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265 Cards in this Set
- Front
- Back
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where is the hypothalamic hunger center located
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lateral nuclei
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where is the hypthalamic satiety center located
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ventromedial nuclei
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where is the hypothalamic thirsting center located at
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peroptic nuclei
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what higher brain areas control feeding
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amygdale = nutrient intake
prefrontal = conscious control of eating behavior |
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what affect does gastrointestinal filling have on feeding
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inhibits feeding
vagus supression good affect in animals very minor in humans |
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what is the affect of CCK on feeding
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inhibit feeding
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what is the affect of Peptide YY on feeding
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inhibits further eating
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what affect does insulin have on feeding
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inhibits feeding
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what affect does ghrelin have on feeding
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increases hunger especially after fasting
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when do we see a increase in cck
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in response to food in the small intestine
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when do we see a increase in peptide yy
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high fat in the small intestine
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when do we see a increase in insulin
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increase of glucose in the blood
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what are the affects of body temperature on feeding
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hot = inhibits feeding
cold = increase caloric intake |
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when is leptin produced
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when adipocytes are stretched they rls leptin to inhibit food intake
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what is the process of carbohydrate metabolism
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begin in mouth with amylase
in small intestine with pancreatic amylase final part in mucosal cell membrane bound disaccharidases put into portal circulation |
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what cell exhibit insulin dependent uptake
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non-neural and liver cells
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what cells exhiit noninsulin dependent uptake
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nural cells and liver cells
insuline improved uptake |
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what is the process by which glucose moves into the cells
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facilitated diffusion
because it is changes to G6P inside cells this allows there to be a gradient |
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which cells have the ability to reverse G6P to glucose
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liver, renal tubular, intestinal epithelial
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what enzyme is neccessary to convert G6P to glucose
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glucose phosphatase
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what are the absorbable forms of carbohydrates
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monosaccharides
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what is the absorbable form of protein
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amino acids
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what is the absorbable form of lipids
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monoglycerides and 2 fatty acids
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what is a anorexigenic hormone
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a hormone that reduceds feeding
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what are some example of anorexigenic hormones
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alpha MSH
leptin serotonin norepinephrine corticotropin rlsing hormone insulin CCK GLP CART Peptide YY |
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what is a orexigenic hormone
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hormone that increases feeding
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what are some examples of orexigenic hormones
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neuropeptide Y
AGRP Melanin concentrating MCH Orexins A and B Endorphins Galanin Amino Acids cortisol ghrelin |
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where is pyruvate converted into acetyl coa
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in the mitochondrial matrix
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what is the energy outcome from glucose in a cell
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36 or 38 atp
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what is glycogenolysis
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break down of glycogen to form glucose
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what is glycogenesis
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the formation of glycogen from glucose
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why doesn't muscle glycogen contribute to blood glucose
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because it lacks the enzyme to converts G6P to glucose so its glycogen must be used by the muscle cell for energy
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what is gluconeogenesis
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the formation of glucose form non carbohydrate molecules
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what is the main molecule used in gluconeogeneis
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amino acids
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what is the problem encountered when we use amino acids for gluconeogenesis
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there are no amino acid stores in the body so body protein must be broken down to supply the cells with amino acids for gluconeogenesis
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what is the function of bile salts in lipid metabolism
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helps to emlusify lipid globules to increase surface area for enzymes
