Let’s go through a little bit of physiology again. We talked about how calcium is important for contraction when we mentioned calcium channel blockers used for relaxing muscles. Now let’s review in detail about the action potential so then we could talk about how pharmacology comes into play here.
- Sino-atrial node (pacemaker)
- Atrio-ventricular node (regulator/gate)
- Bundle of His
- Purkinje Fibers
- The SA node is the pacemaker. Nature put this for our safety. A person can survive with atrial fibrillation but not ventricular fibrillation.
- The AV node comes next and it’s good to think of it as a regulator or a gate that opens and closes. This gate may not let all electrical activity go through. We’ll talk about that in detail later, but if the electrical activity goes through, it goes to the…
- Bundle of His which leads to the…
- Purkinje fibers.
Electrical activity hits, calcium is released to the sarcoplasm, which then interacts with troponin, actin-myosin couples, and we have a contraction.
- PHASE 0 – Fast sodium Channel
- PHASE 1 – Mild repolarization
- PHASE 2 – Slow calcium channel
- PHASE 3 – Repolarization (potassium exits the cell)
- PHASE 4 – Resting (sodium/potassium pump)
Let’s look at this graph. If you put a probe on any particular area on the heart, you could see the electrical activity that takes place.
At Phase 4, the cell is resting. Electrical activity will rest at -70mV. Electrical activity either hits strong enough to cause an AP or it doesn’t (all or none phenomenon; either something happens or nothing happens).
At Phase 0, the fast sodium channel opens up and sodium enters the cell. This is phase 0, known as depolarization.
At Phase 1, we have a mild repolarization.
At Phase 2, we have a plateau because calcium is entering and it’s called the slow calcium channel. Contraction will take place here.
At Phase 3, potassium leaves the cell and this is repolarization, taking us back to phase 4, the resting phase. The cell doesn’t exactly rest in phase 4. because the sodium potassium pump is still working getting it ready for the next AP.
Between Phase 1 and 4 is the refractory period. If electrical activity occurs during the refractory period, nothing happens. Anti-arrhythmic drugs extend this refractory period so that it helps correct the arrhythmia.
We’re going to graph cardiac output on the Y and on the X is Left Ventricular End Diastolic Pressure (LVEDP).
Cardiac output is defined as multiplying stroke volume and heart rate. CO = (SV x HR)
Cardiac output increases with LVEDP. If you blow a balloon up and you blow it up a bit too much, it will lose its elasticity. There will be a ton of pressure in the balloon, but if you let it go it won’t collapse as much as before. If you look at the x-ray of heart failure, it looks large because it has lost its elasticity. If you stretch the heart too far with too much pressure, the output decreases and that’s what we see in an individual with heart failure. Cardiac Output increases with pressure up to a point of congestive heart failure. Cardiac glycosides shift this curve so the cardiac output becomes greater.
Low output failure (congestive heart failure) is when the demand for blood flow is normal but the heart cannot keep up with the demand and fails.
High output failure means the heart is healthy but the body is asking too much from it.