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46 Cards in this Set
- Front
- Back
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Path of blood through body?
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Right atrium
Right ventricle --> pulmonary arteries Lungs --> pulmonary veins Left atrium Left ventricle Aorta Inferior/superior vena cava |
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Blood pressure gradient
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greatest to smallest pressures:
aorta arteries arterioles capillaries venules veins venae cavae |
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Resistance and Flow
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Resistance is proportional to inverse radius to the 4th power.
Flow is inversely proportional to resistance |
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Velocity of flow
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Velocity = Flow rate (Q) / cross-sectional area (A)
flow is in cm cubed/min |
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Ohm's Law
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MAP=CO*TPR
Mean Arterial Pressure = Cardiac Output * Total Peripheral Resistance |
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MAP and SNS
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Direct relationship: MAP decreases as SNS decreases and vice versa
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Cardiac Output
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MAP(P) = CO (Q) X TPR (R)
Q = [(p1-p2)*radius^4] / (length * viscosity) ALSO CO = HR * SV (heart rate, stroke volume) |
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Heart Valves
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Right atrium -> Right ventricle: right AV (tricuspid) valve
Left atrium -> left ventricle: left AV (bicuspid) MITRAL valve Pulmonary artery: pulmonary semilunar valve |
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Cardiac vs. Skeletal muscle
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- Smaller and have single nucleus per fiber
- Have intercalated disks - Desmosomes allow force to be transferred - Gap Junctions provide electrical connection - T-tubules are larger and branch - Sarcoplasmic reticulum is smaller - Mitochondria occupy one-third of cell volume |
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Excitation/relaxation in cardiac muscle cells
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1. Action potential enters from adjacent cell.
2. Voltage-gated Ca2+ channels open. Ca2+ enters cell. 3. Ca2+ induces Ca2+ release through ryanodine receptor-channels (RyR). 4. Local release causes Ca2+ spark. 5. Summed Ca2+ Sparks create a Ca2+ signal. 6. Ca2+ ions bind to troponin to initiate contraction. 7. Relaxation occurs when Ca2+ unbinds from troponin. 8. Ca2+ is pumped back into the sarcoplasmic reticulum for storage. 9. Ca2+ is exchanged with Na+. 10. Na+ gradient is maintained by the Na+-K+-ATPase. |
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Graded cardiac potential
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- Can be graded
- SNS -> NE -> b1 -> increased Ca2+ influx - Ca2+ channel blockers - b1 blockers - Sarcomere length affects force of contraction - Action potentials vary according to cell type |
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Refractory period
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Skeletal muscle: short refractory period, exhibit summation and tetanus
Cardiac muscle: long refractory period prevents tetanus |
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Sympathetic vs. Parasympathetic on heart rate
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Sympathetic: more rapid depolarization, faster heart rate, NE
Parasympathetic: slower depolarization (hyperpolarizes membrane potential), slower heart rate, ACh |
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Electrical Conduction in Heart
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1. SA node depolarizes
2. Electrical activity goes rapidly to AV node via internodal pathways 3. Depolarization spreads more slowly across the atria. Conduction slows through AV node 4. Depolarization moves rapidly through ventricular conducting system to apex of the heart 5. Depolarization wave spreads upward from the apex |
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AV vs. SA node
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AV node: Direction of electrical signals, delay the transmission of action potentials
SA node: Set the pace of the heartbeat at 70 bpm, AV node (50 bpm) and Purkinje fibers (25-40 bpm) can act as pacemakers under some conditions |
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Einthoven's Triangle
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R arm: -, -
L arm: +, - L leg: +, + |
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ECG and electric events in heart
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P wave: start depolarization
PQ/PR segment: conduction through AV node and A-V bundle; atria contract ST segment: ventricles contract T wave: ventricle repolarization |
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Mechanical events of cardiac cycle
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1. Late diastole: both sets of chambers are relaxed and ventricles fill passively
2. Atrial systole: atrial contraction forces a small amount of additional blood into ventricles 3. Isovolumic ventricular contraction: first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves 4. Ventricular ejection: as ventricular pressure rises and exceeds pressure in arteries, the semilunar valves open and blood is ejected 5. Isovolumic ventricular relaxation: as ventricles relax, pressure in ventricles falls, blood falls back into cups of semilunar valves and snaps them closed. |
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Reflex control of heart rate
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Sympathetic:
- NE - Beta-1 receptors of autorhythmic cells - Na+ and Ca2+ influx - Rate of depolarization faster, faster heart rate Parasympathetic: - ACh - Muscarinic receptors - K+ efflux, Ca2+ influx - hyperpolarizes cell, decreases depolarization rate, decreases heart rate |
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Preload
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Frank-Starling law: Stroke volume increases as EDV increases
Increasing venous return increases EDV - Skeletal muscle pump - Respiratory pump - Blood volume Length-tension increases |
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Afterload
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What the heart must pump against
- Arterial pressure - Aortic stenosis Increasing afterload - Decreases ejection fraction - Increases ESV |
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Contractility and effects on SV
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SV = EDV-ESV
(End Diastolic Volume - End Systolic Volume) Increasing contractility reduces ESV at the same EDV (elevates SV) Contractility increases with sympathetic stimulation (NE) |
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Immediate Effect compensation
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1. Immediate effect – consider only changes in variables up to the point at which a highly regulated physiological variable is disrupted.
