Cardiac Muscle and Conducting Systems Flashcards
Describe the pressure and volume changes and pathway of blood flow through the heart and circulation.
Each chamber of the heart has two basic states in their cycle of pumping: systole (contracting) and diastole (relaxing).
1. Diastole
- AV valves (tricuspid and mitral) open.
- Semilunary valves closed.
- Atria and ventricles relaxed
- Atria and ventricles fill passively
- Pressure and volume in the atria and ventricles increase
2. Late ventricular diastole-atrial systole
- AV valves (tricuspid and mitral) open
- Atria contract emptying last bit of blood into ventricles (10-20% at rest)
- Ventricles relaxed.
- Pressure in the atria and and ventricles increases, volume in the atria decreases and volume in the ventricles increases.
3. Ventricular systole (ejection phase)
- AV valves (tricuspid and mitral) closed
- Ventricles contract
- Atria relaxed
- Semilunar valves open
- Pressure in the atria and ventricles increases, volume in the atria increases and volume in the ventricles decreases.
Revisit the concepts of resting membrane potential and action potentials and apply them to cardiac muscle.
The resting membrane potential is the electrochemical equilibrium which occurs when the movement of K+ out of the cell down the concentration gradient is balanced by the movement of K+.
The electrical potential difference between the inside and outside of cell (E) at equilibrium for any ion is described by the Nerst equation. The actual calculation for the E of the cell takes all ions into account, and is termed the **Goldman-Hodkin-Katz **equation.
It demonstrates that if you change the permeability of the cell to a specific ion, the electrical gradient of the membrane will shift closer to the Nerst equation value of that ion.
Therefor,e if we increase the permeability of the membrane to Na+ or Ca+, the membrane depolarises (inside becomes relatively more positive) because the E of Na+ and Ca2+ are 71mV and 132 mV, respectively.
This forms the basis of electrical signaling in excitabile tissues i.e. the action potential.
In cardiac muscle, opening Na channels depolarises the membrane, so that the membrane potential will be somewhere between the Nerst potentials for Na+ and K+ (according to the GHK equation).
During an action potential (AP), depolarisation is caused by opening of Na and Ca channels. These open when the membrane hits a threshold voltage, but only transiently. The membrane then repolarises as K+ efflux becomes dominant (also extra K+ channels open)
There are ‘phases’ of an action potential in cardiac muscle.
Phases of cardiac muscle AP
Phase 0 = rapid depolarisation
- Voltage gates Na channels open rapidly at threshold (-70mV)
- Na influx
- Membrane rapidly depolarises
- Open only for a few milliseconds
Phase 1 = early repolarisation
- Na channels are closed
- Additional K+ channels open briefly
- K+ efflux
- Membrane transiently repolarises
Phase 2 = plateau
- Voltage gated L-type Ca channels open slowly at threshold (40mV)
- Ca2+ influx
- Balanced by K+ efflux
- Potential plateaus
Phase 3 = repolarisation
- Ca channels close
- Additional K+ channels open
- K+ efflux
- Membrane repsolarises
Difference between skeletal muscle and cardiac muscle
Plateau and repolarisation take a long time in cardiac muscle compared to skeletal muscle. This is for two main reasons:
- Excitaton-contraction coupling: plateau phase results in prolonged increase in Ca2+, leads to a relatively long contraction.
- Refractoriness (ie means you cannot restimulate again quickly), avoids multiple APs summating like in skeletal muscle (eg tetanus)
Other differences
- Branching fibres connected in series and in parallel.
- Central nuclei.
- Much higher mitrochondrial density in cardiac muscle.
- Cardiac muscle acts as a functional syncytium via gap junctions
- Automaticity and rhythmicity
- They release calcium differently (Ca induced Ca release)
What is the process of excitation-contraction coupling in cardiac muscle?
- Local potential arrives
- Fast sodium channels open i.e. action potential
- L-type calcium channels open
- Influx of Ca2+ triggers Ca2+ released by SR. This is called calcium-induced calcium release (CICR).
Calcium causes contraction of the sarcomere, by forming cross-bridge cycling and thus contraction of the sarcomere and therefore, muscle.
Refractoriness
There are two types of refractoriness:
Effective refractory period: Na channel either all open (phase 0) or are locked (phases 1,2 and some of 3). It is not possibel to generate another AP.
Relative refractory period: not all Na channels are availbe. Greater than normal stimulus is required to generate another AP.
Intercalated disks
Cardiac myocytes are physically and electrochemically joined end-to-end at the intercalated disks. These are coposed of:
- *desmosomes; *and
- gap junctions
Gap junctions are pores that allow AP to propagate from cell to cell. An AP initiated in one part of an atrium or ventricle will propagate throughout the chambed. This is termed a ‘functional synctium’ and in the heart there are two: atria and the ventricles.
A band of fibrous tissue keeps the atrial and ventricular synctia isolated.
Outline the basic conduction system of the heart
The action potential originates in collections of specialised myocytes that form pacemakers. These pacemakers generate APs automatically at regular intervals:
- Sinoatrial node: at junction of right atrium and SVC, is the physiological pacemaker under normal conditions.
- AV node: between atria and ventricle, can take over if the SA node is damaged.
The AP does not just propagate along atrial and ventricular muscle, as *this would be too slow and too uncoordinated. *
- The top of the ventricle would start to contract while the bottom of the atria was still in systole.
- Contraction of ventricle from top to bottom is not very efficient when outlets (aorta and pulmonary artery) are at the top.
The conduction pathway is composed of specialised cardiomyocytes (non contractile) which conduct APs at variable speeds, and coordinates a sequence of contraction that is efficient for pumping.
- SA node depolarises (0 ms)
- AP spreads across the atria surfaces and reaches the AV node (50ms)
- AV nodal delay of 100ms. Atrial systole occurs during this time (150ms)
- AP rapidly travels along the bundle branches and purkinje fibres to the apex (175ms)
- AP distributed by purkinje fibres and spreads along ventricular myocytes. Ventriclular systole occurs (225 ms).
Understand how the automic nervous system can modify HR, contractility and conduction within the heart.
The heart intrinsically generates it’s own rhythm which results in a sustained AP that is conducted through the heart in a coordinated sequence ot generate contraction in an efficient way. While this happens automatically, the ANS (and some other states e.g. drugs, ischaemic, electrolyte changes and hormones) can modify the:
- Rate of SA node firing
- Speed of conduction including delay at the AV node
- Force of contraction
PNS (vagus) innervates mainly:
- SA node (decreases rate)
- AV node (slows conduction, and increases AV delay - can competely block it if strong enough signal)
Sympathetic nerves innvervates everything:
- SA node (increases rate)
- AV node (speeds conduction, reduces AV delay)
- Conduction network (speeds conduction)
- Ventricular muscle (increases contractility)
Increasing HR
Decreasing HR
