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Cvs > Circulation > Flashcards

Circulation Flashcards

1
Q

Stressed volume

A

Vol of blood in arteries

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2
Q

Value of pressure change in arterioles and it’s regulated by_____ alpha-1 and beta-2 adrenergic receptors are found in

A

35 mmhg( highest R of CVS)
ANS
Alpha -1 —> veins,renal circulation,skin
Beta-2 —-> skeletal muscles

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3
Q

where is found Largest cross sectional area and largest R

A

Largest area —> capillaries (therefore least v)

Largest R—> arterioles(highest pressure drop)

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4
Q

Velocity of blood flow

Where it’s highest

A

V=Q/A
Q-> flow rate

V is highest in aorta because of least cross sectional area

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5
Q

Whats the flow equation and it’s mean

MAP

A

Q(Blood flow)=delta P/R
Or
CO=MAP-RAP/(TPR
RAP(right atrial pressure)

MAP=120+80+80/(3). (Because more time is spent in daistole)

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6
Q

Calculate Value of TPR ,PVR

A

TPR=105-5/5=20

PVR=40-20/5=4

Pulmonary vascular resistance

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7
Q

Write poiseuilli equation

On what it’s factors depends

A

R=meu(viscosity)length/pi(radius)4

Polycythemia ,multiple myeloma(more extra protein),spherocytosis—> î viscosity

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8
Q

Resistance in series and parallel curcuit … our body combination of arteries…..

A

In parallel resistance total resistance is less than that of individual…. in parallel all organs receive same pressure….. our body has parallel combination of arteries…… in series pattern total resistance is more than individual

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9
Q

Why are korotkoff sounds are produced

A

Because of turbulent flow

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10
Q

What is capacitance (compliance) when it !

What happens when it !

A

It’s the stretchness or distensibility of blood vessels . It decreases in hypertensive and old aged persons

It î pulse pressure

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11
Q

Pulse pressure .

It’s main determinant is

A

PP=Systolic Blood pressure -D bp

Sv and compliance

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12
Q

Change in pressure depends on

A

The amount of pressure lost in a particular segment is proportional to the resistance of that segment.

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13
Q

Effect of vasodilation on blood flow

A

Dilation of arterioles decreases arteriolar resistance, which increases flow, decreases upstream pressure (MAP), and increases downstream pressure (capillary pressure).

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14
Q

Sinusoid and fenestrations

Where they are present

A

Sinusoids are large intercellular pores and are present in liver intestine bone marrow peptidal glands etc
Fenestrations are small intracellular pores

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15
Q

Starling equation

A

The Starling equation (Figure 3.18)
J v=[(pc-pi)-(pi.c-pi.i)]
where:

J v = fluid movement (mL/min) K f = hydraulic conductance (mL/min⋅mm Hg) P c = capillary hydrostatic pressure (mm Hg) P i = interstitial hydrostatic pressure (mm Hg) π c = capillary oncotic pressure (mm Hg) π i = interstitial oncotic pressure (mm Hg)

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16
Q

Edema and causes of edema

A

Pathological condition when interstitial fluid î than the capacity of lymph to return to circulation
Causes are îpc
!pi.c
î kf

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17
Q

What are factors that î pc ,! pi.c and îkf

A

Îpc—> arteriolodilation,venoconstriction, î venous pressure,standing, venous thrombus, venous compression (e.g in breast cancer or bands on hand),right ventricular failure(edema in systemic circulation
!pi.c—>!plasma proteins,severe liver disease, protein malnutrition
Î kf—> burn , inflamation

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18
Q

What maintains osmotic pressure

A

Plasma proteins

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19
Q

Where and How hypertension can cause edema

A

Hypertension may cause pulmonary edema. Because when afterload î for long time then left ventricle instead of it’s full hypertrophy cannot pump blood —> cardiac failure(can’t pump what it receives—>back pressure î—> pulmonary edema occur

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20
Q

Laplace law

A

T@P*r

Wall tension is directly proportional to pressure times radius

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21
Q

Relationship between compliance and elasticity

A

Elasticity (ability of vessel to come back to it’s normal position) is inverse of vessel compliace(ability of vessel to stretch