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what is the function of pancreatic lipase
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break down of lipid globules
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what is the process of abosorption of lipids
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-absorbed as monoglyceride and two fatty acids
-resynthesized into triglyceride -small amount of apoprotein B applied to outer surface to form chylomicron -absorbed into lymphatic lacteals -transported through thoracic duct and emptied into venous circulation |
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what happens to the chylomicron on intial transport
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triglycerides are hydrolyzed by lipoprotein lipase releasing fatty acids and glycerol fatty acids pass inot lipocytes and liver cells
-inside cells resythesized into triglycerides using newly synthesized glycerol |
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what happens to triglycerides, lipoproteins, and cholesterol not taken up by cells
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transported to liver to be repackaged into lipoproteins for lipid transport
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what is the purpose of VLDL
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transport of triglycerides
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what is the purpose of LDL
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transport of cholesterol
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what is the purpose of HDL
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transport of lipids back to liver
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how are LDL and HDL tranported into the cell
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by to receptor and whole thing is taken into the cell and then contents are rlsd
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what is hyper cholesteral anemia
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genetically based body does not produce LDL receptors therefore some cholesterol will diffuse but not enough and you can't remove the LDL from blood therefore you get build up in blood and heart attacks
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where are lipids stored
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in lipocytes in adipose tissue unlimited storage
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what are nonessential amino acids
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aa that can be synthesized by human cells from cellular metabolites
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what are essential aa
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aa cannot be synthesized internally so must be supplied by diet
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what is the process for protein digestion
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gastric pepsin in stomach starts the digestion
-pancreatic trypsin, chymotrypsin, and carboxypeptidase cut into smaller chains -intestinal peptidases and dipeptidases break down short chains into single aa -absorbed and put into portal circulation |
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what happens to excess amino acids
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placed in urine where they are reabsorbed up to threshold and the rest are pied out
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by what process are aa taken into the cell
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active transport
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what stimulated aa uptake
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HGH and insulin
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what is the process of protein catabolism
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tissue proteins
amino acids removal of amine group conversion of NH2 to NH3(toxic) NH3 to urea by liver excreted in urine |
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what does high NH3 mean
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liver failure
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what does high Urea mean
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kidney failure
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what is the main hormone of the fed state
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insulin
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what hormones stimulate protein synthesis
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insulin HGH thyroid hormone
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what are the predominant hormone of the fasting state
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glucagone, epinephrine, cortisol
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what stimulates glycogenolysis
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glucagon and ephinephrine
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what stimulates lipolysis
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epinephrine, norepinephrine, cortisol, HGH, thyroid,
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what stimulates protein breakdown
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cortisol
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what stimulates gluconegenesis
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glucagon and cortisol
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what is the bodies first major shift to dealing with prolonged fast
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slow down base metabolic rate
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what is the second major shift
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brain and nervous tissue shift to using ketone bodies for energy derivation
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what are the components of a functional endocrine control system
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-proper dvlpmnt of the endocrine organ and control organ during fetal dvlpmnt
-structural and metabolic integrity of the endocrine organ -ability to respond to control signals and to sythesize and rls hormone -functional receptors on target tissue -target tissue capable of producing proper biologic response |
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how do water soluble hormone communicate
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with suface cell receptors
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how do steriod and lipid soluble hormones communicate
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with intracellular receptors
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what are the hormone of the anterior pituitary
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GH
TSH ACTH FSH and LH Prolactin |
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what are the hormones of the thyroid gland
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thyroxine
calcitonin |
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what are the hormones of the adrenal cortex
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cortisol
