ShockandManagement ConceptHardi Darmawan, MD, MPH&TM, FRSTMDept of Physiology ,Sriwijaya Medical SchoolRK Charitas HospitalPalembang

What is shock?

SHOCK SYNDROMEShock is a condition in which the cardiovascular system fails to perfuse tissues adequatelyAn impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissuesInadequate tissue perfusion can result in:generalized cellular hypoxia (starvation)widespread impairment of cellular metabolismtissue damage organ failuredeath

DefinitionInadequate peripheral perfusion leading to failure of tissue oxygenation may lead to anaerobic metabolismShock is a major critical illness that involves almost every organ system. It is not simply a problem of decreased blood pressure. Rather, it is a problem of inadequate tissue perfusion (Rice,1991)

DefinisiHipotensiTekanan Darah Sistolik < 90 mmHgTekanan Darah Sistolik berkurang > 40 mmHgHipoperfusiPerubahan status mentalOliguriaAsidosis laktat

Diagnosis of ShockMAP < 60 Clinical s/s of hypoperfusion of vital organs

PATHOPHYSIOLOGY OF SHOCK SYNDROMEImpaired tissue perfusion occurs when an imbalance develops between cellular oxygen supply and cellular oxygen demand.

All types of shock eventually result in impaired tissue perfusion & the development of acute circulatory failure or shock syndrome.

Oxygen transport and utilization

CARDIAC OUTPUT = HR X SVSympathetic n. systemCatecholamine releaseIncrease EDV via:VenoconstrictionArteriolar constrictionRenal reabsorptionIncreased contractility

PATHOPHYSIOLOGY OF SHOCK SYNDROME

Cells switch from aerobic to anaerobic metabolism

lactic acid production

Cell function ceases & swells

membrane becomes more permeable

electrolytes & fluids seep in & out of cell

Na+/K+ pump impaired

mitochondria damage

cell death

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal ResponseSNS - Neurohormonal response Stimulated by baroreceptorsIncreased heart rateIncreased contractilityVasoconstriction (SVR-Afterload)Increased Preload

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal ResponseSNS - Hormonal: Renin-angiotension systemDecrease renal perfusionReleases renin angiotension I angiotension II potent vasoconstriction &releases aldosterone adrenal cortexsodium & water retention

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal ResponseSNS - Hormonal: Antidiuretic HormoneOsmoreceptors in hypothalamus stimulatedADH released by Posterior pituitary glandVasopressor effect to increase BPActs on renal tubules to retain water

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal ResponseSNS - Hormonal: Adrenal CortexAnterior pituitary releases adrenocorticotropic hormone (ACTH)Stimulates adrenal Cx to release glucorticoidsBlood sugar increases to meet increased metabolic needs

Failure of Compensatory ResponseDecreased blood flow to the tissues causes cellular hypoxia Anaerobic metabolism begins Cell swelling, mitochondrial disruption, and eventual cell deathIf Low Perfusion States persists:

IRREVERSIBLE DEATH IMMINENT!!

Hypovolaemia and Shockdecreased blood volumedecreased cardiac outputdecreased oxygen deliveryimpaired macrocirculationvasoconstrictionInadequate perfusionErythrocyte aggregationimpaired micro circulationtissue ischemiaorgan failurekidneybowelendotoxin releaseseptic shockDampak Syok

Perfusi normalPompa jantungVolume sirkulasiTahanan pembuluh darah perifer

Pathophysiological causes of shock. After about an hour most patients will demonstrate a dysfunction of all components and it may be difficult to identify the original cause.

Reduced Cardiac Outputpump problem(Cardiogenic - Ischaemic)

Reduced Intravascular volumefluid problem(Hypovolaemic)

Reduced Vascular Resistancepipe problem(Neurogenic - Septic - Anaphylactic)

CLASSIFICATIONS OF SHOCK

Cardiogenic Hypovolemic Distributivesepsis, anaphylaxis, and neurogenic (spinal or epidural anaesthesia, and spinal cord injury). Obstructivepulmonary embolism, dissecting aortic aneurysm, pericardial tamponade and tension pneumothorax Combined

Dissecting ThrorecicAortic Aneurysm

Pulmonary Embolism

Pulmonary Emboli

Tamponade

Stages of ShockInitial stage - tissues are under perfused, decreased CO, increased anaerobic metabolism, lactic acid is building Compensatory stage - Reversible. SNS activated by low CO, attempting to compensate for the decrease tissue perfusion. Progressive stage - Failing compensatory mechanisms: profound vasoconstriction from the SNS ISCHEMIA Lactic acid production is high metabolic acidosisIrreversible or refractory stage - Cellular necrosis and Multiple Organ Dysfunction Syndrome may occur DEATH IS IMMINENT!!!!

