and reactive hyperemia

The most important local vasodialtor for the cerebral circualtion is \_\_\_\_\_\_\_\_

CO2

Primary regulato of blood flow to the skeletal muscle at rest

Sympathetic innervation

Stimulation of alpha 1 receptors cause\_\_\_\_\_\_\_

vasoconstriction

stimulation of B2 receptors causes \_\_\_\_\_\_\_\_\_\_\_\_

vasodialtion

During exercise, when demand is high these \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_are dominant

local metabolic mechanisms

is the principal fucntion of cutaneous sympathetic nerves.

Temperature regulation

Changes occur when an individual moves from a supine to a standing position

* significant volume of blood pools in the lower extremities because of high compliance of the veins * Increased local venous pressure. - \> edema * venous return decreases - \> **SV and cardiac output decreases** * Arterial pressure decreases * Compensatory mechanis will attempt to increase BP * carotid sinus baroreceptors - \> decrease the firing rate of the carotid sinus nerves

Summary of responses to standing

Summary of Effects of exercise

Cardiovascular response to exercise

Summary of compensatory response to Hemorrhage

cardiovascular response to hemorrhage

CARDIOVASCULAR Flashcards

(222 cards)