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TOPICSII > Exam 1 REVIEW > Flashcards

Exam 1 REVIEW Flashcards

1
Q

The conductive system consists of the following components

A

The sinoatrial (SA) node, the internodal tracts, the AV node, the AV bundle, and the Purkinje system

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2
Q

SA node primary pacemaker, rate

A

60-100

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3
Q

AV node only pathway between Atria and ventricles, rate

A

40-60

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4
Q

Small mass of specialized cells and collagenous tissue located along the epicardial surface

A

The SA node (the Keith-Flack node)

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5
Q

At the junction of the superior vena cava and the RA.

A

SA node

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6
Q

Three major internodal tracts exist:

A

the anterior, middle, and posterior internodal tracts.

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7
Q

The anterior internodal tract, or

A

Bachmann bundle

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8
Q

Sends fibers to the LA and then travels down

through the atrial septum to the AV node.

A

Bachmann Bundle

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9
Q

The middle internodal tract, or

A

Wenckebach tract,

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10
Q

Curves behind the superior vena cava before descending to the AV node.

A

Wenckebach tract,

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11
Q

Finally, the posterior internodal tract, or

A

Thorel tract,

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12
Q

continues along the terminal crest to enter the atrial septum and then passes to the AV node.

A

Posterior internodal tract

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13
Q

The AV node causes a

A

delay in the transmission of action potentials

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14
Q

Is the preferential channel for conduction of the action

potential from the atria to the ventricles

A

AV bundle

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15
Q

Where is the site with the greatest resistance to the transmission of action potential?

A

Within the AV node

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16
Q

Speed of conduction to adjacent cells within the SA is

A

0.5m/sec

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17
Q

Intrinsic PM cells of the AV node depolarizes at what rate

A

40-60

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18
Q

Conduction velocity from Bundle of his to left and right BBB is

A

Rapid 2m/sec

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19
Q

Purkinje system firing rate is

A

20-40 beats/min

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20
Q

Purkinje fibers velocity of impulse conduction

A

4m/sec (rapid velocity of impulse conduction) which allows for rapid depolarization of ventricular myocytes.

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21
Q

Necessary to inhibit actin and myosin from interacting and initiating muscle contraction

A

Troponin complex

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22
Q

When catecholamines interact with B1 receptors, they stimulate intracellular

A

G protein activation

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23
Q

Myocardium oxygen demand is determined by

A

preload, afterload, contractility and HR.

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24
Q

Myocardial oxygen supply is determined by

A 
Arterial blood content
Diastolic BP 
Diastolic time (as dtermined by HR)
Oxygen extraction 
Coronary Blood flow
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25
Q

HR affects both

A

Supply and demand

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26
Q

Increasing HR does what

A

Increases demand

decreases diastolic time

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27
Q

Diastolic filling time is

A

80-90 % coronary filling and myocardial perfusion occurs.

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28
Q

What is the most important factor that negatively affects ?

A

MvO2

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29
Q

Doubling the HR

A

Doubles MvO2

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30
Q

Primary substance responsible for coronary vasodilation is

A

Adenosine

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31
Q

Determinants of MvO2 include

A 
myocardial contractility
Myocardial wall tension (preload)
HR 
MAP 
Afterload
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32
Q

Oxygen extraction is determined by measurement of the

A

Difference between the oxygen tension in the pulmonary arterial blood and that in the coronary sinus.

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33
Q

Arterial Oxygen content equation (CaO2) =

A

(SaO2 x Hgb, 1.34) + 0.003 x PaO2

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34
Q

Under normal physiologic conditions, the coronary circulation, like other tissues beds in the body, exhibits

A

Autoregulation

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35
Q

Autoregulation is the

A

ability to maintain coronary blood flow across a range of MAP by dilating or constricting.

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36
Q

Coronary blood flow is maintained at a constant flow rate through a MAP range of

A

60-140 mmHg.

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37
Q

Autoregulation: When arterial pressure is less or exceed these pressure limits what happens?

A

Coronary blood flow becomes pressure dependent.

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38
Q

Autoregulation: During HYPOTENSION, when the coronary arteries are

A

maximally dilated, coronary blood flow is determined by MAP - RAP

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39
Q

Where is the SA node located?

A

Junction of RA and VC

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40
Q

AV node depends on________ for propagation of action potentials

A

L-type Calcium channels

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41
Q

Ions is the major determinant of the resting membrane potential.

A

Potassium

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42
Q

Cardiac muscle fibers resemble skeletal muscle fibers in that they are_______ they differ in that they form_______ a, which means that all fibers are electrically connected via

A

striated; functional syncytium;gap junctions.

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43
Q

Normal Coronary Perfusion Pressure is

A

60-160 mmHg

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44
Q

Normal EF

A

= 60-70%

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45
Q

Normal MAP =

A

70-105 mmHg

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46
Q

Normal SVR =

A

800-1500 dynes/sec/cm^5

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47
Q

Normal PVR =

A

150-250 dynes/sec/cm^5

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48
Q

Normal CI =

A

2.8 – 4.2 L/min

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49
Q

Factors that increases myocardial oxygen demand:

THS inWACEd

A 
Tachycardia
HTN
SNS stimulation
  increased : 
Wall tension
Afterload
Contractility
EDV
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50
Q

Factors Decreases myocardial oxygen demands

A

Decrease coronary blood flow (tachycardia, Decreased aortic pressure, decreased vessel diameter, increase EDP

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51
Q

Decreased CaO2 caused by

A

Hypoxemia, Anemia

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52
Q

Decreased Oxygen Extraction caused by

A

Left shift of Hgb dissociation curve: decreased p50, Decreased capillary density

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53
Q

Affect both sides of the supply/demand equation (HAP)

A

HR
Aortic diastolic pressure
Preload.

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54
Q

Which factor most negatively affects myocardial oxygen consumption?

A

HEART RATE

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55
Q

How does Tachycardia affect supply?

A

A shorter diastolic time means that there is less time to deliver oxygen to the L ventricle.

