CV a&p Flashcards

1
Q

do skeletal myocytes or ventricular myocytes contain more mitochondria?

A

ventricular myocytes contain more mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

normal ventricular RMP and what regulates it

A

-90mV, regulated by potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does hypocalcemia and hypercalcemia do to threshold potential respectively?

A

hypocalcemia decreases TP (cells depol more easily bc its closer to RMP)
hypercalcemia increases TP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

the wave of depolarization throughout the heart is regulated by gap junctions or t tubules?

A

gap junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

equilibrium potential

A

no net movement across cell membrane. inside potential equals outside potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

which equation relates to equilibrium potential

A

nernst equation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

automaticity

A

ability to generate AP spontaneously ex) SA node and HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

excitability

A

ability to respond to electrical stimulus by depolarizing and firing an AP. ex) conduction and contractile CV cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

conductance

A

ability to transmit electrical current. ions are charged and therefore require an open channel.
open ion channel increases conductance of that ion (duh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

lusitropy

A

rate of myocardial relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

dromotropy

A

conduction velocity through heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

RMP is determined by 3 things

A

chemical force (concentration gradient)
electrostatic counter force
Na/K/ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the primary determinant for RMP

A

K. the nerve cell continually leaks this at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

decreased serum K makes RMP more

A

negative, cells become more resistant to depol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

increased serum K makes RMP more

A

positive, cells depol more easily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the primary determinant of threshold potential

A

calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

a cell depolarizes when what enters the cell

A

Na or Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what happens during repolarization

A

K leaves the cell or Cl- enters the cell
resistant to subsequent depol during refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

hyperpolarization

A

movement of cells membrane potential to a more negative value beyond baseline RMP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

purpose of Na/K/ATPase

A

restores ionic balance towards RMP
1. removes Na that enters the cell during depol
2. returns K that has left the cell during repot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

for every _______ ions the Na/K/ATPase pump removes, ___________ ions go back into the cell

A

for every 3 Na ions it removes, 2 K ions go back into cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what happens during cardioplegia with high K

A

Na channels get locked in their closed inactive state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

5 phases of myocyte AP

A

0: depol (Na in)
1: initial repol (K in, Cl- out)
2: plateau (K in, Ca2+ out)
3: repol (K out)
4: maintenance of trans membrane potential (K+ out and Na/K/ATPase fx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what’s the point of the plateau phase in a cardiac myocyte (that neurons dont have)

A

gives myocytes time to contract and eject SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

relation of myocyte AP to EKG

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

myocyte events during phase 0: depolarization

A

TP of -70 is met
activation of fast VgNa channels
slope indicates conduction velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

myocyte events during phase 1: initial repolarization

A

inactivation of Na channels
K and Cl- channels open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

myocyte events during phase 2: plateau

A

activation of slow VgCa channels counters loss of K to maintain depolarized state
delays repolarization
maintains fast Na channels in inactivated state
prolongs absolute refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

myocyte events during phase 3: final repol

A

k channels open, delayed rectifier
K leaves cell faster than Ca2+ enters- repol
slow Ca2+ channels deactivate
restores transmembrane potential to -90mV RMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

myocyte events during phase 4: resting phase

A

K leak channels open (to maintain RMP)
Na/K/ATPase (removes 3 Na gained during depol and replaces 2 K lost during repol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

channel that is the primary determinant of the pace makers intrinsic HR (SA node)

A

I-f (funny channels). sets rate of spontaneous phase 4 depol. funny channels are activated from hyper polarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

conduction of AP from SA node

A

SA–> internal tracts –> AV –> bundle of his –> left and right bundle branches –> purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

RMP of SA node

A

-60mV (higher than cardiac myocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

SA node AP in relation to EKG

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

order of SA node AP

A

phase 4
phase 0
phase 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

SA node events during phase 4: spontaneous depolarization

A

Na in (via I-f channels) and Ca2+ out via T type channels
at -50mV, t type Ca2+ channels open to further depol the cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

SA node events during phase 0: depolarization

A

Ca2+ in via L type channels
Na and T type Ca2+ channels close

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

SA node events during phase 3: repolarization

A

K channels open and K exits the cell making it more negative
K efflux repolarizes cell to return it to phase 4
repol decreases calcium conductance by closing L type calcium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

intrinsic firing rate of SA node

A

70-80 (faster in denervated heart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

intrinsic firing rate of AV node

A

40-60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

intrinsic firing rate of purkinje fibers

A

15-40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what 3 variables can we manipulate to alter HR?

