Cardiac Lecture 2 Flashcards
what is the equation for stroke volume
EDV-ESV
what is the equation for EF
SV/ EDV
equation for cardiac output
HR x SV
what does pre-load refer to?
amount of blood returned to the heart/ the amount eh ventricles are stretched
what does afterload refer to?
the amount of arterial pressure
does cardiac output increase or decrease with age?
decrease
what is the normal cardiac output for men?
5.6 L/min
what is the normal cardiac output for a woman?
4.9 L/min
what is the max cardiac output for an average person?
15-20 L/min (3X increase)
does max HR increase or decrease in old age?
decrease
equation for HR based on age
220-age = HR
what is the gold standard to measure cardiac output
echocardiography
-measures SV by measuring blood flow through left ventricular outflow tract
what is swan Ganz pulmonary wedge pressure
- measures cardiac output
- catheter in pulmonary artery and occludes vessel
- equal to left atrial pressure
the Fick Principle
- measures cardiac output
- VCO2/ (Ca02-Cv02)
the role of angiotensin II
- circulating hormone
- induce the release of Ca2+ in cardiac myocytes
- facilitates the release of NE from nerve terminals
- positive inotropic
the role of thyroid hormones
- regulate metabolism
- positive chronotropic and inotropic effects
the role of insulin
- increases the uptake of glucose
- positive inotropic effects
the role of glucagon
- increases blood glucose
- chronotropic (increases cAMP) and inotropic effects
what effect does hypokalemia have on the cardiac myocyte cells
low extracellular K+ increases the gradient so intracellular K+ will want to move out of the cell quicker
- inside of the cell becomes more negative as positive charge leaves
- HYPERPOLARIZATION of the cell membrane, makes harder to get an action potential
what effect does hyperkalemia have on cardiac contraction
- high extracellular K+ decreases the gradient and causes DEPOLARIZATION
- muscle weakness from inadequate action potential
- blocks conduction
what vessels serve as reservoirs for blood
- pulmonary circulation
2. veins, venues, and venous sinus
what tissues does an artery have
- fibrous tissue
- elastic tissue
- both expand and contract rapidly - endothelium: to secrete nitric oxide
- smooth muscle: to constrict and vasodilate
what tissues does the arteriole have
- endothelium
- smooth muscle
- major function is to constrict and dilate
- lot of smooth muscle and surface area to change blood flow to different tissues
tissues of a capillary
- endothelium
- gas exchange; allows one RBC to pass at a time
tissues of a venule
- endothelium
2. fibrous tissue
tissues of a vein
similar to arteries
what dictates flow and resistance of where the blood goes
arterioles
what is CO equation for flow
Change in pressure / resistance
MABP- CVP/ SVR
systolic and diastolic pressure in the aorta
120/5
pressure in the systemic capillaries
17
central venous pressure
2= right atrium
systolic and diastolic pressure in the right ventricle
25/1
systolic and diastolic pressures in pulmonary arteries
25/8
pressure in pulmonary capillaries
7
pressure in pulmonary veins
2
what will happen to MABP if there is an increase in resistance but CO stays the same?
MABP will increase
what will happen to MABP if you increase CO with the same resistance?
MABP will increase
what two things effect pulse pressure
- stroke volume
- the greater the SV the greater the PP - Compliance
- the less the compliance the greater the PP (systolic pressure)
equation for vascular compliance
change in volume/ change in pressure
does MABP increase or decrease with age?
