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1.) Electrophysiology
a. Action potentials & conduction velocity differs within the heart
b. Compared to other tissues the heart has a relatively long AP and Refractory period
2.) Phase zero, the upstroke of the action potential is: ( see graph on page 3)
a. Relatively fast in Atrial myocytes, Ventricular myocytes, and conduction fibers
b. Relatively slow in SA & AV node
i. This is essential for ventricular filling
3.) Membrane potentials
a. Na & Ca are in higher concentration outside the cell & K is higher in the cell
b. Phase 4:
i. Ventricles, Atria, & His-Purkinje system
Stable Resting membrane potential (-90 mv)
1.
Potential is determined by K, which has the highest conductance
2.
Na plays a minor role, because it is not very permeable
3.
Current is Ik1
4.
c. Phase 0 the Upstroke
i. Transient increase in Na conductance=> Na influx
d. Phase 1
i. Transient repolarization
ii. due to (1) decreased Na conductance ( inactivation gates are closing) and (2) the concentration and charge
gradients favor K outflow
e. Phase 2
i. Plateau
ii. Due to increase in Ca conductance & decrease K conductance
L type Ca channels
1.
iii. These forces oppose each other
f. Phase 3
i. Repolarization
ii. Ca conduction decreases & K increases
iii. Outward Ik repolarizes the cell
4.) Slow response (SA & AV)
a. Phase 4 in SA & AV nodal cells
Resting membrane is not stable (max is -65mv)
1.
Ik1 is very low or absent
2.
If , a Na current, is responsible for the spontaneous depolarization ( automaticity) of the SA node
3.
If is turned on by repolarization ensuring that a new AP is always generated
4.
b. Phase 0
i. is due to a Ca current, not Na
T-type Ca Channels
1.
ii. not as rapid or sharp as in other cardiac tissue
c. Phase 1 & 2 are absent
d. Phase 3 due to outward K current
5.) Conduction velocity trend: Purkinje > ventriclesatria> SA AV
a. Conduction velocity depends on the size of the inward current during the AP upstroke & cable properties
b. Length of the AP does not matter
6.) Frequency of firing
a. SA>AV>His-Purkinje
7.) Activation Sequence of Heart
a. SA=> Left and Right atria via intermodal tracts=>AV node=>Bundle of His=>Purkinje systems
8.) The SA normally serves as the pace maker
a. AV node & His-Purkinje are latent pace makers
b. The fastest rate of phase four depolarization determines what myocardial component will act as the pace maker
c. Under normal circumstances: fastest-SA>AV> His-Purkinje-slowest
d. Ways to change pace maker activity
i. Alter (1) phase four rate of depolarization (2) max negativity of phase four (3) threshold potential
ii. Lecture Examples:
Sympathetic Stimulation increases SA phase 4 depolarization
1.
Parasympathetic (vagal) stimulation decreases SA phase 4 depolarization
2.
Drugs can decrease SA depolarization, by increasing the threshold potential ( see graph pg 10)
3.
a. Ex: Quinidine
A reduction of Ca current in slow response cells can also influence automaticity (graph pg 15)
4.
a.
b.
