Cardiology 2 Flashcards

1
Q

how does atrial fibrillation appear on venous pressure wave?

A
  • -A-wave = LOST

- -C-wave = Prominent

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2
Q

split S2 sound physiologic explanation?

A

-deep breath in; decreases intrathoracic pressure. sucking more blood back to R side of heart; filling R side more than L side. So Right sided pulmonic valve closes later in systolic bc R side has more blood to eject.

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3
Q

what’s a gallop?

A

all four sounds together

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4
Q

In aortic pressure tracing, what is representative of aortic valve closing? what PHASE does this occur in?

A
  • dicrotic notch

- Phase 4 of cardiac cycle

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5
Q

what heart sound correlates with dicrotic notch?

A

S2 (it’s when aortic valve closes)

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6
Q

measure CO clinically with what principle?

A

FICK

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7
Q

what is Fick principle?

A

can know what the FLOW is, if you measure something being carried along with the FLOW, that can be extracted/added along with the flow.

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8
Q

what things are needed for Fick principle calc?

A
  • entrance to lung blood measure
  • sample blood on arterial side
  • rate of oxygen useage
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9
Q

what other methods/products can be used to implement the Fick Principle?

A

-indicator dye
(measure concentration at later point)
-thermodilution
(bolus of saline at different temp, measure temp at later point in circuit to back-calculate the flow)

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10
Q

normal CO?

A

3-5 L/min

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11
Q

how calculate cardiac index?

normal range?

A

CI = CO/BSA

2.5-4.2
L/min/m^2

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12
Q

muscle fiber length prior to contraction, which affects SV, is known as?

A

PRELOAD

-how much blood before

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13
Q

tension against which the muscle must contract?

A

AFTERLOAD

-how much pressure pushing against

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14
Q

intrinsic property of cardiac muscle that adjusts SV?

A

Contractility

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15
Q

Which Law addresses PRELOAD?

A

Laplace

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16
Q

what is the equation for law of laplace?

A

(for spherical chamber); tension in the wall is equal to pressure times the radius of the chamber; divided by 2*wall thickness

T=Pxr/2h

T = LVEDP*LVEDR/2h

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17
Q

what indicators (however unreliable) have been used to estimate SV?

A

PCWP and CVP

further from ventricle, more unknown things intervene

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18
Q

other methods?

A
  • PPV (pulse pressure variation)

- echo

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19
Q

Preload equals what?

A

TENSION

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20
Q

what factors affect PRELOAD?

A

(same as in law)

  • pressure
  • radius
  • wall thickness
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21
Q

Preload INVERSELY proportional to which variable

A

(2 x) the Wall thickness

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22
Q

End Diastolic filling pressure affected by

A
  • how much blood came back to fill
  • compliance of heart chamber
  • venous compliance
  • atrial contraction
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23
Q

end diastolic radius affected by what issue?

A

-dilated cardiomyopathy (decompensated)

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24
Q

tension developed in ventricle during PEAK systolic contraction

A

AFTERLOAD (what ventricle pushes against)

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25
Q

normal SVR?

A

900-1500 dynscm^-5

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26
Q

SVR formula?

A

SVR = 80*(MAP-CVP/CO)

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27
Q

what things affecet ventricular systolic pressure?

A

aka - output impedence

-SVR; Total periph resistance; total blood volume

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28
Q

normal PVR

A

50-150 dynscm^-5

PULMONARY

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29
Q

PVR formula?

A

80*(PAP-LAP/CO)

for PULMONARY

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30
Q

intrinsic ability of myocardium to generate force

A

contra

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31
Q

what is basic element that affects length-tension relationship in isometric contraction?

A

actin-myosin overlap

optimized

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32
Q

according to force velocity curve, if you INCREASE preload only, for same afterload (force generated), what happens to speed of shortening?

A

(see page 16 of Cardiology worksheet - Pass Machine)

  • -increase shortening velocity
  • -essentially ALL reach same max velocity

[ if you are stronger, you will lift things at a faster rate ]

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33
Q

if you increase INOTROPY, for same afterload (force), what happens to speed of shortening?

A

increases proportionately

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34
Q

how measure contractility?

