Cardiac Function Flashcards
What is the function of the SA node + what type of cells is it made up of ?
- pacemaker
- generates spontaneous action potentials
- action potentials pass to atrial muscle cells and AV nose
- made of specialised cardiac muscle cells, continuous with atrial syncytium
Why are action potentials conducted more slowly in the AV node ?
- ensures ventricles contract after atrial has contracted fully and have emptied blood into ventricle
What is the function AV bundle ?
- passes through hole in cardiac skeleton to reach inter ventricular septum
Where so the right and left bundle branches extend ?
- beneath endocardium to apices of right and left ventricles
What is the role of purkinje fibres ?
- has many gap junctions
- large diameter cardiac muscle with few myofibrils
- conduct action potential to ventricular muscle cells (myocardium)
Stages of conduction through the heart ?
- SA node initiates impulse
- stimulates artia to contract
- impulse is delayed in the AV node so that atria can empty blood into ventricles before ventricular contraction
- impulse at AV bundle and divides into left and right branches which carry impulse along septum
- impulse reaches purkinje fibres which distribute impulse to ventricular myocardium
- this triggers ventricular contraction
Structure of cardiac muscle ?
- mononucleated
- faintly striated
- connected by intercalated discs
Why is action potentials conducted propagation slower in cardiac muscle compared to skeletal ?
- slower because of gap junctions + smaller diameter of fibres in cardiac cells
- faster is skeletal cause of larger diameter fibres
Sliding Filament Theory of Cardiomyocyte contraction ?
- Ca2+ binds to troponin C (TN-C) on thin filaments
- exposes binding site on actin for myosin head
- ATP hydrolysis provides energy for actin-myosin conformational change
- ‘ratcheting’ of actin-myosin and shortening of the sarcomere occurs
• Ca2+ dissociates from TN-C and myosin unbinds from actin with energy from ATP
• Cycle ends when ATP binds to myosin and the sarcomere returns to original length.
Stages of cardiomyocyte contraction ?
- Ca2+ enters the cardiomyocyte through L-type channels.
- CICR (Calcium-Induced Calcium Release) = Ca2+ triggers the release of more Ca2+ from the sarcoplasmic reticulum (SR).
- Intracellular Ca2+ Rise: Intracellular Ca2+ rises to ~0.5-2 µM.
- Ca2+ binds to troponin-C, freeing the myosin binding site on actin.
- Actin moves over myosin, leading to myocyte contraction.
- Ca2+ is reabsorbed into the SR by the SERCA pump and removed from the cell via the Na+/Ca2+ exchanger and an ATP-dependent Ca2+ pump.
- Ca2+ dissociates from troponin-C, inhibiting the binding site on actin.
- ATP is required to unbind myosin from actin and reset the sarcomere to its normal length.
What are the 5 phases of cardiac action potential in contractile cells ?
- phase 0 - rapid depolarisation = rapid influx of Na+ through fast Na+ channels
- phase 1 - initial repolarisation = K+ begins to leave the cell causing slight dip in potential
- phase 2 - plateau phase = Ca2+ enters via L-type channels, balances K+ leaving so plateaus also generates contraction
- phase 3 - repolarisation phase = k + efflux through delayed rectifier, decreased membrane potential
- phase 4 = resting potential
What are the K+ channels in ventricular cardiac cells + what’s their role in action potential ?
- Inward Rectifier (IK1):
• maintains phase 4 resting membrane potential by allowing K+ to flow into the cell, helping to stabilize the negative potential. - Transient Outward (Ito):
• contributes to phase 1 (initial repolarization) by allowing a brief efflux of K+ from the cell, causing a small dip in the action potential. - Delayed Rectifier (IKr, IKs):
• important for phase 3 (repolarization) by facilitating K+ efflux, which helps return the membrane potential to its resting state.
What is pacemaker tissue + pacemaker potential ?
- areas of the heart where ‘resting potential is unstable
- after action potential, membrane becomes more positive until threshold potential reached, triggers new AP
- pacemaker potential = slow depolarisation of membrane between 2 successive AP
What is automaticity in pacemaker tissue ?
- Ability to spontaneous depolarise and trigger Action potential without external stimulation
Where is packemaker tissue found + not found ?
- active in SA node
- AV node
- bundle of His
- not in ventricular muscle cardiomyocytes
What are the phases of action potential in SA node ?
Pacemaker Cells: No true resting potential, generate regular, spontaneous action potentials.
Phase 4: Spontaneous Depolarization
• Mechanism: Inward movement of Na+, outward movement of K+.
• K+ movement decays over time.
• Pacemaker potential depolarizes to -55 mV.
• Ca2+ inward current accelerates from -55 to -40 mV (threshold potential).
Phase 0: Depolarisation
• Ca2+ influx increases due to L-type Ca2+ channels.
Phase 3: Repolarisation
• Voltage-controlled K+ channels open, K+ efflux, repolarizing the cell.
• Ca2+ channels inactivate during this phase.
How does the parasympathetic nervous system regulate the cardiac cycle?
• The cardioinhibitory centre in the medulla oblongata controls the vagus nerve, which branches to the SA and AV nodes.
• Ach is released, causing hyperpolarization of the heart.
• This results in a decreased heart rate (dominant effect).
How does the sympathetic nervous system regulate the cardiac cycle?
• The cardioaccelerator centre activates sympathetic neurons (cardiac nerves).
• These neuron’s release norepinephrine, which has a minor effect on heart rate
- but increases the force of contraction and contractility.
How does parasympathetic + sympathetic nervous system affect action potential ?
- refer to graph
- parasympathetic = increases hyperpolarisation
- sympathetic = rapid depolarisation
What is a P wave ?
- atrial depolarisation / contraction
What is QRS complex ?
- ventricular depolarisation
What is T wave ?
- repolarisation of ventricles
What is the PR interval ?
- Start of atrial depolarisation to start of ventricular depolarisation
What is the Q-T interval ?
- time required for ventricles to undergo single cycle of depolarisation and repolarisation
What is Ischaemic heart disease ?
• Deprivation of blood supply to cardiac tissue
• Angina Symptoms (chest pain)
• can cause HEART ATTACK
- eg. Coronary heart disease
What are Cardiac dysrhythmias ?
- Disruption of contraction control
• an cause CARDIAC ARREST
What is cardiac failure ?
- Inability of heart to distribute blood
• can cause HEART FAILURE
What are beta blockers ?
- block β1 receptors which adrenaline/ noradrenaline binds to
- so slows down SA-node which initiates heartbeat
- slows down heart rate + lowers blood pressure
What are calcium channel blockers ?
- block L-type Ca2+ channel
- no influx of Ca2+ ions
- so slows SA-node
- so lowers heart rate + blood pressure
