chap 9, 10- cardiac muscle + excitation/conduction Flashcards
(41 cards)
2 types of circulation
-
pulmonary circulation: carries deoxygenated blood from right side (right ventricle) of heart to lungs & returns oxygenated blood to the left side of heart
- function: picks up O2 from lungs, removes CO2 from blood -
systemic circulation: carries oxygenated blood from the left side (left ventricle) of the heart → all body tissues → returns deoxygenated blood to the right side of the heart.
- function: deliver O₂ and nutrients to tissues,
remove CO₂ and waste products from tissues
2 types of myocardium
-
myocardial contractile/structural cells: cells that contract & pump blood
- includes: atrial muscle cells & ventricular muscle cells (ones that make up atria & ventricles) -
myocardial autorhytmic & conducting cells: these cells generate & conduct electrical impulses (control heart rate- aka pacemaker cells) - HEART HAS INNATE ABILITY TO GENERATE ACTION POTENTIAL
- include:
- SA node: natural pacemaker; starts the heartbeat
- AV node: delays the impulse so atria can contract first
- Internodal fibers: pathways that carry impulses from SA node to AV node
- bundle of His (AV bundle): carries impulses from AV node to ventricles
- purkinje fibers: spread impulse through ventricles for contraction
List the fundamental properties of cardiac muscle LO
- Structure and Striations
- Involuntary nature
- Gap junctions: allow electrical signals to pass quickly from one cell to the next
- Functional syncytium: all heart muscle cells work together as a unit (when one cell is excited, whole chamber contracts)
- Excitability: ability to respond to a stimulus (electrical signal)
- Refractory period: prevents tetany (sustained contraction)
- Contractility
- Autorhythmicity: generates own electrical impulses (action potentials) without external nerve input
- Conductivity: ability to transmit electrical impulses throughout heart
- Endocrine function: atria releases hormone called ANP (atrial natiruetic peptide) which helps lower blood pressure by promoting salt & water excretion in the kidneys
where does cardiac action potential normally originate?
in the sinoatrial (SA) node
cardiomyocyte (cardiac muscle cell) structure
is a striated, involuntary muscle - similar to skeletal muscle in appearance but functionally unique
striations: due to arrangement of actin & myosin microfilaments in sarcomeres
t-tubules: fewer in number but wider than in skeletal muscle; help in conducting action potential into interior of cell
intercalated discs: specialized cell junctions connecting cardiomyocytes that contain gap junctions & desmosomes
branching & uniting fibers: that form a lattice work (helps heart contract as a unit)
sarcoplasmic reticulum!!!: less developed; stores less Ca²⁺ than skeletal muscle.
- cardiac muscle relies more on extracellular Ca²⁺!!!
gap junctions & desmosomes in intercalated discs purpose
Gap junctions: electrical junctions,
low resistance areas that allow rapid spread of cardiac impulse (action potential)
Desmosomes: mechanical junctions, strong mechanical links that hold cells together during contraction of heart as syncytium
function syncytium of heart + 2 types
syncytium: group of interconnected cells that function as a single unit because of electrical coupling through gap junctions
2 types-
- atrial syncytium: made of walls of 2 atria, both atria contract together
- ventricular syncytium: made of walls of 2 ventricles, both ventricles contract together
- these 2 syncytium (atria & ventricles) are separated by fibrous tissue
division into these 2 allows atrium to contract short time before ventricles do
2 types of action potentials in heart (list them + where they are found)
action potential WITH plateau: fast response action potential (initial depolarization is very fast), for strong contraction & impulse conduction (not just speed of repolarization)
- present in: ventricular & atrial muscle, bundle of His, Purkinje cells
action potential W/O plateau: slow response APs (depolarization is slow and gradual)
- present in: SA node, AV node
action potential with plateau in cardiac muscle (all phases, physiological basis, channels) IMP
Phase 0 (rapid depolarization): opening of fast voltage-gated Na+ channels causes rapid influx of Na+
- voltage: from -85 mV to +20 to +20 mV
Phase 1 (initial repolarization): inactivation of Na+ channels & opening of transient K+ channels that let K+ out
- voltage: slight drop from +30 mV
Phase 2 (plateau): opening of L-type (long duration) voltage gated Ca2+ channels & delayed rectifiers K+ channels causes balance of the influx of Ca2+ with balance of efflux of K+ (sustains the plateau)
- voltage: ~0 to 5 mV
Phase 3 (rapid repolarization): L type Ca2+ channels close, delayed rectifier K+ channels remain open, inward rectifier K+ channels (K+ leak channels OPEN to allow K+ to come back in
- voltage: returns to -85 mV
Phase 4 (resting membrane): maintained resting membrane potential by Na+/K+ pump, NCX, K+ leak channels (inward rectifier K+ channels)
- voltage: -85mV
how long does plateau phase last in ventricular muscle?
around 0.2 - 0.3 secs
Which phase of the ventricular action potential is primarily altered by inhibiting voltage-gated sodium channels that resulted in slow conduction velocity in the ventricles?
