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262 Cards in this Set
- Front
- Back
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What is the relationship between the cardiac outputs of the left and right sides of the heart?
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They are equal
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Which sides of the heart are responsible for which circulations?
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Left heart: systemic circulation
Right heart: pulmonary circulation |
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What is the course of blood flow?
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Left atrium
Left ventricle (mitral valve) Aorta (aortic valve) Systemic arteries and tissues Systemic veins Vena cava Right atrium Right ventricle (tricuspid valve) Pulmonary artery (pulmonic valve) Lungs Pulmonary vein |
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What is the function of the arteries?
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Deliver oxygenated blood to the tissues under high pressure
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What types of walls do arteries have?
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Thick walls, with extensive elastic tissue and smooth muscle
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What is the "stressed volume?"
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The volume of blood contained in the arteries
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What are the smallest branches of the arteries?
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Arterioles
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What is the site of highest resistance in the cardiovascular system?
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Arterioles
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Describe the important features of the arteriolar walls
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Smooth muscle is extensively innervated by the ANS
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What types of adrenergic receptors are found in the arterioles?
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alpha 1: skin, splanchnic, and renal arterioles
beta 2: skeletal muscle arterioles |
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What part of the cardiovascular system has the largest total cross-sectional and surface area?
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Capillaries
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What are some important features of capillary walls?
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Single layer of endothelial cells
Thin walls Site of exchange for nutrients, water, and gases |
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What are venules?
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Formed from merged capillaries
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What part of the cardiovascular system contains the highest amount of blood?
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Veins
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What are some important features of veins?
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Progressively merge to form larger veins, the largest of which is the vena cava
Low pressure Thin-walled |
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Are the walls of veins innervated by the ANS?
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YES! The walls have alpha 1 adrenergic receptors
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What is the "unstressed volume?"
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The volume of blood contained in the veins
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Formula for the velocity of blood flow
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V = Q/A
Q = blood flow A = cross-sectional area Velocity is directly proportional to blood flow and inversely proportional to the cross-sectional area |
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Where in the cardiovascular system is blood velocity the highest?
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The aorta, because the cross-sectional area is the smallest
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Formula for blood flow
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Q = delta P/R
Q = flow or cardiac output delta P = pressure gradient R = resistance |
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Formula for cardiac output
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CO = (mean arterial pressure - right atrial pressure) / total peripheral resistance
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What is the driving force for blood flow?
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A pressure gradient. Blood flows from high to low pressure
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How does blood flow relate to the resistance of blood vessels?
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Blood flow is inversely proportional to resistance
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Formula for resistance
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R = (8nl)/(pi x r^4)
n = viscosity l = length of blood vessel r = radius of blood vessel |
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How does resistance relate to the radius of a blood vessel?
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It is inversely related to the 4th power of the radius, so if radius decreases by a factor of 2, resistance increases by a factor of 16 (2^4), and blood flow will also decrease by a factor of 16
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Formula for resistances in parallel
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1/Rtotal = 1/R1 + 1/R2 + ...
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Are most organ resistances in series or in parallel?
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In parallel (except for the kidneys)
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Formula for resistances in series
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Rtot = R1 + R2 + ...
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Where in the body do we find resistances in series?
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Blood vessels within a given organ (that is supplied by one artery)
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What is the difference between laminar and turbulent flow?
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Laminar flow moves in straight lines or lamina, and turbulent flow does not
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What calculation do we do to determine if flow will be turbulent?
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Calculate Reynolds number
Increased Reynolds number (over 3000) = turbulent flow |
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What are bruits?
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Audible vibrations in the blood vessels due to turbulent flow
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How does blood viscosity affect Reynold's number?
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Decreased viscosity (from low hematocrit or anemia) increases Reynold's number (low viscosity = high Reynold's number)
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How does blood velocity affect Reynold's number?
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Increased velocity (from narrowing of a vessel) increases Reynold's number
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What is capacitance?
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Describes the distensibility of blood vessels
Compliance is inversely related to elastance (stiffness) -- the more elastic tissue there is, the higher the elasticity, and the lower the compliance |
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Formula for capacitance
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C = V / P
V = volume P = pressure |
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Which has greater capacitance, veins or arteries?
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Veins, so more blood volume is contained in the veins
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What happens if there is a decrease in venous capacitance?
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This decreases unstressed volume, so blood is shifted from the veins to the arteries
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What happens to the capacitance of arteries with age?
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Decreases (they become stiffer, more elastic)
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Where in the cardiovascular system is pressure the highest? The lowest?
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Highest in the aorta and large arteries
Lowest in the venae cavae |
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What is the mean pressure of the aorta?