Pathophysiology Systemic LevelNet results of cellular shock:systemic lactic acidosisdecreased myocardial contractilitydecreased vascular tonedecrease blood pressure, preload, and cardiac output

Tanda dan gejala syokSistem KardiovaskulerGangguan sirkulasiPucat, dingin, sianosisVena perifer kolapsNadi cepat dan halusTekanan darah rendah kurang bisa jadi peganganVena jugularis penting.CVP

Tanda dan gejala syokSistem RespirasiNafas cepat dan dangkalSistem susunan saraf pusatPerubahan mental / kesadaranSistem saluran cernaMual dan muntahSistem saluran kencingProduksi urin < cc/kg/jam

Clinical Presentation: Generalized ShockMental status: (LOC) restless, irritable, apprehensive unresponsive, painful stimuli only

Decreased Urine output

Shock SyndromesHypovolemic Shockblood VOLUME problemCardiogenic Shockblood PUMP problemDistributive Shock [septic;anaphylactic;neurogenic]blood VESSEL problem

Hypovolemic ShockLoss of circulating volume Empty tank decrease tissue perfusion general shock responseETIOLOGY: Internal or External fluid lossIntracellular and extracellular compartmentsMost common causes:HemorrhageDehydration

Hypovolemik Shock

A 25 year old woman was admitted in the ERShe had given birth 2 hours ago helped by dukun

Hypovolemic Shock: External loss of fluid

Fluid loss: Dehydration Nausea & vomiting, diarrhea, massive diuresis, extensive burns

Blood loss: trauma: blunt and penetrating BLOOD YOU SEE BLOOD YOU DONT SEE

BP 60, pulse just palpable, over 160 per minuteCold clammy skin, unconscious

Multiple iv line were inserted and hemodilution started

Hypovolemic Shock: Internal fluid loss

Loss of Intravascular integrity

Increased capillary membrane permeability

Decreased Colloidal Osmotic Pressure (third spacing)

Pathophysiology of Hypovolemic ShockDecreased intravascular volume leads to.Decreased venous return (Preload, RAP) leads to...Decreased ventricular filling (Preload, PAWP) leads to. Decreased stroke volume (HR, Preload, & Afterload) leads to ..Decreased CO leads to...(Compensatory mechanisms)Inadequate tissue perfusion!!!!

Assessment & ManagementS/S vary depending on severity of fluid loss:15%[750ml]- compensatory mechanism maintains CO15-30% [750-1500ml- Hypoxemia, decreased BP & UOP30-40% [1500-2000ml] -Impaired compensation & profound shock along with severe acidosis40-50% - refactory stage: loss of volume= death

On arrivalAfter infusion

Guidelines for the clinical use of red cell transfusionsBritish Journal of Hematology 2001, 113, p24-3115% loss (750 ml)crystalloids, no transfusion15-30% loss (800-1500 ml)crystalloids, colloids, no transfusions30-40% loss (1500-2000 ml)crystalloids, colloids, probably transfusion> 40% loss (> 2000 ml)crystalloids, colloids, requires transfusion

Clinical PresentationHypovolemic ShockTachycardia and tachypneaWeak, thready pulsesHypotension Skin cool & clammyMental status changesDecreased urine output: dark & concentrated

Hypovolemic Shock: Hemodynamic Changes Correlate with volume lossLow CO Decreased RAP ( Preload)Decreased PAD, PAWPIncreased SVR (Afterload)

Initial Management Hypovolemic ShockManagement goal: Restore circulating volume, tissue perfusion, & correct cause:Early Recognition- Do not relay on BP! (30% fld loss)Control hemorrhageRestore circulating volumeOptimize oxygen deliveryVasoconstrictor if BP still low after volume loading