A

rate of spontaneous phase 4 depolarization (slope increases like with NE admin)
threshold potential (TP becomes more negative, closer to RMP)
RMP (RMP becomes more positive, closer to TP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how does Ach slow HR

A

stimulates M2 receptor, increases K conductance and hyper polarizes SA node. decreases slope of phase 4 conduction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

baseline CaO2

A

20 mL/O2/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

baseline DO2

A

1000mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

baseline VO2

A

250mL/min or 3.5mL/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

baseline CvO2

A

15mL/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

DO2 equation

A

CO x [(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)] x 10
=CO x CaO2 x 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

CaO2 equation

A

(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)

50
Q

MAP equation

A

(CO x SVR)/ 80 + CVP

51
Q

poiseuilles law

A

Q= BF
R= radius
Pa-Pv is change in arterial pressure gradient
viscosity
l= length of tube

52
Q

when radius to the fourth power is tripled, what is the increase in flow

A

81 x increase

53
Q

when radius to the 4th power is quadrupled, what is the increase in flow

A

256 x increase

54
Q

SV equation and normal value

A

CO x (1000/HR)
50-110mL/beat

55
Q

EF equation

A

[(EDV-ESV)/EDV)] x 100 aka
SV/EDV x 100

56
Q

SVR equation

A

[(MAP-CVP)/CO] x 80

57
Q

CI formula and normal value

A

CO/BSA
normal: 2.8-4.2L/min^2

58
Q

SVI and normal value

A

SV/BSA
normal: 30-65mL/beat/m^2

59
Q

SVRi and normal value

A

(MAP-CVP)/CI x 80
normal 1500-2400 dynes/sec/cm-5 per m^2

60
Q

PVR equation and normal value

A

(MAP-PAOP)/CO x 80
normal: 150-250 dynes/sec/cm^-5

61
Q

PVRi and normal value

A

(MPAP-PAOP) x CI / 80
normal: 250-400dynes/sec/cm-5 per m^2

62
Q

surrogate measures of LVEDV

A

LVEDP, LAP, PAOP, CVP

63
Q

surrogate measures for ventricular output

A

CO, SV, LVSW, RVSW

64
Q

surrogate measures for EDV include

A

RVEDV
LVEDV

65
Q

describe how B2 increases contractility

A
  1. activation of more L type ca channels (more ca enters the cell)
  2. stimulation of ryanodine 2 receptor to release more Ca
  3. stimulation of SERCA 2 pump to to increase Ca uptake with subsequent Ca2+ release

net effect is more forceful contraction over shorter time with enhanced relaxation between beats

66
Q

SV is decreased by (3)

A

decreased preload
decreased contractility
increased afterload

67
Q

law of laplace equation in relation to wall stress

A

wall stress = intraventricular pressure x radius / ventricular thickness

68
Q

review the wiggers diagram (EKG, aortic pressure, LAP, LVP)

A
69
Q

review the left ventricular volume as it relates to left atrium, left ventricle, and mechanical events in the heart (wiggers diagram format)

A
70
Q

key events in isometric ventricular contraction

A

LVP>LAP
MV closes (first heart sound)

71
Q

key events in isometric ventricular relaxation

A

aortic pressure > LVP –> AV closes (2nd heart sound)

dichromic notch occurs here because AV closure initiates small retrograde flow that terminates when valve is all the way closed which is where the dichrotic notch happens

lusitropy: where Ca2+ is pumped back into SR

72
Q

two events that happen during systole include

A

isometric ventricular contraction and ventricular ejection

73
Q

name the 6 stages of the cardiac cycle and whether they belong to diastole or systole

A
  1. rapid filling (diastole)
  2. reduced filling (diastole)
  3. atrial kick (diastole)
  4. isovolumic contraction (systole)
  5. ejection (systole)
  6. isovolumic relaxation (diastole)
74
Q

when the LV is compliant, does LV filling increase pressure?

A

no, the LV should stay around 2-3mmHg during filling (until atrial kick that increases LVP to 5-7mmHg)

75
Q

what is the typical stroke volume

A

LVEDV-LVESV=
120-50=
70 is typical SV

76
Q

normal EF
mild dysfunction
moderate dysfunction
severe dysfunction

A

normal >50%
mild: 41-49%
moderate 26-40%
severe < or = 25%

77
Q

this pressure volume loop represents

A

increased preload (ex fluid bolus)
loop gets wider but returns to original ESV. SV increased

78
Q

this pressure volume loop represents

A

decreased preload (ex furosemide)
loop gets narrower but returns to original ESV. SV decreased.

79
Q

this pressure volume loop represents

A

increased contractility (ex B1)
loop gets wider, taller, and shifts to the left.

80
Q

this pressure volume loop represents

A

decreased contractility (ex HFrEF)
decreased SV, decreased chamber emptying, increased ESV. loop gets narrower, shorter, shifts to the right.

81
Q

this pressure volume loop represents

A

increased after load (ex acute HTN or phenylephrine)
decreased SV, decreased chamber emptying, increased ESV. loop gets narrower, taller, and shifts ESV to the right.

82
Q

this pressure volume loop represents

A

decreased after load (ex vasodilators such as Na nitroprusside)
increased SV, increased chamber emptying, decreased ESV. loop gets wider, shorter, shifts ESV to the right.

