Download Transcripts/4_15 2

S3: Cardiology 2:00-3:00
Scribe: Sally Hamissou
Wednesday, April 15, 2009
Proof: Meagan Jarrell
Dr. Parks
Cardiology
Page 1 of 6
Abbreviations: CO = Cardiac Output, CI = Cardiac Index, SV = Stroke Volume, HR = Heart Rate, EDV = End
Diastolic Volume, EF = Ejection Fraction, VR = Venous Return, RAP = Right Atrial Pressure
I. Cardio Output [S1]
a. Concept
II. Objectives [S2]
a. Know functions of veins and how their structural and mechanical properties aid in these functions.
b. Understand the mechanisms by which blood is propelled back to the heart.
c. Understand physiological importance of central venous pressure and factors affecting it.
d. Know why venous pressure is major determinant of cardiac output.
e. Understand the difference between cardiac and vascular function curves
III. Objectives Continued [S3]
a. Understand relative contribution of arterial and venous capacitance to changes in blood volume
b. Understand why CO is determined by inter-section of cardiac and vascular function curves
c. Know effects of contractility, blood volume, venous tone and arteriolar tone on CO and VR
d. Know relationship between HR and CO and basic parameters
e. Know the effects of cardiac imbalance on central venous pressure and the physiological and pathological
consequences
IV. The Cardiovascular System [S4]
a. Systemic Circuit
i. There is a high pressure and low pressure systems, the heart pumps out blood into a capillary network
which comes back to the heart.
ii. It is a closed network
b. Pulmonary circuit
i. Has high and low pressure systems
c. Comprised of High and Low Pressure Systems
d. Most of blood volume contained in venous system this is important
e. Most of vascular resistance in small arteries and arterioles
V. Cardiac Output [S5]
a. Amount of blood pumped out by the heart, into the aortic arch by the heart each minute
VI. Average Cardiac Output [S6]
a. Men ~ 5.6 liters/min
b. Women ~ 10-20% less
c. Based on size
d. How much heart is pumping out, in terms of blood, in one minute
VII. Cardiac Index CI [S7]
a. CO varies by body size and is not corrected for that
b. CI is used to correct the body surface area and size, important for anesthetics. You need the give the right dose
to the person, especially in overweight people
c. CI=CO per sq. meter body surface are
d. Average 70 kg man has 1.7 sq. meter surface area
e. Average CI ~3 L/sq. meter
VIII. Stroke Volume [S8]
a. The difference between EDV and ESV = SV
b. End Diastolic Volume – volume in ventricle before ejection. The heart is filled up, at the end of diastole, fully
relaxed and full of maximum amount of blood.
c. End Systolic Volume – volume in ventricle after ejection, when it is contracted and pushed all of the blood out,
left over after systolic ejection
d. The difference between the maximum and the minimum is the SV
IX. Stroke Volume [S9]
a. Heart pumps intermittently ~ 72 bpm
b. Stroke Volume = vol. of blood ejected per beat
c. CO = all stroke volumes ejected over one minute, factor of 72
d. CO = HR x SV
e. Anything the changes HR or SV will change CO
X. Ejection Fraction [S10]
a. Ejection Fraction= fraction of the EDV ejected in one stroke
b. Every stroke is the percent how efficient the heart is pumping out the blood
c. Typically, EF = 0.55 or 55% is normal, that is the percent of blood that is being ejected with every SV
S3: Cardiology 2:00-3:00
Scribe: Sally Hamissou
Wednesday, April 15, 2009
Proof: Meagan Jarrell
Dr. Parks
Cardiology
Page 2 of 6
d. Indicator of Contractility (Ventricular Efficiency) better the pump, the more that it will eject. The more poorly the
pump is, the less it will eject.
e. If the EF fails, the heart fails, it fails as a pump and as it does that the EF goes down to a point where you can’t
keep up with the needs of the body.