Penanganan Syok HipovolemikMengembalikan volume intravaskulerTekanan DarahNadiPerfusi organPilihan cairanKristaloidKoloidPRC

American Soc of Anesthesiologists 1996

21Hemorrhage

Loss of IVFPoor sluggish perfusionIncreasing pulse rateDecreasing BP2. Partially compensated by ISF (transcapillary refill)

21Crystalloids for hemorrhage

Rapid Infusion to normalize IVFAfter IVF stabilized, infusion is intended for ISFVolume required thus 2-4x initially lost IVF12Ringer LactateRinger AcetateNaCl 0.9%

Pulmonary Edema Neurogenic

Hb 3Hb 3edemaHb 8RL 7-8000 mlPlasma Subs1500-2000mlBP and pulse normalize faster|shortershock time3.1.2.Hemorrhage2500 ml

TreatmentImpaired perfusion secondary to reduced volumerestore volume Restoration of circulating volume can be achieved by the infusion of 3 mL of balanced electrolyte solution for each milliliter of blood lost.Fluids are infused through two large-bore intravenous lines

TreatmentAdministration of supplemental oxygenControl bleedingFoley catheter to monitor renal functionestablishment of urine output at approximately 50 cc/hr for the adult

Penanganan Syok HipovolemikPasang jalur IV satu/lebih no. 18 / 16Infus cepat Kristaloid / kombinasi+ koloidBila perdarahan, ambil contoh darahBila vena sudah terisi, peningkatan isi nadi dan tekanan darah, infus lambatkanJangan kelebihan cairan

Cardiogenic Shock

DEFINISISimply stated, cardiogenic shock is lack of perfusion from pump failure.Cardiogenic shock is related to the inability of the myocardium to produce sufficient flow and/or pressure to maintain adequate tissue perfusion.

Cardiogenic ShockThe impaired ability of the heart to pump bloodPump failure of the right or left ventricleMost common cause is LV MI (Anterior)Occurs when > 40% of ventricular mass damageMortality rate of 80 % or >

Etiologies of Cardiogenic ShockI. Ischemic heart diseaseA. Acute myocardial infarction, usually anteroseptalB. Ventricular septal defect C. Papillary muscle ruptureD. Ventricular aneurysmII. Valvular heart diseaseA. Acute mitral or aortic insufficiencyB. Severe aortic stenosis

Etiologies of Cardiogenic ShockIII. ArrhythmiasSupraventricularVentricularIV.TraumaTension pneumothoraxPericardial tamponade, may include nontraumatic causesCardiac contusion

Cardiogenic Shock: PathophysiologyImpaired pumping ability of LV leads toDecreased stroke volume leads to..Decreased CO leads to ..Decreased BP leads to.. Compensatory mechanism which may lead to Decreased tissue perfusion !!!!

Cardiogenic Shock: PathophysiologyImpaired pumping ability of LV leads toInadequate systolic emptying leads to ... Left ventricular filling pressures (preload) leads to... Left atrial pressures leads to . Pulmonary capillary pressure leads to Pulmonary interstitial & intraalveolar edema !!!!

Diagnosa Syok KardiogenikCardiac Output berkurangLV filling pressure meningkatSVR meningkat

Clinical PresentationCardiogenic ShockSimilar catecholamine compensation changes in generalized shock & hypovolemic shockMay not show typical tachycardic response if on Beta blockers, in heart block, or if bradycardic in response to nodal tissue ischemiaMean arterial pressure below 70 mmHg compromises coronary perfusion (MAP = SBP + (2) DBP/3)

Cardiogenic Shock: Clinical Presentation Abnormal heart sounds

MurmursPathologic S3 (ventricular gallop)Pathologic S4 (atrial gallop)

Clinical PresentationCardiogenic ShockPericardial tamponademuffled heart tones, elevated neck veinsTension pneumothoraxJVD, tracheal deviation, decreased or absent unilateral breath sounds, and chest hyperresonance on affected side

CLINICAL ASSESSMENT Pulmonary & Peripheral Edema JVD CO HypotensionTachypnea, Crackles

