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Patient Care > Cardiology 1 > Flashcards

Cardiology 1 Flashcards

1
Q

Automaticity

A

Cells depolarize without impulse from outside source

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2
Q

Conductivity

A

Cells propagate the electrical impulse from cell to cell

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3
Q

Contractility

A

Specialized ability of cardiac muscle to contract

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4
Q

Excitability

A

Cells respond to electrical stimulus

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5
Q

Types of cardiac muscle cells

A

Pacemaker
Contractile

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6
Q

Groups of cardiac muscle

A

Atrial
Ventricular
Excitatory/conductive

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7
Q

Sodium

A

Major extracellular cation, role in depolarization

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8
Q

Potassium

A

Major intracellular cation, role in repolarization

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9
Q

Calcium

A

Intracellular cation, depolarization and myocardial contraction

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10
Q

Chloride

A

Extracellular anion

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11
Q

Magnesium

A

Intracellular cation

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12
Q

Resting Potential

A

Approximately -90mv
More intracellular negative anions than extracellular

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13
Q

Membrane Potential

A

Separation of charges across the membrane

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14
Q

Depolarization

A

Sodium enters cell change stop positive intracellular charge
Reversal of charges at the cell membrane
Slow influx of calcium

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15
Q

Repolarization

A

Returning to resting potential state
Sodium influx stops and potassium leaves cell
Sodium pumped to outside cell

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16
Q

Absolute refractory period

A

Cell will not respond to repeated action potential regardless of how strong

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17
Q

Relative refractory period

A

Cell responds to second action potential but must be stronger than usual

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18
Q

Myocardial Cell

A

Specialized cells of conduction system able to generate action potentials spontaneously

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19
Q

Cardiac Myocytes

A

Involuntary
Striated
Branched
Tissue arranged in interlacing bundles of fibres

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20
Q

Phase 4

A

Resting potential phase
Inside of cell negative to outside
Na/K pump maintains concentration gradient through Na/K pump

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21
Q

Phase 0

A

Rapid Depolarization
Membrane reaches threshold potential and voltage gated fast Na channels open
Na exceeds permeability to K, membrane reaches Na equilibrium
Inside of cell becomes positively charged
Sodium Influx

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22
Q

Phase 1

A

Partial Repolarization
Chloride ions enter cell cause inactivation of Na channels
K still lost from cell
Slight drop in membrane potential

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23
Q

Phase 2

A

Plateau
Voltage gated calcium channels open
Contraction of muscle
K leaves cell slowly
Prolonged state of depolarization allowing for muscle contraction

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24
Q

Phase 3

A

End of rapid repolarization
Ca channels close
K gates open, membrane depolarization
Na/K pump restores membrane potential

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25
Q

SA + AV Node AP Morphology

A

Phase 4
Phase 0
Phase 3

Progressive depolarization in 4 until threshold

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26
Q

Late Diastole

A

Both chambers relaxed
Ventricular filling

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27
Q

Atrial systole

A

Atrial contraction forces small amount of blood to ventricles

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28
Q

End diastolic Volume

A

Maximum amount of blood in ventricles at end of ventricular relaxation
135mL

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29
Q

Isovolumic ventricular contraction

A

Pushes AV valve closed, not enough pressure to open semilunar valves

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30
Q

Ventricular Ejection

A

Ventricular pressure rises and exceeds pressure in arteries
Semilunar valves open and blood ejected

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31
Q

End Systolic Volume

A

Minimum amount of blood in ventricles
65mL

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32
Q

Iosvolumetric Ventricular Relaxation

A

Ventricles relax, pressure in ventricles drop
Blood flows back into cups of semilunar valve and snaps them closed

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33
Q

P Wave

A

First upward deflection
Atrial depolarization
0.1s or less
Followed by QRS

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34
Q

Inverted P waves

A

When pacing or if initial impulse originates at or below AV node

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35
Q

P wave axis shift

A

Inverted P waves in II, III, aCF
Left atrial enlargement

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36
Q

PR Interval

A

Time for impulse to move through atria and AV node
Beginning of P wave to next deflection on baseline
0.12 - 0.2s

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37
Q

Causes of short PRI

A

Retrograde junctional P waves
WPW pattern
Lown-Ganong-Levine Syndrome

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38
Q

QRS complex

A

Ventricular depolarization
<0.12s

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39
Q

Q wave

A

First negative deflection after P wave
Depolarization of septum
Can be normal or pathological