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56
Q

LV subendocardium Best perfused during

A

Diastole

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57
Q

Why is RV subendocardium not affected?

A

The RV usually isn’t affects, because it is well perfused throughout the cardiac cycle.

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58
Q

How does Tachycardia increases demand?

A

Cardiac contraction and relaxation require ATP, therefore increase the number of cardiac Cycles per minutes increases ATP and oxygen utilization

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59
Q

How does INCREASE Aortic diastolic pressure affect supply/demand?

A

Increase supply and demand

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60
Q

How does supply increases with increases aortic diastole pressure?

A

Increase in aortic pressure increase the pressure head that perfused the coronary artery (P1-P2)

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61
Q

Increase aortic DBP – LV EDP =

A

Increased Coronary Perfusion pressure.

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62
Q

How does demand increases with increases aortic diastole pressure?

A

An increased in aortic pressure also increases wall tension and afterload. The myocardium requires more Oxygen as it generates a higher pressure to open the aortic valve.

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63
Q

As a general rule the benefits of a increase coronary perfusion pressure

A

outweighs the drawback of an increase wall tension

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64
Q

How does an increased preload affect supply/demand?

A

Increase preload decrease supply and increase demand

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65
Q

How does an increase in preload decrease supply?

A

Increase EDV decreases coronary prefussion pressure
Because of the CPP formula
CPP = Aortic DBP - (increased) LVEDP = decrease CPP

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66
Q

How does an increase in preload increase demand?

A

Increase preload increases wall stress.

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67
Q

Most determines coronary blood flow is

A

myocardial metabolism

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68
Q

VALLEY: Myocardial Oxygen demand: 4 factors determine

A

1) Heart rate
2) Diastolic wall tension (preload)
3) Systolic wall tension (afterload)
4) Contractility

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69
Q

Myocardial oxygen demand is affected by the following important factors:

A

(1) HR; (2) ventricular wall tension (as determined by preload, afterload, and wall thickness); and
(3) myocardial contractility

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70
Q

The rate of myocardial oxygen consumption (MvO2) increases with

A

increases in HR, increases in wall tension, and increases in contractility.

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71
Q

The rate of MvO2 generally decreases with a

A

decreasing HR, decreasing wall tension, and decreasing contractility.

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72
Q

As stated previously, the rate of myocardial oxygen extraction is quite high; further increases in metabolic demand are met primarily by

A

an increase in coronary blood flow.

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73
Q

Tachycardia increases myocardial

A

oxygen demand

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74
Q

Only site where impulse travels to pass from atria to ventricles is the

A

AV node

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75
Q

Conduction velocities from fastest to slowest:

A

a) Purkinje fibers (4m/s)
b) Ventricular myocytes (1m/s)
c) Atrial myocytes (1m/s)
d) Bundle of His (1m/s)
e) SA and AV nodes (0.01-0.02 m/s)

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76
Q

Phase 4 of SA nodal action potentials is generated in part by

A

Funny” currents produced by inward movement of positively charged ions

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77
Q

The duration of the effective refractory period in cardiac cells can by increased by

A

inhibiting potassium channels

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78
Q

Normal SV

A

50-110 ml/beat

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79
Q

Normal SVI

A

30-65ml/beat/m^2

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80
Q

Normal pulse pressure is

A

40 mmHg

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81
Q

Normal SVR Index (SVRI)

A

1500 - 2400 dynes/sec/cm^5/m^2

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82
Q

Normal PVR Index (PVRI)

A

250-400 dynes/sec/cm^5/m^2

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83
Q

Slopes of the graph indicates

A

Conduction velocity

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84
Q

Absolute refractory period represent what on EKG?

A

QT interval

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85
Q

Relative refractory period represent what on EKG?

A

End of T wave

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86
Q

Current responsible for slow phase 4 depolarization in SA node?

A

I-f (funny current)

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87
Q

Cardiac action potential sequence

A

SA node –>Internodal tract –> AV node –> Bundle of HIS –> left and Right Bundle Branches –> Purkinje fibers.

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88
Q

Conduction velocity in non-nodal cardiac cells is decreased by doing what?

A

by decreasing the slope of phase 0

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89
Q

A patient who has mitral valve stenosis. Which of the following occurs as they exercise?

A

Increased Pulmonary capillary wedge pressure (PCWP)

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90
Q

Valve defects is not associated with an increase in PCWP

A

– PULMONIC VALVE STENOSIS

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91
Q

Stenotic aortic valve and PCWP:

A

Elevated pulmonary capillary wedge pressure

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92
Q

Aortic valve regurgitation and SV

A

Increase LV stroke volume

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93
Q

Responsible to keep the TMP

A

Na-K+ ATPases PUMP

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94
Q

NA-K ATPase ions movement

A

3 Na+ out

2 K+ in

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95
Q

Explain receptor activation

A

Receptor –>G protein–> Effector –> 2nd Messenger –>intracellular action

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96
Q

When myocytes reach about −70 mV (“threshold”),

A

fast sodium channels open and an influx of sodium

ions increase the membrane potential to +30 mV (phase 0).

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97
Q

DO2 Formula

A

CO x {(HgbxSaO2x1.34) + (PaO2 x0.003)} x10

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98
Q

Normal CaO2

A

20ml/dL

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99
Q

Normal DO2

A

1000 ml/min

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100
Q

Normal Oxygen Extraction Ratio

A

25%

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101
Q

Normal VO2

A

250 ml/min

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102
Q

Normal CvO2 (venous oxygen content)

A

15 ml/dL

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103
Q

Blood flow relationship to hematocrit

A

Inversely proportional

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104
Q

Ventricular myocytes Resting Membrane potential is

A

-90mV

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105
Q

Nodal Tissues Resting membrane potential is

A

-60mV

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106
Q 
5 Phases of  FAST ventricular action potential and ionic movement during each phase
Phase 0 =
Phase 1 =
Phase 2 =
Phase 3 = 
Phase 4=
A