PaO2 UOP LOCHemodynamic changes: PCWP,PAP,RAP & SVR

COLLABORATIVE MANAGEMENTGoal of managementTreat Reversible CausesProtect ischemic myocardiumImprove tissue perfusionTreatment is aimed atEarly assessment & treatment!!!Optimizing pump by:Increasing myocardial O2 deliveryMaximizing CODecreasing LV workload (Afterload)

COLLABORATIVE MANAGEMENTLimiting/reducing myocardial damage during Myocardial Infarction:Increased pumping action & decrease workload of the heartInotropic agentsVasoactive drugsIntra-aortic balloon pumpCautious administration of fluidsTransplantationConsider thrombolytics, angioplasty in specific cases

Management Cardiogenic ShockOPTIMIZING PUMP FUNCTION:Pulmonary artery monitoring is a necessity !! Aggressive airway management: Mechanical VentilationJudicious fluid managementVasoactive agentsDobutamineDopamine

Management Cardiogenic ShockOPTIMIZING PUMP FUNCTION (CONT.):Morphine as needed (Decreases preload, anxiety)Cautious use of diuretics in CHFVasodilators as needed for afterload reductionShort acting beta blocker, esmolol, for refractory tachycardia

Hemodynamic Goals of Cardiogenic ShockOptimized Cardiac function involves cautious use of combined fluids, diuretics, inotropes, vasopressors, and vasodilators to :Maintain adequate filling pressures (LVEDP 14 to 18 mmHg)Decrease Afterload (SVR 800-1400)Increase contractilityOptimize CO/CI

Treatment of Cardiogenic ShockDeterminants of MyocardialOxygen ConsumptionHeart rateContractilityWall tension, preloadAfterload

TreatmentCardiogenic shock cannot be managed appropriately without the ability to measure right and left ventricular filling pressures, cardiac index, and arterial blood pressure or the ability to calculate oxygen delivery, oxygen consumption, and pulmonary and systemic vascular resistance. The pulmonary artery catheter,therefore, is mandatory.

TreatmentBroadly based on four methods(a) increasing contractility (b) altering preload and afterload(c) providing mechanical support(d) controlling arrhythmias.

TreatmentIncreasing ContractilityThe three drugs commonly used to increase cardiac contractility are dobutamine, dopamine, noradrenalin and isoproterenol.Reducing Preload and AfterloadDiuretics may be used as an adjuvant in the treatment of cardiogenic shock but not as a primary agent. vasodilator therapy may be added to reduce preload and afterload, thereby enhancing cardiac output and reducing myocardial oxygen needs

TreatmentMechanical Interventionstension pneumothorax, relief of tension in the chest cavity pericardiocentesis in the case of pericardial tamponadeintraaortic balloon pump

Treatment Common Drugs for ArrhythmiasSupraventricular tachycardia Digitalis VerapamilPropanololProcainamideQuinidineVentricular ectopy LidocaineProcainamideBretyliumQuinidine

DISTRIBUTIVE SHOCKMaldistribution of blood to the tissues.Acute vasodilation without concommitant increase in intravascular volume.Inadequate tissue perfusion. This type of shock is seen in :sepsis, anaphylaxis, and neurogenic (spinal or epidural anaesthesia, and spinal cord injury).

Mechanism of distributive shockhttp://content.nejm.org/cgi/reprint/345/8/588.pdf

Sepsis

Anaphylaxis

Neurogenic

Septic Shock

DEFINISIResult of the systemic effects of infection, primarily with bacterial or fungal organismsinadequate oxygen delivery supernormal oxygen demand by the increased metabolism of septic cells metabolic derangement of cellular metabolism such that cells cannot utilize oxygen

PathophysiologyEarly Septic Shock (Warm Shock)low systolic blood pressurea relative normal pulse pressure and stroke volume normal or high cardiac outputBecause these patients tend to be vasodilated and have a low systemic vascular resistance, the skin is usually warm (or even flushed) and dry. (a "relative" hypovolemia)

PathophysiologyEarly Septic Shock (Warm Shock)Tachycardia and tachypnea Arterial blood gases usually reveal a moderate respiratory alkalosisLactate levels are usually normal or only mildly increased initially

PathophysiologyLate Septic Shock (Cold Shock)Impaired organ functionintravascular fluid retentiondepletion of the functional extracellular fluid volumeCardiac index usually falls below normal Lactate levels begin to rise rapidly bicarbonate levels fall

PathophysiologyLate Septic Shock (Cold Shock)pH becomes increasingly acidoticThe skin becomes cold, clammy, mottled, and cyanoticOliguria and depressed mental status are common accompaniments of severe sepsis.

