Physio Memory Cardiovascular

8/13/2019 Physio Memory Cardiovascular

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11. Atrial

Fibrillation

Well tolerated and common in the elderly.

Complications: bloodpools in parts of atria-forms clots.

Normal but irregular QRS complexes; no P

waves but the baseline may show irregular

fibrillation waves. AF may be paroxymal,

persistent or permanent.

May be asymptomatic or may cause

palpitations, breathlessness and fatigue.

Digitalis is used for A-Fib, increases

contractility.

106. Body's

response to

hemorrhage

(flow chart)

10. Bundle

Branch

Block

A block in both bundles will cause 3rd degree

block, but an interruption of the right or left

bundle of his will delay conduction to the

appropriate ventricle.

Ventricular depolarization is then

asynchronous and the QRS complex is

prolonged. Left bundle branch block generally

a serious condition often underlying

significant heart disease.

2. Cardiac action

potential of a

ventricular

myocyte

Phase 4: REsting- stable pot at -85mV

Phase 0: Rapid depolarization- inward

Na current ina

Phase 1: Initial Rapid Repolarization- Na

inactivation and outward K current ito

Phase 2: Plateau Phase- Inward flow of

Ca- ica

Phase 3: Rapid repolarization- Outward K

current ik through the delayed rectifier

channels

Phase 4: Resting phase- Voltage gated Na

channels and Ca channels are closed- ib

and iK1 are counterbalanced by the Na/K

pump.

NO HYPERPOLARIZATION!!!

108. Decompensated

shock

31. Definition of

stroke work

and kinetic

work

Stroke work is the work done to eject a

volume of blood into the aorta against a

resistance

Kinetic work is the work done to

accelerate blood to its velocity of ejection

through the aorta and pulmonary valves.

55. Describe

metabolic andreactive

hyperemia

77. Draw a cardiac

performance

curve

Physio Memory: CardiovascularStudy online at quizlet.com/_610pr


2/13

78. Draw a vascular

function curve.

What alters VR

curve?

MSFP = pressure at +7 = pressure that

would be measured throughout the CVS if

the heart stopped beating. There would be

no pressure gradient to drive the blood

around the circulation.

Blood volume, venomotor tone and

arteriolar resistance (TPR) affect VR.

Increased BV and venomotor tone

increase VR.

Increased TPR DECREASES VR because

the blood is 'held' in the arterial side.

13. Draw a wigger

diagram of the

ventricular

phase.

3. Draw the

absolute and

relative

refractory

periods of a

cardiac action

potential

67. Draw the

baroreceptor

reflex

(intervention)

69. Draw the baroreceptor reflex when

there is a fall in BP

26. Draw the cardiac myocyte action

potential and the SA node action

potential

see special sheets

82. Draw the effect of changing blood

volume on the Guyton Cross Plot

79. Draw the effect of different blood

volumes/venoconstriction/venodilation

on the vascular function curve.

Venoconstriction = increased

volume

Venodilation = decreased bloo

80. Draw the effects of changing TPR on the

vascular fxn curve


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83. Draw the effects of

increased and

decreased TPR on the

Guyton Cross Plot

81. Draw the effects of

increasing or

decreasing

contractility on the

guyton cross plot.

57. Draw the epinephrine

MOA as far as nerve

endings, NT,

receptors, etc.

32. Draw the pressure

volume loop and

indicate diastole,

systole, EDV, ESV,

Isovolumetric

contraction/relaxation

and where the valves

open and close

4. Draw the

relationship

between muscle

action potential

and muscle

twitch in skeletal

vs. cardiac m.

71. Draw the renin

angiotensin

system in terms

of organs

72. Draw the renin-

angiotensin

system in terms

of a flow chart

58. Draw the time

vs. blood

flow/blood

pressure graphs

of coronary

circulation


4/13

63. Effect of exercise

on skeletal

muscle blood

flow

59. Effects of

exercise on

coronary blood

flow

50. Explain

metabolic

control of blood

flow- metabolic

hyperemia and

reactive

hyperemia

52. Explain MOA of

Nitroglycerin

34. Explain the

effect of changes

in contractility

on force-velocity

relationship. In

which does

Vmax stay the

same?