5 Phases of FAST ventricular action potential and ionic movement during each phase
Phase 0 = Depolarization  Na+ influx
Phase 1 = Initial repolarization  K+ efflux and Cl- influx
Phase 2 = Plateau  Ca2+ influx
Phase 3 = repolarization  K+ efflux
Phase 4= Na/K ATPase restore resting membrane potential

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107
Q

On the other hand, slow action potentials utilized by cells of the SA or AV node yield a similar result but lack the

A

phase 1 and 2 components

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108
Q

3 phases of the SA node action potential and the ionic movement during each phase
Phase 4=
Phase 0 = Depolarization  Ca2+ influx
Phase 3 = Repolarization  K+ efflux

A

Phase 4= Spontaneous depolarization: Leaky to Na+ (Ca2+ influx occurs at the very end of phase 4)
Phase 0 = Depolarization : Ca2+ influx
Phase 3 = Repolarization: K+ efflux

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109
Q

Nodal tissues have 2 types of leaky channels

A

Both sodium and potassium leaky channels

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110
Q

Phase 4 depolarization is fastest in the_____less than fastest in the ______SLOWEST in______

A

SA node, AV node; purkinje fibers

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111
Q

What ion controls the RMP →

A

Potassium ions control RMP

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112
Q

SA node: What ion controls the Threshold Potential?

A

Calcium controls the threshold potential

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113
Q

Hypokalemia and excitability?

A

decreased excitability, RMP becomes more polarized (HYPERPOLARIZED ) like -80mV or -90mV (the difference between the resting and the threshold potential increases making the tissue less excitable.

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114
Q

Hypokalemia relationship with excitabilty

A

Directly proportional

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115
Q

Hyperkalemia and excitability?

A

Hyperkalemia increased excitability, RMP become less polarized (depolarized) like -30 numbers. The difference between the resting potential and the threshold potential decreases, THEREBY MAKING it more excitable

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116
Q

Hypocalcemia and excitability ?

A

increases membrane excitabiliy (Decrease stability) The TP increases becomes more negative. The RMP and the TP approach each other, and nerve and cardiac cells become more excitable.

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117
Q

Excitability of nerve and muscle is increased when.

A

hypocalcemia is present

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118
Q

As Calcium levels increases, excitability

A

Decreases.

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119
Q

P-wave represents

A

atria depolarization

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120
Q

T wave represents

A

ventricular repolarization

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121
Q

Most diastolic ventricular filling occurs

  • Phases part of systole  Phase 2 - Isovolumetric contraction Phase 3 - Rapid Ejection Phase 4 - Reduced Ejection Isovolumetric Relaxation  Pasive filling (diastasis)
  • During what phase of the cardiac cycle does most of ventricular filling occur? Phase 6 Rapid filling.
  • The first heart sound signifies closure of which heart valves? Closure of the AV valves
  • The second heart sound signifies closure of which heart valves? Aortic and pulmonic valves.
  • Ejection phase is complete with closure of the semilunar valves and the start of the relaxation phase. On the ECG, this represents the ST segment
  • A dicrotic notch would be detected on the arterial waveform to indicate the closure of the aortic valve
  • Preload is also the same LVEDV.
  • Curve shift to the left means decrease EDV
A

passively before atrial contraction.

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122
Q

Contraction of atria contributes

A

20-30% of the ventricular filling

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123
Q

a Wave is

A

Atrial systole

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124
Q

c Wave is

A

Ventricular systole

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125
Q

C wave is displayed due to

A

Bulging of the tricuspid valve into the right ventricle.

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126
Q

V venous return before

A

AV valves open again VENOUS RETURN

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127
Q

Phases part of Diastole (4 phases)

A

Isovolumetric Relaxation
Rapid ventricular filling
Reduced (Passive filling) (diastasis)
Atrial systole.

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128
Q

Phases part of systole

A

Isovolumetric Ventricular contraction

Ventricular Ejection

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129
Q

During what phase of the cardiac cycle does most of ventricular filling occur?

A

Phase 6 Rapid Ventricular filling.

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130
Q

The first heart sound signifies closure of which heart valves?

A

Closure of the AV valves

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131
Q

The second heart sound signifies closure of which heart valves?

A

Aortic and pulmonic valves.

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132
Q

-Ejection phase is complete with

A

closure of the semilunar valves and the start of the relaxation phase.

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133
Q

EJECTION pHase: On the ECG, this represents the

A

ST segment

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134
Q

A dicrotic notch would be detected on the arterial waveform to indicate the

A

closure of the aortic valve

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135
Q

Preload is also the same

A

LVEDV.

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136
Q

Curve shift to the left means

A

decrease EDV

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137
Q

Curve to the right

A

Increased preload

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138
Q

Curve to the left

A

Increase contractility

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139
Q

Filling phase has 2 phases: rapid phase

A

rapid phase based on the pressure gradient comprising 75% of blood volume, and (2) the slower active atrial systole phase (“atrial kick”) accounting for the remaining (25%) blood volume.

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140
Q

Most vulnerable to ischemia is the subendocardium why?

A

because it has the greatest metabolic demands and is most compressed (NO BLOOD FLOW) during SYSTOLE

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141
Q

The Subendocardium has the

A

densest network of capillaries.

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142
Q

LV subendocardium is best perfused during diastole. As aortic pressure increases, the LV tissue

A

compresses its own blood supply and reduces blood flow.

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143
Q

The high compressive pressure in the LV subendocardium coupled with a decreased coronary artery blood flow during systole increase

A

coronary vascular resistance and predispose this region to ischemia

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144
Q

Aortic Stenosis , goal Heart rate

A

Slow to normal (SINUS RHYTHM)

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145
Q

Aortic Stenosis, goal preload

A

Increase (you don’t want low BP ever) because valve is already stenotic, you need enough volume to pass _)

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146
Q

Aortic stenosis where do you want SVR and contractility

A

Maintain normal

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147
Q

Aortic stenosis where do you want PVR?

