Dr Chris - SHOCKHYPOVCVSSEPSIS.ppt

DIAGNOSIS AND MANAGEMENT OF SHOCKChris A johannes SpAn KICIntensive Care DepartementGatot Subroto Central Army Hospital.JAKARTA

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

ShockAlways a symptom of it cause.Abnormally low organ perfusion.Usually associated with decreased blood pressure.Sign of organ hypoperfusion, mental status change, oliguria, acidosis.

Diagnosis of ShockMAP < 50 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.

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!!

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

Clinical Presentation: Generalized ShockVital signsHypotensive:(may be WNL or due to compensatory mechanism) < 90 mmHgMAP < 50 mmHgTachycardia: Weak and Thready pulseTachypneic-blow off CO2 Respiratory alkalosis

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

Shock SyndromesHypovolemic Shockblood VOLUME problemCardiogenic Shockblood PUMP problemDistributive Shock [septic;anaphylactic;neurogenic]blood VESSEL problemObstructive Shock ( Tension Pneumothorax, Tamponade )

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

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

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 CO

15-30% [750-1500ml- Hypoxemia, decreased BP & UOP

30-40% [1500-2000ml] -Impaired compensation & profound shock along with severe acidosis

40-50% - refactory stage: loss of volume= death

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)

Hypovolemic ShockVolume resuscitation Crystaloid, colloid.Initial crystalloid choices: - Lactated Ringers solution. - Normal saline ( high chloride may produce hyperchloremic acidosis ).Match fluid given to fluid lost. Blood, cristalloid, colloid.

Fluid TherapyCrystalloids - Lactated Ringers/ Acetate Ringer Solution. - Normal Saline.Colloids - Hetastarch - AlbuminPacked red blood cells.Infuse to physiologic endpoints

Fluid TherapyCorrect hypotension first Decrease heart rateCorrect hypoperfusion abnormalitiesMonitor for deterioration of oxtgenation

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

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 >

Cardiogenic Shock : EtiologiesMechanical: complications of MI:Papillary Muscle Rupture!!!!Ventricular aneurysmVentricular septal rupture

Other causes:Cardiomyopathiestamponadetension pneumothoraxarrhythmiasvalve disease

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 !!!!

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 management :Treat Reversible CausesProtect ischemic myocardiumImprove tissue perfusionTreatment is aimed at :Early 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

Distributive ShockInadequate perfusion of tissues through maldistribution of blood flowIntravascular volume is maldistributed because of alterations in blood vesselsCardiac pump & blood volume are normal but blood is not reaching the tissues

Vasogenic/Distributive ShockEtiologiesSeptic Shock (Most Common)Anaphylactic Shock Neurogenic Shock

Anaphylactic ShockA type of distributive shock that results from widespread systemic allergic reaction to an antigenThis hypersensitive reaction is LIFE THREATENING

Pathophysiology Anaphylactic ShockAntigen exposurebody stimulated to produce IgE antibodies specific to antigendrugs, bites, contrast, blood, foods, vaccines

Reexposure to antigenIgE binds to mast cells and basophilsAnaphylactic response

Anaphylactic ResponseVasodilatationIncreased vascular permeabilityBronchoconstrictionIncreased mucus productionIncreased inflammatory mediators recruitment to sites of antigen interaction

Clinical Presentation Anaphylactic ShockAlmost immediate response to inciting antigenCutaneous manifestationsurticaria, erythema, pruritis, angioedemaRespiratory compromisestridor, wheezing, bronchorrhea, resp. distressCirculatory collapsetachycardia, vasodilation, hypotension

Management Anaphylactic ShockEarly Recognition, treat aggressively AIRWAY SUPPORTIV EPINEPHRINE (open airways)Antihistamines, diphenhydramine 50 mg IVCorticosteroids IMMEDIATE WITHDRAWAL OF ANTIGEN IF POSSIBLEPREVENTION

Management Anaphylactic Shock

Judicious crystalloid administration Vasopressors to maintain organ perfusionPositive inotropesPatient education

NEUROGENIC SHOCKA type of distributive shock that results from the loss or suppression of sympathetic toneCauses massive vasodilatation in the venous vasculature, venous return to heart, cardiac output.Most common etiology: Spinal cord injury above T6 Neurogenic is the rarest form of shock!

