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Physiology > 21. Heart stuff not sure exactly > Flashcards

21. Heart stuff not sure exactly Flashcards

1
Q

2 types of cardiomyocytes

A

Working- involved in pumping function of heart

Conduction/pacemaker- form excitation/conduction system of heart.Pacemaker cells are smaller and lighter with rounded shape, that contain less
contractile elements and mitochondria.

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2
Q

Morphological features cardiac muscle

A

Striated: filaments arranged in sarcomeres

Smaller in size,

mononuclear

connected by intercolated disks (btw endings of each cell)

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3
Q

What is the function of the intercalated disks

A

They build up mechanical connections using desmosomes so cardiomyocytes are held tightly together

This is a necessary prerequisite for
performing the pumping function of
the heart.

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4
Q

Gap junctions in cardiomyocytes

A

Located in the peripheral part of the disks

Type of synapse so allows excitatory process from one cell to another

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5
Q

Do cardiomyocytes have a well developed T tubule system

A

YES

imp for making link btw excitation and contraction
condicts the AP from sarcolemma to sarcoplasmic reticulum

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6
Q

What are cisterns and diads

A

Myofibrils are enveloped by SR

The T-tubules and the terminal
branches of the SR called cisterns
together form a structures called
diads.

Many mitochondria found in them bc cardiomyocytes rely on aerobic metabolism

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7
Q

What is resting membrane potential of cardiomyocytes

A

-90mv

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8
Q

What are the 3 layers of the heart
Which layer is more suspectable to stretching

A

endocardium,myocardium, epicardium/pericardium

epicardium stretches so heart can take in greater amounts of blood - when heart is filled more, it contracts stronger

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9
Q

Are ventricular cardiomyocytes connected with atrial cardiomyocytes

A

NO

Connected via conducting system

Imp bc 2 functional synctiums ( atrial/ventricular)

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10
Q

Do pacemaker cells have a stable resting potential

A

no

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11
Q

Both cells generate action potentials

How do cardiomyocytes generate action potential

A

PHASE 0: Steep depolarization due to Na+ voltage gated channels open until +35 mv

PHASE 1: short term, small amplitude repolarization due to K+ channels opening and inactivation of Na+ channels

PHASE 2: Plateu. Membrane potential retained at 0Mv bc some K+ close and Ca2+ channels open which are also voltage gated but inactivated more slowly than Na+

PHASE 3: Opening of several types of K+ channels leads to repolarization

PHASE 4: resting memebrane potential

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12
Q

What is the biological significance of long duration of phase 2

A

To increase intracellular Ca2+ concentration

The entry of calcium ions into the cell causes calcium ions to be released by the SR for excitation/ contraction coupling
THIS IS CALCIUM DEPENDENT CALCIUM RELEASE

Their DHP recptor lets in more calcium ions than in skeletal

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13
Q

What is the result bc duration of contraction and action potential is same

A

No tetanus in the heart (when it doesnt hv time to fully relax)

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14
Q

When is absolute refractory period

A

Very long (toprevent tetanic contraction) bc there are no Na+ channels at phase 2.3.4

ARP starts at the beginning of phase 0 and
ends around the middle of phase 3 and MP
of -50 mV.

ARP coincides with the period of systole
and the onset of diastole.

During this period, myocardial cells cannot
be re-excited!

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15
Q

What is the supranormal period

A

Period hwere fast Na+ channels are responsive near threshold

weaker than normal stimulus will cause action potential

But these contractions are useless

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16
Q

What is automaticity of the heart

A

Ability of pacemaker cells to generate action potential without need of external stimuli

Due to spontaneous depolarization of their cell membranes

Conducted to working cells by gap junctions

17
Q

Generation of action potential in pacemaker cells

Phase 4

A

It is generated by pacemaker channels
also called “If” channels, during phase
4 of the membrane potential (MP) in
pacemaker cells.

These channels open spontaneously as
the MP returns to its resting value of
-60 mV.

Leads to Na+ entry and K+ exit.

Na+ depolarize and at -50mv, T type Ca2+ channels open where threshold met t -40mv

18
Q

Phase 0 and 3 of pacemaker AP generation

A

PHASE 0: Once threshold of -40mv met, L type Ca2+ channels open

PHASE 3: The repolarization phase is
associated with the opening of
several types of potassium channels
and the release of K+ from the cell.

MP returns to its resting value (-60
mV) leading to opening aging of
pacemaker channels.

