Shock
Transcript of Shock
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Jessica Powers RN, MSN, CEN
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SHOCK = INADEQUATE PERFUSION OF TISSUES WITH OXYGENATED BLOOD
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Response to Hypoxia Response to poor perfusion
Respiratory:•Increased RR and Depth
Cardiovascular: •Increased HR •Increased SVR
•Blood is shunted•Increased preload•Increased contractility
Cardiovascular:•Increased cardiac output
Liver:Mobilization of stored blood
Baroceptors stimulated sympathetic response
Compensatory MechanismsCompensatory Mechanisms
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What is our goal when we treat shock?
to maximize the body’s ability to supply oxygen to the cells in order to preserve tissue and organ function.
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Stages of ShockStages of Shock
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Types of ShockHypovolemic
Distributive
Cardiogenic
Inadequate Venous Return
Pump Failure
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Hypovolemic ShockCaused by excessive loss of intravascular
volumeHemorrhageVomiting/DiarrheaBurns
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Hypovolemic ShockDecreased blood volume = decreased venous
returncompensatory mechanisms initiated
Increased HR, RR, SVR Increased workload on heart more oxygen
demand Blood volume is shunted
Anaerobic metabolism lactic acidosis Cellular inflammation -> increased capillary
permeability -> more decreased volume
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AssessmentHistoryPhysical Findings
Neuro
Respiratory
Skin
Pulses
•Vital Signs?•Urine Output?
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Laboratory StudiesSerum lactate
increasedABG
Acidosis, increased base deficitCBC
Hemoconcentration/hemodilutionBMP
Renal functionElectrolyte abnormalities
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Management of Hypovolemic ShockFix the causeRestore circulating volume
Isotonic fluidsBlood loss
PRBCsVolume expanders in resuscitation phase
Oxygenation
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CautionsPulmonary congestionHypothermiaCoagulopathies
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QuestionThe nurse suspects that a patient injured in a
motor vehicle accident is going into hypovolemic shock. Which of the following compensatory mechanisms will help maintain a patient’s blood pressure?
A. Increased urinary output
B. Decreased respiratory effort
C. Decreased preload
D. Increase in systemic vascular resistance (SVR)
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AnswerD. Increase in systemic vascular resistance
(SVR)
Rationale: The release of catecholamines causes a peripheral vasoconstriction and therefore an increase in the systemic vascular resistance (SVR) as well as venous vasoconstriction, which increases the preload. Respirations increase to supply more oxygen to the tissues. Urinary output decreases to conserve sodium and water under the influence of ADH.
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Cardiogenic ShockPump Failure (Extreme CHF)Causes:
MI MyocarditisValvular diseaseVentricular Septal RuptureDysrythmias
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Mr. Wells89 year old male s/p LV MI with PCIHx: CAD –CABG x1 in 2009, DM, GERD,
Prostate CA in 1980, hypercholesterolemia, HTN, AVR, CRF, Afib, DVT in 1995
Which of these factors make Mr. Wells at high risk for developing cardiogenic shock?
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Current TreatmentsO2 @ 4LNCNSS @ 150cc/hr x 2LCardiac dietDiltiazem gtt @ 10mg/hrMorphine 2mg IV Q 4H PRN
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Your Initial AssessmentVS: T- 97.9, RR-20, BP 102/60, HR 94, P.Ox- 94%
on 4L NC
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Your Initial AssessmentA+Ox2Mild JVDPulse irregular, threadyAbdominal retractions and
distentionInspiratory crackles,
wheezing+2 pitting edemaPallor5/10 midsternal CP20 cc UO in 1 hour
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Labs and DiagnosticsCBC:
WBC 9.1, Hgb 12 g/dL, Hct 45%BMP:
Na 140 , K 6.2, Cl 110, CO2 15, BUN 48, Cr 2.4Trop: 6.0BNP: >4000INR: 2.1CXR – pulmonary congestionEcho – EF 35%
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Another look at Mr. WellsVS: T- 97.9, RR-46, BP 78/43, HR 126, P.Ox- 88% on
4L NC
DiaphoreticIncreased confusionNo urine output x 1hr
ABG: pH 7.50, H 30, paO2 50, paCO2 24, HCO3 26.0
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Cardiogenic Shock
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Management of Cardiogenic ShockWhat will we do for Mr. Wells and pts like
him?OxygenationAttention to preload (LVEDP)
How do we measure it? IVF Diuresis
Electrolyte replacementNarcotics
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Management of Cardiogenic ShockIncreasing contractility
Sympathomimetics: norepinephine, epinephrine Problem – increased HR and SVR (workload)
Postive inotropes: dopamine, dobutamine, amrinone, milnorone Problem – increased workload
Reducing SVR and LVEDPVasodilators: nipride, tridil, ACE inhibitors
Increasing BPVasoconstrictors: Phenylephrine, pitressin
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Mechanical Support IABP LVADInflates during diastolePerfusion of Coronary
arteries Increases CO
Mechanical pump