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100 mmHg
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What is the mean pressure of the arterioles?
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50 mmHg
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What is the mean pressure of the capillaries?
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20 mmHg
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What is the mean pressure of the vena cava?
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4 mmHg
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What happens to arterial pressure over the course of a cardiac cycle?
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It fluctuates and is not constant; it is pulsatile
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What is systolic pressure?
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Measured after heart contraction (systole) and blood is ejected into the arterial system
This is the highest arterial pressure in the cardiac cycle |
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What is diastolic pressure?
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Measured when the heart is relaxed (diastole) and blood is returning to the heart via the veins
This is the lowest arterial pressure in the cardiac cycle |
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What is the pulse pressure?
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The difference between the systolic and diastolic pressures
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What is the most important determinant of pulse pressure?
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Stroke volume
As blood is ejected from the left ventricle, arterial pressure increases because the arteries have relatively low capacitance (ie systolic pressure increases) Diastolic pressure stays the same |
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What happens to pulse pressure as we age?
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It increases because the capacitance of the arteries decreases
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What is the mean arterial pressure?
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The average arterial pressure over time
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Formula for mean arterial pressure
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MAP = Pdiastolic + (pulse pressure / 3)
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Why is venous pressure so low?
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The veins have high capacitance
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What is pulmonary wedge pressure?
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A way of estimating left atrial pressure (should be slightly lower than venous pressure). A catheter is inserted into the smallest branches of the pulmonary artery, and the measured pulmonary artery pressure is approximately equal to left atrial pressure
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What does the P wave on an EKG represent?
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Atrial depolarization
Does NOT include atrial repolarization; this is buried in the QRS complex |
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What does the PR interval on an EKG represent?
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Conduction velocity/time through the AV node
There is an increase in the PR interval if there is a AV nodal block |
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How does autonomic stimulation affect the duration of the PR interval?
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Sympathetic stimulation decreases the interval by increasing conduction velocity
Parasympathetic stimulation increases the interval |
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What does the QRS complex on an EKG represent?
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Depolarization of the ventricles
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What does the QT interval on an EKG represent?
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The entire period of depolarization and repolarization of the ventricles
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What does the ST segment on an EK represent?
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The period where the ventricles are depolarized
This segment is (or should be) isoelectric |
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What does the T wave on an EKG represent?
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Ventricular repolarization
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What ion determines the resting membrane potential of the cardiac tissue?
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K
Em is determined by K conductance, and approaches Ek |
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What effect does inward current have upon the cardiac membrane potential?
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Inward current brings positive charge into the cell
This depolarizes the membrane potential |
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What effect does outward current have upon the cardiac membrane potential?
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This causes positive charge to leave the cell
Hyperpolarization of the membrane potential |
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What maintains the ionic gradient across the cardiac cell membrane?
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Na-K ATPase
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What is the Em of the ventricles, atria, and Purkinje system?
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-90 mV
This approaches Ek |
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How long are the action potentials of the ventricles, atria, and Purkinje system?
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Long, especially in the Purkinje fibers where they are 300 ms
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What are the phases of a cardiac action potential?
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Phase 0: upstroke/depolarization
Phase 1: brief period of repolarization Phase 2: plateau Phase 3: repolarization Phase 4: resting membrane potential |
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What causes phase 0 (upstroke)?
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There is a transient increase in Na conductance, resulting in an inward Na current that depolarizes the membrane
At the peak of the action potential, Em approaches Ena |
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What causes phase 1 (initial repolarization)?
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There is a small outward current, due to efflux of K and a decrease in Na conductance
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What causes phase 2 (plateau)?
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There is a transient increase in Ca conductance
This causes an inward Ca current This is followed by an increase in K conductance (outward K current) Because the inward and outward currents are approximately equal, the membrane potential is stable |
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What causes phase 3 (repolarization)?
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Ca conductance decreases
K conductance increases and therefore predominates The high conductance results in a large outward K current (Ik) which hyperpolarizes the membrane back towards Ek |
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What causes phase 4 (resting membrane potential)?
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The inward and outward currents (Ik1) are equal
Em approaches Ek |
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What part of the heart is the pacemaker?
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The SA node, which exhibits unstable resting potential (automaticity)
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What are the latent pacemakers of the heart?
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The AV node and Purkinje fibers
These regions also exhibit automaticity and can override the SA node if it is suppressed |
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What is the order of the cardiac pacemakers from fastest to slowest?
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SA node > AV node > Purkinje fibers
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How does the phase 0 of the SA node differ from that of the rest of the heart?
