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Physiology III - Freedman > Unit 1: Cardiac Physiology- Pt.2 > Flashcards

Unit 1: Cardiac Physiology- Pt.2 Flashcards

1
Q

(Pick) the Atrial and Ventricular heart muscles are squamous/striated elongated grouped into irregular/regular anatamosing columns with 1-2/over 3 centrally located nuclei.

A

striated elongated

irregular

1-2 nuclei

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2
Q

What are the specialized excitatory and conductive muscle fibers? Do they contract strong or weakly? Are there many for few fibrils?

A

SA node, AV node, Purkinge fibers

contract weakly
few fibrils

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3
Q

Cardiac muscle has a syncytial nature. What is syncytium and how does it occur?

A

= many acting as one
Due to presence of intercalated discs
- low resistance pathways connecting cardiac cells end to end
- presence of gap junctions

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4
Q

What is the duration of an action potential in cardiac muscle?

A

from .2-.3 sec

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5
Q

What are the three channels found in cardiac muscle?

A
  1. fast Na+ channels
  2. slow Ca++/Na+ channels
  3. K+ channels
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6
Q

What is the permeability changes of cardiac muscle, as in when they increase?
Na+
Ca++
K+

A

Na + sharp increase at onset of depolarization

Ca++ increased during plateau

K+ increased during the resting polarized state

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7
Q

Describe the membrane permeability changes for Na+ during an action potential in cardiac tissue.

A

increase at onset of depolarization, decrease during repolarization (same with Ca++)

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8
Q

Describe the membrane permeability changes for Ca++ during an action potential in cardiac tissue.

A

increase at onset of depolarization, decrease during repolarization (same as Na+)

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9
Q

Describe the membrane permeability changes for K+ during an action potential in cardiac tissue.

A

decreases at onset of depolarization, increases during repolarization

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10
Q

During depolarization of typical cardiac muscle, what types of channels open? (fast/slow)

A

both fast Na+ channels and slow Ca++/Na+ channels open

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11
Q

During depolarization, what channels are operational for specialized excitatory cells like the SA node? What does that do to the depolarization time?

A

only slow Ca++/Na+ channels are, therefore increasing depolarization time

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12
Q

What does Tetradotoxin do?

A

blocks fast Na+ channels, therefore changing a fast response into a slow response

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13
Q

Passive ion movement across a cell takes into consideration what 3 things?

A
  1. concentration gradient (high to low)
  2. electrical gradient (opposite charge attract, like charge repel)
  3. membrane permeability (dependent on ion channels (open or closed)
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14
Q

What is the Nernst equilibrium potential?

A

it is what an ion will seek to meet if its ion channel is open; it is why a cell repolarizes to a certain voltage b/c finds that balance where are NEP

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15
Q

How is the concentration gradient favoring ion movement in one direction offset?

A

by the electrical gradient (+ or -)

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16
Q

During the resting membrane potential (Er) in cardiac muscle, which channels are open and which are closed?

A

fast Na+ and slow Ca++/Na+ channels are closed

ONLY K+ channels are open, therefore K+ ions are free to move and when reach their Nerst equilibrium potential, a stable Er is maintained

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17
Q

The ________ is energy dependent and pumps ____ Na+ out and ___ K+ into cardiac cells.

A

Na+/K+ ATPase (pump); 3 Na+ out; 2 K+ in

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18
Q

When the Na+/K+ ATPase pump is in action, what is occuring when it comes to the charge of the cell?

A

there is a net loss of one + charge form the interior each cycle, helping the interior of the cell remain negative

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19
Q

What drug will bind to the Na+/K+ ATPase pump and inhibit it? What other pump does that effect?

A

Digitalis

is tied to Ca++ exchange protein and therefore will inhibit that pump and will increase Ca++ which will increase contraction strength

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20
Q

What is the Ca++ exchange protein? What is it “tied” to?

A

it is in cardiac cell membrane and exchanges Ca++ from the interior in return for Na+ that is allowed to enter the cell
- fxn of this exchange protein is tied to the Na+/K+ pump

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21
Q

When does the Absolute Refractory Period occur? And how is re-stimulation impacted?

A

occurs during the plateau (before Relative RP); unable to re-stimulate cardiac cell, no matter how strong the stimulus

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22
Q

When does the Relative Refractory Period occur? And how is re-stimulation impacted?

