VASOPRESSORS & INOTROPES

8/18/2019 VASOPRESSORS & INOTROPES

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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 –

VASOPRESSORS & INOTROPES

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