(09) Flashcards
(Overview)
(T-tubules)
- lumen is an extension of what? increased surface area facilitates what?
- Important for activation of what?
(sarcoplasmin reticulum)
- intracellular network of what?
- regulates what?
- the extracellular space; AP transmission
- SR Ca++ release
- tubules (network, juctional (cisternae), spec. non-junctional
- intracellular Ca++ movement
(Myofibrils)
(myofilaments)
- thick is what?
- thin?
- myofibril regions?
(…)
- sarcomere is segment between what?
- what are the contractile proteins?
- what are the regulatory proteins?
- myosin
- actin, troponin, tropomysin
- z-lines
- myosin and actin
- troponin and tropomyosin
(Contraction overview)
- heart acts as “functional syncytium)
- action potential –> ? –> ?
- Ca++ triggers what?
- increase Ca in cytosol promtes what?
- in order for contraction to be over what needs to happen?
- once caclcium gets put away what happens?
- Na and Ca; into cell
- more calcium release into SR (Ca induced Ca release)
- actin-myosin interaction (requires ATP)
- Ca seqeustration (requires ATP)
- actin-myosin disengages
(Excitation - Contraction Coupling)
- The provess that links the wave of electrical excitation to what?
- depends largely on what?
- Concentrations of what are important for optimal cardiac function (plus their role)
- mechanical contraction
- Ca fluxes (Ca induced Ca release)
- Na (excitablility)
K (resting membrane potential, repolarization)
Ca (contractile strength, AP duration)
(Actin - Myosin Interaction)
- What inhibits actin-myosin binding?
- Ca++ binding to troponin C –> ?
(look at this figure a little bit)
- troponin I-tropomyosin
- conformational change in tropomyosin to expose myosin attachment sites
(Contraction)
- Patrial hydrolysis of ATP (ADP & Pi) causes what?
- Completion of ATP hydrolysis with ADP/Pi release cuases what?
- Oar-like motion drives actin filament along myosin –> ?
- avid myosin binding to actin (actin-myosin crossbridges)
- myosin head to flex
- Z-lines get closer (Sarcomere “shortens)
first imporant movemnt of Ca is during AP - it comes in - binds to rianidine receoptrs o SR which triggers releas of Ca - lots of free calcium in cell - lots to hook up with troponin C - and allow contraction
catecholamines allow more calcium to come in - allow greater amount of Ca in cell - more actin myosin interactions
another source of increase Ca into cell is a Na-Ca exchange mechanism that is usually important in getting Ca out of cell - in some cases this can be reversed (this isn’t very critical…. at this point she says)
(Cardiac Contraction and Relaxation)
(Tension)
- develops by recuitment or more crossbridge cycles as what hapens
(Intracelular fluxes and the SR)
- How much Ca enter and leave the cell with each cycle?
- Most Ca ions come from where?
(During Relaxation:)
- Most Ca rapidly taken up by what?
- lesser amount Ca –> ?
- cytosolic [Ca] rises to a peak
- only small amounts
- intracellular stores
- SR Ca pump (ATP)
- extracellular space or mitochondira
(for each contraction of the heart:)
(brief perioed when cytosolic Ca increases to a peak)
- Ca binds increasingly to what? which does what?
- get thousands of mini-contractile cycles as long as what?
- from physiologic standpoint what is this considered?
- how do you determine systole on physical exam? what does heart sound like? what causes lub? what causes dub? systole is when? diastole?
(then rapid decrease in free cytosolic Ca)
- As Ca decreases, more actin becomes unavailable to what? leads to what?
- When is contraction over?
- referred to as what?
- Troponin-C all over the actin filaments; turns on increased length of actin to interact with myosin
- Ca is high
- physiologic systole (there is a time shift - starts before we can detect with physical exam)
- pulse and sounds; lub dub; closure of mitral and tricupsid (they cause vibration); closure of aortic and pulmonary valves; between lub and dub; between dub and lub
- myosin heads; decrease in number of mini-contractile cycles
- when possibility of A-M interaction is near zero
- “physiologic diastole”
(physiologic starts before lubs and dubs)
verapimil is a drug that block Ca channels
CRT = capillary refill time
pulmonary crackles = can be caused by fliud buildup in lung
sinus rhythm - normal rhythm
secondary AV block - not every P wave conducted (intermittent)
SO WHAT HAPPENEDD
will have weaker contraction = less CO = increasing venous pressure
what happens when we have higher than normal pulmonary veinous pressure? higher than normal hyrdostatic pressure in pulmonary capillaries - favored increased filtration out of capillares - get edema in lungs
will get slower sinus node firing cause - take longer to get to threshold and get to AP cause of less Ca being able to get in - will also slow conduction potential - important in AV node
will also get vasodilation cause Ca is needed for contraction in vessels
(Intracellular Ca Regulators)
(Phospholamban (PL))
- a major regulator of what?
- is an integral part of what?
- When phosphorylated, PL causes what? phosphoyrlated by?
(Remeber - Ca uptake by SR requires what?)
- the Ca pump of the SR
- SR membrane
- increased uptake of Ca; protein kinase activated by cAMP or calmodulin (ie increased Ca)
(ATP)
(Intracellular Ca Regulators)
(Calmodulin)
- what is it?
- calmodulin decreaes what?
(when intracelluar Ca is high…)
- Ca-calmodulin complex increases what?
- inhibits what?
- intracellular sensor and Ca regulator protein
- cystolic Ca
- Ca pump activity on SR (via PL) and sarcolemma
- Ca release channel of SR (decreases opening time)
(Ventricular Load)
- what is the load before the heart called? determined by what?
- What is the load after the ventrilcle called? determined by factors that do what?
- Are preload and afterload normally in equilibrium?
- the preload; EDP (end diastolic pressure) (filling: venous return, compliance of ventricle)
- the afterload (the amount of force ventricle has to generate to eject blood); oppose myofiber shortening (esp. Ao P; impedance)
- yeshh
(Ventricular load –> increase preload)
- What happens if we have an increase in preload?
- we strech ventricle further - results in an increased output from ventricle (increase output)
- What happens if we increase afterload (aortic pressure)?
(make it harder for blood to get out of ventrcile)
- harder to get blood out
(Estimation of Preload)
- ideally measure what?
- next best?
- usually - measure/estimate what?
- How can a catheter in the PA estimate EDP in the LV?
- how a catheter in the pulmonary artery could help us estimeate what the filling pressure is in the left ventricle?
- end diatolic fiber length
- end diastolic volume
- EDP (end diastolic pressure)
- estimate pressure in left ventricle during diastole
- if cather pressure is tight - will record the pressure on the side that equilirating with the capillary bed - capillary bed pressure is equilibrated pulmonary venous pressure - left atrial pressure is about the same as pulmonary venous pressure - and this helps us estimate the filling pressure of the left ventricle - during diastole the mtiral valve is open so these two pressures are the same (atrial and ventricle) - so we are actually estimating pressure in left ventricle during filling phase - this is called capillary wedge pressure - and is one way of measuring prelod in the left ventricle
