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401 Cards in this Set
- Front
- Back
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What are the pre and postsynaptic PS NT?
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ACh
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What are the pre and postsynaptic SNS NTs?
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o Pre- ACh
o Post- NE |
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\What kind of receptor exists where the presynaptic and postsynaptic neuron synapses for parasympathetics
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Pre-Nicotine
Post-Muscarine |
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• What is an M receptor?
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o Muscarine type ACh Receptor
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• Where are the muscarinic/nicotinic receptors located?
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o Nicotinic – located in ganglia
o Muscarinic – located in effector organ |
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• What is a Cholinergic drug?
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o One that mimics ACh (an agonist, has the same action as)
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anticholinergic drugs?
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o Antagonize ACh
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• What drug antagonizes N receptors in the ganglia?
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o Hexamethonium
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• What does Atropine do?
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o Antagonizes M receptors in end organ
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• What is the presynaptic parasympathetic NT and its respective receptor?
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o ACh and the Nicotinic ACh receptor
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• Is there a drug that will block the N receptor in the ganglia for SYMPATHETIC NS?
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Hexamethonium binds that shit no matter
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• What is the NT used to activate the target, and its receptor for the SNS?
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o NE to the Adrenergic Receptor
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• What is unique about the innervation of the Adrenal medulla?
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There is no post ganglionic receptor (no actual synapse in a ganglia)Instead there is a Chromaffin cell in the actually medulla itself
• They are undifferentiated postganglionic cell that secretes epinephrine (and a bit of NE) • They have a Nicotinic Receptor that binds ACh from the presynaptic side |
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• Where do Chromaffin cells secrete?
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o To the blood, thus the whole body sees a bunch of epinephrine
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• What are the adrenergic NTs?
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o From postganglionic neuron
Norepinephrine o From adrenal medulla Epinephrine |
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• What are the types of adrenergic receptors?
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alpha and beta
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• What are the alpha adrenergic receptors?
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o Alpha 1
o Alpha 2 |
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• What are the Beta adrenergic receptors
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o Beta 1, 2, 3
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• What are the Alpha adrenergic receptors agonists and antagonists?
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o agonists:
Bind NE>E Also bind Phenylephrine (alpha adrenergic agonist) o Antagonists:Phentolamine |
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B1 adrenergic receptor agonists
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Epinephrine=NE
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B2 agonists
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Epinephrine>>>>>NE
Way higher affinity |
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B receptor ANTAGONIST
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Propranolol
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• Name the general function of the ANS
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• Innervates and helps control smooth muscule throughout the body, cardiac muscle, exocrine glands, endocrine glands
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• 2 divisions of the ANS and their function?
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• Sympathetic
• Fight or flight • Parasympathetic • Rest and digest |
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• Where are the cell bodies lay for the sympathetic NS
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• T1-L2
• In the IML (intermediolateral horn) |
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• Where does the Parasympathetic originate?
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• Brainstem to sacral spinal cord
• CN 3, 7, 9, 10 • Sacral spinal cord • S2,3,4 |
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• How do the presynaptics in the SNS and the PNS differ?
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• In the sympathetic, they are very short
• In PNS they are very long |
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• Do parasympathetics control blood vessels?
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• HELL NO! Damn alligator bit my hand off! OH MY GOD, ya I was in a tournament down in Florida, hooked my ball down in the rough by the lake, damn alligator just POPPED up! Cut me down in my prime…
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• Lets talk about synergy Lemon, please list some synergistic roles with respect to PNS and SNS
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• Heart rate
• At rest • Strong parasympathetic tone, with weak sympathetic tone (HR 70bpm) • Exercise • Decrease parasympathetic tone (allowing it to increase, you don’t tell it to increase) HR 90bpm • More exercise • Increase sympathetic tone (130 bpm) |
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• What are special cases that are controlled ONLY by the SNS
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• Peripheral blood vessels
• Glyocogenolysis • Late pregnant uterus is the opposite and gets NO SNS innervation (so you don’t contract on an 8 month uterus) |
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1. What does sympathetic stimulation do to the eye?
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a. Assist with far vision
b. Let more light in to the pupil c. Focus on far objects by flattening the lens |
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3. In general what activity does alpha one receptors undertake?
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a. Alpha 1 receptors on smooth muscle cause contraction
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4. How does the lens change focus?
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a. Contract and relax the ciliary muscle
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5. At rest of the ciliary muscle has what effect on the lens
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a. Suspensory ligament has high tension, lens is thin
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6. For far vision, how do we want the ciliary muscle to be?
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a. Relaxed
i. With tension on the suspensory ligaments 1. So the lens is thin |
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7. What do B2 receptors on smooth muscle do?
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a. Cause smooth muscle relaxation
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8. What is the effect of EPI on the ciliary muscle?
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a. Hits the B2 receptor and relaxes the ciliary muscle
b. This allows for far vision |
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9. What does parasympathetics do to the eye?
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a. Pupil constriction and lens thickening for near vision
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10. Pathway for pupil constriction
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a. PS synapses on iris sphincter smooth muscle at an AChM receptor
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describe pupil constriction
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a. PS synapses on iris sphincter smooth muscle at an AChM receptor, causes contraction
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12. How does thickening of the lens occur?
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a. PS synapses on muscle
i. ACh release on AChM receptor on ciliary muscle 1. Muscle contracts releasing tension on the zonula fibers a. Lens thickens, near vision |
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13. What happens in Horner’s Syndrome
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Damage to sympathetic nerves
i. Symptoms 1. Pupil constricts in one eye 2. Superior eyelid droops 3. Dilation of ipsilateral blood vessels 4. No sweating on ipsilateral side |
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14. What causes Horner’s syndrome
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a. Damage to sympathetic nerves of the face
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15. What does parasympathetic stimulation do to the salivary gland
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a. Increase salvation
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16. What role do sympathetic play on salivary glands?
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a. Very little
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17. What receptor is activated by the Neurotransmitter released from the Parasympathetic nerve to the salivary gland?
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a. Muscarinic
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18. What is a drug that stops asthma attacks
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a. Albuterol (B2 agonist)
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19. How does Albuterol help stop an acute asthma attack
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a. It is a Beta 2 Agonist
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20. Are there sympathetic innervations to the lung?
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essentially no; but there are B receptors in the bronchioles...
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21. In the lung, what type of receptors can be found that could be targeted by Albuterol?
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a. B2 adrenergic receptor site (binds NE and some Epi)
i. Causes bronchodialation |
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22. What is COPD?
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a. Chronic obstructive pulmonary disease
b. High parasympathetic tone to their lungs |
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23. How would you vasoconstrict the lung, as in COPD?
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a. PS innervation to MAChR
i. Causes bronchoconstriction and secretion |
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24. What happens to your heart when you think about starting exercise
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a. HR goes up
b. Contractile force goes up |
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25. If you denervate the heart, can it continue to beat
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a. YES, the SA node has automaticity
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26. What is the extrinsic control system of the heart?
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a. Sympathetics
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28. What do sympathetics do to the SA node
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a. Increases the rate at which we depolarize the cells from -60 to threshold
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29. What effect do B1 Receptors have on the heart?
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a. stimulatory
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30. What is the rate of depolarization directly from the SA node (on the atria)?
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a. Fast
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31. What is the rate of depolarization across the AV node?
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a. VERY SLOW
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32. What is the rate of depolarization across the ventricle?
