1-7 Cardiovascular Flashcards Preview

PHYSIOLOGY Exam 1 > 1-7 Cardiovascular > Flashcards

Flashcards in 1-7 Cardiovascular Deck (68):
1

A: The [HIS/Purkinje System] is a ______ conduction system which allows ______ cells to ALL contract synchronously!

vs.

B: SA and AV node which are both ______-response conduction systems

C: AV node ______[quickens/Slows] nerve impulse it receives from SA node to allow Good ______ Filling AND to protect ______ from high ______ rates!
It exhibits a ______ refractory period (known as ______) and has slow [Action Potential ______]. These are both due to ______.
AV nodal conduction time is clinically determined on EKG by [______]

A: The [HIS/Purkinje System] is a RAPID conduction system which allows Ventricular cells to ALL contract synchronously!

vs.

B: SA and AV node which are both slow-response conduction systems

C: AV node SLOWS nerve impulse it receives from SA node to allow Good Ventricular Filling AND to protect Ventricles from high atrial rates!
It exhibits a LONG refractory period (post-repolarization refractoriness) and has slow [Action Potential upstroke] due to [slow inward Ca+ current].
AV nodal conduction time is clinically determined on EKG by [PR Interval]

2

1A. L Ventricle generates more ______/force (___ mm Hg) BECAUSE [______ circulation resistance] that it works against is HIGHER than ______ resistance for the R Ventricle

1B: L Ventricle and R Ventricle have EQUAL ______ ______ even though L Ventricle generates much more pressure

2. Purkinje fibers sends nerve impulses from ______ ----> ______ for ventricular contraction sync BUT FIRST sends contracting signals to ______ to hold on to [______ ______] during Systole. This All happens during [______] of an EKG

1A. L Ventricle generates more pressure/force (120 mm Hg) BECAUSE [systemic circulation resistance] that it works against is HIGHER than pulmonary resistance

1B: L Ventricle and R Ventricle have EQUAL Cardiac Output even though L Ventricle has much more pressure

2. Purkinje fibers sends nerve impulses from Endocardium ----> EPIcardium for ventricular contraction sync BUT FIRST sends contracting signals to Papillary m. to hold on to [Chordae Tendinae] during Systole. This All happens during [QRS interval] of an EKG

3

A: On an EKG the [P-R interval] is AKA the ______ and is the time nerve impulses travels from Atria---> ______---> ______---> ______

B: On an EKG the [____ interval] is the time nerve impulse travels from Endo--->EPIcardium. This interval can represent ______ ______! The interval should be LESS than ___ ms. If More than __ ms = DEC in ______

C: ______ is NOT apart of QRS but enables for the QRS to occur because it brings impulse to ______ surface!

D: P-S interval should be no more than ____ ms

E: On an EKG the [Q-T] interval represents ______

A: On an EKG the [P-R interval] is AKA the [AV nodal conduction time] and is the time nerve impulse travels from Atria--->AV Node--->[HIS Purkinje System]--->Ventricles

B: On an EKG the [QRS interval] is the time nerve impulse travels from Endo--->EPIcardium. This interval can represent CONTRACTION STRENGTH! The interval should be LESS than 100 ms. If More than 100 = DEC in strength

C: [HIS Purkinje System] is NOT apart of QRS but enables for the QRS to occur because it brings impulse to Endocardium surface!

D: P-S interval should be no more than 200 ms

E: On an EKG the [Q-T] interval represents Action Potential duration

4

A: Resting Membrane Potential of the Heart = -___ mV (Same as __+)
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B: Nernst equation is a ______ equilibrium potential based on ______ ion vs. [Goldman-Katz equation] which is ______ resting membrane potential . [GK] considers Na, K, Cl and their ______ ______.

B2: ACTUAL Resting Membrane Potential is more [+] than Nernst prediction because of what 2 things?
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C: The [Na/K+ pump] requires ___, maintains ____ gradient and IS inhibited by [______ ______]. [______ ______] causes an INC of contraction in CHF patients. [Na/K+ pump]= 3 Na+ ___ and 2 K+ ___= electrogenic net ______(______ + charges)
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D: The [Na/Ca+ pump] purpose is to MAINTAIN ______ INTRACELL Ca+ so it pumps Ca+ ______. Pump is driven by __ gradient and so can be indirectly affected by changes in [____ pump]. It exchanges [3 Na+ __] for [1 Ca+ __] but because Ca+ has a +2 charge = electrogenic net ______ (______ + charges)
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E: Contractures are ______ caused by ______[High/Low] INTRACELLULAR Ca+

A: Resting Membrane Potential of the Heart = -90 mV (Same as K+)
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B: Nernst equation is a THEORETICAL equilibrium potential based on ONE ion vs. [Goldman-Katz equation] which is ACTUAL resting membrane potential . [GK] considers Na, K, Cl and their relative permeabilities.
B2: ACTUAL Resting Membrane Potential is more [+] than Nernst prediction because
1. Na+ leaks INTO cell
2. [Inward anomalous Rectification] will occur at low extracell voltages --->K+ WON'T leak out
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C: The [Na/K+ pump] requires ATP, maintains Na/K+ gradient and IS inhibited by [Digitalis glycosides]. [Digitalis glycosides] causes an INC of contraction in CHF patients. [Na/K+ pump]= 3 Na+ OUT and 2 K+ in = electrogenic net OUTWARD(LOSING + charges)
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D: The [Na/Ca+ exchanger] purpose is to MAINTAIN LOW INTRACELL Ca+ so it pumps Ca+ out. Pump is driven by Na+ gradient and so can be indirectly affected by changes in [Na/K+ pump]. It exchanges [3 Na+ IN] for [1 Ca+ OUT] but because Ca+ has a +2 charge = electrogenic net inward(gaining + charges)
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E: Contractures are LOCKED UP States of muscle contraction caused by HIGH INTRACELLULAR Ca+

5

A: [Inward anomalous Rectification] is a LOCKDOWN DEC of __ permeability (via ___ receptors) to protect it from _____ cell.

B: This Occurs when there is an electrical {______} or chemical{______} gradient driving ___ ______ of the cell

C: When [IAR] Stops __ from flowing ______ of cell during {Action Potential Plateau} prevents premature ______ during an ______ ______

A: [Inward anomalous Rectification] is a LOCKDOWN DEC of K+ permeability (via IK1 receptors) to protect it from leaving cell.

B: Occurs when there is an electrical {Action Potential Plateau} or chemical{hypokalemia} gradient driving K+ OUT of the cell

C: When [IAR] Stops K+ from flowing out of cell during {Action Potential Plateau} prevents premature REPOLARIZATION during an Action Potential

6

A:
ºWhen intracell Voltages are ______ than K+ Equilibrium
--->K+ rushes into cell

ºWhen intracell Voltages are ______ than K+ Equilibrium (such as during ______ ______ ______) K+ channels DON'T ALLOW K+ to leave cell = ______

ºDuring Action Potential Plateau, K+ permeability ______ which is why ______ is delayed and allows for ______[shorter/longer] refractory period
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B: HYPERkalemia ______ K+ concentration gradient across membrane---> ______ K+ membrane permeability. This will make [Resting Membrane Potential] more ______ and ______ to depolarize. This also ______ [Na+ channel] availability ---> ______[strong/weak] CONDUCTIONS

A:
ºWhen intracell Voltages are negative/LOWER than K+ Equilibrium --->K+ rushes into cell

ºWhen intracell Voltages are Positive/GREATER than K+ Equilibrium (such as during action potential plateau) channels DON'T ALLOW K+ to leave cell = IAR

ºDuring Action Potential Plateau, K+ permeability DEC which is why repolarization is delayed and allows for longer refractory period
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B: HYPERkalemia DEC K+ concentration gradient across membrane---> INC K+ membrane permeability. This will make [Resting Membrane Potential] more POSITIVE and easier to depolarize. This also DEC [Na+ channel] availability ---> WEAK CONDUCTIONS

7

A: hypOkalemia ______ concentration gradient across membrane (K+ starts to rush ______) which is not good. Cell prevents this by using [______ ______ ______] which ______ K+ membrane permeability and locks K+ ______ the cell!

B: [T or F] hypOkalemia has no change in membrane potential

hypOkalemia INC concentration gradient across membrane (K+ starts to rush out) which is not good. Cell prevents this by using [Inward anomalous rectification] which DEC K+ membrane permeability and locks K+ inside the cell!

TRUE! hypOkalemia has no change in membrane potential.

8

Describe the Ventricular Phases and activity that occurs

*Phase 0 = ______ channels open until ______ is reached and [______ channels turn OFF]--->RAPID ______. Slow ___ Channels ALSO are activated during initial [______ ______ Upstroke] but at this time they aren't important.

*Phase 1= Na+ channels Close and ______ TRANSIENTLY opens for small ______ right before ______ locks it up!

*Phase 2= Ca+ channels open for [______ ______ ___current], Ventricles start [______ ______ ______] and [______ ______ ______] occurs in [______ channels] --> [______ channels] LOCKING DOWN K+ membrane permeability

*Phase 3= ______ activation of K+ channel [iK channels]
--->finally allows K+ to ______ cell = reverses ______ and starts ______

*Phase 4 = background ___ conductance via [______ receptors] is High, ___ channels recover from inactivation but are still closed and Ca+ channels and [delayed ___ channels] remain closed. This is the ______ ______ ______

B: SA and AV node are only active in what phases?

Describe the Ventricular Phases and activity that occurs

*Phase 0 = Na+ channels open until E(Na+) is reached and [iK1 K+ receptors turn OFF]--->RAPID DEPOLARIZATION. Slow Ca+ Channels ALSO are activated during initial [Action Potential Upstroke] but at this time they aren't important.

*Phase 1= Na+ channels Close and [K+ channel iTO receptor] TRANSIENTLY opens for SMALL Repolarization right before IAR locks it up!