A

occurs during repolarization (after Absolute RP); requires a supra-normal stimulus have an effect

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23
Q

T/F. In a Slow response cardiac muscle cell the Relataive Refractory Period is shortened and the refractory period is about 25% shorter.

A

False–the Relative Refractory period is PROLONGED, and the refractory period is about 25% LONGER

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24
Q

What purpose does the prolonged refractory period in a Slow response cardiac muscle cell serve in an AV node and bundle?

A

it serves to protect the ventricles from supra-ventricular arrhythmias
(so if atrium is abnormal, like in A-fib, ventricles will be protected)

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25
Q

What is the normal pacemaker of the heart?

A

the SA node; which is self excitatory in nature

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26
Q

SA node self excitatory nature:

  1. Is the Er more or less neg.?
  2. What ions is the membrane leaky to?
  3. Is there a plateau?
  4. is spontaneous depolarization faster or slower?
  5. Contracts stronger or weaker?
A
  1. less neg. Er
  2. leaky to Na+/Ca++ (LACKS A STABLE RESTING Er)
  3. No plateau
  4. at faster rate (overdrive suppression)
  5. contracts feebly (lacks strength/force)
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27
Q

What is Overdrive Suppression?

A

if you drive a self-excitatory cell at a rate faster than its own inherent rate–> you will suppress cell’s own automaticity

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28
Q

What cells are under overdrive suppression by the SA node?

A

cells of the AV node and purkinje system

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29
Q

What mechanisms is thought to cause Overdrive Suppression?

A

due to increased activity of Na+/K+ pump–> creating more negative Er (resting membrane potential)

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30
Q

Where is the AV node located?

A

located in wall of base of right atrium

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31
Q

What is the function of the AV node?

A

it delays the wave of depolarization from entering the ventricle –> this allows atria to contract slightly ahead of the ventricles (.1 sec delay)

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32
Q

What occurs in the absence of the SA node?

A

the AV node may act as pacemaker but as a slower rate

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33
Q

T/F. The AV node has a slower conduction velocity due to smaller diameter fibers.

A

true

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34
Q

What is occurring during systole? What about diastole?

A 
systole = heart is contracting
diastole = heart relaxed
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35
Q

What happens to the cycle length as the heart rate increases?

A

the cycle length decreases

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36
Q

At a resting HR, what is the relationship between Systole and diastole?

A

Systole is lesser than diastole

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37
Q

As heart rate increases what happens to systole and diastole?

A

duration for both shorten, BUT diastole shortens at a greater extent (therefore at high HR, ventricle may not fill adequately)

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38
Q

Comparative example:
HR = 75 BPM and the Systole = .3s, and Diastole = .5s. What is the Cycle Length?

HR = 150 BPM, S= .2s, D=.2s, CL =?

A

CL = .8 seconds

CL = .4 seconds

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39
Q

During systole, what is occurring to the blood flow to the myocardium?

A

perfusion of the myocardium is restricted–> by the contracting cardiac muscle compressing blood vessels (esp. LV)

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40
Q

When does the left coronary artery flow peak?

When does the right coronary artery flow peak?

A

at the onset of diastole

at mid systole, due to more compression of small blood vessels in wall of LV during systole

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41
Q

What is the “equation” for Cardiac Output?

A

CO = HR x SV (stroke volume)

CO will be in L/min

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42
Q

What does isovolumic mean?

A

volume fixed and is a sealed chamber

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43
Q

The Cardiac Cycle is divided into what two parts?

A

Systole and Diastole

44
Q

Systole is divided into what two things?

A
  1. isovolumic contraction = pressurization*

2. ejection = muscle shorten and push blood out, opening of aortic valve*

45
Q

During ejection of systole, what valve is opening?

A

aortic valve

46
Q

What are the parts of Diastole?

A
  • isovolumic relaxation
  • rapid inflow –> 70-75% and mitral valve opens
  • diastasis = period of passive filling has slowed
  • artrial systole –> 25-30%
47
Q

Change of pressure in the heart is either due to ______ or ______.

A

change of volume; or tone

48
Q

How is stoke volume calculated?