Normally the Ca current is activated at the end of phase 4 depolarization and accelerated
the rate of diastolic depolarization
Decreases in extracellular Ca or use of Ca antagonist decreases the amplitude and slope
of the slow diastolic depolarization in the SA node
When current is flowing at an angle away from the positive end of the EKG some negative
decrease on EKG
o When current is flowing perpendicular to lead flat line
o When there is no current flat line
EKG Leads 12 total leads, 6 on limbs and 6 on chest (precordial
leads)
6 limb leads:
o 3 standard or bipolar (have a positive and negative
direction)
Lead I = R arm to L arm
Lead II = R arm to L leg
Lead III = L arm to L leg
o 3 augmented or unipolar (have only a positive direction)
aVR = from body wall twds R arm
aVL = from body wall twds L arm
aVF = from body wall twds L foot
o the limb leads only detect cardiac vectors on the frontal
plane of the body
o the normal average mean electrical axis is approximately +60
o the magnitude of the deflection reflects how parallel the electrical force is to the axis of the
lead being examined
6 chest/precordial leads: all unipolar (have only a positive
direction)
o From R to L: V1, V2 (straight down), V3, V4, V5, V6
(straight towards L side of body)
o V1 and V2 = record mainly electrical activity of right
ventricle
o V3 and V4 = record mainly electrical activity of the
septum
o V5 and V6 = record mainly electrical activity of the left
ventricle
o The chest leads detect cardiac activity in a horizontal plane
Electrical Conduction
Normal beat starts at the SA node (junction of RA and SVC)
Electrical propagation through the heart: SA node atria AV node common bundle bundle
branches Purkinje fibers ventricles
o Reflected by 3 major deflections on the EKG P wave, QRS complex, and T wave
o SA and AV node have slow response
o Repolarization of the atria are hidden in QRS during depolarization of ventricles (dont see it)
P wave = atrial depolarization
QRS complex = ventricular depolarization
T wave = ventricular repolarization
Y-axis is voltage 1.0mV produces a deflection of 10mm (each small box represents .10mV and
each large box is .5mV)
EKG Analysis
1) Voltage calibration
In some cases of hypertrophy or bundle branch blocks, QRS complexes are larger than normal
recording is made at standard voltage 1.0mV = 1 large box (instead of normally where 1.0mV
= 2 large boxes)
2) Rhythm
Normal rhythm is called the SINUS RHYTHM, which has 4 components:
o Every P wave is followed by a QRS complex
o Every QRS complex is preceded by a P wave
o The P wave is upright in leads I, II, and III
o The PR interval is greater than 0.12sec (three small boxes)
3) Rate
Normal rate is between 60-100 beats/min
There are three methods for calculating rate
o Count the number of mm between 2 consecutive QRS complexes to use the equation:
Memorize the value that corresponds to HR of each sequential large box after the first QRS
peak
1st = 300, 2nd = 150, 3rd = 100, 4th = 75, 5th = 60, 6th = 50 (use this to estimate the
HR depending on where the next QRS peak is)
o Count the number of QRS sequences between a 3 second interval and multiply by 20
This is particularly useful for determining irregular HR
4) Intervals (PR, QRS, QT)
PR = from the beginning to P to the beginning of Q (normal = 0.12-0.2 sec)
QRS = from beginning of Q to end of S (normal < 0.1 sec)
QT = from beginning of Q to the end of T (normal = 0.3-0.4 sec)
5) Mean QRS Axis
EKG represents the average electrical activity
QRS axis is usually -30 to +90
QRS axis is primarily upwards in leads I and II
o If it is not, the axis is abnormal (not +60) and should be determined from the limb leads by
finding the most isoelectric limb lead, then looking at the lead perpendicular to it the
mean axis points to the positive pole of that lead if it is a +QRS
6) Abnormalities
Look for variance in voltage, rhythm, rate, interval durations, and axis and combine with variances
in shape of the wave forms
Atrial Enlargement
o RA enlargement P wave has double bump with left side of bump (which
represents the RA) larger than the right side (represents the LA)
o LA enlargement P wave had double bump with right side of bump larger
than left side
Sinus Bradycardia APs originate at SA at slow pace slowing of HR
o All complexes are normal and evenly spaced but the rate is <60bpm
Sinus Tachycardia APs originate at SA at fast pace rapid HR
o All complexes are normal and evenly spaced but the rat is >100bpm
Wandering Atrial Pacemaker impulses orginate from varying points in atria
o Variation in P wave contour, PR intervals, PP and thus RR intervals, normal QRS and T
o
o
o
After normal delay at AV node, also get impulses via regular route double depolarization
P wave is immediately followed by short delta wave, producing slurred upstroke on wide QRS
w/short or no PR interval
Third-Degree (complete) AV Block no relationship between P and QRS, ARS rate slower than P rate
o Impulses orginate at SA node and below the AV node block
o Junctional Rhythm atria and ventricles depolarize independently, QRS less frequent,
regular at 40-55/min but normal in shape
Idioventrical Rhythm atria and ventricles depolarize independently, QRS less frequent,
regular at 20-40/min but with wide and abnormal shape
L ventricular block extra vector of depolarization on the L side (R), widening of QRS and R
*when reading an EKG, find the most isoelectric lead and use the one perpendicular to it to get your info!