A

rate change in time trace; SLOPE of curve. (dP/dT)

-covaries with rate, preload and afterload, however

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35
Q

what’s MAIN graph used to estimate contractility now?

A

Pressure-volume loop

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36
Q

what affects Pressure volume loop?

A

HEART RATE!

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37
Q

sympathetic stimulation of myocardial musc, what happens?

A
  • phosphorylate G-proteins, etc

- ALSO facilitate Calcium mobilization overall, so get greater RATE and FORCE of contraction.

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38
Q

contractility decreased by what things? (3 min)

A

1) anoxia
2) acidosis
3) catecholamines

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39
Q

what does increased contractility mean, based on same volume?

A

for given volume, can generate MORE pressure

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40
Q

what measure of the systolic function curve represents CONTRACTILITY?

A

slope of the systolic function curve (STEEPER SLOPE = increased contractility

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41
Q

diastolic function curve’s change in position represents what?

A

COMPLIANCE

more compliance can hold more vol and pressure not increase as much

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42
Q

which measurement represents total work/energy by cardiac muscles during cycle?

A

PVA = PE +SW
(pressure volume area)

PE=potential energy d/t stretch remaining in wall at end of systole

SW=stroke work (d/t contraction); work Ventricle is doing thru contraction and relaxation

43
Q

measure of work is represented by WHAT graphical representation on PV loop?

A

Work = PxV (area)

  • -STROKE WORK is normal shaded area btwn curves between isovolumetric lines and filling/ejection lines
  • -TOTAL work , is total area between two curves (under right side of loop)
44
Q

what other marker can be generally measured based on PVA (pressure volume area)?

A

MVO2

  • myocardial oxygen consumption
  • potential energy and stroke work
45
Q

how calculate ejection fraction?

A

EF = (EDV-ESV)/EDV

46
Q

at constant contractility, how do preload and afterload affect SV?

A
  • INCREASE preload INCREASE SV

- INCREASE afterload DECREASE SV

47
Q

ECG changes d/t Calcium are because?

A

secondary to altered trans-membrane potentials that affect conduction times

48
Q

Hypercalcemia on EKG?

A
  • MC finding = shortened QT interval 2ndary to shortened ST
  • widened or flattened T-wave
  • SIGNIFICANT HYPERCALCEMIA - can mimic acute MI
49
Q

Hypocalcemia on EKG?

-arrhythmias possible?

A

Intermittent QT prolongation (or QTc)

  • Torsades de pointes
  • VT
  • complete heart block
50
Q

what’s E/A ratio?

A

-extent to which heart fills normally

E = early diastolic filling
A = Atrial filling

SHOULD be faster E than A in normal heart

51
Q

what’s normal E/A?

A

0.8-1.2

52
Q

What are limitations of E/A ratio to diagnose diastolic dysfunction of heart?

A

-if A-fib, don’t have A-wave, cuz no atrial contraction

53
Q

what’s the PRIMARY determinant of myocardial oxygen demand?

A

HEART RATE

heart rate is only way to increase amount of oxygen since maximally extract already

54
Q

what is equation for pressure as it relates to Force and resistance?

A

(delta pressure) = FxR

55
Q

name of pressure equation for BP?

A

ohm’s law

flow version

56
Q

what happens to pressure that expended by ventricle once gets to greater cross-sect area?

A

pressure drops

57
Q

what component of the vascular tree accounts for the steady flow of pressure that travels to organs?

A

arterioles

58
Q

what substance do arterioles NOT have?

A

no elastic

59
Q

which blood vessels DON’T have any direct sympathetic innervation?

A

capillaries

60
Q

resistance equation for blood?

A

R = (8nL)/(pi x r^4)

L = vessel length
n = viscosity of blood
61
Q

alpha mediators do what to peripheral vessels?

A

vasoconstriction

62
Q

beta2 receptors mediate which action at peripheral?

A

vasodilation

63
Q

viscosity is measure of?

A

slipperiness between 2 layers of fluid

64
Q

blood viscosity is affected by what THREE things?

A

1) hematocrit (less hct decr viscos)
2) temp (more cool = more visc)
3) vessel radius

65
Q

viscosity in LARGE vessels relates to resistance how?

A

viscosity INDEPENDENT of Resist in LARGE vessels?

66
Q

viscosity in small vessels relates to resistance how?