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a. Fast
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33. Discuss the different effects of sympathetic to different portions of the heart
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a. B1 at SA node causes increased rate depolarization
b. NE on B1 at AV node increases conduction velocity c. NE on the B1 on the actual ventricle causes a positive Inotropic effect, causing an increased force of contraction on the atria and ventricles |
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34. Why do B receptor antagonists decrease mortality after MI
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a. helping to prevent cardiac arrhythmias
i. this tells you that sympathetics have the potential to increase arrhythmias |
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35. What negative effect could sympathetics have on heart rate?
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a. Irregular heart rhythm, arrhythmia
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2. Describe how you dilate the eye
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a. Sympathetic alpha 1 nerves synapse on iris radial smooth muscle
i. Release NE 1. Causes contraction of the iris radial smooth muscle a. Contraction and pupil dilation |
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10. Pathway for pupil constriction
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a. PS synapses on iris sphincter smooth muscle at an AChM receptor
i. This is a circular muscle that moves inward causing the pupil to constrict |
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36. What is the role of parasympathetics on the heart?
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a. SA Node
i. M receptors 1. Decrease depolarization rate 2. Decrease heart rate b. AV node i. M receptors 1. Decrease conduction velocity |
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37. What parasympathetic effect is there on the ventricular muscle?
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a. Very little because there are nearly no M receptors
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38. What effect do M receptors have on the heart?
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a. INHIBITION
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1. What are the 2 components of BP?
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a. Cardiac output (liters of blood pushed out by the Left ventricle per minute) (normal is 5L/min)
b. Peripheral vascular resistance |
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What is cardiac output
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liters of blood pushed out by the Left ventricle per minute) (normal is 5L/min)
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2. Are there parasympathetic innervation to blood vessels?
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a. Essentially no, mostly sympathetic
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3. What do alpha 1 receptors do to blood vessels?
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a. vasoconstriction
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4. What do B2 receptors do to blood vessels?
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a. Vasodilation (relax the smooth muscle)
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5. Do all areas of the body have B2 receptors on the vascular bed?
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a. Nope! Only some
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6. When you exercise where do you want blood to go
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a. Shunt it from the gut and skin to the heart, skeletal muscle, and liver (for energy)
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7. What type of receptors are more present in blood vessels to liver/skeletal muscle?
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a. B2 (more than alpha 1)
b. Causes Vasodilation |
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8. What type of receptors are more present in blood vessels to everywhere BUT the liver/skeletal muscle?
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a. Alpha one (more than beta 2)
b. More vasoconstriction |
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9. What do parasympathetics do in the gut?
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a. Help move food down the gut
b. Increases peristalsis c. Relaxes sphincters |
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10. How do parasympathetics act in the gut (detailed receptors etc.)
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a. PS to MAChR to pyloric sphincter
b. PS to M ACh R to rest of intestine to increase tone/motility |
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11. How do sympathetic act on the gut
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a. NE acting on alpha 1 at pyloric sphincter to contract the sphincter
b. NE acting on the alpha 2 and Beta 2 receptors in the intestine to decrease tone and motility |
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12. What is the role for sympathetics in the urinary bladder
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a. Filling
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13. What is the parasympathetic role in the bladder
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a. Emptying
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14. Where do sympathetics to the bladder originate
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a. L2
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15. Where do parasympathetics to the bladder originate
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a. S2, 3, 4 (pudendal)
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16. Describe the specific role of sympathetic in filling the urinary bladder
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a. Sympathetics activated
b. Relax detrusor muscle i. Activate B2 receptors c. Contract the trigone and internal sphincter i. Activate alpha 1 receptors |
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17. Describe the specific role of parasympathetics in emptying the urinary bladder
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a. Parasympathetics activated
b. Contract the detrusor muscle i. Activate M receptors c. Relax the trigone and internal sphincter i. Activate M receptors |
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18. Discuss the Micturation spinal reflex
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a. Stretch receptors in the urinary bladder send afferent message to the spinal cord at sacral level
b. Parasympathetic NS sends efferent message to contract the detrusor muscle, and relax the trigone and internal sphincter |
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19. So if micturation is a spinal reflex, how do we have control over when we Make’a Da’ Pee’ Pee’?
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a. It is a spinal reflex with superimposed higher brain center efferents
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What is an exception to if you are cortically inhibiting mictiration?
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i. Critical closing pressure for smooth muscles
1. If the pressure in the bladder exceeds the contractile force of the trigone and sphincter, you will still piss yourself |
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20. What happens if you crush the sacral cord (with respect to the bladder)
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a. Can’t relax trigone and sphincter, so you then can’t release urine
b. Need to catheter |
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21. What happens if you have SUPRAsacral cord damage (with respect to the bladder)
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a. Reflex intact but no higher inputs for initiation
b. Reflex may return after initial trauma |
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22. What is the issue if you have uninhibited neurogenic bladder?
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a. Damaged higher brain centers for inhibition
b. Any filling stretch initiates reflex micturition i. Constant dribbling |
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23. What type of innervation does the skin get?
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a. ONLY SYMPATHETICS
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24. What type of receptors do smooth muscle on hair use?
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a. a1 receptors
b. Contraction and piloerection |
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25. Is sweating a sympathetic or parasympathetic response
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a. sympathetic
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26. How does sweating on the palms of the hands occur?
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a. EPI acts on alpha 1 receptor
i. Causes sweating |
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27. How does sweating occur on most sweat glands in the body?
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a. Sympathetic AcH acting on M receptor of sweat gland
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28. What role do sympathetics play in the kidney?
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a. Release NE on B1 receptors on the Juxtaglomerular cells
i. This causes rennin release 1. Causes vasoconstriction |
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29. What is the role of autonomics in the adrenal medulla?
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a. Sympathetic PREGANGLIONIC innervation of chromaffin cells release epinephrine and norepinephrine
b. Preganglionic neuron releases ACh binds to N receptor in adrenal medulla, causes release of EPI (and some NE) |
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30. What role do autonomics play in male genitalia (Erection)
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i. Parasympathetics cause dilation of arteries to corpora cavernosa of penis and corpus cavernosum of urethra
ii. Venus sinus fills |
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What role do autonomics play in male genitalia (Emission)
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i. Sympathetics cause contraction of epididymis, vas deferens, seminal vessicles, prostate
ii. Propels fluid and semen into posterior urethra iii. Sympathetics also close the internal sphincter of the bladder |
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What role do autonomics play in male genitalia (Ejaculation)
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i. Sympathetics contract bulbocavernosus and ischiocavernosus muscles and pelvic floor
ii. Expels semen |
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What role do parasympathetics play in female genitalia?
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i. Vasocongestion of genitalia
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What role do parasympathetics plus sympathetics play in female genitalia?
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i. Transudation of epithelial mucous through the vaginal wall
ii. Secretion from Bartholin’s glands iii. Orgasmic platform 1. Contraction of outer vagina 2. Shortening of uterus 3. Dilation of cervix iv. Higher brain centers very involved |
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1. What is sympathetic/parasympathetic tone?
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the firing/messaging rate to a target
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2. What happens if you cut a sympathetic/parasympathetic nerve?
