biol155 lecture 27
Lecture 27 Question Sheet
What are 2 structural similarities between skeletal and cardiac myofibers?
Both are striated (contain sarcomeres)
Both contain thin and thin filaments/contain myosin and actin filaments
Both contain sodium, potassium, and calcium channels
What are 2 structural differences between skeletal and cardiac myofibers?
Cardiac myocytes have a branched structure, while skeletal myocytes span the whole muscle
Cardiac myocytes have one nucleus per cell, while skeletal myocytes have multiple
Cardiac myocytes are only about 0.2 mm long, while skeletal muscle cells can be much longer
Cardiac myocytes have fewer t tubules and sarcoplasmic reticulum compared to skeletal muscle
Cardiac myocytes lack a neuromuscular junction
Cardiac myocytes are connected by intercalated discs
Cardiac myocytes are activated through gap junctions
Cardiac myocytes have L type (long length) voltage gated calcium channels in the sarcolemma
What are 2 physiological similarities between skeletal and cardiac myofibers?
Both are excited through action potentials
Both have the same parts to their action potential (depolarization, action potential, refractory period, repolarization)
Both require depolarization, calcium release and repolarization to contract
A single AP generates a single twitch for both
What are 2 physiological differences between skeletal and cardiac myofibers?
Cardiac myocytes have a longer plateau of depolarization (due to L type VCG)
For excitation contraction coupling, skeletal muscle uses mechanical coupling while cardiac muscle uses biochemical coupling
Cardiac muscles cannot produce tetanus, while skeletal muscles can produce tetanus
What are the phases of a cardiac action potential and which ion channels are involved?
0: depolarization begins - sodium channels open
1: height of depolarization - sodium channels close, potassium channels start to open
2: repolarization starts - calcium channels open, potassium channels open
3: more repolarization- calcium channels close
4: resting potential
What are the types of coupling involved in skeletal muscle vs cardiac muscle?
Mechanical: depolarization triggers the dihydropyridine receptor (DHPR) to pull on the ryanodine receptor (RyR), which releases calcium
Biochemical: depolarization triggers DHPR to open and let in calcium
The calcium triggers the RyR to release more calcium
Why can’t cardiac muscles produce tetanus?
The length of the action potential is much longer, meaning the absolute refractory period is longer
Compared to the length of the contraction, the relative refractory period lands close to the end of the contraction
This means that another AP cannot be generated until the contraction period of the myocyte is almost done
What are the conduction pathways made of?
Highly modified myocytes
What is the direction that action potentials travel through the heart?
Sinoatrial node > internodal pathways > atrioventricular node > AV bundle/bundle branches > purkinje fibres
What is the SA node?
It’s a “pacemaker cell” meaning it generates an intrinsic rhythm of constant depolarization/repolarization
It sets the rhythm of the heartbeat
It does not require conscious trigger through through the nervous system
It also causes atrial contraction
How does the membrane potential change in the SA node, what channels are involved?
There are 2 main steps: pacemaker potential and action potential
Action potential: depolarization and repolarization
Depolarization is triggered by T type (transient) voltage gated calcium channels
repolarization is triggered by voltage gated potassium channels
Pacemaker potential: automatic depolarization that slowly starts after each repolarization
Triggered by the funny channel/HCN channel: a voltage gated ion channel that only opens after hyperpolarization, letting sodium into the cell
(This system is what allows for the contraction cycle to happen constantly and independently)
What is the AV node?
Node responsible for triggering ventricular contraction, since electrical signals can’t spread to the ventricles through the atria
It also has pacemaker properties but has a slower rhythm
It causes a delay of 100ms in depolarization
How does the membrane potential change in the AV node, and what causes the difference in speed of depolarization?
It is depolarized due to the depolarization of the internodal pathways
It also uses VGCC and VGKC
There are much fewer gap junctions, which causes the AP to be slower
How does the ANS impact the SA node?
It changes the pacemaker potential
Parasympathetic: second synapse releases ACh, causes extra potassium channels to open
This slows down heart rate by increasing the time it takes to depolarize
Sympathetic: second synapse releases NE, which activates the funny channels
This increases the amount of depolarization, which in turn increases heart rate
How does SA and AV node excitation relate to atrial and ventricular contractions?
SA node: excitation causes the atrial myocardium to contract, as it’s coupled to the nearby myocytes, allowing the signal to spread through the jap junction
It forwards the signal to the internodal pathways, which are coupled with the other atria, so both atria contract first
It also forwards the signal through the conduction pathway
AV node: delays signal as atrium contracts, forwards signal to av bundle (in septum)
Av bundle branches forward signal purkinje fibres
Purkinje fibres distribute signal to ventricular myocytes, causes ventricular contraction
What is an ECG?
An electrocardiogram: a measurement of the electrical impulses of the hearth using electrodes
What are the different points that can be measured in an ECG, and what part of the contraction cycle do they represent?
P wave: atrial depolarization - happens once signal from SA node reaches AV node
Q wave: beginning of ventricular depolarization - happens while single makes it to the purkinje fibres
QRS complex: completion of ventricular depolarization - happens when all the myocytes in the ventricle depolarize and repolarize at the same time
T wave: repolarization of the ventricular myocytes:
What is an arrhythmia?
Unusual patterns of cardiac electrical activity
Tachycardia: heart rate above 100 bpm
Bradycardia: heart rate below 60 bpm
Patient b has a prolonged QT interval - the t interval is shown to be much later
Patient a has a reduced p wave - the p wave is much smaller
Patient a has retained damage to the SA node - the atrial depolarization is much smaller
Patient b has received damage to the ventricular myocytes - the repolarization is taking much longer