A

SV = End-diastolic volume – End-systolic volume

49
Q

A normal heart beat makes a “Lub-Dub” sound. What is the Lub sound ass with? What is the Dub sound ass. with?

A 
Lub = mitral valve closes
Dub = aortic valve closes
50
Q

In the Volume-Pressure Loop, what is occurring A –> B?

A
  • ventricular filling
  • AV(atrioventricular) valves open
  • Semiluar valves closed
51
Q

In the Volume-Pressure Loop, what is occurring B –> C?

A
  • isovolumic contraciton
  • AV (atrioventricular) valves close
  • semiluar valves closed
52
Q

In the Volume-Pressure Loop, what is occurring C–> D?

A
  • ejection
  • semilunar valves open
  • AV valves close
53
Q

In the Volume-Pressure Loop, what is occurring D –> A?

A
  • isovolumic relaxation
  • semilunal valves close
  • AV valves remain closed
54
Q

In the Volume-Pressure Loop, what is occurring, what occurs at point A?

A
  • AV valves open

- = ESV (end systolic volume)

55
Q

In the Volume-Pressure Loop, what is occurring at point B?

A
  • AV valves close

- = EDV (end diastolic volume)

56
Q

In the Volume-Pressure Loop, what is occurring at point C?

A
  • semilunar valves open
57
Q

In the Volume-Pressure Loop, what is occurring at point D?

A
  • semilunar valves close
58
Q

What does the area enclosed by the Volume-Pressure loop a measure of?

A

measure of work (EW)

EW = (change of Volume) x (change of pressure)

59
Q

What is the volume in ventricles at the end of filing called?

A

End diastolic volume (EDV)

- is maximum volume

60
Q

What is the volume in the ventricles at the end of ejection called?

A

End Systolic volume (ESV)

- is minimum volume

61
Q

What is the volume ejected by the ventricles called?

A

Stroke volume

SV = EDV - ESV

62
Q

What is the Ejection Fraction? What is normal?

A

the percent of EDV ejected
= (SV/EDV) x 100%

Normal = 50-60%

63
Q

What does exercise do to the ejection fraction?

A

increase ejection fraction due to increase in SNS

64
Q

Example: If EDV = 160 and ESV = 80.

What is the SV? What is the Ejection Fraction?

A 
SV = 80 (due to 160-80)
EF% = 50% (due to SV/EDV, so 80/160)
65
Q

What is the stretch on the wall prior to contraction?

A

Preload (proportional to the EDV–max vol)

66
Q

What is the changing resistance that the heart has to pump against as blood is ejected?

A

Afterload

i.e. changing aortic BP during ejection of blood from the LV

67
Q

What are the three kinds of Atrial Pressure Waves?

A

A wave
C wave
V wave

68
Q

What is the Atrial Pressure A wave associated with?

A

ass. with atrial contraction

69
Q

What is the Atrial Pressure C wave ass. with?

A

ass. with ventricular contraction

- bulging of AV valves and tugging on atrial muscle

70
Q

What is the Atrial Pressure V wave ass. with?

A

ass. with atrial filling

71
Q

When would a valve open?

A

opens with a forward pressure gradient

- Ex: when LV pressure > the aortic pressure; the aortic valve is open

72
Q

When would a valve close?

A

close with a backward pressure gradient

- Ex: when aortic pressure > LV pressure; the aortic valve is closed

73
Q

What are the two AV valves?

A

Mitral and Tricuspid

74
Q

What are the two Semilunar valves?

A

Aortic and pulmonic valves

75
Q

Are AV valves or semilunar valves stronger?

A

AV valves = thin and flimsy

Semilunar valves = stronger construction

76
Q

Which valves contain chorda tendineae? Which contain papillary muscles? What do each do?

A

AV valves have both (Mitral and Tricuspid)

Chorda tendineae = act as check lines to prevent prolapse

Papillary muscles = increase tension on chorda tendineae

77
Q

What is a valve called that does not open fully?

A

stenotic

78
Q

What is a valve called when it is not closing fully?

A

insufficient/regurgitant/leaky

79
Q

What creates vibration noise in the heart?