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-Over time you will get some function back
-Receptors are still able to respond to NT or mimetic drugs -And the number of receptor sites increase in cell membranes |
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describe the example of a Superior cervical ganglionectomy
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a. Knock out sympathetic to eye
i. Pupil constricts (parasympathetic tone high) ii. Nonresponsive to light iii. After weeks normal dilation returns |
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what is an example of convergence of a message
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Parasympathetic preganglionic cells synapse with few postgangionic cells
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what is an example of divergence of a message
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Sympathetic preganglionic cells synapse with many postganglionic cells
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Discuss presynaptic inhibition
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Many preganglionic neurons have inhibitory type of receptors that shut off transmitter release
NE released from presynaptic nerve terminal --Alpha 2 receptor on the SAME NERVE that released the NE bind the NE ---Then it turns off its own signal |
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Discuss inhibition of the GI tract
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a. Normally ACh is released to post synaptic M receptors for peristalsis
i. If EPI or NE is present (do to fight/flight response) it binds to the presynaptic alpha 2 receptor 1. This prevents ACh release |
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Give an example of resting firing for sympathetics
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medulla oblongata controlling the firing rate for blood vessels..increase firing, constrict; decrease--dilate
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Please discuss the referred pain example of gallbladder infection
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a. Pain afferents from gallbladder synapse at the same spinal level with cutaneous sympathetics to vasculature
b. Inhibition of cutaneous vasoconstriction causes vasodilation and a red area results c. Simultaneous synapse with motorneurons to abdominal musculature – stimulate and get localized tightening |
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10. What is hyperesthesia
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a. Increased sensitivity to touch
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11. Hyperalgesia
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Increased sensitivity to pain
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12. What are hyperalgesia and hyperesthesia due to?
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These phenomenon are due to convergence of peripheral and abdominal afferents which go to pain centers of cortex
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13. Spinal level for heart, stomach, liver/gallbladder, large intestine?
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a. Heart: T1-3
b. Stomach: T7-8 c. Liver/gallbladder: T7-8 d. Large Intestine: T12-L1 |
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14. Function of the medulla oblongata?
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a. Circulatory center
b. Respiratory control center |
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15. Pons function?
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a. Micturition
b. Suprapontine input from hypothalamus and cortex for cognitive control – usually for inhibition of micturition |
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16. What is the job of the hypothalamus
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Receives afferents from midbrain
Receives humoral messages from CSF and blood Central monitoring of ANS control |
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• List the functions of the cardiovascular system.
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o Distribute hormones
o Humoral and cellular inflammatory mediators o Temperature regulation o Removes waste o Helps with exercise to move energy |
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• Explain why diffusion as a mechanism is insufficient on its own for the distribution of oxygen around the body.
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o For diffusion to get all the way through your body it would take nearly 5 years to get Oxygen to your toe
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o How do both bulk flow and diffusion play a role in the delivery of oxygen to the body?
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- Diffusion for O2 from the lung to pulmonary circulation
- Bulk flow to pump the O2 in the blood by pumping the heart ---Diffusion of O2 unloading to the tissues |
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• Describe the role of the heart in generating the bulk flow of blood through the cardiovascular system.
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o The heart is the pump
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• Explain the functional advantages of having two interdependent pumps in the heart
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Right heart= pumps to lungs
Left heart= to rest of body o Why are they interdependent? Must pump the same amount of blood (same output or blood will accumulate) Most coordinate contraction time |
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how do you calculate mean blood pressure
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Mean= diastolic + (1/3 x (systolic-diastolic))
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• Describe the arrangement of the individual circulations to different organs with respect to the heart
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o Circulation is in parallel
Aka the blood is divided up and sent to different parts of the body at the same time |
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What is an exception to the idea that blood is distributed in parallel
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• The one exception of this is the LIVER
o In the liver, you have portal system It gets blood from the GI via the portal vein • THIS IS A SERIES arrangement |
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• Explain how blood flow to different organs can be varied
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o By controlling vascular smooth muscle tone
Aka sympathetic tone o This occurs mostly at the level of arterioles |
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list the local and systemic factors that control blood flow
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Local:Metabolic factors, Paracrine Agents
Systemic:SNS, Hormones |
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o Transmural pressure
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PT = PIN - POUT
-Pressure of fluid inside pushing up on the walls -Minus the interstitial pressure pushing from out to in -This has to be a positive number or the vessel will collapse |
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o Compliance
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Change in volume per unit change in pressure;
= ΔV / ΔPT ; Great veins have large compliance, they are thin walled so when you get a little change in pressure they expand out considerably |
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o Capacitance
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Volume/PT
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• Describe and explain the distribution of blood in the systemic circulation by blood vessel type.
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o Veins hold the most blood because they are highly compliant
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• Explain how arterial stretch during systole contributes to diastolic pressure
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o Systole occurs and artery stretches
- The stored energy from the elastic recoil will be transferred back to the blood • This prevents the diastolic pressure from dropping down too low |
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• Describe and explain the distribution of blood in the systemic circulation by blood vessel type.
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o Veins hold the most blood because they are highly compliant
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Dichrotic notch
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• Seen in the graph of systolic diastolic pressure
• It is when the aortic valve SLAMS shut |
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Flow equals?
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Q=(P1-P2)/R
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• Define the terms pressure, flow, resistance and velocity as they relate to cardiovascular hemodynamics.
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o Pressure: Force per unit area
o Flow: volume transferred per unit time o Resistance: opposition to flow o Velocity: flow per cross sectional area |
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Cardiac output=?
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o Cardiac Output= Paorta/Total peripheral resistance
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• Describe the dependence of vascular resistance on vascular radius
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Resistance is inversely proportional to radius^4
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• Describe the dependence of vascular resistance on vascular length
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Longer the length the more resistance
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Describe the dependence of vascular resistance on blood viscosity
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increase viscosity, increase resistance
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Q= (consider resistance)
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Q= [(P1-P2)x pie r^4]/ 8nl
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• Explain how total peripheral resistance is calculated by the sum of individual vascular resistances in series
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Simply add resistance
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Explain how total peripheral resistance is calculated by the sum of individual vascular resistances in parallel
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1/Rtotal=(1/x)+(1/y)+(1/z)
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• Name and explain the main site of resistance in the systemic circulation
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o ARTERIOLES (not capillaries)
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Why are capillaries not the main site of resistance in circulation considering that they have the smallest radius?
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-You have to sum the radius of ALL the capillaries
• This is the equivalent of a really huge radius |
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At a given flow, blood velocity depends on ?
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Cross sectional area
increase CSA decrease velocity decrease CSA increase velocity |
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what happens to lateral pressure against a blood vessel wall as you increase velocity?
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it goes down
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Velocity (for blood flow) =
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Flow/CSA
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o Bernoulli principle
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As kinetic energy goes up, potential energy goes down and vice versa
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• Name and explain the site of lowest blood velocity in the systemic circulation
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Capillaries; due to large CSA; and velocity=flow/CSA
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• Describe the dependence of blood viscosity on hematocrit, blood velocity
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o As viscosity increases % hematocrit increases, but blood flow velocity decreases
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• Explain how artery or valve stenoses can cause audible murmurs.
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o You go from laminar flow to turbulent flow due to increased velocity when there is a stenosis
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• Describe what turbulent blood flow would sound like with auscultation.
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o Laminar: silent
o Turbulent: makes sound (bruit) |
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• List the 3 patterns of blood flow and where they typically occur in the cardiovascular system
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o Laminar
Arteries Arterioles Venules Veins o Turbulent In smooth vessels Promoted by high blood flow rates In ventricles and stenosed arteries o Single File: capillaries |
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What is the Reynolds number?
