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113 Cards in this Set
- Front
- Back
|
Absolute Refractory Period
|
from Na and Ca inactivation - from 0 to 3 - increase DRK activity, delay repol and ARP is longer - decrease Ca activity and AP shorter
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Relative Refractory Period
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from Ca's slowly becomming activated - decrease Ca activity and increase RRP - from mid 3 to 4
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How SA node works
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Na's always inactiviated - fewer IRK's so max diasole potential at -60 - IF channels activate at negative MPs so allows Na influx (K too but small driving force) - around -50, Ca's activate -> slow Ca based AP
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How AV node works
|
same as SA but fewer gap jxns so even slower than SA - no phase 1, shorter plateau
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The effects of a change in depol rate in 4
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increase rate, increase pace - do this by:
- increase If activity - increase DRK closing - increase Ca activation |
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The effects of changing the max diastole depolarization on pace
|
higher MDD, faster pace - do this by:
- decrease IRK's - decrease DRK's |
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The effects of changing threshold on pace
|
lower threshold, higher pace - do this by
- increase Ca activation |
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Sympathetic effects on heart
|
Increase pace and force
- ACh gets nicotinic receptors on post gang, which gets As, Vs, and nodes - relase NE (E from adrenal) - increase Ca activity to decrease threshold and have more SR relase for force - resequester rate increased too so heard can fill - If is increased - DRKs increased to increase repol rate |
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Parasympathetic effects on heart
|
Vagus relases ACh to get nicotinic on post - post gets A's and nodes (NO Vs!!) and releases ACh which gets muscarine receptors
- decrease Ca activity to increase threshold - increase IRK channels (more hyperpolarized) - decrease If |
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ECG divisions
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horizontal big - 0.2 sec
vertical big - .5 mV |
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P wave
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from DP over atria (from SA) - atrial systole - positive in I, II, and aVF - negative in aVR
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PR segment
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from delay of excitation (slow AV) from A to V
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Q wave
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from DP spread over IV septum - small negative - L to R, apex to base - negative in I, II, aVL - none in aVF or III
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R wave
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from DP spread throught apex - large positive (apex big) -
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S wave
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from larger stages of ventrical depol - spread through L, some R V and walls - negative in aVF, II, III - not in I or aVL
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QRS wave
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represents ventricular systole -
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ST segment
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when V is most depolarized (no signal, all DP'd)
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T wave
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from V repol (epi -> endo) - usually positive in I and II, neg in aVR
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QT interval
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duration of electrical V systole
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Lead I
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0 degrees
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Lead II
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60 degrees
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Lead III
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120 degrees
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aVR lead
|
-150 degrees
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aVL lead
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-30 degrees
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aVF lead
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90 degrees
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Premature Atrial Contraction
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ectopic pacemaker in atria - rhythm is is irregular - QRS normal - can come from stress, caffeine
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Premature Ventricular Contraction
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ectopic pacemaker in ventrical - prolonged QRS, no P