aldosterone |
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what are the gonad hormones
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female=estrogen and progesterone
male=testosterone |
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what are the hormones of the posterior pituitary
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oxytocin
vasopressin |
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what are the hormones of the adrenal medulla
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epinephrine
norepinephrine |
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what is the hormone of the parathyroid gland
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parathyroid hormone
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what are the hormone of the pancreas
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insulin and glucagon
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what are the hormones of the kidneys
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renin
angiotensin erythropoietin |
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what are the hormones of the GI tract
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CCK
Gastrin |
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what is rathkes pouch
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upgrowth of the stomodeum that will eventually form the anterior pituitary
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what is the neurohypophyseal bud
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the downgrowth of the floor of the diencephalon that will eventually form the posteior pituitary
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what is the andohypophysis
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anterior pituitary or glandular portion of the pituitary
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what is the neurohypophysis
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posterior pituitary or nervous portion of the pituitary
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how does the hypothalmus control the anterior pituitary
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rls neurotransmitters at infundibular stalk which are picked up by the primary venous plexus and distributed to the anterior pituitary via the secondary venous plexus where they bind to receptors
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how does the hypothalmus control the posterior pituitary
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through neurons groups in the hypothalmus that terminate in the posterior pituiatry and rls their neurotransmitters(hormones) there which are carried away via venous plexus
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hormones rlsd by posterior pituitary
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ADH (vasopressin)
Oxytocin |
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what does lack of ADH lead to
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diabettes insipidis
dilute water urine and fluid imbalances |
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what are the pituitary direct acting hormones
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ADH
oxytocin prolactin MSH |
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TSH
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thyroid gland
thyroid hormone TRH |
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ACTH
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Adrenal cortex
glucocorticoid secretion CRH |
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FSH women
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follicle cells in ovaries
estrogen GnRH |
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LH women
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follicle cells in ovaries
ovulation, formation of corpus luteum, progesterone secretion GnRH |
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FSH MEn
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sustentacular cells of testes
sperm maturation GnRH |
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LH men
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interstitial cells in testes
testosterone GnRH |
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prolactin
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mammary glands
production of milk PIH and PRF |
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GH
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all cells
growth, protein synthesis, lipid mobilization and catabolism GHRH GHIH |
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MSH
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melanocytes
increased melanin sythesis in epidermis MSHIH |
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ADH
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kidneys
reabsorption of waters elevation of blood volume and pressure supraoptic nucleus |
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oxytocin
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uterus, mammary glands, prostate gland
labor contractions, milk ejection, prostatic contractions transported over asons from paraventricular nucleus |
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what is the indirect actions of GH
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in liver produces somatomedins which increase protein synthesis and cell proliferation and increased skeletal growth
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what are the direct actions of GH
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activated cortisol which increases lipolysis and anti insulin affects
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what does GH do befor closure of plates
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increases height
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what does GH do after closure of plates
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increase size of short bones
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most important growth hormone in prenatal growth
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thyroid hormone
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most important growth hormone early childhood
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growth hormone
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most important growth hormone in adolesents
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androgens
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what things stimulate the rls of ADH
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vomiting cntr
increases osmotic pressure pain and stress and emotion decrease blood volume decrease in blood pressure hypoxia |
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what are characteristics of over production of the pituitary
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acromegaly
large structure secondary sexual characteristics changes in hand structure |
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what are signs of underactive pituitary
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lack of growth