*Phase 2= Ca+ channels open for [slow inward Ca+ current], Ventricles start [Action Potential Plateau] and [Inward anomalous Rectification] occurs in [iK1 channels] --> [iK1 channels] LOCKING DOWN K+ membrane permeability

*Phase 3= DELAYED activation of K+ channel [iK channels]
--->finally allows K+ to leave cell = reverses IAR and starts Repolarization

*Phase 4 = background K+ conductance via [iK1 channels] is High, Na+ channels recover from inactivation but are still closed and Ca+ channels and [delayed iK channels] remain closed. = [Resting Membrane Potential ]

B: SA and AV node are only active in Phase 0, 3 and 4

9

A: All ______ Responses contain weak ______ responses

B: Tetrodotoxin (TTX) only blocks [______ channel] used for rapid depolarization BUT this forces the [______ channel influx] to take over for [phase __] ______ and slowly ______ the heart---->fatal ______ from ______[fast/slow] Action Potential Conduction and ______ of ______ IN VENTRICLES.

C:Example: Myocardial Infarctions causes ______ of Resting membrane potential--->Inactivates ____channels
----> local change of ______ to ______ response ---> ______ Conduction

D: What this means is that ______ responses can become ______ responses under certain abnormal conditions

A: All Fast Responses contain weak Slow responses

B: Tetrodotoxin (TTX) only blocks [fast Na+ channel] rapid depolarization BUT this forces the [slow Ca+ channel influx] to take over for [phase 0] upstroke and slowly depolarize the heart---->fatal Arrhythmia from slow Action Potential Conduction and reentry of excitation IN VENTRICLES.

C:Example: Myocardial Infarctions causes depolarization of Resting membrane potential--->Inactivates Na+ channels----> local change of Fast to sloow response --->Slows Conduction

D: What this means is that Fast responses can become slow responses under certain abnormal conditions

10

Comparing [SA/AV node] to [HIS-Purkinje]


1. Membrane potential
2. Threshold
3. Upstroke and Conduction
4. Duration
5. Size Diameter and [space length] constant
6. Purpose
7. # of Gap Junctions
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Atrial & Ventricular Muscle have a ______sized diameter, ______ [space length] constant and ______ [Gap Junction] connections with ______ myofibrils. It can contract AND conduct but is mostly used for ______

Comparing [SLOW SA/AV node] to [FAST HIS-Purkinje]

[SLOW SA/AV node]
1. Membrane potential = low
2. Threshold = low (-40 mV)
3. Upstroke and Conduction= sloooow
4. Duration = short!
5. small diameter with short [space length] constant
6. Purpose = Pacemaker
7. Few Gap Junctions
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[FAST HIS-Purkinje]
1. Membrane potential = HIGH
2. Threshold = HIGH (-65 mV)
3. Upstroke and Conduction= FAST
4. Duration = LONG
5. LARGE DIAMETER with LONG [space length] CONSTANT
6. Purpose = rapid conduction
7. Few Gap Junctions
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Atrial & Ventricular Muscle have a medium diameter, medium [space length] constant and MANY [Gap Junction] connections and MANY myofibrils. It can CONTRACT and conduct but is mostly used for CONTRACTION

11

A: ______ Disc are regions of connections between ______ Cells. 3 types of adhering junctions:
Describe Each:
1) [Fascia Adherens]

2) [Desmosome Macula Adherens] = holds cells together during ______ by binding ______ ______

3) [Gap Junctions] which are ______ resistance connections tht use ______ channels to transfer ______ ______ between cardiac cells. These are the primary source of ______ ______ in cardiac tissue and are VERY sensitive to INTRACELLULAR ______ and ______ .
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B1: [Gap Junctions] will CLOSE UP if exposed to too much INTRACELLULAR ______ and ______ = ______ ______

B2: What is the BENEFIT of the process in B1?

B3: How is this related to the way a old MI appears on EKG?

A: Intercalated Disc are regions of connections between Cardiac Cells. 3 types of adhering junctions:
1) [Fascia Adherens] = Adherens that connects actin of 1 sarcomere to next sarcomere

2) [Desmosome Macula Adherens] = holds cells together during contraction by binding intermediate filaments

3) [Gap Junctions] which are low resistance connections tht use Connexon channels to transfer ACTION POTENTIALS between cardiac cells. These are the primary source of internal resistance in cardiac tissue and are VERY sensitive to INTRACELLULAR Ca+ and H+.

B: [Gap Junctions] will CLOSE UP if exposed to too much INTRACELLULAR Ca+ and H+---> [Healing Over]

B2: Benefit= Damaged areas usually have high intracell Ca+ and H+ and so with closed [Gap Junctions] this area will be isolated from healthy tissue.

B3: MI will appear to look normal on an EKG due to [Healing Over]. Damaged area of the heart is shut down.

12

**Factors that determine Cardiac Conduction**
1. Membrane resistance
2. Internal resistance
3. [Rate of Rise AND Action Potential Amplitude]
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1. ______ Membrane resistance = less chance for K+ to flow out /DEC [K+ permeability] --> ______[More/Less] K+ current to travel down the cell = [length space] constant is ______

***INC Membrane resistance = ______ [K+ permeability] = ______ [length space] constant***
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2. INC [Internal resistance] occurs from DEC ______ or ______

3. [Rate of Rise AND Action Potential Amplitude] is based on [______ ______ ______ speed] and is affected by what 2 things?

**Factors that determine Cardiac Conduction**
1. Membrane resistance
2. Internal resistance
3. [Rate of Rise AND Action Potential Amplitude]
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1. INC Membrane resistance = less chance for K+ to flow out /DEC [K+ permeability] --> More K+ current to travel down the cell = [length space] constant is LARGER

***INC Membrane resistance = DEC [K+ permeability] = INC [length space] constant***
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2. INC [Internal resistance] occurs from DEC [Gap Junctions] or [DEC in Cell Diameter]

3. [Rate of Rise AND Action Potential Amplitude] is based on [Action Potential Upstroke speed] and is affected by:

-premature depolarizations during relative refractory period and
-[Resting Membrane Potential] since it determines # of Na+ channels available and thus UPSTROKE RATE

13

**3 Factors that affect [Action Potential Upstroke speed] as a result of messing with the [Resting Membrane Potential] level

1. Hyperkalemia ---> ______ Resting Membrane Potential and makes more ______---->less ___ channels available
---> weak ______

2. Premature ______ dring ______ refractory period(AKA ______ ______ period)

3. ______ or MI that prevents __ from being physically removed from the area OR INC [______ ______] from [______ ______] closure .

**3 Factors that affect [Action Potential Upstroke speed] as a result of messing with the [Resting Membrane Potential] level

1. Hyperkalemia ---> INC RMP and makes more POSITIVE---->less Na+ channels available--->weak [Action Potential Upstroke speed]!

2. Premature depolarizations dring relative refractory period(AKA Vulnerable Heart period)

3. Ischemia or MI that prevents K+ from being physically removed from the area or INC [Internal resistance] from [Gap Junction] closure .

14

Why does Conduction SLOW DOWN in damaged regions of the heart??

After ischemia/infarct intracell ___ leaks out of damaged cells into extracell environment--->LOCAL ______. LOCAL ______ ______ Resting Membrane Potential making it more ______ and inactives Voltage-dependent __ channel availability----> ______ conduction of Action Potentials----> ______ of ______ ---> Fatal ______


B: K+ milliMolar of more than ___ is considered lethal!

Why does Conduction SLOW DOWN in damaged regions of the heart??

After ischemia/infarct intracell K+ leaks out of damaged cells into extracell environment--->LOCAL Hyperkalemia. LOCAL Hyperkalemia INC RMP/makes more POSITIVE and inactives Voltage-dependent Na+ channel availability----> poor conduction of Action Potentials---->Re-entry of excitation ---> Fatal Arrhythmias

B: K+ milliMolar of more than 10 is considered lethal!

15

AV nodal Conduction Blocks!
A:
1st degree heart block = Gap between P and R is greater than ______ ms. This indicates that ______ are taking too long to send signal to ______.
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2nd degree heart block= Sometimes ______ is NOT followed by a ______ which means ______ are depolarizing but ______ aren't following sometimes

There are two types: ______ I and ______ II.

[______ I = Wenckebach which is when....]
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3rd degree heart block = ______ = NO CONSISTENT ______ = SA node depolarizes ______ but ______ are being depolarized by some unrelated ______ pacemaker
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B: ______ Degree heart block and ______ degree heart block DOES NOT change HR or [______ ______] = Both don't need tx until sx occur. ______ Degree Heart Block can lead to A-Fib!

AV nodal Conduction Blocks!
A:
1st degree heart block = Gap between P and QRS is greater than 200 ms = Atria are taking too long to send signal to Ventricle.
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2nd degree heart block= Sometimes P-wave is NOT followed by a QRS-wave = Atria are depolarizing but Ventricles aren't following sometimes

There are two types: Mobitz I and Mobitz II.

[Mobitz I = Wenckebach = prolongation of PR interval and then a beat drop]
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3rd degree heart block = COMPLETE AV NODAL CONDUCTION BLOCK = NO CONSISTENT [P - R INTERVAL]= SA node depolarizes Atria but Ventricles are being depolarized by some unrelated latent pacemaker
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B: 1st Degree heart block and 2nd degree heart block DOES NOT change HR or [Cardiac Output] = Both don't need tx until sx occur. 1st Degree Heart Block can lead to A-Fib!