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It predicts the probability of turbulent flow
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What factors affect the Reynolds number?
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Reynolds number predicts turbulence: bigger diameter/velocity-->larger reynolds (more likely to be turbulent)
-more viscous=lower reynolds number |
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• Describe what turbulent blood flow would sound like with auscultation.
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o Laminar: silent
o Turbulent: makes sound (bruit) |
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• Explain how artery or valve stenoses can cause audible murmurs
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o You go from laminar flow to turbulent flow due to increased velocity when there is a stenosis
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• Describe the dependence of blood viscosity on hematocrit, blood velocity and vessel diameter.
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o As viscosity increases % hematocrit increases, but blood flow velocity decreases
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• Describe the pattern of blood flow in laminar flow
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o Around the wall of the vessel there is mostly plasma (this is the idea of zero velocity being due to plasma skimming at the edge of the vessel)
o As a result, the RBCs undergo axial streaming, in which they move to the middle of the vessel and are sucked along |
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• Describe the sequence of electrical excitation of the heart.
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o Action potentials initiate contraction of the heart
o Atria contract before the ventricles due to the sequence of electrical excitation |
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• Explain what is meant by the heart being ‘myogenic’ in origin.
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o Certain areas are able to depolarize on their own
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list the specialized areas of cardiac tissue which demonstrate automaticity
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o SA node, AV node, Purkinje fibers (some)
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• List the ion currents that produce diastolic depolarization and underlie the action potential in the SA node.
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o Ik
- Causes repolarization o If (funny channels) - Hyperpolarizing dependent Na channels - Inward current for Na to start depolarization o Ica, L - Causes the quick spike that does the actual AP |
|
|
• Explain the mechanisms by which sympathetic stimulation changes heart rate
|
Increases the funny channel opening
This changes the rate of phase 4 depolarization Makes it so you open the L type Ca channels sooner |
|
|
Explain the mechanisms by which parasympathetic stimulation changes heart rate
|
Slows the opening of the funny channels
Opens an ACh dependent K channel • Causes more hyperpolarization • Thus slowing the depolarization to prevent opening of L type Ca channels |
|
|
• Explain why the rate of firing of the SA node, and not other pacemaking sites, determines heart rate
|
o SA node is the fastest that can initiate the depolarization
This suppresses the spontaneous depolarization of the AV and purkinje fibers • You will depolarize those sooner than they could on their own o SA: 80/sec> AV:50/sec>Purkinje 20/sec |
|
|
• Describe how SA Nodal firing causes electrical excitation of the atria. Explain why this process occurs rapidly.
|
o On the right atria, the signal spreads at .05 m/s which is fast
o After the signal crosses to the left atria, it becomes even faster (1m/s) |
|
|
• Describe the relative rate of electrical conduction through the AV node
|
o In the AV node the speed of conduction decreases (.01-.05 m/s)
This is really slow |
|
|
• Describe the conduction pathway from the AV node to the ventricles.
|
o First hits the bundle of His (left and right bundle)
Left specifically will go more posterior on the heart o Signal runs down the septum Then climbs back up the walls of the ventricles o This is occurring very fast 2-5 m/s |
|
|
Discuss the 4 phases of the ventricular AP
|
o 4: due to the IK1 inward rectifier
o 0: voltage gated Na channels, very fast o 1: due to outward currents Ito (transient outward), fast • Lets out K+ quickly Ito, slow • Lets out K+ slowly Also a Cl- channel opens Because they are transient they will not take us all the way down o 2: Plateau Around 0 mV Open L type Ca channels A bit later you open Na channels If this were it, you would have a upward sloping potential So 2 K channels balance this • IKr and IKs: let out K+ o 3: Rapid repolarization Massive opening of 2 K currents (IKr, IKs) o 4: IK1 inward rectifiers |
|
|
• Describe how electrical excitation of ventricular muscle is achieved
|
o The AP is propagated through ventricular tissue by the spread of passive current cell to cell
This is done by gap junctions • They have low electrical resistance and allow for the current to pass through |
|
|
o 2 things determine the speed of conduction across the ventricle
|
Cell diameter (bigger diameter=faster)
Density of tight junctions |
|
|
• Explain why ventricular electrical excitation does not re-excite the atria under normal circumstances.
|
o It is prevented by the annulus fibrosus cordis
Insulating layer between the atria and ventricle o AV node refractoriness |
|
|
As a depolarizing wave moves towards a recording electrode, what is recorded?
|
an upstroke
|
|
|
As a depolarizing wave moves away from a recording electrode, what is recorded?
|
downstroke
|
|
|
How does depolarization travel in the heart
|
Endo to epi, apex to base
|
|
|
How does repolarization occur in the heart, in what order?
|
The last to depolarize is the first to repolarize (remember order of depolarization is endo to epi, apex to base)
|
|
|
When reading an ECG, every box is how many mm?
|
1 mm
|
|
|
On an ECG, how many seconds are the equivalent of 5mm (or 5 boxes)
|
0.2 seconds
|
|
|
What can direction (up or down) tell you about an ECG
|
direction of the wave
|
|
|
What is an interval on an ECG
|
it includes AT LEAST one wave
|
|
|
what can the magnitude of the deflection tell you on an ECG
|
the amplitude of the wave
|
|
|
what can the horizontal portion of an ECG tell you?
|
1) time btw events
2) breadth of the wave (how long it takes depol/repol to spread; size and/or speed of conduction) |
|
|
What is seen in the P-R segment of an ECG
|
AV node
|
|
|
What does the P-R interval tell you on an ECG?
|
P wave plus P-R segment
conduction through the atria and the AV node |
|
|
What does the P wave show us on an ECG
|
atrial depolarization
|
|
|
What does the QRS interval tell you on an ECG?
|
activation of the ventricles, all about ventricular depolarization
|
|
|
What is occurring during the S-T segment tell you?
|
ventricle is fully depolarized, represents plateau phase (this is isoelectric because the electrodes aren't seeing a difference btw. one another)
|
|
|
T- wave
|
rapid ventricular repolarization
|
|
|
S-T interval
|
all of repolarization of the ventricles
|
|
|
Q-T interval
|
duration of ventricular systole (includes depolarization of ventricle, plus repolarization of ventricle; starts at QRS and ends at T)
|
|
|
What is clinically important about the Q-T interval
|
see arrhythmia there often, since it covers all of systole
|
|
|
What is the U wave?
|
repolarization of myocardial m cells
|
|
|
What is the T-P segment
|
end of one cycle to the beginning of the other cycle; assumed to be zero baseline
|
|
|
What is assumed to be the zero baseline?
|
the T-P segment
|
|
|
if conduction is slowed through the AV node, what happens to the PR interval?
|
it becomes prolonged
|
|
|
if conduction is slowed through the bundle of his, or purkinje fibers, what happens to the PR interval?
|
you will not see prolongation of PR interval, but a widening of the QRS
|
|
|
What does long QT syndrome normally cause?
|
cardiac DEATH
|
|
|
What are the bipolar leads?
|
I, II, III
|
|
|
What is Itobin(?)'s triangle?