29. Explain the

effects of

hyperkalemia

and

hypokalemia on

the heart.

75. Factors that affect

CVP

1. Blood volume (increased, causes

increased CVP)

2. Venomotor tone (Venoconstriction

increases CVP)

3. Arteriolar tone (arteriolar

vasoconstriction decreases venus return,

whereas vasodilation increases venous

return. Increased TPR > decreased VR

and vice versa. ***Arteriolar tone is the

major determinant of TPR!!!6. First degree heart

block

Slowed conduction through the AV node.

PR interval prolonged. Not life

threatening.

30. How do hyper

and hypokalemia

look on an ECG?

27. How do

parasympathetics

affect the heart?

Decreases heart rate, causes bradycardia.

ACh causes a slower rate of rise for the

pacemaker potential = decreased heart

rate. Slower depolarization.

Opening of the K channels is fast which

explains why the vagus quickly slows

down the heart. Ex include:

Slowing of heart during expiration (sinus

arrhythmia)

low heart rate of a trained athlete

slowing of heart during a dive (dive

reflex)

transient arrest of the heart at the onset of

fainting (vasovagal attack)


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28. How do

sympathetics

affect the heart?

1. increases HR (+chronotropic effect)

-increases rate of pacemaker

depolarization- threshold is reached

sooner

- increased conduction through av node

-reduced duration of atrial and ventricular

myocyte action potentials

2. Increases force of contraction

(+inotropic effect)

68. How do thecardiovascular

centers in the

CNS work?

40. How does a

graph of the

Aorta differ

from the Vena

Cava in terms ofcompliance?

Compliance = Volume/Pressure

14. How does an

increase of

stroke volume

affect pulsepressure?

Pulse pressure increases

15. How does

decreased

arterial

compliance

affect pulse

pressure?

Increases pulse pressure

70. How does the

cerebral

ischemic

response work?

51. How is Nitric

Oxide made?

Synthesized in endothelial cells

L-Arginine > NO (by iNOS)

Stimulates guanylyl cyclase > increases

cGMP > vasodilation

Continually modulates basal vascular

tone

Responsible for-flow-induced vasodilation of exercise

-vasodilation of erection

-vasodilation of inflammation

41. How is Pulse

pressure related

to:

Stroke Volume

Arterial

Stiffness

Increased stroke volume increases pulse

pressure

Decreased arterial compliance increases

pulse pressure (as in aging)

113. Hypovolemic

shock- effects

56. In general what

are the

consequences of

vasoconstriction

in response to

sympathetic

stimulation

114. Management ofshock

Ensure adequate lung ventilation andprovide extra oxygen

Restore blood volume by infusion of blood

or other fluids

Use interventions that improve cardiac

performance


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33. Mechanism by

which NE and E

increase the

force of

contraction

In general, factors or drugs which

increase contractility do so by increasing

[Ca]i.

Increased iCa

increased rate of uptake of Ca into the SR

> increased stored Ca in SR

Inhibiting the Na-Ca exchanger

103. Neurogenic or

stress

hypothesis foressential

hypertension

61. Pathway of

angina

60. The pathway of

atheromatous

plaque to

cardiac

problems

45. Pathways of

Right ventricular

failure and Left

Ventricular

failure?

1. Pumps and

Exchangers

Na/K-atpase. Na out, K in

Na-H exchanger- Na in, H out

Na/Ca exchanger- 3Na in, 1 Ca out

Ca ATPase: pumps Ca back into the

sarcoplasmic reticulum.

107. Renin

Angiotensin

System in

hemorrhage

104. Salt

Imbalance/Renal

hypothesis of

essential

hypertension

7. Second DegreeHeart Block-

Mobitz Type I

PR interval gets progressively longer until

you miss an R. Conduction block is seen

in kids and athletes with increased vagal

tone.

Benign, due to conduction block in AV

node.


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8. Second

Degree Heart

Block- Mobitz

Type II

Every nth QRS is missing.

