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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
What is the normal pacemaker of the heart?
the SA node; which is self excitatory in nature
26
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?
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)
27
What is Overdrive Suppression?
if you drive a self-excitatory cell at a rate faster than its own inherent rate--> you will suppress cell's own automaticity
28
What cells are under overdrive suppression by the SA node?
cells of the AV node and purkinje system
29
What mechanisms is thought to cause Overdrive Suppression?
due to increased activity of Na+/K+ pump--> creating more negative Er (resting membrane potential)
30
Where is the AV node located?
located in wall of base of right atrium
31
What is the function of the AV node?
it delays the wave of depolarization from entering the ventricle --> this allows atria to contract slightly ahead of the ventricles (.1 sec delay)
32
What occurs in the absence of the SA node?
the AV node may act as pacemaker but as a slower rate
33
T/F. The AV node has a slower conduction velocity due to smaller diameter fibers.
true
34
What is occurring during systole? What about diastole?
``` systole = heart is contracting diastole = heart relaxed ```
35
What happens to the cycle length as the heart rate increases?
the cycle length decreases
36
At a resting HR, what is the relationship between Systole and diastole?
Systole is lesser than diastole
37
As heart rate increases what happens to systole and diastole?
duration for both shorten, BUT diastole shortens at a greater extent (therefore at high HR, ventricle may not fill adequately)
38
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 =?
CL = .8 seconds CL = .4 seconds
39
During systole, what is occurring to the blood flow to the myocardium?
perfusion of the myocardium is restricted--> by the contracting cardiac muscle compressing blood vessels (esp. LV)
40
When does the left coronary artery flow peak? When does the right coronary artery flow peak?
at the onset of diastole at mid systole, due to more compression of small blood vessels in wall of LV during systole
41
What is the "equation" for Cardiac Output?
CO = HR x SV (stroke volume) CO will be in L/min
42
What does isovolumic mean?
volume fixed and is a sealed chamber
43
The Cardiac Cycle is divided into what two parts?
Systole and Diastole
44
Systole is divided into what two things?
1. isovolumic contraction = pressurization* | 2. ejection = muscle shorten and push blood out, opening of aortic valve*
45
During ejection of systole, what valve is opening?
aortic valve
46
What are the parts of Diastole?
- isovolumic relaxation - rapid inflow --> 70-75% and mitral valve opens - diastasis = period of passive filling has slowed - artrial systole --> 25-30%
47
Change of pressure in the heart is either due to ______ or ______.
change of volume; or tone
48
How is stoke volume calculated?
SV = End-diastolic volume -- End-systolic volume
49
A normal heart beat makes a "Lub-Dub" sound. What is the Lub sound ass with? What is the Dub sound ass. with?
``` Lub = mitral valve closes Dub = aortic valve closes ```
50
In the Volume-Pressure Loop, what is occurring A --> B?
- ventricular filling - AV(atrioventricular) valves open - Semiluar valves closed
51
In the Volume-Pressure Loop, what is occurring B --> C?
- isovolumic contraciton - AV (atrioventricular) valves close - semiluar valves closed
52
In the Volume-Pressure Loop, what is occurring C--> D?
- ejection - semilunar valves open - AV valves close
53
In the Volume-Pressure Loop, what is occurring D --> A?
- isovolumic relaxation - semilunal valves close - AV valves remain closed
54
In the Volume-Pressure Loop, what is occurring, what occurs at point A?
- AV valves open | - = ESV (end systolic volume)
55
In the Volume-Pressure Loop, what is occurring at point B?
- AV valves close | - = EDV (end diastolic volume)
56
In the Volume-Pressure Loop, what is occurring at point C?
- semilunar valves open
57
In the Volume-Pressure Loop, what is occurring at point D?
- semilunar valves close
58
What does the area enclosed by the Volume-Pressure loop a measure of?
measure of work (EW) EW = (change of Volume) x (change of pressure)
59
What is the volume in ventricles at the end of filing called?
End diastolic volume (EDV) | - is maximum volume
60
What is the volume in the ventricles at the end of ejection called?
End Systolic volume (ESV) | - is minimum volume
61
What is the volume ejected by the ventricles called?
Stroke volume | SV = EDV - ESV
62
What is the Ejection Fraction? What is normal?
the percent of EDV ejected = (SV/EDV) x 100% Normal = 50-60%
63
What does exercise do to the ejection fraction?
increase ejection fraction due to increase in SNS
64
Example: If EDV = 160 and ESV = 80. | What is the SV? What is the Ejection Fraction?
``` SV = 80 (due to 160-80) EF% = 50% (due to SV/EDV, so 80/160) ```
65
What is the stretch on the wall prior to contraction?
Preload (proportional to the EDV--max vol)
66
What is the changing resistance that the heart has to pump against as blood is ejected?
Afterload | i.e. changing aortic BP during ejection of blood from the LV
67
What are the three kinds of Atrial Pressure Waves?