body
pulmonary artery
aorta
lungs
aortic semilunar valve left ventricle (mitral valve) left atrium pulmonary vein
IV) Cardiac cycle and Electrocardiograms
A) Diastole
1) Isovolumetric relaxation
Looks like end of systole, but actually beginning of diastole
(b) Semilunar valves and AV valves closed
(i) Pressure in ventricles is higher than pressure in atria
(ii) Pressure in ventricles is lower than pressure in aorta
(iii) Aorta > Ventricle > Atria
(c) No volume change
(d) Pressure starts to decrease in ventricle
(e) Transient increase in atrial pressure = dicrotic notch, imp. to blood pressure measurement
2) Passive filling
(a) Atria start to fill with blood from venae cavae
(i) Pressure increases a little
(ii) AV valves open
(iii) Rapid filling of ventricles
(b) Both atria and ventricles are relaxed
(i) Blood is filling in the atria
(ii) Blood is also entering the ventricle through the open AV valve, reduced filling
(c) Pressure in left atria slightly higher than in left ventricle
(d) Volume rises in the ventricle
3) Atrial Contraction
(a) End of Diastole = Atrial depolarization
(b) SA node fires action potential
e.
II.
III.
IV.
V.
flow through the tube will increase as pressure gradient is increased; flow will decrease as either viscosity or length
increases; radius is critical because it is raised to 4th power; flow is directly proportional to radius
at this point, his lecture goes into a number of slides indicating many of the relationships indicated above; basically,
understand the equation and how changing any of the variables will affect the others
Resistance to Flow
a. similar to Ohms Law for electrical circuits: R= E / I
b. for fluid dynamics:
R = Pi Po / Q = 8l / r4
c. vessel diameter is principal determinant of resistance
i. this makes sense, since the resistance will be inversely proportional to the radius to the 4 th power; other
factors will not have such a major effect
ii. arterial occlusion has a large effect on flow: if the radius of an artery (with P=120mmHg) is decreased by
20%, flow will drop from 100ml/min to 41ml/min and it will take a P=293mmHg to restore normal flow
d. Total resistance in a series arrangement equals the sum of individual resistances
i. Rt = R1 + R2 + R3 +
e. Total resistance in a parallel arrangement equals the sum of reciprocals of individual resistances:
i. 1/ Rt = 1/ R1 + 1/ R2 + 1/ R3 +
f. thus, total resistance in parallel arrangement will be less than similar resistance in series arrangements
g. Advantages to parallel arrangement of resistors:
i. can regulate flow to certain destinations
ii. total resistance is less than the resistance of any one resistor
iii. impact of changes in resistance of a few vascular beds on blood pressure is minimized
iv. optimizes gas and substrate distribution dynamics
Laminar Flow and Turbulence
a. turbulent flow occurs when fluid does not flow in definite laminae (layers), but rapid mixing occurs (this will
happen in blood)
b. in turbulent flow, the pressure drop is approximately proportional to the square of flow rate (compared to first order
in laminar flow)
i. i.e., a heart will have to pump harder if turbulent flow develops
c. laminar vs. turbulent flow is determined by the Reynolds number NR using the following equation:
NR = Dv/
VI.
d.
Diastole ventricular filling pressure in the aorta moves blood back towards ventricles, but it is stopped by the semilunar
valves.
o Dichrotic notch aortic valve closure produces a brief period of retrograde flow from aorta back to the valve, there
is a slight decrease in aortic P which creates this extra hump.
Loss of Elasticity in Arteries:
Systole the volume of blood equal to the entire stroke volume must flow through capillaries but, if no distension in
arteries:
o When arteries are rigid, none of the SV can be stored in the arteries, walls are not compliant.
Diastole flow through the capillaries stops during diastole rigid arteries cant recoil appreciably cant keep constant
flow intermittent flow results.
Low hydraulic filtering requires more energy.
Increased Energy requirement in a Rigid Conduit:
o More energy and O2 is required in a rigid (low hydraulic filter) system plastic tubing vs. native aorta.