|
Right arm, Left Arm, Left Leg
|
|
|
In itobin's triangle, what is the configuration of positive and negative leads
|
I: left arm positive, right arm negative
II: right arm negative, left leg positive III: left arm negative, left leg positive |
|
|
For lead I what direction will the drawing be for atrial, ventricular and repolarization
|
atrial, ventricular and repolarization will all be up
|
|
|
for lead II, what will the EKG look like
|
atrial: up
ventricular: up repolarization: up |
|
|
for lead III, what will the EKG look like
|
atrial: up
ventricular: up repolarization: up |
|
|
What is the EKG electrode configuration for AVF
|
Positive electrode is on the Left Foot; there are 2 electrodes on the hands that act as grounds (to act as negative electrode)
|
|
|
What is the EKG electrode configuration for AVR
|
Positive electrode on Right Arm, left foot and left arm act as ground (to act as negative electrode)
|
|
|
What is the EKG electrode configuration for AVL
|
Positive electrode on left arm, right arm and left foot ground (to act as negative electrode)
|
|
|
What do V1-V6 measure for an EKG?
|
measure electrical depolarization in the horizontal plane
|
|
|
Why is repolarization causing an upstroke (aka going in the same direction as the depolarization on the EKG)
|
as repolarization occurs, the positive electrode will start to see a positive charge building up outside the cell because that portion is becoming negative inside the cell first. (remember the whole repolarization occurring in the opposite direction as depolarization)
|
|
|
What is an arrhythmia?
|
Abnormality of impulse initiation, conduction, or both
|
|
|
What is the intrinsic rate of the normal pace makers?
|
a. SA: 60-100bpm
b. Atria conducting: 60-80 c. AV junction: 40-60 d. Purkinje fibers: 20-40 |
|
|
3. What is sinus tachycardia
|
>100 bpm at SA Node pacemaker
|
|
|
5. What generally causes SA arrhythmias?
|
Altered autonomics
|
|
|
What generally causes SA bradycardia? Is this always abnormal?
|
Increases in vagal outflow
b. No athletes can have lowered BPM |
|
|
What does inspiration/expiration do to the heart rate?
|
Inspiration: Accelerates
b. Expiration: deceleration |
|
|
How do arrhythmias emerge?
|
a. Higher order pacemaker becomes depressed
b. Conduction block c. Lower order pacemaker can emerge (be enhanced) |
|
|
9. What makes latent pacemakers emerge?
|
a. High PARASYMPATHETIC tone (SA node gets slow)
b. Other things i. High catecholamine concentration ii. Hypoxemia iii. Drug use (cocaine, like it was 1980) iv. Ischemia v. Stretch vi. Electrolyte disturbances |
|
|
What is abnormal tissue automaticity
|
a. Tissue that is not normally automatic becomes automatic
b. Key is that rhythms often cannot be overdrive suppressed |
|
|
11. What is Early afterdepolarization (EAD)
|
a. Get a prolonged plateau
b. Causes a depolarization to occur before repolarization can fully happen c. This is an arrhythmia d. L type Ca channel gets opened up again |
|
|
10. What is abnormal tissue automaticity
|
a. Tissue that is not normally automatic becomes automatic
b. Key is that rhythms often cannot be overdrive suppressed |
|
|
15. Where are conduction delay/blocks most likely to occur?
|
a. AV node
|
|
|
13. What is a Delayed afterdepolarization?
|
a. Oscillation in membrane potential after repolarization
b. Causes another depolarization, until it reaches threshold |
|
|
14. What are conduction abnormalities?
|
a. Conduction delay or block
b. Re-entry |
|
|
16. What is a 1st degree block
|
a. Every pulse conducts
b. Consistent prolongation of P-R interval, but nothing fails c. Every P has a QRS |
|
|
What is a 2nd degree block?
|
a. Some, not all, pulses conduct
b. Have some P’s that are not connected to QRS |
|
|
What is a 3rd degree block?
|
NO pulses conduct
|
|
|
What are the two types of 2nd degree block?
|
a. Wenckeback
b. Mobitz |
|
|
Wenckebach
|
2nd degree block; Result of abnormality of the AV node
b. Progressive prolongation of PR c. Then a dropped beat d. Series repeats |
|
|
Mobitz
|
2nd degree block;
a. Anatomical lesion in the His or purkinje fibers b. No prolongation of PR (usually) Can have 2:1 or 3:1 block |
|
|
What is a 2:1 block?
|
Mobitz 2nd degree block;
i. For every 2 p you have 1 QRS ii. Dropping every other beat |
|
|
What is a 3:1 block?
|
Mobitz 2nd degree block;
i. 3 p for every 1 QRS ii. Dropping 2 beats |
|
|
22. What mechanisms contribute to AV block
|
a. Increased vagal tone
b. Ca+ channel block c. Beta-blocker d. Digitalis e. Hyperkalemia |
|
|
23. What things are necessary for re-entry to occur?
|
a. Unidirectional block (or transient)
b. Slowed conduction over an alternate pathway c. Re-excitation of tissue proximal to block (Thus, the effective refractory period of the reentered region must also be less than the propagation time around the loop) -THIS IS BAD |
|
|
So what is re-entry promoted by?
|
a. Things that slow conduction velocity, shorten the refractory period, or a combination of both
|
|
|
s re-entry ordered or random?
|
It can be either
|
|
|
What does WPW do to PR and QRS?
|
This shortens PR, and widens QRS
|
|
|
What is Wolf-Parkinson-White Syndrome? (WPW)
|
a. Patients have an accessory pathway between the atria and ventricle (called bundle of Kent)
b. Can get pre-excitation c. Sometimes get re-entry |
|
|
What happens in pre-excitation seen in WPW?
|
i. Meaning you get excitation of the ventricle from the accessory pathway BEFORE the AV node
ii. This shortens PR, and widens QRS |
|
|
What happens with re-entry seen in WPW?
|
i. Pathway: atria, AVN, ventricle, accessory pathway, atria
ii. Basically the signal from the AV node, travels back up the accessory pathway |
|
|
SUPRAventricular tachycardia
|
a. Signal runs down AV node, and re-enters through the accessory pathway
b. This is just another name for WPW re-entry |
|
|
What is electrical axis?
|
direction of depolarization
|
|
|
What is a vector?
|
an arrow that symbolizes the direction of depolarization
|
|
|
What is the clinical usefulness of vectors?
|
pattern of excitation, orientation of the heart, change in heart mass (hypertrophy), alteration in dipoles (infarction)
|
|
|
What is a horizontal heart?
|
vector pointing to zero, seen in obese people
|
|
|
what is a vertical heart?
|
vector pointing straight down, at +90
|
|
|
If a vector is in the northwest what is going on?
|
extreme right OR left axis deviation
|
|
|
if lead I is up, and avF is up, where is the vector and what does this mean?
|
vector is in normal quadrant, this is a good thing
|
|
|
If lead I is up, and avF is down, where will the vector be?
|
Left axis deviation
|
|
|
if lead I is DOWN and avF is UP where is the vector?
|
Right Axis deviation
|
|
|
If lead I is down and avF is down, where is the vector?
|
Northwest quadrant
|
|
|
Using an Isoelectric lead, what is another way you can find the vector?
|
Identify the lead that is perpendicular to the isoelectric lead, then see if the perp lead's QRS is up or down. If Up go towards positive electrode, if down, go away from positive electrode
|
|
|
Hypertrophy effect on vector
|
the larger the mass, the more the area contributes to the vector (higher amp QRS), so the vector will move TOWARDS hypertrophy
|
|
|
Infarction effect on a vector
|
they vector will move away from infarction because you will not get depolarization there!
