MAP Regulation Flashcards
NE effect on HR
mild direct increase in HR and CTY
BUT… reflex bradycardia overall from increased SVR
which types of tissue have more density of a1 receptors
skin, splanchnic, renal, skel muscle- non essential
sparse receptors need perfusion even w/ low BP or CO, such as brain, heart, lungs
timeframe of hormonal component of arterial baroreflex
onset in 2-3 min, steady in 10-15
effect of hormonal component of baroreflex
support SNS, retention of Na and water and vasoconstriction
when does capillary oncotic pressure decrease
low plasma proteins (such as albumin) can happen w/ liver failure or malnutrition
factors that determine capillary hydrostatic pressure
MAP, capillary flow, ratio of resistance b/w arteriole and venules
impact of arteriolar constriction on ultrafiltration
favors absorption, upstream constriction lowers flow to capillaries which reduces hydrostatic pressure and filtration rate
(think about kinking a hose like constricting arterioles)
local regulation of vascular tone
metabolites that accumulate during high metabolism cause vasodilation
eg. active skeletal muscle w/ more H+, CO2, adenosine
change in venous pressure effect on ultrafiltration
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
when does edema occur
when volume of filtration out of capillaries exceeds capacity of lymphatic system
SNS impact on filtration (increase or decrease of SNS activity)
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
dehydration effect
pro absorption, oncotic pressure is increased due to less plasma water
hypoproteinemia effect on ultrafiltration
pro edema, less oncotic pressure
define shock
state w/ reduction in systemic perfusion and O2 delivery to tissues- becomes irreversible
results from profound insult to MAP regulation
hypovolemic shock impact on PCWP, CO, SVR
decreases (lower preload), decreases (same reason), increases via SNS
cardiogenic shock impact on PCWP, CO, SVR
increase (lower CTY), decrease (lower CTY), increased via SNS
distributive shock impact on PCWP, CO, SVR
not much impact, increase CO (tachy and low afterload), low SVR (cause of shock)
cause of hypovolemic shock
acute blood loss or dehydration- leads to loss of preload and low SV
compensation and Tx of hypovolemic shock
tachy and increased SVR
IV saline, maybe blood transfusions
cause of cardiogenic shock
insufficient CO- usually low SV from poor CTY (HF or STEMI) or very low/high HR
compensation and Tx of cardiogenic shock
increased preload, tachy, SNS increases SVR
tx w/ inotrope, diuretic, ACEi (or other afterload reducer)
important physical exam findings on cardiogenic shock
JVD and cold extremities
cause of distributive shock
sepsis, anaphylaxis, neurogenic- cause vasodilation and profoundly lower SVR
compensation and tx of distributive shock
tachy- usually high SV/CO when combined w/ low afterload
tx w/ fluids, pressors, and underlying cause (eg antibiotics for sepsis)
physical exam findings for distributive shock
warm extremities (vasodilation)
septic effect on vessels
cause vasodilation and vascular leak- both causing hypotension, increase filtration rate and cause low blood volume
sympathomimetic therapy w/ shock, cardio vs distributive
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)
