Scullard Shock and Infection PDF

Images have been removed from the PowerPoint slides in this handout
due to copyright restrictions.
Shock
• A state of inadequate perfusion relative to tissue
demand
Shock • Inadequate oxygen delivery relative to tissue demand
• Systemic tissue perfusion is
Lynelle Scullard RN MSN CCRN‐K CNRN a product of CO and SVR
Critical Care Clinical Educator Cardiac Output = SV x HR
Hennepin County Medical Center
Cardiac Output 4 Types of Shock:
• A normal CO is 4‐8 liters per minute •1. Cardiogenic
CO = SV X HR •2. Hypovolemic
• *Stroke volume = amount of blood ejected by the left
ventricle with each contraction •3. Distributive: ‐ Neurogenic
(A normal SV is 60‐100ml)
• *Heart rate = beats per minute
‐Anaphylactic
(A normal HR is 60‐100 bpm) ‐ Sepsis
4. Obstructive
Shock is a result of inadequate: Shock

• Oxygen supply • Components needed for oxygen supply
• Oxygen delivery (DO2) • Adequate ventilation(exchange of air between lungs and
atmosphere so that O2 can be exchanged with Co2
• Oxygen utilization (VO2) • Adequate hemoglobin to carry oxygen to the tissue cells
Hemodynamic, Shock, and Infection in Critical Care

1 ©TCHP Education Consortium, October 2014
Shock Shock
• Components necessary for oxygen delivery • Components necessary for oxygen utilization
• Adequate pump = cardiac output • Adequate functional vascular bed
• Adequate volume = stroke volume
• VO2 = represents “Oxygen utilization”
**DO2=Oxygen delivery (the result of cardiac output)
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

Types of Shock Shock
• Cardiogenic – pump • Heart and brain
• Hypovolemic – volume • Increase metabolic rates
• Decreased stores of energy substrate
• Distributive – vascular bed • Require perfusion pressure >60 to perfuse organs and
• Neurogenic prevent cell death
• Anaphylactic
▼Septic
Neuroendrocrine Response Sympathetic Activation
• Baroreceptors and chemoreceptors • Alpha receptors
• Norepi produces vaso and splenic constriction • Vasoconstriction
• Reduce vagal response • Beta receptors
• Vasopressin • Dilation of circulation to brain and heart
• Constriction
• Renal tubules water reabsorption
• Aldosterone
• Reabsorption of Na
Cellular Response Cardiovascular Response
• Hypoperfusion • Decrease stroke volume causes increase HR
• Decrease filtration • CO = SV x HR
• Ion pump dysfunction
• Aerobic to anaerobic metabolism
• Venoconstriction
• 2/3 of volume is in the
• Increase metabolites increase osmolarity
venous bed
• Reabsorbtion of fluid into intravascular bed
• Increase interstitial fluid
• Lactic Acidosis
• Cell death

Pulmonary Response Renal Response
• Increase RR and depth of breathing • Conserve water and Na
• By relaease of ADH, aldosterone
In decompensation In decompensation
• Increase PVR reduces tidal volume, increases dead space‐ • Tubular obstruction by cellular debris
decrease gas exchange • Decrease blood flow
• Increase work of breathing • Toxic injury
• Increase demand on resp muscles
• Lung injury ARDS
Stages of Shock Stages of Shock
• Initial stage (preshock) • Compensatory Stage
• Change from aerobic to anaerobic (Warm shock, compensated shock)
• Glycogen stores used early
• Slowly build up lactic acid
• Neural
• No signs or symptoms • SNS
• Hormonal
• ADH
• Chemical
• CO2
Stages of Shock Stages of Shock
• Progressive • Refractory
• Compensatory mechanisms fail • Irreversible damage and death
• Cell death
• Organ failure

Multi‐system Failure Metabolic Acidosis
• Cellular anoxia results from: • Metabolites override vascular tone
• Cellular depletion of ATP • Hydrogen ions build up
• Energy debt • Lactate
• Accumulation of anaerobic end‐product metabolism‐ • Cell swelling and leaking
(waste)further impairs cells
Shock‐ Compensatory Stage
Diagnosis
moving to Progressive Stage
• Medical history • Assessment
• Physical exam • BP
• HR
• Laboratory evaluation • Neuro
• Na, K, Chloride, serum bicarb, creat & bun, coags, liver function, cardiac
enzymes, ABG, lactate • Renal
• “non‐invasive” monitoring • Skin
• Lungs
• Pulmonary artery catheterization* • Hemodynamic
Treatment of any Type of Shock Goal for Treatment
• Identify cause • Restore Oxygen Transport
• Type of shock
• Oxygen
• Hemoglobin
• Saturation
• Support Blood Pressure
• Volume
• Inotropic agents
• Psychological
• Patient
• Family (all shock mortality = 35‐ 60%)