|
|
|
if transitional leads (which are which ones?) shift to the right, what do you have?
|
(V3/V4) rightward rotation
|
|
|
if transitional leads (which are which ones?) shift to the left, what do you have?
|
(V3/V4) leftward rotation
|
|
|
32. What happens when you have trauma to the skin?
|
a. Histamine is releases (vasodilator)
b. Get the triple response i. Reddened line ii. Flare (circle of red as the histamine spreads) iii. Wheal (edema) |
|
|
31. When you are outside exercising what happens to skin?
|
a. You shut down sympathetics, cause vasodilation, get red and flushed
|
|
|
30. What happens when you walk in the cold and your face is exposed
|
a. Get sympathetic alpha 1 vasoconstriction
b. Pale and white looking |
|
|
29. Do we use local metabolic products to control dilation of skin?
|
a. Nope
|
|
|
28. During exercise, what do we do to the cutaneous sympathetic tone?
|
a. We inhibit it, causing dilation of arterioles
|
|
|
27. What is the primary control for body temperature?
|
a. Autonomics to the skin
|
|
|
26. What kind of innervation does the skin get?
|
a. Dense sympathetic innervation
|
|
|
25. What is active hyperemia?
|
a. You get lactate, adenosine, and K+ build up
|
|
|
24. What is reactive hyperemia?
|
a. When a muscle sustains a contraction, you are compressing down arteries
b. This mechanically reduces blood flow to the muscle c. When you relax, you get way more blood flow than it would normally get at rest d. This flushes out adenosine, K+, lactate (wastes) |
|
|
23. What is the main form of control of skeletal muscle during exercise?
|
a. Local metabolic control
|
|
|
22. At rest, what kind of innervation is skeletal muscle getting (for blood flow regulation)
|
a. Sympathetic (NE at alpha 1 receptors)
|
|
|
21. What is the major determinant of total peripheral resistance (TPR)?
|
a. The degree of vasoconstriction in skeletal muscle
|
|
|
20. How do skeletal muscles control blood flow? (What mechanisms)
|
a. Local metabolites and autonomics
|
|
|
19. What does hypoxia cause in the lung? Why?
|
a. Vasoconstriction
b. Shunt blood away from poorly ventilated areas c. Put the blood where there is better gas exchange |
|
|
18. What primarily controls pulmonary circulation?
|
a. Oxygen
|
|
|
17. What does edema do to cerebral blood flow?
|
a. Increase in pressure will significantly impair flow
|
|
|
16. Is cerebral blood flow sensitive to neurotransmitters?
|
a. Nopers
|
|
|
15. What mechanisms allow the autoregulatory effect in the brain?
|
a. 1st: myogenic arteries (they contract when the artery expands)
b. 2nd: metabolic products |
|
|
14. What does chronic hypertension do to cerebral blood flow
|
a. The brain “resets the computer” for autoregulation
b. It shifts the autoregulation curve up c. Changes mean arterial pressure d. Can see hemorrhagic stroke |
|
|
13. What is the difference in pressure in the right coronary artery between diastole and systole?
|
a. It is pretty much the same through both phases
|
|
|
12. What happens to the right coronary artery pressure during systole?
|
a. Constriction only during isovolumetric contraction
b. Other than that, it is mostly sustained i. Due to Less constriction of capillary bed |
|
|
11. During the cardiac cycle, where is there most likely to be a blockage in the heart?
|
a. In the left coronary artery, during the beginning of systole
i. This is due to very low pressure |
|
|
10. What happens to the left main coronary artery pressure during diastole?
|
a. Pressure becomes its maximum
|
|
|
9. What happens to the left main coronary artery pressure during ejection?
|
a. It goes up (note that there is some valve impairment)
|
|
|
8. What happens to the left main coronary artery pressure during isovolumetric contraction?
|
a. It is very low
i. Due to subendocardial constriction |
|
|
7. With respect to the heart, which layer(s) are the worst at autoregulation?
|
a. The subendocardium
b. The middle and outer are better |
|
|
6. What are the starting and exercise blood flows from the heart (ml/min)
|
a. Normal: 250
b. Exercise: 1200 |
|
|
5. How does the heart meet its oxygen demand?
|
a. By increasing blood flow
|
|
|
4. Does the heart use anaerobic glycolysis?
|
a. To a very small degree
|
|
|
3. When does the heart best extract oxygen?
|
a. At rest
|
|
|
2. What mechanisms play a role in autoregulation?
|
a. Metabolic control
b. Myogenic control c. NO (vasodilator) |
|
|
1. Explain the concept of organ blood flow autoregulation
|
a. At low pressure, organs get more flow than you would expect
b. At high BP, the flow will be lower than expected |
|
|
2. What is pulse pressure?
|
a. Systolic-Diastolic pressure
|
|
|
3. What is MAP and how is it calculated?
|
a. Mean arteriole pressure
b. MAP=P(diastole)+1/3(Systolic Pressure-Diastolic Pressure) |
|
|
4. How does a sphygmomanometer measure blood pressure?
|
a. When cuff pressure exceeds systolic pressure, blood will no longer flow through the artery, and no sounds can be heard through the stethoscope. When pressure is released, blood flow resumes and diastolic pressure is determined.
|
|
|
Besides using diastolic and systolic pressures how else could you calculate MAP?
|
MAP=COxTPR
CO=cardiac output=SVxHR TPR=total peripheral resistance |
|
|
6. What happens to mean arterial pressure if you increase cardiac output?
|
a. MAP=COxTPR
b. So increase CO, increase MAP |
|
|
7. What happens to MAP if you decrease TPR?
|
a. MAP=COxTPR
b. Decrease TPR decrease MAP |
|
|
8. How does adrenergic receptor activation affect blood vessels?
|
a. If B2 is activated, vasodilation will occur. This is prevalent in BV to liver, skeletal muscle, coronary, and cerebrum.
b. If A1 is activated, expect vasoconstriction. (chronic vasoconstriction, see dilation due to backing off vasoconstriction) |
|
|
9. How does M receptor activation affect blood vessels?
|
Although parasyms do not typically influence BV, there are exceptions such as salivary, some GI, and erectile tissue. In these cases, PSNS can cause vasodilation of smooth muscle cells.
b. ACh is responsible for this activity c. Note that this is not a direct innervation |
|
|
10. By what two mechanisms do parasympathetics cause indirect vasodilation?
|
a. Vascular smooth muscle cells have M3 endothelial receptors for ACh
i. That cell then releases NO 1. This moves to vascular smooth muscle cell and causes vasodilation b. M2 receptor on adrenergic presynaptic neuron (which is dumping NE) is activated by ACh i. This inhibits the release of NE 1. Causes vasodilation |
|
|
11. What effect do alpha one receptors have on veins? What does this do?
|
a. They constrict
b. This forces blood back to the heart |
|
|
13. Describe the general distribution of blood in the body.
|
a. 80% is in systemic circulation
i. Most of this is in the veins. ii. Why? Because veins are 20X more compliant that arteries b. Central BV contains 20-25% i. This is the central vena cava, IVC, RA, RV, Pulmonary circulation, LA. ii. This can be measured by central venous pressure. |
|
|
How can you change central blood volume?
|
a. Change total BV
i. Increase: infuse fluid, retain salt and H2O, shift fluid from interstitial to plasma ii. Decrease: Hemorrhage, sweat, shift plasma fluid to interstitial b. Redistribute the BV you already have. |
|
|
15. Describe the vascular function curve.
|
a. Pressure in the right atrium (Pra) depends on CO and venous return (VR). At the same time, Pra is defined by CO and VR. Through this, CO = VR.
