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Quarter 2 > Physiology Exam 2 > Flashcards

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
Q

S-T segment corresponds to :

A

plateau phase of Fast ventricular action potential
(when ca L type influx)
Ventricles are contracting!

26
Q

P-R interval

A

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
Q

Another way to think about S-T segment

A

Ventricular contraction and emptying

28
Q

Q-T interval

A

All of ventricle activity
Depol-Repol
Ventricles are contracting, relaxing, and filling.

29
Q

We need to know this timing for exam

P-R interval! time it takes atria to depolarize and get signal to ventricles

A
  1. 12-0.20 seconds is normal

longer: conduction delay or AV block

30
Q

1st degree AV block

A

prolonged PR interval due to delayed conduction thru AV node or Bundle of HIS

one P wave for every QRS

31
Q

2nd degree AV block

A

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
Q

3rd degree AV block

A

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
Q

S2 2nd sound

“Dub”

A

closing of Semilunar valves (to body and lungs) to CLOSE

34
Q

End systolic volume

A

All valves closed

Ventricular blood volume is at lowest after ejection completed

35
Q

Difference between End diastolic volume and End systolic voluem

A

tells us how much blood was actually pumped out into the body

Stroke volume = ~70 mL

36
Q

S3 = normally not heard

A

Rapid ventricular filling
may indicate tensing of chordae tendinae and AV valve ring
-normal in chidren
-pathologic in adults, cause dby ventricular dilation

37
Q

Longest phase of the cardiac cycle

A

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
Q

How does increased HR affect Reduced Cardiac filling?

A

decreases the time available for the ventricles to finish filling

decreases filling OR
reduces preload and thus Stroke Volume decreases

39
Q

“Lub” sound

A

pressure increase in ventricles causes AV valves to close`

40
Q

S1

A

Isovolumic contraction
“Lub”
AV valves closing

41
Q

S2

A

Isovolumic relaxation
“Dub”
two components (the aortic valve closing and the pulmonary valve closing)

42
Q

S3

A

Ventricles filling rapidly

normal in children, not audibly normal in adults

43
Q

S4

A

Atrial systole

where ventricular compliance is decreased- Ventricular Hypertrophy

44
Q

S4

A

Ventricular Hypertrophy

Quarter 2 (16 decks)

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