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It is caused by an increase in Ca conductance instead of Na
The inward Ca current drives the membrane potential toward Eca |
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Does the SA node exhibit phases 1 or 2?
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No!
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What causes phase 3 of the SA node?
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Repolarization, caused by increased K conductance that results in outward K current
This repolarizes the membrane |
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How does phase 3 of the SA node differ from the rest of the heart?
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Repolarization is mediated by outward K current only, not outward K and inward Ca
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How does phase 4 of the SA node differ from the rest of the heart?
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It is a slow depolarization, not steady state/flat. This is what accounts for the automaticity of the SAN
Caused by an increase in Na conductance; the inward Na current is known as If |
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What turns on the If current?
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Repolarization of the membrane potential
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How does phase 0 of the AV node differ from the rest of the heart?
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Mediated by Ca (like the SA node), not Na
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What is cardiac conduction velocity?
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The time it takes for excitation to spread throughout the cardiac tissue
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What determines the conduction velocity?
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The size of the inward current during the upstroke of the action potential. Larger inward current = higher velocity
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Where is cardiac conduction velocity fastest? Slowest?
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Fastest in the Purkinje system
Slowest in the AV node |
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Why is conduction velocity slowest in the AV node?
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This allows time for the ventricles to fill before ventricular contraction. If this duration is too short, ventricular filling may be compromised
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What is cardiac excitability?
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The ability of cardiac cells to initiate action potentials in response to inward, depolarizing current
It is a function of the extent to which ion channels recover such that they can carry the inward current |
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Does cardiac excitability change or stay constant?
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It changes over the course of the action potential; this is reflected in the existence of refractory periods
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What is the absolute refractory period?
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The time during which no new action potential can be generated, regardless of the magnitude of the inward current
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What is the duration of the absolute refractory period?
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Begins with the upstroke of the action potential (phase 0)
Ends after the plateau (phase 2) |
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What is the effective refractory period?
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The period during which a conducted action potential cannot be elicited
Seems to be the same as the absolute refractory period except slightly longer |
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What is the relative refractory period?
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The period during which an action potential can be elicited, but a larger inward current is required
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What is the duration of the relative refractory period?
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Begins immediately after the absolute refractory period, when repolarization is almost complete
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What is a chronotropic effect?
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Produces a change in heart rate
Negative chronotropic effect decreases the heart rate by decreasing the firing frequency of the SA node |
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What are the sympathetic adrenergic receptors in the heart?
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Beta 1 receptors
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What are the parasympathetic cholinergic receptors in the heart
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Muscarinic receptors
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What are the sympathetic adrenergic receptors in the vascular smooth muscle?
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Alpha 1 and beta 2
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What happens when you stimulate the B1 receptors of the heart?
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This would be sympathetic stimulation:
Increased HR Increased conduction velocity Increased contractility |
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What happens when you stimulate the muscarinic receptors of the heart?
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This is parasympathetic stimulation:
Decreased HR Decreased conduction velocity Decreased contractility |
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What sympathetic adrenergic receptor mediates vasoconstriction?
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Alpha 1
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What are dromotropic effects?
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Produce changes in conduction velocity, primarily in the AV node
A negative dromotropic effect decreases conduction velocity by slowing the conduction of action potentials from the atria to the ventricles |
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A negative dromotropic effect would have what effect upon the PR interval?
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It would increase it, because the conduction velocity through the AV node is decreasing
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What parts of the heart have parasympathetic vagal innervation?
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SA node
Atria AV node |
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What is the chronotropic effect of vagal stimulation of the heart?
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Decreases heart rate by decreasing the rate of phase 4 depolarization of the SA node
This is accomplished by decreasing If, the inward Na current that mediates phase 4 in the SA node |
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What is the dromotropic effect of vagal stimulation of the heart?
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Decreased conduction velocity through the AV node
This is because there is a decreased inward Ca current and an increased outward K current |
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What is the chronotropic effect of sympathetic stimulation of the heart?
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Increases the heart rate by increasing the rate of phase 4 depolarization in the SA node
If is increased |
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What is the dromotropic effect of sympathetic stimulation of the heart?
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Increases conduction velocity through the AV node
This is due to an increased inward Ca current |
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What is the structure of the cardiac sarcomere?
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This is the contractile unit of the myocardial cell
Delineated as the area between two adjacent Z lines Contains thick filaments (myosin) and thin filaments (actin, troponin, tropomyosin) |
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How does the cardiac sarcomere shorten?
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Like in skeletal muscle, this occurs using the sliding filament model
Thin filaments slide along thick ones by forming and breaking cross-bridges between actin and myosin |
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What are intercalated disks?