True Emergency! Cardiogenic Shock
• Cardiogenic shock is the most difficult type of shock • Most common cause of death in hospitalized
to treat and has one of the highest mortality rates of patients with MI
the different shock types. • Mortality Range 70%‐80% in 70’s
50%‐60% in 90’s
• Goal is to save the patient’s life and treat the cause 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 Cardiogenic Shock ‐ Intrinsic

• Pathophysiology • Cause
• Decrease stroke volume • Severe ischemia or infarction
• Decrease cardiac output • Cardiomyopathy
• Increase heart rate • Valvular disease or dysfunction
• Vasoconstriction • Low cardiac output syndrome
• Decrease urine output • Severe brady or tachy rhythms
• Pulmonary congestion • Free wall rupture
Signs and Symptoms Cardiogenic Shock Diagnosis
• Low blood pressure and tachycardia • History –past cardiac disease?
• • Skin cool, clammy and possibly dusky; slow • Shock assessment
capillary refill • EKG
• • Hemodynamic monitoring is usually instituted • ECHO
• • Lung sounds with crackles; patient short of breath • Enzymes‐Troponin,
or dyspneic CK‐MB
• • Restlessness, anxiety, and possibly lethargy and
confusion

EKG Treating Cardiogenic Shock
• T wave inversion
• Ischemia
• ST segment elevation • • Requires an aggressive strategy
• Injury • • Specific goals:
• Q wave • * Identify and correct underlying cause
• infarction • * Improve tissue perfusion. Especially important in
the case of MI.
*Acute coronary
syndrome
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 Hypovolemic Shock
• Cause • Pathophysiology
• Hemorrhagic • Decrease circulating volume
• Non hemorrhagic • Cellular hypoxia
• Diarrhea/vomiting‐increase fluid output • Cellular death and acidosis
• Heat stroke‐lack of H2O
• Burn/ascites‐fluid shift
• “Third spacing”

Classification of Hypovolemia
Pathophysiologic Process
• 1. Mild <20% Mild tachycardia
• • Decreased circulating volume leads to decreased ________________________No BP changes
preload and stroke volume, decreased cardiac • 2. Moderate 20% ‐ 40% Same plus:
output, and finally hypotension and inadequate
tissue perfusion Increase HR >120
Orthostatic changes
Oliguria
• Begins when 15% or appx. 750 ml of intravascular
volume has been lost _______________________ Tachypnea
• 3. Severe >40% Same plus:
Hemodynamic instability
Multi‐system failure
Treatment
Hypovolemic Shock
• Best to prevent its occurrence by monitoring for
signs of fluid loss and correcting before shock
• Assessment
occurs • BP‐ low
• HR‐ increase
• Treatment includes finding the cause and
• Neuro‐ irritable, coma
correcting it by replacing specific fluid lost.
(**Place 2 large bore) IV catheters. • Renal‐ decrease output
• Skin‐ pale cool clammy
• Lungs clear
• Specifics of treatment:
• Hemodynamic assessment
* Fluid and blood • CVP, RA, PW‐ low
* Colloid fluids • CO, CI‐ low
* Transfusion • SVR‐ increase
Hypovolemic Shock Intravenous Fluid Replacement
•Treatment replace what’s lost! •Crystalloids •Colloid

• Volume • Saline, ringers • Albumin,
• Blood • Distribute freely Hespan
• Fluids • 2 – 6 times more • More expensive
required than
estimated fluid •Not proven
loss more effective

Electrolyte Imbalances Electrolyte Imbalance
• Hyponatremia • Hypernatremia
• Overcorrection can lead to paralysis and coma • Overcorrection can lead to cerebral edema
• Prolonged can lead to Neuro injury • Free water to correct gradually
• 115 mEq/l and symptomatic = nonaggressive therapy • Change no faster than 1 – 2 mEq/hr to max 15 – 20 mEq
• If symptoms or severe (< 115) 1 – 2 mEq/hr to 120 to 125 in 24hr
• Lasix if fluids adequate
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 Goal for Treatment

• ABC’s • Restore Oxygen Transport
• Stasis
• Early stabilization of FX*
• Debridement of devitalized and contaminated
tissue*
• Evacuation of Hematoma*
* Decrease inflammatory response

Case Study #2
Uncontrolled Hemorrhage Houston Study
Case Study #2 598 Adults Penetrating Injuries Bp<90
• 20 year old male gun shot wound with uncontrolled
bleeding .
What are you going to do? • Immediate fluid flushes • Delayed fluid
• 62% survived • 70% survived
BP = 60/30 • 30% complication • 23% complication
HR = 120 • ARDS, ARF, pneumonia • Hospitalization shorter
RR = 26 clear lungs • Wound infection
Neuro = unconscious
Skin = cold
Now what?
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!

