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Hemodynamic, Shock, and Infection in Critical Care
©TCHP Education Consortium, October 20141
ShockShockLynelle Scullard RN MSN CCRN‐K CNRN
Critical Care Clinical Educator
Hennepin County Medical Center
Shock
• A state of inadequate perfusion relative to tissue demand
• Inadequate oxygen delivery relative to tissue demand• Systemic tissue perfusion is
a product of CO and SVR
Cardiac Output = SV x HR
Cardiac Output
• A normal CO is 4‐8 liters per minute
CO = SV X HR• *Stroke volume = amount of blood ejected by the left ventricle with each contraction
(A normal SV is 60‐100ml)
• *Heart rate = beats per minute
(A normal HR is 60‐100 bpm)
4 Types of Shock:
•1. Cardiogenic•2. Hypovolemic
•3. Distributive: ‐ Neurogenic‐Anaphylactic
‐ Sepsis
4. Obstructive
Shock is a result of inadequate:
• Oxygen supply
• Oxygen delivery (DO2)
• Oxygen utilization (VO2)
Shock
• Components needed for oxygen supply• Adequate ventilation(exchange of air between lungs and atmosphere so that O2 can be exchanged with Co2
• Adequate hemoglobin to carry oxygen to the tissue cells
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Shock
• Components necessary for oxygen delivery• Adequate pump = cardiac output
• Adequate volume = stroke volume
**DO2=Oxygen delivery (the result of cardiac output)
Shock
• Components necessary for oxygen utilization• Adequate functional vascular bed
• VO2 = represents “Oxygen utilization”
4 Factors effect SVO2 Balance
• Cardiac Output‐(oxygen delivery)
• Hemoglobin‐(oxygen delivery)
• SAO2(oxygen supply)
• VO2‐(oxygen utilization)
Stages
Initial - At this stage, shock is reversible
Compensatory - Compensatory mechanisms kick in to return cells to preshock state
Progressive – Compensatory efforts begin to fail and irreversible cellular damage occurs
Refractory - Progressive end organ dysfunction becomes irreversible and unresponsive to therapeutic interventions
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Types of Shock
• Cardiogenic – pump
• Hypovolemic – volume
• Distributive – vascular bed• Neurogenic
• Anaphylactic
▼Septic
Shock
• Heart and brain • Increase metabolic rates
• Decreased stores of energy substrate
• Require perfusion pressure >60 to perfuse organs and prevent cell death
Neuroendrocrine Response
• Baroreceptors and chemoreceptors• Norepi produces vaso and splenic constriction
• Reduce vagal response
• Vasopressin • Constriction
• Renal tubules water reabsorption
• Aldosterone• Reabsorption of Na
Sympathetic Activation
• Alpha receptors• Vasoconstriction
• Beta receptors• Dilation of circulation to brain and heart
Cellular Response
• Hypoperfusion • Decrease filtration
• Ion pump dysfunction
• Aerobic to anaerobic metabolism
• Increase metabolites increase osmolarity
• Reabsorbtion of fluid into intravascular bed
• Increase interstitial fluid
• Lactic Acidosis
• Cell death
Cardiovascular Response
• Decrease stroke volume causes increase HR• CO = SV x HR
• Venoconstriction • 2/3 of volume is in the
venous bed
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Pulmonary Response
• Increase RR and depth of breathing
In decompensation • Increase PVR reduces tidal volume, increases dead space‐decrease gas exchange
• Increase work of breathing
• Increase demand on resp muscles
• Lung injury ARDS
Renal Response
• Conserve water and Na• By relaease of ADH, aldosterone
In decompensation • Tubular obstruction by cellular debris
• Decrease blood flow
• Toxic injury
Stages of Shock
• Initial stage (preshock)• Change from aerobic to anaerobic
• Glycogen stores used early
• Slowly build up lactic acid
• No signs or symptoms
Stages of Shock
• Compensatory Stage(Warm shock, compensated shock)
• Neural• SNS
• Hormonal• ADH
• Chemical• CO2
Stages of Shock
• Progressive• Compensatory mechanisms fail
• Cell death
• Organ failure
Stages of Shock
• Refractory• Irreversible damage and death
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Multi‐system Failure
• Cellular anoxia results from:• Cellular depletion of ATP
• Energy debt
• Accumulation of anaerobic end‐product metabolism‐(waste)further impairs cells
Metabolic Acidosis
• Metabolites override vascular tone• Hydrogen ions build up
• Lactate • Cell swelling and leaking
Diagnosis
• Medical history
• Physical exam
• Laboratory evaluation• Na, K, Chloride, serum bicarb, creat & bun, coags, liver function, cardiac enzymes, ABG, lactate
• “non‐invasive” monitoring
• Pulmonary artery catheterization*
Shock‐ Compensatory Stage moving to Progressive Stage
• Assessment• BP
• HR
• Neuro
• Renal
• Skin
• Lungs
• Hemodynamic
Treatment of any Type of Shock
• Identify cause• Type of shock
• Oxygen• Hemoglobin
• Saturation
• Support Blood Pressure• Volume
• Inotropic agents
• Psychological• Patient
• Family (all shock mortality = 35‐ 60%)
Goal for Treatment
• Restore Oxygen Transport
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True Emergency!
• Cardiogenic shock is the most difficult type of shock to treat and has one of the highest mortality rates of the different shock types.
• Goal is to save the patient’s life and treat the cause
Cardiogenic Shock
• Most common cause of death in hospitalized patients with MI
• Mortality Range 70%‐80% in 70’s
50%‐60% in 90’s
48% in 2004 NRMI database
•Occurrence 5 to 7%• 40% LV
• RV, VSD, Pap muscle rupture, free wall rupture, hypovolemia
Braunwald 7th edition
Cardiogenic Shock
• Pathophysiology• Decrease stroke volume
• Decrease cardiac output
• Increase heart rate
• Vasoconstriction
• Decrease urine output
• Pulmonary congestion
Cardiogenic Shock ‐ Intrinsic
• Cause• Severe ischemia or infarction
• Cardiomyopathy
• Valvular disease or dysfunction
• Low cardiac output syndrome
• Severe brady or tachy rhythms
• Free wall rupture
Signs and Symptoms
• Low blood pressure and tachycardia
• • Skin cool, clammy and possibly dusky; slow capillary refill
• • Hemodynamic monitoring is usually instituted
• • Lung sounds with crackles; patient short of breath or dyspneic
• • Restlessness, anxiety, and possibly lethargy and confusion
Cardiogenic Shock Diagnosis
• History –past cardiac disease?• Shock assessment
• EKG
• ECHO
• Enzymes‐Troponin,
CK‐MB
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EKG•T wave inversion
• Ischemia
•ST segment elevation• Injury
•Q wave• infarction
*Acute coronary syndrome
Treating Cardiogenic Shock
• • Requires an aggressive strategy
• • Specific goals:
• * Identify and correct underlying cause
• * Improve tissue perfusion. Especially important in the case of MI.