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40
Q

R wave

A

First positive deflection following P or Q

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41
Q

S wave

A

Negative deflection following R wave

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42
Q

QRS Interval

A

Time impulse takes to depolarize ventricles
Beginning of Q to ST segment
<0.12s

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43
Q

What to look for in QRS

A

Height/Amplitude
Width/duration
Morphology
Presence of Q waves in infarct pattern
Axis along frontal plane
R wave progression

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44
Q

Tall QRS Complexes

A

Increased hypertrophy of ventricles
Increased abnormal pacer
Increased aberrantly conducted beat

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45
Q

Criteria of Small Complex

A

Voltage in all limb leads <5 mm
Waves <10mm high in precordial leads

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46
Q

Causes of Small QRS complexes

A

Obesity
COPD
Pericardial effusion
Severe hypothyroidism
Subcutaneous emphysema
Massive myocardial damage/infarction
Infiltrative/restrictive disease such as amyloid cardiomyopathy

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47
Q

QRS Width

A

Anything >0.12 is abnormal

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48
Q

Causes of Wide QRS

A

Hyperkalemia
V-tach
Idioventricular rhythms
Drug effects and overdoses
WPW
BBB and inter ventricular conduction delay
Ventricular premature contractions
Aberrantly conducted complexes

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49
Q

5 Steps to ECG interpretation

A

Rate
Rhythm
P waves
PR interval/relationship
QRS duration

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50
Q

T wave

A

Repolarization of ventricles
End of ventricular systole

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51
Q

Bi Polar Leads

A

I/II/III

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52
Q

Unipolar leads

A

Vector point midpoint of the axis
Augmented limb leads and precordial leads

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53
Q

Augmented limb leads

A

aVR/aVL/aVF

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54
Q

Augmented chest leads

A

V1-V6

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55
Q

Vectors from precordial leads

A

Limb leads: frontal plane
Precordial leads: horizontal plane

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56
Q

R wave progression

A

Increasingly large R wave in V3-V6

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57
Q

Male QT(c)

A

<450ms

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58
Q

QT(c) women

A

<470

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59
Q

QT(c) > 500

A

Risk of torsades

60
Q

QT(c)

A

Estimates QT interval as a standard HR of 60

61
Q

Prolonged QT(C) men

A

> 440

62
Q

Prolonged QT(c) women

A

> 460

63
Q

Abnormally short QT(c)

A

<350ms

64
Q

Causes of QT prolongation

A

Drugs: Type IA + III anti arrhythmic, TCAs/phenothiazines
Lytes: Hypokalemia, hypomagnesemia, hypocalcemia
CNS: stroke, seizure bleed

65
Q

Normal Axis

A

-30 to 90 degrees

66
Q

Importance of Axis

A

Provides insight into chamber enlargement, abnormalities of conduction system, MI and origin of arrhythmias

67
Q

Electrical Axis

A

Average direction of depolarization during ventricular contraction of the heart

68
Q

Causes of Non-Pathological Axis Deviation

A

Age
Body type

69
Q

Age axis deviation

A

Moves leftward with age

70
Q

Body type Axis deviation

A

Vertical: tall + thin
Leftward: short and obese

71
Q

Normal Axis

A

QRS positive in I and aVF

72
Q

LAD

A

Positive QRS lead I, negative aVF

73
Q

RAD

A

Negative Lead I, positive aVF

74
Q

Extreme RAD

A

Negative I and aVF

75
Q

Pathological Left axis deviation

A

Lead I positive, aVF negative
II more negative than positive

76
Q

Causes of Extreme RAD

A

V tach
Ventricular pacing

77
Q

Causes of RAD

A

Right ventricular hypertrophy
Chronic pulmonary disease
PE
Left posterior fascicular block
Sodium channel blocker
Hyperkalemia

78
Q

Causes of LAD

A

Left ventricular hypertrophy
LBBB
Ventricular pacemaker
Left anterior fascicular block
V tach
Inferior MI
Anterior MI
WPW
Ascites
Obesity
Pregnancy