83
Q

which arteries arise from aortic root

A

LCA and RCA

84
Q

what does LCA divide into

A

LAD and circumflex

85
Q

what does LAD perfuse

A

anterolateral and apical walls of left ventricle as well as anterior 2/3 of intraventricular septum

86
Q

what does CXA perfuse

A

left atrium as well as lateral and posterior walls of LV

87
Q

what does RCA perfuse

A

RA, RV, inter arterial septum, posterior third of interventricular septum

88
Q

what does the posterior descending artery perfuse

A

inferior wall. origin of this vessel defines coronary dominance

89
Q

define right dominance

A

in 70-80% of patients, RCA gives rise to posterior descending artery

90
Q

define left dominance

A

circumflex or RCA and circumflex supply PDA which can also be defined as co dominance

91
Q

where do these conduction points receive blood supply from

A

SA and AV node usually get perfused by RCA
bundle of his and left bundle branches usually get perfused by LCA

92
Q

which artery runs alongside these veins
great cardiac vein
middle cardiac vein
anterior cardiac vein

A

great cardiac vein LAD
middle cardiac vein PDA
anterior cardiac vein RCA

93
Q

describe the thesbian veins

A

blood returning to left side of the heart by way of thesbian circulation contributes to small amount of anatomic shunt. volume of deoxygenated blood dilutes PaO2 of oxygenated blood that passes through lungs.

94
Q

go through coronary artery relation and EKG table

A
95
Q

best view (and second best view) for diagnosing LV ischemia for TEE

A

mid papillary muscle in short axis is first best
second best view is apical segment also in short axis

96
Q

ID these arteries

A
97
Q

coronary BF equation and normal value

A

coronary perfusion pressure / coronary vascular resistance
OR
aortic DBP - LVEDP

normal value: 225-250mL/min or 4-7% of CO

98
Q

at rest, myocardium consumes O2 at a rate of

A

8-10mL/min/100g with an extraction ratio of ~70%

99
Q

most important determinant of coronary vessel diameter

A

local metabolism

100
Q

MOA of adenosine at coronaries

A

potent coronary vasodilator and byproduct of ATP metabolism
as MVO2 increases, adenosine is released

101
Q

effect of histamine 1 at coronary arteries

A

increases Ca2+ and causes constriction

102
Q

effect of histamine 2 at coronary arteries

A

increased cAMP, decreased MLCK sensitivity to Ca2+

103
Q

which waveforms correlate with coronary perfusion for aortic pressure, LCA flow, and RCA flow

A

in LCA, flow is greatly diminished during systole
in RCA, blood flow is a little more constant because RV doesn’t generate a blood pressure high enough to occlude during systole

104
Q

how does decreased P50 influence O2 supply to myocardium

A

shifts curve to the left and decreases supply.

105
Q

factors that decrease coronary flow

A

decreased aortic pressure (less P1-P2 gradient) and vessel diameter
increased LVEDP

106
Q

how does increased aortic diastolic pressure affect supply and demand for coronaries/myocardium

A

increases supply and demand
increased aortic DPB increases LVEDP and coronary perfusion pressure
increased aortic pressure increases demand via wall tension and afterload

107
Q

how does increased preload influence supply and demand for coronaires/myocardium

A

decreased supply and increased demand
increased EDV decreases CPP
increased demand because increased preload increases wall stress

108
Q

general overview of 3 important pathways that influence calcium concentration in vascular smooth muscle

A
  1. G protein cAMP pathway –> vasodilation
  2. NO cGMP pathway–> vasodilation
  3. PLC pathway –> vasoconstriction
109
Q

effect of cAMP and PKA in VSMC’s versus cardiac myocyte

A

cardiac myocyte: PKA and cAMP increase intracellular calcium
VSMC: increased PKA decreases intracellular calcium

110
Q

steps in the NO cGMP pathway

A
  1. NOS (nitric oxide synthase) catalyzes conversion of L arginine to nitric oxide
  2. NO diffuses from endothelium to smooth muscle
  3. NO activates guanylate cyclase
  4. guanylate cyclase converts GTP to GMP
  5. increased cGMP increases intracellular Ca2+ leading to smooth muscle relaxation
  6. PDE5 activates cGMP to guanosine monophosphate
111
Q

activators of the PLC pathway include (4)

A

neo, NE, AT2, and endothelin 1

112
Q

NO production is increased by (7)

A

Ach, substance P, bradykinin, serotonin, vasoactive peptide (VAP), thrombin, shear stress

113
Q

list the following arteries in the correct order as they arise from the aorta (first being most proximal to aortic valve):
innominate
left SCA
L coronary artery
L common carotid

A
  1. left coronary artery
  2. innominate artery (brachycephalic)
  3. left common carotid
  4. left subclavian artery
114
Q

list the following vessels that arise from the transverse aortic arch from most proximal to most distal:
left common carotid
innominate (sometimes called brachycephalic)
left subclavian

A

most proximal: 1. innominate (sometimes called brachycephalic)
2. left common carotid
3. left subclavian

115
Q

Define frank starling curve and what influences it

A

relationship between ventricular volume and ventricular output

116
Q

a reduction of which factor would most likely augment SV

A

afterload

117
Q

best TEE view for diagnosing LV ischemia
and second best

A

mid papillary muscle level in short axis
apical segment also in short axis

118
Q

what does this graph represent

A

LCA flow through cardiac cycle (RCA flow is more constant)

119
Q

what does this graph represent

A

LCA flow through cardiac cycle (RCA flow is more constant)

120
Q

right vagus nerve and left vagus nerve innervate which nodes respectively

A

right: SA
left: AV