no secondary sexual characteristics early aging lack of skin coloration |
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what is the thyroid diverticulum
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the outgrowth from which will form the thyroid
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what are the steps in the formation of thyroxine
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intake of dietary iodine
iodide trapping thyroglobulin complexed with iodine on the tyrosine molecules this is what is stored in the follicles |
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what are the steps in the release of thyroxine
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pinocytotic vesicles(engulf a portion of thyroglobulin)
lysosomal protease splits of T3 and T4 this is what is released into the blood |
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how is thyroxine transport in blood
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most of thyroxine is bound to thyroxine binding prealbumin T4 has greater affinity than T3
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how does thyroxine affect the cell
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thyroxine will cross the membrane and bind to receptor in the cell
then it will turn on specific enzymes, synthesis, and genes |
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what affects does thyroxine have on metabolic activity
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increase number of mitochondria
increase activity of mitochondria increase activity of sodium potassium pump increase permiability to glucose |
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what affects does thyroxine have on lipid metabolism
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increase lipolysis and free fatty acids in serum
increase uptake and metabolism of free fatty acids increase uptake and metabolism of cholesterol and phospholipids and removal of triglycerides from serum increase rate of cholesterol secretion in the bile through inducing increasing LDL receptors |
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what affects does thyroxine have on vitamin metabolism
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possible deficency dut to used up resources
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what affects does thyroxine have on protein metabolism
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protein are broken down to aa to make glucose
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affects on body weight
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drop in weight
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affects on cardiovascular
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increase heart rate, arterial blood pressure, blood volume, vasodilation and blood flow
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affects on respiratory
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increase oxygen for increase energy demand
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affects on gastrointestinal
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diaherra or poor absorbtion
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affects on nervous system
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improper neural transmission
more ready to fire shortened or abnormal sleep |
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what are the affects on endocrine function
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increase in insulin
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what are the affects on sexual function
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hypo=diminshed libido
hyper=no real association |
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how is the release of thyroxine controlled
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via TRH rlsd in hypothalmus carried via blood flow to anterior pituitary where it is picked up by receptors which activate a 2nd messanger system then rls TSH
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what are the affects of TSH
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splits the thyroxin from thyroglobulin
increased activity of the iodide pump increased iodination of tyrosine increased size and activity of thyroid cells increase number of thyroid cells |
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how is thyroxine rls controlled
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feedback on pituitary and hypothalmus
sympathetic neural stimulation cold temp increase thyroxine |
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what does thiocyanate do
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it is a competitive inhibitor for iodide trapping
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what other mechanisms are used to treat hyperthyroidism
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bind iodide in serum and not make it available for transport into thryoid gland
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what does blockage of peroxidase do
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makes it so the body cant iodinate tyrosine propylthiouricil but we sometimes lose feedback mechanism here so the TSH overwhelms the drug
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what are symptoms of hyperthyroidism
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toxic goiter
thyrotoxicosis(weight loss) graves disease(wide eye) thyroid adenoma exophthalmosis(bulging eyes)you can see white on all sides |
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what other symptoms might be associated with hyperthyroidism
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increased BMR
intolerance to heat increased sweating mild to extreme weight loss diarrhea muscular weakness fatigue insomnia hand tremors psychic and hallucinatory manifestations |
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what are the symptoms of hypothyroidism
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fetal/neonatal cretinism
endemic colloid goiter(no production of T3 or T4) idiopathic nontoxic goiter myxedema arterioslerosis |
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what other symptoms might be associated with hypothyroidism
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fatigue
somnolence(excessive sleeping muscular sluffishness bradycardia decreased blood volume increased weight constipation mental sluggishness depressed hair growth edema husky voice |
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what are the three layers of the adrenal cortex
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Zona glomerulosa=aldosterone
fasciculata=glucocorticoid reticularis=gonadocorticoid |
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what is produced in adrenal medulla
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epinephrine
norepinephrine |
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what adrenocorticoids have mineralcorticoid activity
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aldosterone
deoxycorticosterone corticosterone cortisol cortisone |