79
Q

NSR

A

60-100
Regular
PR constant
QRS normal
Normal heart function

80
Q

Sinus bradycardia

A

<60
Regular
PR constant
Normal QRS

81
Q

Causes of Sinus bradycardia

A

Normal, beta blocker OD, digoxin, AMI/ischemia, increased ICP

82
Q

Significance of Bradycardia

A

Profound bradycardia could decrease CO

83
Q

Sinus tachycardia

A

> 100 <200
Regular
PR constant
QRS normal

84
Q

Causes of sinus tachy

A

Exercise, anxiety/stress, drugs

85
Q

Significance of Sinus tach

A

Usually benign, treat cause

86
Q

Sinus Arrhythmia

A

60-100
Irregular
P waves and PR constant
QRS normal

87
Q

Sinus Node Dysfunction

A

Abnormalities in SA impulse formation and conduction including sinus brad, sinus pause/arrest, sinoatrial exit block, tachy/brady syndrome

88
Q

Sinus Pause/Arrest

A

Failure of impulse formation in sinus node
Rate varies with arrest
Irregular
Normal P waves
Normal QRS

89
Q

Short Sinus Pause

A

<2.5s

90
Q

Long Sinus Pause

A

> 2.5s

91
Q

S/sx of Sinus arrest

A

Lightheaded, syncope, death if escape rhythm does not kick in

92
Q

Causes of Sinus Arrest

A

Heart disease, AMI, sinus node dysfunction

93
Q

Sinus Exit Block

A

Failure of conduction of SA node impulse
Variying rate
Irregular rhythm, pause same as distance between 2 other P-P intervals

94
Q

Causes of Sinus exit block

A

Increased vagal tone
Sinus node dysfunction
Inferior AMI
Digitalis, Ca beta blockers, amiodarone

95
Q

Tachy-brady syndrome

A

Rate alternates between too fast and slow
Long pause between heartbeats especially after tachycardia

96
Q

Atrial Fibrillation

A

Atrial Rate: 350-650
Ventricular rate: variable
Regularly irregular
No consistent P waves
No PR interval

97
Q

Clinical significance of A fib

A

Atrial kick lost
Thrombus from pooled blood common cause of CVA

98
Q

Atrial Flutter

A

Atrial rate: 300/min
Regular but not always
Saw toothed pattern of flutter waves, varying ratios
QRS narrow, no true marriage

99
Q

Origin of A flutter

A

Single ectopic focus in atria with re-entry mechanism

100
Q

Ectopic Atrial Dysrhythmias

A

Site outside of sinus node but in atria creating AP faster than sinus node

101
Q

Wandering Atrial Pacemaker

A

Variable rate depending on site of pacemaker, usually 45-100
Irregular
Variable PR
Normal QRS
Variable impulses from atria

102
Q

Multi-Focal Atria Tachycardia

A

Wandering Atrial Pacemaker with rates >100

103
Q

Junctional Rhythm

A

Default rate at 40-60
Regular
Normal if P waves present
Normal QRS

104
Q

Causes of junctional rhythm

A

ACS
Drugs: beta blocker, CCB, amiodarone, digoxin
Sinus node dysfunction

105
Q

Accelerated Junctional

A

60-100

106
Q

Junctional Tachycardia

A

> 100

107
Q

4 Features of classic SVT

A

Fast between 140 and 250
Regular
Narrow QRS
NO P waves

108
Q

AVNRT Pathways

A

Alpha path: slower, fast refractory
Beta: faster, slower refractory

109
Q

AVRT

A

Caused by abnormal anatomical conduction pathway between atria and ventricles
Bypasses AV node, bundle of HIS or both
Early depolarization of ventricle

110
Q

WPW

A

Impulse normally in SA passes thru AV nod and accessory pathway
PAC reaches pathway when refractory but AV is not
Re-entry circuity

111
Q

Delta wave

A

Slurred upstroke in QRS

112
Q

Adenosine and WPW

A

Contraindicated and lethal

113
Q

V-Tach

A

120-250 (typical 170)
Regular
Absent p wave
Wide QRS

114
Q

Origin of Vtach

A

Ectopic focus in ventricle, possibly accessory pathway

115
Q

Causes of Vtach

A

AMI, hypoxia, acidosis, hypokalemia, R on T

116
Q

ECG Criteria Favouring VT

A

AV dissociation
Negative or positive concordance in precordial leads
Very broad complexes
Extreme RAD (positive QRS aVR)
Captur beats or fusion beats
Rsr’ in V1
Distance from onset of QRS to S wave is >100ms
Notched S wave (Josephson’s sign)