16

A: Heart Resting Membrane Potential is PRIMARILY created by [Passive ______ Diffusion of ___]. This wouldn't occur UNLESS ______ pump first created a high intracell ___ to diffuse ______

2. ______ is usually a result of Renal Failure! and it Inactivates __ channels because it makes Resting Membrane Potential more ______! (This is similar to TTX toxin) which will convert _______ response---> ______ response locally!
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3. Two things that cause Phase __ [Action Potential Plateau]

A: Heart Resting Membrane Potential is PRIMARILY created by [Passive Outward Diffusion of K+]. This wouldn't occur UNLESS [Na+/K+] pump first generated high intracell K+ to diffuse out

2. Hyperkalemia is usually a result of Renal Failure! and it Inactivates Na+ channels because it makes Resting Membrane Potential more Positive! (This is similar to TTX toxin) which will convert Fast response--->Slow response locally! meaning Ca+ will have to take over
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3. Two things that cause Phase 2 [Action Potential Plateau]
*Less Outward K+ Current secondary to IAR locking up [iK1 channels] ) --->More + inside cell
*More inward Current of Ca+ ----->More + inside cell

17

1A. ______ QRS complex indicates SLOW ventricular conduction and is associated with [______ ______ ______]

1B: Causes = ______, ischemia and ______
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2A: A NOTCHED QRS complex indicates ______ electrical activation of L and R ______. It looks like a ______ on EKG

2B: Causes= ______
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1A. WIDENED QRS complex indicates SLOW ventricular conduction and is associated with [Abnormal Wall Motion]

1B: Causes = HYPERkalemia, ischemia and V-tach
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2A: A NOTCHED QRS complex indicates asynchronous electrical activation of L and R Ventricles. It looks like a "bunny ear fork" on EKG

2B: Causes= L or R Bundle Branch Block
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18

A: V-Tachycardia is any HR greater than ______ bpm and is NOT necessarily an ______. It occurs when impulse route changes from ______ TO ______ This is AKA an [______ ______ ______]----> ______ QRS complex---> ______ conduction/contraction -----> ______ Cardiac OUTPUT

B: Different Types of V-Tach
1. ______ tachycardia (abnormal conditions) is the same as ______ tachycardia (Normal conditions). It involves ______ and does NOT affect ______ ______ {specifically ______ volume} by Much. In SVT.. ______ duration, ______ Wall motion and [conduction through ______ is rapid] but still ALL NORMAL

2. VENTRICULAR TACHYCARDIA IS when impulse originates within the ______ and does not utilize the ______----> ______ QRS complex----> ______ ______ ______ ----> ______ Cardiac Output
**Ventricular Tachycardia eventually degenerates into ______**

3. During ______, you have 2 minutes to cardiovert before pt dies. It and ______ are both due to ______
--->asynchronous pumping

C: In [______ tachycardia] (normal conditions).. ______ is the phase that shortens the most/takes biggest blow!.. ______ shortens a little but that's only to compensate for loss in ______

A: V-Tachycardia is any HR greater than 100 bpm and is NOT necessarily an arrhythmia. It occurs when impulse route changes from [Endo---->Epicardium ] TO longitudinal "long" route. This is AKA an [Abnormal Wall Motion]----> WIDENS QRS complex---> DEC conduction/contraction -----> DEC Cardiac OUTPUT

B: Different Types of V-Tach
1. Supraventricular tachycardia (abnormal conditions) is the same as Sinus tachycardia (normal conditions). It involves ATRIA and does NOT affect Cardiac Output {specifically stroke volume} by Much. In SVT.. QRS duration, Ventricular Wall motion and [conduction through ventricles is rapid] but ALL NORMAL

2. VENTRICULAR TACHYCARDIA IS when impulse originates within the Ventricle itself and does not utilize the [HIS-Purkinje system]!----> Widened QRS complex----> Abnormal Ventricular Wall Motion ---->DEC Cardiac Output
**Ventricular Tachycardia eventually degenerates into V-Fib!!**

3. During V-Fib, you have 2 minutes to cardiovert before pt dies. It and A-Fib are both due to re-entry of excitation--->asynchronous pumping

C: In [Sinus tachycardia] (normal conditions)..Diastole is the phase that shortens the most/takes biggest blow!..Systole shortens a little but that's only to compensate for loss in Diastole

19

Effects of Autonomic System on Heart:
1. ACh is used by ______ to act on ______ receptors and INHIBIT both ______ (lengthens PR interval) and ______ =____ HR)
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How does ______[sympathetic/PARAsympathetic] ACh do this?
A-______ K+ permeability using __-proteins
---> ______ Resting Membrane/DIASTOLIC Potential and pulls it AWAY from ______ and ______ slope of [Diastolic depolarization]

B- INHIBITS ______ synthesis by blocking ______. This allows ACh to ______ [L-type slow inward Ca+ current] which is responsible for ______ node conduction

C-DIRECTLY blocks ______ muscle --> [______ inotropic effect] = ______ Contraction STRENGTH.

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2.[ ______(sympathetic/PARAsympathetic) ACh] has NO DIRECT effect on ______ Function!!!!!!!!
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3. inotropic effect = ______ ______

Effects of Autonomic System on Heart:
1. ACh is used by [PARAsympathetic Vagus nerve] to act on Muscarinic receptors and INHIBIT both AV node conduction (lengthens PR interval) and SA node pacemaker (slows HR)
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How does PARAsympathetic ACh do this?
A-INC K+ permeability using G-proteins --->HYPERpolarizes Resting Membrane/DIASTOLIC Potential pulling it AWAY from threshold and DEC slope of [Diastolic depolarization]

B- INHIBITS [cAMP stimulant] synthesis by blocking [adenylate cyclase]--->allows ACh to DEC [L-type slow inward Ca+ current] which is responsible for Ventricular contraction

C-DIRECTLY blocks atrial muscle --> [negative inotropic effect] =DEC Contraction STRENGTH.

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2.[ PARAsympathetic ACh] has NO DIRECT effect on Ventricle Function!!!!!!!!
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3. inotropic effect = Contraction STRENGTH

20

Effects of Autonomic System on Heart:

1. ______ is used by [Sympathetic] to act on [Beta-1 ______ receptors] which INC [______ stimulant]. This [______ stimulant] will INC [__-type slow inward ___ current]---> ______ inotropic effect/Contraction Strength.

2.It also Uses [______ stimulant] to INC slope of [______ ______] by having it stimulate ____________ -->more steep depolarization! **

3. ______(used by Sympathetic Nervous System) acts on what parts of the heart?
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B: ![INC Rate = ______ Interval] --> ______ Relationship

Effects of Autonomic System on Heart:

1.NorEpi is used by [Sympathetic] to act on [Beta-1 adrenergic receptors] which INC [cAMP stimulant]. This [cAMP stimulant] will INC [L-type slow inward Ca+ current or (SICC)]---> POSITIVE inotropic effect/Contraction Strength.

2.It also Uses [cAMP stimulant] to INC slope of [Diastolic depolarization] by having it stimulate {i.F.} Na+ channel current -->more steep depolarization! **

3.NorEpi acts on ALL areas of the heart
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B: ![INC Rate = DEC Interval] -->Inverse Relationship

21

Difference between [EFFECTIVE Refractory Period (ERP)] and [Relative Refractory Period (RRP)]

ERP occurs when channels needed for [______ ______ ______] are COMPLETELY ______ = NO ______ ______! Occurs during [Phase __ -->Phase __]
------------------- ---------- ------------------ -------- ------------ -------- ----
RRP occurs when channels needed for [______ ______ ______] are ______________

B: Refractory periods are conducted ______ and referred to as the "______ ______ period". They're carried out by
1. ___ channels (FAST response and ______-dependent)
and
2. ___ channels ( slllooooowww response and ______-dependent)

Difference between [EFFECTIVE Refractory Period (ERP)] and [Relative Refractory Period (RRP)]

ERP= channels needed for [Action Potential upstroke] are COMPLETELY INACTIVATED = NO Action Potentials! Occurs during [Phase 1 -->Phase 3]
------------------- ---------- ------------------ -------- ------------ -------- ----
RRP= channels needed for [Action Potential upstroke] are "partially" recovered and can be somewhat used during this time.

B: Refractory periods are conducted slowly and referred to as the "vulnerable heart period". They're carried out by
1. Na+ channels (FAST response and Voltage-dependent)
and
2. [Ca+ channels] ( slllooooowww response and Time-dependent)

22

A: [R on T phenomena] is a ______ that occurs when an R wave transects a previous T-wave during ______ ______ ______. --->eventually this results in ______ and INC more ______.

A2: [R on T phenomena] can also precipitate ______ which is polymorphic V-Tach. [R on T phenomena] can also cause the Rare ______ ______ or "Agitation of the heart"

B: [T or F] [R on T phenomena] happens to All of us sometimes but can be fatal with underlying heart dz.

C: [______ ______] is a lethal Blow to the [______ Heart] DURING vulnerable [Relative Refractory Period] that causes PVC and V-Fib and is 80% Fatal! It's most common in young ______ and can be sometimes reversed with ______.

A: [R on T phenomena] is a PVC (Premature Ventricular Contraction) that occurs when an R wave transects a previous T-wave during the vulnerable [Relative Refractory Period]. --->may result in re-entry of excitation in INFARCTED tissue and INC more PVC.

A2: [R on T phenomena] can also precipitate [Torsades de pointes] which is polymorphic V-Tach. [R on T phenomena] can also cause the Rare [Commotio Cordis] or "Agitation of the heart"

B: TRUE! [R on T phenomena] happens to All of us sometimes but can be fatal with underlying heart dz.

C: [Commotio Cordis] is a lethal blow to the [Precordial Heart] DURING vulnerable [Relative Refractory Period] that causes PVC and V-Fib and is 80% Fatal! It's most common in young boys and can be sometimes reversed with defibrillation.

23

A: [Post-Repolarization Refractoriness] occurs when the voltage of the ______ ______ has fully REpolarized BUT Cell is still ______! This occurs because recovery period of the ______ is Dependent on ______ and these have to fully recover before a new [______ ______ ______] can occur in the_____

B: how does this help to protect our Ventricles?
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2. Caffeine is a ______ INHIBITOR and thus ______ [cAMP stimulant] levels --> ______ HR

A: [Post-Repolarization Refractoriness] occurs when the voltage of the Action Potential fully REpolarized BUT Cell is still refractory! This occurs because recovery period of the T-Type SICC [slow inward Ca+ current] is more Dependent on TIME and these have to fully recover before a new [Action Potential Upstroke] can occur in the SA or AV node

B: This prevents Ventricular activation during atria-tachycardia like a-fib and atrial flutter
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2. Caffeine is a Phosphodiester (breaks down cAMP) inhibitor and thus INC [cAMP stimulant] levels --> INC HR

24

A: Atrial Fibrillation can be easily recognized on EKG by its __________. Although many people can live with A-fib (because it only ACTIVELY PUMPS __% of blood
-->Ventricle) it also INC risk of developing ______ ______ {i.e. ______ or ______}

B: [Prolonged QT syndrome] can be either Congenital due to ___ or ___ channel _____OR caused by ____cardia, ____kalemia or [______ drugs].
**[Prolonged QT syndrome] can lead to ______
---------------------------------------------------------------------------------------
C: Polymorphic Ventricular Tachycardia can result from [______ de Pointes], ______ OR EAD (Early ______).

