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Quarter 3 > Cardio II New > Flashcards

Cardio II New Flashcards

1
Q

p-wave

A

atrial depolarization

right and left atrial action potentials

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2
Q

Length of p-wave

A

0.08 sec

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3
Q

What represents ventricular depolarization on an ECG?

A

QRS

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4
Q

What represents ventricular repolarization on an ECG?

A

T-wave

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5
Q

What interval represents atrial contraction?

A

PR interval

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6
Q

Length of PR interval

A

0.2 sec

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7
Q

What do long PR intervals indicate

A

heart block

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8
Q

Why is the ECG isoelectric during the PR interval?

A

annulus fibrosus breaks the electrical circuit

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9
Q
A

A - SA node

B - Atrial cell

C - Venricular cell

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10
Q

What causes the t-wave to be upright?

A

subepicardial myocytes have ~3x mroe repolarizing iK channels than subendocardial, so they repolarize first

[repolarization occurs in reverse sequence to depolarization]

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11
Q

Why does atrial repolarization not register on an ECG?

A

it is asynchronous and slow

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12
Q

Length of QRS

A

0.1 sec

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13
Q

Lead II

A

left leg (+) to right arm (-)

angle of view = 60o

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14
Q

Lead III

A

left leg (+) to left arm (-)

angle of view 120o

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15
Q

aVL

A

left arm to + terminal

angle of view -30o

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16
Q

aVR

A

right arm to + terminal

angle of view -150o

looks into the inside of the ventricles

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17
Q

aVF

A

foot to + terminal

angle of view 90o

records the inferior surface of the heart

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18
Q

Where does the first depolarization occur

A

left side of the interventricular septum

activated by the left bundle branches

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19
Q

electrical axis of the heart

A

direction of largest dipole in the frontal plane

Can be determined by comparing the height of the R wave in leads I and aVF:

  • if the largest R wave is in lead II, the electrical axis is closer to 60o
  • the lead with the smallest QRS complex, with R and S waves of nearly equal height, must be at 90o angle to electrical axis
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20
Q

Shift of electrical axis in left ventricular hypertrophy

A

shifts to the left

(left axis deviation)

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21
Q

shift of electrical axis in right ventricular hypertrophy

A

right axis deviation

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22
Q

When is dipole the largest

A

midway through excitation

roughly half the wall is negative and half positive

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23
Q

Which lead displays the biggest R wave

A

Lead II

aligned at 60o, it is roughly in line with the biggest dipole

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24
Q

Sinus arhythmia

A

normal, regular, physiological slowing of the heart during expiration and speeding up during inspiration

fall in left ventricular SV during inspiration

fall in LV filling during inspiration

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25
Q

First-degree heart block

A

lengthening of the PR interval

( > 0.2sec)

caused by slowing of conduction between the AV node and the ventricle

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26
Q

Second-Degree Heart Block

A

intermittent failure of excitation to pass from the atria to the ventricles

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27
Q

Wenkebach Phenomenon

A

PR interval lengthens with each beat until a transmission fails completely

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28
Q

Third-Degree Heart Block

(complete)

A

atria and ventricles beat independently and at different rates

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29
Q

Stokes-Adams attacks

A

sudden and temporary syncope due to heart block

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30
Q

Wolff-Parkinson-White Syndrome

A

episodes of paroxysmal tachycardia (palpitations) resulting from a re-entry pathway (accessory bundle of Kent)

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31
Q

Bundle of Kent

A

extra electrical connection across the annulus fibrosus, additional to the bundle of His

  • Seen in WPW syndrome
  • produces a self-perpetuating circus pathway
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32
Q

Pharmalogical therapy for Re-Entry dysrhythmias

A

Disrupt the timing of re-entry using:

  • Ca2+ channel blocker
    • verapamin
  • K+ channel activator
    • Adenosine
  • Na+ channel blocker
    • Procainamide or quinidine
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33
Q

