Heart details Flashcards

1
Q

CO and right atrial pressure relationship

A

-increase in venous return -> increase right atrial pressure (to a point), end-diastolic volume and end-diastolic fiber length
-Increases in end-diastolic fiber length -> increases CO
-volume of blood leaving the LV (cardiac output) = the volume it receives in venous return
-
*more venous return -> more pressure in right atrium since more blood is accumulating
-too much pressure in right atrium -> pressure gradient that drives venous blood into right atrium is decreased
-Decreased pressure gradient = less venous return to the right atrium

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2
Q

mean arterial pressure

A

-pressure that would be measured throughout the cardiovascular system if the heart were stopped
-2 factors that influence MAP- blood volume and distribution of blood between stressed and unstressed volume

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3
Q

stressed vs unstressed

A

-Unstressed: volume of blood in the VEINS; volume that produces no pressure
-Stressed: volume in the arteries; volume that produces pressure by stretching elastic fibers in blood vessels
-When blood volume is 0-4 L -> all blood in the unstressed volume (the veins) -> producing no pressure -> MAP = 0
-When the blood volume is greater than 4 L -> some blood will be in stressed volume (the arteries) -> produce pressure
-when blood volume increases past 4 L unstressed volume remains the same (max) -> stressed increases
-Redistribution of blood -> changes MAP
-decrease in venous compliance= venoconstriction= the veins can hold less blood= blood shifts from the unstressed to stressed volume= increase cardiac output= increase in right atrial pressure
-increase in venous compliance= venodilation= the veins can hold more blood= blood shifts from stressed to UNSTRESSED volume= decrease cardiac output= decrease right atrial pressure

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4
Q

total peripheral resistance

A

-total blood volume is unchanged during shift of blood -> but it increases the mean systemic pressure and the vascular curve shifts to the right
-If there is venodilation -> unstressed volume will increase -> stressed volume and mean systemic pressure will decrease and the vascular curve shifts to the left
-decrease in TPR= easier for blood to flow from arteries to veins
-Decrease in atrial pressure= decrease in afterload
-Decrease in TPR= increased venous return= increases atrial pressure (increase flow back into the heart
-**The higher the right atrial pressure, the higher the cardiac output
-increase in TPR= more difficult for blood flow from arteries to veins

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5
Q

positive ionotropic agents

A

-increase in contractility, increase in stroke volume, and increase in CO for any level of right atrial pressure
-CO is increased and right atrial pressure is decreased-> more blood is leaving the heart on each beat due to the increased contractility and increased SV -> less pressure in the atrium

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6
Q

negative ionotropic agents

A

-decrease in contractility and a decrease in CO for any level of right atrial pressure
-CO is decreased and right atrial pressure is increased-> less output= more pressure
-less blood is leaving the heart on each beat, due to decreased contractility and decreased stroke volume

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7
Q

effects of increase/decrease of blood volume

A

-Increase in blood volume -> increase in amount of blood in stressed volume (arteries) -> increase the mean systemic pressure -> shifts the curve right in a parallel manner (right means increase in right atrial pressure) -> CO increased and right atrial pressure is increased
-Decrease in blood volume -> decreases the amount of blood in the stressed volume and mean systemic pressure -> vascular function curve is shifted to the left in a parallel manner -> CO is decreased and right atrial pressure is decreased

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8
Q

effects of changes in venous compliance

A

-Decreases in venous compliance -> shift of blood out of unstressed and into stressed volume -> increase mean systemic pressure -> shifts the curve right in a parallel manner (right means increase in right atrial pressure) -> CO increased and right atrial pressure is increased
-increases in venous compliance -> shift of blood into the unstressed -> decrease mean systemic pressure -> vascular function curve is shifted to the left in a parallel manner -> CO is decreased and right atrial pressure is decreased

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9
Q

increase/decrease TPR

A

-increase in TPR -> restricting flow of blood out of arteries -> increase in BP and decrease in venous return
-BP increase bc resistance is “holding” blood in arteries -> increases pressure
-increase in afterload (arterial blood pressure) -> decrease CO
-decrease venous return

-De­­creases TPR -> decrease arterial pressure -> decrease in afterload -> increase venous return -> increases CO -> decreases right atrial pressure (more blood is pumped out of the heart)
-decrease in TPR increases venous return, which increases right atrial pressure (increased flow back to the heart)
-Depending on relative magnitude of the effects, right atrial pressure can be slightly increased, slightly decreased, or unchanged.

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10
Q

starling

A

-know everything
-know all laws -> finks, etc.

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11
Q

how much blood in your system

A

-5L
-1 L of blood loss -> no BP -> heart has no blood
-stressed volume is 0 -> unstressed has 4 L
-volume depleted -> baroreceptors alerted -> HR and contractility is higher -> hearts trying harder (BP might not be high bc ur depleted still
-volume depleted -> kidneys alerted -> renin angiotensin system (anti-diuretic) -> increase volume -> increase Na retention -> water follows -> compensation
-

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12
Q

baroreceptors and aortic arch receptors

A

-sinus baroreceptors -> glossopharyngeal gives feedback to increase parasympathetic tone -> HR slow
-aortic arch only looks at if your hypertensive (baroreceptors detect low and high pressure)
-aortic arch -> CN X -> slows cardiac accelerator + vasodilation -> slows HR, contractility, decrease pressure in arteries and veins

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13
Q

kidney BP regulation

A

-ACE inhibiotor - angiotensin 2 blocker -> decrease BP
-increase aldosterone -> increase Na reabsorption -> increase ECF volume
-

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14
Q

starlings force - cont.

A

-capillary permeability
-closed loop circuit system
-hydrostatic pressure- arterial pressure at capillary bed
-osmotic pressure- protein at level of capillary
-net filtration- pressure in
-remaining fluid- lymphatic drainage

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15
Q

increase capillary hydrostatic pressure

A

-arteriolar dilation
-venous constriction
-increased venous pressure
-heart failure
-extracellular fluid volume expansion

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16
Q

decrease capillary oncotic pressure

A

-decreased plasma protein concentration
-severe liver failure (failure to synthesize protein)
-protein malnutrition
-nephrotic syndrome (loss of protein in urine)

17
Q

increase hydraulic conductance

A

-burn
-inflammation (release of histamine - cytokines)

18
Q

impaired lymphatic drainage

A

-standing (lack of skeletal muscle compression of lymphatics)
-removal or irradiation of lymph nodes
-parasitic infection of lymph nodes

19
Q

exercise

A

-central command -> increase sympathetic outflow and decrease parasympathetic (heart rate only) -> increase HR, increase contractility, increase CO, increase SV, constriction of arterioles, constriction of veins (decrease unstressed and increase stressed) -> INCREASE FLOW TO SKELETAL MUSCLE
-local response -> increase vasodilator metabolites -> dilation of skeletal muscle arterioles (decrease TPR) -> INCREASE FLOW TO SKELETAL MUSCLE

20
Q

standing

A

-pooling blood in veins -> decrease arterial pressure -> less flow detected -> baroreceptor reflex -> increase sympathetic outflow -> increase HR, contractility, CO, constriction of arterioles (increase TPR), constriction veins (decrease unstressed volume and decrease venous return) -> INCREASE ARTERIAL PRESSURE TOWARDS NORMAL