week 3 Flashcards
What are the 3 types of Cardiac muscle cells
- Contractile Cells (>99%)
- pacemaker cells
- Conduction Fibers
Contractile Cells
- Contain contractile machinery like skeletal muscle including sarcomeres, troponin and tropomyosin
- Connected by gap junctions in 2 syncytia (collection of cells with cytoplasmic continuity - atrial and ventricular)
Pacemaker cells
- Specialized cells that create heart rhythm
- very few myofibrils
- different fiber shape
- doesn’t have contractile fibers
Conduction fibers
- Conduct action potentials around heart in coordinated manner
- connect atrial and ventricular syncytia
- very few myofibrils
- no contractile fibers
Which ions have high concentrations in the extracellular fluid
Na+ and Ca++
Which ions have high concentrations in the intracellular fluid
K+
What is the resting membrane potential of cardiac muscle and how does that vary from other cells such as neurons
Resting membrane potential: -80 to -90
- more negative than neurons
What factors maintain a negative resting membrane potential
- Greater K+ membrane permeability compared to Na+
- the Na+/K+ ATPase (3 Na+ out/ 2K+ in)
What is the main difference between cardiac and neuron/skeletal muscle APs causing long-lasting depolarization in cardiac fibers
Increased Ca++ permeability and reduced K+ permeability
Cardiac Muscle Action Potential
- Threshold depolarization opens voltage-gates Na+ channels in cell membrane
- influx of Na+ - Voltage- gated Na+ channels close (inactivate) and K+ channels in cell membrane close
- Voltage-gated Ca++ channels (L-type) in cell membrane open
- Ca++ influx - Ca++ channels close and K+ channels re-open
- Ca++ influx stops, K+ efflux - Na+/K+ ATPase and Na+/Ca++ exchangers in cell membrance and Ca++ ATPase in sarcoplasmic reticulum help re-establish ion concentrations, resting membrane potential maintained
Excitation-Contraction Coupling in Contractile cells
- AP spreads to interior of cell via T tubules
- Ca++ flows into cytoplasm from extracellular fluid
- Ca++ influx stimulates opening of Ryanodine receptor channels (RyR) in the SR membrane
- More Ca++ flows into the cytoplasm form the SR
- Ca++ then binds to troponin, which causes a conformational change of tropomyosin that exposes myosin binding sites on actin, and cross-bridge cycling starts
Why is there a greater effect on cardiac muscle than skeletal muscle when reducing extracellular Ca++
- Cardiac muscle relies more on extracellular Ca++ (more T tubules)
- Skeletal relies more on SR Ca++ (more developed SR)
Differences in permeability seen in pacemaker cells
- High resting membrane Na+ permeability leads to slow depolarization (Not voltage-gated)
- Voltage-gated Ca++ channels open more slowly, so the rate of depolarization is slower than in contractile cells
Why are many voltage-gated Na+ channels in inactivated states in pacemaker cells
the resting potential is never strongly negative
- many inactivation gates don’t open and many activation gates don’t close
Which cells in the heart have pacemaker properties
sinoatrial node, atrioventricular node, purkinje fibers
What sets rhythm of heart and what is the rate? What are the back up pacemaker rates
Heart rate set by S-A Node: 70 to 80 beats per min
A-V node: 40 to 60 beats per min
Purkinje fibers: 15-40 beats per min
Ectopic Pacemaker
when somewhere other than the S-A node becomes the dominant pacemaker
- Causes abnormal sequence of contraction and weakens heart pumping
At what rates do conduction fibers conduct APs
- Internodal pathways: 1m/s
- Purkinje Fibers: 1.5-4.0 m/s
At what rate is an AP propagated between contractile cells
0.3-0.5 m/s
Why do conduction fibers have faster rates of propogation
Large diameter and lots of gap junctions between cells
What is the purpose of conduction fibers
coordinate contraction so different regions of the heart contract at appropriate times
Sequence of excitation in the heart
- An action potential is initiated in the SA node
- AP are conducted from the SA node to the atrial muscle
- APs spread through the atria to the AV node where conduction slows
- APs travel rapidly through the conduction system to the apex of the heart
- APs spread upward through the ventricular muscle
- The entire heart returns to the resting state, remining there until another AP is generated in the SA node
Speed of excitation through the heart
- Rapid through atria via internodal pathways
- delayed in the A-V node and A-V bundle due to fewer gap junctions
- fast conduction through purkinje network for rapid contraction across ventricles
Frank-Starling Mechanism
The more the heart is stretched during filling, the greater the force of contraction and thus the greater stroke volume
Why does the Frank-Starling mechanism cause an increase in contractile force
- Stretching increases sarcomere length such that there is a greater overlap of actin and myosin filaments increasing contractile force
- Too much stretch will go past optimal zone causing too few CB to form, decreasing force of contraction
What determines the end-diastolic pressure-volume relationship
The volume of blood that fills the heart during diastole
- increased volume causes a gradual increase in pressure at first
- at high volumes there will be a dramatic increase in pressure as the heart has to start to stretch and the pericardium puts pressure on the ventricle
What determines end-systolic pressure-volume relationship
- the force of contraction at each filling volume
- At lower volumes there is a gradual increase as the greater stretch causes a greater pressure produced by the myocardium
- At high volumes the pressure produced dips due to decreased CB formation
How do pressure-volume loops relate to pressure-volume curves?
The changes during the cardiac cycle lie between the EDPVR and ESPVR
How do pressure-volume loops change with and without pre-load compared to a control loop?
WITH PRELOAD
- increased end diastolic volume
- greater pressure created during isovolumetric contraction
- higher end systolic presure and higher end systolic volume
WITHOUT PRELOAD
- lower EDV
- less pressure during isovolumetric pressure
-lower ES pressure and volume
What is an example of intrinsic regulation of CO
Frank-Starling mechanism
What is an example of extrinsic regulation of CO
Sympathetic and parasympathetic nervous systems
The role of the sympathetic nervous system on regulation of CO
Neurons innervate S-A and A-V nodes, conduction fibers, and contractile cells and act to increase SV and HR (Contract Harder and faster)
- Increase pressure produced (ESPVR) at a given volume
The role of the parasympathetic nervous system on regulation of CO
Neurons innervate the S-A node and A-V nodes and primarily act to reduce HR
-Also innervate contractile cells creating a modest effect on SV by reducing ventricle filling
How does the SNS regulate SV (physiological level)
- Activates beta1 receptors in contractile cells, enhancing the components of Ca++ cycling
- pathway activates through G protein and cAMP activating protein kinase which upregulates Ca++ channels
How does the SNS and PNS regulate HR
Change rate of spontaneous depolarization
SNS
- increase # of Na+ leak channels open
PNS
- Increase the number of K+ leak channels offsetting the effect of the Na+ leak channels
How do the contributions of SV and HR increase change throughout higher intensity exercise
- SV more significant at first
- SV plateaus due to limitation of pericardium
- HR increases rather steadily throughout