19
Q

SA node is pacemaker of our heart.
What has to happen to it to be our heart rate

A

Has to be suppressed

w/o innervation it contracts 105-110/min so has to be suppressed to get to 65-85/min

20
Q

How is excitation conducted from atria to ventricles

A
  • AP generated in right atrium, SAN
  • Impulse conducted to AVN an dleft atrium
  • AP delayed in AVN, allows atrai to fully contract
  • AP to Bundle of HIS near interventricular septum
  • AP spreads along Purkinje fibers which disperses it to rest of cells
21
Q

Where is the highest and lowest sponataneous depolarization

A

SAN= 105-110/min which is why it is the pacemaker

Bundle if His= 30-40/min

22
Q

Mechanism of excitation/contraction coupling

A
  1. AP spreads from sarcoplasmic membrane
    to T - tubules.
  2. As a result L-type voltage-gated Ca2+
    channels open, leading to entry of Ca2+ ions
    into sarcoplasm.
  3. Increased concentration of Ca2+ ions in
    sarcoplasm induces Ca2+ release from SR by
    activation of ryanodine receptor-channels
    (RyR) - Ca2+ induced Ca2+ release.
  4. The release of Ca2+ from SR causes Ca2+
    spark.
  5. Ca2+ ions bind to troponin to initiate
    contraction.
23
Q

Action of contraction in myocardium

A
  1. ATP binds to actinmyosin complex breaking the crossbirges
  2. ATPase activity of myosin increases
  3. The ATP molecule is broken down
    into ADP and inorganic P. This leads to formation of a new
    strong bound between myosin and
    actin.
  4. Myosin moves 10 nm towards the M-line of the sarcomere.
  5. ADP is released, allowing a new ATP molecule to bind to myosin, and the cycle
    starts over.
24
Q

Relaxation in the heart

A

Ca2+ unbinds from troponin leading to increase in ECF and SR

Ca2+ is pumped back into SR by Ca2+ pump
for storage.

On the cell membrane Ca2+ is exchanged
with Na+ by NCX antiporter.

Na+ gradient is maintained by Na+ - K+
pump.

25
Q

When can extrasystoles be produced

A

In phase 3 during relative refractory period

premature beat

26
Q

Depending on the place of their generation, how many types of
extrasystoles can be discriminated?

A

Atrial, nodal, ventricular

27
Q

What are extrasystoles divided into

A

supraventricular and ventricular

28
Q

What happens in supraventricular extrasystoles

A

Excitatory process carried out by the 2 ventricles

Resulting supraventricular extrasystole is
also conducted to the SAN, exciting it and thus
shifting forward in time the generation of the
next normal systole.

29
Q

What happens in ventricular extrasystoles

A

the excitatory
process is usually not conducted back to the
atria, bc it is difficult for the AVN to conduct in this direction

Atria are not affected by the extrasystoles that are generated in the ventricles.

30
Q

Differences btw extrasystole and normal systole on cardiomechanogram

A
  • ES smaller amplitude than S (part of voltage gated Na+ channels is inactivated
  • After ventricular ES, there is a long pause
    called compensatory pause (CP). (ventricles cannot
    respond to the normal impulse coming at that
    time from SAN, because of the refractory state
    induced by ES)
  • The systole following ES, called
    compensatory systole (PES), has a larger
    amplitude than usual. (long CP
    preceding the compensatory systole,
    during which more blood enters into the
    ventricles, and the concentration of
    intracellular Ca2+ increases more than
    usual.)
31
Q

How is cardiac activity regulated
Intercardiac

A

Homometric- w/o change in sarcomere length
BOUDICH EFFECT: stronger contraction due to
increased heart rate bc more calcium ions

Heterometric- Change in sarcomere length
ANREP EFFECT?

32
Q

How is cardiac activity regulated
Extracardiac

A

ANS: sympathetic and
parasympathetic regulation

Humoral regulation: endocrine,
and paracrine.

Electrolyte regulation.

33
Q

Effects of the sympathetic system

A

+ CHRONOTROPIC- increase heart rate by increasing permeability of pacemaker chnnels in SAN

+IONOTROPIC- increases contraction strength by opening of Ca2+ ion channels through β1 receptors

+ DROMOTROPIC- increases conduction velocity by increasing permeability of Ca2+ channels

+ BATHMOTROPIC- increases excitability of myocardium

34
Q

Effects of parasympathetic system

A

negative chrono, iono,dromo, bathmo tropic

opening of K+ channels by M2 receptors

35
Q

Where are parasympathtic/ sympathetic nerve endings

A

The parasympatetic
postganglionic nerve endings
innervate primarily the atria and
the border between the atria
and ventricles

Postganglionic
sympathetic fibers are present in
both the atria and ventricles.

36
Q

what is postive lysotropic effect (Parasympathetic) negative for sympathetic

A

for greater ease of relaxation

37
Q

Frog heart anatomy

A

2 atria 1 ventricle
venous sinus contracts first

38
Q
A

Physiology (20 decks)

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