Cardiogenic Shock Treatment
(Thrombolytic Agents)• Aspirin, Heparin,
• GP 11b/111a inhibitors
(Hemodynamic monitoring)• Assess volume
• Assess response to treatment
(Angioplasty/Surgery)
(Inotropes, Vasodialators, Ventricular assist devices)
(Sedatives, Analgesics, rest, oxygen)
Hypovolemic Shock
• Cause• Hemorrhagic
• Non hemorrhagic• Diarrhea/vomiting‐increase fluid output
• Heat stroke‐lack of H2O
• Burn/ascites‐fluid shift
• “Third spacing”
Hypovolemic Shock
• Pathophysiology• Decrease circulating volume
• Cellular hypoxia
• Cellular death and acidosis
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Pathophysiologic Process
• • Decreased circulating volume leads to decreased preload and stroke volume, decreased cardiac output, and finally hypotension and inadequate tissue perfusion
• Begins when 15% or appx. 750 ml of intravascular volume has been lost
Classification of Hypovolemia
• 1. Mild <20% Mild tachycardia
________________________No BP changes
• 2. Moderate 20% ‐ 40% Same plus:
Increase HR >120 Orthostatic changes
Oliguria
_______________________ Tachypnea
• 3. Severe >40% Same plus:
Hemodynamic instability
Multi‐system failure
Treatment
• Best to prevent its occurrence by monitoring for signs of fluid loss and correcting before shock occurs
• Treatment includes finding the cause and correcting it by replacing specific fluid lost. (**Place 2 large bore) IV catheters.
• Specifics of treatment:
* Fluid and blood
* Colloid fluids
* Transfusion
Hypovolemic Shock
• Assessment• BP‐ low
• HR‐ increase
• Neuro‐ irritable, coma
• Renal‐ decrease output
• Skin‐ pale cool clammy
• Lungs clear
• Hemodynamic assessment• CVP, RA, PW‐ low
• CO, CI‐ low
• SVR‐ increase
Hypovolemic Shock
•Treatment replace what’s lost!•Volume
• Blood• Fluids
Intravenous Fluid Replacement
•Crystalloids•Saline, ringers
• Distribute freely • 2 – 6 times morerequired than estimated fluid loss
•Colloid•Albumin, Hespan
• More expensive
•Not proven more effective
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Electrolyte Imbalances
• Hyponatremia• Overcorrection can lead to paralysis and coma
• Prolonged can lead to Neuro injury
• 115 mEq/l and symptomatic = nonaggressive therapy
• If symptoms or severe (< 115) 1 – 2 mEq/hr to 120 to 125
• Lasix if fluids adequate
Electrolyte Imbalance
• Hypernatremia• Overcorrection can lead to cerebral edema
• Free water to correct gradually
• Change no faster than 1 – 2 mEq/hr to max 15 – 20 mEq in 24hr
Hypovolemic Shock ‐ Trauma
• If trauma associated with hypovolemia • Tissue injury and inflammatory response
• Increase fluid going to inflammation
• Mal‐distribution of blood flow
Treatment Hypovolemia ‐ Trauma
• ABC’s
• Stasis
• Early stabilization of FX*
• Debridement of devitalized and contaminated tissue*
• Evacuation of Hematoma*
* Decrease inflammatory response
Goal for Treatment
• Restore Oxygen Transport
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Case Study #2
• 20 year old male gun shot wound with uncontrolled bleeding .
What are you going to do?
BP = 60/30HR = 120RR = 26 clear lungsNeuro = unconsciousSkin = cold
Now what?
Case Study #2 Uncontrolled Hemorrhage Houston Study 598 Adults Penetrating Injuries Bp<90
• Immediate fluid flushes
• 62% survived
• 30% complication• ARDS, ARF, pneumonia
• Wound infection
• Delayed fluid
• 70% survived
• 23% complication
• Hospitalization shorter
International resuscitation research center
Case Study # 2
• Timing of fluid resuscitation• Early 2L bolus delays hemostasis
• 2L Bolus at hemostasis trigger rebleeding• Vulnerable clot 0‐34min
Mapstone, J of Trama 03
Hirshberg J of Trama 06
Lunch time!
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ReferencesBarber, A.E. Cell damage after shock. New Horizons. 1996; 4:161.
Rodgers, K.G. Cardiovascular shock. Emergency Medicine Clinics North America. 1995; 13:793.
Shoemaker, W.C. temporal physiologic patterns of shock and circulatory dysfunction based on early descriptions by invasive and noninvasive monitoring. New Horizons. 1996; 4:300
Tuchschmidt, J.A., Mecher, C.E. Predictors of outcome from critical illness. Critical Care Clinics. 1994; 10‐179
Kinch, J.W., Ryan, T.J. Right ventricular infarction. New England Journal of Medicine. 1194. 330:1211.
ReferencesHochman, J.S. Cardiogenic shock complicating acute myocardial infarction: expanding the
paradigm. Circulation 2003; 107:2998.
Mimoz, O. etal. Pulmonary artery catheterization in critically ill patients. Critical Care Medicine 1994; 22:573
Conners, A.F.Jr, Speroff, T. et al. The effectivness of right heart catheterization I the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996; 276:889.
Harvey, S., Harrison, D.A. et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC‐Man): a randomized controlled trial.
Lancet 2005; 366:472
ReferencesMoscucci, M. Bates, E.R. Cardiogenic shock. Cardiology Clinics. 1995; 13:391.
Hichman, J.S., et al. Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Circulation 1995; 91:873.
Mapstone, J., et al. Fluid resuscitation strategies: A systematic review of animal trials. The Journal of Trauma. 55(3) 571‐589, September, 2003.
Hirshberg, A., et al. Timing of fluid resuscitation shapers the hemodynamic response to uncontrolled hemorrhage: Analysis using dynamic modeling. The Journal of
Trauma. 60(6): 1221‐1227, June, 2006.