A

AVOID Increase

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148
Q

Aortic stenosis avoid 2 things

A

Tachycardia

Increase PVR

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149
Q

Aortic Regurgitation goal HR : avoid

A

AVOID bradycardia and increase in SVR

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150
Q

Aortic regurgitation : SVR: Where do you want it

A

You want Decrease in SVR

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151
Q

Aortic regurgitation :preload

A

Same to elevated (maintain intravascular volume)

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152
Q

Aortic regurgitation :PVR and contractility

A

Maintain

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153
Q

Mitral Stenosis: HR where do you want it?

A

Slow NSR

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154
Q

Mitral stenosis PVR

A

Avoid increase

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155
Q

Mitral stenosis maintain

A

SVR, preload, contractility

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156
Q

Mitral stenosis : THIS condition must be treated aggressively and how?

A

Atrial fibrillation ; Cardioversion

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157
Q

Mitral regurgitation : Mitral insufficiency HR where do you want it

A

Elevated

158
Q

Mitral regurgitation : avoid this

A

Increase in PVR

159
Q

2 conditions that benefit from Tachycardia

A

MR

AR

160
Q

Holodiastolic descrescendo murmur is

A

Mitral stenosis

161
Q

AS hypotension should be avoided due to

A

Decrease in CPP

162
Q

Aortic regurgitation avoid what kind of medications?

A

Alpha agonists, the increase afterload and reflex bradycardia will make the regurgitant condition worst? because it will increase SVR and slow HR

163
Q

Mitral regurgitation avoid: 3 conditions (HAH)

A

Hypoxia
Hypercabia
ACidosis

164
Q

Mitral regurgitation treat hypotension with

A

EPHEDRINE

165
Q

Chronic increase in pressure leads to

A

PCP (pressure - Concentric Hypertrophy - Parallel saracomeres)

166
Q

Chronic increase in volume leads to

A

VES (Volume- Eccentric Hypertrophy –Series)

167
Q

A 60-year-old female with mitral stenosis has the following post-induction vital signs: HR 125, BP 70/45
followed by sudden supraventricular tachycardia (SV). What will you do first?

A

Cardioversion

168
Q

In which valvular disease is the pulmonary capillary wedge pressure (PCWP) an overestimation o the left
ventricular end-diastolic pressure (LVEDP)?

A

MITRAL STENOSIS

169
Q

Which pathologic state will not cause giant, “cannon” a-waves on the CVP wave form?

A

TRICUSPID REGURGITATION

170
Q

What is the goal of hemodynamic management for the patient with mitral stenosis?

A

MAINTENANCE OF NORMAL SINUS RHYTHM

171
Q

Mitral stenosis is associated with left atrial and pulmonary hypertension due to the

A

stenotic transvalvular pressure gradient.

172
Q

The patient with mitral stenosis has impaired

A

left ventricular filling

173
Q

An adult patient with moderate aortic regurgitation receives a spinal anesthetic. A blood pressure drop to 68/42 is treated with 100 μg o phenylephrine. How will this dose impact the patient’s underlying disease state?

A

It will exacerbate the regurgitation.

174
Q

Which valvular disorder leads to the largest ventricular volume?

A

AORTIC REGURGITATION

175
Q

Which valve disorder most likely predisposes a patient to coronary ischemia with hypotension?

A

AORTIC STENOSIS

176
Q

Which risk actor contributes to myocardial ischemia in a patient with aortic regurgitation?

A

Heart rate 110-120 beats/minute

177
Q

What arterial line waveform might you observe in a patient with severe aortic regurgitation?

A

(C) Pulsus bisferiens

178
Q

What compensatory mechanism is commonly seen with aortic regurgitation?

A

(A) Eccentric hypertrophy (because of volume overload)

179
Q

In which valvular disorder is the left ventricular volume approximately normal, but left ventricular pressure higher than normal?

A

Mitral regurgitation

180
Q

What increases stroke volume?

A

Increased Ventricular EDV

181
Q

Mitral regurgitation, in general, factors such as _____HR AND ______SHOULD BE AVOIDED

A

slow heart rate and acute increases in afterload should be avoided

182
Q

Which actors will exacerbate mitral regurgitation?

A

Bradycardia and acute increases in afterload.

183
Q

With which patient would the anesthetist most want to maintain spontaneous ventilation?

A

AORTIC STENOSIS

184
Q

What is the goal of hemodynamic management of the patient with severe mitral valve regurgitation under general anesthesia?

A

AFTERLOAD REDUCTION (maintain forward flow)

185
Q

AVOID (HAH) → HYPOXIA, HYPERCARBIA and ACIDOSIS

A

MITRAL REGURGITATION

186
Q

MITRAL Stenosis how to avoid Pulm. HTN?

A

minimize pulmonary HTN (avoid hypoxemia, hypercarbia, acidosis, hypothermia)

187
Q

Coronary blood flow is autoregulated between

A

MAP of 60-140 mmhg .

188
Q

Role of autoregulation ?

A

This allows a constant coronary blood flow over a wide range of BPs. When MAP falls below the range of autoregulation , coronary perfusion becomes entirely dependent on coronary perfusion pressure.

189
Q

When MAP falls below the range of autoregulation , coronary perfusion becomes entirely dependent on

A

coronary perfusion pressure.

190
Q

Autoregulation is the NET effect of 3 things:

A

Local Metabolism
Myogenic Response
ANS

191
Q

Autoregulation? What is the most important determinant of coronary vessel diameter?

A

Local metabolism

192
Q

Autoregulation: ADENOSINE is a

A

byproduct of ATP metabolism and is a POTENT CORONARY VASODILATOR.

193
Q

Autoregulation: As MVO2 increases, the coronary endothelium release as

A

adenosine as well as a variety of other vasodilator substances including NO, prostaglandins, hydrogen, potassium and CO2.

194
Q

Autoregulation: Note the HYPOCARBIA causes.

A

coronary vasoconstriction

195
Q

Autoregulation: As MVO2 increases, the tissue has a mechanism to

A

increase its own blood flow.

196
Q

Autoregulation: Vasodilation decreases

A

vascular resistance, increases coronary perfusion and flushed out products of metabolism

197
Q

Autoregulation: What is the myogenic response?