References References
Barber, A.E. Cell damage after shock. New Horizons. 1996; 4:161. Hochman, J.S. Cardiogenic shock complicating acute myocardial infarction: expanding the
paradigm. Circulation 2003; 107:2998.
Rodgers, K.G. Cardiovascular shock. Emergency Medicine Clinics North America. 1995; 13:793.
Mimoz, O. etal. Pulmonary artery catheterization in critically ill patients. Critical Care Medicine
Shoemaker, W.C. temporal physiologic patterns of shock and circulatory dysfunction based on early 1994; 22:573
descriptions by invasive and noninvasive monitoring. New Horizons. 1996; 4:300
Conners, A.F.Jr, Speroff, T. et al. The effectivness of right heart catheterization I the initial care of
Tuchschmidt, J.A., Mecher, C.E. Predictors of outcome from critical illness. Critical Care Clinics. critically ill patients. SUPPORT Investigators. JAMA 1996; 276:889.
1994; 10‐179
Harvey, S., Harrison, D.A. et al. Assessment of the clinical effectiveness of pulmonary artery
Kinch, J.W., Ryan, T.J. Right ventricular infarction. New England Journal of Medicine. 1194. catheters in management of patients in intensive care (PAC‐Man): a randomized controlled trial.
330:1211. Lancet 2005; 366:472
References:
• TCHP Education Consortium –Hemodynamic
Monitoring Primer
References • Hypovolemia retrieved from

en.wikipedia.org/wiki/Hypovolemia
Moscucci, 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
• Take a rapid treatment approach to cardiogenic
revascularization on mortality. Circulation 1995; 91:873.
Mapstone, J., et al. Fluid resuscitation strategies: A systematic review of animal trials.
shock retrieved from
The Journal of Trauma. 55(3) 571‐589, September, 2003. www.nursingcenter.com/library/Journal
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. Article.asp?Article_ID=800728
References: References:
• Cardiogenic Shock retrieved from emedicine.medscape.com/article/152191‐ • Critical Care Medicine‐ Venous Oximetry‐ The concept of SvO2 and ScvO2
overview retrieved from icucare.blogspot.com/2009/08/venous‐oximetry‐concept‐of‐
• Critical Care Medicine Tutorials‐The patient is hypotensive: is this due to svo2‐and.htlm
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

Space
Infection in Patient placement
Critical Care Bedside procedures

Ventilation
Environmental contamination
Hand Washing Handwashing

• Compliance:
• RN….52%
Compliance
• MD….23%
Frequency
• Michigan study bacteria on hands:
Skin irritation • Nails…before 73%
• After ….68%
Jewelry • No nails 32% .. 26%
Nails
Another study Patient Susceptibilty

• RN’s washed %
• Before care 62 • Age
• After care 87 • Why they are in the hospital
• Move dirty to clean 60 • Co-morbid conditions
• After remove gloves 80
• Contacts with carriers
• Before invasive procedures 57
• Nutrition
• After direct contact fluids 87
• Before touching own eyes etc 3 • Stress

Fever Fever
• Benefit • SCCM: Consequences
• >100.4 (38C) • 100.4 ‐ 38C fever
kills bugs, helps • 101.5 ‐ 38.6C treat
neutrolphils • 102‐ 38.9C most likely dehydration febrile seizures
and antibodies, infection increased metabolism confusion
potentiates increased cardiac output delirium
antibiotic increased MVO2 patient discomfort
activity Each 1* raises metab rate 13%
Fever Cultures
• Management of non‐beneficial • Why? • Where?
fever:
• Thermoregulation is impaired at • Blood
104*/40 C
To
• • Urine
• Evaporative cooling best
• Meds accurately • Sputum
• antibiotics
identify
• Lines
bacteria
• CSF
Blood Sputum
• Bacteria showers 1 hr after temp spike • Color, amt, odor?
• Draw blood before antibiotics • QBAL (qualitative bronchial alveolar lavage) vs
• Peripheral sticks, usually 2 sets suction
• Redraw 24 hrs later
• Prep site, allow to dry
• Don’t change needle
• 8‐10cc’s per bottle
• Contamination risk