Compliance
Compliance (C, capacitance) describes the volume of blood the vessel can hold at a given pressure.
o Compliance is related to distensibility.
o C = V/P
o Veins are the most compliant can hold the largest volume of blood at low pressure (unstressed volume)
o Arteries much lower compliance, hold much less blood and at higher pressures (stressed volume), most elastic.
o in compliance of veins causes redistribution of blood b/w veins (unstressed volume) and arteries (stressed
volume).
o Compliance of arteries as age walls become stiffer, less distensible, less compliant, hold less blood at any
given arterial pressure.
Elastance
Elastance is the tendency of arterial walls to recoil.
Elastance = P/ (D/D)
o D = max amount aorta distends, D = diameter
Elastance 1/Compliance (opposites).
Elastance is greatest in arteries, smallest in veins.
More elastic tissue leads to more elastic recoil.
Mean Arterial Pressure, Pa
Pulse pressure = Systolic pressure Diastolic pressure
o If all other factors are equal, magnitude of pulse pressure reflects Stroke Volume (volume of blood ejected from L
ventricle on a single beat)
o Largest pressure drop is at the level of the arterioles.
o Pressure greatest in aorta, and decreases steadily to veins (lowest pressure)
o Mean Pressure integral of Aortic P
Pa = Pd (diastolic P) + 1/3 Pulse Pressure
More weight is given to diastolic P because more time spent in this state.
Factors that Determine Arterial BP
Physiological Factors 1) CO (HR x SV), 2) Peripheral Resistance
Physical Factors Arterial blood volume, Arterial compliance
o Physiological factors modify physical ones, both modify arterial BP
1) Increasing CO increases BP
o If instantaneously, Q doubles CO (b/c SV and HR), but P hasnt yet.
o As reach steady-state, P to maintain constant flow
Recall: Q = P/R
o As CO, rate of in BP is lower in younger adults arteries are more distensible and more compliant.
2) Increasing Peripheral resistance increases BP
o If resistance in arterioles (by diameter), initial response is to flow, but get a build up of blood in the system, so
BP to push more blood through arteries and maintain constant flow therefore P.
Arterial Pulse pressure:
stroke volume
\
If nutrients are not needed, the sphincter will close, blood will go through the met arteriole and directly to the vein (it bypasses the
capillaries) this way you are conserving nutrients/ gases for the areas in which they are needed
In contrast, active tissues which are in need of nutrients/ gases, the precapillary sphincter will relax so blood will flow through it to the
capillaries
This system also regulates how much blood goes where
If youre older, there is less elasticity in the arterioles, they cannot vasodilate as much, which leads to decreased blood flow which
leads to an oxygen debt which can lead to pain
The capillaries still need pressure in order to move the blood forward
How can they withstand this pressure with just thin layer of endothelium?
Law of Laplace!
Tension = pressure times radius (P X r)
Bigger radius = bigger tension
Tension is how much force needs to be applied to make the wall split
(capillaries are small and so there is little tension as opposed to the aorta for example)
Ex) aneurysm diameter increases therefore tension increases, more prone to break
Pinocytosis, diffusion and filtration are the three methods used for exchange of nutrients
Field pores- aqueous holes in the endolthelial wall that allow exchange
Plasma proteins are usually relatively large and stay in the blood
Pinocytosis- is the movement of larger proteins through the use of vesicles out of the capillaries
Ions/glucose/ amino acids- pass through the water pores- diffusion based on concentration gradient
O2, CO2 (lipid soluble) can cross the endothelial wall
Flow limited diffusion- the more flow you have in one tissue, the more flow of blood
The more open capillaries= greater blood flow
He then drew a graph explaining how on the arteriolar side of the capillaries there is a high concentration of molecules
You will see a decrease in the concentration of small molecules in the capillaries as you go from arteriolar to venous side because most
of them are small enough to go into the tissues whereas the concentration of medium to large sized molecules will not decrease as
much as more of them will stay in the capillary
Also, notice that some cells are farther from the capillary than usual and this leads to edema because the molecules do not reach the
tissue cells and this leads to a build up of fluid in the interstitia
Endothelial lining has fenestrations where the endothelium is discontinuous
Fenestrations are bigger in kidney/intestine/liver, form= function!!