|
|
|
17. If you have a dramatic decrease in cardiac output, what will be the effect on pressure in the right atrium?
|
a. Not translocating as much blood from the right side out
b. This will cause an increase in atrial pressure |
|
|
18. If you increase right atrial pressure, what will happen to venous return?
|
a. It will decrease
b. It slams shut the door, not as much blood can return to the heart |
|
|
19. So what is the relationship between cardiac output, pressure in the right atrium, and venous return?
|
a. Increase cardiac output
i. Decrease pressure in right atrium 1. Increase venous return |
|
|
20. If you increase pressure in the right atrium, what happens to cardiac output?
|
it decreases
|
|
|
21. What is mean circulatory filling pressure (Pmc)?
|
a. Measure of fullness of the system or tightness of the container
b. So if you stopped the heart, the volume in the right atrium should equal the Pmc |
|
|
22. What are the three factors that can affect the vascular function curve?
|
a. BV (blood volume)-how full the system is. This is also an effect on the mean circulatory filling pressure (Pmc).
b. Capacitance on the system (the tightness of the container) c. Slope of the curve, or total peripheral resistance. |
|
|
23. What happens if you increase volume or venous tone to the vascular function curve?
|
a. Vascular function curve is the Cardiac output vs. pressure in right atrium graph
b. It shifts the curve up c. Think UP, UP, UP d. Thus you get increased cardiac output |
|
|
24. What happens to the vascular function curve if you decrease volume or venous tone?
|
a. Decrease CO
b. Curve shifts down c. (baby are you…) DOWN DOWN DOWN |
|
|
25. What is a decrease in venous compliance (Cv) equivalent to?
|
a. An increase in venous tone
|
|
|
26. What happens to venous return when you have vasoconstriction? (sudden increase in resistance)
|
a. The pressure decreases
|
|
|
27. What happens to the vascular function curve (venous return) when systemic resistance decreases?
|
a. It increases
|
|
|
28. At any PRA, increasing arteriolar resistance (increases or decreases) venous return (cardiac output)?
|
a. DECREASES
|
|
|
29. At any PRA, decreasing arteriolar resistance (increases or decreases) venous return (cardiac output)?
|
a. Increases
|
|
|
30. What happens to Pmc (mean circulatory filling pressure) when arteriolar resistance changes?
|
a. Nothing, doesn’t really change
|
|
|
31. What happens if you increase right atrial pressure, what happens to cardiac output?
|
a. Increase cardiac output
|
|
|
32. What can cause enhanced cardiac function? 3 things
|
a. Decrease afterload
b. Increase inotropy c. Increase heart rate |
|
|
33. What can depress the cardiac output? 3 things
|
a. Increase afterload
b. Decrease inotropy c. Decrease heart rate |
|
|
34. If you give a patient digitalis, will you increase, decrease, or keep cardiac output the same?
|
a. Digitalis increases Ca2+, thus increases contraction, thus you get enhanced cardiac output
|
|
|
35. Right atrial pressure determines what?
|
a. Cardiac output
|
|
|
36. What does cardiac output determine?
|
right atrial pressure
|
|
|
37. What is the equilibrium point? (with respect to the vascular function curve)
|
a. Where cardiac output equals venous return
|
|
|
38. When you have a mismatch in cardiac output and venous return, what happens with each beat?
|
a. Eventually you will return to the equilibrium point
|
|
|
1. Explain the concept of organ blood flow autoregulation
|
a. At low pressure, organs get more flow than you would expect
b. At high BP, the flow will be lower than expected |
|
|
2. What mechanisms play a role in autoregulation? 3
|
a. Metabolic control
b. Myogenic control c. NO (vasodilator) |
|
|
3. When does the heart best extract oxygen?
|
a. At rest
|
|
|
4. Does the heart use anaerobic glycolysis?
|
a. To a very small degree
|
|
|
5. How does the heart meet its oxygen demand?
|
a. By increasing blood flow
|
|
|
6. What are the starting and exercise blood flows from the heart (ml/min)
|
a. Normal: 250
b. Exercise: 1200 |
|
|
7. With respect to the heart, which layer(s) are the worst at autoregulation?
|
a. The subendocardium
b. The middle and outer are better |
|
|
8. What happens to the left main coronary artery pressure during isovolumetric contraction?
|
a. It is very low
i. Due to subendocardial constriction |
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9. What happens to the left main coronary artery pressure during ejection?
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a. It goes up (note that there is some valve impairment, and it is not at maximum pressure)
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10. What happens to the left main coronary artery pressure during diastole?
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a. Pressure becomes its maximum
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11. During the cardiac cycle, where is there most likely to be a blockage in the heart?
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a. In the left coronary artery, during the beginning of systole
i. This is due to very low pressure |
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12. What happens to the right coronary artery pressure during systole?
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a. Constriction only during isovolumetric contraction
b. Other than that, it is mostly sustained i. Due to Less constriction of capillary bed |
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13. What is the difference in pressure in the right coronary artery between diastole and systole?
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a. It is pretty much the same through both phases
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14. What does chronic hypertension do to cerebral blood flow
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a. The brain “resets the computer” for autoregulation
b. It shifts the autoregulation curve up c. Changes mean arterial pressure d. Can see hemorrhagic stroke |
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15. What mechanisms allow the autoregulatory effect in the brain?
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a. 1st: myogenic arteries (they contract when the artery expands)
b. 2nd: metabolic products |
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16. Is cerebral blood flow sensitive to neurotransmitters?
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no
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17. What does edema do to cerebral blood flow?
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a. Increase in pressure will significantly impair flow
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18. What primarily controls pulmonary circulation?
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O2
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19. What does hypoxia cause in the lung? Why?
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a. Vasoconstriction
b. Shunt blood away from poorly ventilated areas c. Put the blood where there is better gas exchange |
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20. How do skeletal muscles control blood flow? (What mechanisms)
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a. Local metabolites and autonomics
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21. What is the major determinant of total peripheral resistance (TPR)?
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a. The degree of vasoconstriction in skeletal muscle
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22. At rest, what kind of innervation is skeletal muscle getting (for blood flow regulation)
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a. Sympathetic (NE at alpha 1 receptors)
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23. What is the main form of control of skeletal muscle during exercise?
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a. Local metabolic control
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24. What is reactive hyperemia?
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a. When a muscle sustains a contraction, you are compressing down arteries
b. This mechanically reduces blood flow to the muscle c. When you relax, you get way more blood flow than it would normally get at rest d. This flushes out adenosine, K+, lactate (wastes) |
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25. What is active hyperemia?
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a. You get lactate, adenosine, and K+ build up
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26. What kind of innervation does the skin get?
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a. Dense sympathetic innervation
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27. What is the primary control for body temperature?
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a. Autonomics to the skin
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28. During exercise, what do we do to the cutaneous sympathetic tone?
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a. We inhibit it, causing dilation of arterioles
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29. Do we use local metabolic products to control dilation of skin?
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no
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30. What happens when you walk in the cold and your face is exposed
|
a. Get sympathetic alpha 1 vasoconstriction
b. Pale and white looking |
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31. When you are outside exercising what happens to skin?