Phase 0
what causes the plateau phase in ventricular action potential and what 3 channels are responsible + what is physiological role of plateau?
role of plateau: maintains depolarization to allow sufficient Ca2+ entry = long contraction duration = complete ejection of blood
- also prevents tetany by extending absolute refractory period
cause: balance b/w inward Ca2+ current & outward K+ currents
3 channels
1. L-type voltage gated Ca2+ channels: slow opening causes Ca2+ to come in slowly
- delayed rectifiers K+ channels: open slowly to allow K+ to leave slowly
- Na+/Ca2+ Exchanger (NCX): exchanges 1 Ca2+ ion out for 3 Na+ ion in (in phases 2-4)
which 3 channels maintain the RMP in cardiac AP with plateau?
- Na+/K+ pump (ATPase)
- Na+/Ca2+ exchanger (NCX)
- Inward Rectifier K+ channels (leaky K+ channels)
Which phase of the ventricular action potential is most directly affected by blocking voltage-gated K+ channels leading to prolonged repolarization?
Phase 3
absolute & relative refractory period in cardiac muscle + cause & duration
absolute refractory period: period during which no second action potential can be initiated, no matter how strong the stimulus is during phase 0, 1, 2, and half of 3
- cause: inactivation of voltage-gated Na+ channels (not just closed- inactivation gates are shut)
- duration: ~250-300 milliseconds (nearly entire duration of AP)
relative refractory period: time when a second action potential is possible, but it requires a stronger-than-normal stimulus
- cause: some Na+ channels have reset however K+ channels still open so membrane is hyper polarized
- duration ~50 milliseconds
significance of refractory period in cardiac muscle
heart muscle can’t be tetanized:
long refractory period thats almost equal to entire muscle twitch means heart cant summate contractions (vital bc contracted heart cant pump)
prevents reentry & arrhythmias:
ensures regular, rhythmic contraction + heartbeat
ensures coordinated contraction:
allows sufficient time for ventricular filling during diastole = synchronized contraction
limits max heart rate: max heart rate is about 170-240 bpm, beyond this ventricles dont have enough time to fill & pump effectively
What is the physiological basis of the unstable resting membrane potential in pacemaker (SA node) cells?
due to the “funny” Na⁺ current (If), T-type Ca²⁺ current, and reduced K⁺ efflux during phase 4. These currents gradually depolarize the cell, so pacemaker cells never have a true resting potential — instead, they continuously drift toward threshold, leading to spontaneous action potentials
pacemaker potential/prepotential
slow drift of membrane potential toward threshold due to unstable resting potential
- action potential w/o plateau (occurs in the SA/AV nodes)
auto-rhythmic cells of the heart
autorhythmic/pacemaker cells: specialized cells that generate their own electrical impulses, initiating the heartbeat
SA node: main pacemaker of heart
- much faster so “wins the race”
AV node: secondary pacemaker (slower)
- latent pacemaker
Bundle of His: conducts signal from AV node to ventricles
Purkinje fibers: distribute impulse to ventricular muscle
atrial & ventricular muscle: normally do not self-excite, but can under special conditions (e.g., damage to SA node)
- ectopic beats
action potential w/o plateau (SA nodal action potential)
no phase 1 or 2 b/c dont need plateau phase
phase 0 (depolarization): actual action potential “spike”, L-type Ca2+ channels open causing rapid influx of Ca2+ → sharp depolarization
- voltage: -40 mV to 0mV
phase 3 (repolarization): cell resets itself to be ready for next impulse, L-type Ca2+ channels close, voltage gated K+ channels OPEN, K+ leaves making the membrane more negative
- voltage: back to -60 mV
phase 4 (unstable resting potential/prepotential): phase responsible for autorhythmicity, Funny Na+ current (If) aka HCN (hyperpolarization-activated cyclic nucleotide-gated) channels (open b/w -40 to -60 mV, called funny bc Na+ doesnt usually operate at this voltage)
- T-type Ca2+ channels (transient): open briefly to allow small amount of Ca2+ influx
- decreased K+ permeability
this is the chart that looks like lehrey
what 3 factors are responsible for the pre-potential or pacemaker potential (phase 4)?
-
Funny Na⁺ current (If) aka HCN (hyperpolarization-activated cyclic nucleotide-gated) channels: open when membrane becomes more negative (after repolarization)
- allow slow Na⁺ influx, slowly depolarizing the membrane -
T-type Ca²⁺ channels (Transient): open briefly as membrane becomes more positive
- allow small amount of Ca²⁺ influx - Decreased K⁺ permeability: fewer K⁺ ions leave the cell, helping membrane potential move toward threshold
why is there no role of voltage gated Na+ channels in SA nodal action potential?
- In ventricular muscle, resting membrane potential is –90 mV, so Na⁺ channels are ready to open
- In SA node, resting membrane potential is –60 mV, normally voltage gated Na+ channels are inactivated at this voltage
Ca2+ plays this role instead
What is the primary ion channel responsible for the spontaneous depolarization during phase 4 (pacemaker potential) of the SA nodal action potential?
Hyperpolarization-activated cyclic nucleotide-gated channels
Which of the following best explains why the SA node sets the heart rate as the primary pacemaker?
It has the fastest rate of phase 4 depolarization
