Cardiology Flashcards
What is an intercalated disc and why do we care?
This is the division between cardiac cells, gap junctions liver here to allow rapid diffusion of ions. This means that action potentials can travel super easily from one cardiac muscle to the next via the intercalated discs. Thus, cardiac muscle is a synctium
What is the cause of long QT syndrome
Congenital: mutations in sodium and potassium channel genes.
Hypocalcemia, hypomagnesemia, hypokalemia
Administration of excess antiarrhythmics like quinidine or fluorquinolones and erythromycin
What are some differences between cardiac and skeletal muscle action potential?
- Slow calcium channels: After fast sodium channels open, the calcium channels open. These are slow to open, and remain open for longer. This allows for influx of sodium and calcium. This is important becuase it causes plateau phase of action potential
- The calcium ions that enter also trigger muscle contraction, whereas in skeletal musclethis comes from sarcoplasmic reticulum
- After onset of cardiac AP, the permeability to potassium decreases fivefold. This does NOT happen in skeletal muscle. May be due to excess calcium influx from calcium channels. Anyways, it prevents outflux of potassium ions during plateau phase. When slow calcium-sodium channgels close, then the permeability for potassium increases and potassium leaves cell to restore to resore resting membrane potential
What is the refractory period of cardiac muscle?
There is a refractory period, and a relative refractory period. Relative refractory period is when cardiac muscle can be excited by a very strong excitatory signal.
Where does calcium come from for the cardiac muscle contraction? How is it removed?
Sarcoplasmic reticulum, but most comes from T tubules themselves. Calcium ions entering cell from T tubules during action potential trigger opening of calcium release channels (ryanodine receptor channels). This triggers release from sarcoplasmic reticulum. The sarcoplasm in the heart is way less well developed than in the skeletal muscle, so without T tubules heart contraction would be much weaker.
At the end of the cardiac action potential, calcium ions in the sarcolemma are pumped out of the muscle fibers into sarcoplasmic reticulum and T tubule ECF space. This is done via calcium ATP-ase
Wigger’s diagram! know this!
What is preload?
End diastolic pressure when the ventricle has been filled.
What is afterload?
Pressure in the aorta - arterial pressure against which the heart must contract
Frank Starling Mechanism
Intrinsic ability of the heart to adapt to increasing volumes of inflowing blood. The greater the heart muscle is stretched during filling, the greater is the force of contraction and the greater quantity of blood pumped into the aorta.
Explanation for it;
When extra blood enters heart, this stretches the heart, which causes muscle to contract with greater force because actin and myosin filaments are brought to a more optimal degree of overlap.
Parasympathetic stimulation of the heart?
- Distributed mainly to atria and not ventricles
- Slows heart rate, but doesn’t really have huge effects on cardiac contraction
Effect of potassium on heart function?
Hyperkalemia causes heart to become dilated and flaccid, and slows the heart rate.
Can block condution via AV node. High K depolarizes thecell membrane, and also makes action potential intensitiy weaker
Hypercalcemia is going to make the heart spastic because of effects on calcium in cardiac contraction. Hypocalcium makes heart flaccid.
This is a stupid question!
Resting membrane potential for sinus node?
-55 to -60 mV
The reason for this is that the cell membranes of sinus node are naturally leaky to sodium and calcium ions
What causes depolarization of the sinus node?
At -55, the fast sodium channels have become inactivated so that only slow sodium calcium channels can open. Thus, the atrial nodal action potential is slower to develop.
The sinus node is leaky to sodium and calcium, so between heartbeats, the sodium slowly leaks into the membrane, becoming gradually more positive. When it reaches a threshold of -40, the sodium calcium channels become activated, causing action potential.
What prevents sinus node from remaining constantly depolarized?
- Sodium-calcium channels become inactivated very soon after opening
- Greatly increasednumbers of potassium chnnels open after sodium calcium channels open. The potassium channels remain open for a little while after depolarization, so makes cell membrane hyperpolarized, which then allows for leakage of sodium and calcium into cell, to make cell more positive, to start new AP
Why is AV node transmission slow?
Decreased number of gap junctions causes delay in transission because cells slower to become excited