A

viscosity decreases in very small vessels (???)

67
Q

laminar flow = ?

A

columns of fluid slide across each other without interaction; EFFICIENT

68
Q

turbulent flow?

A

disorganized flow; have NO linear relationship between driving pressure and FLOW

69
Q

how predict turbulence of fluid?

A

Reynold’s number

70
Q

Reynold’s equation?

A

Re = 2rv*p/n

r-radius
v-velocity
p-density
n-viscosity

71
Q

how is reynold’s number translated?

A

INVERSELY proportional to viscosity

more viscous you are, more likely you are to behave in laminar manner

72
Q

what NUMBER Reynold’s value correlates to laminar flow?

A

Re

73
Q

what percentage of blood is in PULMONARY circulation at any given time?

A

9%

74
Q

how much of circulation is in VENOUS system?

A

65% !!!!

75
Q

unstressed vs stressed volume in your body?

A

unstressed (venous blood; big compliance)

stressed (arterial blood under pressure)

76
Q

increased venous return how?

A
  • muscle pumping forces blood upward
  • respiratory pump (increased inhalation)
  • trendelenburg
77
Q

hydrostatic pressure vs osmotic pressure?

A
  • hydrostatic pressure (push out of vessel)

- oncotic pressure (pull into vessel)

78
Q

which pressure (oncotic vs hydrostatic) is greater at arterial end?

A

hydrostatic

79
Q

which vessel pressure is higher at VENOUS end?

A

oncotic

80
Q

lymphatic drainage/pump does what?

A

pick up extra fluid that was extravasated during blood travels

81
Q

how does permeability of capillaries affect flow?

A

(SEPSIS) increased permeability allows greater extravasation of fluid

82
Q

HOW calculate MAP?

A

(diast press + pulse press) /3

PP=SBP-DBP

83
Q

what law relates calculation of BP?

A

Ohm’s law

84
Q

Ohm’s law?

A

P=QR

85
Q

what three things control autonomics CENTRALLY?

A
  • hypothal
  • pons
  • medulla
86
Q

peripheral baroreceptors?

A
  • carotid baroreceptors

- aortic baroreceptors

87
Q

where aortic baroreceptors?

A

-in arch of aorta

88
Q

where are carotid baroreceptors?

A

at bifurcation of carotids

89
Q

how is afferent information carried about BP? (aortic)

A

Vagus nn

90
Q

how is afferent information carried about BP? (carotid)

A

Hering’s nerve (CN9)

91
Q

Inhalational that has LEAST depressant effect on baroreceptor response?

A

isoflurane

92
Q

what other function in Carotid and Aortic bodies also present?

A

-CHEMOreceptors

pH, Co2, O2

93
Q

what regulatory control centers are the signals ultimately sent to?

A

cardioregulatory and vasomotor control centers (IN MEDULLA OBLONGATA)

94
Q

initial controller/regulator of RAS?

A

kidney

(renin….which converts angiotensinogen [from liver] to angiotensin I

95
Q

angiotensin II does what things?

A

1) stimulates the release of aldosterone from ADRENALs (stim na reabsorption in distal tubules of kidney)
2) vasoconstrictor

96
Q

uncomplicated post-pregnancy reflex?

A
Bainbridge reflex
(autotransfusion from uterus)
97
Q

Bezold-Jarisch Reflex is from what?

A

response to noxious stimuli to ventricle

ex: ischemia

98
Q

what happens in Bezold-Jarisch reflex?

A

TRIAD:

  • hypotension
  • bradycardia
  • coronary artery dilation

(these all PROTECT the heart!!)

99
Q

Bainbridge reflex?

A

R atrium sense sudden INCREASE in VOL; inputs into medullary reg center to INCREASE HR

100
Q

oculo cardiac reflex?

A

pushing on your eye INCREASES PARASYMPATHETIC tone and BRADY

101
Q

how occulo-cardiac reflex travel?

A

ciliary nn —> ophthalmic division of TRIGEM –> gasserian ganglion

102
Q

gasserion ganglion from where? to where?

A

FROM - ophthalmic division of trigeminal

TO - parasympathetic centers

103
Q

tx of occulocardiac reflex?

A

-antimuscurinic (atropine or glycopyrrolate)