BRS Booknotes Flashcards
Arteries contain what volume
Stressed volume
Arterioles have the highest __________ in the CV system
Resistance
What controls the arterioles of the skin, splanchnic, and renal circulation
α1
What controls the arterioles of the skeletal muscle
β2
What has the largest cross sectional area in the circulation
Capillaries
What volume is present in veins
Unstressed volume
What receptor is present on veins
α1
Capacitance is ___________ of stiffness
Inverse
How do you calculate capacitance
Volume/pressure
How do you calculate the velocity of blood
Flow/area
Which blood vessels have higher capacitance
Veins
Capacitance __________ with age
Decreases
What is the most important determinant of pulse pressure
Stroke volume
How do you calculate the mean arterial pressure
Diastolic pressure + 1/3 pulse pressure
How can one estimate the LA pressure
Inserting a catheter into the pulmonary arterioles near the capillaries and measuring pressure here approximates the LA pressure
Pulmonary wedge pressure
What does the p wave represent
Atrial depolarization
Where does the atria repolarize
QRS complex
What does the PR interval represent
Initial depolarization of the ventricles
What does the PR interval depend on
Depends on velocity through AV node
What increases the PR interval? Decreases?
Parasympathetic; sympathetic
What does the QRS complex represent
Ventricular depolarization
What does the QT interval represent
Entire ventricle depolarization and repolarization
What does the ST interval represent
Isoelectric
What does the T wave represent
Ventricle repolarization
What determines the resting membrane potential
K conductance
What is phase 0 in normal contraction
- upstroke of AP
- increased Na conductance causes Na influx
What is the peak of phase 0
Na equilibrium
What is phase 1 of normal ap
K efflux from fast channels and brief repolarization
What is phase 2 of the normal AP
Plateau of the AP
What causes the plateau at phase 2
K goes out but Ca comes in so repolarization stalls
What happens at phase 3 of normal AP
Repolarization continues as Ca conductance decreases but the slow K channels open so the K drives repolarization
What is phase 4 of normal AP
Resting potential
What has the fastest action potential
SA node > AV node > purkinje fibers
What are the AV node and purkinje fibers called
Latent pacemakers
Why is the SA node the pacemaker
It has an unstable resting potential
How is the nodal AP different from normal ones
There is no phase 1 or 2
What is phase 0 of the nodal AP
Ca influx which is the same as the AV node
What is phase 3 of the nodal AP
Repolarization; K flows in
What is phase 4 of nodal AP
Na influx called If; turned off by repolarization
What determines the conduction velocity
Ca influx during depolarization
What portion of the heart has the fastest conduction velocity
Purkinje
What is the difference between absolute and effective refractory period
Absolute means no AP can be initiated
Effective means no AP can be conducted
What is the relative refractory period
The period where AP is not likely but can be initiated with more force
What is a chronotropic change
Change in HR
What is a negative chronotropic change
Decreases in HR caused by decrease in SA node firing
What is a positive chronotropic change
Increase in HR caused by increase in SA nodal firing
What is a dromotropic change
Change in conduction velocity
What is a negative dromotropic change
Slower speed through AV node and longer PR interval
What is a positive dromotropic change
Faster conduction through AV node and shorter PR interval
What portions of the heart have vagal innervation? What does it do
SA node, atria, AV but NOT ventricles
Parasympathetic vagal innervation
What is the mechanism of negative chronotropic change
Decreases in HR due to slowing phase 4 depolarization (Na entering cells of AV and SA node)
What is the mechanism of negative dromotropic changes
Slower conduction through AV node; more K out and less Ca in
What is the mechanism of positive chronotropic changes
Faster phase 4 depolarization from faster I_f which is the Na flow responsible for phase 4 at SA node
What is the mechanism of positive dromotropic change
- faster conduction through AV node
- ventricle filling can be compromised
- increased Ca current
- decreased RR interval
Contractability is called what
Inotropism
What causes an increase in contractability
Increasing intracellular Ca
What is a normal ejection fraction
60%
What does a positive inotropic activity? Negative inotropic activity
Increase in contractability; decrease in contractability
What causes positive inotropism
Increased HR
Increased sympathetic activity via β1 receptor
Cardioglycosides (digitalis)
How does increased HR cause positive inotropism
Causes a building of Ca intracellular concentration = positive staircase or Bowditch staircase
Postextrasystolic potentiation = next beat is stronger from extra Ca in the cell and causes an extra boost of power from the Ca
