Anesthesia for PACU, ICU, MODS dicttaed slides 71-98

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History of the ICU:

History of the ICU First ICU at Johns Hopkins for postop neurosurgical patients in 1923 Late 1950’s-1960’s: when multidisciplinary ICU’s evolved Development due to: Advances in surgical techniques Polio epidemic resulting in respiratory failure Recognition of ARDS

ICU outcomes:

ICU outcomes Leapfrog Group Utilization of checklists to reduce errors of omission Outlining daily goals of care on rounds Strict attention to aseptic technique during CVL insertion

Sepsis cycle:

Sepsis cycle

Definitions of Sepsis and Organ Failure:

Definitions of Sepsis and Organ Failure Septic shock can occur in ICU patients From of distributive shock with activation of systemic inflammatory response High cardiac output, low SVR, hypotension, regional blood flow redistribution  tissue hypoperfusion Can also be associated with pancreatitis, burns, fulminant hepatic failure, trauma, toxic shock syndrome, anaphylaxis/anaphylactoid reactions, drug/toxin reactions (insect bites, transfusion reactions, heavy metal poisoning).

Septic Shock:

Septic Shock Influenced by physiological changes Hypovolemia Vasodilation Cardiac depression Global decrease in cardiac contractility Inability of left ventricle to dilate Metabolic acidosis


Sepsis Systemic inflammatory response syndrome (SIRS) May not have evidence of infection Response manifested by 2 or more of the following conditions Core temperature <36*C or >38*C Tachycardia >90 b/min Tachypnea > 20 b/min while breathing spontaneously White blood count >12,000 cells/mm3, <4000 cells/mm3, or >10% immature forms Sepsis: manifested by 3 or more of the above conditions with clinical or microbiological infection


Sepsis Severe sepsis: associated with organ dysfunction, hypoperfusion, or hypotension May include lactic acidosis, oliguria, altered mentation Septic shock: severe sepsis with: Hypotension despite adequate fluid resuscitation SBP <90 mmHg or reduction of >40 mmHg from baseline Presence of other perfusion abnormalities Multiple organ dysfunction syndrome (MODS) Presence of several (>2) altered organ functions in an acutely ill patient such that homeostasis cannot be maintained without intervention

Multiple organ dysfunction syndrome (MODS) :

Multiple organ dysfunction syndrome (MODS) Previously known as multiple organ failure (MOF) or multisystem organ failure (MSOF) Final stage of SIRS + infection  sepsis  severe sepsis  MODS Current investigation is looking at genetic targets and gene therapy to manage MODS Mortality ranges from 30-100%

Pathophysiology of MODS:

Pathophysiology of MODS Gut hypothesis Intestinal mucosa vulnerable to hypoperfusion/ischemia Gut implicated as the “motor” of MODS and splanchnic resuscitation is advocated as central objective in treatment Increased gut permeability, immune dysfunction, and increased translocation of bacteria Hepatic dysfunction  toxins escape into systemic circulation and acitvate immune response tissue injury and organ dysfunction Intramucosal pH and pCO2 monitoring proposed technique to assess splanchnic metabolic state

Pathophysiology of MODS:

Pathophysiology of MODS Endotoxin macrophage hypothesis Gram negative infections common in MODS Cytokines produced and released with pro-inflammatory mediators (TNF-alpha, interleukin-1,-6, thrombaxane A2, prostacyclin, platelet activating factor, and nitric oxide Tissue hypoxia microvascular hypothesis Due to micro-and macrovascular changes, tissue hypoxia which leads to organ dysfunction


Diagnosis Stage 1 Increased volume requirements, mild resp. alkalosis, oliguria, hyperglycemia, increased insulin requirements Stage 2 Tachypneic, hypocapnic, hypoxemic, mod. liver dysfunction, possible hematologic abnormalities Stage 3 Shock with azotemia, acid-base disturbances, coagulation abnormalities Stage 4 Vasopressor dependent, oliguric or anuric, ishcemic colitis, lactic acidosis

Neurosurgical/neurological ICU care:

Neurosurgical/neurological ICU care Mild hypothermia (32-34*C) for 12-24 hours after admit Neuromonitoring modalities Transcranial doppler ultrasonography (TCD) Measures mean, peak systolic and end-diastolic flow velocities and indirectly estimates CBF Can identify migraines, stenosis, emboli, vasospasm in SAH and TBI by monitoring trends in flow velocities detecting ischemic patterns

Neurosurgical/Neurological ICU care:

Neurosurgical/Neurological ICU care Brain tissue oxygenation (PbrO2) Non-invasive cerebral oximeters (INVOS) measures regional oxygen saturation (rSO2) Measures NIRS via sensors on both sides of forehead Invasive oxygen-sensitive catheters are advanced into brain tissue Monitors local cerebral oxygenation Increased ICP, decreased CPP or arterial oxygenation and hyperventilation may result in decreased PbrO2 Normal PbrO2 values: 25-30 mmHg PbrO2 < 15 mmHg: threshold to inititate treatment PbrO2 < 10 mmHg for > 15 min: associated with unfavorable neurologic outcomes


LICOX PbtO2 monitoring system

Traumatic Brain Injury (TBI):

Traumatic Brain Injury (TBI) Highest predictors of poor outcomes from TBI Age >55 years Poor pupillary reactivity Low GCS Hypotension Hypoxia Poor CT scan Level of diffuse injury I-IV Early hyperglycemia (> 200 mg/dL) Stroke Anoxic Brain Injury

