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76 Cards in this Set
- Front
- Back
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systemic circulation
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left heart and arteries
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pulmonary circulation
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right heart and arteries
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smooth muscle in walls of arterioles is innervated by
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sympathetic adrenergic nerve fibers
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a1-adrenergic receptors are found
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on the arterioles of many vascular beds (skin, splanchnic, etc)
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a1-adrenergic receptors, when activated, cause
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contraction/constriction of vascular smooth muscle
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B2-adrenergic receptors are found
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less common....in skeletal muscle
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B2-adrenergic receptors, when activated, cause
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relaxation of vascular smooth muscle
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selective perfusion
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not all capillaries are perfused with blood at all times
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what contain the largest percentage of blood in the cardiovascular system?
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veins
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velocity =
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Q/A (flow/cross-sectional area)
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as vessel diameter increases, velocity
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velocity of flow through the vessel decreases
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Ohm's law
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Q = delP/R
flow = pressures diff / resistance |
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Poiseuille equation
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R = 8nl/piR^4
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Series Resistance
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Rtot = R1 + R2 + R3 + ...
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where does the greatest decrease in pressure occur?
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in the arterioles....because they contribute the largest portion of resistance
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parallel resistance
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1/Rtot = 1/R1 + 1/R2 + ...
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laminar blood flow
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streamlined, non-turbulent
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murmurs
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audible sound of turbulent flow
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Reynold's number
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predicts whether blood flow will be laminar or turbulent
Nr = pdv/n |
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Reynold's number < 2000
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laminar
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what allows glood to flow?
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pressure differences throughout our system!
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pulse pressure
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the difference between systolic and diastolic pressure
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stroke volume
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the volume of blood ejected from the LV on a single beat
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mean arterial pressure
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diastolic press + 1/3 pulse press
the average pressure in a complete cardiac cycle (more time in each cardiac cycle is spent in diastole than in systole) |
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arteriosclerosis
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plaque deposits in arterial walls ==> decrease diameter --> make stiffer --> arterial pressure (and all pressures) is increased
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aortic stenosis
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aortic valve is narrowed
less blood enters aorta on each beat --> all pressures decrease |
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aortic regurgitation
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blood that was ejected into the aorta flows backward into the ventricle
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by the time blood reaches the venules and veins, pressure is
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less than 10mmHg
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Cardiac output
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the amount of blood pumped per minute
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BP =
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Cardiac Output X Resistance
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what can generate action potential spontaneously?
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SA node
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pacemaker
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SA node
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what types of Ca channels do cardiac APs open?
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L-type (L for long-lasting)
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myocardial tissue cells are connected by
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gap junctions --> electrical coupling
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chronotropic effects
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the effects of the autonomic nervous system on heart rate
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positive chronotropic effects
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increases in heart rate
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how does sympathetic nervous system increase heart rate?
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release norepinephrine --> activates B1 receptors in SA node
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negative chronotropic effects
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decrease heart rate
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how does parasympathetic system decrease heart rate?
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release acetylcholine --> activate M2 (muscarinic) receptors in SA node
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dromotropic effects
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effects of ANS on conduction velocity
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heart block
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action potential not conducted at all from the atria to the ventricles
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P wave represents
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depolarization of atria
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PR interval
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time from atrial depolarization to beginning of ventrical depolarization
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PR segment
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AV node conduction
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QRS complex
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depolarization of ventricles
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T wave
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repolarization of ventricles
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QT interval
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represents time from first ventricular depolarization to last ventricular repolarization
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cycle length
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R-R interval
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heart rate
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=1/cycle length
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arrhythmias
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abnormal heart rhythms
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cardiac cells made up of
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sarcomeres
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sarcomeres
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Z-to-Z line
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sarcomeres made up of
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thick and thin filaments
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thick filaments made of
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myosin
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thin filaments made of
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actin
tropomyosin troponin |
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T tubules invaginate cardiac muscle cells at
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the Z lines
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sarcoplasmic reticulum
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site of storage and release of Ca for excitation-contraction coupling
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Ca-induced Ca release
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Ca goes in via L-type Ca channels --> triggers release of more Ca from sarcoplasmic reticulum
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Ca release binds to
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troponin C subunit
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what happens when Ca binds to troponin?
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moves tropomyosin out of the way --> allows actin and myosin to bind
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magnitude of the tension developed by myocardial cells is proportional to
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intracellular Ca concentration
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how does Ca get back into SR?
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Ca-ATPase
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positive inotropic effects
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increase rate of tension development and the peak tension
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the amount of Ca released from the SR depends on 2 factors:
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1) size of the inward Ca current
2) amount of Ca previously stored in the SR |
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phospholamban
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a protein that regulates Ca-ATPase in the SR
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phospholamban phosphorylation states
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phosphorylated --> stimulates Ca-ATPase --> faster relaxation and more stored Ca for next release
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increase in heart rate causes
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increase in contractility
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effects of cardiac glycosides
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foxglove/digitalis --> inhibits Na/K-ATPase --> increases intracellular Na conc --> Ca-Na exchanger decreases --> intracellular Ca conc increases --> positive inotropic effect
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intercalated disks
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low resistance electrical junctions that adhere adjacent myocytes
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thick filaments
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myosin
dark A-band |
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thin filaments
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actin
light I-band |
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sarcomere
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the portion of the myofibril bounded by adjacent Z-discs
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titin
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flexible cytoskeletal protein that binds at its one end to the Z-disk and thin filament and at its other end to thick filaments
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Binding of the myosin head to the actin thin filament increases
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the myosin ATPase rate by several hundred fold
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which two additional proteins bind to the actin thin filaments?
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tropomyosin and troponin
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Each time a cross bridge attaches and detaches to actin via a power stroke
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1 ATP is split
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