f. EF = SV/EDV
g. Overall: EF is indicator of efficiency
XI. Contractility [S11]
a. Ability of heart to eject
b. Intrinsic ability of myocardial cells to develop force at given muscle length and they contract
c. Correlates with Intracellular Ca2+ concentration, higher the calcium the more effective the pump
d. How effective is contractility
XII. Figure [S12]
a. Vascular component and the heart itself
b. Pressure gradient, from high P to low P (down the gradient) the gradient will push blood down the vascular
component
c. On the venous side to the heart where it dumps into the heart
d. In the heart, there is a system that must overcome the aortic P, so you must eject beyond the resistance. It is
opposing the heart, ejecting blood, and this is the force that drives the blood towards the heart
XIII. Systolic and diastolic left ventricular pressure-volume curves [S13]
a. Systolic curve
i. Shows active pressure as a function of end-diastolic volume (fiber length). Look at the fiber length and how
it forces blood out of the chamber.
ii. All active forces. As you start to increase the volume (P) to a point, there is a certain maximum efficiency
(you are putting/stretching the blood out). Maximal overlap of fibers, and you get to a point where there is a
cross bridge, overlap is not optimal and you start to lose force. That is the relationship.
b. Diastolic curve
i. Shows passive pressure as a function of end-diastolic volume
ii. If you put blood into the chamber, it stretches because of the volume increases. The more you stretch it
passively, the more ventricular pressure you will see.
c. Figure 4-21 Systolic and diastolic left ventricular pressure-volume curves. The systolic curve shows active
pressure as a function of end-diastolic volume (fiber length). The diastolic curve shows passive pressure as a
function of end-diastolic volume.
XIV.
Preload vs AfterloadS14]
a. Preload
i. What pushes things to the heart
ii. Pushes the blood into the heart and is “priming the pump”
iii. Capitance Vessels
b. Afterload
i. What opposes the blood coming out of the heart, usually the arterioles
ii. Heart
iii. Resistance Vessels
XV. Stroke Volume [S15]
a. SV depends on how much volume is there, ejected per beat. Whatever feeds blood back into the chamber is
going to help, the more blood back into the chamber, the more you can pump.
b. EDV- the more you have loaded into chamber, the higher the SV.
c. If you have to pump against resistance, there is another effect on SV because something has to pump against
the gradient is greatest when the pressure is high on one side and low on the other side, and it starts to raise
where it is equal, and there is no flow, which is the afterload
d. Ionotropic is a pump effect and that’s going to effect this as well. How effective it is.
e. This determines SV and the basic parameters.
XVI.
Regulation of heart rate: Sympathetic [S16]
a. Can see a different pattern of HR because of the sympathetic nervous system (the curve in light blue)
b. Sympathetic nerves release norepinephrine
c. Changes rhythm at SA node to increase HR
d. Increases HR = tachycardia
XVII. Regulation of heart rate: Parasympathetic [S17]
a. The parasympathetic system is the opposite now your beat from here to here slows down, less active HR
b. Vagus releases ACh
c. Acts on muscarinic receptors on sinoatrial (SA) node
S3: Cardiology 2:00-3:00
Scribe: Sally Hamissou
Wednesday, April 15, 2009
Proof: Meagan Jarrell
Dr. Parks
Cardiology
Page 3 of 6
d. Decreases heart rate = bradycardia
XVIII. Effect of sympathetic and parasympathetic stimulation on HR [S18]
a. This is a summary from slides [16, 17]
b. Sympathetic- sympathetic stimulation increases the HR
c. Parasympathetic- parasympathetic stimulation decreases the HR
d. Normal- normal firing pattern of the SA node
e. Figure 4-16 Effect of sympathetic and parasympathetic stimulation on the SA node action potential. A, The
normal firing pattern of the SA node is shown. B, Sympathetic stimulation increases the rate of phase 4
depolarization and increases the frequency of action potentials. C, Parasympathetic stimulation decreases the
rate of phase 4 depolarization and hyperpolarizes the maximum diastolic potential to decrease the frequency of
action potentials.
XIX.
