Lecture 3 Flashcards

1
Q

intercalated discs

A

specialized structures in cardiac muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

intercalated discs contain 2 key types of cell jns

A

gap junctions = electric coupling
allows functional syncytium = heart contracts as a synchronized unit.

desmosomes = fro strong cell/cell adhesion during contractions,
don’t want cells to rip off from e/o under high force

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

the big picture of cardiac muscle

A

pacemaker cells stimulate the contraction. auto rhythmic

heart contracts as a unit, all or none

influx of Ca from extracellular fluid, then triggers Ca release from sacroplasmic reticulum

—- 10-20% of Ca needed to support contraction from ECF = a jumpstart

absolute refractory period.
cannot stimulate a 2nd contractile response, prevents tetanus, relaxation occurs for 250 msec vs 1-2 msec for skeletal. allows it to fn continuously as a pump

relies only on aerobic rep, so coronary circulation is vvvvvv imp.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Contractile cardiac muscle cells

A

1)depolarization = Na influx through voltage gated channels
positive feedback cycle opens many more Na channels

2)plateau phase
Ca influx, through slow Ca channels
keeps cell depolarized bc few K channels are open
Ca+ in and K+ leaving so almost equal/balanced

3) repolariation
Ca channels inactivate
more K channels open = K efflux
bring voltage of mb back to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

auto rhythmic vs contractile

A

contractile = 99% of cells in heart
generate force of contraction
don’t initiate AP, just follow it through

autorhytmic = pacemaker cells
1%
Initiate and regulate heart rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

auto rhythmic cells

pacemaker potentials

A

SA node = rate of pumping
sinus rhythm= det. heart rate
capable of spontaneous depolarization

pacemaker potentials lead to action potentials

AP due to voltage gated Ca channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

auto rhythmic cells steps

A

1)pacemaker potentials =
slow depolarization is Na channels open and K channels close
mb potential is never a flat line

2)depolarization=
AP begins when pacemaker potential reaches threshold
Ca influx through Ca channels

3)repolarization
Ca channels inactivating
K channels open
K efflux
bring back to (-) voltage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

intrinsic conduction system of heart

A

AP generated by SA node
passes through AV node
slows down at AV bundle
branches into L/R bundle brancehes
branches further into the purkinje fibres
now called = subendocardial conducting network.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

there is a bottleneck from A to V, bc

A

only 1 pathway
provides time fro A to full V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

SA node is te pacemaker bc

A

the further we get from the node, the slower they spontaneously depolarize

bc it depolaries the fastest + on its own.

on its own, it could be 90x/min, but ParaNS slows down the rate of depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

influence of PNS and SNS on cardiac fn

A

ParaNS = dec depol. rate, slows heart rate
SNS = inc depol. and repol. rate, fastens heart rate

tonic ParaNS output has a dampening effect on heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

bradycardia
tachycardia
sinus rhythm

A

Bradycardia = heart rate slower than usual
tachycardia = heart rate faster than usual
sinus rhythm = normal rhythm of the heart, set by SA node firing.

1 and 2 are variable person to person based on fitness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ECG tracing + events at each step

A

P-wave = atrial depolarization -NOT CONTRACTING
SA node is firing

QRS complex = ventricular depolarization
atrial depolarization
T wave = ventricular repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

abnormal activation of heart

A

1)ventricular fibrillation =
absolute mess of squiggly and round ups and downs
both V contract at diff times,
absolute mess, can’t just live w it

2) 2nd degree heart block
every 2nd time, the SA node doesn’t get through to AV node, SA is firing but nothing else happens
so P wave, QRS, T wave, P wave ——no activity**, P wave, QRS, T wave, etc,
no activity bc firing doesn’t go through