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Occur at the ends of myocardial cells
Maintain cell-cell cohesion Contain gap junctions |
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What are gap junctions?
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Low-resistance paths between cells that allow for rapid electrical spread of action potentials
These are responsible for the heart's behavior as an electrical syncytium |
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Are mitochondria more or less numerous in cardiac tissue relative to skeletal muscle?
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More numerous
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What are T tubules?
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Contiguous with the cell membrane
They invaginate the cells at the Z lines and carry action potentials to the cell interior Well developed in the ventricles, less developed in the atria Form dyads in the sarcoplasmic reticulum |
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What is the sarcoplasmic reticulum?
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Small-diameter tubules that are in close proximity to the contractile elements of the cell
Site of storage and release of Ca for excitation-contraction coupling |
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What are the steps of cardiac excitation-contraction coupling?
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Action potential spreads from the cell membrane into the T tubules
During the action potential plateau, Ca conductance increases and there is inward Ca current This triggers the release of more Ca from the SR (Ca-induced Ca release) As intracellular Ca increases, Ca binds to troponin C Tropomyosin is moved out of the way, removing the inhibition of actin-myosin interaction Actin and myosin bind, the thick and thin filaments slide past each other, and the myocardial cell contracts The magnitude of the tension generated is proportional to the intracellular Ca concentration Relaxation happens when the Ca goes back into the SR via an active Ca-ATPase |
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What determines the amount of Ca released from the sarcoplasmic reticulum?
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The amount of Ca previously stored
The magnitude of the inward Ca current |
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What is contractility?
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The intrinsic ability of the heart to develop force at a given muscle length (also known as inotropism)
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What determines cardiac contractility?
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The intracellular Ca concentration
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What index is used to estimate the contractility of the heart?
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The ejection fraction, which is normally 0.55 (55%)
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Formula for ejection fraction
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EF = SV / EDV
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What effect do positive inotropic agents have upon the heart? What about negative inotropes?
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Positive -- increase contractility
Negative -- decrease contractility |
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What are some positive inotropic factors?
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Increased heart rate
Sympathetic stimulation Cardiac glycosides (digitalis) |
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How does increased heart rate increase contractility?
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There are more action potentials per unit time
More Ca enters the myocardial cells during the plateaus More Ca is released from the SR Greater tension is produced during contraction |
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What is a "positive staircase?"
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Also known as a Bowditch staircase or Treppe
Increased heart rate increases the force of contraction in a stepwise fashion as the intracellular Ca accumulates over several beats |
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How does postextrasystolic potentiation increase contractility?
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This is when there is an extrasystolic beat
The beat that occurs after the extrasystolic beat will have increased force of contraction due to the higher intracellular Ca concentration |
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How does sympathetic stimulation increase contractility?
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It increases the inward Ca current during the plateau of the action potential
It increases the activity of the Ca pump of the SR via phosphoryation of phospholamban |
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How do cardiac glycosides increase contractility?
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Digitalis inhibits the Na-K ATPase
This causes intracellular [Na] to increase, diminishing the Na gradient Na-Ca exchange (which extrudes Ca) depends on the size of the Na gradient, so if this is abolished, less Ca is transported out of the cell This means the intracellular Ca concentration is higher |
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How does parasympathetic stimulation decrease contractility?
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Decreases the force of contraction in the atria by decreasing the inward Ca current during the plateau
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What is preload?
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It is the end-diastolic volume (which is related to right atrial pressure)
When venous return increases, EDV increases and stretches/lengthens the ventricular muscle fibers |
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What is afterload?
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The pressure in the artery leading away from the ventricle (ie aortic or pulmonary artery pressure)
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When is the velocity of cardiac contraction highest?
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When the afterload is 0, ie when there is low pressure in the arteries
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How do increases in afterload affect the velocity of contraction?
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They decrease velocity of contraction
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What is the Frank-Starling relationship?
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When EDV/venous return increase, there is an increase in SV and cardiac output
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What is the Frank-Starling relationship based upon?
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The length-tension relationship in the ventricle
Increases in EDV cause an increase in ventricular fiber length This produces an increase in the developed tension |
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How does the Frank-Starling relationship match cardiac output to venous return?
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The greater the venous return, the greater the cardiac output
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How do changes in contractility affect the Frank-Starling relationship?
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Increased contractility shifts the curve up, causing an increase in cardiac output for any EDV
Decreased contractility shifts the curve down, causing a decrease in cardiac output for any EDV |
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Refer to the pressure-volume loop on BRS p82. What is represented in 1-->2?
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Isovolumetric contraction
Diastole begins at point 1 The ventricle is beginning to contract but there is no pressure change yet All valves are closed |
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Refer to the pressure-volume loop on BRS p82. What is represented in 2-->3?