CO Flow Chart [S19]
a. These are the parameters that determine CO
b. CO = SV X HR
i. Things that effect HR means more ejections per minute
ii. SV- how much is pumping out per beat.
c. What determines those two things?
i. SV is more blood it gets, the more it pumps. Venous return (blood back to heart). So more blood in it, it will
have more coming out of it
ii. HR- the faster it beats, the more it will eject per minute. It is effected by sympathetic and parasympathetic
nervous system, and VR is affected by this as well.
d. Both of these factors will determine CO.
XX. Frank Starling’s Law of the Heart [S20]
a. Within physiologic limits, heart pumps all the blood that comes into it. The more blood that comes into it, the
more it pumps
b. The more you stretch the heart, the more powerful the force to oppose it, the more that is ejected
c. When increased volumes of blood enter the heart, chamber walls stretch. Cardiac muscle contracts with greater
force to empty chamber.
d. All extra blood is automatically pumped into the aorta and into the systemic circulation.
XXI.
Starling’s Law of the Heart [S21]
a. If VR increases, stroke volume (SV) increases; if VR decreases, SV decreases.
b. Remember that SV directly affects CO (CO=SV*HR)
i. VR is important and determines SV and CO. As VR increases, SV increases
XXII. Frank Starling Law of the Heart [S22]
a. Control Line
i. Dark line is the normal and at the bottom should be: EDV curve (x) and cardiac output (y).
ii. As you get higher on the curve, CO increases as you get more volume. There are ways to increase or
decrease the volume by ionotropics. You can shift the curve up or down depending on what happens in the
heart. The less effective pump, the less that is ejected and the more effective pump, the more that is
ejected.
b. The heart length relationship is related to the volume, how much it is stretched
XXIII. Venous Return [S23]
a. Quantity of blood flowing from the veins into the right atrium each minute
b. At equilibrium VR = CO
XXIV. Mechanisms to Maintain Venous Return [S24]
a. One way valves
i. Valves in the veins prevent backflow of blood and direct it towards the heart, helps VR
b. Muscle pump
i. Veins are between skeletal muscle layers which contract and relax to help squeeze blood back towards
heart.
c. Respiratory pump
i. Same effect in pulmonary cavity
ii. During exercise, breathing becomes deeper and/or faster, which causes pressure changes in the thorax
and abdomen. This increases the pressure in the abdomen, squeezing the large veins in that area and
forcing the blood back to the heart.
d. Smooth muscle
i. Contraction and relaxation of smooth muscle in the middle layer of the vein walls also helps to push blood
towards heart.
e. Gravity
S3: Cardiology 2:00-3:00
Scribe: Sally Hamissou
Wednesday, April 15, 2009
Proof: Meagan Jarrell
Dr. Parks
Cardiology
Page 4 of 6
i. Blood from upper body is aided by gravity as it descends to heart.
ii. It determines where the blood goes.
XXV. Factors Aiding Venous Return [S25]
a. Muscular part is constricting the vessel and propelling it back up beyond the valves.
b. VR is assisted by the pumps
c. Venous return is aided by:
i. Respiratory pump
1. Pressure changes created during breathing suck blood toward the heart by squeezing local veins
ii. Muscular pump
1. Contraction of skeletal muscles “milk” blood toward the heart
d. Valves prevent backflow during venous return
XXVI. Left and Right Heart in Series [S26]
a. VR coming into the heart, CO out of the heart, the two must be the same
b. If right heart is different by 1 ml per beat in 60 minutes, can get 6 mL to the lung in 90 minutes, so it must be
regulated precisely. If you get fluid in the lung, you can get heart failure.