A

valvular dysfunction
AKA murmurs
- but, NOT all murmurs are valvular defects

80
Q

During systolic timing, list the valves and if open or closed:

A 
Tricuspid = closed
Pulmonary = open
Mitral = closed
Aortic = open
81
Q

During Systole, list the valves, if they should be open or closed and the potential heart murmur issue.

A

Tricuspid (closed) insufficiency
Pulmonary (open) – stenosis
Mitral (closed) – insufficiency
Aortic (open) – stenosis

82
Q

During diastolic timing, list the valves and if open or closed:

A 
Tricuspid = open
Pulmonary = closed
Mitral = open
Aortic = closed
83
Q

During Diastole, list the valves, if they should be open or closed and the potential heart murmur issue.

A

Tricuspid (open) – stenosis
Pulmonary (closed) – insufficiency
Mitral (open) – stenosis
Aortic (closed) – insufficiency

84
Q

If a heart murmur is heart during both systole and diastole what could the issue be? (2)

A
  • patent ductus arteriosus (didn’t close at birth–connects pulmonary artery to aorta)
  • combined valvular defect
85
Q

What is the Law of Laplace?

A

Wall tension = (pressure)(radius) / 2

  • at given pressure, as ventricular radius increase, developed wall tension increases
86
Q

For the Law of Laplace, as tension increases what occurs to force?

A

increase force of ventricular contraction

87
Q

Example: If you have two ventricles operating at the same pressure, but with different chamber radii, which will consume more energy and oxygen?

A

the larger chamber will have to generate more wall tension, consuming more energy and oxygen

88
Q

How does the Law of Laplace explain how capillaries can withstand high intravascular pressure?

A

“very small radius”

- capillaries are’t strong, but if minimize radius, the wall tension is lowered, therefore won’t rupture

89
Q

What is the term for anything that affects the heart rate?

A

chronotropic
(+ increases)
(- decreases)

90
Q

What is the term for anything that affects conduction velocity?

A

Dromotropic

91
Q

What is the term for anything that affects the strength of contraction?

A

Inotropic

92
Q

What would be a + chronotropic agent?

A

caffeine b/c it increases the heart rate

93
Q

What is an exampel of a + chronotropic?

A

NE, Epinephrine, caffeine

94
Q

What is an exampel of a negative chronotropic?

A

beta-blocker

95
Q

What has control over heart pumping?

A

intrinsic properties of cardiac muscle cells –>

- Frank-Starling Law of the Heart

96
Q

What is the Frank-Sterling Law of the Heart?

A

w/in physiological limits, the heart will pimp all the blood that returns to it w/o allowing excessive damming of blood in veins
(“heart pumps whatever comes back to it”)

97
Q

When referring to the mechanism of the Frank-Sterling Law of the Heart, increased venous return will cause what?

A

will increase the stretch on cardiac muscle fibers (intrinsic effects)

98
Q

When cardiac muscle are stretched what else occurs?

A

Increase force of contraction by:

  • increased cross-bridge formation
  • increased Ca++ influx

Increase HR b/c:
- increase stretch on SA node

99
Q

When referring to the mechanism of the Frank-Sterling Law of the Heart— what is heterometric and homeometric autoregulation? (in general)

A

Heterometric = stretch to greater length

Homeometric = keep length constant

100
Q

What autoregulation is it called when cardiac fibers are stretched and the force of contraction is increased, within limits?

A

Heterometric autoregulation

- more Ca++ influxed into cell

101
Q

What autoregulation is it called when there is the ability to increase strength of contraction, independent of a length change?

A 
Homeometric autoregulation
(- no change in length, but change in force)
102
Q

What three ways can Homeometric autoregulation be induced?

A
  1. Flow induced
  2. Pressure induced
  3. Rate induced
103
Q

How would flow induce homeometric autoregulation of the heart?

A

increased stroke volume maintained, even as EDV decreases back to initial levels; ESV would be reduced

104
Q

How would pressure induce homeometric autoregulation of the heart?

A

increase in aortic BP (afterload) will stimulate force of LV contraction

105
Q

How would rate induce homeometric autoregulation?

A

increased heart rate (therefore decreased cycle length), will stimulate force “treppe”

“treppe” = stair-cased

106
Q

What will direct stretch on the SA node cause?

A

it will increase Ca++ and/or Na+ permeability, which will increase heart rate

Physiology III - Freedman (18 decks)

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