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Ventricular ejection
The aortic and pulmonary valves open at point 2, when ventricular pressure exceeds arterial pressure Blood is ejected into the arteries so ventricular volume decreases (the volume ejected is the stroke volume) The SV can be measured graphically as the width of the pressure-volume loop The volume remaining in the ventricle is the EDV |
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Refer to the pressure-volume loop on BRS p82. What is represented in 3-->4?
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Isovolumetric relaxation
The ventricle relaxes at point 3 When arterial pressure exceeds ventricular pressure, the arterial valves close All valves are closed |
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Refer to the pressure-volume loop on BRS p82. What is represented in 4-->1?
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Ventricular filling
When atrial pressure exceeds ventricular pressure, the mitral and tricuspid valves open and the ventricles fill This causes the ventricular volume to increase |
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How does increased preload affect the ventricular pressure-volume loop?
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It increases the stroke volume, and therefore increases the width of the loop
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How does increased afterload affect the ventricular pressure-volume loop?
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This decreases the stroke volume and decreases the width of the loop
The decrease in stroke volume is equal to the increase in end-systolic volume |
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How does increased contractility affect the ventricular pressure-volume loop?
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The ventricle has increased tension during systole, and this increases stroke volume, so the loop is wider
This causes a decrease in end-systolic volume |
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What does the cardiac function curve show?
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It demonstrates that cardiac output is a function of EDV
Cardiac output increases as EDV (preload) increases |
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What does the vascular function (venous return) curve show?
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Venous return decreases as atrial pressure increases
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What is the mean systemic pressure?
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The point at which the vascular function curve intersects the x-axis
It is equal to the right atrial pressure when blood flow is arrested throughout the body (cardiac output and venous return are 0, and pressure is the same everywhere) Measured when the heart is experimentally stopped |
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What factors increase the mean systemic pressure?
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Increase in blood volume
Decrease in venous compliance (shift of blood into the arterial compartment) |
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What effect does an increased mean systemic pressure have upon the vascular function curve?
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It shifts it to the right (you are increasing the pressure for a given cardiac output)
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What determines the slope of the vascular function curve?
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The resistance of the arterioles
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What effect does decreased total peripheral resistance have upon the vascular function curve?
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It decreases the slope, because when resistance decreases, there is an increase in venous return due to the vasodilation
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What is the equilibrium point?
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The point of intersection between the cardiac output and vascular function curves
It is where cardiac output equals venous return |
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How do inotropic agents change the cardiac output curve?
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They increase contractility and cardiac output, so stroke volume increases
This shifts the cardiac function curve up |
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How do changes in blood volume or venous compliance change the vascular function curve?
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Increased blood volume or decreased venous compliance both increase mean systemic pressure, which shifts the curve to the right
This increases both cardiac output and right atrial pressure |
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How do changes in total peripheral resistance affect the cardiac output and vascular function curves?
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Increased resistance will shift the cardiac function curve down, and decrease the slope of the vascular function curve (because there is decreased venous return)
This establishes a new equilibrium point where both CO and venous return are decreased, but right atrial pressure is unchanged |
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What is stroke volume?
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The volume ejected from the ventricle on each beat
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Formula for stroke volume
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SV = EDV - ESV
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Formula for cardiac output
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CO = SV x HR
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What is the ejection fraction?
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The amount of EDV that is ejected in each stroke volume
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What factor determines ejection fraction?
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Contractility
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What is the normal value for ejection fraction?
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55%
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What is stroke work?
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The work that the heart performs on each beat
Fatty acids are the primary energy source |
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Formula for stroke work
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Stroke work = arterial pressure (aortic or pulmonary) x stroke volume
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What factors determine cardiac oxygen consumption?
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Increased afterload
Increased size of the heart Increased contractility Increased HR Oxygen consumption is directly related to the amount of tension developed by the ventricles |
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Formula for cardiac output using the Fick principle
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CO = O2 consumption / (O2 conc in pulmonary vein - O2 conc in pulmonary artery)
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What does it mean for a phase of the cardiac cycle to be isovolumetric?
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All valves are closed so there is no change in volume
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How does atrial systole related to ventricular filling?
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It contributes to ventricular filling, but is not essential
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What produces the fourth heart sound?
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Filling of the ventricle by atrial systole
This sound is not audible in normal adults |
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What produces the first heart sound?
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Closure of the AV valves at the onset of isovolumetric ventricular contraction
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Why might the first heart sound be split?
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The mitral valve closes before the tricuspid valve
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What are the periods of ventricular ejection?
