Cardiovascular Physiology Flashcards
Dr. Mike Wacker (UMKC)
What membrane channel does each phase of a cardiac action potential indicate?
Permeability changes during an AP in cardiac muscle cells
Mostly L type VGCC
How long are the absolute and relative refractory periods in cardiac muscle cells (seconds)?
What is the main difference between the AP and refractory period between skeletal and cardiac muscle cells?
- Cardiac has a lot longer absolute refractory period so another action potential can’t be generated until the relative refractory period (in which a large stimulation is needed to cause contraction)
- In cardiac cells, calcium ions also diffuse into the sarcoplasm from the T tubules themselves at the time of the action potential. The SR in cardiac cells is less developed but much wider, and the reason why T tubules have to make up for the internalization of calcium to cause contraction.
What is the role of phospholambin in cardiac cells?
Phospholamban tonically inhibits the SERCA pump by increasing its Km for Ca2+. Phosphorylation of phospholamban relieves this inhibition, speeding up the SR Ca-ATPase at any given [Ca2+] and therefore lowering the cytoplasmic [Ca2+].
Therefore, when epinephrine binds to B1 receptors, the activation of PKA phosphorylates phospholamin (inhibiting the inhibitor) resulting in quicker relaxation (Ca2+ reuptake in SR) of cardiac muscle cells
What are the different forms of cardiac hypertrophy, and what genes can cause this?
What are ways that you can augment force of contraction and ways in which you can decrease the force of contraction?
What are the pacemaker cells of the heart, and some attributes that make them unique?
What is the If (funny current) in pacemaker cells? What is it also known as?
HCN - Hyperpolarization activated cyclic nucleotide gated
The If is caused by leaky Na+ channels at “resting potential” in which enough slow depolarization occurs to reach the threshold for opening of Ica (mostly t but some L-type voltage gated Ca2+ channels) which rapidly depolarizes the SA/AV nodal cells until Ik (voltage gated K+ channels open) hyperpolarizing the cell back to resting potential
SA nodal fiber discharges have a negativity of about _______mV, in comparison with _______mV for the ventricular muscle fiber
SA nodal fiber discharges have a negativity of about _-55 to -60_mV, in comparison with _-85 to -90_mV for the ventricular muscle fiber
This is due to the SA membranes being naturally leaky to Na+ and Ca2+ ions
When the membrane potential remains less negative than about -55mV for more than a few ms, what happens to the Na+ inactivation gates on the inside of the cell membrane?
The fast sodium channels become closed and remain so, therefore only the slow Na+ and Ca2+ channels can open (activated) and cause the AP
What are the intrinsic depolarization rates of SA, AV and Purkinje Fibers?
What is unique about the ventricular perkinje system?
- *1. Very large fibers
2. Transmit AP very fast (1.5-4.0m/sec)
3. High level of gap junction permeability
4. Very few myofibrils**
After the delay of the action potential from the AV node, the purkenje fibers are activated through the AV bundle into the ventricles. Purkinje fibers are very large, and t__ransmit action potentials at a velocity of 1.5-4.0 m/sec (6X faster than ventricular muscle and 150X faster than some AV nodal fibers). This fast conduction is due to a very high level of permeability of the gap junctions at the intercalated discs between cells in addition to few myofibrils, meaning they contract little or not al all during the course of impulse transmission.
What does chronotropic, isotropic, and lusitropic mean?
Chronotropic - Increasing HR
Isotropic - Increasing contractility
Lusitropic - Increasing relaxation
How does sympathetic stimulation alter heart rate?
- cAMP increases funny channel opening increasing heart rate (chronotropic)
- PKA phosphorylates phospholambin (inhibits SERCA) increasing the rate of muscle relaxation (lusitropic)
How does parasympathetic stimulation alter heart rate?
- G protein stimulation inhibits AC that decreases cAMP and PKA
- This hyperpolarizes the cell and K+ goes more towards it’s equilibrium potential
Mediated through the Vagus nerve!
What are some special considerations of the AV node that slows down conduction from the SA node to the rest of the heart?
What are some common cardiac inotropic agents used for short term treatment of heart failure?
Of all the inotropic agents (Digoxin, Dobutamine, Milrinone, Levosimendan), which ones increase HR, increase Ca2+, and cause arrythmias?
What can a P-R interval tell you?
How wide is a normal QRS complex? What can a widened QRS indicate?
Widened QRS can indicate a left bundle branch blockage, that condution is going through the muscle instead of the normal conduction pathway
How long is a normal QT interval? What can result on a long QT or short QT, and implications of each?
Normal QT = 0.35-0.43 sec
QTc = corrected QT interval
What usually causes ST-segment changes?
What is the first area to repolarize in the heart after the action potential was generated?
The ventricles are the last to depolarize and the first to repolarize
What will happen if the first area to depolarize is the first area to repolarize? What can cause this?
Inverted T wave
What can cause sinus bradycardia?
What can a block in conduction of the SA node result in? What can cause it?
What can cause an AV-block, what are the different types of AV blockage?
Different causes of sinus tachycardia? What are the three types?
During junctional tachycardia, the AV node takes over pacing of the heart >100bpm. What will happen to the p wave?
Indications of supraventricular tachycardia from atrial tachycardia? Difference between multifocal and unifocal?
What happens when there is hyperexcitability in the ventricles?
Ventricular tachycardia (V-tach)
How would you reduce SVT? (5)
What is this electrocardiogram indicative of?
What are the three major types of hyperexcited/premature contractions?
- Premature atrial contractions
- AV node premature complex
- Premature ventricular contractions
What are signs of a premature atrial contraction (PAC)?
What are signs of a premature junctional complex?
What are signs of premature ventricular contractions?
What are treatment options for A-fib?
What is the cause of ventricullar fibrillation?
Autonomic nervous system effects on HR and contraction
