Cardio II New Flashcards
1
Q
p-wave
A
atrial depolarization
right and left atrial action potentials
2
Q
Length of p-wave
A
0.08 sec
3
Q
What represents ventricular depolarization on an ECG?
A
QRS
4
Q
What represents ventricular repolarization on an ECG?
A
T-wave
5
Q
What interval represents atrial contraction?
A
PR interval
6
Q
Length of PR interval
A
0.2 sec
7
Q
What do long PR intervals indicate
A
heart block
8
Q
Why is the ECG isoelectric during the PR interval?
A
annulus fibrosus breaks the electrical circuit
9
Q
A
A - SA node
B - Atrial cell
C - Venricular cell
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]
11
Q
Why does atrial repolarization not register on an ECG?
A
it is asynchronous and slow
12
Q
Length of QRS
A
0.1 sec
13
Q
Lead II
A
left leg (+) to right arm (-)
angle of view = 60o
14
Q
Lead III
A
left leg (+) to left arm (-)
angle of view 120o
15
Q
aVL
A
left arm to + terminal
angle of view -30o
16
Q
aVR
A
right arm to + terminal
angle of view -150o
looks into the inside of the ventricles
17
Q
aVF
A
foot to + terminal
angle of view 90o
records the inferior surface of the heart
18
Q
Where does the first depolarization occur
A
left side of the interventricular septum
activated by the left bundle branches
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
20
Q
Shift of electrical axis in left ventricular hypertrophy
A
shifts to the left
(left axis deviation)
21
Q
shift of electrical axis in right ventricular hypertrophy
A
right axis deviation
22
Q
When is dipole the largest
A
midway through excitation
roughly half the wall is negative and half positive
23
Q
Which lead displays the biggest R wave
A
Lead II
aligned at 60o, it is roughly in line with the biggest dipole
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
25
First-degree heart block
lengthening of the PR interval
( \> 0.2sec)
caused by slowing of conduction between the AV node and the ventricle
26
Second-Degree Heart Block
intermittent failure of excitation to pass from the atria to the ventricles
27
Wenkebach Phenomenon
PR interval lengthens with each beat until a transmission fails completely
28
Third-Degree Heart Block
| (complete)
atria and ventricles beat independently and at different rates
29
Stokes-Adams attacks
sudden and temporary syncope due to heart block
30
Wolff-Parkinson-White Syndrome
episodes of paroxysmal tachycardia (palpitations) resulting from a re-entry pathway (accessory bundle of Kent)
31
Bundle of Kent
extra electrical connection across the annulus fibrosus, additional to the bundle of His
* Seen in WPW syndrome
* produces a self-perpetuating circus pathway
32
Pharmalogical therapy for Re-Entry dysrhythmias
Disrupt the timing of re-entry using:
* Ca2+ channel blocker
* verapamin
* K+ channel activator
* Adenosine
* Na+ channel blocker
* Procainamide or quinidine
33
Delayed afterdepolarization (DAD)
can reach threshold, triggering an action potential and poorly co-ordinated ectopic beat (extra systole)
34
When is the "vulnerable period"
in the later half of the T-wave
## Footnote
readily triggers re-entry based arrhythmias
35
ECG of myocardial infarct
elevated ST segment
later on, Q and T-waves invert
36
Size (mV) of an EKG
1 mV
37
12-Lead EKG
recording of small potential differences in the frontal plane (3 bipolar limb leads and three unipolar limb leads) and transverse plane (6 precordial leads)
38
Lead I
left arm to right arm
horizontal (0o)
39
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
40
Automaticity
ability of a cell to depolarize itself
Examples: SA node and automaticity foci
41
First 1/3 of p-wave
caused by right atrial activation
42
what does the PR interval reflect?
delay of condution by the AV node
43
What does the t-wave represent on a ventricular myocyte graph?
phase 3 - repolarization
44
QT interval
measures the action potential duration
time in which the ventricles depolarize and repolarize
45
Bazett's formula
QTc = QT/sqrt(RR)
46
What does each large box on an EKG represent?