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Rapid ventricular ejection
Reduced ventricular ejection |
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When is most of the stroke volume ejected?
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The rapid ventricular ejection
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When do the atria begin filling?
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During rapid ventricular ejection
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What is the difference between rapid and reduced ventricular ejection?
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During reduced ejection, the ejection is slower and ventricular pressure begins to decrease
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What produces the second heart sound?
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Closure of the semilunar valves
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What causes the second heart sound to be split?
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Inspiration
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What is the "blip" in the aortic pressure tracing of the cardiac cycle after the closure of the aortic valve?
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The dicrotic notch or incisura
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What produces the third heart sound?
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Rapid blood flow from the atria into the ventricles
Normal in children, but associated with disease in adults |
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Where are the baroreceptors located?
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These stretch receptors are found in the walls of the carotid sinus and in the aortic arch
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How does the baroreceptor reflex work?
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Decreased arterial pressure results in decreased stretch
This decreases the firing rate of the carotid sinus nerve Information is carried to the vasomotor center in the brainstem The vasomotor center decreases vagal stimulation and increases sympathetic outflow This will: increase heart rate, increase contractility and stroke volume, and vasoconstrict the arterioles and veins (this increases venous return and increases cardiac output) |
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How is the Valsalva maneuver used to demonstrate the baroreceptor mechanism?
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You are expiring against a closed glottis
This increases intrathoracic pressure and decreases venous return If the baroreceptor reflex is intact, you will increase the heart rate |
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What is the purpose of the RAS?
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Adjustment of blood volume
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What is the first enzyme to come into play in the RAS?
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Renin -- cleaves angiotensinogen to angiotensin I
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What is the physiologically active compound in the RAS?
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Angiotensin II
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What degrades angiotensin II?
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Angiotensinase
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What are the steps of the RAS?
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There is a decrease in renal perfusion pressure
Juxtaglomerular cells in the afferent arteriole produce renin Renin cleaves angiotensinogen to angiotensin I Angiotensin I goes to the lungs and is cleaved by ACE to give angiotensin II |
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What is the mechanism of ACE inhibitors?
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ACE inhibitors block the conversion of angiotensin I to angiotensin II
This decreases blood pressure |
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What is Captopril?
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An ACE inhibitor
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What do AT1 antagonists do?
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They block the angiotensin receptor to prevent angiotensin II from exerting effects
This decreases blood pressure |
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What is Losartan?
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An AT1 antagonist
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What are the effects of angiotensin II?
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Stimulation of the synthesis and secretion of aldosterone
Increases Na-H exchange in the proximal convoluted tubule of the nephron (leads to contraction alkalosis) Increases thirst Vasoconstricts the arterioles, increasing resistance and arterial pressure |
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Where is aldosterone produced?
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The adrenal cortex
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What does aldosterone do?
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Increases Na reabsorption in the distal tubule of the nephron -- increases ECF volume, blood volume, and arterial pressure
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Is the action of aldosterone fast or slow?
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Slow, because it requires new protein synthesis
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How does the chemoreceptor reflex work?
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When the brain is ischemic, PCO2 in the CSF increases
Chemoreceptors in the vasomotor center increase sympathetic outflow This causes vasoconstriction to divert blood flow away from peripheral organs and toward the heart The arterial pressure increases to preserve oxygenation of the brain Note that this reflex can be sustained to life-threatening levels |
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What is the Cushing reaction?
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Increased intracranial pressure compresses the cerebral blood vessels
This leads to cerebral ischemia and increased cerebral PCO2 The vasomotor center increases sympathetic outflow This increases arterial pressure |
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Where are the peripheral chemoreceptors located?
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The carotid and aortic bodies
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What are chemoreceptors sensitive to?
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Decreases in PO2
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Under what physiological conditions does vasopressin come into play?
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Regulation of blood pressure in response to hemorrhage
Not involved in minute-to-minute regulation of normal blood pressure |
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What is another name for vasopressin?
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Antidiuretic hormone (ADH)
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What causes vasopressin to be released?
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Atrial receptors respond to decreased blood volume or decreased blood pressure
Vasopressin is released from the posterior pituitary |
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How does vasopressin increase low blood pressure toward normal?
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Vasoconstriction via activation of V1 receptors on arterioles
Increases water reabsorption in the renal tubule via activation of V2 receptors |
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What conditions cause ANP to be produced?
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Released from the atria in response to increased blood volume and atrial pressure
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What are the effects of ANP?
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Vasodilation
Increases excretion of Na and water Inhibits renin secretion |
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What structure is found at the junction of the arterioles and the capillaries?
