Heart Flashcards
what structural detail is unique to the heart as a muscle? How does this effect its contractile motion?
origin and insertion is on the same CT, wringing contraction
What is the all or none law of the heart?
cannot recruit additional muscle fibers in order to increase developed tension
why is the length of the refractory periods of the heart so important functionally?
cannot get tetany of the heart
What is the SNP?
supranormal period, increased susceptibility to AP with stimulus
What determines cardiac output?
preload (Frank starling law of Heart/ VR), Contractility (positive inotropic agents, heart rate, state of heart- failure, hypoxia, ischemia), afterload (aortic diastolic pressure plus impedence), HR
How does an increase in developed tension in working heart muscle change velocity of shortening?
as tension increase time for contraction remains relatively the same therefore velocity increases
How does norepinephrine effect the Frank Starling curve?
upward shift along developed tension without changing the length, this meansthere is an increase in tension and work without changing length, this means it changes contractility
If we are following the all or none law how does norepinephrine increase contractility?
more calcium available quicker so there is an increase in available actin myosin binding sites this increases the velocity of shortening and tension/work
what is capillary wedge pressure? How is measurement achieved?
catheter feed venous system through to lungs just before LA, balloon is inflated to measure pressure on proximal venous side
What causes a change in Vmax in cardiac tissue?
only norepinephrine due to increase in binding sites,
what type of contraction does cardiac muscle use and why?
isometric due to the resistance from pressure
what is stroke work?
SV*MAP (or area within PV loop)
What is Cardiac work?
HR*SW
which type of work done by the heart is harder? What is the other kind of work?
pressure work, volume work
What effect does valve stenosis have on pressures?
decreased pressure after valve and increased pressure before valve
What effect does mitral regurgitation have on pressures?
increase in pressure after valve closure
What effect does aortic regurgitation have on pressures?
decrease in pressure after valve closure, no dicrotic notch observed
If preload and afterload are fixed how does stroke volume change with changing contractility?
in PV loop upper sloped line changes its slope and starting height as a function of contractility, increased contractility increases stroke volume, decreased contractility decreases stroke volume
what changes in a PV loop with a systolic dysfunction?
decreased contractility-> decreased SV; downward shift of upper sloped line
what changes in a PV loop with a diastolic dysfunction?
compliance of ventricle decreased, therefore there is less filling and thus stroke volume is decreased; upward shift in bottom sloped line
What causes the splitting of S2 with inspiration?
inspiration: decrease in intraplural pressure pulls blood into lungs and the right heart. More blood in right heart requires more time for ejection thus increased period for systole and a delayed S2. at the same time decreased intraplural pressure causes decreased venous return to the left side and decreased volume for ejection so less time needed to a shorter systole and an earlier S2
How do the S2 sounds move back together on expiration?
expiration increases intraplural pressure which forces blood out of lung into left side of heart, increasing volume thus systole and delaying S2, increased plural pressure also impedes venous return on right side thus decreasing volume and systole causing a sooner S2
How is cardiac output measured?
via O2 consumption, 200-150, consumption of 50 mL/L difference between before lungs and after, 250 mL O2/min; 250/50= 5mL/min CO
What is cardiac output?
HR*SV (mL/min)
What is venous return?
volume of blood returning to right atrium/min, determine preload
What is inotropic?
change in contractility
what does chronotropic mean?
change in rate
What is another way to measure cardiac output other than oxygen consumption?
dye or thermal dilution, 1g of dye to a barrel, stir then measure concentration, inject into blood then measure dye concentration downstream
What is the frank starling law of the heart?
heart pumps all that comes to it; preload determined by VR, CO=VR
What all affects preload?
VR, TPR (Q=deltaP/R) and Tissue control cardiac output (CO=sum of flow through all systemic vascular beds, flow through vascular bed is determined by the needs of that vascular bed, each vascular bed with few notable exceptions determines amount of blood that it receives- autoregulation of blood flow); cardiac output is determined by the needs of the peripheral tissues
How is venous return and its interrelationship with cardiac performance?
CV system is a closed system with variable capacitance; capacitance is about 20x greater in venous system than the arterial system. Cap=dV/dP; increasing heart rate decreases venous pressure
On a graph with CO vs. venous pressure the point where line crosses venous is what? The slope is what?
MSFP or mean systemic filling pressure- avg pressure when no flow, changing resistance does not change MSFP; slope is based on resistance- dilation increases slope and constriction decreases slope
How does volume changes effect the graph of CO vs venous pressure?
slope remains the same but entire line shifts left for hemorrhage and right for a transfusion; changes MSFP but not resistance