Delayed afterdepolarization (DAD)

A

can reach threshold, triggering an action potential and poorly co-ordinated ectopic beat (extra systole)

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34
Q

When is the “vulnerable period”

A

in the later half of the T-wave

readily triggers re-entry based arrhythmias

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35
Q

ECG of myocardial infarct

A

elevated ST segment

later on, Q and T-waves invert

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36
Q

Size (mV) of an EKG

A

1 mV

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37
Q

12-Lead EKG

A

recording of small potential differences in the frontal plane (3 bipolar limb leads and three unipolar limb leads) and transverse plane (6 precordial leads)

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38
Q

Lead I

A

left arm to right arm

horizontal (0o)

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39
Q
A

Intracellular Potential of Ventricular Myocyte

  • 0 - rapid inflow of Na+
  • 1 - transiently outward K+
  • 2 - inward Ca2+
    • L-type calcium channels
    • Na/Ca exchanger
    • K efflux
  • 3 - K+ outflow
  • 4 - resting membrane between -80 to -90mV
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40
Q

Automaticity

A

ability of a cell to depolarize itself

Examples: SA node and automaticity foci

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41
Q

First 1/3 of p-wave

A

caused by right atrial activation

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42
Q

what does the PR interval reflect?

A

delay of condution by the AV node

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43
Q

What does the t-wave represent on a ventricular myocyte graph?

A

phase 3 - repolarization

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44
Q

QT interval

A

measures the action potential duration

time in which the ventricles depolarize and repolarize

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45
Q

Bazett’s formula

A

QTc = QT/sqrt(RR)

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46
Q

What does each large box on an EKG represent?

A

0.20 seconds

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47
Q

Normal P-wave length

A

0.08-0.12 seconds

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48
Q

PR Interval length

A

0.12-0.20 seconds

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49
Q

QRS length

A

0.06-0.11 seconds

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50
Q

Frontal Plane leads

A

I, II, III, and aVR, aVL, and aVF

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51
Q

Horizontal plane leads

A

V1-V6

View the heart as if the body were cut in half

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52
Q

Which leads are bipolar

A

I, II, and III

53
Q

Augmented Limb Leads

A

aVR, aVL, aVF

amplify the votlage of the waves in Leads I, II, and III

unipolar

54
Q

Hexaxial Reference System (HRS)

A

demonstrates the heart’s electrical axis in the frontal plane

based on the first six leads of the 12-lead

Normal Axis: -30 to +90o

Left Axis: -30 to -90o

Right Axis: +90 to +180o

Extreme axis deviation: -90o to -180o

55
Q

Precordial leads

A

(chest leads)

views across the horizontal plane

each lead is positive

56
Q

V1 placement

A

right side of sternum, 4th intercostal

57
Q

V2 placement

A

left side of sternum, 4th intercostal

58
Q

V4 Placement

A

left midclavicular line, 5th intercostal

59
Q

V5 placement

A

left anterior axillary

60
Q

V6 Placement

A

left midaxillary line

61
Q

Which leads correspond to the high lateral wall of the left ventricle?

A

Leads I and aVL

62
Q

Which leads correspond to the inferior wall of the left ventricle?

A

Leads II, III, and aVF

63
Q

Which leads correspond to the septal wall of the left ventricle?

A

Leads V1 and V2

64
Q

Which leads correspond to the anterior wall of the left ventricle?

A

V3 and V4

65
Q

Which leads correspond to the lateral wall of the left ventricle?