0.20 seconds
47
Normal P-wave length
0.08-0.12 seconds
48
PR Interval length
0.12-0.20 seconds
49
QRS length
0.06-0.11 seconds
50
Frontal Plane leads
I, II, III, and aVR, aVL, and aVF
51
Horizontal plane leads
V1-V6
View the heart as if the body were cut in half
52
Which leads are bipolar
I, II, and III
53
Augmented Limb Leads
aVR, aVL, aVF
amplify the votlage of the waves in Leads I, II, and III
unipolar
54
Hexaxial Reference System (HRS)
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
Precordial leads
(chest leads)
views across the horizontal plane
each lead is positive
56
V1 placement
right side of sternum, 4th intercostal
57
V2 placement
left side of sternum, 4th intercostal
58
V4 Placement
left midclavicular line, 5th intercostal
59
V5 placement
left anterior axillary
60
V6 Placement
left midaxillary line
61
Which leads correspond to the high lateral wall of the left ventricle?
Leads I and aVL
62
Which leads correspond to the inferior wall of the left ventricle?
Leads II, III, and aVF
63
Which leads correspond to the septal wall of the left ventricle?
Leads V1 and V2
64
Which leads correspond to the anterior wall of the left ventricle?
V3 and V4
65
Which leads correspond to the lateral wall of the left ventricle?
V5 and V6
66
Pacemaker centers of Automaticity
SA node, Atrial foci, junctional foci, and ventricular foci
67
Ventricular Escape Rhythm
20-40 bpm
essentially regular rhythm
p waves usually absent or appear after QRS
QRS \> 0.12sec
68
Enhanced automaticity
increase in slope of phase 4 repolarization resulting in the cell reaching threshold more often per minute
69
Early afterdepolarizations
occur during the inciting action potential
can lead to torsades de pointes
70
Normal QT length
450ms in men; 460ms in women
71
Bradycardia
\< 60 bpm
72
Tachycardia
\> 100 bpm
73
Second degree AV Block - Type II
dropped P wave not preceded by PR prolongation
disease of His-Purkinje system
74
LBBB
bunny ear R wave on V6
75
Trifasciular Block
1st degree AV block, RBBB, and LAFB or LPFB
76
Premature Ventricular Contractions (PVCs)
heartbeat is initiated by the ventricles instead of the sinus node
wide QRS, followed by compensatory pause
77
Ventricular Tachycardia
run of 3+ PVCs in a row
78
Stroke Volume
influenced by energy of contraction and aortic pressure
79
How does arterial pressure affect stroke volume?
Atrial pressure **depresses** stroke volume
## Footnote
ejection cannot begin until ventricular pressure exceeds aortic pressure
80
Afterload-Shortening Relation
if afterload increases, rate and degree of shortening decrease
81
the ejection phase is roughly equivalent to \_\_\_\_?
isotonic shortening
82
On what part of the length-tension cure do myocytes normally operate?
Ascending part
83
Anrep Effect
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
Cardiac muscle has a much steeper curve than skeletal msucle because stretch increases Ca sensitivity of cardiac myocytes
85
Frank's experiment
energy of contraction increases as a function of diastolic distension
86
'law of the heart'
the greater the stretch of the ventricle in diastole, the greater the stroke work acheived in systole
87
Stroke Work Equation
change in pressure \* change in volume
88
What represents the area inside the pressure-volume loop
Stroke work
89
upper boundary of the pressure-volume loop
isovolumetric pressure relaxation
## Footnote
systolic pressure that would be generated if ejection were prevented
90
Is increasing afterload good or bad?
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
What (5) factors affect volume distribution
* gravity
* peripheral venous tone
* skeletal muscle pump
* heart
* breathing pattern
92
How does gravity effect CVP?
decreases
venous pooling causes more of the blood supply to go to the lower limbs
93
If CO is suddenly reduced (as in a heart attack), what happens to the filling pressure
it rises
94
How does respiration affect CO and pressure?