A

It’s the vessel’s innate ability to maintain a constant vessel diameter.

198
Q

Autoregulation –>With myogenic response: When the vessel’s diameter is increased, it will have the tendency to and

A

contract,

199
Q

Autoregulation –>With myogenic response when the diameter decreases, it will have a tendency to

A

dilate.

200
Q

Autoregulation : ANS =>

A

Can affect coronary vascular tone, although the effects are overshadowed by the products of local metabolism.

201
Q

There are times when the ANS effects

A

prevail. For examples in patients with PRINZMETAL angina (Vasospastic myocardial ischemia ) are believed to have overactive coronary alpha receptors that can cause intense vasoconstriction and chest pain.

202
Q

Substance that Causes Coronary Artery Constriction how?

A

Alpha (epicardial) and HISTAMINE-1

Increase IP3 increases, Increase intracellular Calcium

203
Q

Causes Coronary Artery Dilation - Beta 2

A

Beta-2 (endocardial) -> Increases cAMP -> Decrease intracellular Ca2+

204
Q

Causes Coronary Artery Dilation - Histamine 2

A

Increases cAMP -> Decrease intracellular Ca2+

205
Q

Causes Coronary Artery Dilation

A

Muscarinic –> Increases NO

206
Q

3 substances causing coronary artery dilation

A

Beta-2
Histamine-2
Muscarinc

207
Q

Metabolic coronary vasodilation in response to enhanced myocardial oxygen consumption during exercise occurs, at least in part, as a result of

A

enhanced local release of metabolic substrates (e.g., adenosine, ADP) combined with sympathetic nervous system stimulation of the coronary vasculature.

208
Q

CO definition:
HR is controlled by the spontaneous depolarization of the sinoatrial (SA) node (which is controlled by the autonomic nervous system), SV is a function of the following
four factors: (1) preload; (2) afterload; (3) contractility; and (4) wall motion abnormalities.

A

defined as the volume of blood pumped systemically by the left ventricle each minute.

209
Q

The SV usually ranges between

A

70 and 120 mL

210
Q

CO men vs women:

A

CO of 5.6 L/min in men and 4.9 L/min in women

211
Q

Formula CO=

A

HR x SV

212
Q

Both HR and SV are (relationship)

A

directly proportional to CO, such that increases in either the HR or the SV produce an increase in CO

213
Q

HR is controlled by the

A

spontaneous depolarization of the sinoatrial (SA) node (which is controlled by the autonomic nervous system)

214
Q

Spontaneous depolarization of the sinoatrial node controlled by the

A

ANS

215
Q

SV is a function of 4 factors

A

Preload
Afterload
Contractility
Wall motion abnormalities.

216
Q

Preload is described with the

A

Frank Starling Mechanism

217
Q

Afterload →

A

Ventricular wall tension during systole approximate ventricular afterload

218
Q

SV and afterload have what kind of relationship

A

inversely proportional

219
Q

Contractility

A

The sympathetic nervous system has the most profound effect on myocardial contractility as the sympathetic adrenergic fibers release norepinephrine, which stimulates the myocardial beta-1 adrenergic receptors to enhance contractility and CO

220
Q

Which has the most profound effect on myocardial contractility?

A

SNS

221
Q

Basic components of the circuit?

A
  1. Venous reservoir
  2. Oxygenator
  3. Heat exchanger
  4. Main pump
  5. Arterial filter
  6. Tubing -> venous blood to the venous reservoir.
    Tubing –> oxygenated blood back to the patient.
222
Q

CPB priming

A

CBP circuit must be primed with typically 1200-1800 ml free of bubbles

223
Q

Reservoir is placed

A

Below the level of the patient to allow for gravity drainage.

224
Q

Reservoir serves at the

A

Large mixing chamber for all blood return.

225
Q

The amount drain to reservoir is a factor of

A

CVP
Gravity
Resistance found in circuit

226
Q

Arterial pump function:

A

Pull blood from reservoir

Driving it through the oxygenator (gas exchanger: artificial lung, a heat exchanger, and arterial line filter)

227
Q

Oxygenated warm blood return to patient’s arterial system via an

A

Arterial line positioned in the ASCENDING AORTA

228
Q

Preferred cannulation method is:

A

Aorto-atriocaval cannulation

229
Q

CPB is associated with

A

Severe inflammatory response becauce of contact of blood with nonendothelial extracorporeal surface.

230
Q

CPB response lead to

A

Platelet, endothelium, leukocyte activation, initiation of the coagulation cascade, decrease levels of coargualtion factors.

231
Q

Aorto-atriocaval cannulation : the blood is drained from

A

The right atrium and returned to the ascending aorta.

232
Q

Roller pump : Flow and air

A

continuous pulsatile flow ; MAY ENTRAIN AIR

233
Q

Centrifugal Pumps Advantages:

A

Less traumatic to blood than roller pumps

Centrifugal pumps DO NOT ENTRAIN AIR IN PATIENT

234
Q

Centrigugal pumps is between the

A

Oxygenator and the VENOUS RESERVOIR.

235
Q

Disadvantage of centrifugal pumps:

A

NO well defined volume

236
Q

Five major functions of CPB:

-

A 
Circulation of blood
Oxygenation
Ventilation
Systemic cooling, rewarming
Diversion of blood from the heart to provide a bloodless surgical field.
237
Q

The CPB allows the surgeon

A

to operate on a non-beating heart in the setting of a bloodless field while maintaining adequate whole body tissue oxygenation and perfusion.

238
Q

What is the Role of the LV vent?

A

LV vent removes blood from the LV. This blood usually comes from the Thebesian veins and bronchial circulation (anatomic shunt)

239
Q

Which patient is most at risk or catastrophic bleeding upon midline sternotomy?

A

Patient with previous coronary artery bypass grafting undergoing mitral valve repair

240
Q

In general, one should wait how long after heparinization before initiating CPB

A

3-5 minutes (after heparinization)

241
Q

For inintiation of CPB ACT should be >

Heparin 300-400 units /kg

A

400 seconds

242
Q

Should be given prior to cannulation? and why?