A

V5 and V6

66
Q

Pacemaker centers of Automaticity

A

SA node, Atrial foci, junctional foci, and ventricular foci

67
Q

Ventricular Escape Rhythm

A

20-40 bpm

essentially regular rhythm

p waves usually absent or appear after QRS

QRS > 0.12sec

68
Q

Enhanced automaticity

A

increase in slope of phase 4 repolarization resulting in the cell reaching threshold more often per minute

69
Q

Early afterdepolarizations

A

occur during the inciting action potential

can lead to torsades de pointes

70
Q

Normal QT length

A

450ms in men; 460ms in women

71
Q

Bradycardia

A

< 60 bpm

72
Q

Tachycardia

A

> 100 bpm

73
Q

Second degree AV Block - Type II

A

dropped P wave not preceded by PR prolongation

disease of His-Purkinje system

74
Q

LBBB

A

bunny ear R wave on V6

75
Q

Trifasciular Block

A

1st degree AV block, RBBB, and LAFB or LPFB

76
Q

Premature Ventricular Contractions (PVCs)

A

heartbeat is initiated by the ventricles instead of the sinus node

wide QRS, followed by compensatory pause

77
Q

Ventricular Tachycardia

A

run of 3+ PVCs in a row

78
Q

Stroke Volume

A

influenced by energy of contraction and aortic pressure

79
Q

How does arterial pressure affect stroke volume?

A

Atrial pressure depresses stroke volume

ejection cannot begin until ventricular pressure exceeds aortic pressure

80
Q

Afterload-Shortening Relation

A

if afterload increases, rate and degree of shortening decrease

81
Q

the ejection phase is roughly equivalent to ____?

A

isotonic shortening

82
Q

On what part of the length-tension cure do myocytes normally operate?

A

Ascending part

83
Q

Anrep Effect

A

stretch causes an immediate force increase with no increase in systolic Ca2+

If the stretch is maintained, there is a slow increase in force due to increased Ca2+

84
Q
A

Cardiac muscle has a much steeper curve than skeletal msucle because stretch increases Ca sensitivity of cardiac myocytes

85
Q

Frank’s experiment

A

energy of contraction increases as a function of diastolic distension

86
Q

‘law of the heart’

A

the greater the stretch of the ventricle in diastole, the greater the stroke work acheived in systole

87
Q

Stroke Work Equation

A

change in pressure * change in volume

88
Q

What represents the area inside the pressure-volume loop

A

Stroke work

89
Q

upper boundary of the pressure-volume loop

A

isovolumetric pressure relaxation

systolic pressure that would be generated if ejection were prevented

90
Q

Is increasing afterload good or bad?

A

Bad

raising arterial blood pressure requires more energy, leaving less for ejection; therefore, stroke volume declines

There could be maximum systolic pressure without useful work

91
Q

What (5) factors affect volume distribution

A
  • gravity
  • peripheral venous tone
  • skeletal muscle pump
  • heart
  • breathing pattern
92
Q

How does gravity effect CVP?

A

decreases

venous pooling causes more of the blood supply to go to the lower limbs

93
Q

If CO is suddenly reduced (as in a heart attack), what happens to the filling pressure

A

it rises

94
Q

How does respiration affect CO and pressure?

A
  • inspiration raises right ventricular stroke volume
    • decreases LVSV
      • overcome by tachycardia
  • inspiration boosts filling pressure of right ventricle
95
Q

Traube-Hering Waves

A

synchronous oscillations in arterial pressure due to breathing

96
Q

Why does CVP change less than arterial pressure?

A

venous compliance is greater than arterial compliance

97
Q

Coughing

A
  • raises intrathoracic pressure
  • reduces or can reverse ventricular transmural pressure in diastole
98
Q

Negative Inotropic influences

A
  • parasympathetic (vagal) activity
    • cholinergic agonists
  • B-blockers
  • CCB
  • hyperkalemia
  • barbituates
  • acidosis and hypoxia
  • chronic cardiac failure
99
Q

Why are diuretics used in heart failure?

A

in heart failure an excessively high CVP over-distends the heart

increased radius impairs the conversion of active wall tension into internal pressure

100
Q

How do you increase ventricular contractility?