D: [T or F] [______ de Pointes] is VERY SERIOUS!

A: Atrial Fibrillation can be easily recognized on EKG by its [FAST and IRREGULAR Ventricular Rate]. Although many people can live with A-fib because it only ACTIVELY PUMPS 5% of blood -->Ventricle, it also INC risk of developing blood clots = CVA or PE.

B: [Prolonged QT syndrome] can be either Congenital due to [Na+ OR K+ channel lesions] OR caused by bradycardia, hypOkalemia or [Quinidine drugs].
**Can lead to [Torsades de Pointes]
---------------------------------------------------------------------------------------
C: Polymorphic Ventricular tachycardia that can result from [Torsades de Pointes], [R on T phenomena] OR EAD (Early AfterDepolarizations).

D: TRUE! [Torsades de Pointes] is VERY SERIOUS!

25

A: What is the Hierarchy of Pacemakers in the Heart
SA node >>> [______ pacemaker] >> ______ > ______ ______ > Purkinje fibers

B: SA node is the primary pacemaker because of what 2 reason?

A: What is the Hierarchy of Pacemakers in the Heart
SA node >>> [latent atrial pacemaker] >> (jnctional AV node/[bundle of HIS] ) > bundle branches > Purkinje fibers

B: SA node is the primary pacemaker because
1. HAS the fastest inherent beating rate and
2. has ability to suppress other pacemakers from activating

26

DIASTOLIC DEPOLARIZATION for [SA nodes] occurs during PHASE __ and is activated either thru:

A: SA Node via..
1) [______-activated inward current] via ______ channels! ----> Inward __ current. This channel Is unique because it is the ONLY heart current-channel activated by ______

2) Deactivate ___ current by blocking ____ channels

3) __-type Ca+ current (which can NOT be adjusted with ______ ______ ______)

4) INWARD ______ exchange current activated by intracell ______

DIASTOLIC DEPOLARIZATION occurs during PHASE 4 and is activated either thru:

A: SA Node via..
1) [Hyperpolarization-activated inward current] via {i.F.} funny channels! ----> Inward Na+ current. Is unique because it is the ONLY heart current activated by HYPERpolarization

2) Deactivate K+ current by blocking {i.K.} channels

3) T-type Ca+ current (which can NOT be adjusted with Calcium channel blockers)

4) INWARD Na/Ca exchange current activated by intracell SR Ca+ release {Ca+ will want to leave}

27

A: Mechanisms responsible for Heart Rate Changes
1. Change in [______ ______] Slope
2. Change in MAX ______ potential
3. Change in Threshold
4. ______ Site shifts --->causes abrupt changes in HR because hierarchy of ______ changes
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B: [______ ACh] ----> ______[INC/DEC] K+ conductance and thus causes [______ Depolarization] to shift ______ and threshold to occur at ______ time

C: [______ NorEpi] ----> stimulates ______ channels and ______[INC/DEC] depolarization thus causing [______ Depolarization] to shift ______ and threshold to occur ______

A: Mechanisms responsible for Heart Rate Changes
1. Change in [Diastolic Depolarization] Slope
2. Change in MAX Diastolic potential
3. Change in threshold
4. Pacemaker Site shifts --->causes abrupt changes in HR because hierarchy of pacemaker changes

B: [PARAsympathetic ACh] ----> INC K+ conductance and thus causes [Diastolic Depolarization] to shift Right and threshold to occur at later time

C: [Sympathetic NorEpi] ----> stimulates {i.F.} channels and INC depolarization and thus causes [Diastolic Depolarization] to shift LEFT and threshold to occur EARLIER

28

A: What is Overdrive Suppression?
______ Node "Overdrives" all other [______ ______ pacemakers] and therefore suppresses ______ ______ activity.

B: If a daughter Pacemaker is stimulated/driven at a frequency ______ than ITS OWN by a Parent, stopping That Parent Pacemaker will do what to the daughter?

C:Clinical Applications of Overdrive Suppression include:
1. ______ and ______ degree AV node Block
2. Stopping ______ ______
3. ______ Sinus Syndrome

A: What is Overdrive Suppression?
SA Node "Overdrives" all other [subsidiary ectopic pacemakers] and therefore suppresses ectopic pacemaker activity.

B: If a daughter Pacemaker is stimulated/driven at a frequency higher than ITS OWN by a Parent, stopping That Parent Pacemaker ----> temporarily suppress the daughter

C:Clinical Applications
1. 2nd and 3rd degree AV node Block
2. Stopping Artificial pacemakers
3. Sick Sinus Syndrome

29

A: What is Sinus Arrhythmia
Normal Event during ______ that's caused by PARAsympathetic ______ ______ to ______ Node

B: Athletes have MORE pronounced ______ ______
---->More pronounced Sinus Arrhythmia


**What occurs in Sinus Arrhythmia***

C: Inspiration --> ______ cardiac cycle length---> ______ HR by ______[Stimulating/Blocking] PARAsympathetic activity

D: Expiration----> ______ cardiac cycle length-----> ______ HR by ______[Stimulating/Blocking] PARAsympathetic activity

E: Having a ______ basal HR (like Athletes have) is good because it requires ______ OXYGEN to function

F: Bradycardia = HR lower than ______ and can be result of HIGH ______ ______ in athletes

A: What is Sinus Arrhythmia
Normal Event during breathing that's caused by PARAsympathetic Vagal Tone to SA Node

B: Athletes have MORE pronounced Vagal Tone---->More pronounced Sinus Arrhythmia
**What occurs in Sinus Arrhythmia***

C: Inspiration --> DEC cardiac cycle length--->INC HR by blocking PARAsympathetic activity

D: Expiration---->INC cardiac cycle length----->DEC HR by Stimulating PARAsympathetic activity

E: Having a low basal HR (like Athletes have) is good because it requires LESS OXYGEN to function

F: Bradycardia = HR lower than 60 and can be result of HIGH VAGAL TONE in athletes

30

A: Cardiac dysrhythmias cause alteration in ______ ______ and result from disturbing IMPULSE ______ or IMPULSE ______...OR BOTH!

B: What are the 3 ways you can disturb IMPULSE phenomena?
1) Altered automaticity = altering ______ ______ by changing pacemaker ______. This can lead to ___ or ___

2) ______ = MOST COMMON

3) ______ activity

A: Cardiac dysrhythmias cause alteration in Cardiac Output and result from disturbing IMPULSE FORMATION or IMPULSE CONDUCTION...OR BOTH!

B: Caused by..
1) Altered automaticity = altering pacemaker rate by changing pacemaker mechanisms --> Tachy or Brady

2) Re-Entry of Excitation= MOST COMMON

3) Triggered activity

31

A) Altered automaticity = altering ______ ______ by changing pacemaker ______ = ______ or ______

1. Possible causes of TACHY-dysrhythmias
-[______ NorEpi]
-Stimulants like Cocaine which prevent ______
-______--->"current of injury"
-______ during Ventricular aneurysm
-______ Sinus Syndrome (______ node having strange rhythm), fever(______ Pacemaker actvity) or ______ (can lead to afib)

2A. Explain Ventricular aneurysm.
2B: Ventricular aneurysm can also be caused by ______ Trauma

A) Altered automaticity = altering pacemaker rate by changing pacemaker mechanisms = tachy or brady

1. Possible causes of TACHY-dysrhythmias
-[Sympathetic NorEpi]
-Stimulants like Cocaine which prevent reuptake of NorEpi
-Ischemia--->current of injury
-stretching during Ventricular aneurysm
-Sick Sinus Syndrome (SA node having strange rhythm), fever(INC Pacemaker actvity) or HYPERthyroidism (can lead to afib)

2. Explain Ventricular aneurysm = infarct damages Vt cells and weakens it--->pressure from contracting bulges it out. Can also be caused by BLUNT TRAUMA

32

A) Altered automaticity = altering ______ ______ by changing pacemaker ______ = ______ or ______

2. Possible causes of BRADY-dysrhythmia
-Drugs (______ / ANTagonist / ______)
- ______ & anesthetics
- ISCHEMIA & ______
-______ Sinus Syndrome (______ node having strange rhythm)
-Aging (because of ______ formation)

A) Altered automaticity = altering pacemaker rate by changing pacemaker mechanisms = tachy or brady

2. Possible causes of BRADY-dysrhythmia
-Drugs (Digitalis / ANTagonist / blockers)
- barbiturates & anesthetics
- ISCHEMIA & INFARCT
-Sick Sinus Syndrome (SA node having strange rhythm)
-Aging (because of Fibrosis formation)

33

Ca+ has NO influence on [______ ______ ______] BECAUSE ______. This is true for any ion that isn't ______

Ca+ has NO influence on [Resting Membrane Potential] BECAUSE it is NOT permeable. This is true for any ion that isn't permeable

34

K+ change does NOT AFFECT ______ NODE because ______ Node don't have ______ receptors BUT hypokalemia----> ______ HR by making inside of cell more ______ -----> [______ ______] of ____ ______ becomes MORE STEEP---> bring it closer to ______ ______ ______.

K+ change does NOT AFFECT SA NODE because SA/AV Node don't have Ik1 receptors BUT hypokalemia---->INC HR by making inside of cell more [+] -----> [Diastole Depolarization] OF LATENT PACEMAKERS BECOMES MORE STEEP---> bring it closer to Action Potential threshold.

35

A: [Re-Entry of Excitation] can occur ______ in the HEART and is MOST COMMON cause of ______
What are the 3 Requirements?

