Exam review Flashcards
collaterals
multiple arteries that contribute to 1 capillary bed
arterial anastomosis
fusion of 2 collateral arteries
arterial anastomosis function
allows capillary circulation to continue if an artery is blocked
arteriovenous anastomoses
direct connections between arteries and venules to bypass the capillary bed and flow directly into venous circulaion
3 factors the affect circulation
pressure, resistance, and venous return
amount of blood in veins & venules at rest
60-65%
amount of blood in arteries and arterioles at rest
13%
capillary blood flow in peripheral tissues and organs maintained by
ΔP (pressure gradient) = the difference between pressure of left side (at heart), and pressure returning to right side (at peripheral capillary beds)
capillary blood flow equals
cardiac output
capillary blood flow determined by
pressure and resistance (ΔP/R = force/flow)
how are pressure and resistance related to flow
pressure= directly related
resistance= inversely related (R increase, flow decrease)
laminar flow
turbulent flow
abnormal turbulence caused by
4 factors associated with blood pressure
systolic pressure
diastolic pressure
systolic pressure
diastolic pressure
pulse pressure
pulse pressure formula
mean arterial pressure (MAP)
MAP formula
CO x TPR
factors that affect MAP
3 regulatory mechanisms
autoregulation, neural mechanisms, and endocrine mechanisms
regulatory mechanism purpose
control CO & BP to restore adequate blood flow
autoregulation is
the ability to make changes as needed by demand for O2 and waste removal
autoregulation is adjusted by
peripheral resistance while CO stays the same
local vasodilators dilate precapillary sphincters
to accelerate blood flow at tissue level in response to physical changes
local vasodilator examples
low O2 or high CO2 levels
low pH
histamines
warmer temp
local vasoconstrictors released by
damaged tissues
local vasoconstrictor examples
prostaglandins and thromboxanes
neural mechanisms
autoregulation, neural mechanisms, and endocrine mechanisms
cv centers adjust
CO & peripheral resistance
each cardiac center has
cardioacceleratory center (increase CO thru SNS)
cardioinhibitory center (decrease CO thru PNS)
sympathetic nervous system
increase HR & contractility
fight or flight
parasympathetic nervous system
decreases HR
rest or digest
vasomotor center controls
the activity of sympathetic motor neurons (vasodilation & vasoconstriction)
vasoconstriction
controlled by adrenergic nerves (NE)
stimulates smooth muscle contraction
vasodilation
controlled by cholinergic nerves (NO)
relaxes smooth muscle
vasomotor tone
produced by constant action of sympathetic vasoconstriction nerves
keeps arterioles partially constricted
hormonal regulation
has short and long term effects on CV regulation
types of hormones
anti diuretic (ADH)
angiotensin II
erythropoietin (EPO)
atrial natriuretic peptide (ANP)
anti diuretic (ADH)
released by posterior lobe of pituitary to elevate BP & reduce water loss at kidneys
anti diuretic (ADH) responds to
low blood volume
high plasma osmotic concentration
circulating
angiotensin II
appears in blood when decrease in BP or decreased blood flow to kidneys
release of renin results in
formation of angiotensin II and aldosterone
angiotensin II important functions
aldosterone production
secretion of ADH
stimulates thirst
stimulates CO & triggers constriction of arterioles
aldosterone
H2O & Na+ reabsorption
increase total blood volume
erythropoietin (EPO)
is released at kidneys to stimulate RBC production
erythropoietin (EPO) responds to
low BP
low O2 content
atrial natriuretic peptide (ANP)
is produces by cells in right atrium to lower blood volume and pressure
reduces stress on heart
atrial natriuretic peptide (ANP) responds to
excessive diastolic stretching
shock
failure of CV system to deliver enough O2 & nutrients
what happens in shock
inadequate perfusion
cells forced to switch to anaerobic respiration
lactic acid builds up
cells & tissues become damaged and die
hypovolemic shock
due to loss of blood or body fluids (hemorrhage, sweating, diarrhea)
venous return to heart declines, output decreases
cardiogenic shock
caused by damage to pumping action of the heart (ischemia, valve problems, arrhythmias)
vascular shock
causing drop inappropriate vasodilation
head trauma
obstructive shock
caused by blockage of circulation
pulmonary embolism
homeostatic responses to shock
activation of renin-angiotensin-aldosterone
secretion of ADH
activation of SNS
release of local vasodilators
CV response to light exercise
extensive vasodilation
venous return increases
CO rises
CV response to heavy exercise
CV centers activate the SNS
CO increases
blood flow to most tissues is diminished
skin perfusion increases because temp increases
diffusion
substances move down concentration gradient to pass freely thru lipid bilayer, fenestrations, or channels