increase
what is general term for hardening of the arteries
arteriosclerosis
4 side effects of arteriosclerosis
- loss of compliance (hardening of arteries)
- destroys endothelium ( reduces nitric oxide)
- increase in systolic pressure (increase in afterload)
- leads to hypertrophy and hypertension
the most common form of arteriosclerosis
atheroslerosis
-plaque in arteries
the volume that passes a given point over time
flow rate ( how much)
distance the volume of blood will travel in time
velocity of flow (how fast)
equation for velocity
flow rate/ cross sectional area
- the narrower the vessel the faster the velocity of flow
is velocity of flow proportional or inversely proportional to to cross sectional area
inversely proportional to cross sectional area
-the bigger the cross sectional area, the slower the velocity of flow
what has the biggest cross sectional area
capillaries
-good thing, allows more time for gas exchange
what has the slowest velocity of flow
capillaries
what has the fastest velocity of flow
aorta
3 things that determine resistance
- length of the tube
- viscosity of fluid
- radius of the tube (biggest factor)
blood flow in series
R= R1 + R2 = R3
branching of blood vessels forms ____ circuit
parallel
R= 1/ (1/R1 + 1/R2 + 1/R3)
-less resistance, more flow
_____ are arranged in parallel
arterioles
the flow through individual arterioles is dependent on _____
resistance
increased resistance = _____ flow to that arteriole
decreased
blood is diverted from ___ resistance arterioles to ____ resistance arterioles
high, low
-sympathetics can shunt blood away to other organs
arterioles control blood flow in ___ regions
local
total blood flow of all the arterioles in the body is always equal to
cardiac output
blood flow to individual tissues is possible because arterioles are arranged in
parallel
increase in metabolic products during tissue metabolism that induces vasodilation and increases blood flow
metabolic (active) hyperemia
-autoregulation
will get ___ blood flow to an area of higher metabolism
more
5 vasodilators produces with increased tissue metabolism
- CO2
- K+
- adenosine
- H+ (acidosis)
- phosphates
as arterial oxygen saturation decreases, blood flow will _____
increase
method of auto regulation of blood flow that causes endothelial cells to release NO and induce vasodilation
shear stress
vasoconstriction; released by endothelium
endothelin
vasoconstriction; secreted by posterior pituitary
vasopressin (antidiuretic hormone)
mostly vasoconstriction; released by platelets; intestine
seretonin
vasoconstriction; released by platelets; smooth muscle
thromboxane
vasodilation; released by endothelial cells
prostacyclin; PGI2
vasodilation; in blood plasma; released during inflammation
bradykinin
vasodilation; released during inflammation; allergies by mast cells
histamine
vasodilation; released by heart during stretch
ANP and BNP
what is the biggest dictator of blood flow in the heart
metabolism ( metabolic hyperemia)
3 things that alter coronary blood flow
- contraction
- metabolism
- neuronal control (alpha and beta receptors)
the carotid sinus has baroreceptors associated with _____nerve
glossopharyngeal
the aortic arch has baroreceptors associate with the ____ nerve
vagus
where do the baroreceptors travel to signal what the blood pressure is
medulla
when the blood pressure increases, the baroreceptors fire ____ action potentials
more
these constantly send action potentials to the brain and alert the medulla what the blood pressure (MABP) is
baroreceptors
what happens when you have a high BP sensed by the baroreceptors
- sensed by baroreceptors in the carotid sinus and aortic arch
- this increases firing in the glossopharyngeal nerve and vagus nerve
- action potentials reach medulla
- medulla sends a vagal efferent output to SA and AV node to decrease HR and decrease CO and decrease BP
- inhibit sympathetics
what happens when you have a low BP
same as high blood pressure but slow action potentials and medulla sends vagal efferent to SA and AV node to increase HR, increase CO, and increase BP
-inhibit parasympathetics
condition when baroreceptors do not work properly
orthostatic hypotension
2 long term regulations of BP
- antidiuretic hormone
2. RAAS system
where is the antidiuretic hormone (vasopressin) released from?
posterior pituitary when you have low BP or low blood volume
mechanism of antidiuretic hormone
- promotes water retention
- kidneys excrete water and blood vessels reabsorb the water - vasoconstriction
mechanism of the RAAS system to raise BP
- low BP is sensed by kidneys
- increase renin production
- renin convertis angiotension (liver) to angiotension I
- in the prescence of ACE from the lung/ kidneys, angiotension I is converted to angiotension II
- angiotension II activates the sympathetic nervous system and cause Na+ reabsorption and water retention
- adrenal cortex secretes aldosterone that also helps with Na+ retention and water retention
- angiotension II induces vasoconstriction
- induces secretion of ADH from posterior pituitary to promote water reabsorption
the best target for hypertension
RAAS system
why does obesity correlate with hypertension
adipocytes carry angiotension, renin, angiotension I, and ACE— all necessary for aldosterone and Angiotension II to promote vasoconstriction and increase Na+ and water reabsorption
atrial and brain natriuretic peptides
another mechanism for blood pressure regulation
what natriuretic peptides increase as atria and ventricles stretch?
increase in ANP and BNP
what natriuretic peptides should you look for in patients with heart failure
elevated ANP and BNP
effects of elevated ANP and BNP
- decrease renin
- direct vasodilation
- increase in globular filtration rate
= naturesis and diuresis (excrete salt and water)
=decrease BP and blood volume
response by kidneys from hemorrage
secrete renin and angiotension to induce vasoconstriction
response by hormones released by the heart from hemorrage
decrease in ANP and BNP
neural response by baroreceptors from hemorrage
baroreceptors tell the sympathetic nervous system to increase firing of action potentials and increase HR
high blood pressure medications reduce the afterload or preload on the heart
afterload