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Paroxysmal Atrial tachycardia
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re-entry near AV node - no P, irregular QRS
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Atrial Flutter
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re-entry at atria - rhythmic, high frequency oscillations for P - partial AV block
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Atrial Fibrillation
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chaotic atrial excitation - no P, corse or fine oscillations - ventricular rate varies - 2:1 block
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1st degree AV block
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prolonged, uniform PR - minor defect
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2nd degree AV block
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from worsening AV conduction - PR may increase until conduction fails and V is missed, or more consistent
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3rd degree AV block
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V rhythm independent , need artificial pacemaker
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VOCC and SR Ca channels
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VOCC open when AP get cardiac cell surface and cause EC influx - Skeletal muscle doesn't have them so cardiac drugs target - SR open when AP hits T-tubules - in exercise, NE and E bind B1 and increase cAMP which increases VOCC and inhibits SR less (so increase)
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Relaxation during diastole
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repol closes VOCC and SR Ca's - ATP-Ca pumps Ca back outside the cell
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3 variables determine # and rate of crossbridge pulling
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- CTY - level of IC Ca in systole - can be graded w/ NE and EPI
- preload - amt of overlap determined by amt of stretch - afterload |
|
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how smooth muscle depolarized
|
depol mainly from EC - IP3 receptors on SR for Ca release - Ca can be grated like cardiac - No Na channels - NTs bind or strech load changes, which aters K conductance -> Em change - > change in VOCC conductance
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5 stimuli of Smooth muscle
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- Neural - NE, ACh
- Hormonal - Stretch -> depol - Metabolic changes - tone, H, O - Paracrine/Autocrine |
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Smooth muscle consrtiction and dilation mechanisms
|
- NE from sym, angiotensin from kidney, or vasopressin from pituitary - bind receptors which cause IP3 release
- Adeonosine (from activity) and epi activate adenylate cyclase -> cAMP - or NO can activate SMC guanylate cyclase which form cGMP |
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P in arms and legs
|
95
|
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P in lungs
|
15
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P in coroary
|
100
|
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P in vena cava
|
1-3
|
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P in veins other than vena cava
|
10
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Q =
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delta P/R
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MAP =
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CO * SVR (SVR determined by arteriole diameter)
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BP =
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(MAP - CVP)/CO
|
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CO =
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HR * SV
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4th heart sound
|
flow from A to V - chordae tendinae vibrations - will hear if LV hypertrohpy
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1st heart sound
|
lub - M then T valves closing
|
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SV value
|
75 mL for a 75 kg person
|
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CO value
|
5L / min
|
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2nd Heart sound
|
A then P closing
|
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3rd heart sound
|
rapid filling of A and V - from chordae tendinae vibrations - a dilated V will make you hear it
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L Mechanical Diastole lasts from ____ to _______
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from A closure through iso relax, V filling and atrial contraction
|
|
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L Mechanical systole lasts from ____ to _______
|
mitral closing to aortic closing
|
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Question
|
Answer
|
|
|
Absolute Refractory Period
|
from Na and Ca inactivation - from 0 to 3 - increase DRK activity, delay repol and ARP is longer - decrease Ca activity and AP shorter
|
|
|
Relative Refractory Period
|
from Ca's slowly becomming activated - decrease Ca activity and increase RRP - from mid 3 to 4
|
|
|
How SA node works
|