What are some highly regulated physiologic variables? O2/CO2 pH Blood pressure Temperature Osmolality Blood volume Blood glucose |
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Short-Term compensation
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2. Short-term compensation
This is what the body does in an attempt to bring the disrupted critical physiological variable back into homeostasis – RIGHT NOW. What can we do right now? Neural effects – osmosis – things that can happen quickly |
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Long-Term compensation
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3. Long-term compensation
If the problem persists what can the body do to help maintain homeostasis over a period of days/months/years? Hormones Facilitation/inhibition of cellular responses Neural pathways change over time (set-points) |
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Angiogenesis
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New blood vessel development
Necessary for normal development Wound healing and uterine lining growth Coronary heart disease -Collateral circulation |
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Elastic recoil in arteries
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1. Ventricle contracts
2. Semilunar valve opens 3. Aorta and arteries expand and store pressure in elastic walls 1. Isovolumic ventricular relaxation occurs 2. Semilunar valve shuts, preventing flow of blood back into ventricle 3. Elastic recoil of arteries sends blood forward into the rest of the circulatory system |
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Pulse pressure and MAP
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Pulse Pressure = systolic P – diastolic P
Valves ensure one-way flow in veins MAP = diastolic P + 1/3(systolic P – diastolic P) MAP is proportional to cardiac output * resistance |
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Blood pressure control
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Increased blood volume -->
Increased blood pressure --> 1. FAST RESPONSE Compensation by cardiac system (vasodilation or decreased cardiac output) 2. SLOW RESPONSE Compensation by kidneys Excretion of fluid in urine; decreased blood volume |
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Vasoconstrictors/Vasodilators
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1. Vasoconstrictors
- NE Sympathetic nerves - Vasopressin (ADH) Hormone from posterior pituitary - AngiotensinII Plasma hormone (Involves Kidney (renin) & Lungs) 2. Vasodilators - NO Produced from endothelial cells - Metabolites Low O2, High CO2, lactate, adenosine, temperature |
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Active Hyperemia
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Increased tissue metabolism
Increased release of metabolic vasodilators in ECF Arterioles dilate Decreased resistance Increased blood flow Blood flow matches metabolism |
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Reactive Hyperemia
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Decreased tissue blood flow due to occlusion
Metabolic vasodilators accumulate in ECF Arterioles dilate, but occlusion prevents bloodflow Remove occlusion Decreased resistance Increased blood flow As vasodilators wash away, arterioles constrict and blood flow returns to normal |
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Arteriole diameter and NE
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Arteriole diameter is controlled by tonic release of NE
Increase NE on alpha receptors - blood vessel constricts Decrease NE on alpha receptors - blood vessel dilates |
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Capillaries: Exchange
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Plasma and cells exchange materials across thin capillary wall
Capillary density is related to metabolic activity of cells Capillaries have the thinnest walls - Single layer of flattened endothelial cells - Supported by basal lamina Bone marrow, liver and spleen do not have typical capillaries but sinusoids |
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Continuous capillaries
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Leaky junctions
Water and small dissolved solutes pass |
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Fenestrated capillaries
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Large pores
Proteins and macromolecules across endothelium Some vesicles may fuse to create temporary channels |
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Capillary exchange
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Exchange by paracellular pathway or transendothelial transport
Small dissolved solutes and gasses by diffusion is determined by concentration gradient Large solutes and proteins by vesicular transport - In most capillaries, large proteins are transported by transcytosis Bulk flow - Mass movement as result of hydrostatic or osmotic pressure gradients Absorption: fluid movement into capillaries - Net absorption at venous end Filtration: fluid movement out of capillaries - Caused by hydrostatic pressure - Net filtration at arterial end |
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Lymphatic system
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Returning fluid and proteins to circulatory system
Picking up fat absorbed and transferring it to circulatory system Serving as filter for pathogens |
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Baroreceptor reflex
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Change in BP (Carotid and aortic baroreceptors)
Medullary cardiovascular control center Para/sympathetic neurons - SA node Sympathetic neurons - Ventricles - Arterioles - Veins |
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CVD factors
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Not controllable
- Gender - Age - Family History Controllable - Smoking - Obesity - Sedentary lifestyle - Untreated hypertension Uncontrollable genetic but modifiable lifestyle - Blood lipids -- Leads to atherosclerosis -- HDL-C versus LDL-C Diabetes mellitus - Metabolic disorder contributes to development of atherosclerosis |
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Hypertension
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Carotid and aortic baroreceptors adapt
- Set-point in brain is now higher! Risk factor for atherosclerosis - Disrupts endothelium ( NO -> vasodilation) Heart muscle hypertrophies - Increased afterload - Pulmonary edema - Congestive heart failure Treatment - Calcium channel blockers, diuretics, beta-blocking drugs, and ACE inhibitors |
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Monosynaptic reflex
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single synapse between afferent and efferent neurons
Stimulus -> receptor -> sensory neuron Spinal cord integrating center Efferent neuron -> target cell receptor -> response |
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Polysynaptic reflex
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Two or more synapses
stimulus -> receptor -> sensory neuron interneuron efferent neuron -> target cell receptor -> response |
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Skeletal muscle reflexes
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Proprioceptors are located in skeletal muscle, joint capsules, and ligaments
Proprioceptors carry input sensory neurons to CNS CNS integrates input signal Somatic motor neurons carry output signal - Alpha motor neurons Effectors are contractile skeletal muscle fibers |
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Proprioceptors
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Muscle spindle
Golgi tendon organ Joint receptors - Are found in capsules and ligaments around joints |
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Muscle spindles
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1. Extrafusal muscle fibers at resting length
2. Sensory neuron is tonically active 3. Spinal cord integrates function 4. Alpha motor neurons to extrafusal fibers receive tonic input from muscle spindles 5. Extrafusal fibers maintain a certain level of tension even at rest |