References:
• TCHP Education Consortium –Hemodynamic Monitoring Primer
• Hypovolemia retrieved from en.wikipedia.org/wiki/Hypovolemia
• Take a rapid treatment approach to cardiogenic shock retrieved from www.nursingcenter.com/library/JournalArticle.asp?Article_ID=800728
References:
• Cardiogenic Shock retrieved from emedicine.medscape.com/article/152191‐overview
• Critical Care Medicine Tutorials‐The patient is hypotensive: is this due to hypovolemia retrieved from www.ccmtutorials.com/cvs/clinshock/clinshock3.htm
• Critical Care Medicine Tutorials‐The patient is hypotensive is this pump failure retrieved from www.ccmtutorials.com/cvs/clinshock/clinshock4.htm
• Critical Care Medicine Tutorials‐The patient is hypotensive is there Abnormal Vasodialation retieved from www.ccmtutorials.com/cvs/clinshock/clinshock5.htm
• Critical Care Medicine Tutorials‐Invasive Cardiovascular Monitors When I use them retrieved from www.ccmtutorials.com/cvs/clinshock/clinshock7.htm
• Shock, Cardiogenic retrieved from emedicine.medscape.com/article/759992‐print
• Shock retrieved from www.merckmanuals.com/professional/sec06/ch067/ch067b.htlm
References:
• Critical Care Medicine‐ Venous Oximetry‐ The concept of SvO2 and ScvO2 retrieved from icucare.blogspot.com/2009/08/venous‐oximetry‐concept‐of‐svo2‐and.htlm
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Infection in Critical Care
Space
Patient placement
Bedside procedures
Ventilation
Environmental contamination
Hand WashingCompliance
Frequency
Skin irritation
Jewelry
Nails
Handwashing• Compliance:
• RN….52%
• MD….23%
• Michigan study bacteria on hands:• Nails…before 73%
• After ….68%
• No nails 32% .. 26%
Another study
• RN’s washed %
• Before care 62
• After care 87
• Move dirty to clean 60
• After remove gloves 80
• Before invasive procedures 57
• After direct contact fluids 87
• Before touching own eyes etc 3
Patient Susceptibilty• Age
• Why they are in the hospital
• Co-morbid conditions
• Contacts with carriers
• Nutrition
• Stress
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Fever•Benefit
•>100.4 (38C) kills bugs, helps neutrolphils and antibodies, potentiates antibiotic activity
• SCCM:
• 100.4 ‐ 38C fever
• 101.5 ‐ 38.6C treat
• 102‐ 38.9C most likely infection
FeverConsequences
dehydrationincreased metabolismincreased cardiac outputincreased MVO2Each 1* raises metab rate 13%
febrile seizuresconfusion
deliriumpatient discomfort
Fever• Management of non‐beneficial fever:
• Thermoregulation is impaired at 104*/40 C
• Evaporative cooling best
• Meds
• antibiotics
Cultures•Why?
• To accurately
identify bacteria
• Where?
• Blood
• Urine
• Sputum
• Lines
• CSF
Blood• Bacteria showers 1 hr after temp spike
• Draw blood before antibiotics
• Peripheral sticks, usually 2 sets
• Redraw 24 hrs later
• Prep site, allow to dry
• Don’t change needle
• 8‐10cc’s per bottle
• Contamination risk
Sputum• Color, amt, odor?
• QBAL (qualitative bronchial alveolar lavage) vs suction
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Urinary Tract Infections:• Treatment
• Remove catheter
• Culture
• Antibiotics
• Sterile technique
S/S
•Fever
•Urgency
•Frequency
•Dysuria
•Supra-pubic tenderness
•Positive urine culture 40% infections
Sepsis in immunosuppressed
CAUTI prevention
• Need for Foley
• Alternatives
CMS Hospital Compare: CAUTIFor time period October 1, 2017‐ September 30, 2018
September 2019 Infection Prevention Update
Urinary Catheter DeviceStandardized Utilization Ratio (SUR)
September 2019 Infection Prevention Update
What is the Standardized Utilization Ratio (SUR)?• A summary measure used to
track device use at a national, state, or local, or facility level over time.
• Adjusts for various facility and location-level factors that contribute to device use; allows users to summarize data by more than a single variable
• Factors included in the SUR analysis are:
• unit type, • facility bed size, • medical school
affiliation
• A SUR > 1.0 means more device days were observed than predicted,
• A SUR < 1.0 means fewer device days were observed than predicted
Pneumonia: S/S
Sputum
Positive culture
Fever
Tachypnea
Auscultation
quiet over area, coarse
around
Pneumonia: Risks
Host factors
Bacterial colonization
Aspiration
Contaminated equipment
Aerosolization
Inadequate pulmonary clearance
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Ventilator Associated Pneumonia (VAP)
Issued 01/2008
Author: Marianne Chulay, RN, DNSc, FAAN
Consultant, Clinical Research and Critical Care Nursing
Reviewers: Suzi Burns, Mary Jo Grap,
Judy Verger, and Lori Jackson
Nosocomial Pneumonias
• Account for 15% of all hospital associated infections
• Account for 27% of all MICU acquired infections
• Primary risk factor is mechanical ventilation (risk 6 to 21 times the rate for nonventilated patients)
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2004
Craven, Chest 2000; 117:186S-187S.
Primary Route of Bacterial Entry into Lower Respiratory Tract
• Micro or macro aspiration of oropharyngeal pathogens
• Leakage of secretions containing bacteria around the ET cuff
Significance of Nosocomial Pneumonias
• Mortality ranges from 20 to 41%, depending on infecting organism, antecedent antimicrobial therapy, and underlying disease(s)
• Leading cause of mortality from nosocomial infections in hospitals
Significance of Nosocomial Pneumonias
• Increases ventilatory support requirements and ICU stay by 4.3 days
• Increases hospital LOS by 4 to 9 days
• Increases cost ‐ > $11,000 per episode
• Estimates of VAP cost / year for nation > $ 1.2 billion
VAP Prevention
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Continuous Removal of Subglottic Secretions
Use an ET tube with continuous suction through a dorsal lumen above the cuff to prevent drainage accumulation.
HOB Elevation
HOB at 30‐45º
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2004 ATS / IDSA Guidelines for VAP 2005
HOB Elevation Leads to Significant Deduction in VAP
0
5
10
15
20
25
% V
AP
Supine HOB Elevation
Dravulovic et al. Lancet
1999;354:1851‐1858
Is HOB Elevation Done?
Despite effectiveness
of HOB elevation,
compliance is poor.
• Grap et al. Am J Crit Care1999;8:475‐480
• Grap et al. Am J Crit Care2005;14:325‐332
0
20
40
60
% w
ith
HO
B E
leva
tio
n
0 to 20
21 to 30
31 to 40
> 40
Degrees of
HOB Elevation
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2004
Frequency of Equipment Changes
Ventilator
Tubing
Ambu
Bags
Inner Cannulas of Trachs
No Routine Changes
BetweenPatients
Not Enough
Data
VAP Prevention
Wash hands or use an alcohol‐based waterless antiseptic agent before and after suctioning, touching ventilator equipment, and/or coming into contact with respiratory secretions.
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2004
AACN Practice Alert for VAP, 2007
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VAP Protection
• Use a continuous subglottic suction ET tube for intubations expected to be > 24 hours
• Keep the HOB elevated to at least 30 degrees unless medically contraindicated
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2004
AACN Practice Alert for VAP, 2007
No Data to Support These Strategies
• Use of small bore versus large bore gastric tubes
• Continuous versus bolus feeding
• Gastric versus small intestine tubes
• Closed versus open suctioning methods
• Kinetic beds
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2004
Oral Care
• Role of oral care, colonization of the oropharynx, and VAP unclear – dental plaque may be involved as a reservoir
• Limited research on impact of rigorous oral care to alter VAP rates
• Surveys indicate most nurses use foam swabs rather than toothbrushes in intubated patients
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2004
Grap M. Amer J of Critical Care 2003;12:113-119.