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what are the synthetic mineralcorticoids
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fluorocortisol
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what are the glucocorticoids
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cortisol
corticosterone |
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what are the synthetic glucocorticoids
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cortisone
prednisone methylprednisone dexamethasone |
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what are the adrenocorticoids
|
androsterone
testosterone |
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how is cortisol transported in the body
|
CBG
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when do we see elevated levels of CBG in the blood
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pregnancy
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we do we see decreased levels of CGG in the blood
|
cirrhosis and nephrosis
|
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how is aldosterone transported in the blood
|
albumin 50% and 50% free
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what is process of metabolism for adrenocorticoids
|
degraded in the liver
conjugated to form glucuronides or sulfated 25% excreted in bile 75% in urine |
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what is the product of adrogens and cortisol in the urine
|
17-ketosteriods
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what are effects of adrenocorticoids on cells
|
diffuse to cell cytoplasm
bind to internal receptor steriod receptor migrates to nucleus binds to DNA to activate specific gene transcription formation of proteins based on the type of cell it is affecting |
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what are the affects of the glucocorticoids on cells metabolism
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stimulation of gluconeogenesis
-increase enzymes for gluconeogenesis -mobilization of aa -increased glycogen storage in liver -reduce glucose uptake -mobilization of fatty acids -fatty acid oxidation -ketogenic affect -hyperglycemia |
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what are the affects of glucocorticoids on immune system
|
anitinflammatory and immunosuppresive affects
-stabilization of lysosomal membrane -decrease migration of WBC from vascular to site in tissues -decrease capillary permeability -reduced lymphocyte activity -reduces rls of endogenous pyrogens |
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what are the affects of mineral corticoids on cells
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retention of Na and loss of K in urine
reabsorbtion of Na from sweat saliva gastric juices |
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what is the main target mineralcorticoids
|
kidney tubules and collecting ducts causing cells to reabsorb Na and transport K into urine
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what stimulates aldosterone secretion
|
na and k concentrations
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what controls aldosterone secretion indirectly
|
angiotensin 2
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how does aldosterone regulate blood pressure
|
blood pressure drops
kidney rls renin renin converts angion to angio 1 angion1 converted angio 2 angio 2 -constricts arterioles -caused aldosterone to be secreted -aldos increases na and water retention -returns na water balance -increases extracellular vol -raises blood vol -raises blood pressure to normal |
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how is aldosterone metabolized
|
converted into tetrhydrogluconoride and rlsd in urine
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effects of gonadocorticoids on cells
|
responsible for 2/3 of daily androgens
affects gonadal, brain, secondary sex organs |
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what is the hypotalamic control of adrenal cortex
|
CRH
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what is the anterior pituitary control of adrenal cortex
|
ACTH
|
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what causes adrenal atrophy
|
autoimmune attack tuberculosis, neoplasic invastion
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what happens with aldosterone deficiency
|
failure of reabsorption of Na from urine
-Na and Cl, water loss -decrese ECF vol and hyperkalemia -decrease plasma volume -increase RBC concentration -decrease cardiac output -shock -death |
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what happens with cortisol deficiency
|
decreased gluconeogenesis
-hypoglycemia decrease mobilization of aa and fatty acids decrease energy and normal cell metabolism increased susceptibility to stress |
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what are symptoms of addisons disease
|
adrenal atrophy
aldosterone deficiency cortisol deficiency increased formation of MSH |
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when do we see cushings syndrome
|
excess cortisol
|
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when do we see buffalo hump
|
mobilization of fat from lower body to upper body
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when do we see moon face
|
excess corticosteroids
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when do we see facial hair
|
excess androgens
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what do we see with adrenal cortex hyperactivity
|
hyperplasia of adrenal cortex
buffalo hump cushings syndrome moon face facial hair hypertension hyperglycemia bone loss |
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what happens with aldosterone producing tumors
|
hypokalemia
-increased ecf and blood volume -hypertension -periods of muscular paralysis |
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what happens with androgen producing tumors
|
adrenogenital syndrome
-virilization in female -virilization in prepubescent male |
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what happens with Congenital adrenal hyperplasia
|
inability to produce one or more enzymes responsible for cortisol systhesis during fetal development leads to virilization of fetus or neonate
|
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what happens with 3 beta hydroxysteroid dehydrogenase deficiency
|
no adrenocorticoids
marked salt excretion in urine early death |
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what happens with 17 alphs hyroxylase deficiency
|
sex hormones and cortisol not produced
sodium and fluid retention patient phenotypically female but unable to mature |
|
|
what happens with 21 alpha hydrxylase deficiency
|
commenest form of CAH
acth levels elevated causing flux in sex hormones and masculinization ambigious genetalia |
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what happens with 11 beta hydroxylase deficiency
|
decrease in serum cortisol, aldosterone, corticosterone
fluid retention and hypertension masculinization |
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what do beta cells produce
|
insulin
|
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what do alpha cells produce
|