XXVII. Determinants of cardiac output [S27] ROS
a. 4 factors:
i. Preload- Initial stretching of the cardiac myocytes prior to contraction (related to sarcomere length)
ii. Afterload- load that the heart must eject blood against (related to aortic pressure). Force that stops heart
from pushing out the blood.
iii. Contractility- Inherent ability of myocardial cells to develop force at given muscle lengths (related to
Calcium). How effective the heart is at pumping.
iv. HR- controlled by autonomic nervous system and how fast the heart beats
XXVIII. Factors Determining RV Preload [S28]
a. Contractility, compliance, venous pressure, HR (can oppose it)
XXIX. Determinants of Cardiac Output [S29-30]
a. Other coupling and cardiac factors
b. HR and contractility determined by the heart itself
c. CO is affected by the resistance in the periphery by a force and an opposing force (P gradients)
XXX. CO Equation [31]
a. CO = arterial pressure / total peripheral resistance
XXXI. Low Cardiac Output [S32]
a. Cardiac Factors
i. Severe myocardial infarction
ii. Valvular heart disease
iii. Cardiac tamponade (which is blood outside the heart itself)
iv. Myocarditis
b. Vascular Factors
i. Decreased blood volume
ii. Acute venous dilatation like a massive response in an allergic reaction
iii. Obstruction of the large veins (seen in pregnancy)
XXXII. Cardiac Output Curves [S33]
a. Three basic factors determine the characteristics of the CO curve
i. Effectiveness of the heart as a pump (contractility)
ii. HR
iii. Extracardiac pressure
XXXIII. Cardiac Output Curves [S34]
a. Based on Frank Starling Relationship for the left ventricle
b. Cardiac Output equals Venous Return
c. Right Atrial Pressure related to:
i. Venous return (how much blood gets back)
ii. EDV (at end of diastole)
iii. ED fiber length
d. When RAP = +4 mmHg, CO can not keep up with VR and cardiac function plateaus. It is effective to a point
then to after a point/plateau there is a flattening of the curve
XXXIV. Effect of stressed volume on mean systemic pressure [S35]
a. Unstressed Volume
i. Blood and veins (about 4 liters) no increase in pressure in periphery, so no BP. If you go beyond the 4
liters, you get an increase in BP.
S3: Cardiology 2:00-3:00
Scribe: Sally Hamissou
Wednesday, April 15, 2009
Proof: Meagan Jarrell
Dr. Parks
Cardiology
Page 5 of 6
b. Stressed Volume
c. If you measure at this point (5 or 6 liters) it is 7 mmHg is mean systemic pressure. At this level there is a certain
passive pressure that is determined by the total BV.
d. Figure 4-27 Effect of changes in stressed volume on mean systemic pressure. Total blood volume is the sum of
unstressed volume (in the veins) and stressed volume (in the arteries). Increases in stressed volume produce
increases in mean systemic pressure.
XXXV. Mean Systemic Filling Pressure [S36]
a. Heart, arterial side, venous side, arterioles
b. Pa (arterial P) = Pv (venous P)
c. At equilibrium- 7 mm Hg (all the way around) due to filling of blood itself, the vessel, determined by arteriole side
XXXVI. Venous and Arterial Compliance [S37-38]
a. Start at 7, turn pump on and the pressure increases, when you start to pull the blood out of the system and back
into the heart it goes back to the venous.
b. Arterial pressure, Pa= 7, Pa= 26, Pa= 102 determines the pressure
c. Venous pressure- Pv= 7, Pv= 6, Pv= 2 pressure before the heart.
XXXVII. Venous Return Curve [S39]
a. Used to look at CO in terms of how it relates to RAP to VR.
b. As you decrease RAP (more negative), you increase the amount of VR.
c. The RAP (in the heart) is the force opposing the blood coming to the heart. If the pressure is low and high, the
flow is going to go easily in the heart because the gradient is greater, so the flow will be greater. You start to get
to a point of negative pressure.
d. Negative pressure- BV collapses because of the negative pressure due to thin vessels (veins).
e. RAP is characterized by down slope, transition, and plateau.
f. Psf is pressure in systemic circulation when all BF stopped
g. Pressure that forces systemic blood back to heart
h. Determined by Psf and resistance to BF
XXXVIII.
