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Shock Al state 2eT which —T Vv Timinfsheol Cardrac output | Blood Volume | imp airs TISSUE PERFUSION [2 leads to elluLer 4 Sia a Reduced effective, Crealading fo] Oe ¢ Onset —> Reversible Ing Helonged Shock —> Ir. Citoue P: Fatal. ° Comphicates conditons tke 1 MT, Aevere +Hemorrha, 5 o extensive [raumea pulmona = = =) embolism Burns. ca 7) MP SeT A&B @ Gee: Cotegories I. CARDIOGENIC SHOCK = Cardiogenic Myocardial infaotion olow Cardfac Output + of 2p onfacction. pisudeeardl ald Failure of myocardial pump resuiting fromfintrinsic myocardial damage] pales oe Isic compression] or[obstruction to Outfiow] or Ventrzular oleae G eg: Cardlac, Palmon Arby thmfas. Pulmonary embolism al Tamponade. “embolism Cf CHvDBT) = Hypovolemic Fluid loss (@.g., hemorrhage, vomiting, diarrhea, burns, or Inadequate blood or plasma volume trauma) Ss Shock @/w SYSTEMIC Inflamm™ ° Massive ou rin inflam. feggered mediators ie folate ie CN italy oct t adaptive find celts. CarterPal) Shock associated with Overwhelming microbial infections (bacterial and fungal) | Activation of cytokine cascades; peripheral dian and pooling ha systemic inflammation Superantigens (e,g., toxic shock syndrome) of blood; endothelial actvatiorvinjury; leukocyte-induced damage, = Trauma, bums, pancreatitis {disseminated intravascular coagulation 2 Vascular leakage. result a AW QO Trssue Hypoper fusion. — @) Cellular Hyponia- si teed @) Metabolic Derang emeuts — | ui Sota severe ORGAN n stunction FAILURE & a 7 f a * polittedt ° Septic Shock: ~ Caused qd microbial. infection — Mortal? Rate — Pa ; 20} ~ Fncideuce wonically :: “-4 , 2p "I 4+ OU mt Aonks of imeunocowpromised te, fi of CHEMOTHERAPY, _ -$MMUNO.SUPPRESION , ADVANCED AGE or Hiv_$NFECTION + F _ Sebtic Shock most commons apes am _-+ve haectena | thee yom -ve ‘bacteria | thew Seg ~ Older Nonym —> os Shock No longer appro pnate . — Macro pha Re s pousible _ neurapidte Hecagyinan Dendattie Cells dothelial Cells A i suse of Smnate fmmunity ( Complement) ¢ Factors _bel?eved to play, mayor roles uw. pathophy siolog- ot a) v sepiic Sheck : t aS) UV T Oo Likely tnsthators snl arematon, pre Sepsis Ls Atanalin athw that Ife. 4) O aoabn strea TJouL- I’ke receptors. & G&- pret coupled rec. | fecegnnns \ reco guise Host op microbe ~ dere Detect bactenalL Aubstances contain Pep tides & PAM Fs ica ass. ‘an (ndot, Nop 2). molecular aiierns ) Nucleatde oli ometcat oomain Prot. * Innate immune activation QS QO el) —~*ricee aa Produce, oe h notte Box - 1 aS, fo] ° efector molecules BEND endothelial cells t) Himulate tokin (2, Pallas CA M z } ¢ gQ product upregule ke, Chemokine 5 producthow. Result : Septic pains “| oscillate bw sypeunflamm “Oe g immuno suppressed totes. Fmmune Auppression. 1° of 0) sh t 2, Dehn inflammatory [T, 4) 1D ot - wal (2) CF eiottnes @ ae Fi anh- Pn Flamm. mediators. (sduble TNF | receptor, IL-| receptor antaponist Q ike lo). si P si @ “yophoggte abo ptosis. (+) ~Smmuno Sup ressive effects of apopteti.c cells. 