These organs are involved in filtration and absorption and thus need many fenestrations
In contrast, the brain has the blood brain barrier and thus has fewer fenestrations and a more continuous endothelium
Forces on capillaries
When resistance on the arteriolar side is reduced, pressure in the capillaries is increased and when vasodilation on the venous side
occurs pressure in the capillary is also increased, this leads to a pressure gradient in the capillaries which favors filtration
(so high pressure in the capillaries favors filtration)
Oncotic pressure- proteins in the capillaries exert oncotic pressure which moves water down its gradient into the capillaries
Filtration- bring fluid out of the capillaries
Absorption- bring water into the capillaries
Ex) kidneys you have mostly filtration and in liver you have mostly absorption
Albumin is important for maintaining protein concentrations in capillaries which is key for maintaining oncotic pressure, without
albumin, there is less movement of water into the capillaries and more risk for edema
Also, pressure increases on either arteriolar or venous side increases pressure in capillaries and this will increase filtration
Most of the fluid filtrated out is reabsorbed by the capillary
Whatever is not reabsorbed will move into lymphatic vessels and go back to the heart for recirculation
Lymphatic vessels have a thin cell lining, cells are not as tightly attached as in the endothelia, this makes lymphatic vessels more
permeable, when excess fluid exists it goes into the lymphatic vessels and then becomes lymph
Lymphatic vessels- unidirectional flow back to the heart because of the presence of valves
In cases of burns, permeability of the capillaries increase, fluid builds up in the interstitial space, lymphatic vessels are not working
properly and so they dont take up all the fluid properly
Decrease in the blood volume leads to a decrease in blood pressure
Less blood goes back to the heart which leads to decreased stroke volume and decreased cardiac output
The body responds by increasing heart rate/ BP
Two factors affecting venous return
Respiratory pump- in horizontal position, body is at atmospheric pressure but pressure in thorax is below that so you have a pressure
gradient in your body
Cardiac pump- opening of the ventricles functions as a suction cup and sucks in more blood from the atria and the veins therefore
increasing venous return
When you stand up, your blood pools at your feet and thus there is less blood going to your heart, your blood pressure will drop and so
your body responds by increasing the heart rate and BP
This sympathetic stimulation increases the pressure in the capillaries as well which we know will increase filtration which is what
leads to the swelling of ankles/ feet
CV #8- Special Circulations
Coronary circulation
The force that is actually used to propel blood compresses the coronary vasculature on the heart
itself, consequently:
Epicardial pressure (outside the cardiac muscle) < endocardial pressure (innermost layer)
When the heart is in systole (compression of heart muscle) endocardial blood flow drops to nearly zero
Flow increases during diastole as a result of local metabolite release (stimulated by O2 debt)
Myocardial oxygen balance flow chart (determinants of coronary perfusion)
Thus as metabolic demand increases coronary resistance decreases coronary perfusion increases
*Clinical tachycardia (rapid heart rate) decreases diastolic time period thus decreasing time for
coronary perfusion increased metabolic demand
*SAME THING OCCURS WITH INCREASED SYMPATHETIC INNERVATION*
Reaction Hyperemia
Basically clamping the coronary artery and upon release you get a corresponding increase in
perfusion to compensate for the blood flow lost during clamping
Local factors such as NO, Adenosine, and ATP sensitive K+ channels mitigate the response via
prolonging K+ effusion shorter plateau of AP
As always, diffusion of O2 is flow limited (depends on number of capillaries and open/closed state)
Clinical: transient ischemia can be temporarily compensated for in the body via collateral circulation
Skin Circulation
Has arterio-venous (A-V) shunts (aka metarterioles)
Properties of A-V shunts
Thick muscular walls
Under sympathetic not metabolic control
Notice that skeletal muscle exhibits both active intrinsic vasodilation and extrinsic vasoconstriction while
skin vessels exhibit only vasoconstriction (NO ACTIVE VASODILATION IN SKIN)
Cerebral Circulation
Regional blood flow is associated with regional neural activity
Little or no sympathetic influence
Local:
PaCO2 vasodilation across BBB
Acidic pH in CSF vasodilation
K+ seizure or hypoxia
Adenosine increased levels during seizure/hypoxia
Autoregulated between 60-160 mm Hg (but at this high pressure BBB is compromised)
Blood vessels in the brain exhibit reactive hyperemia
Gastrointestinal Circulation
25% of Cardiac Output to liver and 10% to SI
Control:
Sympathetic vasoconstriction
Local: metabolic
Adenosine: increases during arterial occlusion (enhances food absorption)
Gastrin/cholecystokinin increase blood flow during digestion
During congestive heart failure fluid accumulates in the right heart fluid from liver enter the abdominal
cavity
Fetal Circulation
Law of Laplace
Assumes shape of heart as a sphere to make conclusions about affect of geometry and tension on
pressure
P = 2HT
r
P: Pressure
H: Thickness (height)
T: Tension
r: radius
In words, the Law of Laplace for a sphere states that the greater the thickness of the wall of the
sphere (ie: the left ventricle), the greater the pressure that can be developed.