Cardiac and Vascular Function Curves [S40]
a. P1 is high and P2 is low, if too high it will oppose the flow. Vessel component and then the heart component.
b. If P2 is so low, it will suck the pressure (BV will collapse) to the plateau.
XXXIX. Ionotropic Effects [S41]
a. Vascular function and cardiac function- vessel component and cardiac component, graphs go in opposite
directions.
b. As you increase RAP, you increase the CO. RAP is on the other side of the heart and the force that pushes
blood into the ventricle, getting ejected. The more blood it gets, the more it will eject. More blood goes higher
and higher until you reach another plateau.
c. Why does this happen? Because as VR decreases, and there is nothing more to be pumped, the heart can’t
pump out anymore blood and that is your maximum (9ml/min). Can’t keep up with the VR and can’t keep up
with CO.
d. Figure 4-28 Effects of positive ionotropic agents (A) and negative ionotropic agents (B) on the cardiac and
vascular function curves. The solid lines show the normal relationships, and the dashed lines show changes.
The circle intersecting the dashed line shows the new steady state operating point
XL. Mechanisms of the positive ionotropic effect of cardiac glycosides [S42 & 41]
a. Cardiac glycosides are positive and negative ionotropic agents.
b. Point of graph: an agent that is poisonous, effects Na, which effects the transport system which depends on Ca
and Na (co-transporter), so get an increases in Ca and contractility depends on intracellular calcium, effects the
pump
c. These drugs can have affects of ionotropic (positive or negative)
d. Contractility is effectiveness of the pump. A failing heart that is not ejecting well, these drugs will cause it to
pump more forcefully and effectively.
e. Positive or negative ionontropic agent. Venous curve is not affected, because you are only changing the heart
function and doesn’t affect the vasculature, so only affects the cardiac function curve.
f. Positive ionotropic shifts it upward, CO increased for any given pressure, more effective as a pump. Increased
CO, the delta, on the graph is the difference
g. Negative ionotropic agent- the heart is not effective, not ejecting as much blood as before
XLI.
Effects of Changes in Blood Volume [S43]
a. The venous side
b. Curve same as CO, change blood volume (determines how much gets to the heart). Preloading phenomenonmore it has in the heart, more in VR, more it can eject
S3: Cardiology 2:00-3:00
Scribe: Sally Hamissou
Wednesday, April 15, 2009
Proof: Meagan Jarrell
Dr. Parks
Cardiology
Page 6 of 6
c. At 7, it is at equilibrium, if you decrease the RAP it will increase to a point and at forces equal to RAP the
vascular forces collapse.
d. If you go from 7-10, you get more blood volume, no change in resistance, the vascular curve increases the CO
and VR. Transfusion reaction can increase that.
e. Taking blood back out (hemorrhage curve): The normal red curve pressure at 4, if you lose blood volume, you
won’t pump out the blood, and that is a problem. You can give a transfusion reaction, which can increase the
CO because the vascular curve increases (they are parallel).
XLII.
Effects of Total Peripheral Resistance [S44]
a. Peripheral resistance in the arterioles
b. Increase TPR: down stream putting a resistor there, the heart has to work harder to eject blood and have less
CO because it has to go against a higher pressure, with resistance it has to pump harder and loses some CO as
a result
c. If you take away the peripheral resistance, it is more effective, and it shifts graph in the other direction by
decreasing peripheral resistance
d. Now you can see a change in the other curve too because we are changing something else and the blood
volume can now get to the heart so VR is paralleling it and it starts to fall. The resistance can affect both the
vascular and the cardiac curve
XLIII. Arterial Pressure Curve [S45]
a. Different examples that can cause this
b. Can see normal arterial pressure
c. What changes CO? Certain conditions can change it: physiological conditions- pulmonary disease and anemia
it changes resistance and CO
d. There are a lot of physiological conditions that can determine this and affect it
XLIV. End Lecture [S46]***Dr. Parks briefly went back over and made comments on a few of the graphs**
a. [44] this is the hardest to measure physiologically, because parameters are changing and affecting each other
[45] diseases can change it
b. [End 33:48]