glucagon
|
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what is glucose starvation
|
inability for cells to take up glucose
|
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what is hyperglycemia
|
glucose left in circulation
|
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how do glucose levels contribute to dehydration
|
glucose beyond reabsorptive capability
-glucose in urine -water trapped with urine -polyuria -water and electrolyte loss |
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how does insulin affect hunger
|
loss of intracelllurlar calories
|
|
|
what happens when there is a lack of feedback inhibition
|
increase rls of hgh, glucagons, epinephrine, cortisol
|
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type 1
|
no production of insulin
|
|
|
type 2
|
receptors do not respond
|
|
|
what are the principle affects of insulin
|
increase glycogenesis
decrease gluconeogenesis increase triglyceride synthesis decrese trigly breakdown increase protein syn decrease protein breakdown |
|
|
how does glucose get into brain
|
GLUT 1 noninsulin dependent
GLUT 2 noninsulin dependent GLUT 4 insulin dependent |
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what is preproinsulin
|
signal sequence and c peptide still attached
|
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what is proinsulin
|
no signal sequence attached clipped off in ER
|
|
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what is insulin
|
just the beta chain no c peptide attached clipped off in golgi
|
|
|
how does insulin affect glucose uptake
|
binds to receptor which starts a signaling cascade which transports more transporters to the surface for the uptake of glucose
|
|
|
what is the effects of insulin on glycogen metabolism
|
activate enzymes to make glycogen
down regulate glycogenolysis |
|
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what are insulins effects on gluconegenesis
|
inhibits protein breakdown
increase aa uptake reduced enzymatic activity promotes use of glucose as energy source |
|
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what are insulins effects on fate metabolism
|
uptake and storage of triglycerides
decrease enzymes that mobilize fats |
|
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what are insulins effects on protein metabolism
|
stimulatory effect on muscle cell protein synthesis
inhibits breakdown of protein |
|
|
what are the affects of insulin on ion transport
|
increases na k pump
increase kidney na retention increase activity of Na H exchange pump |
|
|
what stimulates insulin release
|
glucose
AA CCK, Gastrin, Secretin |
|
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what inhibits insulin
|
epinephrine
|
|
|
what are the phases of insulin rls
|
1= rapid releasable pool
2=reserve pool |
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what happens with release in type 2
|
no rapid release pool to suck up glucose then an ever increasing release of insulin
|
|
|
what is the path of blood through the heart
|
enter r atrium
through tricuspid valve into r ventricle through pulmonary valve into pulmonary artery to lungs into l atrium through bicuspid valve into l ventricle through aortic valve into aorta |
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how does the heart propel blood
|
postive hydrostatic pressure
|
|
|
why can all cardiac fibers fire together and what is this called
|
due to gap junctions
functional sycitium |
|
|
how are the atria and ventricles connected electrically
|
av node
|
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what is the pacemaker of the heart
|
sa node
|
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how many phases are in atrial and ventricular action potentials
|
5 phases
|
|
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what does phase 2 in atrial and ventricular action potential correspond to
|
systole or contraction
|
|
|
what is phase 0
|
rapid depolarization
-fast sodium channels open |
|
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what is phase 1
|
rapid partial repolarization
-fast sodium channels close |
|
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what is phase 2
|
plateau depolarization
-slow sodium and calcium channels open(200-300mSec) |
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what is phase 3
|
rapid repolarization
-slow sodium and calcium channels close and potassium channels open |
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|
what is phase 4
|
rest
-normal high K permeability |
|
|
what other cells can act as pacemakers
|
internodal fibers
av node bundle of his perkinje fibers |
|
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why is sa node the pacemaker
|
starts at a more postive number and faster closing k channels
|
|
|
what is the role of the AV node
|
to delay conduction
|
|
|
what is total av nodal delay
|
.16 sec
|
|
|
how do we produce delay
|
decreasing the number of gap junctions which increases resistance and slows velocity
|
|
|
how does the ventricle depolarize
|
from endocardium to epicardium and from base to top or up and out
|
|
|
what is the spacing in contraction when sa node is pacemaker
|
.75-.85 sec
HR 70-80 |
|
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what is the space in contraction if av node is pacemaker
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1-1.3 sec
HR 40-60 |
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what is the space in contraction in purknje fibers are pace maker
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1.3-4 sec
HR 15-40 |
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what is an ectopic pacemaker
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when some cells depolarize faster than SA node usually the AV node
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what are the effects on the heart under sympathetic control
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increased heart rate
increased strength of contraction decrease av nodal delay |
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what are the effects on the heart under parasympathetic control
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decreased heart rate
increase av nodal delay |
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where does lead 1 run
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left shoulder positive
right shoulder negative |
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where does lead 2 run
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right shoulder negative
right groin positive |
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where does lead 3 run
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left groin positive
left shoulder negative |
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what is happening electrically as the atria contract
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current is moving from right to left causing positive inflection known as the p wave
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what would cause a negative defelection of the pin
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if the first cells the depolarized are the first to repolarize we get negative deflection of the pin because positive is moving towards positive