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22
Q

Importance of veins in compliance and blood volume

A

Veins are 20% more compliant and 70% of blood remains in vein

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23
Q

Veinous return formula ,formula of it’s factors and dependence of its factors

A

VR=psf-RAP/(R
Psf=Volume/compliace
We can increase psf either by increasing volume of decreasing compliance (sympathetic constriction and muscle pump)
We can decrease psf by increasing compliance(venodilation,sympathtic inhibition, alpha block)

Psf(systematic filling pressure) is the pressure in vessels when there is no blood flow

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24
Q

What causes and increase in pulse pressure

A

Î sv and

! Compliance

25
Q

Baroreceptors , where are they found, what is difference between different baroreceptors function and when they are stimulated

A

Baroreceptors in carotid sinus sense both î and ! arterial bp while those of aortic arch sense î in bp but less sensitive to ! In bp . They increase para sympathetic(vagul) activity.
Abundant in walls of carotid sinus and aortic arch
They are stimulated when stretched

26
Q

How baroreceptor reflex works and what happens in the last when sns is stimulated

A

Baroreceptors in walls of carotid sinus and aortic arch are stimulated by î bp. Afferent activity is relayed to the medulla(vasomotor center) via cranial nerves IX (carotid sinus) and X (aortic arch).
Baroreceptor activity exists at the person’s resting arterial blood pressure.
Afferent activity stimulates the parasympathetic nervous system and inhibits the sympathetic nervous system.when bp ! Then vasomotor center does this does 4 things (1) î heart rate (2) î contractility and SV (3) arterial vasoconstriction (4) venoconstriction

27
Q

How barorecptor reflex is inhibited

A

A fall in arterial blood pressure evokes a reflex decrease in para sympathetic activity and increase in sympathetic activity. This is a negative feedback system to bring blood pressure back to its original level.

28
Q

arterial baroreceptors inhibits the secretion of ——- hormone

A

Activation of arterial baroreceptors inhibits the secretion of ADH.

29
Q

What a carotid massage does

Afferent activity is relayed to medulla by which nerves

A

It stimulates baroreceptor reflex mechanism

Cranial nerve 9 ( carotid sinus) 10 (aortic arch)

30
Q

Aortic regurgitation , which things increases due to it and which decrease

A

Incomplete closure aortic valve. Blood flows back to LV this î sv and systolic blood pressure and decrease diastolic blood pressure

31
Q

Ways to regulate blood flow

A

Autoregulation(no nerves and hormones are included)
It is done by two mechanisms
1)metobolites:- CO2, H+,k+,adenosine ,amp,lactate , adp.. produce dilation in respective tissue
2) myogenic:- smooth muscles inherently contract when they are stretched
Extrinsic regulation:- by ANS

32
Q

What are vaso-active substances with function

A

Histamine and bradykinin cause arteriolar dilation and venous constriction therefore î Pc and capillary filtration and cause local edema.
Serotonin (5-hydroxytryptamine) causes arteriolar constriction and is released in response to blood vessel damage to help prevent blood loss.
d. Prostaglandins
Prostacyclin is a vasodilator in several vascular beds.
E-series prostaglandins are vasodilators.
F-series prostaglandins are vasoconstrictors.
Thromboxane A 2 is a vasoconstrictor.

33
Q

Autoregulating tissues include (tissues least affected by nervous reflexes):

A

l Cerebral circulation
l Coronary circulation
Skeletal muscle vasculature during exercise

34
Q

Coronary circulation
Controlled by
When Î
Difference between aortic pressure and coronary pressure

A

Blood flow to heart is Controlled mostly by autoregulation (adenosine and hypoxia specially)
During systole compression of coronary vessels occur therefore blood flow ! And after occlusion blood flow î to repay the oxygen debt
Aortic pressure is maximum after qrs but coronary circulation is wavy at that time and maximum after T wave

35
Q

hypovolumic shock does what and what those factors do to compensate

A

Hypovulumic shock ! a)bp b)blood volume…
a)!bp—STIMULATE—>1) !O2–signal—>i)anaerobic respiration(this î lactate,!ph—>stimulate medullary center)…..ii)chemo-sensors of aorta(—signal->medullary center)….iii)—>medullary center-singal—>SNS….iv) —>! Capillary pressure—>H2O influx into capillaries—> i blood volume….v)—>stimulate kidney—>!blood flow—>!GFR—> oliguria —> blood volume Î.