A

Heparin; decrease risk of thrombosis in both the patinet and the CPB circuit

243
Q

What cannulation is achieve first?

A

Arterial cannulation first (ascending aorta)

244
Q

Heparin dose

A

300-400 units/kg

245
Q

Primary method of myocardial protection during CPB remains

A

the administration of CARDIOPLEGIA and the institution of hypothermia

246
Q

Anterograde Cardioplegia: is catheter placed in the

A

Proximal Aorta between aortic clamp and aortic valve

247
Q

Retrograde Cardioplegia: Catheter place in the

A

Coronary sinus. (used for patient with aortic pathologies)

248
Q

Myocardial temperature monitored, wanted myocardial temperature

A

directly 10-15C desired

8-10 C nagelhout

249
Q

Cardioplegia solutions, 2 types

A

Potassium-rich crystalloid or blood-crystalloid solutions.

250
Q

Cardioplegia must be

A

repeated every 30 minutes

251
Q

CARDIOPLEGIA → leads to

A

High K+ , depolarization and cardiac arrest.

252
Q

Cardioplegia is indicated when the

A

aortic cross-clamp is in place because there is no coronary blood at the time.

253
Q

Cardioplegia leads to electrical

A

silence and mechanical silence, reduces Myocardial O2 demand by more than 80%.

254
Q

Bicarbonate is given for buffering

A

excess acid metabolites on bypass

255
Q

Mannitol to reduce

A

edema

256
Q

Potassium for

A

arresting the heart, blood or/and crystalloid as carrier

257
Q

Magnesium is given to

A

Reduce calcium overload

258
Q

Anterograde is delivered to the ____system

A

ARterial

259
Q

Retrograde: Must be

A

monitored, High pressure limit is 40 mmhg in order to avoid hemorrhage from damage to the coronary sinus, and venous systems.

260
Q

Cardioplegia: MOST CASES, A combination of

A

ANTEROGRADE and RETROGRADE is USED for the most complete coverage and protection of the myocardium

261
Q

Dosing of cardioplegia is every ___minutes OR when

A

20 ; cardiac activity is observed.

262
Q

Hypothermia to ____reduces______by _______

A

27C reduces O2 requirements by approximately 60%. Benefits,

263
Q

Hypothermia and SVR

A

increase in SVR caused by hypothermia may offset the decrease in SVR associated with hemodilution alone.

264
Q

3 main good effects of hypothermia:

A

a) Hepatic blood flow and enzymatic activity are decreased, reducing clearance of drugs eliminated by this route
b) Myocardial preservation is enhanced
c) CNS protection

265
Q

2 key steps prior to initiating CPB →

A

Anticoagulation AND Vascular cannulation

266
Q

Onset of Bypass and BP

A

Transient hypotension (MAPs as low as 30 mm Hg) is common following initiation of CPB, and should not be treated unless prolonged.

267
Q

The predominant cause of hypotension following initiation of CPB is

A

decreased SVR (secondary to reduced blood viscosity, dilution of endogenous catecholamines in priming solution, and differences in pO2, pH, and electrolyte concentrations between the priming solution and native blood).

268
Q

What should the activated clotting time be prior to initiation of cardiopulmonary bypass (CPB)?

A

> 400 seconds

269
Q

A 100-kg patient is administered 40,000 units of heparin. Five minutes later the AC was measured to be 182 seconds. What is the next step?

A

Administer two units of fresh frozen plasma( contains antithrombin III)

270
Q

Your patient is undergoing an elective coronary artery bypass graft (CABG). The patient was managed on heparin therapy or five days preoperatively. The patient is now on cardiopulmonary bypass and the perfusionist is having difficulty maintaining total heparinization. What is the most likely cause?

A

( A) Antithrombin deficiency

271
Q

Termination of CPB temp

A

Patient should be normothermic to maximize cardiac contractility and decrease chance of arrhythmias’
<38

272
Q

Termination of CPB electrolytes

A

Acid-base, calcium and potassium abnormalities should be addressed.

273
Q

Termination of CPB and Hgb

A

Hemoglobin should be at least 7 g/dl

274
Q

Infusion, the patient will require this

A

inotropic support, SHOULD be started after removal of the aortic cross clamp

275
Q

Termination of CPB: Potassium should be approaching

A

normal range 4-5

276
Q

Termination of CPB: Lungs should be fully expanded,

A

ventilated and volatile agent administered if patient can tolerate

277
Q

Termination of CPB:Heart rate should be

A

paced at 90 bpm

278
Q

Termination of CPB: Anticoagulation is reversed with

A

protamine sulfate and thoracic incision closed.

279
Q

Rewarming : Nasopharyngeal goal temp

A

36-37C

280
Q

Rewarming: rectal goal temp

A

> 35 but < 37

281
Q

Separation from CPB Hct should be

A

20-25%

282
Q

TERMINATION : 1ST STEP CLAMPING

V -A

A

VENOUS OUTLFOW LINE IS SLOWLY CLAMBED

AORTIC INFLOW LINE IS CLAMPED

283
Q

INITIATION CLAMPING; 1ST STEP

A-V

A

ARTERIAL CANNULATION FIRST

284
Q

Administration of protamine, a heparin antagonist, may have the following adverse reactions:

A

(l) systemic hypotension, (2) pulmonary hypertension, MYOCARDIAL DEPRESSION and (3) allergic reactions.

285
Q

Adverse effects of protamine sulfate are due to

A

Histamine release.

286
Q

Pulmonary artery pressure increases because, with

A

rapid Infusion of protamine pulmonary systemic vascular resistance increases.

287
Q

As you know, protamine also promotes a

A

decrease in systemic vascular resistance and hypertension. These pulmonary and systemic consequences of protamine result from histamine release

288
Q

3 adverse reactions with Protamine sulfate.

A

Severe pulmonary artery vasoconstriction
myocardial depression
Severe systemic hypotension.

289
Q

What is the Most common complication during rewarming as BRAIN normothermia is restored in the setting of_______?