VAPRisk Factors
ETT > 6 days
Re-intubated within 72 hours
Neurosurg, trauma, or burn patient
Decreased LOC + secretions
H2 blockers
NG tube present
WASH HANDS!
Pneumonia: Management
Position side to side
Separate suction canisters
Clean in-line suction catheter
Suction above cuff
Oral care q2-4h
Catheter Related Infections
Increased risk with:
Cultures
tip of line and blood culture
emergency visitmore lumenscentral linelong timeTPN/lipids
inexperienced operator
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CMS Hospital Compare : CLABSIFor time period October 1, 2017‐ September 30, 2018
September 2019 Infection Prevention Update
https://www.medicare.gov/hospitalcompare/compare.html#vwgrph=1&cmprTab=3&cmprID=240004%2C240080%2C240001&cmprDist=0.5%2C1.4%2C5.2&dist=25&loc=55415&lat=44.9758391&lng=-93.2571034
Central Line Device Standardized Utilization Ratio (SUR)
September 2019 Infection Prevention Update
What is the Standardized Utilization Ratio (SUR)?• A summary measure used to
track device use at a national, state, or local, or facility level over time.
• Adjusts for various facility and location-level factors that contribute to device use; allows users to summarize data by more than a single variable
• Factors included in the SUR analysis are:
• unit type, • facility bed size, • medical school
affiliation
• A SUR > 1.0 means more device days were observed than predicted,
• A SUR < 1.0 means fewer device days were observed than predicted
ICU type UTI CLABSI VAP
Interdisp. 3.1 1.5 2.3
Interdisp, major teaching hosp
3.3 2.0 3.3
Surgery 4.1 2.3 5.3
CV surgery 3.2 1.4 4.7
Neurosurgery 6.8 2.5 6.5
Medical 4.1 2.4 2.5
CCU 4.4 2.1 2.5
Burn 7.7 5.6 10.7
Trauma 5.7 4.0 9.3
Peds 2.0 2.9 2.1
CMS’s “Never Events”• Blood incompatibility
• Air embolism
• Surgical site infection CABG
• UTI
• Vascular catheter associated infection
• Fall and trauma
• Pressure ulcer III and IV
Infectious Diarrhea
Signs and Symptoms
Causes• Antibiotics
• tubefeeding
•Fever•Watery diarrhea
•Cramping
Management•DC antibiotics
•Metronidazole, then oral Vanco
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C diff• Isolation
• Contaminates every surface• 78% still contaminated after cleaning
• Wash with soap and water• Alcohol doesn’t kill
• Bleach works
• 20% uniforms
Hospital Onset CDI
September 2019 Infection Prevention Update
TARGET: 36
Common Infections: Sinusitis
Signs and SymptomsFever
Drainage-not oftenPain/Pressure
Smell
Causes and RisksTubes in the nose
AntibioticsOpen head injury
Necrotizing Fasciitis#1 organism =
Group A streptococcus (GAS)
Many other organisms can cause it too!
Gas gangrene: clostridial myonecrosis
4% of bacteria are in us all the time, 1% cause problems
Necrotizing FasciitisNon-specific erythema
Edema
Extreme pain
Pallor/gray discoloration
Anesthesia
Purpura
Hemorrhagic bullae
Gas bubbles on X-ray
Hemorrhagic blistering
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Pustule Blistering
Necrotizing FasciitisSurgical debridement
Antibiotics
Supportive care
Case study• 79 yo male fell 3 days ago, abrasion to (L) arm
• PMHx: metastatic squamous cell CA of the lips with neck dissection 2 months ago
• Arm is now “ecchymotic up and down its entire extent, and the hand is now cool and mottled”
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Case study
• Hypotensive
• OR:• Fascial and muscle debridement
• Amputation mid upper arm
• Culture of tissue:• “many gram negative cocci”
• “many Group A beta hemolytic Streptococcus isolated”
Case study
• No further debridement of wound needed in the OR
• 2 days later a R antecubital A‐line infiltrated. Area white and cold
• 6 hrs later area red with streaks, hand dark and cold
• Debridement with multiple further dressing changes and trimming.
• Cultured same Group A Strep
Meningitis MeningitisViral
Rarely fatalTreatment is symptomaticSymptoms last 7-10 days
Resp secretions
Bacterial
May be fatalTreatment is supportive
Antibiotics a must!Break in dura, URI, strep
Symptoms of MeningitisFever
Severe headache
Nuchal rigidity
Photophobia
Confusion/sleepiness
Diagnose: LP, WBC, glucose
Isolation
Brain AbscessCauses
Signs and Symptoms
HeadacheFever
Focal neuro changesIn 50% - seizures, nuchal rigidity, n/v, papilledema
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Cardiac Valve Infection
CausesGas/rheumatic fever
Drug abuse
Signs and Symptoms
GeneralRegurgitant murmurs
S/S embolizationFever with shaking chills
Cardiac Valve Infection
Diagnosis and Treatment
EchocardiogramBlood cultures
AntibioticsSurgical debridement/excision/replacement
Surgical Wound with Dehiscence
Causes
•Dehiscence
•EviscerationSigns and Symptoms
Pain “boggy”Fever stretching of suture line
Increased WBC
Treatment
If minor, call MD immediatelyIf major, call for help immediately
Sterile NS soaked 4X4’sComfort
Surgical debridement w/wo secondary closureAntibiotics
Surgical Wound with Dehiscence
Candida • Common in mouth (thrush)
• Moist areas, low oxygen
• Systemic difficult to treat
• Multiple antibiotics increase risk
• Treat:
• Nystatin s/s
• Suppositories
• Powder/cream
• Fluconazole or amphotericin B
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MRSA• Penicillin is now completely useless against staph aureus
• Oxacillin on lab results
• Vancomycin treatment of choice
• Nosocomial strains resistant up to 50% time
September 2019 Infection Prevention Update
TARGET: 9
Hospital Onset MRSA Infection (all sites) CMS Hospital Compare: MDRO
For time period October 1, 2017‐ September 30, 2018
MRSA Bacteremia CDI
September 2019 Infection Prevention Update
https://www.medicare.gov/hospitalcompare/compare.html#vwgrph=1&cmprTab=3&cmprID=240004%2C240080%2C240001&cmprDist=0.5%2C1.4%2C5.2&dist=25&loc=55415&lat=44.9758391&lng=-93.2571034
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VRE• Generally effects only debilitated or immunocompromised pts
• Large cause vanco use for MRSA
• Synercid
• Linezolid
Next up:• Pseudomonas
• Klebsiella
• Amphotericin B
Other Bug Fighters
AntifungalFever, chills, rigors, and n/v
May do test dose firstPremedicate
Monitor VS q 15” X 1 hr, then q2hMay give fluid flush before and/or