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Distributive ShockAnaphylactic NeurogenicSeptic
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Anaphylactic ShockAllergic reaction
IgE mediated Immune response to specific antigen
Non-IgE mediated Anaphylactoid reaction Direct activation of mediators Commonly associated with NSAIDS
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PathophysiologyAntibody-antigen reaction causes mast cells
and basophils to secrete:HistamineLeukotrienesEosinophil chemotactic substanceHeparinProstaglandinsNeutrophil chemotactic substancePlatelet-activating factor 2
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PathophysiologyHistamine, prostagandins, and leukotrienes cause:
Systemic vasodilationIncreased capillary permeabilityBronchoconstrictionCoronary vasoconstrictionUrticaria
Other substances cause:Myocardial depressionInflammationExcessive mucous secretionPeripheral vasodialtion
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Management of Anaphylaxis
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Neurogenic ShockSpinal cord injury above T6Other causes: spinal
analgesia, emotional stress, pain, drugs, other CNS problems
Loss of sympathetic tone -> peripheral vasodilation
Hypotension and Bradycardia
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Septic Shock
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Systemic Inflammatory Response Syndrome (SIRS)Systemic response to infection manifested by two
or more of the following:Temperature >38 C or <36C (>100.4 F or <96.8 F)HR >90 bpmRR >20 breaths/min or PaCO2<32 mmHgWBC > 12,000 cell/mm3, <4,000 cells/mm3 or
>10% immature (band) forms
SEPSIS is SIRS with an identified SEPSIS is SIRS with an identified sourcesource
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Severe SepsisSepsis with organ dysfunction,
hypoperfusion, or hypotensionPatient responds to fluids
How can you measure fluid responsiveness?
Signs of hypoperfusion?Lactic acidosis, oliguria, mental status change
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Septic ShockSepsis with hypotension despite adequate
fluid resuscitation along with perfusion abnormalities.
What about patients who are on vasopressors and maintaining an adequate BP?
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Risk Factors For Septic ShockHost Treatment-related
Elderly, young Invasive catheters
Malnutrition Surgical procedures
Chronic illness/debilitation Traumatic/thermal wounds
Drug/alcohol use Invasive diagnostic procedures
Neutropenia Medications – antibiotics, cytotoxic agents, steroids
Splenectomy
Organ failure
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Loss of Homeostasis
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Cardiovascular AlterationsNitric Oxide is released from endothelial cells
Widespread vasodilationTumor necrosis factor-a and endothelin
Vasoconstriction in microvasculatureFormation of small fibrin clots
Hypoxia to distal cells/tissuesInflammatory cascade, NO, lactic acidosis
myocardial depression
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Pulmonary AlterationsCapillaries leak into the pulmonary tissues
Interstitial edemaAreas of poor pulmonary perfusionPulmonary hypertensionIncreased respiratory workloaddecreased pulmonary compliance,impaired gas exchange hypoxemia
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Pulmonary Alterations- ARDSFluid accumulation
spills to alveoli -> infiltrates
Mechanical ventilation = mode of entry
Pneumonia (may even be a different organism)
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Metabolic AlterationsHypermetabolic stateCatecholemines cause excessive glucose
production and insulin resistanceMuscle breakdown accumulation of amino
acidsFat catabolism ketones produced
Liver function decreases lactic acid productionAs shock progresses, body cant use glucose,
protein, and fats for energy no ATP production cell death
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Assessment findingsAltered
mental statusIncreased RRAltered tempEdemaBleedingAltered CO
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Labs and DiagnosticsCBC – increased WBC and bandsBMP – hyperglycemiaABG – metabolic acidosisCT, X-rays, Cultures to find sourceLactateSvO2 – assess oxygen delivery and
consumption
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Management of Septic ShockEarly, goal directed therapyAntibiotics within 6 hours with broad spectrum
Each hour delayed: 8-9% increase in mortalityFluid resuscitation
CVP 10-12, MAP 65Maintain CO
Vasopressors: dopamine and levophed preferred
Oxygenation – add PEEPNutritional support- enteral is preferred Coagulation – Xigris recommended ????
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Multiple Organ Dysfunction Syndrome (MODS)Failure of several organ systemsBody cannot maintain homeostasis without
interventionLungs, heart, and kidneys are usually firstNo organ system is independent
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Case StudiesFive Groups - Each given a type of shockAnswer the questions accompanying the case
studyPresent a summary of the case and answers
to the questions to the class
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Case StudiesGroup 1Group 2Group 3Group 4Group 5
Study GuideGame Questions
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Click to MakeYellow Car Move
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