Diagnosa Syok DistributifCardiac Output normal atau meningkatLV filling pressure normal atau rendahSVR berkurang

Gambaran Hemodinamik Syok

HipotensiBiasanya (tidak selalu) cardiac output berkurang, kecuali Sepsis beratTidak selalu berarti syokHipertensi bisa CO rendah dan hipoperfusi organ (Gagal Jantung)Penting pemeriksaan fisik

PRINCIPLES OF MANAGEMENT identify cause establish adequate ventilation and oxygenation restore optimum intravascular volume maintain adequate cardiac output and renal perfusion maintain optimum internal metabolic environment

Penanggulangan SyokPrinsip dasarMeningkatkan O2 deliveryCararesusitasi cairanmeningkatkan kontraktilitas jantungmeningkatkan SVRMemperbaiki kelainan iramaOptimalisasi O2 content darahPasang kateter urinThe goal of all treatment is to maintain adequate tissue perfusion and treat the underlying cause

Penanganan Syok DistributifSyok SeptikCorrect primary processAntibioticsDrainageResuscitationVentilatory support and 02, as neededFluidsInotropesVasodilators or vasopressors

Resuscitationincrease vascular volumecrystalloid solutions are preferred for raising intravascular volumesevere acidosis may impair cardiac function if the arterial pH is < 7. 1, bicarbonate may be required.Dopamine in doses of 5 to 15 ug/kg/min seems ideal for improving myocardial contractility and cardiac output in hypotensive vasodilated patients.

Syok AnafilaktikEpinephrine SQResusitasi cairanEpinephrine IVPenanganan Syok Distributif

Terapi CairanMengganti volume intravaskulerMenentukan status volume cairan pasienVena leherAuskultasi paruCVP

Resusitasi CairanKoreksi hipotensiTurunkan HRKoreksi hipoperfusiOliguriaPerubahan status mentalAsidosis laktatPantau perburukkan oksigenasi

Prioritas dalam Terapi CairanEMERJENSI : VOLUME INTRAVASKULARCURAH JANTUNGPERFUSI ORGAN VITALSUB-EMERJENSI : INTERSTITIALINTRASELTANDA-TANDA VITALPROD. URIN

Jenis CairanKristaloidRinger Asetat / Ringer LaktatNormal SalineKoloidHetastarchAlbumin 5%PRCMeningkatkan kapasitas angkutan O2Fresh-frozen plasmaTidak diindikasikan untuk mengganti volume

TERAPI CAIRANASERINGRINGER LAKTATNORMAL SALINE

RESUSITASI

KRISTALOID

KOLOID

ELEKTROLIT

NUTRISIMENGGANTIKAN KEHILANGAN AKUT CAIRANDEXTRAN- 40MEMENUHI KEBUTUHAN HARIAN ELEKTROLIT DAN NUTRISIKA-EN 1B KA-EN 3AKA-EN 3BKA-EN 4AKA-EN 4B

AMIPARENAMINOVEL- 600PAN- AMIN GKA-EN MG 3Martos -10TRIPAREN ITRIPAREN II

RUMATANKONSEP MEDIS

KOREKSI- NaCl 3 % - MgSO4 20 % - Mannitol 20 %

TREATMENT CONCEPT OF SHOCK

ENHANCING PERFUSION / OXYGEN DELIVERYOxygen delivery/DO2 = HR X SV X Hb X S02 X 1.34 + Hb X paO2Cardiac outputArterial O2 contentDO2 = CO x CaO2

Cardiac Output x SVRPipe = VascularPump =HeartVolume =BloodHypovolemic ShockCardiogenic ShockDistributive ShockInotropes (Dob,Dop,Adr,Amr)Vasopressor ( NE,PE,ADR,Dop)FluidsObstructive ShockRelease tamponade,etcBlood Pressure

John Collin Warren (1800s)

momentary pause in the act ofdeath.

Samuel D. Gross (late 19th century)rude unhinging of the machinery of life.

Arthur C. Guyton

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