PR is constant.

2:1 heart block (every 2nd R is missing)

Dangerous and needs a pacemaker.

Loss of conduction is BEYOND AV node

5. Sinoatrial

Node action

potential

Phase 4. Pacemaker potential- slow diastolic

potential due to

Inward Na current if, then Inward Ca

current ICa

Phase 0. Rapid depolarization- L-type Ca

channels open. if are closing.

Phase 3. Repolariation- due to closing of Ca

channels and opening of K channels- ik

Phase 4. Pacemaker potential, Na if

channels open and membrane starts to

spontaneously depolarize again.

9. Third Degree

Heart Block

Fairly constant P-P intervals and relatively

constant R-R intervals but there is no

relationship between the P waves and QRS

complexes.

62. Treatment of

Angina

110. Treatment

strategies for

hypertension

105.Vascular

hypertrophy

12. VentricularFibrillation

Medical emergency- life-threatening.

Electrical chaos. No coordinated

ventricular contraction and cardiac output

and blood pressure falls with lethal

consequences. Treatment is DC

cardioversion.

Not useful force

111.What are

characteristicsof shock

94. What are

differences

between static

and dynamic

exercise?

17. What are

factors that

decrease

venous return?

Hemorrhage

Venodilation

16. What are

factors that

increase CVP?

1. Increased blood volume

2. Venomotor tone


8/13

42. What are some

factors that

increase CVP

and what are

some factors

that decrease

CVP?

Increase VR:

Increased blood volume

Increased venomotor tone.

Decrease VR:

Hemorrhage

Venodilation

112.What are the

categories of

shock?

109.What are the

consequences of

Hypertension?

64. What are the

different types

of exercise, and

whichhyperemia is

dominant?

Phasic, Dynamic exercise: eg running

-Active hyperemia is predominant

Isometric exercise: eg weight lifting-blood flow to exercising muscle impaired

-on termination of exercise > Reactive

hyperemia.

73. What are the

different ways

Angiotensin II

effects the

circulating

volume?

98. What are the

effects of age on

blood pressure

in terms of a

graph?

97. What are the

effects of age on

the CVS?

93. What are the

effects of

dynamic

exercise on BP?

Flow chart

39. What are the

effects of

exercise on the

pressure-volume

loop?

20. What are the

heart sounds

made by?

Splitting of

which is

pathological vs.

physiological?

Splitting of 1 is pathological- occurs in

conduction defects on 1 side of the heart

Splitting of 2 is physiological and is

enhanced in inspiration

19. What are the

mean pressures

during the

cardiac cycle


9/13

54. What are the

metabolic

vasodilators

66. What are the

principal

determinants of

blood pressure?

What are the

short term and

long term

controllers of

blood pressure?

Cardiac output and Venous return

Baroreceptor reflex- short term

-immediate responses to a change in BP

-minimizes normal daily fluctuation in BP

-returns BP to s urvival levels in the event

of a catastrophic change eg hemorrhage

Renin/Angiotensin system- long term

-maintain the effective circulating blood

volume over days or weeks

-involved in the long term control of MAP

46. What are the

starling forces

in relation tocapillary

pressures?

21. What are the

types of heart

murmers?

1. Incompetent- failure of the valve to seal

properly such that it becomes leaky

allowing blood to regurgitate through it

2. Stenosis- the open valve is narrowed so

that a higher pressure gradient is needed

to drive blood through.

100.What are the

types of

primary

hypertension?

"silent killer"

18. What are the

valve positions

during the

cardiac cycle?

Ventricularfilling,

isovolumetric

contraction,

ejection,

isovolumetric

relaxation

48. What

controls

vascular

tone?

Intrinsic and

extrinsic

mechanisms

Intrinsic- local factors.

-Myogenic Control

--autoregulation

-Metabolic control

--Endothelial secretions

--Metabolic vasodilators

--Autacoids

Intrinsic mechanisms mediate

Autoregulation and active and reactive

hyperemia.

