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181 Cards in this Set
- Front
- Back
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Function of the autonomic NS
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innervate and control smooth m., cardiac m., endocrine and exocrine glands
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Neuron length in sympathetic NS
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Preganglionic = SHORT
Postganglionic = LONG |
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What is unique about the sympathetic innervation of the Adrenal Medulla?
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preganglionic sympathetics go directly to the gland
(still a 2 neuron system) |
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Parasympathetic Cranial Nerves
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CN III, VII, IX, X
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Sympathetic Spinal Nerves
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T1-L2
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Sacral Spinal Nerves of parasympathetics
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S2,3,4
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Neuron length in parasympathetic NS
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Preganglionic = LONG
Postganglionic = SHORT |
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Parasympathetics do NOT innervate _______ ________
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Blood Vessels
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Antagonism
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autonomics oppose each other
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Synergism
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autonomics work together for net effect
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Autonomic Activity and heart rate
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rest - strong parasympathetic tone, weak sympathetic tone (70 bpm)
excercise - decrease parasympathetic tone (90 bpm) more exercise - increase sympathetic tone (130 bpm) |
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Parasympathetic tone dominates at ______
Sympathetic tone ________ with demands on the system |
Rest
Increases (Dangerous Generalizations) |
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What ANS controls glycogenolysis?
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Sympathetic ONLY
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Late pregnant uterus
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-sympathetic innervation disappears
-no sympathetic vasoconstriction but can respond to exogenous drugs |
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Parasympathetics. Which receptor and NT are found in the ganglion?
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Receptor: Nicotinic Receptor
NT: ACh (Nicotinic because nicotine binds to the ACh receptor) |
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Parasympathetics. Which receptor and NT are found at the target tissue (effector organ)?
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Receptor: Muscarinic Receptor
NT: ACh (Muscarinic because Muscarine binds here, but is an antagonist) |
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Cholinergic drug
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mimic the action of ACh
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Anticholinergic drug
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antagonize ACh (cholinergic blocker)
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Hexamethonium
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antichilinergic drug
-antagonize N receptors in the ganglia |
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Atropine
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anticholinergic drug
-antagonizes M receptors in the end organ (prevent salivation) |
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Sympathetics. What is the receptor and NT in the ganglion?
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Receptor: Nicotine receptor
NT: ACh |
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Sympathetics. What is the receptor and NT in the effector organ?
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Receptor: Adrenergic Receptor
NT: NE (adrenergic because is binds adrenaline) |
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Sympathetic stimulation of the Adrenal medulla?
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sympathetic neuron -> ACh on N receptor on Chromaffin cells -> release of mostly epinephrine and a little norepinephrine -> release in the blood
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Where does Norepinephrine and Epinephrine come from?
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Norepinephrine - postganglionic neuron
Epinephrine - Adrenal Medulla |
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2 main types of Adrenergic receptors
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α adrenergic receptor
β adrenergic receptor |
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Agonist and Antagonist of α adrenergic receptor
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Agonist
- norepinephrine > epinepthrine -phenylephrine Antagonist -phentolamine (α blocker) |
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β1 adrenergic receptor agonist
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β1 agonist - epinephrine = norepinephrine
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β2 adrenergic receptor agonist
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β2 agonist - epinephrine >> norepinephrine
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β receptor antagonist
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β antagonist - propranol
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Sympathetic stimulation to the eye?
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Far Vision
-let more light in - pupil -focus on far objects - lens flattens |
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α1 receptors on smooth muscle cause _________
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contraction
(uses NE) |
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Sympathetic stimulation of the iris radial smooth muscle?
(receptor and NT) |
contraction and pupil dilation
Receptor: α1 NT: NE |
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What muscle changes the focus of the lens?
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ciliary muscle
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Describe sympathetic stimulation to the ciliary muscle.
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EPI acts on β2 receptors -> ciliary muscle relax -> increase tension on suspensory ligament -> pulls lens to flatten -> FAR Vision
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β2 receptors on smooth muscle cause ________
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relaxation
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Describe parasympathetic stimulation of the pupil.
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ACh acts on M receptors -> contraction of iris sphincter smooth muscle -> pupil constriction
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M receptors on smooth muscle cause __________
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contraction
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Describe parasympathetic stimulation to the lens.
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ACh acts on M receptors -> contraction of ciliary muscle -> decrease tension of suspensory ligament -> lens curves -> NEAR Vision
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Horner's Syndrome
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loss of sympathetics to affected eye -> constriction of eye
(note: eyelid droops and no sweating on ipsilateral side) |
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parasympathetic stimulation to salivary gland.
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copious secretion of water and enzymes
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sympathetics to salivary glands
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little effect and of minor imporatance
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M receptors on glands cause ________
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secretion
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What causes bronchodilation?