What does increased sympathetic activity do for inotropism? What receptor is used
Increases; β1
How does increased sympathetic activity increase inotropism
- Increases influx of Ca with each AP
2. Increases Ca pump activity (phospholamban)
What do cardioglycosides do? What else are they called
Positive inotropism; digitalis
How do cardioglycosides cause positive inotropism
They inhibit the Na/K ATPase this leaves more Na inside the cell. Since intracellular Na is higher, the Na/Ca pump doesn’t bring in as much Na which leaves intracellular Ca high
What things cause positive inotropism
Inreased HR
Increased sympathetic activity via β1
Digitalis
What causes negative inotropism? How does it work
Parasympathetic activation via vagus N with ACh on muscarinic receptors. This causes a decrease of Ca flow during phase 2
What is preload related to
RA pressure
What increases preload
Increases in venous return causing increased end-diastolic volume and increases fiber length
What is afterload
Aortic pressure (or pulmonary A pressure) working against ventricular ejection
What increases afterload
Increases in pulmonary A pressure or aorta pressure
Increased length of sarcomeres causes increased __________ and allows for _________ cross bridges to form
Tension; more
When is contraction velocity maximal
When there is no afterload
As afterload increases, velocity of ejected blood ____________
Decreases
Increased end diastolic volume causes
Increased SV and CO
Increased venous return
Increased preload
Increased end diastolic volume causes ________ ventricle fibers which causes (increased/decreased) tension
Stretched; increased
Venous return is directly correlated to what
Cardiac output
Upward shift in CO means what? Downward shift means what
Increased contractility; decreased contractility
Increased contractility (increases/decreases) CO
Increases
At point 1 in ventricular pressure volume loops what valve is closing
AV valves close
At point 2 in ventricular pressure-volume loops what is happening with valves
Semilunar valves open
What is happening with valves at point 3 in ventricular pressure volume loops
Semilunar valves closes
What happens at point 4 of pressure volume loops
AV valves open
From 1–>2 in pressure volume loop is called
Isovolumetric
What happens at 2–>3 in pressure volume loops
SV is ejected
-width (Δ x-axis) is the SV
Point 3 in pressure volume loops is what general cardiac event
Diastole
What causes the semilunar valves to close
When pressure in the artery is higher than ventricle
When does isovolumetric contraction occur
3–>4 in pressure volume loops
What event marks 4–>1 in pressure volume loops
Ventricular filling
When does mitral valve open
LV pressure < LA pressure
What does increased preload cause
increased SV by F-S relationship (increased width on X axis)
Caused by increased end diastole volume
What causes increased end diastole volume
Decreased venous capacitance and/or increased venous return
How does increased afterload manifest on pressure-volume loop
‘Skinnier’ graphs; decreased width
Why does afterload decrease SV
The ventricle is ejecting blood against pressure so some energy of contraction goes into opposing that force
What causes increased afterload
Increases in aortic or pulmonary a BP
Increased contractility manifests as what on pressure-volume loop
Increased height and width of the curve
The intersection of vascular function and cardiac curve is what
Venous return and CO since venous return = CO
Where can you find mean systemic pressure on vascular/cardiac function graphs
Where the venous return intersects the x axis
What is mean systemic pressure approximately equal to
RA pressure with no flow
How do you obtain mean sytemic pressure
Stop the heart and wait for the pressure to equilibrate
What increases the mean systemic pressure
Increase in blood volume or decrease in venous capacitance
The slope of venous return is a function of what
Arteriole pressure
Depressing the vascular/cardiac graph causes
Same CO
Decreased flow —> increased TPR (total peripheral resistance)
Caused by increased arteriole constriction and increased RA pressure (preload)
Depressing vascular cardiac graphs is called what for venous return
CCW rotation of venous return
Stretching the vascular cardiac graph vertically results in __________ CO and __________TPR
Increased; lower
Vertically stretching vascular cardiac graph is named what in the vascular system
CW rotation of venous return
CW rotation of venous return does what to RA pressure and arteriole pressure
Decrease; decrease
Increases in TPR causes what changes
Decreased CO decreased venous return
How do you calculate SV
End diastolic volume - end systolic volume
How do you calculate CO
SV*HR
What is normal EF? How do you calculate it
0.6; SV/end-diastolic-volume
or
(EDV-ESV)/(EDV)
How do you calculate stroke work? What is the primary energy source?
