NRS 313 Study Guide - Midterm Guide: Degranulation, Ectopic Pacemaker, Rubber Band
27 May 2018
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W6: Cardiovascular Structure and Function and Dysfunction
• PARASYMPATHETIC stimulation:
o Acetylcholine is the main neurotransmitter
o Parasympathetic stimulation comes from vagus nerve (CN X).
▪ Stimulated by barorecptors with an increase in pressure=> heart rate slows
reduces CO
o Cholinergic stimulation SLOWS the HR
▪ ACh
o NOTE: Strong vagal nerve stimulation (Valsalva) can override the nodes, inhibit
ventricular contraction and decrease cardiac output.
o The parasympathetic nervous system affects the heart through the vagus nerve,
which releases acetylcholine. Acetylcholine causes decreased heart rate, and
slows conduction through the AV node. Acetylcholine also causes coronary
vasodilation.
• Valsalva
o Closed glottis (covers trachea) and holding breath + increased pressure in
abdomen and thoracic cavity
o Occurs due to constipation
o Increase pressure against vagus nerve
• Sympathetic stimulation
o Norepinephrine (alpha receptors) and epinephrine (alpha and beta adrenergic
receptors)
▪ Released from the adrenal glands
▪ Thalamus talks to the hypothalamus
▪ ACTH is released and talks to adrenal glands. Release of NE and E
o Alpha 1 receptors— slightly vasoconstrict renal, intestinal and peripheral
arteries. There are few Alpha 1 receptors in the heart so the net effect is coronary
vasodilation
▪ Increase in heart rate and heart contraction (ionotropic)
o Decreased blood flow to the kidneys -> decreased water retention -> also the
RAAS is activated
o Beta 1 receptors —stimulation increases heart rate (chronotropic) and strength of
contraction (inotropic) by enhancing calcium influx (shortening refractory period)
o Beta 2 —stimulation vasodilates coronary arteries and pulmonary arteries AND
smooth muscle of bronchial airway.
o Stimulation of the SA note by the sympathetic nervous system rapidly increases
heart rate.
o Furthermore, neutrally released norepinephrine or circulating catecholamines
interface with B-adrenergic receptors on the cardiac cell membranes.
o The overall effect is an increased influx of Ca++, which increases the contractile
strength of the heart and increases the speed of electrical impulses through the
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heart muscle and increases the speed of electrical impulses through the heart
muscles and the nodes.
o Finally, increased sympathetic discharge dilates the coronary vessels.
• Stenosis
o Aortic valve stenosis. Much more dangerous. Normal valve is not thickened or
scarred. Leaflets become thickened and stiff.
o Chronic imflammation
o Hypercalcemia can lead to deposits here
o Hyperparathyroid-> release of PTH-> osteoclast-> Rank L-> Rank L receptors ->
osteoclast-> reabsorbs bone-> release of Ca++
o Hypertrophy-> weaker heart-> decreased intraventricular radius-> lower cardiac
out
• Disruption in conduction and rythm
o May be asymptomatic to fatal
o Caused often by ischemia (Necrosis), electrolyte disturbances (sodium/potassium/
calcium), acidosis, autonomic dysfunction
▪ PNS becomes more activated
• Neurogenic shock: head injury can play a major role.
▪ Excess K+ from crush injury
▪ Hydration
▪ Dietary depletion-chromes disease
▪ Someone with the flu
o Examples:
▪ Heart block – conduction between atria and ventricles is disrupted. Atria
and ventricles beat independently of each other.
▪ Premature Ventricular Complex (PVC) – ectopic pacemaker in
ventricles initiates heart beat.
• Some other pacer in the heart is not wanitng to wait for the SA
Node
▪ Fibrillation – disorganized conduction resulting in quivering without
contraction
• Ischemia + necrosis
• Hypercoagulation
• Heart Sound dysfunction
o Valve Regurgitation (incomplete closure)
▪ Murmur
o Valve Stenosis (constricted/narrowed)
▪ Murmur
o Ventricular Failure – S3 sound
o S1: tricuspid and mitral
o S2: Pumonary and aortic
• Leaky Aortic Valve
o Prolapsed
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Document Summary
Acetylcholine causes decreased heart rate, and slows conduction through the av node. Release of ne and e: alpha 1 receptors slightly vasoconstrict renal, intestinal and peripheral arteries. There are few alpha 1 receptors in the heart so the net effect is coronary vasodilation. Increase in heart rate and heart contraction (ionotropic: decreased blood flow to the kidneys -> decreased water retention -> also the. Atria and ventricles beat independently of each other: premature ventricular complex (pvc) ectopic pacemaker in ventricles initiates heart beat, some other pacer in the heart is not wanitng to wait for the sa. Node: fibrillation disorganized conduction resulting in quivering without contraction. Ischemia + necrosis: hypercoagulation, heart sound dysfunction, valve regurgitation (incomplete closure, murmur, valve stenosis (constricted/narrowed, murmur, ventricular failure s3 sound, s1: tricuspid and mitral, s2: pumonary and aortic, leaky aortic valve, prolapsed, congenital birth defect.
