The Cardiac Pressure-Volume Cycle Flashcards
If is what type of channel?
HCN
hyperpolarisation activated, cyclic nucleotide gated channel
Some ion channels are voltage gated. Some are —- dependent.
time
open or close with a delay
Two K+ channels to know for cardiac cycle?
- inward rectifier K+ channels
- delayed rectifier K+ channels
Inward rectifier K+ channels
- open when Vm goes below -60mV
- unusual, most open when cells
are at rest
- unusual, most open when cells
- function: to clamp membrane
potential (Vm) at rest - lets K+ out of cell, repolarising it
Delayed Rectifier K+ channels
- opens when membrane
depolarises - but both opening and closing takes
place with a delay
Basic action potential:
Example of a positive feedback loop in depolarisation:
Na+ enters cell, causing more depolarisation causing more Na+ channels to open, causing more depolarisation
At rest what occurs in action potential:
- *** inward rectifier K+ channels are
open - K+ leaving cell is dominant current
Depolarisation stage of action potential
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!!!
After hyperpolarisation stage of action potential:
- insert diagram
insert slide
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
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
Ventricular Myocyte action potential phases name:
- phase 0
- phase 1
- phase 2
- phase 3
- phase 4
Cardiac action potential is ——– than skeletal
broader
Ventricular myocyte action potential: phase 0:
insert diagram: where is P0?
- depolarisation
- Na+ channels open with positive
feedback
insert diagram
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
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
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
Ventricular myocyte action potential: phase 4:
insert diagram: where is P4?
- resting potential
- K+ leaves myocyte
- inward rectifier K+ channels
Comparison of action potentials: which action potential time always stays the same?
Nerve cells
1 millisecond
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
comparision of AP 3 diagram
label lines
insert diagram
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!!!
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
- desmosome, adherens 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