Pressure*SV
Fatty acids
The tension of ventricles α ________
Cardiac O2 consumption
What causes cardiac O2 to increase
- Increase afterload
- Increase size of heart
- Increase in contractility
- Increase HR
How do you calculate cardiac output without stroke volume
(O2 consumed in body)/([O2]pulmonary v - [O2]pulmonary a)
What immediately proceeds atrial systole
P wave
Atrial systole causes what change in venous pressure graph
A wave (increase)
In ventricular hypertrophy, atrial systole causes what
4th heart sound
Isovolumetric contraction happens during what
QRS
What causes the first heart sound
AV valves
What is a split 1st heart sound
Mitral valve can shut faster than tricuspid
How much blood is ejected during isovolumetric contraction
None, the aortic valve is closed so no blood leaves
What portion of heart contraction has the highest ventricular pressure
Rapid ventricular contraction
What ends rapid ventricular contraction
T wave
What happens with the atria during rapid ventricular contraction
Atrial filling begins
When is the remainder of the SV ejected
During reduced ventricular ejection
What wave on the venous pulse correlates to reduced ventricular ejection
V wave
What is the second heart sound? What happens when it’s split
Aortic and pulmonic valve close; inspiration can interrupt pulmonary valve
During what stage on contraction do we see the dicrotic notch
Isovolumetric ventricular relaxation
What phase starts with the AV valves opening
Rapid ventricular filling
What is the third heart sound
Mitral valve opening; normal in kids, but means disease in adults
What is the longest phase of the cardiac cycle
Reduced ventricular filling
What are the 7 phases of the cardiac cycle
Atrial systole Isovolumetric ventricular contraction Rapid ventricular ejection Reduced ventricular ejection Isovolumetric ventricular relaxation Rapid ventricular filling Reduced ventricular filling (diastasis)
What is the dicrotic notch also called
Incisura
What is the fast method of altering arterial pressure? Slow?
Baroreceptors
Slow is RAAS
Where are the baroreceptors located
They are stretch receptors located in the walls of the carotid sinus near the bifurcation of the common carotid arteries
What is the primary mechanism of baroreceptors
Fast and neural
What are the general steps in the baroreceptor reflex
- Decrease in arterial pressure
- Decreased stretch decreases the firing rate of the carotid sinus nerve (hering’s nerve CN IX)
- This new level of stretch is compared to the set point in the vasomotor center (about 100 mm Hg)
- The vasomotor center decreases parasympathetic (vagal) outflow to the heart and increases sympathetic flow to the heart and blood vessels
What are the four ways that arterial pressure can be raised quickly
Increase HR
Increase contractility and stroke volume
Increase vasoconstriction of the arterioles
Increase vasoconstriction of the veins
How does contractility and stroke volume increase BP
When they are both raised this raises CO which increases arterial pressure
What does the valsava maneuver do? What is it
It is trying to expire against a closed glottis
This increases interthoracic pressure which decreases venous return, this decreases Pa, baroreceptors detect change and increase sympathetic activity to blood vessels and heart
What produces the greatest response from baroreceptors
Rapid changes in pressure
What is unique about the baroreceptors in the aortic arch
They respond to increases in pressure but not decreases
How does RAAS regulate blood pressure
Changes in blood volume
What does renin do
Enzyme from the kidney which converts angiotensinogen to angiotensin I
What converts angiotensin I to II? Why is this important
Angiotensin converting enzyme (ACE) is in the lungs and angiotensin II is the active form
What degrades angiotensin II
Angiotensinase
What are the steps in the renin-angiotensin-aldosterone system
- Decrease in renal perfusion pressure causes juxtaglomerular cells of the afferent arteriole to secrete renin