117
Q

1st Degree Block

A

Normal rate
Regular
P wave present
PR interval >0.20s
Normal QRS

118
Q

Causes of 1st degree block

A

Age, heart disease slowing conduction through AV node

119
Q

2nd degree Type I

A

Normal to brady
Irregular rhythm
Normal P wave
PR increases until QRS dropped

120
Q

Origin of 2nd degree Type I

A

SA node with block at or below AV node

121
Q

Causes of 2nd degree Type I

A

Ischemia, digoxin toxicity, acute inferior AMI

122
Q

2nd Degree Type 2

A

Usually brady
Irregular
P wave Present
PR interval constant until QRS randomly dropped
Uniform ratio 2:1, 3:1, 4:1

123
Q

Origin 2nd degree Type 2

A

SA node with block at or below AV

124
Q

3rd degree Block

A

Atrial rate: normal
Ventricular rate: 20-50
Regular R-R interval
P wave present
QRS present
No relationship between P and QRS

125
Q

Origin of 3rd Degree Block

A

SA node with complete block at AV
Ventricles AV node signal, bundle or ventricles

126
Q

RBBB

A

QRS >0.12
Right side of heart last to depolarize, last vector of complex moves towards V1
Upright rsr’ in V1
Negative deflection in V6 as large S wave

127
Q

LBBB

A

Left side of heart last to depolarize, terminal vector moves away from V1
Negative deflection in V1

128
Q

Smith-Modified Sgarbossa Criteria

A

ST Elevations >1mm in >1 lead
ST depression >1mm in >1 lead of V1-V3
Excessive discordant STE in >1 lead anywhere with >1mm STE, >25% depth of preceding S wave

129
Q

Atrial Enlargement

A

Left atrial enlargement commonly caused by mitral valve disease
Right atrial enlargement caused by lung disease

130
Q

Ventricular Hypertrophy

A

Sustained HTN forces left ventricle to work too hard
Right VH far less common

131
Q

right atrial enlargement

A

Height of P wave >2.5mm in lead II or >1.5mm in V1
Increased amplitude of first portion of P wave

132
Q

Left atrial Enlargement

A

Duration of P wave >0.12s in II
P wave notched in II
Pwave inverted or biphasic in V1

133
Q

Right Ventricular Hypertrophy

A

RAD
Right atrial enlargement
Tall R wave in V1 >7mm
R wave greater than S in V1
Rsr’ in V1 > 10mm

134
Q

LVH

A

Deepest S wave in V1 or V2 and tallest R wave in V5 or V6 >/= 35mm
R in aVL > 12mm
S wave in V1 or V2 >20-25
R wave in V5 >20 or V6 >25

135
Q

Hypertrophic Cardiomyopathy

A

Septal hypertrophy positive R wave in V1, LVH and septal Q waves in v5 and v6

136
Q

RCA

A

Right ventricle
SA and AV node
Posterior wall
Posterior descending artery to inferior wall

137
Q

LCA

A

LAD + Circumflex

138
Q

Left anterior descending artery

A

Septum
Left + right BB
Anterior wall
Lateral wall

139
Q

Circumflex Artery

A

Lateral and posterior wall
Inferior wall 10%

140
Q

Ischemia and NSTEMI ECG

A

Hyperacute T wave
Inverted T wave
ST depression

141
Q

necrosis ECG

A

Pathological Q waves
>1mm wide >1/3 R wave

142
Q

Wellens Syndrom

A

LAD coronary T wave syndrome
Biphasic/deeply inverted T waves in V2 and V3 persisting after resolved ischemic chest pain

143
Q

Significance of Wellens Syndrome

A

Acute Mi in 6-8.5 days post admission
Acute Mi 21.4 days from symptoms

144
Q

De winter’s T waves

A

Anterior STEMI equivalent without obvious ST elevation
Tall peaked T waves in precordial leads starting below isoelectric line

145
Q

RV failure

A

Preload dependent

146
Q

Morphology of ST depression

A

Upsloping non-specific for myocardial ischemia
Horizontal or downsloping = ischemia

Patient Care (11 decks)

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