This is important in explaining why the left ventricular wall is thicker than the right ventricular wall
because the left ventricular wall must develop a greater pressure to eject blood.
It is also important in seeing the compensatory affect
Ventricular wall thickness will increase if the ventricle has to pimp against increased aortic pressure
(ie: hypertension).
Therefore, in systemic hypertension, the left ventricle will hypertrophy.
In pulmonary hypertension, the right ventricle hypertrophies.
Stroke Volume, Cardiac Output, and Ejection Fraction
1. Stroke Volume (SV)
Is the volume ejected from the ventricle on each beat.
Expressed by:
SV= EDV ESV
SV: Stroke Volume
EDV: End Diastolic Volume
ESV: End Systolic Volume
2. Cardiac Output (CO)
Expressed by:
CO = SV x HR
CO: Cardiac Output
SV: Stroke Volume
HR: Heart Rate
3. Ejection Fraction (EF)
Parameter
Heart Rate, HR
Stroke Volume, SV
Cardiac Output, CO
Arterial Pressure
Pulse Pressure
Total Peripheral Resistance, TPR
Arteriovenous 02 difference
Effect
(slightly)
(due to increased stroke volume)
(due to vasodilation of skeletal muscle beds)
(due to increased O2 consumption)
Frank-Starling Relationship
Describes the increase in SV and CO that occur in response to an increase in VR or EDV.
Is based on the length-tension relationship in the ventricle:
o EDV cause Ventricular fiber length, which produce Tension developed.
Is the mechanism that matches CO to VR; the greater the VR, the greater the CO.
Changes in contractility shift the Frank-Starling curve up (ed Contractility) or down (ed
Contractility).
Increases in contractility cause in increase in cardiac output for any level of right atrial
pressure or EDV.
Decreases in contractility cause a decrease in cardiac output for any level of right atrial
pressure or EDV.
Contractility
Is the intrinsic ability of cardiac muscle to develop force at a given muscle length.
Is also called inotropism.
Is related to intracellular [Ca2+].
Can be estimated by ejection fraction.
Positive inotropic agents produce increase in contractility.
Negative inotropic agents produce decrease in contractility.
What Causes Increase in Contractility? (aka What are Positive Inotropic Agents?)
1. Increased HR
When more action potentials occur/unit time, more Ca2+ enters the myocardial cells
during the AP plateaus, more Ca2+ is released from the SR, and greater tension is
produced during contraction.
Examples of Increased HR:
o Positive Staircase (Bowditch staircase): Increased HR increases the force of
contraction in a stepwise fashion as the intracellular [Ca2+] increases
cumulatively over several beats.
o Postextrasystolic Potentiation: The beat that occurs after an extrasystolic beat has
increased force contraction because extra Ca2+ entered the cells during the
extrasystole.
2. Sympathetic Stimulation
Sympathetic Stimulation is by catecholamines acting on 1 Receptors
Increases Contractility by Increasing the inward Ca2+ current during the plateau of
each cardiac AP.
Catecholamines (ie: Norepinephrine) act on GPCRs. This Activates Adenyl Cyclase, which
increases cAMP levels, which activate kinases (ie: PKA) to P-late enzymes (such as
Phospholamban).
Sympathetic Simulation also increases the activity of the Ca2+ pump of the SR; this
occurs by P-lation of Phospholamban.
As a result, more Ca2+ is accumulated by the SR, therefore more Ca2+ is available
for release in subsequent beats.
3. Cardiac Glycosides (digitalis)
Increase force of contraction by inhibiting the Na+/K+ ATPase in the myocardial cell
membrane.