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a. You shut down sympathetics, cause vasodilation, get red and flushed
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32. What happens when you have trauma to the skin?
|
a. Histamine is releases (vasodilator)
b. Get the triple response i. Reddened line ii. Flare (circle of red as the histamine spreads) iii. Wheal (edema) |
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1. What is microcirculation?
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a. That portion of the systemic and pulmonary circulations adapted for the exchange of gases, nutrients and waste products.
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2. What does an A-V shunt do?
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a. It is a straight shot vessel from arteriole to venule
b. It allows blood to go to venous supply even if capillaries are closed off by sphincters |
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3. What does the capillary bed consist of?
|
a. Capillaries and thoroughfare channels (A-V shunts)
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4. How big are capillaries?
|
a. 7-10 microns in diameter
i. Just a touch larger than RBC |
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5. What are the 3 types of capillaries? (think histo)
|
a. Continuous
b. Fenestrated c. Discontinuous |
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6. What are the two types of continuous capillaries and what kind of tissue do they supply?
|
a. Low: muscle, nerve, adipose
b. High: lymph, thymus |
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7. What are the two types of fenestrated capillaries and what kind of tissue do they supply?
|
a. Open: renal glomeruli
b. Closed: endocrines and intestinal villi |
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8. What tissues have discontinuous capillaries?
|
a. Liver, bone marrow, spleen
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9. What is vasomotion?
|
a. The mechanism by which we allow blood to go through a capillary bed
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10. How do we control vasomotion at the capillary bed?
|
a. Sympathetic alpha adrenergic vasoconstriction
i. Occurs at the metarterioles and arterioles 1. Note: there are some B2 vasodilators (high affinity for epi) |
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11. Aside from sympathetic control, how else is vasomotion at the capillary bed controlled?
|
a. Local control
i. Metabolic product control of precapillary sphincter opening and closing ii. This is local AUTOREGULATION (it determines how much blood it is getting by itself) |
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12. What is myogenic regulation?
|
a. Increased pressure causes relaxation of vasculature
b. Relaxation causes active contraction c. Prevents edema with sudden BP increase d. This is a form of autoregulation |
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13. What is active hyperemia?
|
a. Increased blood flow with increased metabolism
b. Many products are capable of relaxing sphincter smooth muscle (H+, O2, CO2 etc.) c. Basically, more products made, the more vasodilation to get rid of waste d. Note that other things in combination that will lead to vasodilation |
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14. What causes shear force?
|
a. Movement of fluid across a membrane
b. Such as plasma moving across membrane of blood vessel |
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15. How is NO made and how does NO work as a vasodilator?
|
a. Arginine + endothelial cell shear + endothelial NO synthase
i. Forms NO 1. NO goes to vascular smooth muscle a. stimulate active guanylate cyclase through cyclic guanosine monophosphate i. causes inhibition of contraction (Ca) 1. thus vasodilation |
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16. How do you calculate the rate of diffusion across a membrane? (J)=?
|
a. J=PS(dc/dx)
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17. In calculating rate of diffusion, what is PS and what factors change this value
|
J=PS(dc/dx)
a. PS: permeability and surface area b. Changed by i. Temp, molecular radius, and viscosity ii. % of capillaries open iii. Type of endothelium |
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|
18. In calculating rate of diffusion, what is dc/dx and what factors change this value
|
a. Concentration difference between blood and interstitium
b. (change in concentration across the change in space) |
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19. What are the two limitations of diffusion?
|
a. Flow limited
b. Rate Limited |
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|
20. What is flow limited diffusion?
|
a. Diffusion is superfast on its own (for say, oxygen)
b. Thus the amount of diffusion is limited by the amount of blood that is perfused to that tissue c. (capillary blood flow limited) |
|
|
21. What is rate limited diffusion?
|
a. Larger molecules have difficulty moving through pores, thus diffusion is limited
|
|
|
22. How does diffusion change in the case of pneumonia?
|
a. O2 and CO2 normally are flow limited (that is they travel superfast and are only limited by the amount of blood that perfuses)
b. When you have fluid buildup in the lung, it adds diffusion distance and viscosity c. Diffusion of gases shifts from flow-limited to rate (diffusion) limited |
|
|
23. What does water movement depend on?
|
a. Pressure differences across the capillary
b. Hydraulic conductivity and area of diffusion |
|
|
24. What is the Starling-Landis Equation for filtration of water?
|
a. J = KA[(CHP-THP)-(COP-TOP)
|
|
|
When considering diffusion of water, what two pressures cause water to move from the capillary to the interstitial space?
|
CHP, TOP
|
|
|
When considering diffusion of water, what two pressures cause water to move from the interstitial space to the capillary
|
THP, COP
|
|
|
26. What is the California Gangster Rule
|
a. At equilibrium CHP=COP
i. That is to say the outward flow from capillary to interstitium is equal to the inward flow of Force of water from interstitum trying to dilute protein in blood |
|
|
27. What happens to capillaries in burn victims?
|
a. You destroy the capillary integrity, so permeability increases
i. Causes loss of water and even albumen in extreme cases |
|
|
28. What is happening when you have increased capillary hydrostatic pressure? Examples?
|
a. CHP>COP
b. Heart failure, DVT c. This is edema |
|
|
29. What is happening with low plasma proteins? Examples?
|
a. COP<CHP
b. Quashiorkor, severe burns, nephrosis c. Protein malnutrition i. b/c no plasma proteins, COP goes down, water moves from capillary to interstitium |
|
|
30. What happens in lymphedema?
|
a. Protein is left in tissue
b. Protein in interstitium goes up b/c lymph is blocked up c. CHP + TOP > COP d. Water moves from plasma to intersitium |
|
|
1. Define cardiac output (CO).
|
Volume of blood pumped per ventricle per minute (L/min)
|
|
|
2. Define Stroke volume (SV).
|
a. Volume of blood ejected per beat (L/beat).
|
|
|
Define the relationship between SV and HR.
|
a. CO= HR * SV. This is approx. 5L/min.
|
|
|
4. Describe the blood volumes at end diastole and end systole.
|
At the end of diastole, the LV is full of blood and ready to contract. At the end of systole, blood volume is significantly decreased, but not completely gone from the LV.
|
|
|
5. How is SV computed from end diastolic volume (EDV) and end systolic volume (ESV)?
|
a. SV = EDV – ESV.
|
|
|
6. How is ejection fraction (EF) computed and what is a normal value?
|
a. EF = SV/EDV. A healthy adult produces as EF OVER 55%.
|
|
|
7. Define preload.
|
a. Preload is the amount of stretch at the end of diastole. An increase in preload is related to stretch generating force.
|
|
|
8. What is afterload and why is it a consideration in myocardial performance?
|
a. Afterload is the resistance the ventricle must overcome to empty its contents into the aorta. Since systole cannot occur without afterload being surpassed, an INCREASE in afterload may lead to less ventricular ejection.
|
|
|
9. What are two factors that can have an effect on end systolic volume?
|
a. Afterload
b. Ionotropy |
|
|
10. What factors can affect preload? And in turn, what does preload effect?
|
a. Compliance, HR (diastolic filling time), increased inflow resistance (e.g. tricuspid valve stenosis)
b. Preload effects EDV |
|
|
11. How is ventricular wall stress calculated? (afterload)
|
afterload = (ventricular pressure x ventricular radius)/(ventricular wall thickness x 2) .
|
|
|
29. Do you cha cha?
|
a. YES. I lika do da cha cha.
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