A

Intraoperative AWARENESS decrease anesthetic concentration.

290
Q

May be needed during rewarming?

A

Additional anesthetic dosing

291
Q

CBP pump flow at normothermia pump flow should be between

A

50 and 70 ml/kg/min)

292
Q

During rewarming, increased SVR is usually due to

A

inadequate anesthesia, volatile anesthetic preferred in that case if the patient has good ventricular function. If patient does not have good ventricular function, inhalational agents are avoided because of the potential for myocardial depression after CPB.

293
Q

Aortic cross clamp placed above the

A

artery of Adamkiewicz can cause ischemia to the lower portion of the anterior spinal cord can result ANTERIOR SPINAL ARTERY SYNDROME also known as BECK’s syndrome.

294
Q

Signs of Anterior spinal artery syndrome

A

Flaccid paralysis of the LE
Bowel and bladder dysfunction
Loss of temperature and pain sensation
Preverve touch and proprioception

295
Q

Most sensitive intraoperative monitor for detecting MI is

A

TEE

296
Q

The single best lead for detecting myocardial ischemia

A

V5.

297
Q

Where do you place V5?

A

4th intercostal space midclavicular line

298
Q

Not recommended for monitoring perioperative ischemia?

A

3-lead ECG

299
Q

SA artery

A

prominent central artery that is a branch of the RCA

300
Q

3 internodal tracts

A

Anterior middle posterior

301
Q

Equillibrium potential of K

A

-94

302
Q

Equillibrium potential of Na

A

60

303
Q

Severe mitral stenosis atrial kick %

A

40%

304
Q

Cardiac surgery you need to monitor

A

Automated ST segment monitoring

305
Q

CO =

A

VO2 / (Ca-Cv) O2

306
Q

Normal ACT is

A

80 -120 Seconds

307
Q

During aortic cannulation, systolic BP should be

A

100 mmHg to minimize the risk of dissection.

308
Q

RMP is a balance of 2 opposing forces

A

Movement of K+ down its concentration gradient, and the electrical attraction of the negative interior for the positive potassium ions. (opposite attracts)

309
Q

Action potential of myocardial cell raises the membrane potential to

A

+20 mV

310
Q

How long does the plateau phase lasts

A

0.2 to 0.3 second

311
Q

Whereas the action potential for skeletal muscle and nerve is caused by ___________in cardiac muscle, it is due to opening of both

A

Fast Na+ Channels

fast Na channels and slower calcium channels

312
Q

Depolarization is also accompanied by a

A

Transient decrease in Potassium permeability

313
Q

SA node has a less negative RMP because (-60mV) why

A

Slow influx of Na+ lead to

Fast Na+ Channels are inactive
Action potential threshold is -40 mV (caused by ION MOVEMENT OF SLOW CALCIUM CHANNELS)

314
Q

When threshold reach is Nodal tissues?

A

Calcium channels open

Potassium permeability decreases –> Action potential

315
Q

For nodal tissues, what return the normal RMP?

A

normal potassium permeability.

316
Q

Anesthetic effects: VA on SA node and AV node

A

Depress SA node automaticity

Modest effects on the AV nodes.

317
Q

Opioids on Sa node

A

Increases AV node conduction and refractory period

318
Q

Myocardial cells contract because of 2 proteins

A

Actin and myosin

319
Q

Connect actin to the cell membrane

A

Dystrophin

320
Q

What normally prevent the interaction of troponin and tropomyosin?

A

Actin and myosin

321
Q

Troponin has 3 subunits?

A

Troponin I
Troponin C
Troponin T

322
Q

Mechanisml of contraction of myocardial cells: Increase in Intracellular Ca2+ promotes

A

contraction as calcium Binding to troponin C –> results in conformational changes of those proteins exposes active site on actin that allow interaction with myosin bridges. (active site on myosin function as magnesium-dependent ATPase whose activity) is enhanced by the increased in intracellular calcium concentration
Relaxation occurs as calcium is pumped back into the Sarcoplasmic recticulum by a Ca2+-Mg 2+ ATPase; the resulting drop in calcium allow the troponin-tropomyosin complex to prevent actin and myosin interaction.

323
Q

The force of contraction is directly dependent on

A

Magnitude of initial calcium influx

324
Q

Parasympathetic receptors

A

Muscarinic M2 –> Negative chronotropy, dromotropy and inotropy

325
Q

Sympathetic fibers of heart originate in

A

Thoracic spinal cord T1-T4 and travel through heart initially through CERVICAL GANGLIA (stellate)

326
Q

v wave is the

A

Result of the pressure buildup from venous return

327
Q

Decline in pressure between the c and v wave, Pulling down of the atrium by ventricular contraction

A

x-descent

328
Q

Notch in the aortic pressure tracing is referred to as the

A

INCISURA : transient backflow of blood into left ventricle just before aortic valve closure.

329
Q

Ventricular preload aka

A

EDV

330
Q

In the absence of pulmonary or RV dysfunction, venous return is a major determinant of

A

LV preload.

331
Q

Venous return is affect by PPT

A

PPV
Posture
Tachycardia.

332
Q

The larger the ventricular RADIUS, the ______wall tension

A

GREATER

333
Q

An increase in ventricular THICKNESS, Reduces

A

Ventricular WALL TENSION

334
Q

Contraction depends on the

A

Intracellular calcium concentration during systole.

335
Q

Most anesthetics and antiarrhythmic agents are (inotropy)

A

Negative.

336
Q

Ventricular wall abnormalities; Hypokinesis

A

Decreased contraction

337
Q

Ventricular wall abnormalities; Akinesis

A

Failure to contract

338
Q

Ventricular wall abnormalities; Dyskinesis

A

Paradoxic bulging

339
Q

Stenosis of an AV valve reduces SV how?

A

decreasing ventricular preload

340
Q

Stenosis of a semilunar valve reduces SV how?

A

increasing ventricular afterload.