B: Causes of Re-Entry Excitation
1A. Congenital bypass tract such as [Wolff-Parkinson-White]= [PAC--> ______]. This occurs because impulses traveling to Ventricles use the ______ instead of the ______--->RAPID ______ conduction and DEC in ______ intervals!
1B. IN WPW: Initial Ventricular Depolarization is ______ because heart is using ______ vs. the ______ = ______ WAVE which is the now ______ upstroke of the ______

2. Another Cause of Re-Entry of Excitation is ______ and ______ which are actually the MOST COMMON

A: [Re-Entry of Excitation] can occur ANYWHERE IN THE HEART and is MOST COMMON cause of dysrhythmia
3 Requirements:
1) Slowed Delayed conduction
2)Unidirectional Conduction Block
3) Geometry for an actual conduction loop

B: Causes of Re-Entry Excitation

1A. Congenital bypass tract such as [Wolff-Parkinson-White]= [PAC-->SVT] occurs because impulses traveling to Ventricles escape from AV node AFTER refractory has ended and then use [Accessory Bundle of Kent] to travel back UP to atria (re-entering) ---> [Premature Atrial Contraction]

1B. IN WPW: Initial Ventricular Depolarization is SLOWWED because heart is using [fiber-to-muscle fiber conduction] vs. the faster [HIS-purkinje system] = DELTA WAVE which is the now SLOW upstroke of the QRS --->RAPID AV conduction and DEC in PR intervals!

2. Another Cause of Re-Entry of Excitation is Ischemia and Infarction which are actually the MOST COMMON

36

A: Triggered Activity is a Dysrhythmia that occurs in ______ OR ______. Two types = DAD or EAD

DAD [______ Afterdepolarization] is caused by HIGH Intracell ___ (usually from ______ toxicity). It leads to ______ and ______.
Other causes include High [______] or HIGH ______

B: What's another mechanisms behind DAD?
Action Potentials can trigger release of ______ from ______ ______ even AFTER the Action Potential is already over. This ____ is typically pushed out of the cell via ______ but then 3 ___ get pumped into cell --->DAD.

C: If DAD amplitude is large enough to bring membrane potential to ______ you'll develop a second premature ______ ______[ single or multiple] ---> ______ `

A: Triggered Activity is a Dysrhythmia that occurs in Atrial OR Ventricles. Two types = DAD or EAD

DAD [Delayed Afterdepolarization] is caused by HIGH Intracell Ca+ (usually from digitalis toxicity). It leads to PAC/PVC and tachycardia.
Other causes include High [Catecholamines] or HR

B: What's another mechanisms behind DAD?
Action Potentials can trigger release of Ca+ from SR AFTER the Action Potential is already over. Although this Ca+ will be released via Na/C exchanger, 3Na+ get pumped in this --->DAD.

C: If DAD amplitude is large enough to bring membrane potential to threshold = second premature AP[ single or multiple] --->tachycardia `

37

A: Triggered Activity is a Dysrhythmia that occurs in ______ OR ______. Two types = DAD or EAD

EAD [______ Afterdepolarization] is a ______ of an already occurring [action potential duration] which is caused by prolonged ______. Mechanism occurs Usually Reactivating ______ and will eventually cause "bouts" of tachycardia episodes

B. Possible Causes of EAD:
1. _______ [______ ______ ______ ______]
2. ___kalemia, ____cardia and ______ drugs which all
[______ Action Potential duration]
3. ______ (from Ischemia)

C: What are the 3 EKG manifestations of EAD? include:

A: Triggered Activity is a Dysrhythmia that occurs in Atrial OR Ventricles. Two types = DAD or EAD

EAD [Early Afterdepolarization] is a PROLONGATION of an already occurring [action potential duration] caused by [prolonged QT syndrome]. Mechanism occurs by Reactivating [L-type SICC [slow inward Ca+ current]] and will eventually cause "bouts" of tachycardia episodes or [Polymorphic Ventricular Tachycardia]

B. Possible Causes:
1. ReActivated SICC
2. hypOkalemia, Bradycardia and [Class I quinidine]--->
[INC Action Potential duration]
3. Infarct (from ischemia)

C: EKG manifestation include:
1. PAC/PVC
2. [Torsades de Pointes] polymorphic ventricular tachycardia
3. BiGeminy Deep-Cut Forks

38

A: BLOCKING K+ conductances = ______ [Action Potential duration] = ______ [space length constant]

B: What are the 4 Anti-Arrythmic Therapies

C: What is DC Cardioversion?

D: ICD have __ atrium leads that travel out the ________
--->device--->[________ lead]

A: BLOCKING K+ conductances = INC [Action Potential duration] = INC [space length constant]

B: What are the 4 Anti-Arrythmic Therapies
1) Drugs
2) Radio-freq. ablation
3) DC Cardioversion
4) Implantable Cardioverter Defibrillator [ICD]

C: DC Cardioversion = HUGE CHARGE is sent thru heart to place all cells onto same Depolarization accord

D: ICD have R atrium leads that travel out the L subclavian --->device--->[subcutaneous lead]

39

Normal EKG Values!
1. [PR interval] = ______ ms

2. [QRS complex] = ______ ms

3. [QT interval] = ______ ms

4. Tachycardia = HIGHER than ____ bpm OR [cycle length less than _____ ms]

5. bradycardia = lower than ____ bpm OR [cycle length GREATER than ______ ms]

Normal EKG Values!
1. [PR interval] = 120-200 ms

2. [QRS complex] = 70-100 ms

3. [QT interval] = 250-430 ms

4. Tachycardia = HIGHER than 100 bpm OR [cycle length less than 600 ms]

5. bradycardia = lower than 60 bpm OR [cycle length GREATER than 1000 ms]

40

A: Sarcolemma of Cardiac Cells control ____ influx via activation of ______. Action potential travels in ______ located at Z-lines to activate outer ______. The ___+ activate (______) receptors. These (______) receptors open up SR channels to let A BULK of __+ Out for Phase 2 ______ and ______ Contraction! Contraction is maintained as long as _________
A2: In Skeletal muscle (______) receptors open when triggered by ______

B: [Terminal cisternae] = ______ site where ___+ triggers the ______ of BULK ___+ RELEASE. This is also where __+ is ______.

C: Longitudinal Cisternae = ______ site where ______ + is ReUptook by ______ to initiate muscle relaxation

D: What is Phospholamban?

E: [Na/Ca exchanger] ______ vs.
the [Ca+ ATPase pump] which ______

F: Relaxation of Cardiac muscle occurs what 3 ways? (Rank in order from most common to least)

A: Sarcolemma of Cardiac Cells control Ca+ influx via activation of SICC[slow inward Ca+ current]. Action potential travels in T-tubules located at Z-lines to activate outer SICC. The Ca+ activate (RyR) receptors. These (RyR) receptors open up SR channels to let A BULK of Ca+ Out for Phase 2 SICC and Vt. Contraction! Contraction is maintained as long as cytosolic Ca+ remains high
A2: In Skeletal muscle (Dihydropyridine) receptors open when triggered by VOLTAGE

B: [Terminal cisternae] = SR site where Ca+ triggers the opening of BULK Ca+ RELEASE. This is also where Ca+ is STORED.

C: Longitudinal Cisternae = SR site where Ca+ is ReUptook by [Ca+ ATPase pump] to initiate muscle relaxation

D: Phospholamban = structure that BLOCKS and regulates [Ca+ ATPase pump] --->which BLOCKS relaxation

E: [Na/Ca exchanger] removes Ca+ from the cell vs.
the [Ca+ ATPase pump] removes Ca+ from cytosol back into SR!

F: Relaxation of Cardiac muscle occurs when
1. Ca+ uptake via SR (80%)
2. Ca+ EFFLUX out of cell using [Na/Ca exchange pump](18%)
3. Ca+ EFFLUX out of cell using Sarcolemma Ca+ pump (2%)

41

1. Global ischemia and HYPERkalemia will both ______ QRS Complex


B: The Relative Refractory period on EKG = ______

C: ______% of Atrial muscle cells DONT have/need T-tubules because ______

D: The ______ has the LONGEST refractory period because it has the LONGEST ______

E: Extracell K+ Does NOT affect on ______ because these HAVE NO IK1 receptors but it can affect what 3 things?

A: 2 Ways you can Widen QRS complex
1. Global ischemia
2. HYPERkalemia

B: The Relative Refractory period on EKG = the 2nd Downward part of the T-wave

C: 50% of Atrial muscle cells DONT have/need T-tubules because Atrial muscle is Thin and AP relay is easier!

D: The [HIS-purkinje system] has the LONGEST refractory period because it has the LONGEST [Action Potential Duration]

E: Extracell K+ Does NOT affect SA/AV Node because these HAVE NO IK1 receptors but they can affect
1) [HIS-purkinje system]
2) Ventricles
3) Latent Pacemakers

42

Cardiac Cells
1. small or long
2. Made of ______
3. Activated by ______ conduction
4. Contraction dependent on ______
5. Contraction AMPLITUDE determined by ______ via ______
6. No ______ or tetanus
7. AEROBIC with LOTS OF ______

Cardiac Cells
1. small cells
2. Made of Syncytium = electrically connected w/gap junctions
3. Activated by Cell-to-Cell conduction
4. Contraction dependent on [Ca+ induced Ca+ release]
5. Contraction amplitude determined by Ca+ influx via SICC
6. No summation/tetanus
7. AEROBIC with LOTS OF MITOCHONDRIA

43

**Skeletal Muscle Cells**
1. small or long
2. Made of ______ muscle cells
3. Activated by ______ at ______

4. contraction NOT dependent on ______ but rather on ______-sensor for ____ channel opening

5. Contraction AMPLITUDE determined by ______ of ______ ______ and ______ Recruitment of muscle fibers

6. Summation & tetanus ---> ______ ______

7. ______ metabolism with not many mitochondria (Doesn't need a lot of O2)

**Skeletal Muscle Cells**
1. Fibers can run full length of muscle
2. Individual muscle cells
3. Activated by ACh at [neuro-muscular jnction]

4. contraction NOT dependent on Ca+ influx but rather on Voltage-sensor for Ca+ channel opening

5. Contraction amplitude determined by FREQUENCY of Action Potentials and Central Recruitment of muscle fibers

6. Summation & tetanus --->MAX tension

7. AnAerobic metabolism with not many mitochondria (Doesn't need a lot of O2)

44

Catecholamines (______ & ______) are ______ inotropic agents that bind to [______ receptors] to activate [______ ______ ---> INC [cAMP stimulant]. [cAMP] activates ______ which Phosphorylates:
1. Ca+ channels to allow Ca+ ______[Influx/Efflux]