36
Q

What is the compensation for ! In blood volume

A

b)!blood volume—STIMULATE->1)volume sensors of atria—signal—> pituitary gland —> release ADH—signal—> kidneys—> î re-absorption of water—>oliguria —> î blood volume

37
Q

What SNS does after stimulation

A

Sympathetic nervous system—signal—> 1) heart—> î heart rate….2) Renin—>convert angiotensinogen to angiotensin II —signal—>i)adrenal cortex—> release aldosterone(i re-absorption of Na)ii)ADH

38
Q

Hypovolumic shock and it’s causes

A

Circulatory shock is inadequate supply of blood to tissue and that’s due to less volume of blood then it’s said to be hypovolumic
Causes…1) blood loss—due to—>GIT,AAA,trauma,postpartum haemorrhage,ETP,hemoptysis(blood loss during cough)…..2)Non-blood fluid loss—due to—> 3rd degree burn,vomiting,diarrhoea,bowl obstruction,acute pancreatitis, diabetes mellitus, diabetes insipidus, high-dose diuretic treatment

39
Q

Symptoms of hypovolumic and cardiogenic shock

A

Hypovolemic and cardiovascular shock are characterized by decreased blood pressure (weak pulse) increased heart rate, pallor with cold sweats (not observed with shock caused by vasodilatation), reduced urinary output (oliguria) and extreme thirst.

40
Q

Treatment of circulatory shock

A

BLOOD TRANSFUSION
Transfusion of whole blood is done in hypovolemic shock except burn shock.
•PLASMA TRANSFUSION
Plasma transfusion is very useful in burns
• ADMINISTRATION OF PLASMA SUBSTITUTES
Plasma substitutes are used when plasma is not available.
Commonly used Plasma Substitutes
i. Plasma expanders (solutions of sugar with high molecular weight such as dextran); such substances do not escape through capillary membrane
ii)Concentrated human serum albumin
iii. Hypertonic solutions, which cause drawing of fluid into blood from interstitial space.

41
Q

Cardiogenic shock causes

A

1) acute heart failure or ischemia
2) arrhythmiasis( both tachy and brady)
3) multiple MI
4) congenital heary disease
5) dilated cardiomapathy
6) myocarditis(inflamation of myocardium) may be due to virus
7) mpairment of cardiac filling, e.g. in pericardial tamponade. T

42
Q

What does Renin-Angiotensin-Aldosterone system do, how it’s initiated

A

It is a slow, hormonal mechanism and is used in long-term blood pressure regulation by adjustment of blood volume.
A decrease in renal perfusion pressure causes the juxtaglomerular cells of the afferent arteriole to secrete renin.
Renin is an enzyme which convert Angiotensinogen into angiotensin I
Hence process initiated

43
Q

How and where angiotensin II is formed and what it’s four majestic functions

A

Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II, primarily in the lungs.

1)It stimulates the synthesis and secretion of aldosterone by the adrenal cortex.it î Na re-absorption but it’s slow
2)It increases Na+–H +exchange in the proximal convoluted tubule.
This action of angiotensin II directly increases Na + reabsorption.
3) î thirst
4) causes vasoconstriction of the arterioles and î TPR

44
Q

What chemoreceptors in the carotid and aortic bodies do

A

They are located near the bifurcation of the common carotid arteries and along the aortic arch.

They have very high rates of O 2 consumption and are very sensitive to decreases in the partial pressure of oxygen (Po2 ).

Decreases in Po 2 activate vasomotor centers that produce vasoconstriction, an increase in TPR, and an increase in arterial pressure.

45
Q

When ADH is released and what are it’s functions

A

Atrial receptors respond to a decrease in blood volume (or blood pressure) and cause the release of vasopressin from the posterior pituitary.

a. It is a potent vasoconstrictor that increases TPR by activating V1 receptors on the arterioles.
b. It increases water reabsorption by the renal distal tubule and collecting ducts by activating V 2 receptors.