A

noradrenaline and adrenaline

result is a stronger, shorter contraction, a bigger stroke volume, ejection fraction and systolic pressure, and a reduced end-systolic volume. The pressure–volume loop becomes wider, taller and is shifted leftwards.

101
Q

Cardiac Index equation

A

CI = CO / BSA

102
Q

Cardiac Output equation

A

CO = (MAP - CVP) / SVR

or

CO = SV * HR

103
Q

What affects ESV

A

afterload (increases) and iontropy (decreases)

104
Q

How does preload affect EDV?

A

increases

105
Q

What 2 things decrease right ventricular preload?

A

increased HR and increased inflow resistance

106
Q

What increases venous pressure (CVP)

A

venous volume

  • venous return
  • total blood volume
  • respiration
  • muscle contraction
  • gravity
107
Q

What (5) things increase right ventricular preload

A
  • ventricular failure
  • increase atrial contractility
  • increase ventricular compliance
  • increase venous pressure
  • increase outflow resistance and afterload
108
Q

Transmural pressure

A

Pinside - Poutside

(venous pressure - intrathoracic pressure)

109
Q

Normal range for intrathoracic pressure

A

-5 to -10 cmH20

110
Q

Law of Laplace

A

P = 2T/r

T = wall stress * thickness

111
Q
A

first arrow = Frank-Starling Law

second (top) arrow = LaPlace’s Law

112
Q
A

A - Mitral valve opens

B - isovolumetric relaxation

C - End-systolic volume

D - ejection

E - aortic valve opens

F - isvolumetric contraction

G - end-diastolic volume

113
Q
A

line = ESPVR (inotropic state)

1 = Normal

2 = increased EDV

  • increased stretch due to increased preload

3 - increased afterload

4 - maximum afterload (no SV)

114
Q

Intrinisic and extrinsic regulation of Contractility

A

Intrinsic = Frank-Starling mechanism

Extrinsic = sympathetic nervous system

115
Q

SNS effect on cardiac function

A
  • increased
    • ventricular pressure
    • ejection fraction
    • stroke volume
  • decrease
    • diastolic volume
    • duration of systole
116
Q

Circulating Inotropes

A
  • Catecholamines (adrenal medulla)
    • epinephrine, norepinephrine
  • Angiotensin
  • Calcium ions
  • insulin, thyroxine, glucagon
117
Q

Bowditch Effect

A

Changes in heart rate affect contractility

  • increased heart rate causes increased contractility
  • due to increase SR calcium store
  • relatively small contribution in exercise
118
Q

What decreases inotropy?

A

systolic failure

119
Q

Increase CO in exercise

A
  • increase sympathetic discharge
    • increase in EF and HR
  • increase preload
    • venoconstriction, skeletal muscle pump
  • decrease afterload
    • arterial vasodilation
120
Q

Darcy’s Law

A

Q = (P1 - P2) / R

clinically applied:

CO = (PMAP - PCVP) / RSVR

121
Q

Bernoulli’s Relationship

A

E = P + p*g*h + (p*v2)/2

122
Q

Laminar Blood Flow

A

Q is proportional to change in pressure

  • areas of laminar flow
    • arteries, arterioles, venules, veins
123
Q

Turbulent Blood Flow

A

Q proportional to sqrt(change in pressure)

*Darcy’s law does not apply

124
Q

Where does bolus flow occur?

A

exchange vessels

125
Q

shear stress

A

friciton betwen molecules in lamina

126
Q

Shear rate

A

change in fluid velocity per unit distance normal to direction of flow

127
Q

Fahraeus-Lindqvist effect

A

viscosity decreases as tube diameter decreases

  • < 1mm diameer
  • bolus flow
    • decrease friction with wall
    • decrease resistance, less pressure needed for flow
  • Viscosity decreases as shear rate increases
128
Q
A
  • Reflection wave
    • diastole in young
      • aids in coronary perfusion
    • systole in old
      • adds to afterload
129
Q
A

Quarter 3 (12 decks)

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