Cardiac Output, BP, Blood flow Flashcards
1st heart sound
AV valves closing
2nd heart sound
semilunar valves closing
look and label wiggers diagram
PPT 2 Slide 3
look and label the pressure volume curve
PPT 2 Slide 4
cardiac output equation
CO= HRxSV
normal CO for men and women
men= 5.6L/min women= 4.9L/min
what can the average cardiac output get up to during exercise?
15-20 L/min
~3 fold increase
Does cardiac output increase or decrease with age?
decrease
angiotensin II
circulating hormone
induce release of Ca
release of NE
positive inotropic
thyroid hormone
regulate metabolism
positive chronotropic and inotropic
hyper/hypo
inotropic
increase contraction
insulin
increase glucose uptake
positive inotropic effects
PI3K signaling pathway
glucagon
increased blood glucose
positive chronotropic and inotropic effects
increases cAMP
hypokalaemia
low K+ extracellular
hyperpolarizes
cardiac arrest
hyperkalaemia
excess K extracellular
depolarizes membrane potential
muscle weakness
blocks conduction
hypocalcemia
cardiac muscle weakness
hypercalcaemia
increased contraction potentially spastic
frank-starling mechanism
greater the stretch on resting muscle (preload) the greater the contraction
what is stretch determined by?
end diastolic volume/pressure
starlings law of the heart
the energy of contraction of a cardiac muscle fiber is proportional to the initial fiber length at rest
venous return
amount of blood flow back to the heart
how does increased preload change the pressure-volume curve
increased preload usually means increased EDV and increased stroke volume
curve gets wider
afterload
the force that contracting myocytes must overcome
what can increase afterload
increases in arterial pressure, aortic pressure and aortic stenosis
how does afterload change the pressure-volume curve?
height increases due to increase in pressure the LV must create and increases ESV
what is the percent of blood in pulmonary circulation
9%
what is the percent of blood in the veins, venules, venous sinouses
64%
what determines blood pressure and blood flow
vasoconstriction and vasodilation
endothelial nitric oxide synthase
constitutively expressed (eNOS) inducible (iNOS)
what can NO bioavailability be reduced by?
presence of free radicals
neural stimulation
sympathetic vasoconstriction (NE)
endocrine/paracrine
CO2, H+, adenosine
artery components
endothelium
elastic tissue
smooth muscle
fibrous tissue
arteriole components
endothelium
smooth muscle
capillary components
endothelium
venule component
endothelium
fibrous tissue
vein components
endothelium
elastic tissue
smooth muscle
fibrous tissue
arteries
expand to hold blood, compliant
elastic recoil maintains consistant pressure
arterioles
smooth muscle and surgace area and can change BF to different tissues
capillaries
endothelial cells allow only 1 RBC to pass at a time
veins
large diameter
reservoir for blood
what do veins induce and how?
one way blood flow
one way valves
varicose vein
damaged and allows backflow of blood
Left ventricle pressure
120/5
aorta/ systemic pressure
120/80
CVP
7
right ventricle pressure
25/1
pulmonary arteries
25/8
MAP calculation
diastolicx2 + systolic / 3
pulse pressure
the difference between systolic and diastolic BP
BP equation
MABP= CO x SVR
as SV increases what happens to pulse pressure
pulse pressure increases
compliance
ability to distend and increase volume with increasing blood pressure
as compliance decreases what happens to pulse pressure
pulse pressure increases
vascular compliance=
change in volume/change in pressure
arteriosclerosis
hardening of arteries
loss of compliance
collagen replaces elastic fibers
increases systolic pressure
atherosclerosis
form of arteriosclerosis fat/cholesterol clogs it up
new BP goal
<130/80
recommendations for stage 1 high blood pressure
lifestyle changes
exercise
recommendations for stage 2 high blood pressure
medication
how much do exercise interventions reduce systolic pressure by on average?
4.8 mmHg
how much does antihypertensives reduce systolic pressure by on average?
8.8mmHg
common causes of Htn
obesity atherosclerosis renal endocrine sympathetic overactive
problems from Htn
endothelial damage stoke MI pathological hypertrophy HF
should you put low risk patients on antihypertensives?
no they did not improve mortality or CV outcomes and lead to adverse events
flow rate
volume that passes a given point over time (how much)
velocity of flow
distance volume of blood will travel in time (how fast)
velocity equation
velocity= flow rate/cross sectional area
how is velocity related to cross sectional area
velocity is inversely related to cross sectional area
blood flow
quantity of blood that passes a given point in the circulation in a given period
pressure
blood flows because of pressure gradients
resistance
decreases flow
ohms law
Flow= change in pressure/ resistance
ohms law other equation
CO= (MABP-CVP)/ TSR
does absolute pressure drive flow?
no the change in pressure
resistance determined by what? what law?
length of tube
radius of tube
viscosity of fluid
poiseuilles law
what is radius determined by?
local control- metabolic needs, paracrine agents
circulating horomones
sympathetic reflexes
what are arteries, arterioles, capillaries, venules and veins arranged in? why is that important for resistance?
series
Rtotal= R1+R2+R3
what forms parallel? why is that important for resistance?
branching of blood vessels
less resistance overall, more flow
Rtotaly= 1/(1/R1 + 1/R2 + 1/R3)
what is the flow through individual arterioles depended on?
dependent resistance of that arteriole
increased resistance in arteriole does what to flow?
decreases
what is the total blood flow through all the arterioles equal to?
cardiac output
why is variation in blood flow to individual tissues possible?
arterioles in the body are arranged in parallel
metabolic hyperemia
increase in metabolic products during tissue metabolism induces vasodilation which increases blood flow
shear stress control of blood flow
Nitric Oxide
shear stress causes release of NO and induces vasodilation
endothelin
vasoconstriction, released by endothelium
NE/E
vasoconstriction
angiotensin II
vasoconstriction, found in blood plasma
vasopressin (antidiuretic hormone)
vasoconstriction, secreted by posterior pituitary
serotonin
mostly vasoconstriction
released by platelets intestine
thromboxane
vasoconstriction released by platelets smooth muscle
postacyclin
vasodilation released by endothelial cells
bradykinin
vasodilation, in blood plasma, released during inflammation
histamine
vasodilation, released during inflammation, allergies by mast cells
NO
vasodilation released by endothelial cells
ANP/BNP
vasodilation released by the heart during stretch
coronary blood flow altered by
contraction
local metabolism
neuronal control
baroreceptor locations
carotid sinus (glosso) aortic arch (vagus)
as BP increases does the firing rate of baroreceptor increase or decrease?
increases and then levels out at max
ADH
antidiuretic hormone
secreted by posterior pituitary
water retention
vasoconstriction
long term regulation of BP RAAS
renin angiotensin aldosterone system
what 5 things does angiotensin II cause?
increase in sympathetic h2o retention aldosterone secretion vasoconstriction ADH secretion
many cases of HTN can be ascribed to excess weight why?
adipocytes have the angiotensin renin, and ACE that cause HTN
ANP, BNP
atrial and brain natriuretic peptides
released by heart when it is stretched
FAIL SAFE FOR VOLUME OVERLOAD
(excrete salt and water)
what happens if blood volume decreases due to dehydration or hemorrhage? (hypovolemic)
increase RAAS, decrease baroreceptor firing (increase sympathetic output)
what are the common targets of high blood pressure medicines?
blood volume cardiac output (HR or SV) resistance (vasoconstriction)