46
Q

From where atrial natriuretic peptide is released and what are it’s function

A

Atrial natriuretic peptide (ANP) is released from the atria in response to an increase in blood volume and atrial pressure.

1) causes relaxation of vascular smooth muscle.
2) causes increased excretion of Na + and water by the kidney.
3) inhibits renin secretion.

47
Q

Active hyperemia vs reactive hyperemia

A

b. Active hyperemia Blood flow to an organ is proportional to its metabolic activity.
c. 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.

48
Q

How blood flow to skeletal muscles is controlled…. which receptors are present and what they do

A

By both auto regulations and SNS

There are both α 1 and β 2 receptors on the blood vessels of skeletal muscle.
Stimulation of α 1 receptors causes vasoconstriction.
Stimulation of β 2receptors causes vasodilation

49
Q

Constriction of carotid artery causes….

A

It causes ! In blood pressure which provokes sympathetic activity of baroreceptors and ! Vagal tone

50
Q

High secretion of aldosterone affects the following… 1)bp 2)k+ level 3)renin

A

It increases na re-absorption and k+secretion therefore water intake î and so do bp . Hence 1)bpî 2)k+! 3) renin !

51
Q

What causes growth of blood vessels in tumor and how

A

A decrease in tissue oxygen tension is thought to be an important stimulus for vascular endothelial growth factor and the growth of blood vessels in solid tumors.

52
Q

Flow through a blood vessel is 100ml/min , if we î vessel diameter by 4 times…what will be the value of blood flow

A

According to Poiseuille’s law, flow through a vessel increases in proportion to the fourth power of the radius. Therefore blood flow will be 25600

53
Q

What happens when a person stands from supine position …. also tell 1)how that can be prevented…. 2)what may occur due to it….3)what happens to venous return, cardiac output ….4) arterial pressure affect and what may occur

A

blood increases in veins because of their less compliance Thats called venous pool . It can be prevented by muscular activity
2) venous pooling in legs may îPc of veins and fluids will flow in interstium and if net filtration exceeds the limit that lymph can carry back to circulation, edema will occur..3)! in venous return will decrease SV n CO (frank-starling mechanism…4)it will cause ! in Pa and hence cerebral blood flow will ! And if it’s low enough than fainting may occur

54
Q

What’s the compensatory mechanism for decrease in bp (name the specific site) due to venous pool and what happens then!

A

less bp in arteries will ! Firing of carotid baroreceptors reflex to vasomotor center and hence sympathetic activity will î. as a result, heart rate, contractility, TPR, and venous return increase, and blood pressure increases toward normal.

55
Q

What’s orthostatic hypotension and it’s more common in…?

A

Orthostatic hypotension (fainting or light-headedness on standing) may occur in individuals whose baroreceptor reflex mechanism is impaired (e.g., individuals treated with sympatholytic agents) or who are volume depleted.

56
Q

What are sympatholytic drugs .. name some

A

Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals….. examples…..Guanethidine (Magnesium-ATPase inhibitor),
Indoramin (α1 antagonist),
Doxazosin (alpha blocker)

57
Q

What happens after anticipation of exercise and how

A

Central command originates in the motor cortex or from reflexes initiated in muscle proprioceptors when exercise is anticipated.and it 1)î sympathetic activity and ! Vagal tone—> îî HR,î sv 2)ÎÎ CO because of primarily î HR 3) îî VR because of muscular activity and vasoconstriction—>sv (frank-starling mech) 4) Arteriolar resistance in the skin, splanchnic regions, kidneys, and inactive muscles is increased. Accordingly, blood flow to these organs is decreased.

58
Q

What happens due to local metabolites after exercise

A

Local metabolites (k,adenosine and lacate) î this causes vasodilation and active hyperemia due to muscular activity. Oxygen supply to muscles î and arteriovenous oxygen difference increases. OVERALL TPR DECREASES after exercise ,remember just stimulation by central command î TPR

Cvs (3 decks)

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