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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
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
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