As a result of this inhibition, intracellular [Na+] increases, diminishing Na+ gradient
across the cell membrane.
Na+-Ca2+ exchange (a mechanism that takes Ca2+ OUT of cell) depends on the size of
the Na+ gradient.
So, no Na+ gradients means no Ca2+ leaves the cell!
What Causes Decrease in Contractility? (aka What are Negative Inotropic Agents?)
1. Parasympathetic Stimulation
Parasympathetic Stimulation is by ACh acting on Muscarinic Receptors.
Decreases Contractility by Decreasing the inward Ca2+ current during the plateau of
each cardiac AP.
2. Decreases in pH (Acidosis), decreases force development and contractility.
NOTE: Vagal Effects predominate! There is quick on/off response of vagal effects and sympathetic affects
in absence of vagal are strong.
Indices of Contractility
1.) Peak Rate of Pressure Rise (dP/dt)
2.) Peak Aortic Flow Velocity (dV/dt)
3.) Ventricular Ejection Fraction (SV/EDV)
Excitation-Contraction Coupling: Cardiac vs. Skeletal
NOTE: this is from previous exam, for more detailed explanation see notes from EXAM1
Basically, in Cardiac CICR predominates and in Skeletal VICR predominates.
5) How do changes in myocardial contractility and blood volume produce a compensation in heart failure?
-
Inc preload inc vent filling, inc EDV, and inc end-diastolic P. but
NO CHANGE in afterload more forceful contraction inc
ejection P inc ejection fraction inc SV
Inc afterload = inc aortic P must develop greater P in vent to
overcome it inc ejection P, inc ESV, inc end-systolic P, dec
SV.
B/c aortic P is higher, valve will close sooner inc ESV and ESP dec SV
In the 2nd beat, the system will compensate towards a more normal SV at the expense of a higher EDV leading to inc
tension (T) on vent walls eventually causing vent hypertrophy and eventual dilated cardiomyopathy in the long term
(heart failure)
o Increasing symp stimulation of the heart leads to inc contractility inc vent P at any given EDV. There is a
decrease in vent P at any EDV with heart failure and the system compensates by increasing symp stim to return vent
pressure closer to normal.
Increased contractility inc endsystolic P inc SV dec ESV.
o On the 2nd beat, same endsystolic P as beat one dec EDV dec ESV returns SV to normal.
SLIDE 24: understand how diseases affect pressure volume loops.
With exercise, you get (inc venous return inc EDV) and also (inc contractility dec ESV). Both work together to
increase SV.
o
o
Contractility: Contractility is the intrinsic ability of cardiac muscle to develop force for a given muscle length.
An increase in Contractility = an elevated stroke volume at each End Diastolic Volume; and less End Diastolic Volume is required to
generate a given Stroke Volume (Top line of the graph)
Preload: Preload is the muscle length prior to contractility, and it is dependent on ventricular filling (or end diastolic volume.) This
value is related to right atrial pressure. The most important determining factor for preload is venous return.
An increase in Preload causes an increase in End Diastolic Volume and an increase in cardiac output. (he does not have a picture for
this in lecture)
Afterload: Afterload is the tension (or the arterial pressure) against which the ventricle must contract. If arterial pressure increases,
afterload also increases. Afterload for the left ventricle is determined by aortic pressure, afterload for the right ventricle is determined
by pulmonary artery pressure.
An increase in Afterload causes a reduced stroke volume at each End Diastolic Volume; and an elevated End Diastolic Volume to
achieve the same Stroke volume (bottom line of the graph.)
3. Calculate the Cardiac Output using the Fick Principle and determine the Cardiac Index
Fick Principle can be used to compute cardiac output (CO) indirectly from whole body oxygen consumption (VO 2) and the mixed
venous (O2ven) and arterial oxygen contents (O2art).
The principle states that the oxygen quantity delivered to the lungs in the pulmonary arteries plus the oxygen quantity added by the
lungs must equal the amount carried away from the lungs in the pulmonary veins.
CO =
VO2
_____________
(O2vein O2artery)
Pressure work is more expensive than volume work. This is measure by the oxygen consumption required by the heart to do each.
