vasopressors & inotropes
TRANSCRIPT
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VASOPRESSORS &
INOTROPES
Critical Care Internship
ProgramDr. T. Madaag
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Smpathomimetics & Catecholamines
• Dopamine! epinephrine &norepinephrine – Prod"ced nat"rall in the #od to
acti$ate the smpathetic ner$o"ssstem #• Initiating the %ght or ight
•
Stim"lating the alpha and #eta receptorsth"s – Increased cardiac o"tp"t
– $asoconstriction
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• Cholinergic transmission ismediated # Ach
• Adrenergic transmission ismediated # – epinephrine 'adrenal med"lla(
– norepinephrine 'post ganglionic
ne"rons(
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Ach E)ects
• *EART – Decreased heart rate # red"ction in
SA %ring
– Increased cond"ction thro"gh the AVnode
• VESSE+S
– Vasodilation
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Receptor Phsiolog
• Alpha ,
• Alpha -
•
eta ,• eta -
• Dopaminergic
•
Vasopressin 'V,(
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Alpha ,
• +ocated in the arteriolar /allsind"cing $asoconstriction
• Present in the heart – Stim"lation leads to constriction o0
the $asc"lar smooth m"scle!splanchic $essels
– Increases SVR
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Alpha -
• 1hen #loc2ed ca"ses $asodilation #inhi#iting the release o0norepinephrine
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eta Receptors
• eta , – Most common in the heart
• Stim"lation ca"ses – Increased rate 'Chronotropic e)ect( – Contractilit 'Inotropic e)ect(
– Increased CO & per0ormance
– Rela3ation o0 smooth m"scles• Vasodilation
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Dopamine Receptors
• 4 s"#5tpes – Present in renal! splanchnic! coronar
& cere#ral $asc"lar #eds
– D6 receptors identi%ed in the heart
• Increases CO # – Impro$ing contractilit
–*eart rate
• D,! D- receptors stim"latedi"resis & nat"resis in the 2idnes
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Vasopressin 'V,( Receptors
• Present in smooth m"scles o0peripheral arterioles
• Stim"lation ca"ses – Increased $asc"lar resistance
• 77Main compensator mechanism inhpo$olemic shoc2
–
Increased P d"e to #aroree3
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Rationale 0or Vasopressor &
Inotrope 8se
• Shoc2 – A %nal common path/a in
• MI
• Sepsis
• P"lmonar em#olism
• Tra"ma
• Anaphla3is
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• Tpes o0 shoc2 – *po$olemic
– Cardiogenic
– Ne"rogenic
– O#str"cti$e
– Distri#"ti$e
– Septic
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• Pathologic processes in septicshoc2 – Vasodilation '$asoplegia(
– Maldistri#"tion o0 #lood o/
– Mocardial depression
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Management o0 Shoc2
• Management o0 ade9"atesstemic press"re 0or optimaltiss"e per0"sion – Maintain MAP o0 :; mm *g
•
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Vasopressors & Inotropes
• Vasopressors – Increase SVR> increase P
• Inotropes – Increases CO # ?contractilit
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• Note – Dr"gs ma in"ence se$eral
receptor sites
– Ma #e dose dependent
– P ma increase $ia direct &indirect responses
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• Phenlephrine 'neosnephrine(
• Vasopressin
•
Norepinephrine '+e$ophed(• Epinephrine
• Dopamine
•
Do#"tamine
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• Phenlephrine 'neosnephrine(
• Vasopressin
• Norepinephrine '+e$ophed(
• Epinephrine
• Dopamine
• Do#"tamine
Increased SVR
Decreased SVR
Decreased CO
Increased CO
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• Treatment o0 shoc2• Characteri=ed # inade9"ate tiss"e per0"sion
• Res"lts in impairment o0 o3gen & n"trient deli$er
• Ca"ses hpotension
• Progresses to m"lti organ sstem ds0"nction
– Re$ersal o0 the pro#lem & correctinghemodnamics
–
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Dr"g O$er$ie/
• Phenlephrine 'Neosnephrine(• 8se0"l in ne"rogenic shoc2
• Also /hen the SVR4;; & CO not impaired
• *perdnamic sepsis
–
P"re alpha acti$it> $eno & arteriororalconstriction
– Minimal direct e)ects on inotrop or chronotrop
– ? s@dP! MAP
– Ree3 #radcardia
– Minimal e)ects on heart rate or contractilit'arrhthmia potential minimal(
– Decreased renal & splanchnic per0"sion
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Epinephrine
• Potent #eta5, receptor acti$it
• eta5- and alpha5, receptor e)ects
• ? CO! SVR! $aria#le e)ects on MAP
• eta5, e)ects ma pro$o2e arrhthmias• Breater degree o0 splanchnic
$asoconstriction
•
AC+S! anaphla3is! second line agent inshoc2! hpotension post CAB@openheart
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Vasopressin 'AD*(
• Reg"lates retention o0 /ater 'notsalt(
• Stim"lates smooth m"scle V5,receptors – Vasoconstriction
• 8sed in – DI
– Esophageal $ariceal #leeding
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Norepinephrine '+e$ophed(
• Acts on Alpha5, and eta5,receptors – Potent $asoconstriction> $eno"s
ret"rn increases – +ess increase in CO
– Ree3 #radcardia
– +o/ doses '- mcg@min(5 #etaadrenergic receptors
– mcg@min5 alpha receptors >$asoconstriction
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Dopamine 'Intropin(
• Prec"rsor o0 epinephrine&norepinephrine
• Mediated # dopaminergicreceptors
• Dose dependent – +o/ doses '-5 mcg@2g@min(
• D5, receptors in renal! mesenteric!coronar! & cere#ral #eds leads to$asodilation
– 8se o0 dopamine 0or ac"te renal 0ail"re not
s"pported and sho"ld #e eliminated
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Dopamine 'Intropin(
• Moderate doses '5,; mcg( – Stim"lates 5, receptors
– Increases CO # increasing SV
– Varia#le e)ects on *R
• *igher Doses – P"re alpha
– Vasoconstriction
– Increases SVR
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Dopamine 'Intropin(
• Ad$erse E)ects – Tachcardia!
– Tacharrhthmia
– E3cessi$e $asoconstriction 'dosedependent(
– Increased mocardial O- demand
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Do#"tamine 'Do#"tre3(
• Not a $asopressor
• Inotrope that ca"ses $asodilation
• Predominant #eta5, receptor acti$it –
?inotrop & chronotrop – +V %lling press"res
• Net e)ect – ? CO
–
Decreased SVR '/ith or /itho"t a smallred"ction in P(
– 7CO ma #e decreased as a res"lt o0 mar2eddecrease in SVR 'a0terload(
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Deciding on the right $asopressor
• In all shoc2 states• Vasopressors sho"ld onl #e initiated /ith@a0ter
ade9"ate res"scitation is pro$ided /ithcrstalloids! colloids! and@or #lood prod"cts
• Septic shoc2 – Maintain MAP F: mm *g
– Norepinephrine '+e$ophed( is the %rst lineagent /hen $asopressors indicated
• Re0ractor septic shoc2 – Add $asopressin! dopamine or epinephrine
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• Cardiogenic shoc2
– In lo/ o"tp"t cardiogenic shoc2!• Norepinephrine '+e$ophed(! Dopamine G@5
Do#"tamine
• *po$olemic shoc2 –