B1W3: Cardiac Muscle Flashcards
AV Valves
LAB RAT bicuspid/mitral tricupid Chordae tendae pull back Between atria and ventricles
Aortic/pulmonary valves
Prevent backflow from aorta/pulmonary artery into ventricles
Prolapsed valve
Mitral valve that accidently lets blood leak through backwards
Rheumatic fever
Causes high instance of valvular stinosis (interferes with transfer of blood)
Mitral regurgitation
Elevates arterial pressure because blood is not moving forward, staying put
This elevates the atrial pressue a little more each cycle, messing up end diastolic volume and diastolic pressure
S1 heart sound
the “lub”
- marks beginning of systole/end of diastole
- closure of mitral/tricuspid valves
S2 heart sound
The “dub”
End of systole/beginning of diastole
Closure of aortic/pulmonary valves
Additional heart sounds
- swishing means there’s a problem with laminar flow
- 3rd sound=increased atrial pressur
- 4th sound=stiffened left ventricles
It is important to listen to the nature and timing of the sound
Three different types of cells in myocardium
- Myocardial muscle: in atria and ventricles, generates force
- Conducting: bundle of His, purkinje fibers; coordinates contraction
- Pacemaker: SA node and AV node; initiates heart-beat, and control of heart beat
Cardiac muscle ccomponents
- actin/myosin
- intercalated disks, i.e. gap junctions
Major conducting pathways
- Atrial syncytium
- AV node
- Bundle of His
- Ventricular syncytium
- Action potential in cardiac muscle
- due to influx of Na+ and Ca2+
- Calcium causes plateau phase, where calcium enters and binds to troponin
- Abslutely refractory period and relative refractory period
Cardiac excitation-contraction coupling
Needs external calcium to contract–DEPENDENT ON IT
- Ca2+ enters cell via L type Ca2+ channels during plateau for calcium-induced-calcium released
- T tubule helps Ca2+ released from SR using RyR receptors
- Ca2+ also stays in T tubules!
End diastolic volume
Volume of blood filling the ventricle during rapid filling
Stroke volume
Volume of blood ejected as the ventricles contract during systole
End-Systolic Volume
Volume remaining in each ventricle after contraction
Ejection fraction
Fraction of the end-diastolic volume that is ejected; will be reduced in people at end stage of heart disease
Equation for Stroke Volume
Stroke Volume=EDV - ESV
Calcium’s role in contraction
Binds to Troponin C once released from SR, T-tubules or extracellular fluid
Troponin C does conformation chainge on tropomyosin
Active sites on actin are uncovered for myosin to bind
Ejection fraction equation
EF=SV/EDV
Volume-Pressure Relationship
As you fill heart, pressure increases
Just adding volume generates pressure
This works to a point until you pass the Frank-Starling relationship
Stroke work
Output of heart
(work=force x distance)
Chronotropic action
effecting the heart rate
inotropic
effecting the strength of cardiac contraction
lusitropic action
effect on rate of relaxation
preload
The load in heart before systole (i.e. EDV)
afterload
effects ESV
resistance in aorta against ventricular pumping
determinants of stroke volume
preload
contractility
afterload
length tension relationship in cardiac muscle
Tension of heart increases, length will increase too
What affects EDV
Ventricular performance increases as we increase EDV
- venous tone
- total blood volume
- body position
- pumping of skeleatl muscle
- atrial contribution to ventricular filing
- intrathoracic pressure
- intrapericardial pressure, ventricular compliance
Effect on preload of compliance
Compliance of ventricles
If they’re stiff, more pressure at less volume
If too compliant, more volume out with little pressure
- extrinsic compression (pleural pressure, tumor), thickness of LV wall (edema, muscle) and elasticity due to cross-bridges will all affect
How is contraction measured?
Using isovolumic pressure-volume curve
Clamp aorta, fill ventricle with varying amounts, can see the max amount of tension heart can have at any volume
factors affecting myocardial contractility
- sympathetic/parasympathetic impulses/hormones circulating
Role of sympathetic on heart
Chronotrophic and inotrophic (increases heart rate and stroke volume)
SA node discharge rate increased
Role of parasympathetic on heart
Innervates only nodes, not ventricles (unlike sympathetic)
Slows heart rate
SA discharge rate decreased
Catecholamines on heart contractility
increases
B blockers on contractility
block stimulation of Ca2+ channels and Na+/Ca2+ exchangers
Constant depolarization
Ca2+ channel blockers
Block L-type Ca2+ channels
Digitalis glycosides
Inhibit Na/K pump and Ca channels; increases cytosolic Ca2+
Cardiac output and arterial pressure
Cardiac output not affected by increases in afterload until over 160 (hypertension)
–CO is determined almost entirely by ease of blood flow
Increase in afterload on volume/pressure curve
Narrows and moves upward
Volume/pressure curve under increase of volume
widens
Increase in contractile state on volume/perssure curve
Widens; pushes up isovolumetric-volume curve (makes line steeper)
Sinus nodal fiber compared to ventricular muscle fiber
- no plateau
- looks like “normal” action potential
Purpose of AV node
Delays transmission from SA node to ventricles
Allows time for atria to empty
Pacemaker Node Contraction
No plateau
Unstable resting potential–Funny Na+ channels (IF) slowly open until threshold, then Ca2+ channels open
Pulmonary system
low resistance/pressure
Systemic system
high resistance/pressure
increase in preload causes…
increase in stroke volume
thick and thin filaments stretch, overlap, more cross bridges
positive inotropic effect
increase contractility
negative inotropic effect
decrease contractility
increasing contractility means…
greater stroke volume
Frank Starling curve becomes near vertical…for that given EDV, more blood will be pumped out
Cardiac output equation
CO=HR x SV
if afterload increases:
higher pressure needed to open aortic valve
ejection phase shortened
stroke volume decreases
if preload increases
stroke volume increases
end systolic volume does not change
Accumulation of what solute is responsible for tetanus?
Ca2+
