Heart lecture 2 week 1 Flashcards
What is the purpose of gap junctions in cardiac muscle? What protein forms them? What other proteins are found in intercalated disks?
- They decrease the longitudinal resistance of cardiac cells (cytoplasmic resistance of ion flux) to allow for quick spread of APs from one cell to another. remeber gap junctions are bi-directional and also allow for flow of nutrients, metabolites, and water (depending on permeability of connexon pore). have no synaptic delay!
- connexon proteins
- desmosomes and fascia adherens-mechanically connects cardiac cells
How long is a typical cardiac (ventricular) action potential? How large is the depolarization? What is its shape? What is the reason for the plateau phase?
- 250-300 msec
- 110-120 mV (from -90 mV to +20-+30 mV)
- sharp rise, slow repolarization with a plateau
- plateau phase is due to Ca2+ entry into the myoplasm at the same time that K+ is leaving the cell. This resists repolarization and prolongs the AP
How is Ca2+ released in cardiac muscle for interaction with troponin?
Ca2+ is released from the SR and from Ca2+ channels in the surface membrane that open during an AP. Ca2+ release is required for full contraction of cardiac muscle and is the trigger that initiates contraction.
Discuss the cardiac cycle as it pertains to pressures, heart sounds, EKG, and ventricular volume.
see slide 5 of course notes. be sure to discuss the normal pressures of the ventricles, atria, and aorta. note that it is a graph of the left side of the heart. the same events occur on the right side of the heart with lower observed pressures in the right ventricle.
The EKG is an ______ potential difference btwn points on the body surface.
extracellular
Where are the AV nodal delays and ST segments seen on an EKG and what are they correlated with?
The AV nodal delay is (normally) the only electrical connection btwn the atria and ventricles and the AP moves very slowly through this region. It is seen on the EKG as the interval btwn the end of the P wave and the start of the Q wave.
The ST segment is the region btwn the end of the QRS comples and the start of the T wave and is associated with the plateau of the ventricular AP. During this period, the ventricle is essentially uniformly depolarized.
What is normal ejection fraction? How is it calculated?
During diastole, the ventricles fill with approximately 130 ml of blood. During systole, they end up with about 50 ml of blood. This means they eject about 80 ml of blood.
ejection fraction: 80 ml/130 ml=.61
normal ejection fraction is 50-60%
Discuss the packemaker activity of the SA node and AV nodes. What ion is responsible for the upstroke of the SA node AP? Why is the SA node the pacemaker for the heart?
Cells of the SA (sinoatrial) node and AV (atrioventricular) node do not have well defined resting potentials. Instead, the potential across their membranes continuously changes, leading to periodic action potentials-pacemaker activity. Note cells of the SA node have a less negative threshold than ventricular cells. The SA node is the pacemaker for the whole heart bc the AV node normally has a slower rate of pacemaker activity than the SA node so that the AP spreading from the SA node will reach it before it has had a chance to iniate an AP of its own. Ca2+ is responsible for the upstroke in SA node APs. Note that Ca2+ channels are inactivated at a much higher membrane potential than Na+ channels
What pumps are responsible for the maintenance of ion gradients at rest (resting membrane potential) in cardiac muscle and where are they located? What is the primary ion responsible for resting membrane potential? What would occur if there is no ATP in the cell as in myocardial infarction?
- Na+/K+ ATPase, Ca2+ pumps, and Na+/Ca2+ exchangers are responsible for the maintenance of ionic gradients. Note that the typical intracellular concentration of Ca2+ is 50 nm in resting myocytes but goes up to 1 micromolar during contraction. Ca2+ pumps are located in the sarcolemma and the SR membrane
- K+ (resting membrane potential is -90 mV, Ek is -95 mV)
- If there was no ATP, Na+ and K+ gradients would dissipate and the membrane potential would become 0 mV. This would lead to resting inactivation of Na+ channels and APs could not be conducted.
Contrast the contractile (ventriclar and atrial) cells of the heart and SA and AV node APs. Also talk about Purkinje cell APs.
APs in ventricles and atria are fast response APs. Note that ventricular APs are of longer duration (0.25-.30 seconds) than atrial APs (0.15-0.20 seconds). APs of Purkinje fibers are very similar to those of ventricular muscle but have few contractile proteins.
APs of the SA and AV nodes are slow response APs. The APs of these two nodes are very similar. Both show pacemaker activity and a relatively slow upstroke.
The concentration differences establised by pumps can be utilized by cells to change the membrane potential (to produce an AP). To produce the cardiac AP, the cell membrane changes its permeability to what ions?
Na+, K+, and Ca2+
Discuss the spread of excitation throughout the heart.
Remember that APs propagate. An AP initiated at any point in a cell will spread throughout the cell and can spread from one cell to the next if the cells are connected by gap junctions.
- APs are normally initated in the SA node.
- The AP then spreads through the atria, requiring less than 0.1 seconds (from the time of inititation at the SA node) to reach all of the atrial contractile cells
- The AP spreads to the AV node. Despite its small size, spread of the AP through the AV node is slow (0.1 seconds for the AP to move the the AV node form the atria to the ventricles)
- After the AP leaves the AV node, it spreads to a specialized ventricular conduction system consisting of bundle of His, right and left bundle brances, and the Purkinje fiber network (frequently the entire conducting system is simply called the Purkinje system). The cells making up the Purkinje system are specialzed ventricular myocytes that occur on the endocardial surface and partially penetrate into the ventricular walls. Propagation through this conducting network is very fast, requiring only about 0.03 seconds to spread throughout the ventricles.
- Spreadof the AP through the rest of the ventricles beyond Purkinje fibers. Spread is predominantly from the endocardial (inner) surface of the ventricular wall to the epicardial (outer) surface and requires roughly another 0.03 seconds.
What is the reason for the observed QRS complex occurring before the pacemaker spike?
Arrythmia. An AP is being initated somewhere in the ventricle before the pacemaker initates the ventricular AP.
What are cardiac arrythmias and what are the potential results?
abnormalities in the electrical rhythm of the heart resulting from changes in the spread of the AP throughout the heart. Can involve either an abnormal site of AP initiation or abnormalities in AP conduction (or both). see pg 48 of course notes for diff types of cardiac arrythmias.