341
Q

Most tissue beds regulate

A

Their own blood flow

342
Q

2 causes of autoregulation can be because of

A

Intrinsic response of vascular smooth muscle to stretch

Accumulation of vasodilatory metabolic byproducts

343
Q

Vasodilatory metabolic produces may increase

A

K+, H+, CO2, Adenosine and lactate.

344
Q

Vascular endothelium secretes and modifies substances that control BP-> Vasodilators

A

Nitric oxide, prostacyclin, PGI2

345
Q

Vascular endothelium secretes and modifies substances that control BP-> Vasoconstrictors

A

Thromboxane A2, Endothelins

346
Q

Vascular endothelium secretes and modifies substances that control BP-> anticoagulants

A

Thrombomodulin, protein C

347
Q

Vascular endothelium secretes and modifies substances that control BP-> Fibrinolytics

A

TPA

348
Q

Vascular endothelium secretes and modifies substances that control BP-> Inhibit platelet aggregation

A

NO and PGI2

349
Q

Vascular tone and autonomic influences on the heart are controlled by

A

Vasomotor centers in the reticular formation of the medulla and LOWER Pons.

350
Q

Vasomotor centrers in the reticular formation are also responsible for

A

Adrenal secretion of catecholamines as well as enhancement of cardiac automaticity and contractility.

351
Q

Coronary vessel tone can be autoregulated between

A

CPP 50-120mmHg

352
Q

Most vulnerable to ischemia during decrease in CPP

A

Subendocardium (Endocardium)

353
Q

Dose dependent abolition of autoregulation may be greatest_____and least with ______

A

ISOFLURANE

SEVO

354
Q

Volatile anesthetics reduce ______And are protective against_____

A

Myocardial O2 requirements,

Reperfusion injury.

355
Q

Risk for PERIOPERATIVE MI

A 
Ischemic heart disease
CHF
CVA
High risk surgery
Preoperative insulin therapy
Preoperative creatinine > 2mg/dl
356
Q

Perioperative MI can be caused by

A

Severe HTN or tachycardia
Hypotension, Anemia
Severe AS or AR

357
Q

Sudden this can cause Perioperative myocardial ischemia

A

Sudden withdrawal of antiangianal medication preoperatively , such as Beta BLOCKERS, can lead to rebound HTN, tachycardia or both

358
Q

Symptoms hx at risk for perioperative Myocardial ischemia

A

CP , dyspnea, poor exercise tolerance, syncope

359
Q

Beta blockers should be started at least

A

1 week before surgery

360
Q

If AF, TEE to rule out

A

Left atrial or left atrial appendage thrombuses

361
Q

Thermodilution CO measurements are falsely elevated in a patients with

A

TR

362
Q

Why is slow HR increase regurgitation?

A

Because of the associated disproportionate increase in diastolic time, but increases in diastolic arterial pressure favor regurgitant volume by increasing the pressure gradient for back flow

363
Q

Phenylephrine and MR

A

Large amount of phenylephrine can increase SVR and worsen regurgitation

364
Q

Critical aortic stenosis is _____Valve area and _______transvalvular gradients

A

0.5 to 0.7 cm2 ; 50 mmHg

365
Q

AS wth AF

A

Immediate cardioversion

366
Q

Aortic stenosis and CO

A

CO becomes rate dependent, and bradycardia is poortly tolerated

367
Q

Contraindicated with AS

A

Spinal and epidural anesthesia

368
Q

MVP murmur

A

Midsystolic click

369
Q

Aortic surgeries done with CBP: ascending Aorta?

A

Ascending Aorta are done with CPB

370
Q

Ascending aorta surgeries give 2 medications

A

Nicardipine , nitroprusside

371
Q

Aortic dissection medication that should be used

A

B-Blockers

372
Q

Patient having Ascending aorta surgeries where should the aline be placed and why?

A

For Ascending aorta surgeries, place A-line in Left radial artery because clamping of the innominate may be required.

373
Q

Aortic arch surgeries, are done with

A

CPB and deep HYPOTHERMIC CIRCULATORY ARREST

374
Q

Aortic surgeries that may be done without CPB

A

Descending Thoracic aorta surgeries, may be done through a left thoracotomy without CPB.

375
Q

Where do you place the A-line for the Descending thoracic aorta surgeries

A

Right radial. because left subclavian may be clamped.

376
Q

Aorta is cross-clamped where is HTN, and HoTN

A

HTN in aorta above clamp

HoTN below the lesion (when not using shunt or bypass)

377
Q

After release of aortic clamp you may get

A

Severe systemic hypotension

378
Q

CPB limit times to less than

A

120 minutes

379
Q

The aortic cross clamping required during CPB reduces CBF to

A

0

380
Q

Target K+ , pH, glucose , hct

A

5.5; >7.20 ; >72; >22%

381
Q

Target HR post bypass is

A

80 -100 may need pacing

382
Q

When is HR adequate to wean from CPB

A

HR should start contracting in an empty state for 5-10 minutes before weaning CBP to ensure adequate cardiac rate and rhythm via ECG

383
Q

Pt coming off CPB low SVR tx

A

Positive inotrope (epi, dopa, dobutamine) with milrinone can be started. With pump failure , CPB may be needed

384
Q

During CPB keep blood flow rate at _____L/min or _____ml/kg/min and MAP

A

2 - 2.5 L/min
50-60 ml/kg/min
MAP between 50-80 mmHg

385
Q

CPB glucose check

A

Hourly if DM

once if none

386
Q

CPB for on pump arterial cannulation is usualy in the

A

radial artery in non-dominant hand.

387
Q

When is the ideal time to start beta blockers

A

1 week prior to ensure adequate B-Blockade and to help identify side effects such as HB.

388
Q

For every _______C change in body temperature, Metabolic oxygen requirements decrease by

A

10C ; 50%

389
Q

Side effects of hypothermia

A

Platelet dysfunction
Reversible coagulopathy
Depression of Myocardial contractility

390
Q

Aortic regurgitation treamtne needed?

A

Diuretics and afterload reduction, particular with ACEIO

391
Q

Post bypass you may need heparin reversal as well as

A

FFP and platelets

TOPICSII (4 decks)

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