* inspiration raises right ventricular stroke volume
* decreases LVSV
* overcome by tachycardia
* inspiration boosts filling pressure of right ventricle
95
Traube-Hering Waves
synchronous oscillations in arterial pressure due to breathing
96
Why does CVP change less than arterial pressure?
venous compliance is greater than arterial compliance
97
Coughing
* raises intrathoracic pressure
* reduces or can reverse ventricular transmural pressure in diastole
98
Negative Inotropic influences
* parasympathetic (vagal) activity
* cholinergic agonists
* B-blockers
* CCB
* hyperkalemia
* barbituates
* acidosis and hypoxia
* chronic cardiac failure
99
Why are diuretics used in heart failure?
in heart failure an excessively high CVP over-distends the heart
## Footnote
increased radius impairs the conversion of active wall tension into internal pressure
100
How do you increase ventricular contractility?
noradrenaline and adrenaline
## Footnote
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
Cardiac Index equation
CI = CO / BSA
102
Cardiac Output equation
CO = (MAP - CVP) / SVR
or
CO = SV \* HR
103
What affects ESV
afterload (increases) and iontropy (decreases)
104
How does preload affect EDV?
increases
105
What 2 things decrease right ventricular preload?
increased HR and increased inflow resistance
106
What increases venous pressure (CVP)
venous volume
* venous return
* total blood volume
* respiration
* muscle contraction
* gravity
107
What (5) things increase right ventricular preload
* ventricular failure
* increase atrial contractility
* increase ventricular compliance
* increase venous pressure
* increase outflow resistance and afterload
108
Transmural pressure
Pinside - Poutside
(venous pressure - intrathoracic pressure)
109
Normal range for intrathoracic pressure
-5 to -10 cmH20
110
Law of Laplace
P = 2T/r
T = wall stress \* thickness
111
first arrow = Frank-Starling Law
second (top) arrow = LaPlace's Law
112
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
line = ESPVR (inotropic state)
1 = Normal
2 = increased EDV
- increased stretch due to increased preload
3 - increased afterload
4 - maximum afterload (no SV)
114
Intrinisic and extrinsic regulation of Contractility
Intrinsic = Frank-Starling mechanism
Extrinsic = sympathetic nervous system
115
SNS effect on cardiac function
* increased
* ventricular pressure
* ejection fraction
* stroke volume
* decrease
* diastolic volume
* duration of systole
116
Circulating Inotropes
* Catecholamines (adrenal medulla)
* epinephrine, norepinephrine
* Angiotensin
* Calcium ions
* insulin, thyroxine, glucagon
117
Bowditch Effect
Changes in heart rate affect contractility
* increased heart rate causes increased contractility
* due to increase SR calcium store
* relatively small contribution in exercise
118
What decreases inotropy?
systolic failure
119
Increase CO in exercise
* increase sympathetic discharge
* increase in EF and HR
* increase preload
* venoconstriction, skeletal muscle pump
* decrease afterload
* arterial vasodilation
120
Darcy's Law
Q = (P1 - P2) / R
clinically applied:
CO = (PMAP - PCVP) / RSVR
121
Bernoulli's Relationship
E = P + p\*g\*h + (p\*v2)/2
122
Laminar Blood Flow
Q is proportional to change in pressure
* areas of laminar flow
* arteries, arterioles, venules, veins
123
Turbulent Blood Flow
Q proportional to sqrt(change in pressure)
\*Darcy's law does not apply
124
Where does bolus flow occur?
exchange vessels
125
shear stress
friciton betwen molecules in lamina
126
Shear rate
change in fluid velocity per unit distance normal to direction of flow
127
Fahraeus-Lindqvist effect
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
* Reflection wave
* diastole in young
* aids in coronary perfusion
* systole in old
* adds to afterload
129