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EPI acting on β2 receptors in bronchial smooth muscle
(sympathetic but not via nerve) |
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What causes bronchoconstriction and secretion of bronchial glands?
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PS stimulation (via nerve)
Receptor: M NT: ACh |
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Sympathetics are the ________ control system for the heart
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extrinsic
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What does sympathetic stimualation doe the SA node AP in the heart?
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increases the rate of depolarization
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sympathetic innervation to the heart
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NE acts on a β1 receptor to increase HR
(positive chronotropic) |
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β1 receptors on the heart are __________
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stimulatory
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How does sympathetics affect the AV node
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increase the conduction velocity through the node
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What do sympathetics do to the atria and ventricles?
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increase force of contraction (atria and ventricles)
(postive inotropic) |
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Why would β receptor antagonist be given to a person who just had a MI?
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reduce mortality by preventing cardiac arrhythmias (eliminating sympathetic stimulation)
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M receptors on the heart are ________
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inhibitory
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Parasympathetics to the SA and AV node?
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SA - decrease depolarization rate
AV - decrease conduction velocity |
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Parasympathetics to the heart?
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essentailly no M receptor -> no parasympathetic effect
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What is interesting about ANS innervation to blood vessels?
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essentially no parasympathetic innervation to blood vessels
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Sympathetics in blood vessels
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α1 receptors - vasoconstriction everywhere
β2 receptors - vasodilation to liver, coronary, and skeletal muscle |
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Describe parasympathetic stimulation to the gut.
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Sphincter - ACh acts on M receptor to relax
Intestine - ACh acts on M receptor to increase tone and motility |
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Describe sympathetic stimulation to the gut.
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Spincter - NE acts on α1 receptor to contract sphincter
Intestine - NE acts on α2 and β2 to decrease tone and motility |
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Sympathetics to the urinary bladder
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Fill the bladder
-relax the detrusor m. -> activate β2 receptor -contract the trigone and internal sphincter -> activate α1 receptor |
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Parasympathetics to the urinary bladder
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Emptying the bladder
-contract the detrsor m. -> activate M receptors -relax the trigone and internal sphincter -> activate M receptors (using M receptors to relax and contract) |
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Innervation to the skin
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only Sympathetics!!
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sympathetic innervation to smooth m. on hair.
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α1 receptor - contraction and piloerection
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Innervation of most sweat glands are via sympathetic ______ neurons
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cholinergic
(ACh acting on M receptor) |
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sweat glands on palms of hands
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EPI acting on α1 receptor
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ANS in the kidney
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ANS have minimal role in regulating blood flow in the kidney
(self regulates blood flow) |
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Sympathetic effect on afferent arteriole of the kidney
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NE acts on β1 receptors stimulating juxtaglomerular cells to release renin
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Parasympathetic preganglionic cells (converge or diverge) on postganglionic cells
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converge
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Sympathetic preganglionic cells (converge or diverge) on postganglionic cells
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diverge
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Presynaptic inhibition, how does it work?
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Sympathetic - NE acts on α2 on the presynaptic neuron to turn off release
Paraysmpathetic is turned off by EPI and NE acting on α2 on the presynaptic neuron |
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hyperesthesia
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increased sensitivity to touch
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hyperalgesia
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increased sensitivity to touch
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Medulla oblongata controls...
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circulation and respiration
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Pons controlls...
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micturation
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Organization of blood vessels in the systemic circulation
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Aorta - Muscular Conduit Artery - Arteriole - Capillary - Venule - Vein - Vena Cava
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Is the pulmonary pressure greater or less than systemic pressure?
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less than
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What does ventricular septal defect result in?
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pulmonary congestion and inefficient O2 transport
(increase pressure in the R ventricle) |
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What is unique about the circulation to the liver compared to all other organs?
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circulation is parallel to the heart in all other organs and is perpendicular in the liver
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What is the mechanism to control blood flow in vessels?
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alter the vascular smooth muscle tone
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How do the heart and kidney differ with respect to blood flow and O2 consumption?
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Heart - maximally extract O2 at rest (minimal blood flow)
Kidney - a lot of blood flow with minimal O2 consumption |
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Mean Arteriole Pressure (eq.)
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Mean = diastolic + (1/3*(systolic - diastolic))
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Transmural pressure
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Pt = Pin - Pout
Pin = pressure inside the vessel pushing outward Pout = pressure outside the vessel pushing in |
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What characteristic allows systemic veins to hold the majority of blood volume
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they are compliant
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Flow (eq.)
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Flow = change in pressure/ resistance
Q = (P1 - P2)/R |
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CO eq. with regard to pressure and resistance
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CO = mean arterial pressure/ total peripheral resistance
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Poiseuille's Law for resistance
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R = (8*viscosity*length)/(pi*radius to the 4th)
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Resistance is inversely proportional to _______ to the 4th.