Cardiovascular ICU care:

Cardiovascular ICU care Goal of monitoring is to detect not only global but regional perfusion Invasive monitoring provides information on circulatory status, organ perfusion, tissue microcirculation, and cellular metabolic status Tissues can suffer from hypoxia due to blood flow maldistribution and an inadequate balance between oxygen delivery and utilization from mitochondrial dysfunction and energy failure

Hemodynamic Monitoring:

Hemodynamic Monitoring Pulmonary artery catheter (PAC) Central venous oxygen saturation (ScvO2) Fiberoptic CVC; ScvO2 > 70% associated with reduction in mortality ~ 5 mmHg > SvO2

Medical management of shock:

Medical management of shock Correction of hypotension and restoration of regional blood flow with volume replacement and vasopressors/inotropes Adrenergic agonists (inotropic/vasconstrictor effects) Norepinephrine Dopamine Dobutamine Epinephrine Vasopressin

Medical management of shock:

Medical management of shock Activated Protein C DIC and consumption coagulopathy (increase in D dimer, decreased protein C, thrombocytopenia, increased prothrombin time) present in most septic patients Activated protein C important in modulating the above Works as an antithrombotic agent by inactivating factors Va and VIIIa and in clot lysis by inhibiting plasminogen activator inhibitor 1 In sepsis, inflammatory cytokines (tnf-alpha, interleukin-1beta) down regulate protein C activation complex Replacement of human recombinant activated protein C (Drotrecogin-alfa) at rate of 24 mcg/kg/hr High risk of bleeding

Respiratory ICU care: Acute Lung Injury (ALI) and ARDS:

Respiratory ICU care: Acute Lung Injury (ALI) and ARDS Characterized by a derangement in pulmonary gas exchange or an imbalance between the work or breathing and respiratory muscle capacity Syndromes of acute, hypoxemic respiratory failure with diffuse alveolar damage  increased lung permeability and diffuse alveolar edema

Acute Lung Injury (ALI) and ARDS:

Acute Lung Injury (ALI) and ARDS Reduced static thoracic compliance and severe gas exchange impairment intrapulmonary shunt Criteria for diagnosis: Identifiable cause with acute onset Hypoxemia Diffuse, bilateral radiographic opacities PCWP < 18 or no evidence of left atrial HTN ALI: PaO2/FiO2 ratio < 300 ARDS: PaO2/FiO2 ratio < 200

Acute Lung Injury (ALI) and ARDS:

Acute Lung Injury (ALI) and ARDS Key points of management: Separation from mechanical ventilation rather than “weaning” trials Keep tidal volumes between 5-7 ml/kg in patients with ALI/ARDS Ventilator-induce lung injury (VALI) due to overdistention and cyclic reopening of alveoli (shear injury) Prolong expiratory time limiting MV (low tidal volumes 5-7 ml/kg and low rate 8-12 b/min and keep PEEP/CPAP < 20 cm H2O Nitric oxide administration improves blood flow to ventilated alveoli Diuresis with Lasix and albumin Inhaled beta agonists Fluid resuscitation management and blood products TRALI: transfusion-related acute lung injury Maintain Hgb <7 g/dL

Acute renal failure (ARF) in the ICU:

Acute renal failure (ARF) in the ICU Reported in up to a quarter of ICU patients ARF occurs from prerenal causes and acute tubular necrosis (ATN) in most cases Medical management disappointing New evidence suggests renal replacement therapy may be most effective Daily dialysis as opposed to every other day due to hypovolemic swings Continuous renal replacement therapy (CRRT), including continuous venovenous hemofiltration and hemodialysis, may improve outcomes but evidence is not there yet

Other considerations in ICU patients:

Other considerations in ICU patients Nutritional support Crticially ill patients require 1.0-1.5 g/kg/d protein as compared to nonstressed patients at 0.5 g/kg/d Sedation Nursing driven protocols and daily interruption of sedative infusions reduce duration of intubation and ICU stay

Other considerations in ICU patients:

Other considerations in ICU patients Noscomial infections Ventilator assisted pneumonia (VAP) reduced with strict hand washing and changes in patient position Antibiotic therapy should use a de-escalating scale Venous thromboembolism Acquired neuromuscular disorders

Surviving Sepsis Campaign:

Surviving Sepsis Campaign Early goal directed therapy within 6 hours of onset of sepsis Blood cultures before antibiotics; imaging studies Fluid resuscitation with crystals or colloids Fluid challenges First line vasopressors: dopamine or norepinephrine for target MAP > 65 mmHg Low dose dopamine for renal protection NOT recommended Vasopressin at 0.03 U/min as adjunct

Surviving Sepsis Campaign:

Surviving Sepsis Campaign Dobutamine in low cardiac output states despite adequate fluid resusciation Supranormal oxygen values NOT recommended Stress dose steroids if BP not responsive to fluids and pressors Recombinant activated protein C in high risk patients Target Hgb 7-9 g/dL Appropriate use of FFP and platelets

Surviving Sepsis Campaign:

Surviving Sepsis Campaign Low tidal volumes, limited inspiratory plateau pressure, minimal PEEP for ALI Weaning and sedation protocols Avoid NMB drugs Elevation of HOB PAC NOT recommended Glucose control with BG <150 mg/dL CRRT vs. intermittent hemodialysis Bicarbonate NOT recommended Prophylaxis of DVT, stress ulcer

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