2. Phospholamban (which will ______ Phospholamban) and thus allows ______ to do its job and pump Ca+ back into ______ for stronger release when AP occurs AND ______[INC/DEC] time inbetween relaxation

3. Reduces Affinity of Troponin-__ to Ca+ by phosphorylating [Troponin-__] and thus allows Ca+ to come off Troponin-__ during ______ more easily = ______[INC/DEC] time inbetween relaxation

Catecholamines (NorEpi & Epi) are POSITIVE inotropic agents that bind to [beta-Adrenergic receptors] to activate [adenylate cyclase] ---> INC [cAMP stimulant]. [cAMP] activates PKA which Phosphorylates:
1. Ca+ channels to allow Ca+ Influx

2. Phospholamban (which will INHIBIT Phospholamban) and thus allows [Ca+ ATPase pump] to do its job and pump Ca+ back into SR for stronger release when AP occurs AND DEC time inbetween relaxation

3. Reduces Affinity of Troponin-C to Ca+ by phosphorylating Troponin-I.. and thus allows Ca+ to come off Troponin-C during relaxation more easily = DEC time inbetween relaxation

45

A: Ca+ channel blockers are ______ in Smooth Muscle and ______ in Cardiac
Examples include (Name 3)

B: ______ (MOSTLY SMOOTH MUSCLE) work by ______ SR Ca+ release which ______ contraction

C: In Cardiac Muscle it does this by slowing down ______ nodal upstroke after it slows its ______ . This will ______ refractory period and ______ SVT

D: Unwanted side effect of [Ca+ channel blockers] in Cardiac= ______

A: Ca+ channel blockers are Vasodilators in Smooth Muscle and [Anti-arrhythmics] in Cardiac
Examples include: Verapamil / Diltiazem / Nifedipine

B: Vasodilators (MOSTLY SMOOTH MUSCLE) work by DEC SR Ca+ release which DEC contraction

C: In Cardiac Muscle does this by slowing down AV nodal upstroke after it slows its [slow inward Ca+ current] . This INC refractory period and PREVENT SVT by stopping re-entry of excitation

D: Unwanted side effect = Negative inotropic effects on heart (DEC in contraction)

46

[Force-Frequence relationship] of the heart describes how ______ can affect ______ Cardiac Contraction. This occurs because if you DEC the cycle length you'll alter TIME available for ______

B: INC HR Rate/freq. = ______ cycle length = ______ time available for Ca+ ______ (via Na/Ca exchanger) therefore creating ______ intracell Ca+ = ______ Contractility STRENGTH = [______ ______ STAIRCASE] / ______ INOTROPIC EFFECT

B2: When DEC HR = ______ cycle length = ______ time available for Ca+ ______ (Na/Ca exchanger) and ______ Ca+ INflux

C: Why does Higher Intracell Ca+ INC Contractility STRENGTH?

[Force-Frequence relationship] of the heart describes how [Beating Rate/freq.] can affect STRENGTH Cardiac Contraction. This occurs because if you DEC the cycle length you'll alter TIME available for intracellular Ca+ handling.

B: INC HR Rate/freq. = DEC cycle length = DEC time available for Ca+ efflux (via Na/Ca exchanger) therefore creating HIGHer intracell Ca+ = INC Contractility STRENGTH = [Treppe POSITIVE STAIRCASE] / POSITIVE INOTROPIC EFFECT

B2: When DEC HR = INC cycle length = more time available for Ca+ Efflux (Na/Ca exchanger) and less Ca+ influx

C: Why does Higher Intracell Ca+ INC Contractility STRENGTH
More Ca+ inside cell can be pumped into SR so when AP occurs more Ca+ is released and Contraction is stronger!

47

A: Why does a premature beat have a weak contraction strength?
1) there's Less time for recovery of ______ ______ during phase 4

2)There's ______ time for SR [______ Cisternae] [______ channels] to recover ---> ______ Ca+ is released in muscle contraction

3) There's Less time for SR to redistribute Ca+ from [______ cisternae] --> [______ Cisternae] for final release
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B: What occurs after a premature beat occurs? PESP (Post-______ ______) = ___________

B2: What causes this PESP?
1) there's ______ time for recovery of Pacemaker SICC during phase 4

2)There's ______ time for SR [______ Cisternae] [______ channels] to recover ---> ______ Ca+ is released in muscle contraction

3) There's ______ time for SR to redistribute Ca+ from [______ cisternae] --> [______ Cisternae] for final release

A: Why does a premature beat have a weak contraction strength?
1) there's Less time for recovery of Pacemaker SICC during phase 4

2)There's Less time for SR [Longitudinal Cisternae] [Ca+ release channels] to recover ---> Less Ca+ is released in muscle contraction

3) There's Less time for SR to redistribute Ca+ from [terminal cisternae] --> [Longitudinal Cisternae] for final release
---------------------------------------------------------------------------------------
B: What occurs after a premature beat occurs? PESP (Post-extrasystolic potentiation) = The Beat which follows the premature contraction is STRONGER than normal

B2: What causes this?
1) there's MORE time for recovery of Pacemaker SICC during phase 4

2)There's MORE time for SR [Longitudinal Cisternae] [Ca+ release channels] to recover ---> Less Ca+ is released in muscle contraction

3) There's MORE time for SR to redistribute Ca+ from [terminal cisternae] --> [Longitudinal Cisternae] for final release

48

A: EKG records ______ ______ on the heart surface (which occur during ______ like Depolarization and Repolarization) and ______ & ______ of the Wavefront. This means it ONLY records [___ current] and can NOT record ______ ______.

B: EKG can NOT read activity from [______ ______ ______] because current from here is small and there is ______ resistance on the skin... and so it only reads electrical activity from ______ and ______ muscle

C: UPward and Downward Deflections from EKG waveforms do NOT indicate ______ or ______ but are caused by the [______ ______] moving toward or Away from a ______. EKGs typically don't give information on ______ activity or ______

D: 12 EKG leads
º3 [______ Standard] = Lead I, II and III --> Records ______ Plane
º3 [______ Augmented]= aVR, aVL and aVF-->Records ______ Plane
º6 [______ Precordial]= V1- V6 ----> Records ______ Plane

D2: [Unipolar] leads do NOT have ___ electrodes and [Unipolar ______] just help to create angles for ______ leads to form from its ______ electrode.

E: Leads have different looking EKGs because although the see the same ______ event, they all see it from ______ ANGLES!
E2: Lead __ is typically used in E.R. because it has the largest ______

F: BECAUSE the ___ ventricle is the largest-->it generates MOST ______ ______ --> which is why ______ ______ ______ ______ is down and to the Left

A: EKG records VOLTAGE DIFFERENCES on the heart surface (which occur during wavefronts like Depolarization and Repolarization) and Direction & Amplitude of the Wavefront. This means it ONLY records [AC current] and can NOT record Absolute voltages.

B: EKG can NOT read activity from [specialized conduction system] because current from here is small and there is HIGH resistance on the skin... and so it only reads electrical activity from atrial and vt muscle

C: UPward and Downward Deflections from EKG waveforms do NOT indicate depolarization/repolarization but are caused by the [Voltage Vector] moving toward or Away from a (+) electrode. EKGs typically don't give information on contractile activity or strength

D: 12 EKG leads
º3 [Bipolar Standard] = Lead I, II and III --> Records Frontal Plane
º3 [Unipolar Augmented]= aVR, aVL and aVF-->Records Frontal Plane
º6 [Unipolar Precordial]= V1- V6 ----> Records Coronal Plane

D2: [Unipolar] leads do NOT have (-) electrodes and [Unipolar Augmented] just help to create angles for Bipolar leads to form from its (-) electrode.

E: Leads have different looking EKGs because although the see the same electrical event, they all see it from DIFFERENT ANGLES!
E2: Lead II is typically used in E.R. because it has the largest QRS complex

F: BECAUSE the L ventricle is the largest-->it generates MOST electrical current --> which is why [Normal Mean Frontal plane Vector] is down and to the Left

49

4 Factors that Control Cardiac Output =
ºHR
ºMyocardial Contractility
ºPreLoad
ºAfterLoad
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A1: Describe Preload = This is the LOAD the heart muscle has on it ______ contraction initiates (such as ______ of blood).
A2: When preload fills & stretches ______ muscle = ______ cardiac length by creating _________ AND ______ their sensitivity to Ca+ --> generates passive [______ ______ Tension] ---> ultimately causes INC [______ ______ and ______ tension]!

A3: DRT is dependent on ______ ______
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B: CONTRACTION is a process by which muscle generate ______ or ______. What are the 2 types?

1) [______ contraction] = Contraction WITHOUT SHORTENING!
1B) If muscle is UNABLE to create enough force to match AfterLoad force then contraction remains ______

2) [______ contraction = classic contraction in which muscle SHORTENS with ______ force.
2B) If muscle is ABLE to meet the force of the AfterLoad then contraction turns ______ (shortens)

4 Factors that Control Cardiac Output =
ºHR
ºMyocardial Contractility
ºPreLoad
ºAfterLoad
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A1: Describe Preload = This is the LOAD the heart muscle has on it BEFORE contraction initiates (such as EDV of blood).
A2: When preload fills & stretches cardiac muscle = INC cardiac length by creating better overlap between myosin and actin AND INC their sensitivity to Ca+ --> generates passive [Diastolic Resting Tension] ---> ultimately causes INC [Contraction Strength and ACTIVE tension]!

A3: DRT is dependent on muscle compliance
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B: CONTRACTION is a process by which muscle generate tension or force. What are the 2 types?
1) [isometric contraction] = Contraction WITHOUT SHORTENING!
1B) If muscle is UNABLE to create enough force to match AfterLoad force then contraction remains isometric

2) [IsoTonic contraction = classic contraction in which muscle Shortens with CONSTANT force.
2B) If muscle is ABLE to meet the force of the AfterLoad then contraction turns isotonic (shortens)

50

4 Factors that Control Cardiac Output =
ºHR
ºMyocardial Contractility
ºPreLoad
ºAfterLoad
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A: Describe AfterLoad
This is the LOAD that ______ muscle shortening (such as ______ pressure). It is the Load on the Heart ______ contraction occurs

B: [Myocardial Contractility] is the ability of ______ to form ______ and generate contractile force. IT IS INDEPENDENT OF ______ AND ______!
It is DEPENDENT ON [______] (since more Ca+ ______ cross-bridges in the Lab), but ______ in the Clinic.

