The Cardiac Pressure-Volume Cycle Flashcards by Aarya Sumesh

If is what type of channel?

HCN
hyperpolarisation activated, cyclic nucleotide gated channel

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Some ion channels are voltage gated. Some are —- dependent.

time
open or close with a delay

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Two K+ channels to know for cardiac cycle?

inward rectifier K+ channels
delayed rectifier K+ channels

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Inward rectifier K+ channels

open when Vm goes below -60mV
- unusual, most open when cells
  are at rest
function: to clamp membrane
potential (Vm) at rest
lets K+ out of cell, repolarising it

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Delayed Rectifier K+ channels

opens when membrane
depolarises
but both opening and closing takes
place with a delay

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Basic action potential:

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Example of a positive feedback loop in depolarisation:

Na+ enters cell, causing more depolarisation causing more Na+ channels to open, causing more depolarisation

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At rest what occurs in action potential:

*** inward rectifier K+ channels are
open
K+ leaving cell is dominant current

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Depolarisation stage of action potential

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Repolarisation stage of action potential:

*** delayed rectifier K+ channels
open
Na+ channel inactivation, decrease
in Na+ entry into cells
Delayed Rectifier K+ channels open:
increase in K+ going out

Vm less positive!!!

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After hyperpolarisation stage of action potential:

insert diagram

insert slide

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What channels are open in the stages of action potential?

baseline/rest: inward K+ channels
open, very few Na+
depolarisation: inward K+ close,
Na+ opens
repolarisation: Na+ channels close,
Delayed rectifier K+ open
after hyperpolarisation: Delayed
rectifer close, inward K+ open

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Refractory period of an action potential

amount of time it takes a cell membrane to be ready for a second stimulus after reaching resting state

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Ventricular Myocyte action potential phases name:

phase 0
phase 1
phase 2
phase 3
phase 4

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Cardiac action potential is ——– than skeletal

broader

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Ventricular myocyte action potential: phase 0:

insert diagram: where is P0?

depolarisation
Na+ channels open with positive
feedback
insert diagram

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Ventricular myocyte action potential: phase 1:

insert diagram: where is P1?

transient outward current
delayed rectifier K+ channels
K+ leaves myocyte
myocyte starts to repolarise

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Ventricular myocyte action potential: phase 2:

insert diagram: where is P2?

plateau phase
Ca1+ channels open: time and
voltage dependent
Ca2+ enters as K+ leaves
calcium current into cell just about
balances the K+ current leaving the
cell
very slow repolarisation in this
phase

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Ventricular myocyte action potential: phase 3:

insert diagram: where is P3?

rapid repolarisation phase
Ca2+ channels that maintain
plateau close
delayed rectifier K+ channels open
K+ leaves myocyte

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Ventricular myocyte action potential: phase 4:

insert diagram: where is P4?

resting potential
K+ leaves myocyte
inward rectifier K+ channels

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Comparison of action potentials: which action potential time always stays the same?

Nerve cells
1 millisecond

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Comparison of action potentials: Middle in terms of action potential length?

skeletal muscle
2-5 mins
contraction follows action potential
short refractory period
tetany occurs with repeated stimuli

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comparision of AP 3 diagram

label lines
insert diagram

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Comparision of action potentials: cardiac action potential: time:

varies in size and duration
depending on requirements
(exercise)
can last upto 500 milliseconds
contraction during action potential
long refractory period - prevents
tetany of cardiac muscle!!!

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Cardiac action potentials vary in time and shape depending on which part of heart. Which has lowest plateau phase?

SA node and AV node

Sinus and AV node cardiac action potentials:

- Pacemaker tissues: - spontaneous depolarisation - no inward K+ rectifier current - not stable at rest 0 = depolarisation phase 1 = does not exist 2 = does not exist 3 = repolarisation phase 4 = pacemaker potential Phase 4 is a pacemaker current: If current = funny current depolarisation is due to Ca2+ not Na+ no plateau phase as no inward K+ rectifier repolarisation is due to delayed rectifier K+

If (funny current)

- If increases upon hyperpolarisation - HCN channel - makes SA node spontaneously active - If leads to a NET INWARD CURRENT If involves: - large Na+ current inwards - tiny K+ current outward - depolarises cell to 0mV

What is responsible for cardiac auto-rhythmicity?

