1
Jay Hoying, 626-5273
LSN Rm. 356
CARDIAC PUMP:
1. Define the cardiac cycle; Wiggers Diagram.
2. Describe the Frank-Starling Relationship and pressure volume loops.
3. Describe the affects of pre-load and after-load on heart performance.
Tortora and Grabowski (11th edition):
Berne & Levy (5th edition):
Boron & Boulpaep:
pp 716 - 719
pp 305- 321
pp 508-513, 522-524
Topic Outline:
I. Pressurization of blood
A) Blood moves through the CV system down a pressure gradient.
1. Heart, in coordination with heart valves, serves to "pressurize" blood
right ventricle acts as a bellows
left ventricle acts through a "twisting squeeze"
II. Cardiac cycle
A) Systole
1. active force-generation phase
a) coordinated electrical activation of myocytes
b) emptying phase of heart
2. End Systolic Volume (ESV)
B) Diastole
1. passive phase
a) no contraction (although there may be heart wall tension)
b) filling phase of heart
2. End Diastolic Volume (EDV)
C) Valve activity
1. atrial-ventricular valves
a) Mitral: left side
b) Tri-cuspid: right side
2. semilunar valves (ventricle-to vessel)
a) aortic valve
b) pulmonary valve
3. valves open and close due to pressure differences on either side of valve
II. Wigger's Diagram
A) Diagrams volume, pressure, and electrical activities during the cardiac cycle
1. coordinates the many different events
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Jay Hoying, 626-5273
LSN Rm. 356
B) Isovolumic relaxation and contraction
1. changes in heart wall tension and chamber pressure without a change in volume
a) diastole: ventricle relaxes
b) systole: heart contracts
2. all valves are closed
C) Know this diagram
II. Frank-Starling relationship: contractility
A) as heart muscle (myocardium) is stretched, it is able to generate more force per
contraction
1. positions the contractile machinery of the muscle (sarcomere) to be more
effective for a given contraction.
2. the forces acting to stretch the muscle, filling pressure and atrial contraction,
are called preload.
a) sets the "contractile state" of the muscle
3. more stretching leads to greater pressure generation
B) Pressure-volume relationship: P-V loop
1. in the case of the heart, the volume of the ventricle chamber is analogous to
length
a) e.g. as blood fills the chamber, it's volume increases as the ventricle
wall stretches–leading to an increase in myocyte length.
b) therefore, as volume changes, the heart changes it's ability to contract
according to the Frank-Starling relationship.
2. in the case of the heart, the pressure is analogous to the tension generated
a) contraction of myocytes, which generates tension, leads to increases in
chamber pressure
b) the forces acting against the heart, primarily arterial and chamber
pressures, during contraction defines the afterload.
3. Summary: as ventricle chamber volume changes, then the intrinsic pressure
generated by the heart changes accordingly
a) is defined by the pressure-volume relationship
b) changes in pressure versus volume during one cardiac cycle is a
pressure-volume or P-V loop
3
Jay Hoying, 626-5273
LSN Rm. 356
CARDIAC OUTPUT:
1. Define cardiac output, stroke volume and venous return.
2. List the effects of the autonomic nervous system on cardiac output.
3. Describe the mechanisms of cardiac output regulation.
Tortora and Grabowski (11th edition):
Berne & Levy (5th edition):
Boron & Boulpaep:
pp 683-687
pp 379-383, 387-399
pp 428 - 430, 547 - 557
Topic Outline:
I. Cardiac Output
A) Cardiac Output is the blood pumped by each ventricle per minute
1. Cardiac Output = Stroke Volume X Heart Rate:
CO = SV X HR
a) CO is in L/min
b) SV is in L/beat
c) HR is in beat/min
II. Stroke Volume
A) volume of blood ejected from ventricle after systole
1. Stroke Volume = End Diastolic Volume - End Systolic Volume: SV = EDV ESV
a) SV is in L/beat
b) EDV is in L/beat
c) ESV is in L/beat
B) Effectors of stroke volume
1. on End Diastolic Volume (EDV)
a) venous return
1. volume of blood returning to heart to fill the ventricle
b) heart rate
1. time of filling of ventricle with blood before ventricle contracts
a) an increase in heart rate results in less time between
ventricular contractions
2. on End Systolic Volume (ESV)
a) ventricle muscle contractility
1. strength of contraction of the ventricle walls can determine the
volume of blood ejected
a) depends upon intracellular Ca++ levels
b) Starling's Law
1. relationship between the volume of ventricle and force of
contraction
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Jay Hoying, 626-5273
LSN Rm. 356
2. analogous to skeletal muscle length-tension relationship
3. effect of venous return on this relationship
a) preload
4. principle governing balance between preload and afterload
c) Total Peripheral Resistance (TPR)
1. the resistance of the systemic circulation the heart must work
against to eject the blood
a) termed afterload
III. Autonomic regulation
A) Parasympathetic
1. uses acetylcholine as transmitter
2. innervates primarily the SA node, AV node and atria
a) minor innervation in ventricle muscle
3. general activity is to decrease cardiac function
a) decrease heart rate
B) Sympathetic
1. uses norepinephrine as transmitter
2. innervates primarily the ventricular muscle
a) minor innervation in nodes and atria
3. general activity is to increase cardiac function
a) increase contractility
IV. Regulation of Cardiac Output
A) Increase in cardiac output
1. increase in venous return
a) Starling's Law
b) increase EDV
2. increase in heart rate
a) decrease parasympathetic flow
b) increase sympathetic flow (minor)
3. increase in contractility
a) increase in sympathetic flow
b) decrease in parasympathetic flow (minor)
B) Decrease in cardiac output
1. decrease in venous return
2. decrease in heart rate
a) increase in parasympathetic flow
3. decrease in contractility
a) decrease in sympathetic flow
PERIPHERAL CIRCULATION:
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Jay Hoying, 626-5273
LSN Rm. 356
1. Describe the relationship between cardiac output, total peripheral resistance and mean
arterial pressure.
2. Describe the baroreceptor reflex and its effects on mean arterial pressure.
3. Describe the mechanisms which regulate total peripheral resistance.
4. Describe the role of blood volume in determining mean arterial pressure.
Tortora and Grabowski:
Boron & Boupaep:
pp 718-721, 697-702, 705-717
pp 513-518, 547 - 557, 477 - 481
Topic Outline:
I. Mean Arterial Pressure
A) Main variable of cardiovascular system that is regulated
1. driving force for perfusion through organs
B) Difference in pressures between the aorta and vena cava = Flow X Resistance: ªP =
cardiac output X vascular resistance
1. ªP = mean arterial pressure
a) vena cava pressure near zero
b) mean aortic pressure . mean pressure of major arteries
1. low resistance to flow in large arteries
C) Mean Arterial Pressure = Cardiac Output X Total Peripheral Resistance: MAP = CO
X TPR
II. Total Peripheral Resistance
A) the sum resistance to blood flow offered by the systemic vascular system
1. usually see differences in resistance between the various vascular beds
B) vasoconstriction/vasodilation
1. differences in resistance of vascular beds due primarily due to the diameter of
the arterioles
a) arterioles are the small vessels immediately preceding the capillary beds
b) called "resistance vessels"
2. high ratio of smooth muscle cells to vessel diameter
3. innervated with sympathetic system
a) increase sympathetic activity to arterioles 6 smooth muscle cell
constriction 6 vasoconstriction 6 increase in vascular resistance to
flow
4. effectors
a) sympathetic nervous system
b) humoral agents
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Jay Hoying, 626-5273
LSN Rm. 356
1. epinephrine
c) metabolites
1. pH, CO2, adenosine
d) endothelial cells
1. endothelin, EDRF
C) Effects on Mean Arterial Pressure
1. vasoconstriction (reducing vessel diameter) will increase arterial pressure with
a constant flow (ie. cardiac output)
2. vasodilation (increasing vessel diameter) will decrease arterial pressure with a
constant flow (ie. cardiac output)
III. Regulation of Pressure
A) Arterial Baroreceptors
1. nerve endings located in walls of arteries
a) carotid sinus (before the brain)
b) aortic arch (immediately after the heart)
2. are in reality mechanoreceptors
a) sense stretch of arterial wall in response to pressure
3. stimulation of baroreceptors occurs in response to increases in pressure
a) send impulses to the medullary center in the brain
4. physiological result of baroreceptor activity is a to lower mean arterial
pressure
a) increase in BR activity leads to decrease in sympathetic activity
1. decrease in heart rate--9 in cardiac output
2. decrease in heart contractility--9 in cardiac output
3. vasodilation of arterioles--9 resistance
5. short term regulation
1. rapid response to arterial pressure changes
2. adapt to a new steady state pressure
B) Blood Volume
1. Volume of blood within the cardiovascular system
a) changes in blood volume usually due to changes in water content of the
plasma portion of the blood
1. an exception would be hemhorrage
2. Affects mean arterial pressure by determining venous pressure 6 venous return
6 end diastolic volume 6 stroke volume 6 cardiac output
3. long term response to arterial pressure changes
a) involves coordination with the kidney
ENDOTHELIUM and MICROVASCULAR EXCHANGE:
1. Describe the endothelial cell and its biology.
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Jay Hoying, 626-5273
LSN Rm. 356
2. Describe endothelium-dependent physiology.
3. Describe the mechanisms which regulate microvascular exchange.
Tortora and Grabowski:
Boron & Boupaep:
pp 703-705
pp 464-476
Topic Outline:
I. Endothelium
A) Blood vessels, heart chambers, valves, lymphatics
1. Blood (lymph):tissue interface
2. large vessel vs. microvessel
B) Heterogeneous
1. Continuous, discontinuous, fenestrated
a) organ specific
1. muscle vs liver vs gut
b) function specific
1. exchange, coagulation, biochemistry
2. different cellular markers
C) Function
1. vasoregulation
a) EC-derived relaxing and contracting factors
1. nitric oxide
2. Angiogenesis
a) tissue perfusion
b) vascular architecture
3. Coagulation
a) surface for blood biochemistry
b) synthesizes coagulation/thrombosis factors
4. Inflammation/Immunity
a) blood cell adhesion and diapedesis
b) synthesize/respond to inflammation mediators
1. nitric oxide, prostaglandins, TNFα
c) antigen presentation
II. Microvascular exchange
A) solute exchange
1. diffusion
a) capillary permeability
b) modified Fick’s Law: passive movement of solutes
1. J = -PS(Co-Ci)
2. transport
a) convection
b) vesicular system
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B) water exchange
1. filtration
a) hydrostatic pressure
b) oncotic pressure
1. π = σRT(Ci-Co)
2. Starling hypothesis
a) Qf = k[(Pc+πif)-(Pif + πc)]
Jay Hoying, 626-5273
LSN Rm. 356
9
Jay Hoying, 626-5273
LSN Rm. 356
CARDIOVASCULAR DISEASE:
1. Define ischemia and its relationship to a "heart attack".
2. Describe the main contributing factor to a "heart attack" and the physiological basis for
the various treatment regimes that are used.
Topic Outline:
Myocardial Infarction ("Heart Attack")
A) Coronary Circulation
1. heart perfused by left and right coronary arteries
a) originate from aorta immediately downstream to the aortic valve
2. heart highly vascularized
B) Ischemia
1. lack of (or unacceptably low) blood flow to a tissue
2. result is poor oxygen delivery to the tissue
a) if too severe, cell dysfunction or death occurs
b) since heart is a muscle, contractility is directly compromised due to the
lack of ATP generation
3. usually occurs as a result of an obstruction in the vessel
a) increase in resistance to flow
C) Coronary Obstruction
1. Atherosclerosis
a) chronic decrease in vessel lumen diameter
b) due to thickening of vessel wall into the vessel interior
1. smooth muscle cells
2. lipid accumulation
2. Clot formation
a) blood clots that may get trapped in the coronary circulation
b) can complicate a situation in which a coronary vessel is already
compromised (ie. atherosclerosis)
D) "Heart Attack"
1. cardiac myocyte death
a) lack of oxygen
b) build up of toxic metabolites
2. fibrillation
a) unorganized electrical activation of the heart
1. various parts of the heart are not activated in proper sequence
2. numerous, chaotic contractions
b) improper action potential conduction through the heart
10
Jay Hoying, 626-5273
LSN Rm. 356
1. a dead or compromised myocyte cannot conduct an action
potential
a) imbalanced membrane permeabilities
b) uncoupling of gap junctions
3. blood not pumped
a) damaged cardiac myocytes cannot contract and therefore cannot pump
blood
b) unorganized activation translates into out of sequence contraction
1. blood is not pumped since myocytes of the ventricle are not
contracting in unison
E) Treatment
1. vasodilators
a) dilate coronary vessels permitting an increased flow to the heart tissues
b) decrease in afterload
1. vasodilation of systemic vessels
2. sympathetic nerve blockers (ie. "beta-blockers")
a) decrease oxygen demands of the heart
1. heart is dominated by parasympathetic control
a) lower heart rate
b) lower contractility
3. calcium-channel blockers
a) reduces oxygen demand of heart
1. heart contracts less vigorously
b) reduces afterload
4. coronary artery repair
a) coronary angioplasty
b) coronary bypass