Extrinsic Mechanisms

-ANS- Sympath/parasym

-Circulating hormones- Epinephrine,

angiotensin and vasopressin

Extrinsic mechanisms support the needs of

the whole organism. Involved in teh control

of MAP and TPR.

23. What does a

tricuspid or

mitral

incompetence

sound like?Mitral incompetence- pan systolic-

ventricular systole causes blood to regurgitatethru the mitral valve back into the LA

resulting in a murmur that extends

throughout the ventricular contraction =

pansystolic murmur.

22. What does an

aortic valve

stenosis

sound like

When the aortic valve is narrowed, flow

during the ejection phase becomes turbulent.

The murmur is heard during the ejectionphase of the ventricular cycle. The 1st heart

sound is normal, but during the ejection a

murmur is heard (systolic murmur) which

rises and falls as the ejection waxes and

wanes, loudest over the aortic area. S2 which

is the closure of the aortic valve should be

heard.


10/13

24.What does

aortic valve

incompetence

sound like?

If the aortic valve does not close completely,

blood will regurg back into the ventricle

during diastole. Actual turbulence is

upstream of the aortic valve. Murmur beginsat time of S2 and lasts through the early part

of diastole. S2 may be affected. Pulse pressure

is increased in this abnormality.

53.What does

Endothelin

do?

Vasoconstrictor.

High Endothelin levels found in:

-hypoxia

-pre-eclampsia of pregnancy

-cardiac failure

-cerebrovascular accidents

25.What does

mitral

stenosis

sound like?

Diastolic murmur-

blood is forced through the narrowest mitral

valve during the phase of ventricular filling-

ventricular diastole.

76.What factors

regulate CO?

91.What

happens

during

exercise interms of CNS

and Local

components?

Flow chart

92.What

happens

during

exercise with

the

sympathetic

discharge?

Flow chart

87. What happens

in phase 1 and

phase 2 of the

valsalva

maneuver?

88. What happens

in phase 3 and

phase 4 of a

valsalva

maneuver

96. What happens

in the diving

response?

90. What happens

to exercise as far

as requirements

and

cardiovascular

changes?


11/13

47.What happens

to Oncotic

pressure and

Hydrostatic

pressure across

a capillary?

Oncotic pressure pretty much stays the

same because the plasma protein levels

don't change and fluid volume in the

capillary changes are negligible.

Hydrostatic pressure changes because as

the fluid moves through the capillary it

encounters resistance, so the pressure

drops.

84.What happensto the Guyton

cross plot when

cardiac failure

occurs?

Cardiac contractility is reduced.

Fluid retention > increased blood volume.

Venoconstriction > vascular fxn curve isshifted upwards and MSFP increases.

Overall effect: Slight decrease in CO but

an increase in RAP.

Such CV changes are observed moderate

cardiac failure.

36.What happens

to the pressure

volume loop if

you increase

afterload?

37. What happens

to the pressure

volume loop if

you increase

contractility?

35. What happens

to the pressure

volume loop

when you

increase

EDV/Preload?

99. What happens

to your cvs when

you sleep?

85. What happens

upon standing

from a supine

position in a

flow chartformat?

74. What happens

when blood

volume

increases (use

bainbridge

reflex, ANF)


12/13

43. What happens

with the

Respiratory

pump?

89. What is a

clinical use of

the valsalva

maneuver?

What does a

graph look like

MAP and HR

during the

manoeuvre?

What happens

to BP and HR in

each phase?

101.What is

secondary

hypertension

due to?

3. PHeochromocytoma: increased release

of EPI, NE

4. Pre-eclampsia Toxema: increased BP of

pregnancy- they think it has to do with

endothelin but no one knows why

95. What is thealerting

response?

44. What is the

equation for net

filtration

pressure, and

what is the

mechanism for

fluid transport?

Osmosis.

Positive # favors filtration, Negative #

favors absorption.

38. What is the

ESPVR and in

what cases does

it change?

Changes with contractility

49. What is the

myogenic

response

86. What is the

overall effect of

standing from a

supine

position?

102.What is the

pathology of

hypertension


13/13

65. What keeps blood flow to the brain relatively constant?

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Physio Memory Cardiovascular