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Precapillary sphincters
These are bands of smooth muscle |
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What is the purpose of precapillary sphincters?
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Blood flow through the capillaries is regulation by constriction and dilation of these sphincters
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How do lipid-soluble substances cross the capillary wall?
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Simple diffusion
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How do O2 and CO2 cross the capillary wall?
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Simple diffusion
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How do small water-soluble substances cross the capillary wall?
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They use the water-filled pores between endothelial cells
Proteins are generally too large to cross by this mechanism |
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How do water, glucose, and amino acids cross the capillary wall?
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Endothelial pores
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What is unusual about the capillary endothelium in the brain?
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The pores between endothelial cells are exceptionally tight
This gives rise to the integrity of the blood-brain barrier |
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What is unusual about the capillary endothelium of the liver and intestine?
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The pores are unusually wide and allow passage of protein
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What are sinusoids?
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Capillaries in the liver and intestines
These capillaries have unusually wide fenestrations that permit passage of proteins |
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How do large water-soluble substances cross the capillary wall?
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Pinocytosis
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Formula for the Starling equation
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J = Kf[(Pc - Pi) - (PIc - PIi)]
J = fluid movement Kf = hydraulic conductance P = hydrostatic pressure of the capillary and interstitium PI = colloid osmotic pressure of the capillary and interstitium |
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What does the sign of J indicate in the Starling equation?
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If J is positive, there is net fluid movement out of the capillary (filtration)
When J is negative, there is net fluid movement into the capillary (absorption) |
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What is the significance of Kf?
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It is the hydraulic conductance (water permeability) of the capillary wall
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What determines the hydrostatic pressure of the capillary?
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Arterial and venous pressures and resistances
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How does hydrostatic pressure change along the length of the capillary?
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It is highest at the arteriolar end and lower at the venous end (except for glomerular capillaries, where it is nearly constant)
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What determines the colloid osmotic pressure of the capillary?
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Protein concentration in the blood
Dehydration increases concentration, nephrotic syndrome, protein malnutrition, and liver failure decrease concentration |
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What increases the colloid osmotic pressure of the interstitium?
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Inadequate lymphatic function
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What is the function of lymph?
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Collection of excess filtered fluid from the capillaries
This fluid is returned to circulation Any filtered proteins are also returned to circulation |
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How does lymph flow?
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It is unidirectional
One-way flap valves allow interstitium fluid to enter the lymph vessels, but that fluid is unable to leave One-way valves and skeletal muscle contractions aid in the unidirectionality of flow |
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What is edema and how does it develop?
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Edema occurs when the volume of interstitial fluid exceeds the capacity of the lymphatics to return fluid to circulation
Can be caused by excess filtration or blocked lymphatics |
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What is endothelium-derived relaxing factor?
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Produced by endothelial cells and causes vasodilation via cGMP
One form of EDRF is nitric oxide |
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How does circulating ACh cause vasodilation?
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It stimulates the production of nitric oxide in vascular smooth muscle
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What is autoregulation?
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Blood flow to an organ remains constant over a wide range of perfusion pressures
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What organs exhibit autoregulation
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Heart
Brain Kidneys |
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If the perfusion pressure to the heart suddenly decreased, what would be the autoregulatory response?
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Vasodilation of the arterioles to maintain constant blood flow
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What is active hyperemia?
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When the blood flow to an organ is proportional to its metabolic flow
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What is reactive hyperemia?
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When blood flow to an organ increases after a period of occlusion
The longer the occlusion lasts, the greater the increase in blood flow above pre-occlusion levels |
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What is the myogenic response?
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Vascular smooth muscle contracts when it is stretched
When there is increased perfusion, vasoconstriction increases resistance to maintain constant blood flow |
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What is the metabolic hypothesis?
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Tissue supply of oxygen is matched to the tissue's demand for oxygen
Vasodilator metabolites are produced in response to metabolic activity? |
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What are some vasodilatory metabolites?
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CO2
H K Lactate Adenosine |
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Is sympathetic innervation of vascular smooth muscle constant in all tissues?
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No
Skin has the most sympathetic innervation in the vasculature Coronary, pulmonary, and cerebral circulations have the least innervation |
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How does histamine affect vasoactivity?
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Arteriolar dilation
Venous constriction This results in increased capillary hydrostatic pressure, which can increase filtration and cause local edema |
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What stimulates histamine release?
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Tissue trauma
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How does bradykinin affect vasoactivity
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Arteriolar dilation
Venous constriction Increased capillary hydrostatic pressure favors filtration and can result in edema |
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How does serotonin (5-hydroxytryptamine) affect vasoactivity?
