Physiology Exam 2 Flashcards

1
Q

Two types of junctions in the intercalated discs

A

Desmosomes- do the holding together (MECHANICAL)

Gap Junctions- allow communication b/w the cells so they can work in syncytium (ELECTRICAL)

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2
Q

The only point of Electrical Contact b/w the Atria and Ventricles

A

AV Node

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3
Q

Rate of conduction through AV node

A

SLOW. Allows adequate time for ventricles to fill between beats

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4
Q

Rate of conduction through Purkinje Fibers

A

FAST. allows for efficient contraction & ejection of blood flow

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5
Q

What are the 3 reasons that a latent/intrinsic pacemaker can assume the pacemaker role instead of the SA node?

A
  • If SA node firing rate decreases or stops (vagal stimulation, SA node destroyed, removed, or suppressed by drugs)
  • Latent/intrinsic rate is faster than SA node
  • if SA node action potential conduction to rest of the heart is locked d/t disease in conducting pathways
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6
Q

Pacemaker (Nodal) cells

A

SA and AV node. Slow action potentials.

Major Fx: pacemaker activity (with SA node being the primary pacemaker)

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7
Q

Conductile Cells

A

Bundle of His & Purkinje Fibers
Fast Action Potentials.
Major Fx: rapid spread of electrical signal

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8
Q

Contractile Cells

A

Ventricular and Atrial Cells
Major fx: contraction (pumping)
Fast Action Potentials

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9
Q

Why can we not have summation or tetanus in cardiac cells?

A

The long refractory period occurs in conjugation with the Prolonged Plateau Phase

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10
Q

Why is it important that we have a long refractory period and NO tetanus or summation?

A

This ensures that we have both contraction and relaxation and in order which is essential for pumping blood

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11
Q

Contraction happens during:

A

Refractory period

We need the long refractory period to make sure we can do contraction!

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12
Q

Where does calcium come from for cardiac muscles?

A

Both from the SR and outside of the cell through calcium channels

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13
Q

How are intracellular Ca2+ levels decreased in cardiac cells?

A

Same as smooth muscle!

  • SERCA
  • Sarcolemmal Na+/Ca2+ Exchanger
  • Sarcolemmal Ca2+ ATPase
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14
Q

Force of cardiac muscle contraction depends on:

A

Initial fiber length!

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15
Q

Chronotropy

A

Heart Rate
SA Node
“Impulse Generation”

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16
Q

Dromotropy

A

AV-Conduction
AV Node
“Impulse Contraction”
How fast is the impulse conducted?

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17
Q

Ionotropy

A
Contractility
Electro-Mechanical coupling
How strong (force) is the muscle contraction?
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18
Q

Types of Cardiac Drugs

A
  • Sodium potassium pump blocker (lead to increased contraction)
  • Calcium channel blocker (lead to decreased contraction)
  • B-receptor agonist (lead to increased contraction)
19
Q

Beta receptor agonist drug

A

(+) positive Ionotropy result
via cAMP pathway
given for CHF and Heart Attack (MI)

20
Q

Na-K pump blocker drug

A

leads to increased Ca, and increased contraction!

+ ionotropy

21
Q

Ca channel blocker drug

A
  • ionotropy bc not as much calcium available
22
Q

T wave inversion can be a sign of

A

LVH

or Coronary Ischemia

23
Q

“Peaked” (tall & narrow) T waves can indicate

A

Hyperkalemia

repolarization wave is detected stronger

24
Q

Flat T waves may indicate

A

HypOkalemia

or Coronary Ischemia (again)

25
S-T segment corresponds to :
plateau phase of Fast ventricular action potential (when ca L type influx) Ventricles are contracting!
26
P-R interval
Represents time for Atria to depolarize and get through the AV node ONE LARGE BOX 0.12-0.2 seconds Longer: Conduction delay, AV block
27
Another way to think about S-T segment
Ventricular contraction and emptying
28
Q-T interval
All of ventricle activity Depol-Repol Ventricles are contracting, relaxing, and filling.
29
We need to know this timing for exam | P-R interval! time it takes atria to depolarize and get signal to ventricles
0. 12-0.20 seconds is normal | longer: conduction delay or AV block
30
1st degree AV block
prolonged PR interval due to delayed conduction thru AV node or Bundle of HIS one P wave for every QRS
31
2nd degree AV block
partial dissociation b/w atria & ventricles not every P wave is followed by QRS may have 2 P waves, then 1 QRS. maybe 3 P waves, then QRS
32
3rd degree AV block
Complete Heart Block no correlation b/w P wave and QRS- meaning atria and ventricles are acting totally independent of each other No conduction b/w AV node
33
S2 2nd sound | "Dub"
closing of Semilunar valves (to body and lungs) to CLOSE
34
End systolic volume
All valves closed | Ventricular blood volume is at lowest after ejection completed
35
Difference between End diastolic volume and End systolic voluem
tells us how much blood was actually pumped out into the body Stroke volume = ~70 mL
36
S3 = normally not heard
Rapid ventricular filling may indicate tensing of chordae tendinae and AV valve ring -normal in chidren -pathologic in adults, cause dby ventricular dilation
37
Longest phase of the cardiac cycle
Reduced Ventricular Filling At the very end of the ventricles filling process- eventually the pressure in ventricles increases bc they are filling so much and rate of filling decreases
38
How does increased HR affect Reduced Cardiac filling?
decreases the time available for the ventricles to finish filling decreases filling OR reduces preload and thus Stroke Volume decreases
39
"Lub" sound
pressure increase in ventricles causes AV valves to close`
40
S1
Isovolumic contraction "Lub" AV valves closing
41
S2
Isovolumic relaxation "Dub" two components (the aortic valve closing and the pulmonary valve closing)
42
S3
Ventricles filling rapidly normal in children, not audibly normal in adults
43
S4
Atrial systole | where ventricular compliance is decreased- Ventricular Hypertrophy
44
S4
Ventricular Hypertrophy