Pathophysiology of Neurogenic ShockDistruption of sympathetic nervous systemLoss of sympathetic toneVenous and arterial vasodilationDecreased venous returnDecreased stroke volumeDecreased cardiac outputDecreased cellular oxygen supplyImpaired tissue perfusionImpaired cellular metabolism

Assessment, Diagnosis and Management of Neurogenic ShockPATIENT ASSESSMENTHypotensionBradycardiaHypothermiaWarm, dry skinRAP PAWP CO Flaccid paralysis below level of the spinal lesionMEDICAL MANAGEMENTGoals of Therapy are to treat or remove the cause & prevent cardiovascular instability, & promote optimal tissue perfusion

MANAGEMENT OF NEUROGENIC SHOCKObserve for Bradycardia-major dysrhythmiaObserve for DVT- venous pooling in extremities make patients high-risk>>P.E.Use prevention modalities [TEDS, ROM,Sequential stockings, anticoagulation] NURSING DIAGNOSISFluid Volume Deficit r/t relative lossDecreased CO r/t sympathetic blockadeAnxiety r/t biologic, psychologic or social integrity

Management Neurogenic ShockAlpha agonist to augment tone if perfusion still inadequatedopamine at alpha doses (> 10 mcg/kg per min)ephedrine (12.5-25 mg IV every 3-4 hour)Treat bradycardia with atropine 0.5-1 mg doses to maximum 3 mgmay need transcutaneous or transvenous pacing temporarily

SEPSISSystemic Inflammatory Response (SIRS) to INFECTION manifested by two or > of following:Temp > 38 or < 36 centigradeHR > 90RR > 20 or PaCO2 < 32WBC > 12,000/cu mm or > 10% Bands (immature wbc)

SEPTIC SHOCKSEPSIS WITH:Hypotension (SBP < 90 or > 40 reduction from baseline) & Tissue perfusion abnormalities invasion of the body by microorganisms & failure of bodys defense mechanism.

Risk Factors Associated with Septic ShockAge

Malnutrition

General debilitation

Use of invasive catheters

Traumatic wounds

Drug Therapy

Pathophysiology of Septic shockInitiated by gram-negative (most common) or gram positive bacteria, fungi, or virusesCell walls of organisms contain EndotoxinsEndotoxins release inflammatory mediators (systemic inflammatory response) causes...Vasodilation & increase capillary permeability leads toShock due to alteration in peripheral circulation & massive dilation

Pathophysiology of Septic ShockIMMUNE / INFLAMMATORY RESPONSE Microorganisms enter bodyMediator ReleaseActivation of Complement, kallikrein / kinin/ coagulation & fibrinolytic factors platelets, neutrophils & macrophages>>damage to endothelial cells.ORGAN DYSFUNCTION

Clinical Presentation Septic ShockTwo phases:Warm shock - early phasehyperdynamic response, VASODILATIONCold shock - late phasehypodynamic response DECOMPENSATED STATE

Clinical ManifestationsEARLY---HYPERDYNAMIC STATE---COMPENSATION

Massive vasodilationPink, warm, flushed skinIncreased Heart RateFull bounding pulseTachypnea

Decreased SVR*Increased CO & CISVO2 will be abnormally highCrackles

Clinical ManifestationsL ATE--HYPODYNAMIC STATE--DECOMPENSATIONVasoconstrictionSkin is pale & coolSignificant tachycardiaDecreased BPChange in LOC

Increase SVRDecreased CODecreased UOPMetabolic & respiratory acidosis with hypoxemia

COLLABORATIVE MANAGEMENTPrevention !!!Find and kill the source of the infection Fluid ResuscitationVasoconstrictorsInotropic drugs

Maximize O2 delivery SupportNutritional SupportComfort & Emotional support

Sequelae of Septic Shock

The effects of the bacterias endotoxins can continue even after the bacteria is dead!!!

In summary, Treatment of ShockIdentify the patient at high risk for shockControl or eliminate the causeImplement measures to enhance tissue perfusionCorrect acid base imbalanceTreat cardiac dysrhythmias

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