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what is significant about ventricular depolarization
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it happens at the same time as atrial repolarization
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what happens if current flows perpendicular to the lead
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there would be no deflection
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what should happen when the atria are depolarized and stay depolarized Phase 2
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no deflection since no current is flowing
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what is the p wave
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atrial depolarization
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what is qrs
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ventricular depolarization and atrial repolarization
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what is the t wave
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ventricular repolarization
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what is teh p-r interval
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atrial systole
.16 sec |
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what is the q-t interval
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ventricular systole
.35 sec |
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what is the r-r interval
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distance between heart beats
.83 sec |
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what is the s-t interval
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plateau of ventricle
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what is a major division on the trace paper
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.2 sec
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what is a minor division on the trace paper
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.04 sec
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what is a healthy heart axis
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20-100 degrees
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what would cause a left hand shift of the axis
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left ventricular hypertrophy
-systemic hypertension -aortic stenosis -aortic regurgitation -congenital problems |
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what would cause a right hand shift in the heart axis
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right ventricular hypertrophy
-pulmonary hypertension -pulmonary valve stenosis -interventricular septal defect |
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when would we see a shift in the axis and a notch in QRS
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bundle branch block
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what would a inverted t wave indicate
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left bundle branch block
ischemia at base of ventricles digitalis toxicity |
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what is tachycardia
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fast heart
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what can cause tachycardia
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hyperthermia
sympathetic outflow weak heart |
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what is bradycardia
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slow heart
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what causes bradycardia
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vagal parasym outflow
-due to increased pressure in arterial circulation baroreceptor reflex |
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what is sinus arrythmia
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heart rate isnt steady but within normal range
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what is sinoatrial block
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sa node doesn't discharge
doesn't excite atrial cells no p wave av node takes over |
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how many levels are there in atrioventricular block
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3
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what can cause atrioventricular block
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ischemia of theave node or bundle of his
irritation of bundle high vagal outflow |
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what is first degree heart block
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slowed conduction through av node
increased P-R interval |
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what is second degree heart block
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not all p waves penetrate av node
all p wave there but not all qrs may have 2:1, |
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what is third degree heart block
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complete block of av node
new ventricular pacemaker P-P constant R-R constant P-R interval always changing |
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what is stokes adams syndrome
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third degree heart block
block not constant last from seconds to months -mild ischemia |
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how is stokes adams syndrome treated
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installing a pacemaker
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what are premature atrial contractions
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spontaneous atrial depolarization
one time event shortened P-R Longer delay to next P wave |
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what is premature ventricular contraction
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prolongedand large QRS with inverted T
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what is paroxsmal atrial tachycardia
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sudden onset fast HR originating in atria
abnormal P because new pacemaker |
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what is paroxysmal ventricular tachycardia
|
can lead to
-ischemic cardiac damage -ventricular fibrillation |
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how do we treat PVT
|
increased vagal outflow
-massage carotid sinus -press on eyes -valsava maneuver -quindine or lidocaine |
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what is atrial fibrillation
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enlarged atrial
prolonged conduction path circus rythyms no p waves rapid QRS |
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what is atrial flutter
|
circus rythyms before atrial fibrillation
atrial HR up around 200-350 |
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How do we treat ventricular fibrillation
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placing all cells indepolarized state simultaneously
110 AC 1000 DC |