after
Infection case study• 38yo female from Ontario
• Hx HA for 4 days, felt “crappy”
• ER 6/10 w/ HA, weak/numb LE’s
• Admitted 8pm
• CSF cx, yellow glucose 77, hi protiens
• r/o cord compression, r/o GB, ?viral
• Head CT negative
Case study• 0800 BP 220/110, 120, 20’s, sats 80’s
• SICU ? Guillian‐Barre
• Numb and paralized to above nipple line
• Drowsy, but oriented
• Runs V‐tach, change in voice quality
• Intubated and sedated
• BP 41/28 140
Case study• Back to CT no change
• Norepi, phenyl, dopamine….swan
• Hemodynamics normal
• Flash pulm edema…… no cough
• No brainstem reflexes , fixed pupils
• Ventric ICP 15
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Case study• Work up:
• Infection… culture everything
• Exposed to chicken pox 2 wks ago
• Canada
• HIV
• Infectious disease consult• West nile vs rabies
Case study• Results
• No growth to date
• No herpes simplex seen in CSF
• Viral encephalomyelitis of unknown origin
• + HIV
Case study
• No change in status, drips, neuro
• 6/11 2000 CT• Significant brain stem swelling, hydrocephalaus
MRI
‐inflamm consistent w/ encephalitis
Case study• Repeat CT
• Intraparenchymal hemorrhage in pons and 4th
ventricle
• Removed from support
Sepsis and
Septic Shock
SIRS
•Systemic Inflammatory Response Syndrome
• signs and symptoms of infection without identifiable source
2 or more:
T>100.4/38C or <96.8/36C
HR>90
RR>20
WBC>12,000 or <4000
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Sepsis• HR > 90
• Temp > 38º C (100.4º F) or < 36º C (96.8º F)
• RR > 20 or PaCO2 < 32 mm Hg
• WBC > 12K < 4K, or > 10% bands
• Infection causes inflammatory response
Severe Sepsis
sepsis + signs of organ system failure,
hypoperfusion, or hypotension
Severe Sepsis
• Definition
• Sepsis+• Organ dysfunction
• Hypoperfusion
• Hypotension or
or
Arterial hypoxemiaacute oliguria
creatinine increasecoagulation abnormalities
thrombocytopeniahyperlactemia
arterial hypotension
Sepsis mimics
• Pancreatitis
• Trauma
• Burns
• Cardiac surgery
• ARDS
• Diabetic ketoacidosis
• Neuroleptic malignant syndrome
• Drug reaction
• Aspiration pneumonitis
11/5/2019
Septic Shock
sepsis + hypotension + perfusion defects
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Sepsis is now defined as
• “a life‐threatening organ dysfunction caused by dysregulated host response to infection”
• “life threatening condition that arises when the bodies response to an infection injures its own tissues and organs”
• Response is excessive, creating an increased risk of morbidity and mortality
Early is key
• Infection no longer defined
• SIRS and severe sepsis removed from definitions
• Septic shock:• A subset of sepsis
• Circulatory, cellular, metabolic alterations assoc. with higher mortality than sepsis alone
CMS, research, and you
• CMS still supports SIRS and old definitions
• Research still uses severe sepsis definitions
• YOU need to know when you patient is getting sicker and how to manage them
qSOFA
• Bedside screening tool
• One point for each:
• Altered mentation
• SBP 100 mmHg or less
• RR 22 or greater
• Two or more points is a positive screen
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11/5/2019
Sepsis
• SOFA >2 PLUS
• Suspected or documented infection
• Decrease in P/F ratio
• Decrease in GCS
• Hypotension
• Decrease in platelets
• Increase in bilirubin
• Increase in creatinine levels and oliguria
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Septic shock (In addition to sepsis)
• Vasopressors needed to keep MAP>65, and
• Lactate > 2.0 mmol/L,
• Despite adequate fluid resuscitation.
11/5/2019
Who’s At Risk?• being in a health care setting
• having natural defenses broached
• immunocompromise: age, HIV, diabetes
• co‐morbid conditions
• surgery, trauma, or necrosis of abdomen
Risks
• Artificial devices
• Inappropriate antibiotics
• Poor nutrition
• *** greatest risk may be the pathogens that medical and nursing professionals carry on unwashed hands!***
Causative Organisms
Gram negative organisms
Klebsiella, E.coli, enterobacter
Opportunistic organisms
yeast, aspergillus
C diff
Gram positive organisms
GAS, strep
After Exposure...
Release of Cytokines
Vasodilation
Inadequate tissue
perfusion Third-spacing
Hyperdynamic state
Hypodynamic state
Capillary
permeability
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Cytokine Released by Effect
TNF‐α Dendritic cellsMacrophageNeutrophilT‐cell
Attracts other inflammatory cellsFever, catabolismEdema, vasodilation
IL‐1 Dendritic cellsMacrophageT‐cell
Similar to and synergistic with TNF‐α
NO Many Vasodilation
TGF‐β T‐cell Suppresses lymphocytes
IL‐10 B‐cellT‐cell
Suppresses pro‐inflammatory cytokinesEnhance B‐cell function
11/5/2019
Hyperdynamic Stage
Early ‐ Fix them now!
Tachycardia
Hypotension
High cardiac output
Low SVRBUT
Symptoms More Symptoms
Labs–Lactate/pH
–WBC’s
–Platlets/albumin
–ABG/SVO2
Endocrine– Insulin resistant
Lactate/Lactic acid
• Causes of lactic acidosis:
• Type A: impaired tissue perfusion
• Type B1: disease states (sepsis)
• Type B2: drug‐related
• Type B3: inborn error of metabolism
• Lactate rises in sepsis for many reasons
• Higher lactate levels predict mortality
11/5/2019
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Care of the Septic Patient: Source Control
Find source of infectionCan’t ID bug up to 70 % of the time
Treat source•Surgical
•Medical
•Antibiotics
Prevent new infections
Hemodynamic Support
Fluid resuscitationCrystalloids
Colloids (not trauma)
6-10 L, retain 25%
Vasopressor/Inotropic SupportDopamine
Dobutamine
Norepinephrine
Phenylephrine
Supportive Care
Pulmonary ManagementDecrease O2 demands
ARDS/PEEP
Prone positioning
Nutrition
Family Support
Hypodynamic Stage
Late!Tachycardia
Hypotension
Low cardiac output
High SVRAND
Symptoms Cardiovascular– Tachy, low BP… low HR
– Low CO, hi SVR/PAWP
– Cool, clammy, mottled
– hypothermic
Pulmonary– Crackles, ARDS
– Acidotic
– PEEP, PCV
More Symptoms
•Neurological• Coma
• Gastrointestinal•No BS
•Lg NG output
•Transmigration of bacteria
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More Symptoms
Renal–Anuric
–Hi BUN/Cr
Hepatic–LFT’s up
–DIC ?