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radius
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What vessel provides the most resistance to flow?
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Arterioles (rather than capillaries) because they are in series
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Increase cross sectional area -> ______ Velocity
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decrease
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decrease cross sectional area -> _______ velocity
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increase
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Bernouli's Principle
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conversion of potential energy to kinetic energy when cross-sectional area decreases
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Where is blood velocity the lowest
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capillaries
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What 2 factors play into blood viscosity?
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hematocrit and blood velocity
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Where does turbulent blood flow occur?
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Ventricles and stenosed arteries
(due to high blood flows) |
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What does Reynold's number predict?
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turbulent flow
Reynold's # = (velocity*diameter*density)/viscosity |
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What produces murmurs and bruits?
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turbulent flow either due to stenosed valves or arteries
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How do sympathetics increase the rate of firing in the SA node?
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increase If - depolarizes the cell
(increase the inward Na+ current) |
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How do parasympathetics decrease the rate of firing in the AV node?
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increase Ik + decrease If - hyperpolarize the cell
(open K+ channel and decrease Na+ influx) |
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Pace of...
SA node AV node Purkinje fibers |
80/sec
50/sec <20/sec |
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Rate of excitation across the atria
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0.05 to 1 m/s
Rapid! |
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Rate of excitation across the AV node
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0.01 - 0.05 m/s
Slow |
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AV nodal conduction is dependent on the activation of _____ ______ ___ _______
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voltage gated Ca2+ channels
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Rate of excitation across the ventricles
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2-5m/s
very fast |
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What 2 factors determine the speed of passive current cell to cell?
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1. cell diameter
2. density of tight junctions |
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Anulus Fibrosus
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structure between the atria and ventricle
prevents re-excitation of the atria in conjunction with AV node refractoriness |
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When is a isoelectric potential recorded?
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when region is fully depolarized or fully repolarized
(or when tissue is so small that activity can not be seen) |
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P wave
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atrial depolarization
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P-R segment
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AV node activation
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P-R interval
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measure activation of atria and AV node
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QRS interval
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activation of ventricles
(ventricular depolarization) |
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S-T segment
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isoelectric because ventricles are fully depolarized
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S-T interval
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repolarization of ventricles
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Q-T interval
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duration of ventricular systole
(include depolarization and repolarization of ventricles) |
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T wave
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rapid ventricular repolarization
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ECG speed of paper movement
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25 mm/sec
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What would be seen on an ECG if conduction is slowed through the AV node?
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prolonged PR interval
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What would be seen if there was a block in the bundle branches
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wide QRS complex, rather than a prolonged PR interval
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Channelopathies that can lead to a long QT interval
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gain of function of Na+ channel
lose of function for K+ channel |
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V leads show the wave of depolarization in the _________ plane
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horizontal
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Rate (beats/min) =
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Rate (beats/min) = (60s/min)/ R-R interval (s/beat)
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Abnormal automaticity
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arrhythmias associated with non-pacemaker cells that develop automaticity
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Triggered activity
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oscillations in membrane potential that trigger an action potential
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Sinus arrhythmia
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not abnormal, represents the cyclic variation in rate associated with respiration
[acceleration during inspiration, deceleration during expiration] |
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3 causes of abnormal emergence of a latent pacemaker
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- become enhanced
- higher order pacemaker becomes depressed -conduction block |
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What is a normal occurrence after cardiac tissue damage?
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abnormal automaticity - rythms often can not be overdrive suppressed
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2 classifications of triggered activity
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Early after depolarization (EAD)
-occur before full phase 3 repolarization Delayed after Depolarization (DAD) -occur after phase 3 repolarization |
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1st degree block
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consistant prolongation of the PR interval, but every impulse gets through
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2nd degree block
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not all impulses get through the AV node
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Wenckebach
(2nd degree block) |
Mobitz Type I
-progressive prolongation through the AV node with an eventual dropped beat (cycle repeats) |
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Mobitz
(2nd degree block) |
Mobitz Type II
-dropped beats without the prolongation of the PR interval |
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3rd degree block
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complete block through the AV node
(one of the latent pacemakers below the block my instead excite the ventricle) |
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Mechanisms that could contribute to a block in the AV node?