3)nonfunctional SA node
SA node is damages so AV takes over
no P wave, but everything is slow bc AV spont depolarization is slower than that of SA
at resting, can be lived with, but pacemaker is needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

systole

A

contraction of heart, pumping out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

diastole

A

relaxation of heart, filling in

17
Q

cardiac cycle

A

atrial systole + diastole
+
ventricular systole + diastole

18
Q

cycle

A
  1. ventricular filling. mid to late diastole
    Pressure is low, P atria > P vent.
    AV valve open
    SL valves closed

after vent is 70% full, AV valves begin to close, P wave, and atrial systole.
P atrial inc
final 30% of blood enters w atrial contraction

  1. ventricular systole = QRS complex and T waves
    ventricles contract,
    inc P closes AV valves,
    is-volumetric contraction = constant volume in a closed system
    SL valves open,
    ventricular ejection phase
  2. isovolumetric relaxation.
    vent. relaxes, early diastole.
    P decreases rapidly,
    SL valves close to prevent back flow.
19
Q

chat ai. recap

A

Atrial Systole (Atrial Contraction)
Atria contract → blood flows into ventricles.
AV valves: Open, Semilunar valves: Closed.

Isovolumetric Contraction (Early Ventricular Systole)
Ventricles contract → pressure rises → AV valves close.
No blood ejected yet.
AV valves: Closed, Semilunar valves: Closed.

Ventricular Ejection (Late Ventricular Systole)
Ventricular pressure exceeds arterial pressure → semilunar valves open.
Blood is ejected into aorta/pulmonary artery.
AV valves: Closed, Semilunar valves: Open.

Isovolumetric Relaxation (Early Diastole)
Ventricles relax → pressure drops → semilunar valves close.
No blood enters ventricles yet.
AV valves: Closed, Semilunar valves: Closed.

Ventricular Filling (Late Diastole)
Ventricular pressure drops below atrial pressure → AV valves open.
Blood flows passively into ventricles.
AV valves: Open, Semilunar valves: Closed.

20
Q

2 features driving cardiac cycle

A

blood flow is controlled by P changes
flows from H to low P through any available opening

electrical activity of L/R hearts is almost simultaneous.

21
Q

heart sounds/

A

2 distinguishable sounds heard through stethoscope

1st = closure of AV valve, beginging of Vent systole
2nd = closer of SemiLunar valve, end of vent systole

sounds due to vibration of heart/chest bc of valve closer

22
Q

heart murmurs, due to

A

vascular insufficiency
leakage of blood back
causes sound where there should be silence

valvular stenoses
valve isn’t opening 100% so there is a narrow opening
high velocity jet of blood through narrow opening
higher pitch of sounds
travels in a swirl instead of a straight line through valve

23
Q

CO + calc

A

= cardiac output
volume of blood pumped from each Vent per minute

CO= SV X HR

lets say your heart is beating 75/min = HR
and each contraction/beat is pumping out 70ml/beat = SV

so to find how much blood is pumped from each vent per minute

70 x 75 = 5250 ml/min

24
Q

SV + calculation

A

= stroke volume
amount of blood being pumped out w a single contraction

SV= EDV-ESV
EDV = end diastolic volume
ESV = end systolic volume

25
influences of expertise on HR and SV
CO inc 4-5 in a fit person 7x in a marathon runner,
26
cardiac reserve
can't change V of blood being pumped out but can move that fixed amount more quickly + redirect it to parts that need it more than others.
27
effects ON heart rate BY autonomic NS, epinephrine, plasma electrolytes, body temp
HR is det by rate of spont. depolarization of SA node 1. autonomic NS innervates SA node 2. circulating hormones = epinephrine are NTs for autoNS, allow threshold to be hit faster, inc HR 3. plasma electrolyte conc. (Na, Ca, K, H) are imp, but we don't modify them, however, if they change, will change HR 4. body temp, esp in surgery cools patient down so heart doesn't move as quickly, easier to work on heart, then warms them back up again WE indv don't use, but still a factor
28
sympathetic NS parasympathetic NS on HR
NE= symp inc rate of spont depol. HR inc ACh = parasymp dec rate fo spont depol. by hyperpolariation pacemaker cells dec HR
29
extreme tachycardia more than 150-170 beats/min = reduced CO, why?
heart is going cray, too fast not enough time for vents to fill before pumping so pumping faster but only a small amount