–bleeding
More Symptoms
•Endocrine•Insulin resistance…hi
glucose…low….
•MDF lowers HRLaboratory results
ABG…acid/lactate
Coags up
Platlets low, fibrinogen low
Electrolytes off
P/F ratio
• PaO2/FiO2
• Normal is greater than 380• 80/.21
• 90/.30=300 (ALI)
• 80/.40=200 (ARDS)
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Atelectasis in ARDSDisseminated Intravascular Coagulation
Coagulation &
Inflammation
Fibrinolysis
Inappropriate
clotting
Microemboli Loss of
clotting factors
Widespread cell
death
Bleeding
DIC
• Clotting:• Platlets/ fibrinogen sent to stop bleeding and clot
•Hemorrhage:
• Plasminogen activated…lyses clot
• Develop FSP, FDP, D‐dimer (potent anticoagulants)
• Consumption of platlets/fibrinogen
DIC case study
• 39 yo F, placenta previa, placenta accretia
• 34 wks bleeding… C‐section
• Amniotic fluid embolus
• Coded immediately after delivery and went into fulminate DIC
DIC case study
• LABS
• Hgb ..9.6 (1245) pre op• 6.3 (1846) code troponin
• 3.7 (1950) in SICU 1.2
• 11.4 (2123) SICU
• 4.9 (2225) 5.5
• 0030 9.5
DIC case study
• PT INR PTT fibrin D‐dimer plts
• 13.6 1.3 47.3 94 >1000 140
• 20.6 2.0 129.3 66 >1000 90
• 16.1 1.6 68.3 83 63
• Other labs:glucose >200• Calcium low
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DIC blood products
• PRBC’s: 50 units
• Platlets: 7 6pks
• FFP: 28 units
• Cryo (jumbo): 8
DIC case study
• Summary:• Clotted an 8” section of inf vena cava
• MODS
• Planned transfer to U of M for clot removal, dislodged clot with neuro, renal, and cardiac affected.
• Has since recovered enough to be alert, reorientable, and getting ready for rehab
DIC Relationship of DIC & sepsis
Hemodynamic Support for sepsis/septic shock
Fluid balanceFluids
Diuretics
Dialysis/CVCC
Vasoactive DrugsInotropes
Vasodilators
Vasopressors
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Other measures
• Pulmonary management
• Management of DIC
• Family support
Other Measures
Nitric Oxide
• Vasodilates by inhibiting angiotensin II and sympathetic vasoconstriction
• Inhibits platelet/WBC adhesion
NO Inhibition -N-monomethyl-L-arginine = L-NMMA
Vasopressin
• 0.04 u/min
• Restores responsiveness to vasopressors
• NO mediates inhibition
Insulin
• < 150 recommended by SCCM
• High blood sugar creates sticky leukocytes
Adrenal replacement therapy
• Modulates inflammatory cytokines
Procalcitonin
• Prohormone of calcitonin, released by lung and intestine in response to endotoxin
• More accurate at identifying bacterial sepsis than other available markers
• Can be elevated in major trauma, burns, major abdominal or cardiac surgery, MODS, ESRD
• Can be used to shorten antibiotic courses
11/5/2019
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Other measures
• Nutritional assistance
• Glutamine…. T‐cell improve, bactericidal, essential amino acid
• Selenium …. Less renal problems
• Vit C … radical scavenger
• Vit E ….ATP, less peroxidation
Initial management
• A one‐hour bundle is promoted by SSG:
• Measure lactate level
• Obtain blood cultures before administering antibiotics
• Administer broad‐spectrum antibiotics
• Begin rapid administration of 30mL/kg crystalloid for hypotension or lactate level ≥ 4 mmol/L
• Apply vasopressors if hypotensive during or after fluid resuscitation to maintain MAP ≥ 65 mm Hg
11/5/2019
3 hour bundle
• Measure lactate
• Obtain blood cultures before antibiotics• Delay considered > 45”
• 2 sets
• Administer broad‐spectrum antibiotics• ASAP
6 hour bundle
• In addition to 3 hour
• Vasopressors MAP >65 (after fluids)
• If lactate >4 or hypotension persists reassess volume and perfusion
• Reassess lactate if initially elevated
Unproven/controversial therapies
• Methylene blue
• Vitamin C, hydrocortisone, thiamine
• Sodium bicarbonate
• Steroids
• Also dozens of drugs targeting the inflammatory pathway
• ECMO
11/5/2019
Sepsis case study
• 44 yo MVA unrestrained , ejected
• PMHx: cocaine. ETOH, smoker
• Splenic fracture
• Multiple rib fx with flail chest/hemopneumo
• Intubated
• Labs unremarkable
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Case study
• Day 3
• Attempts at weaning fail
• VS stable except T103
• Labs stable pO2 73
• QBAL culture gram + cocci
• Plan: early tracheostomy, re‐culture
Case study
• Day 4
• Lungs deteriorating
• FiO2 up to 90%
• 99/43 120 14 102T
• +2 pitting edema
• QBAL >100,000 group A strep
• Treat for ARDS
Case study
• Day 5
• Continue with poor ventilatory state, flolan
• Intubated, sedated, paralyzed
• 100/60 110 14 103.2 T
• Swan … SVO2 75% (89%) CO 14 SVR 463
• CT negative for PE
• Cultures GAS, staph
• Troponins rising, afib
Case study
• Day 6
• Echo
• PEEP 15
• PCV
• Troponins continue to rise
• Check cortisol levels
• proned
Case study
• Day 7
• FiO2 70% AC 550 R23 PEEP 12
• Sats low 90’s, SVO2 60’s
• T 102.7
• diuretics
Case study
• Slowly improved to SIMV with periodic trach dome trials
• Transferred to a rehab vent facility after 21 days
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Toxic Shock Syndrome What bugs?