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- increased vagal tone
- Ca2+ channel block - Beta blocker - digitalis - hyperkalemia |
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Re-entry
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cardiac impulse does not die out, rather continues to circulate and re-excite tissue
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3 conditions that are necessary for re-entry to occur
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1. unidirectional block
2. slowed conduction over an alternate pathway 3. re-excitation of tissue proximal to the block |
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Re-entry may be ______ or random
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ordered
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Re-entry may occur around an _________ site or it may be functional
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anatomical
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2 examples of re-entry
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atrial and ventricular fibrillation
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WPW (Wolf-Parkinson-White) syndrome
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pt with an accessory pathway between the atria and ventricle
-atrial impulse my go down pathway to pre-excite the ventricle |
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ECG with bypass tract (WPW)
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shortened PR segment
delta wave widened ORS |
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Orthodromic Atrioventricular Reentrant Tachycardia
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impulse is conducted back to the atria via the accessory pathway
[retrograde P waves] |
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Antidromic Atrioventricular Reentrant Tachycardia
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impulse conducted down the accessory pathway and back up the AV node pathway
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S1 heart sound
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mitral and tricuspid valves closing
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S2 heart sound
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Aortic and Pulmonic valves closing
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S3 heart sound
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passive ventricular filling
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S4 heart sound
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artrial systole, ventricular stiffness
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Sound of aortic stenosis
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cresendo-decrescendo murmur
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Sound of aortic incompetence
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diastolic decrescendo murmur
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Sound of mitral/tricuspid incompetence
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pan-systolic murmur between S1 and S2
(Increased C wave) |
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Max and Min pressures observed in the atria, aorta, pulmonary artery
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Atria 0-4 (RA) & 8-10 (LA)
Aorta 120/80 Pulmonary Artery 25/10 |
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End diastolic pressure in Right and Left ventricles
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Right ventricle 25/4
Left ventricle 120/9 |
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Ejection Fraction
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stroke volume/end diastolic volume
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afterload
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the resistance the ventricle must overcome to empty its content
(ventricular wall stress) |
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Wall stress =
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(ventricular pressure*ventricular radius)/2*h
(h = ventricular wall thickness) |
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Does afterload increase or decrease with an increased wall thickness
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decrease
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Positive inotropes in the heart
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-open Ca channels
-inhibit the Na/Ca changer -inhibit plasma membrane pump |
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effects of activating the beta1 adrenergic receptor in ventricles
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-increase open probability of L-type Ca2+ channels
-increase SR Ca2+ pump |
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Negative inotropes
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-Ca2+ channel blockers
-low extracellular Ca -high extracellular Na |
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Pulse Pressure =
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systolic pressure - diastolic pressure
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β2 receptor on blood vessels causes...
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vasodilation
(liver, skeletal m., coronary, cerebral) Note: no actual innervation, just EPI |
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α1 receptors on blood vessels causes....
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vasoconstriction
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Where are vascular smooth muscle cells found and how are they innervated?
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found in salivary, some GI, erectile tissue
NT, such as NO, causes vasodilation |
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3 things that affect vascular function curve
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1. blood volume (mean circulatory filling pressure)
2. capactiance of the system 3. total peripheral resistance |
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3 things that can change Pmc (mean circulatory filling pressure)
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1. SNS tone
2. Blood volume 3. compression of veins (exercise, elastic stockings) |
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What would enhance cardiac performance (shift curve up an to the left)?
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-increase in HR and inotropy
-decrease in afterload |
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Continuous transcapillary exchange
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Low: muscle, nerve, adipose
High: lymph and thymus |
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Fenstrated transcapillary exchange
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open: renal glomeruli
closed: endocrines and intestinal villi |
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Discontinous transcapillary exchange
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liver, bone marrow, spleen
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Vasomotion - neural control of peripheral ciruclation
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sympathetic α-adrenergic vasoconstriction
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Vasomotion - local control of the periphery
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local metabolic product control of precapillary sphincter opening and closing
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Myogenic regulation of microvascular resistance
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-increased pressure causes active relaxation -> P goes down
-relaxation causes active contraction |
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Active hyperemia regulation of microvascular resistance
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-increased blood flow with an increased metabolism
-relax sphincter smooth muscle |
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adenosine
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potent dilator
(important for the heart and brain) |
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Capillary hydrostatic pressure (CHP)
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blood pressure in a single capillary
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Capillary oncotic pressure (COP)
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force of water in the interstitium trying to dilute plasma protein (trying to come into the vessel)
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Increased capillary hydrostatic pressure
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CHP > COP (outward)
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Low plasma protein
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COP < CHP (outward)
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Lymphedema
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CHP + TOP > COP
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What happens al low perfusion pressures in organ blood flow autoregulation?
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vascular resistance decreases -> more flow
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What happens al high perfusion pressures in organ blood flow autoregulation?
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vascular resistance increase -> less flow
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Describe why edema impairs cerebral blood flow.
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Increase in pressure due to swelling -> reduces flow which is very dangerous to tissue
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Hypoxia causes _______ in pulmonary circulation
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vasoconstriction
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What is the difference between active hyperemia and reactive hyperemia in skeletal muscle?
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Active hyperemia - local metabolic products affect the pre-capillary sphincter
Reactive hyperemia - increased flow after muscle contraction/ischemia |