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Arteriolar constriction
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What stimulates serotonin release?
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Blood vessel damage
This helps to prevent blood loss |
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What vasoactive substance has been implicated in the genesis of migraines?
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Serotonin
Thought to potentially cause vascular spasms |
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Which prostaglandins are vasodilators?
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Prostacyclin (PGI2)
E-series PGs (PGE family) |
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Which prostaglandins are vasoconstrictors?
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F-series PGs (PGF family)
Thromboxane A2 |
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What is primarily responsible for regulation of coronary circulation?
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Local metabolic factors
Hypoxia and adenosine are the most important |
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What is primarily responsible for cerebral circulation?
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Local metabolic factors
CO2 is an important local vasodilator Vasoactive substances in the systemic circulation have little effect because they are excluded by the blood-brain barrier |
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What controls the vasoactivity of arterioles in the skeletal muscle?
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Sympathetic innervation
Local metabolic factors |
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How does sympathetic stimulation affect vasoactivity in the skeletal muscle?
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Sympathetic innervation is the primary regulator of resting tone
Stimulation of alpha 1 receptors causes vasoconstriction Stimulation of beta 2 receptors vauses vasodilation |
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How do metabolic factors affect vasoactivity in the skeletal muscle?
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During exercise, when oxygen demand is high, metabolic factors are the primary determinant of vascular tone
Important metabolic vasodilators are lactate, adenosine, and K |
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How does exercise cause reactive hyperemia?
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Muscular contractions compress the arteries and decrease blood flow
In the post-occlusion period, reactive hyperemia increases blood flow to replenish the oxygen deficit |
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What controls the vasoactivity of blood flow in the skin?
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Sympathetic activity -- contribute to temperature regulation
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How does temperature regulation in the skin work?
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High ambient temperature causes cutaneous vasodilation, which allows excess body heat to dissipate
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What is the "triple response" in the skin?
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The triple response is how skin responds to trauma
A red LINE is produced A red FLARE is produced A WHEAL is produced |
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What is a wheal?
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Local edema resulting from histamine release, which increases capillary filtration
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What happens to the various indices of cardiovascular function when you go from a supine to a standing position?
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Blood pools in the lower extremities because of the high venous compliance
This increases Pc in the legs and fluid is filtered into the interstitium (possibly causing edema) Blood volume and venous return decrease Decreased venous return decreases stroke volume and cardiac output Low cardiac output decreases arterial pressure (can cause fainting) Compensatory mechanisms attempt to increase blood pressure to normal via the baroreceptor reflex |
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What is the compensatory mechanism when you go from a supine to a standing position?
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Carotid sinus baroreceptors detect decreased arterial pressure
Firing rate of the carotid sinus nerves decreases Increased sympathetic outflow from the vasomotor center |
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What is orthostatic hypotension and what causes it?
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It is when you experience fainting or light-headedness upon standing
Happens in people with an impaired baroreceptor reflex (such as people being treated with sympatholytic agents) |
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Where does the central command of exercise (anticipation of exercise) come from?
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The motor cortex, or from reflexes initiated in muscle proprioceptors when exercise is anticipated
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What happens when you are anticipating exercise?
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Sympathetic outflow to the heart and blood vessels increases
Vagal outflow decreases Cardiac output increases (due to increased HR, and to a lesser extent the increased stroke volume) Venous return increases Arteriolar resistance increases to divert blood flow towards the muscles and away from organs |
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What are the metabolic effects of exercise?
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Vasodilators (lactate, K, and adenosine) accumulate from the increased metabolism during exercise
These metabolites cause vasodilation O2 delivery to muscle is increased Vasodilation causes an overall decrease in total peripheral resistance Note that if exercise produced sympathetic effects only, there would be an increase in resistance |
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What happens when you hemorrhage?
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Decreased blood volume decreases cardiac output and arterial pressure
Carotid sinus baroreceptors detect decreased pressure Increased sympathetic outflow and decreased parasympathetic outflow Peripheral chemoreceptors detect hypoxia and supplement the baroreceptor mechanism by increasing sympathetic outflow Cerebral ischemia increases PCO2, which activates central chemoreceptors to increase sympathetic outflow Arteriolar vasoconstriction, which decreases Pc and favors capillary reabsorption Adrenal medulla releases epinephrine and norepinephrine RAS is activated by decreased renal perfusion pressure ADH is released |
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What is the hormonal response to hemorrhage?
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Increased circulation of angiotensin II, aldosterone, epinephrine and norepinephrine, and ADH
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What does ADH do?
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Causes vasoconstriction
Increases water reabsorption Both of these factors tend to increase blood pressure |