• Mild prodromal symptoms
• Precipitous acute illness: high fever, n/v, abdominal pain, severe muscle pain,
headache
• profuse diarrhea, macular erythroderma
Signs/Symptoms
Toxic Shock Syndrome
• Early diagnosis
• Early antibiotics - broad spectrum
• Supportive care
Treatment
Toxic shock case study
• 28 yo F
• 2 previous cases of toxic shock (14, 18)
• c/o fever, myalgia, ® groin pain
• Day 3, neuro change… intub…CT neg w/ free fluid in abd… ex lap… compartment syndrome
• Day 6, abd open, hypotensive on dopamine and levophed, low SVR and hi CO…sepsis
TS case study
• Dx: “distributive shock with multi‐organ dysfunction, possibly toxic shock”
• Summary
• Day 9• Fixed, dilated pupils cerebral edema
• No source of infection ID’d
Multiple Organ Dysfunction Syndrome
• Cardiovascular
• Pulmonary
• Renal
• CNS
• Hepatic
• Splanchic
MSOF
• Causes • Primary
• Aspiration leading to ARDS
• PE
• Trauma to ABD
• Secondary• Hypoperfusion
• Microemboli
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APACHE II criteria
• Cardiovascular failure • HR </= 54/min
• MAP </= 49mmHg
• V‐tach, V‐fib or both
• Serum pH </= 7.24 with
• PaCO2 </= 40mmHg
APACHE II criteria
• Respiratory failure • RR <5/min or > 49/min
• PaCO2 > 50 mmHg
• P(A‐a)O2 .350mmHg
• Vent/CPAP dependent day 4
APACHE II criteria
• Renal failure • UO <479mL/24h or <159mL/8h
• Serum BUN > 100mg/dL
• Serum Creatinine >3.5 mg/dL
APACHE II criteria
• Hepatic failure • Serum Bilirubin >6 mg/dL
• PT >4 seconds over control (without systemic anticoagulation)
APACHE II criteria
• Hematologic Failure • WBC <1000/uL
• Platelets < 20,000/uL
• Hematocrit < 20%
APACHE II criteria
• CNS failure • GCS</= 6 (without sedation)
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Multiple OrganDysfunction Syndrome
Fluid resuscitation
PRBC administration
Supportive care for each organ system
Patient coded at end of previous shift. Previous blood sugar during code 39 and patient given 1 amp D50, recheck at 0000 120. Per Dr Ericson L pupil not reactive to light following code, bilat Pupils noted to be 3mm and sluggish overnight. ICPs overnight 12‐14 and CSF drainage 6‐35, 35 being post code. ABD open and packed to wall suction with large amount of drainage at beginning of shift. 750ml of serosang drainage overnight. 150ml of dark green thick drainage from NG. UO approx 100ml q 2 hours. Bladder pressure at 0330 19, Dr Ericson notified. CVPs 20s, last CVP 0430 24. Post code patients temp 35.8 and bair hugger applied. Bair hugger later removed when patient 37.2, end of shift temp 38.9, Dr Ericson notified. Post code, patient with clear, thin and frothy secretions and HOB in trendelenberg. Patient suctioned frequently. Multiple labs drawn, ABGs q 1 hour d/t having to bag patient and unable to get reliable O2 sat and high vent settings. Patient started on versed and vec. BIS reading 20‐40s, train of 4 ‐1/4 at 0600. Continue to monitor per POC and notify MDs with any change in status.
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Neurogenic & AnaphylacticShock
Sam Johnson was involved in a car accident in which he was driving and hit from behind. When EMS arrived, he was confused but able to indicate that he could not move his arms or feet. VS were stable and
he was immobilized and transferred to the ED. Spine films revealed a C6-C7 fracture of the spinal cord. Physical assessment revealed loss of movement and sensation from 1 inch above his nipple line and down. Sam was started on a methylprednisolone infusion and transferred to
the SICU.
Once in the SICU, Sam’s VS were unstable. His HR dropped to 50 and his BP dropped to 84/44. Neurogenic shock was anticipated.
What is Neurogenic Shock?
Loss of autonomic nervous system
regulation below level of injury causes
massive vasodilation and bradycardia
Causes of Neurogenic Shock
• Spinal Cord Injury• T6 or higher
Anesthesia
Drug overdose
Pain All interrupt SNS and
vasomotor center
Signs of Neurogenic Shock
mentation changes
nausea/vomiting
warm and dry skin below LOI
bradycardia
paralysis
apnea/tachypnea
profound hypotension
May have...
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Interventions for Neurogenic Shock
• ABC’s and oxygen
Check fluid status
Remove underlying cause
Vasopressors x 72 hours
Fluids early to prevent parasympathetic NS from
firing
AnaphylacticShock
1. Blood Transfusion Reaction
Sarah Reed, 68/yo, is admitted to the MICU with a GI bleed. She has received 3 units of blood on your shift and you just started her fourth unit of blood 20 minutes ago. She complains to you that she “feels funny” and her face is flushed and her temperature has gone from
36.5 to 38.9C.
Four Types of Blood Reactions
• Acute Hemolytic Transfusion Reaction
• Rx to ABO/Rh
• Febrile Non‐Hemolytic Transfusion Reaction
• Rx to Antibodies or elements
• Mild Allergic Reaction• Hives/itch
• Anaphylactic Reaction• Severe RX to protiens
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Signs of a Transfusion Reaction
Non‐Hemolytic
(antibodies)
• Fever
• Chills• >1 degree baseline
• Flushed
• Most common
Mild Allergic
Hives
Urticaria
Hemolytic Transfusion ReactionRX to blood type
• Fainting, dizziness, anxiety
• Chest pain
• Hypotension
• Bronchospasm
• Blood urine
• Flank/back pain
• Nausea/vomiting
Emergency Measures for a Blood Transfusion Reaction
• Stop the blood!!!
Remove blood from the line or change
Assess ABC’s
Medications
Send labs
COMPLICATIONS(poor oxygen delivery)
• Discomfort
• Anemia
• Acute kidney failure
• Shock
• Lung dysfunction
• Cardiac ischemia
• DIC
Massive transfusion
• 1 blood volume replaced in 24 hrs
• Mortality 50% (higher in elderly)
• 45% pts with >10units in 24hrs develop ARDS (many researchers feel actually TRALI then ARDS later)
• Infection rate 50% if >7 units
Massive Transfusion
• Complication is diffuse microvascular bleeding or “oozing” coagulopathy
• Labs cannot predict
• Deplete coag factors to 37% after 10 units and still have normal coagulation
• Platelets drop inversely to blood given (50‐20u)
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Massive transfusion complications
• MSOF, ARDS
• 47% develop coagulopathy
• 25u components exposes to 80 different donors
• Febrile non‐hemolytic transfusion Rx• Occurs 20%
• Risk:• 1:5 platelets
• 1:100 RBC’s
• Delayed hemolytic reaction 1:2500• 2‐14 days post TX
• Fever, jaundice
• From clearance of antibody coated RBC’s
Antibodies and TRALI
• Found in donor serum• Most common cause because able to react with entire circulating blood pool of WBC’s
• Can be in recipient• Less frequent because limited # WBC’s in donor product
Radiology
• Bilateral pulmonary infiltrates• Appear at time of reaction and resolve in 96 hrs in 80% pts
• ABG's are altered for same time frame
• Infiltrates persist for 7 days in other 20%
• White out from WBC aggregation and sequestration in lung
2. Anaphylaxis and Anaphylatic Shock
Agnes White is a 56y/o beekeeper who was tending her bees when she accidentally knocked over one hive. It is estimated that she was stung over 100
times. She is admitted to your unit from the ER, where she received 5 liters of fluid. She is edematous, with a
HR of 124, and BP of 70/44.