B2: INC contractility (______ inotropic effect) = shifts SAT curve [______ ______ Tension] ______ and to ______ while also INC [rate of ______]. this means Heart will ______ ______[faster/slower] inbetween contractions.

DEC contractility (______ inotropic effect) = shifts SAT curve ______ and to ______ and DEC [ rate of ______]

4 Factors that Control Cardiac Output =
ºHR
ºMyocardial Contractility
ºPreLoad
ºAfterLoad
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A: Describe AfterLoad
This is the LOAD that RESIST muscle shortening (such as arterial pressure). It is the Load on the Heart AFTER contraction occurs

B: [Myocardial Contractility] is the ability of actin and myosin to form cross-bridges and generate contractile force. IT IS INDEPENDENT OF PRELOAD AND AFTERLOAD!
It is DEPENDENT ON [intracell Ca+] (since more Ca+ INC cross-bridges) in the Lab, but [Overall Contractile Ability] in the Clinic.

B2: INC contractility (POSITIVE inotropic effect) = shifts SAT curve [Systolic Active Tension] up and to Left while also INC [rate of relaxation]. this means Heart will relax faster inbetween contractions.

DEC contractility (negative inotropic effect) = shifts SAT curve down and to right and DEC [ rate of relaxation]

51

A: What is [Systolic Active Tension]? = ______ tension that develops with muscle contractions at specific [______]. It is represented by ______ Volume and determined by ______.

B1: Compliance = {[change in ______ ______] / [change in ______ ______]} . It is the PRIMARY DETERMINANT OF ______ ______ ______

B2: Cardiac muscle has ______ compliance (______ STIFF) than skeletal muscle so has ______ DRT[Diastolic Resting Tension] even at shorter muscle lengths. Since Compliance determines slope of ______, DEC compliance
---> ______ slope ---> ______ pressure

C: Force x ______ = POWER

A: What is [Systolic Active Tension]? = isometric tension that develops with muscle contractions at specific [preloads/muscle length]. It is represented by Stroke Volume and determined by Contractility.

B1: Compliance = {[change in Volume length] / [change in pressure tension]} . It is the PRIMARY DETERMINANT OF DRT[Diastolic Resting Tension]

B2: Cardiac muscle has LOWER compliance (MORE STIFF) than skeletal muscle so has HIGHER DRT[Diastolic Resting Tension] even at shorter muscle lengths. Since Compliance determines slope of [DRT curve], DEC compliance--->INC slope --->INC pressure

C: Force x Velocity = POWER

52

1. INC PREload = ______ [AMOUNT of shortening muscle will do during contraction](AKA INC ______ Contractions) and vice versa

2. INC AFTERLOAD= ______ [AMOUNT of shortening muscle will do during contraction] and this is because there is ______ resistance making it ______[harder/easier] for Contraction to occur

**In NEITHER OF THESE CASES DO YOU CHANGE ______ ______ (AKA ______) because PREload and AFTERLOAD do NOT affect ______. Only Muscle ______ during shortening
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3. INC Contractility =
A. also ______ [AMOUNT of shortening muscle will do during contraction]
B: ______ shortening VELOCITY [even with higher AFTERLOAD]
C: ______ [rate of relaxation] between contractions if it's the ______ NS INC the contractility

4. DEC Contractility =
A: also ______ [AMOUNT of shortening muscle will do during contraction]
B: ______ shortening VELOCITY
C: ______ [rate of relaxation] between contractions if the ______ Contractility is being caused by ______ Sympathetic NS

1. INC PREload = INC [AMOUNT of shortening muscle will do during contraction](AKA INC IsoTonic Contractions) and vice versa

2. INC AFTERLOAD= DEC [AMOUNT of shortening muscle will do during contraction] and this is because there is MORE resistance making it harder for Contraction to occur

**In NEITHER OF THESE CASES DO YOU CHANGE CONTRACTILE FORCE (AKA Contractility) because PREload and AFTERLOAD do NOT affect Contractility. Only Muscle LENGTH during shortening
--------------------------------------------------------------------------------------
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3. INC Contractility =
A. also INC [AMOUNT of shortening muscle will do during contraction]
B: INC shortening VELOCITY [even with higher AFTERLOAD]
C: INC [rate of relaxation] between contractions if it's the Sympathetic NS INC the contractility

4. DEC Contractility =
A: also DEC [AMOUNT of shortening muscle will do during contraction]
B: DEC shortening VELOCITY
C: DEC [rate of relaxation] between contractions if the DEC Contractility is being caused by Blocking Sympathetic NS

53

A: [Maximal isometric force] = is when isometric force has reached ____________ ---> ______ velocity of muscle shortening. This Can be INCREASED with [INC in ______] or [INC ______]

B: INC AFTERLOAD = ______ shortening Velocity
but
INC PREload = ______ shortening Velocity [AT ANY GIVEN ______]

A: [Maximal isoMETRIC force] = is when isometric force has reached its MAX but is still unable to meet force of AFTERLOAD --->zero velocity of muscle shortening. This Can be INC with [INC in PREload] or [INC Contractility]

B: INC AFTERLOAD = DEC shortening Velocity
but
INC PREload = INC shortening Velocity [AT ANY GIVEN AFTERLOAD]

54

A: [Mean Frontal Plane Vector] can normally range from ______ based on persons ______. Taller people have hearts which aren't pushed ______ by the ______ and so will be closer to ____º.

B: When Determining MFPV [Lead _ + Lead _ = Lead _]
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C: TALLER QRS complex in all leads usually indicates ______. This is because if L Ventricle is ______-->generate ______ current in all leads
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D: The (+) electrode is the ______ ______ so [Voltage Vectors] traveling ______ this electrode will display as ______ Deflection on EKG!
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E: PR-interval starts at P and actually ends at ______! QTC stands for "______" QT-interval and indicates [______ QT intervals]

A: [Mean Frontal Plane Vector] can normally range from (-30º - 105º) based on persons ht. Taller people have hearts which aren't pushed horizontally by the diaphragm and so will be closer to 105º.

B: When Determining MFPV [Lead 1 + Lead 3 = Lead 2]
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C: TALLER QRS complex in all leads usually indicates Hypertrophy. This is because if L Ventricle is larger-->generate MORE current in all leads
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D: The (+) electrode is the RECORDING ELECTRODE so [Voltage Vectors] traveling TOWARD this electrode will display as (+) Deflection on EKG!
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E: PR-interval starts at P and actually ends at beginning of Q! QTC stands for "corrected" QT-interval and indicates [Prolonged QT intervals]

55

A: Why is it important that More current flows to LEFT ventricle?

B: ______ ______ ______ and [ _____] can lead to [Left Axis Deviation] (which is a MFPB less than ______ )
vs.
______ ______ ______ and [______] can lead to [RIGHT Axis Deviation] (which is a MFPB MORE than ______)

C: [ST segment] = [Phase __ ______ ______ ______]

D: [U-wave] comes after [___-wave] and represents repolarization of [______] (which is sensitive to ___kalemia)

E: During Repolarization the impulse runs ______ from [______ ---> ______] but is an ______ polarity {returning to + outside cell} --->so the two cancel to make ______ [Voltage Vectors]

A: Why is it important that More current flows to LEFT ventricle? If an equal amount of current flows to both ventricles the currents WILL CANCEL OUT!

B: Left Ventricular Hypertrophy and [L BBB] can lead to [Left Axis Deviation] (which is a MFPV less than -30º )
vs.
RIGHT Ventricular Hypertrophy and [R BBB] can lead to [RIGHT Axis Deviation] (which is a MFPV MORE than 105º)

C: [ST segment] = [Phase 2 Action Potential Plateau]

D: [U-wave] comes after [T-wave] and represents repolarization of [HIS-purkinje system] (which is sensitive to hypOkalemia)

E: During Repolarization the impulse runs BACKWARDS from [Epi --->Endocardium] but is an OPPOSITE polarity {returning to + outside cell} --->so the two cancel to make Positive [Voltage Vectors]

56

A: Shape of [Ejection phase] for the [______-______] Loop is NOT FLAT for CARDIAC muscle like in ______ muscle because ______ during this period gradually INC.

______ INC because
1. sarcomeres are ______ at that point & can't ______

2. blood rushes into aorta and ______ arterial pressure.

Therefore Heart generates [______ contraction] with a ______ afterload during Ejection phase.
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B: [Isovolumic Relaxation phase] occurs after [______ phase] and is represented by the [__-wave] on EKG. The volume of blood in ventricles during this phase = [______-______ ______]

A: Shape of [Ejection phase] for the [Pressure-Volume] Loop is NOT FLAT for CARDIAC muscle like in Skeletal muscle because Afterload during this period gradually INC. Afterload INC because
1. sarcomeres are shorter at that point & can't generate much more Force AND because
2. blood rushes into aorta and INC arterial pressure.

Therefore Heart generates [isoTonic contraction] with a changing afterload during Ejection phase.

B: [Isovolumic Relaxation phase] occurs after [Ejection phase] and is represented by the [T-wave] on EKG. The volume of blood in ventricles during this phase = [End-Systolic Volume]

57

Ejection Fraction = [% of blood] ______ during __ stroke beginning with starting [End-______ Volume] in LEFT Ventricle.
{Formula = ______/ ______} . It is a clinical index of ______ ______ ______ .
A2: Normal EF = ___%

B: Normal EDV = ___ ml // Normal ESV = ____ml

C: A [Venous Pulse] is a ______ recorded in the ______ ______ or [R atrium] . It has an...
[a] wave = ______ ______ /
[c] wave = ______________
[v] wave = filling and emptying of ______ chamber

Ejection Fraction = [% of blood] ACTUALLY EJECTED during 1 stroke from the starting [End-Diastolic Volume] in LEFT Ventricle. {Formula = SV/ EDV} . It is a clinical index of L ventricular contractility.
A2: Normal EF = 60%

B: Normal EDV = 130 ml // Normal ESV = 60 ml

C: A [Venous Pulse] is a waveform recorded in the Vena Cava or [R atrium] . It has an...