The energy requiremens for pressure work are higher than those of volume work. More O2 is consumed to develop pressure gradient
in the heart than is used to eject the blood in cardiac output
5. Use the Law of LaPlace to describe why a dilated heart has greater energy costs
A dilated heart is caused by Cardio Myopathy which causes the thinning of the ventricular walls and therefore a lager radius.
An increase in Radius and End Diastolic volume Increases Tension creating a higher demand for ATP therefore
demanding more O2
Meanwhile, a healthy heart has a comparatively smllaer radius and End Diastolic Volume which Lowers the tension, requires less ATP
and therefore less O2
Circulation and Cardiac Output: CV12
Venous P affect R. Ventricle filling affects CO (cardiac output)
If inc. VP (diff btn VC and peripheral venous pressure) from inc. R. Ventricle filling, inc. end diastolic volume inc. CO
Venous compliance has (-) affect on VP, b/c relaxation of smooth muscle inc. stretchability, which dec. VP
If inc. Venous return (inc. blood flow to central vein), then will inc. VP
o Venous SM contractility
o Inc. total BV (blood volume)
o Resp. movements will inc VP by dec. interthoracic pressure
o Skeletal muscle pump- compresses veins inc. blood flow b/c one way valves
o Gravity- from lying to standing, venous pooling less venous return
o Ventricular compliance (low) can inc. VP
o Atrial contractility inc. VP
HR when above 170 compromises time for vent. Filling, so (-) affect on VP
*Inc. CO dec. BV for next, so has (-) affect on VP
o if dec. CO, that inc. central VP or r. atrial pressure
o where CO = 0, that is the (Pmc) mean circulatory pressure (7mm Hg for normal)
where heart is stopped, all the pressures can equilibrate (identical). Pressures in veins = arteries, etc.
o Only two types of volumes in veins:
1) Unstressed- very little pressure being developed
2)Stressed- after 4L, each addition lead to rapid inc. in of pressure in veins
Observe changes in BV as it relates to central VP(venous pressure) see p.6
o If inc. BV curve shifts rightwhich inc. VPalso inc. Pmc (10.5)
venoconstriction
o If dec. BV curve shifts leftdec. VPalso dec. Pmc (5.2)
Venodilation
Pmc changes with changes in BV
o BV dec. (e.g. hemorrhage)- no change in unstressed volume, but dec. in stressed volume, dec. Pmc
o BV inc. (transfusion)- no change in unstressed volume, but inc. in stressed volume, inc. Pmc
o Venoconstriction dec. unstressed volume, inc. Pmc
o venodilation(syncope/blood pooling) inc unstressed volume, dec. Pmc
this is the same with change from going to reclining to standing position quickly-venous poolingdec.
Pmc
Sympathetic stimulation and Vascular Fxn
o If inc. TPR (art. constriction) shift left, dec. CVP, no change Pmc
o If dec. TPR (art. dilation) shift right, inc. CVP, no change Pmc
Cardiac fxn curve- (looks at VP affect on CVP)
o Inc. CVP inc. CO
Vascular fxn curve (looks at CO affect on CVP)
o Inc. CO dec. CVP, see slide 13!
Interaction of both curves Cardiovascular Operating point- where at equilibrium. Tries to reestablish equilibrium.
o Symp. Stimulationinc contractinc COdec. CVP
o Hemorrhage dec. BVdec COdec CVP
Response to hemorrhage:
1)inc. symp. Stimulationinc HR, contractility, CO
2)venosonstrictinc. Pmc, inc. CVP
3)vasoconstrictinc TPRinc CO
Inc. in MAP (mean art. pressure) dec. CO (because aortic valve cant open)
o Inc. in TPR (hypertension)inc. MAP (or afterload)dec. CO, no change Pmc
Will always get a dec. CO, but CVP can dec/inc.
Heart Failuredec. contractilitycurve to rightdec. CO
o Response: inc. BVby retention of fluid (hypervolemia)inc. CVP, Pmc. The compromise to get back to normal
CO is the inc. in CVP!!!
o Severe is more dec. in CO, and more inc. in CVP. CO is not normal, so there is more pressure to inc. BV
furtherleads to peripheral edema
On flip side, if can inc. symp. stimulation of veinsinc CO = Cardiac Reserve
o Happens in exercise inc. symp, and inc. HR