Anaphylaxis: When the Immune System Goes Nuts
Histamine and other substances released in
mass
Massive vasodilation
Increase in capillary permeability
(IGE stim-mastcell-histamine-platlet activating factor)
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Causes of Anaphylaxis Latex
• Home• Diapers
• Mouse pads
• Erasers
• Rug backing
• Zip lock bags
• lottery tickets
• socks
• Hospital• Ace wraps
• Electric cords
• Shoe covers
• Stethoscope tubing
• Injection ports
• masks
Symptoms of Anaphylactic Shock
• Hypotension
• Tachycardia
• Decreased SVR
• Edema
• Wheezing/SOB
• Nausea/vomiting
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Hemodynamics of anaphylactic shock
• BP‐ low
• HR‐ high
• CO‐ low
• RA/CVP‐ low
• PAOP(wedge)‐ low
• SVR‐ low
Treatment for Anaphylaxis
• ABC’s
• Epinephrine SQ 1:1000 Q10‐15” (or IM?)
• Steroids (hydrocortisone 5mg/Kg)
• Benadryl
All of anaphylaxis interventions
Epinephrine IV 5-10 mcg
Fluid volume resuscitation (lose 40% into interstitium)
Epi or dopamine drips
?Amrinone or milrinone (bronchdilates)
Tx for Anaphylactic Shock
Case studiesPutting It All Together
Ms. E. is a 54 yo female who was admitted for chest pain and MI. She had chest pain for three days before going to
the MD. Physical exam shows:•RR 26 and labored•HR 136, BP 72/48
•Skin cool and pale•Troponin 4.1
What will the CVP/RA be?
-the wedge?
-the CO?
-SVR? (vasodilated or vasoconstricted)
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Putting It All Together
Mr. A, a long-time nursing home resident, comes to the hospital via ambulance. Physical exam shows:
•RR 28, crackles 1/3 up bilaterally•HR 122, BP 70/46
•Skin warm, sweaty•UO 150 with cath; foul smelling, cloudy
What will the CVP/RA be?
-the wedge?
-the CO?
-SVR? (vasodilated or vasoconstricted)
Putting It All Together
Mr. B. is a 57 yo male returning from the PACU after spinal surgery for chronic thoracic back pain. Physical exam
shows:•RR 10
•HR 45, BP 80/44•Skin warm and dry from nipple line down; cool and
clammy from the nipple line up
What will the CVP/RA be?
-the wedge?
-the CO?
-SVR? (vasodilated or vasoconstricted)
Putting It All Together
Ms. C. is a 16 yo female who has had uncontrolled diarrhea and vomiting for three days. Physical exam shows:
•RR 22•HR 136, BP 84/36
•Skin cool and pale•UO 35 through cath; clear
What will the CVP/RA be?
-the wedge?
-the CO?
-SVR? (vasodilated or vasoconstricted)
Putting It All Together
A 46yo female comes to the ER complaining of SOB. Physical exam shows:
•RR 24, labored•Inspiratory and expiratory wheezes progressing to audible stridor
•HR 130, BP 180/94 initially then drops to 80/44, HR 145•Skin warm and red
What will the CVP/RA be?
-the wedge?
-the CO?
-SVR? (vasodilated or vasoconstricted)
Putting It All Together
Mr. D. is a 77 yo patient with a COPD exacerbation and ventilator dependence. Physical exam shows:
•RR 20 on AC 12•HR 106; BP 120/78
•Skin warm and slightly diaphoretic•Temp 39.3 C
What will the CVP/RA be?
-the wedge?
-the CO?
-SVR? (vasodilated or vasoconstricted)
Who Done It????
The Death of a Cell
Images have been removed from the PowerPoint slides in this handout
due to copyright restrictions.
Hemodynamic, Shock, and Infection in Critical Care
©TCHP Education Consortium, October 201450
The Location
In a quaint little town just off of a picturesque river, there sits a popular vacation spot, known for its excellent service.
Seemore Cell
•Has a lot of things to do
•Has not lived a healthy lifestyle
•Lots of folks come and go from his place everyday
Professor Neuro Genic
•Well educated
•Likes to control the world around him
•Kind of “nerdy”
Miss Anna Fillactic
•Has a drug problem
•Loves to dine on fish in strawberry sauce
•Is the heiress to the Benadryl family fortune
Princess Scarlet Heart
•Is essential to her peers
•Likes to be the center of attention
•Likes to “pump” weights
Sir Bach Terria
•Loves adding to his bug collection
•Makes everyone aware of his presence
•He’s really “hot”
Images have been removed from the PowerPoint slides in this handout
due to copyright restrictions.
Hemodynamic, Shock, and Infection in Critical Care
©TCHP Education Consortium, October 201451
Mr. Hy Po Volemic
•Has a “dry” sense of humor
•Enjoys “bloody” Mary’s while watching “bloodbath” horror flicks
Your Mission
Seemore Cell was found dead. Your mission (and you chose to accept it) is to figure out who killed Seemore Cell.
Scenario•All guests were invited to a pool-side party at the Therapy Pool.
•It would be pot luck as the dietary staff’s parking location was moved, and they are now on strike.
•The pool was a bit dirty as all chemicals were used up in preparation for an important inspection earlier in the week.
Scenario
The guests were enjoying drinks and appetizers when Miss Anna Fillactic lets out a very loud scream…. Mr. Cell is at the bottom of the pool!
Scenario
Mr. Cell was removed from the pool and taken to the nearest hospital where he later dies. Upon autopsy, his death was determined to be a homicide. You, Inspector Assessment, are assigned to the case.
Known Facts
Mr. Cell has a past medical history of:•CAD•Diabetes•Alcohol Abuse (many treatments)•Hypertension•“Many allergies” but nothing specific documented
Images have been removed from the PowerPoint slides in this handout
due to copyright restrictions.
Hemodynamic, Shock, and Infection in Critical Care
©TCHP Education Consortium, October 201452
Known Facts
Mr. Cell was on the following medications:
•Zantac•Lisinopril•ASA•Glyburide•Motrin
Clue #1
• BP RANGE 60‐90/35‐48
• Does this rule any type of shock?
Clue #2
• Urine output <30 cc/hr
• Does this rule out any type of shock?
Clue #3
• Upon admission, Mr. Cell was alert and oriented, but quickly became anxious, which progressed to confusion, lethargy and eventually coma.
• Does this rule out any type of shock?
Clue #4
• Hemodynamics
• CO/CI 3.2/1.6
• RAP 5
• PCWP 5
• SVR 537
• Does this rule out any type of shock?
Clue #5
• Skin is warm and flushed.
• Which 3 types of shock can this be?
Images have been removed from the PowerPoint slides in this handout
due to copyright restrictions.
Hemodynamic, Shock, and Infection in Critical Care
©TCHP Education Consortium, October 201453
Clue #6
• Heart rate has been 40‐60 (sinus brady)
• “Dead” giveaway?
SO…….
WHO DONE IT?
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