MAP Regulation Flashcards

1
Q

NE effect on HR

A

mild direct increase in HR and CTY

BUT… reflex bradycardia overall from increased SVR

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2
Q

which types of tissue have more density of a1 receptors

A

skin, splanchnic, renal, skel muscle- non essential

sparse receptors need perfusion even w/ low BP or CO, such as brain, heart, lungs

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3
Q

timeframe of hormonal component of arterial baroreflex

A

onset in 2-3 min, steady in 10-15

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4
Q

effect of hormonal component of baroreflex

A

support SNS, retention of Na and water and vasoconstriction

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5
Q

when does capillary oncotic pressure decrease

A

low plasma proteins (such as albumin) can happen w/ liver failure or malnutrition

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6
Q

factors that determine capillary hydrostatic pressure

A

MAP, capillary flow, ratio of resistance b/w arteriole and venules

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7
Q

impact of arteriolar constriction on ultrafiltration

A

favors absorption, upstream constriction lowers flow to capillaries which reduces hydrostatic pressure and filtration rate

(think about kinking a hose like constricting arterioles)

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8
Q

local regulation of vascular tone

A

metabolites that accumulate during high metabolism cause vasodilation

eg. active skeletal muscle w/ more H+, CO2, adenosine

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9
Q

change in venous pressure effect on ultrafiltration

A

more of an impact than the arteriolar side, in the opposite direction- pro edema because higher capillary hydrostatic pressure

this is because there are less sphincters and other controls on veins

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10
Q

when does edema occur

A

when volume of filtration out of capillaries exceeds capacity of lymphatic system

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11
Q

SNS impact on filtration (increase or decrease of SNS activity)

A

more SNS is pro absorption (higher arterial pressure and less capillary flow)

less SNS is pro edema, arteriole dilation increases flow into capillary and hydrostatic pressure

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12
Q

dehydration effect

A

pro absorption, oncotic pressure is increased due to less plasma water

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13
Q

hypoproteinemia effect on ultrafiltration

A

pro edema, less oncotic pressure

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14
Q

define shock

A

state w/ reduction in systemic perfusion and O2 delivery to tissues- becomes irreversible

results from profound insult to MAP regulation

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15
Q

hypovolemic shock impact on PCWP, CO, SVR

A

decreases (lower preload), decreases (same reason), increases via SNS

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16
Q

cardiogenic shock impact on PCWP, CO, SVR

A

increase (lower CTY), decrease (lower CTY), increased via SNS

17
Q

distributive shock impact on PCWP, CO, SVR

A

not much impact, increase CO (tachy and low afterload), low SVR (cause of shock)

18
Q

cause of hypovolemic shock

A

acute blood loss or dehydration- leads to loss of preload and low SV

19
Q

compensation and Tx of hypovolemic shock

A

tachy and increased SVR

IV saline, maybe blood transfusions

20
Q

cause of cardiogenic shock

A

insufficient CO- usually low SV from poor CTY (HF or STEMI) or very low/high HR

21
Q

compensation and Tx of cardiogenic shock

A

increased preload, tachy, SNS increases SVR

tx w/ inotrope, diuretic, ACEi (or other afterload reducer)

22
Q

important physical exam findings on cardiogenic shock

A

JVD and cold extremities

23
Q

cause of distributive shock

A

sepsis, anaphylaxis, neurogenic- cause vasodilation and profoundly lower SVR

24
Q

compensation and tx of distributive shock

A

tachy- usually high SV/CO when combined w/ low afterload

tx w/ fluids, pressors, and underlying cause (eg antibiotics for sepsis)

25
Q

physical exam findings for distributive shock

A

warm extremities (vasodilation)

26
Q

septic effect on vessels

A

cause vasodilation and vascular leak- both causing hypotension, increase filtration rate and cause low blood volume

27
Q

sympathomimetic therapy w/ shock, cardio vs distributive

A

for cardiogenic- need to increase CO, target CTY w/ dobutamine (B1 agonist) and afterload w/ ACEi

for distributive- need to increase SVR, use phenyleprhine (a1 agonist)