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venous return
- The quantity of blood that flows from the veins into the right atrium each minute
- The venous return and the cardiac output must be equal
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Four factors that directly affect cardiac output
- 1. level of body metabolism
- 2. exercising
- 3. age, with increasing age body activity diminishes
- 4. size
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Average CO
- men 5.6
- women 4.9
- For adults the average is stated to be 5
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cardiac index
- the cardiac output in proportion to body surface area
- CO/BSA
- normal is around 3 L/min/M^2
- Peaks at around 10 years of age, 4 L/min/M^2
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Stretch of the right atrium affect?
- positive inotropic affect
- positive chronotropic effect, bainbridge sympathetic reflex
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When does the heart become the limiting factor in cardiac output
when venous return becomes more then the heart can handle
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Venous return in the sum of
all local blood flow through all the individual segments of tissue
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Blood flow in tissue increases in proportion to
tissue metabolism
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How PVR affects CO
reciprocally, when PVR increases CO decreases
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Ohm's law
- Q = arterial pressure / Total peripheral resistance
- flow = pressure / resistance
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Conductance and resistance are reciprocal
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What amount of venous return can the heart pump without special stimulation
- 13 L/min
- can max out higher or lower if it is hypereffective or hypoeffective respectfully
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Two factors that can cause hypereffectivness
- nervous stimulation
- hypertrophy of the heart muscle
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Two ways nervous stimulation increases effectiveness
- increases heart rate, pos chronotrop, up to 180 - 200 beats/min
- increases the strength of contraction, pos inotrop
- can raise output to 25 L/min
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Factors that cause hypoeffectivness
- coronary blockage
- sympathetic inhibition
- abnormal rate and rhythm
- Valvular disease
- increased arterial pressure
- congenital heart disease
- cardiac hypoxia
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Without nervous control
- you heart cannot respond to changes in arterial pressure
- no compensation
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Tissue metabolites act?
on arterioles
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Distinguishing feature of diseases that increase co
- all result from reduced total peripheral resistance
- non result from increased excitement of the heart
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diseases that decrease peripheral resistance and increase CO
- beriberi - caused by insufficient thiamine vitamin, B1. This lack cause the cell to lose the ability of oxidative phosphorilation and compensate by increasing blood supply
- AV fistula - decreases total peripheral resistance
- hyperthyroidism - increased metabolism of tissues. metabolic byproducts are released that causes dilation
- anemia - reduced viscosity of the blood, decreased delivery of O2 to the tissues
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Two categories of conditions that decrease CO
- abnormalities that cause pumping effectiveness to fall too low
- those that decrease venous return
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Five things that damage the heart and lower CO
- CAD
- valve disease
- myocarditis
- cardiac tamponade
- metabolic derangments
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Cardiogenic shock
when the CO falls so low that the tissues begin to suffer nutritional deficiency
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Four factors that decrease venous return
- decreased blood volume, peripheral vascular pressure falls to a level too low to force blood back to the heart
- acute venous dilation - when the sympathetic nervous system suddenly becomes inactive
- obstruction of large veins -
- decreased tissue mass of skeletal muscle - aging and long period of inactivity. decreases oxygen consumption and blood flow needs resulting in decreased output.
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An increase in intrapleural pressure
- shifts the cardiac output curve to the right
- Right atrial pressure must increase in proportion to the increase in intraplerual pressure
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5 factors that can alter the intrapleural pressure
- cyclic changes during respiration
- breathing against negative pressure shifts the curve to the left
- positive pressure breathing, shifts to the right
- opening of the thoracic cage increases pressure from -4 to 0
- cardiac tamponade, as the chambers of the heart fill the external pressure rises
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Three principle factors that affect venous return from the systemic circulation
- right atrial pressure; exerts a backward flow to impede return
- mean systemic filling pressure;
- resistance to blood flow
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mean systemic filling pressure
- pressure of rt atrium when blood flow stops
- usually around 7
- when arterial and venous pressure come to equilibrium
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rt atrial pressure bill plateau at negative pressure
- this is caused by the collapse of the veins entering the chest
- sucks the walls of the veins together
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Mean circulatory filling pressure
- when blood flow is stops this is the pressure in the circulation
- greater the blood volume the greeted the circulatory filling pressure
- at zero when volume is unstressed
- increased by sympathetic stimulation, decreased compliance
- decreased by parasympathetic
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systemic and circulatory filling pressures are almost always equal
The greater the system is filled the easier it is for blood to return to the heart
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The pressure gradient of venous return
the greater the difference between systemic filling pressure and right atrial pressure the greater the venous return
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Where does most resistance to venous return occur
- in the veins
- some in arterial and small arteries
- In the veins when there is resistance blood begins to dam up, there is little increase in pressure because of the veins are highly distensible
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A decrease in venous resistance =
a increase in venous return
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What is the maximum pressure the rt atrial pressure can rise to
the mean systemic filling pressure
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Affect of an increase in blood
- increase in the mean systemic filing pressure, shifts venous return curve to the right
- distends blood vessels and decreases resistance to venous return , increases slope of venous return curve
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Three compensatory effects in response to increased blood volume
- increased cardiac output increases capillary pressure so fluid begin to transude out. decreases volume
- stress-relaxation of the veins; increased pressure causes veins to distend thus reducing systemic filling pressure
- increased resistance through tissue causing return to decrease
- over a period of 10-40 minutes these effects will return cardiac output to normal
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Effects of sympathetic stimulation on cardiac output
- increased strength of contraction
- increases systemic filling pressure, and increases resistance to venous return
- venous return curve is shifted to the right and slope is decreased
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What can shift the cardiac output curve to the right
increase in intraplerual pressure
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Hexamethonium
blocks sympathetic nervous system
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effects of opening an AV fistula
- decrease resistance to venous return thus increasing the slope of venous return
- slight increase in cardiac output due to the decrease in peripheral resistance
- after sympathetics kick in the CO output curve is increased and the venous return curve is shifted right from the constriction of the veins and increase in systemic filling pressure
- After a couple weeks volume has increased shifting the venous return curve farther right, increase in systemic filling pressure, and an increase in CO
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Fick principle
CO = O2 absorbed by the lungs / AV O2 difference
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