A wave C wave V wave
68
What is the Atrial Pressure A wave associated with?
ass. with atrial contraction
69
What is the Atrial Pressure C wave ass. with?
ass. with ventricular contraction | - bulging of AV valves and tugging on atrial muscle
70
What is the Atrial Pressure V wave ass. with?
ass. with atrial filling
71
When would a valve open?
opens with a forward pressure gradient | - Ex: when LV pressure > the aortic pressure; the aortic valve is open
72
When would a valve close?
close with a backward pressure gradient | - Ex: when aortic pressure > LV pressure; the aortic valve is closed
73
What are the two AV valves?
Mitral and Tricuspid
74
What are the two Semilunar valves?
Aortic and pulmonic valves
75
Are AV valves or semilunar valves stronger?
AV valves = thin and flimsy | Semilunar valves = stronger construction
76
Which valves contain chorda tendineae? Which contain papillary muscles? What do each do?
AV valves have both (Mitral and Tricuspid) Chorda tendineae = act as check lines to prevent prolapse Papillary muscles = increase tension on chorda tendineae
77
What is a valve called that does not open fully?
stenotic
78
What is a valve called when it is not closing fully?
insufficient/regurgitant/leaky
79
What creates vibration noise in the heart?
valvular dysfunction AKA murmurs - but, NOT all murmurs are valvular defects
80
During systolic timing, list the valves and if open or closed:
``` Tricuspid = closed Pulmonary = open Mitral = closed Aortic = open ```
81
During Systole, list the valves, if they should be open or closed and the potential heart murmur issue.
Tricuspid (closed) insufficiency Pulmonary (open) -- stenosis Mitral (closed) -- insufficiency Aortic (open) -- stenosis
82
During diastolic timing, list the valves and if open or closed:
``` Tricuspid = open Pulmonary = closed Mitral = open Aortic = closed ```
83
During Diastole, list the valves, if they should be open or closed and the potential heart murmur issue.
Tricuspid (open) -- stenosis Pulmonary (closed) -- insufficiency Mitral (open) -- stenosis Aortic (closed) -- insufficiency
84
If a heart murmur is heart during both systole and diastole what could the issue be? (2)
- patent ductus arteriosus (didn't close at birth--connects pulmonary artery to aorta) - combined valvular defect
85
What is the Law of Laplace?
Wall tension = (pressure)(radius) / 2 - at given pressure, as ventricular radius increase, developed wall tension increases
86
For the Law of Laplace, as tension increases what occurs to force?
increase force of ventricular contraction
87
Example: If you have two ventricles operating at the same pressure, but with different chamber radii, which will consume more energy and oxygen?
the larger chamber will have to generate more wall tension, consuming more energy and oxygen
88
How does the Law of Laplace explain how capillaries can withstand high intravascular pressure?
"very small radius" | - capillaries are't strong, but if minimize radius, the wall tension is lowered, therefore won't rupture
89
What is the term for anything that affects the heart rate?
chronotropic (+ increases) (- decreases)
90
What is the term for anything that affects conduction velocity?
Dromotropic
91
What is the term for anything that affects the strength of contraction?
Inotropic
92
What would be a + chronotropic agent?
caffeine b/c it increases the heart rate
93
What is an exampel of a + chronotropic?
NE, Epinephrine, caffeine
94
What is an exampel of a negative chronotropic?
beta-blocker
95
What has control over heart pumping?
intrinsic properties of cardiac muscle cells --> | - Frank-Starling Law of the Heart
96
What is the Frank-Sterling Law of the Heart?
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
When referring to the mechanism of the Frank-Sterling Law of the Heart, increased venous return will cause what?
will increase the stretch on cardiac muscle fibers (intrinsic effects)
98
When cardiac muscle are stretched what else occurs?
Increase force of contraction by: - increased cross-bridge formation - increased Ca++ influx Increase HR b/c: - increase stretch on SA node
99
When referring to the mechanism of the Frank-Sterling Law of the Heart--- what is heterometric and homeometric autoregulation? (in general)
Heterometric = stretch to greater length Homeometric = keep length constant
100
What autoregulation is it called when cardiac fibers are stretched and the force of contraction is increased, within limits?
Heterometric autoregulation | - more Ca++ influxed into cell
101
What autoregulation is it called when there is the ability to increase strength of contraction, independent of a length change?
``` Homeometric autoregulation (- no change in length, but change in force) ```
102
What three ways can Homeometric autoregulation be induced?
1. Flow induced 2. Pressure induced 3. Rate induced
103
How would flow induce homeometric autoregulation of the heart?
increased stroke volume maintained, even as EDV decreases back to initial levels; ESV would be reduced
104
How would pressure induce homeometric autoregulation of the heart?
increase in aortic BP (afterload) will stimulate force of LV contraction
105
How would rate induce homeometric autoregulation?
increased heart rate (therefore decreased cycle length), will stimulate force "treppe" "treppe" = stair-cased
106
What will direct stretch on the SA node cause?
it will increase Ca++ and/or Na+ permeability, which will increase heart rate

Physiology III - Freedman (18 decks)

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