Na's always inactiviated - fewer IRK's so max diasole potential at -60 - IF channels activate at negative MPs so allows Na influx (K too but small driving force) - around -50, Ca's activate -> slow Ca based AP
|
|
|
How AV node works
|
same as SA but fewer gap jxns so even slower than SA - no phase 1, shorter plateau
|
|
|
The effects of a change in depol rate in 4
|
increase rate, increase pace - do this by: - increase If activity - increase DRK closing - increase Ca activation
|
|
|
The effects of changing the max diastole depolarization on pace
|
higher MDD, faster pace - do this by: - decrease IRK's - decrease DRK's
|
|
|
The effects of changing threshold on pace
|
lower threshold, higher pace - do this by - increase Ca activation
|
|
|
Sympathetic effects on heart
|
Increase pace and force - ACh gets nicotinic receptors on post gang, which gets As, Vs, and nodes - relase NE (E from adrenal) - increase Ca activity to decrease threshold and have more SR relase for force - resequester rate increased too so heard can fill - If is increased - DRKs increased to increase repol rate
|
|
|
Parasympathetic effects on heart
|
Vagus relases ACh to get nicotinic on post - post gets A's and nodes (NO Vs!!) and releases ACh which gets muscarine receptors - decrease Ca activity to increase threshold - increase IRK channels (more hyperpolarized) - decrease If
|
|
|
ECG divisions
|
horizontal big - 0.2 sec vertical big - .5 mV
|
|
|
P wave
|
from DP over atria (from SA) - atrial systole - positive in I, II, and aVF - negative in aVR
|
|
|
PR segment
|
from delay of excitation (slow AV) from A to V
|
|
|
Q wave
|
from DP spread over IV septum - small negative - L to R, apex to base - negative in I, II, aVL - none in aVF or III
|
|
|
R wave
|
from DP spread throught apex - large positive (apex big) -
|
|
|
S wave
|
from larger stages of ventrical depol - spread through L, some R V and walls - negative in aVF, II, III - not in I or aVL
|
|
|
QRS wave
|
represents ventricular systole -
|
|
|
ST segment
|
when V is most depolarized (no signal, all DP'd)
|
|
|
T wave
|
from V repol (epi -> endo) - usually positive in I and II, neg in aVR
|
|
|
QT interval
|
duration of electrical V systole
|
|
|
Lead I
|
0 degrees
|
|
|
Lead II
|
60 degrees
|
|
|
Lead III
|
120 degrees
|
|
|
aVR lead
|
-150 degrees
|
|
|
aVL lead
|
-30 degrees
|
|
|
aVF lead
|
90 degrees
|
|
|
Premature Atrial Contraction
|
ectopic pacemaker in atria - rhythm is is irregular - QRS normal - can come from stress, caffeine
|
|
|
Premature Ventricular Contraction
|
ectopic pacemaker in ventrical - prolonged QRS, no P
|
|
|
Paroxysmal Atrial tachycardia
|
re-entry near AV node - no P, irregular QRS
|
|
|
Atrial Flutter
|
re-entry at atria - rhythmic, high frequency oscillations for P - partial AV block
|
|
|
Atrial Fibrillation
|
chaotic atrial excitation - no P, corse or fine oscillations - ventricular rate varies - 2:1 block
|
|
|
1st degree AV block
|
prolonged, uniform PR - minor defect
|
|
|
2nd degree AV block
|
from worsening AV conduction - PR may increase until conduction fails and V is missed, or more consistent
|
|
|
3rd degree AV block
|
V rhythm independent , need artificial pacemaker
|
|
|
VOCC and SR Ca channels
|
VOCC open when AP get cardiac cell surface and cause EC influx - Skeletal muscle doesn't have them so cardiac drugs target - SR open when AP hits T-tubules - in exercise, NE and E bind B1 and increase cAMP which increases VOCC and inhibits SR less (so increase)
|
|
|
Relaxation during diastole
|
repol closes VOCC and SR Ca's - ATP-Ca pumps Ca back outside the cell
|
|
|
3 variables determine # and rate of crossbridge pulling
|
- CTY - level of IC Ca in systole - can be graded w/ NE and EPI - preload - amt of overlap determined by amt of stretch - afterload
|
|
|
how smooth muscle depolarized
|
depol mainly from EC - IP3 receptors on SR for Ca release - Ca can be grated like cardiac - No Na channels - NTs bind or strech load changes, which aters K conductance -> Em change - > change in VOCC conductance
|
|
|
5 stimuli of Smooth muscle
|
- Neural - NE, ACh - Hormonal - Stretch -> depol - Metabolic changes - tone, H, O - Paracrine/Autocrine
|
|
|
Smooth muscle consrtiction and dilation mechanisms
|
- NE from sym, angiotensin from kidney, or vasopressin from pituitary - bind receptors which cause IP3 release - Adeonosine (from activity) and epi activate adenylate cyclase -> cAMP - or NO can activate SMC guanylate cyclase which form cGMP
|
|
|
P in arms and legs
|
95
|
|
|
P in lungs
|
15
|
|
|
P in coroary
|
100
|
|
|
P in vena cava
|
1-3
|
|
|
P in veins other than vena cava
|
10
|
|
|
Q =
|
delta P/R
|
|
|
MAP =
|
CO * SVR (SVR determined by arteriole diameter)
|
|
|
BP =
|
(MAP - CVP)/CO
|
|
|
CO =
|
HR * SV
|
|
|
4th heart sound
|
flow from A to V - chordae tendinae vibrations - will hear if LV hypertrohpy
|
|
|
1st heart sound
|
lub - M then T valves closing
|
|
|
SV value
|
75 mL for a 75 kg person
|
|
|
CO value
|
5L / min
|
|
|
2nd Heart sound
|
A then P closing
|
|
|
3rd heart sound
|
rapid filling of A and V - from chordae tendinae vibrations - a dilated V will make you hear it
|
|
|
L Mechanical Diastole lasts from ____ to _______
|
from A closure through iso relax, V filling and atrial contraction
|
|
|
L Mechanical systole lasts from ____ to _______
|
mitral closing to aortic closing
|