- Renin converts angiotensinogen to angiotensin I in the plasma
- ACE converts I to II in the lungs
What is the ultimate effect of ace inhibitors
Block the conversion of angiotensin I to II which decreases blood pressure
What do angiotensin receptor antagonists do
They block the effect of angiotensin II by binding to the receptors and thus cause a decrease in pressure
What are the 4 effects of angiotensin II
- Stimulates the synthesis and secretion of aldosterone in the adrenal cortex
- this increases Na reabsorption which increases blood volume (water follows ions) and increases blood pressure
- slow because protein syn is slow
- Increases Na-H exhange in proximal convoluted tubule
- angiotensin II and aldosterone both increase Na retention (angiotensin is direct aldo is indirect)
- angiotensin II leads to contraction alkalosis
- Increases thirst and water intake
- Causes vasoconstriction of the arterioles and thus increases TPR (total peripheral resistance) and BP
What follows cerebral ischemia
Increase in PCO2 in brain tissue
What reaction is associated with cerebral ischemia
Cushing reaction
What are the effects of cerebral ischemia
Intense peripheral constriction to shunt blood to brain (too much blood is shifted)
Mean arterial pressure can rise to life-threatening levels
What is the cushing reaction
A response to cerebral ischemia which is marked by increases in intercranial pressure. This compresses cerebral blood vessels and causes ischemia and increases PCO2 which causes vasomotor to increase sympathetic outflow to heart and blood vessels
How do the peripheral receptors respond to blood gas
They consume lots of O2 and are sensitive to decreases do they signal vasomotor center to increase vasoconstriction and increase TPR and Pa
What is vasopressin
ADH, causes increase in BP
What does vasopressin mainly react to
Large loss of BP (hemorrhage)
What causes vasopressin release
Decreased pressure in atria cause posterior pituitary to release vasopressin
What are the two effects of vasopressin
- Potent vasoconstrictor that increase TPR by activating V1 receptors on arterioles
- Increases water reabsorption in renal distal tubule and collecting ducts by activating V2 receptors
What increases filtration (movement of fluid out of capillaries)
Increased Pc -increased Pa -increased Pv -arteriolar dilation -venous constriction Decreased Pi Decreased πc -decreased protein concentration in the blood Increased πi -caused by inadequate lymphatic function
What is the fluid effect of histamine
Causes increase in arterial dilation and venous constriction which both cause local edema
Which factor of starling forces does histamine change
Increase in Pc
What is active hyperemia
Blood flow to an organ α metabolic activity
The MoA of NO involves what enzyme and intermediate
Guanylate cyclase; cGMP
NO is one form of
Endothelial-derived relaxing factor
What stimulates production of NO
Circulating ACh
What causes reactive hyperemia
Removal of an occlusion
Bradykinin causes what? What are its other effects similar to
Arterial dilation and venous constriction; histamine
Serotonin is released in response to
Vascular damage
Serotonin is believed to be related to vascular spasms which are related to
Migraines
What does serotonin do to vessels
Arterial constriction and released in response to blood vessel damage
Which prostaglandin is a dilator
Prostacyclin and E series prostaglandins
Which prostaglandins are vasoconstrictors
F-series prostaglandins; thromboxane A2
Hypoxia and adenosine cause what CV effects
Vasodilation
Cerebral circulation exhibits what hyperemia
Active and reactive
What is the most important vasodilator for cerebral circulation
CO2
Vasoactive compounds don’t act on
Cerebral circulation
β2 is responsible for
Vasodilation
What are the local vasodilators related to exercise
Lactate, adenosine, K+
Cutaneous sympathetic nerves are primarily responsible for
Temperature regulation; more flow through cutaneous = more dissipation