[a] wave = atrial contraction /

[c] wave = RIGHT VentriCular contraction which causes TriCuspid valve to bulge UP into R Atrium-->INC Venous Pressure

[v] wave = filling and emptying of atrial chamber

58

A: Skeletal Muscle has a CONSTANT ______ and thus has a resting period that Doesn't change.

A2: INC ______ = DOES NOT CHANGE [MAX Tension Development] because this is essentially ______
(since ______ is the MAX force needed to graduate to ______ contraction). ______ for all ______ amounts is the same regardless of the amount.

A3: [Peak Isometric Tension] is the ______ ______ ______ each PREload amount will generate. This is never used since ______ is all the force needed to overcome.
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B: Ventricular Contractility is AKA __________

A: Skeletal Muscle has a CONSTANT AFTERLoad and thus has a resting period that Doesn't change.

A2: INC PREload = DOES NOT CHANGE [MAX Tension Development] because this is essentially AFTERLoad
(since AFTERLoad is the MAX force needed to graduate to isoTonic contraction) and AFTERLoad for all PREload amounts is the same regardless of the amount.

A3: [Peak Isometric Tension] is the SPECIFIC MAX tension each PREload amount will generate. This is never used since AFTERLoad is all the force needed to overcome.
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B: Ventricular Contractility is AKA [End-Systolic PressureVolume relationship]

59

A: INC AFTERLoad

1. ______ [Tension Development]
2. ______ [AMOUNT of shortening muscle will do during contraction]
3. ______ pressure developed b4 ejection
4. ______ energy consumption
5. ______ stroke volume

A: INC AFTERLoad

1. INC [Tension Development]
2. DEC [AMOUNT of shortening muscle will do during contraction]
3. INC pressure developed b4 ejection
4. INC energy consumption
5. DEC stroke volume

60

A: IN SKELETAL MUSCLE: INC Contractility shifts [Length-Tension] curve ______ and to the ______ which means there's ______ length required to generate ______ Tension!
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B: In Cardiac Muscle: INC Contractility will
1. ______ stroke volume
2. ______ [Ejection Velocity]
3. ______ [Velocity shortening]
4. Shift [______-______] curve

A: IN SKELETAL MUSCLE: INC Contractility shifts [Length-Tension] curve UP and to the Left which means there's less length required to generate same amount of Tension!

B: In Cardiac Muscle: INC Contractility will
1. INC stroke volume
2. INC [Ejection Velocity]
3. INC [Velocity shortening]
4. Shift [Length-Tension]

61

**Heart Failure occurs when heart Fails to provide [______ ______] that's sufficient to meet body needs There are 2 Types**

A1: [Systolic Heart Failure] is associated with [DEC ______ ______]. INFARCT can cause damaged ventricle muscle and disrupt ___+ handling ---> cause DEC in ______ force ------> ______[more/less] fluid being left in ventricle after contraction----> ______ venous fluids and further ______ contractility

A2: [Diastolic Heart Failure] is associated with [DEC ______ ______]

B: Both Heart Failure conditions ______ Stroke Volume

**Heart Failure occurs when heart Fails to provide [Cardiac Output] that's sufficient to meet body needs There are 2 Types**

A1: [Systolic Heart Failure] is associated with [DEC Ventricle CONTRACTILITY]. INFARCT can cause damaged ventricle muscle and disrupt Ca+ handling ---> cause DEC in contraction force ------> more fluid being left in ventricle after contraction---->INC venous fluids and further DEC contractility

A2: [Diastolic Heart Failure] is associated with [DEC Ventricle Compliance]

B: Both Heart Failure conditions DEC Stroke Volume

62

A: What 4 things are PRELoad dependent on?

1) Pressure gradient between atria & ventricle.
(ex. INC [End-Diastolic Pressure] will ______ Ventricular Filling

2) ______ filling Time (AKA ______ RATE)

3) ______ Compliance

4) ______ Kick! = will ______ Ventricular Filling!

A: What 4 things are PRELoad dependent on?
1) Pressure gradient between atria & ventricle. (INC [End-Diastolic Pressure] will DEC Ventricular Filling

2) Ventricular filling Time (AKA HEART RATE)

3) Ventricular Compliance

4) Atrial Kick! = Loss of Atrial functioning (such as a-fib) will DEC Ventricular Filling!

63

What 3 things are AFTERLOAD dependent on?
1. ______ ______ Pressure

2. [______ Outflow ______ Resistance] such as ______ ______ or [______ ______ stenosis]

3. [Ventricular Size & ______ Tension] Dilated Hearts have ______ Wall Tension---> ______ AFTERLOAD

What 3 things are AFTERLOAD dependent on?
1. Aortic Arterial Pressure

2. [Ventricular Outflow TRACT Resistance] such as valve stenosis or [SubAortic Valve stenosis]

3. [Ventricular Size & Wall Tension] Dilated Hearts have HIGHER Wall Tension--->HIGHER AFTERLOAD

64

A: [Systolic murmor] is caused by ______ blood flow through either ______ or ______ heart valve DURING ______. Can occur in ANY the ______ valves

B: [Diastolic murmor] occurs when ______ blood flow through either ______ or ______ heart valve occurs DURING ______. Can occur in ANY the ______ valves
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C: [Physiological splitting] occurs because the ______ valve closes BEFORE ______ valve and aren't synchronized. This NORMAL during ______ and ______ people but otherwise = pathological!

D: Why does Inspiration affect Heart Sounds?
DEC in ______ pressure when chest cage opens will ______ preload because they'll be a ______ pressure develop in the chest and ______ ventricle---->More blood in the ______ ventricle to pump out will delay ______ valve from closing ---->[Physiological splitting]

A: [Systolic murmor] is caused by turbulent blood flow through either stenotic or incompetent heart valve DURING SYSTOLE. Can occur in ANY of the valves

A2: "SM-AVS was a MVP" = Systolic Murmor = [Aortic Valve Stenosis] OR [Mitral Valve Prolapse]

B: [Diastolic murmor] occurs when turbulent blood flow through either stenotic or incompetent heart valve occurs DURING DIASTOLE. Can occur in ANY of the valves
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C: [Physiological splitting] occurs because the Aortic valve closes BEFORE Pulmonic valve and aren't synchronized. This NORMAL during inspiration and younger people but otherwise = pathological!

D: Why does Inspiration affect Heart Sounds?
DEC in thoracic pressure when chest cage opens will INC preload because they'll be a negative pressure develop in the chest and R ventricle---->More blood in the R ventricle will be needed to pump out will delay pulmonic valve from closing ---->[Physiological splitting]

65

A: Paradoxical Splitting is a pathological condition which occurs when ______ Valve closes before ______ Valve (which it isn't supposed to do!) This is because ______ Valve is delayed due to a ______. This will all attenuate during ______.

B: After [Isovolumic Relaxation] Passive ______ filling has 2 stages = Rapid ---> [Reduced ______]. This is followed by [______ ______].

C: [Dicrotic Notch] on {______ Diagram} comes from ______ recoiling after ______ Valve has closed. During the notch, ______ pressure slightly ______ due to elasticity change from recoiling. The ______ is the MOST compliant blood vessel in the body.

D: Which Valves close first?
1st: ______ valves first
2nd: ______ Valve
3rd: ______ Valve

A: Paradoxical Splitting is a pathological condition which occurs when Pulmonic Valve closes before Aortic Valve (which it isn't supposed to do!) This is because Aortic Valve is delayed due to a LBBB. This will all attenuate during Inspiration.

B: After [Isovolumic Relaxation] Passive Ventricular filling has 2 stages = Rapid ---> [Reduced Diastasis]. This is followed by [Atrial Systole].

C: [Dicrotic Notch] on {Wiggers Diagram} comes from Aorta recoiling after Aortic Valve has closed. During the notch, Aortic pressure slightly INC due to elasticity change from recoiling. The Aorta is the MOST compliant blood vessel in the body.

D: Which Valves close first?
1st: AV valves first
2nd: Aortic Valve {A before P}
3rd: Pulmonic Valve

66

A: What is Persistent Splitting and what causes it?

Persistent Splitting is pathological and occurs when [______ Splitting] occurs ______ and all the time. Can be caused by ______ since ______ Ventricle will be slower to depolarize and will therefore delay ______ valve closure even later than usual!

B: [3rd Heart Sound] = occurs as a result of when blood "______" into a ______ VENTRICLE

C: [4th Heart Sound] = occurs when ______ makes Loud Contracting Noise during ______

A: What is Persistent Splitting and what causes it?

Persistent Splitting is pathological and occurs when [Physiological Splitting] occurs more profoundly and all the time. Can be caused by RBBB since R Ventricle will be slower to depolarize and will therefore delay Pulmonic valve closure even later than usual!

B: [3rd Heart Sound] = occurs as a result of when blood "swish turbulent sounds" into a DILATED VENTRICLE

C: [4th Heart Sound] = occurs when Atria makes Loud Contracting Noise during Diastole

67

Table of Normal Values:
1. Cardiac Index = ______ liters/min/sq

2. Venous pressure = ______ mmHg

3. Pulmonary Wedge = ______ mmHg

4. Brachial Artery = ______ mmHg

Table of Normal Values:
1. Cardiac Index = 3.1 liters/min/sq

2. [Central Venous pressure] = 2 mmHg

3. [Pulmonary Wedge/L Atrial] = 6 mmHg

4. Brachial Artery = 95 mmHg

5. [R Atrial pressure] = 2

6. [R VENTRICLE PRESSURE]= 25/2

7. [PULMONARY ARTERY PRESSURE] = 25/10

8. [MEANNN PULMONARY ARTERY PRESSURE]= 15

9. [LEFT VENTRICLE PRESSURE] = 120/6

68

AV nodal conduction time ______ and PR interval ______ During Exercise of healthy people.

AV nodal conduction time INC and PR interval DEC During Exercise of healthy people.