6) Induction of cellular one aa 9. | P4 A \0 () 0) oo CNGoTm eliaL Ficnveatio~w a AMA = — f f) + rr Inflomenator State [ teas to wides read Vesculer Leakage + Pe oue Edema. (im L deled en Gus eff ects on both nutnent ceiver € " waste removel. bd Inflamm. tokmes —> Looser endoth- dP cell tight Gunct's Aecumutaton of ccumuUlaton =—_ lea Vessels prot: - nel of edema _thr.ouwt body , Ld (4) c) a impedez ssue extus1 OL, ress por exacerbated ot IV fiefs. e Act vated endothelrum also | Product” of upreg- No & other Vasc. smoot, Voesoachve muscle relaxation. infl. medictors. Systemic typariersticcn. Cl30,CSa, PAF) 3 Saduction of a. prococ ulent state: Procoagulant Oerongement ss Coogulat” Ab system CJ 5 J sf oee Disseminated thrombi 2 Snhravasculer (0 c) Hemostasfs cpminiam ate the, form” of a stable blood clot. © o P) i tra — Ve r ‘i L lateletr a. Crest Cons um pt P fall os Vv Great i J Defrcien °f sthece factors. Concomitant bleeding & wr (3) Metabolic AbnormaliHes - * SebHe patients —> Gnsulh — Resistance aie ° ™ IL-l, Sdress - induced hor manes C glacegons GH 5 Catecholamine. ) L dnve _gluconeo sogenses ° - FH ate Oo Aubpre ss {nguLm romore insure release VO res! Stance by impairing. surface express” of GLuT-4. ins — | Man meee Funct" Bacten'ctdal Ay Sabbression, 4nittall Proust Te | “C ~ Jecocost? std product’ d | fotows Adrenal usu ff ar 2 pinckenol. a is Yai) * git ebression Syntheli ca act ty op intact ad ond lends frank Adrenol Necros{s \ of Dic. e — ellul Hyphotia 2 Dimintshed odatne OU ospheng N 4 9p 0 Lacte re Qa lacne ‘Attdosts. ° Organ Dysqunchen Systemic Fe mai Intershhel. 5 edema Small vessel Thtambosis 0) Extent & viwwlence of wlect” Immune Po of Host: resence other co- morbid cond”s peter a level of. mediator Production, e Standard of Cere CH treat under lyin ike, peewee (a) Cb mamntau Blood ressure fo |pm5t d1ssue hypoxia.) e Su, ane C Additional Gree of ecrete bactenaL. prot.) | couse y C similor uo) é sepne shock) poem ol a amprogs achvaloek ales HP release av Clinical cytokines | moni fs ; , Steges of Shock: Shock —> pro ressive. disorder —> <£
ae ee = Ties ue operfus" on ng = Onset op worseniHp_ couse camel 2 metab_Colfs not ] embalan eke | imckedtiop correcte LActic Acip ved wid ad <— Rogressive phase. es pre P “eto i fer sistent On deficit L P) replaced Sntracellular aerobic — 1 > A naerobee resp” cf cme sts excessive sod” Tissue pba AACTIC =~ sPLA- Arierfalor AcIDOs!S ton Bluntn Vasomotor response Reoling d of Blood a microcPreulotfon. ( fenphera lL Pool 09 5 - Worsenin C:D- ~ Endoth\ cells = at ask of ANDXIC myur T subsequent Alc cn ~ Vital organs affected —_= Begum to fail. severe cellular 2 thesue to the bod [evens “an Hemodynamic defects are corrected apremie et Sumuval not pn scible. “prosomal Cel) leakage fete ag grey - Shock stote_ * tschemic Bowel —> allows fntest. flora to Bacteremic =— _ enter Cir culation. Shock (may be Supe nm P oGed) e Anuna as a result of Tubular NecrosiS &. Renal fates re. e Hemorrhagic Adrenaltis | fulminant pied o— ac Ya. ° Consumption or platelets R coqlet” fecters _ skin. © ct _ excebt” of Neuronal £ Myocyte. Ischemic loss. | YY vistuall all of these tHssues m revert to (®) L af undivid. Survives, bd —Irrev. omen ges —_ : op Sev Shock ~ ° Clinical Conseqneuces | Hanifestat’s: " U be povoleme + Cardiogenic Shock — HYPOTENSION —- Weak, Rapid pulse — Tachypnea — CooL Claeys Gpanotic skin Sebhe Shock | niall eed Warm & fished Py op perip- vasodil’. Shock ein rise -+to ! © Cardiac Oyefun unchow ° Cerebral or cher Pulm mt sDys-fun chee & even tual Electolyte ‘Btanandd taboli dogs. ( excerbates ie aii | oP pl. ther) 2nd phase. L, dominated ai | ‘Renal. Snot “ Bice all Mie Arh output fluid 2 elect ie Imbalances. 