- If (funny) current makes the SA node spontaneously active

Cardiac myocytes are joined together by

intercalated discs

Intercalated Discs:

- joins adjacent cardiac myocytes - 3 components: - desmosome, adherens junctions, gap junctions - low electrical resistance, high ion permeability - allows action potentials to easily pass from cell to cell

Desmosome

structural holds cells together

Adheres junctions

anchor thin actin filaments to ensure co-ordinated movement

gap junctions

free ion movement between cardiac myocytes gives the intercalated discs a low electrical resistance and allows the action potential to move freely from cell to cell

Functional Syncytium

- syncytium = multinucleated cell due to multiple cell fusions eg skeletal muscle - 2 functional syncitia: - atrial - ventricular - each follows the all or nothing rule

Intercalated discs purpose

allow co-ordinated cardiac contraction

Conduction Velocities in the heart

only connection between atria and ventriculars is the slowest (allows atria to complete contraction)

What controls the AV node conduction velocity?

autonomic nervous system acts via effects on phase 0 depolarisation

Sympathetic AV node conduction

Sympathetic chain NAdr, beta 1, Gs, increased cAMP, adenylate cyclase

Parasymathetic AV node conduction:

Vagal Ach, muscarinic receptors, Gs, decreased cAMP

What drugs and mechanism can slow AV node conduction?

- bisoprolol (beta 1) - verapamil (L type Ca2+ channels) (CCB) - Digoxin (increases vagal tone)

Sarcomere

Sarcomeres and Starling's Law

- myocyte stretch increases overlap of thick and thin filaments -MORE OVERLAP, INCREASES ACTIN MYOSIN CROSS BRIDGING INCREASES FORCE GENERATION - hence increases force and duration of contraction

Intrinsic regulation of contractile force (starling mech) vs extrinsic regulation (sympathetic stimulation)

starling is longer and stronger sympathetic is faster and stronger, same number of cross-bridges working harder

left ventricle pressure

insert

aorta pressure

insert

Maximum pressure in the left ventricle is different to the maximum pressure in the aorta. true or false?

False; both the same

Which pressure is the same during systole?

aorta and left ventricle as aortic semi-lunar valve is open

Which pressure is the same during diastole?

left atrium and left ventricle as mitral valve is open in diastole

cardiac cycel diagram

insert with valves opening and closing isovolumic contracgtion and relaxation

Isovolumic contraction period

period after mitral valve is closed, and before aortic valve is open, when the ventricle is contracting but there is no change to volume of blood, despite increase in pressure

Isovolumic Relaxation period

period after aortic valve closes and before mitral valve opens, where the ventricle is relaxing but there is no change in volume despite decrease in pressure

4 phases of diastole

- isovolumic relaxation (after mitral valve opens and before it closes) - passive filling - diastasis - active filling (+atrial contraction)

2 phases of systole

Isovolumic contraction and ejection

cardiac cycle

heart sounds

P wave is

atrial systole

QRST complex is

ventricular systole

Aortic Stenosis on cardiac cycle draw and shade

Wiggers plot of the cardiac cycle

Wiggers volume loop of left ventricle

Mitral stenosis loop

aortic stenosis loop

mitral regurg loop

aortic regurg loop

Which thin filaments are common biomarkers to all muscle and which are specific to cardiac muscle and detail of biomarkers

Tn-C common to all Tn-T cardiac Tn-I cardia = Tn-T binds the troponin complex to tropomyosin = Tn-C binds Ca2+ during excitation- contraction coupling = Tn-I inhibits cross-bridging to myosin heavy chains

CK-MB

- creatine biomarker specific to cardiac muscle - moves high energy phosphate - from ATP in mitochondria - to ADP in the cytoplasm

Markers of Myocardial damage

list the dayys and markers