Urinary Tract Infections: CAUTI prevention

• Treatment • Need for Foley
S/S • Remove catheter
• Alternatives
• Culture
•Fever • Antibiotics
•Urgency • Sterile technique
•Frequency
•Dysuria
•Supra-pubic tenderness
•Positive urine culture 40% infections
Sepsis in immunosuppressed
CMS Hospital Compare: CAUTI Urinary Catheter Device
For time period October 1, 2017‐ September 30, 2018
Standardized Utilization Ratio (SUR) 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
September 2019 Infection Prevention

September 2019 Infection Prevention Update
Update
Pneumonia: S/S Pneumonia: Risks

Host factors
Sputum Bacterial colonization
Positive culture Aspiration
Fever Contaminated equipment
Tachypnea Aerosolization
Auscultation Inadequate pulmonary clearance
quiet over area, coarse
around

Nosocomial Pneumonias
Ventilator Associated
• Account for 15% of all hospital associated
Pneumonia (VAP) infections
• Account for 27% of all MICU acquired
infections
Author: Marianne Chulay, RN, DNSc, FAAN • Primary risk factor is mechanical ventilation
Consultant, Clinical Research and Critical Care (risk 6 to 21 times the rate for nonventilated
Nursing patients)
Issued 01/2008 CDC Guideline for Prevention of Healthcare
Reviewers: Suzi Burns, Mary Jo Grap, Associated Pneumonias 2004
Judy Verger, and Lori Jackson Craven, Chest 2000; 117:186S-187S.
Primary Route of Bacterial Entry Significance of Nosocomial
into Lower Respiratory Tract Pneumonias
• Micro or macro aspiration of • Mortality ranges from 20 to 41%, depending on
infecting organism, antecedent antimicrobial
oropharyngeal pathogens therapy, and underlying disease(s)
• Leakage of secretions • Leading cause of mortality from nosocomial
infections in hospitals
containing bacteria around
the ET cuff
Significance of Nosocomial
Pneumonias
• Increases ventilatory support requirements and ICU stay
by 4.3 days
• Increases hospital LOS by 4 to 9 days VAP Prevention
• Increases cost ‐ > $11,000 per episode
• Estimates of VAP cost / year for nation > $ 1.2 billion

Continuous Removal of
Subglottic Secretions HOB Elevation
Use an ET tube with
continuous suction HOB at 30‐45º
through a dorsal lumen
above the cuff to prevent
drainage accumulation.
CDC Guideline for Prevention of Healthcare Associated Pneumonias
2004 ATS / IDSA Guidelines for VAP 2005
HOB Elevation Leads to
Significant Deduction in VAP Is HOB Elevation Done?
25 60
Despite effectiveness Degrees of
20 of HOB elevation, HOB Elevation
% with HOB Elevation

40
compliance is poor. 0 to 20
15 21 to 30
% VAP
31 to 40
10 • Grap et al. Am J Crit Care > 40
20
1999;8:475‐480
• Grap et al. Am J Crit Care
5
2005;14:325‐332
Dravulovic et al. Lancet
0
0 1999;354:1851‐1858
Supine HOB Elevation
Frequency of Equipment Changes
VAP Prevention
No
Routine Ventilator Wash hands or use an alcohol‐based waterless
Changes Tubing
antiseptic agent before and after suctioning,
touching ventilator equipment, and/or coming
into contact with respiratory secretions.
Between Not
Patients Enough
Ambu Inner Data
Cannulas
Bags of Trachs
CDC Guideline for Prevention of Healthcare Associated
Pneumonias 2004
Pneumonias 2004 AACN Practice Alert for VAP, 2007

VAP Protection No Data to Support These Strategies
• Use a continuous subglottic suction ET • Use of small bore versus large bore gastric
tube for intubations expected to be > 24 tubes
hours
• Continuous versus bolus feeding
• Keep the HOB elevated to at least 30
degrees unless medically contraindicated • Gastric versus small intestine tubes
• Closed versus open suctioning methods
• Kinetic beds
Pneumonias 2004 CDC Guideline for Prevention of Healthcare Associated
AACN Practice Alert for VAP, 2007 Pneumonias 2004
Oral Care VAP
Risk Factors
• Role of oral care, colonization of the
oropharynx, and VAP unclear – dental plaque ETT > 6 days
may be involved as a reservoir Re-intubated within 72 hours
• Limited research on impact of rigorous oral
care to alter VAP rates Neurosurg, trauma, or burn
• Surveys indicate most nurses use foam swabs
patient
rather than toothbrushes in intubated patients Decreased LOC + secretions
H2 blockers
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2004
Grap M. Amer J of Critical Care 2003;12:113-119.
NG tube present
Pneumonia: Management Catheter Related Infections
Increased risk with:

WASH HANDS!
emergency visit
Oral care q2-4h more lumens
central line
Suction above cuff long time
Separate suction canisters TPN/lipids
inexperienced operator
Clean in-line suction catheter Cultures
Position side to side tip of line and blood culture

CMS Hospital Compare : CLABSI
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&la
t=44.9758391&lng=-93.2571034
Central Line Device ICU type UTI CLABSI VAP

Standardized Utilization Ratio (SUR) Interdisp. 3.1 1.5 2.3
What is the Standardized
Utilization Ratio (SUR)? Interdisp, major 3.3 2.0 3.3
• A summary measure used to
track device use at a national,
state, or local, or facility level
teaching hosp
over time.
• Adjusts for various facility and
location-level factors that
contribute to device use; allows
Surgery 4.1 2.3 5.3
CV surgery 3.2 1.4 4.7
users to summarize data by
more than a single variable
• Factors included in the SUR

analysis are:
• unit type, Neurosurgery 6.8 2.5 6.5
• facility bed size,
• medical school
affiliation Medical 4.1 2.4 2.5
• A SUR > 1.0 means more device
•
days were observed than
predicted,
A SUR < 1.0 means fewer device
CCU 4.4 2.1 2.5
Burn 7.7 5.6 10.7
days were observed than predicted
Trauma 5.7 4.0 9.3

Peds 2.0 2.9 2.1
Infectious Diarrhea
CMS’s “Never Events”
Causes
• Blood incompatibility
• Antibiotics
• Air embolism
• tubefeeding
• Surgical site infection CABG Signs and Symptoms
• UTI •Fever
• Vascular catheter associated infection •Watery diarrhea
• Fall and trauma •Cramping
• Pressure ulcer III and IV Management
•DC antibiotics
•Metronidazole, then oral Vanco

C diff Hospital Onset CDI
TARGET:
36
• Isolation
• Contaminates every surface
• 78% still contaminated after cleaning
• Wash with soap and water
• Alcohol doesn’t kill
• Bleach works
• 20% uniforms
September 2019 Infection

Prevention Update
Common Infections:
Sinusitis Necrotizing Fasciitis
Causes and Risks #1 organism =
Tubes in the nose Group A streptococcus (GAS)
Antibiotics
Many other organisms can cause
Open head injury
it too!
Gas gangrene: clostridial
Signs and Symptoms
Fever
myonecrosis
Drainage-not often
Pain/Pressure 4% of bacteria are in us all the
Smell
time, 1% cause problems
Necrotizing Fasciitis Hemorrhagic blistering

Non-specific erythema
Edema
Extreme pain
Pallor/gray discoloration
Anesthesia
Purpura
Hemorrhagic bullae
Gas bubbles on X-ray

Pustule Blistering
Necrotizing Fasciitis
Surgical 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”

Case study Case study
• Hypotensive • No further debridement of wound needed in the OR
• OR: • 2 days later a R antecubital A‐line infiltrated. Area
• Fascial and muscle debridement white and cold
• Amputation mid upper arm • 6 hrs later area red with streaks, hand dark and cold
• Debridement with multiple further dressing changes
• Culture of tissue:
• “many gram negative cocci”
and trimming.
• “many Group A beta hemolytic Streptococcus isolated” • Cultured same Group A Strep
Meningitis Meningitis
Viral Bacterial
Rarely fatal May be fatal

Treatment is symptomatic Treatment is supportive
Symptoms last 7-10 days Antibiotics a must!
Resp secretions Break in dura, URI, strep
Symptoms of Meningitis Brain Abscess

Fever
Causes
Severe headache
Nuchal rigidity
Signs and Symptoms
Photophobia
Confusion/sleepiness Headache
Fever
Focal neuro changes
Diagnose: LP, WBC, glucose In 50% - seizures, nuchal rigidity, n/v, papilledema
Isolation

Cardiac Valve
Infection Cardiac Valve Infection
Causes Diagnosis and Treatment

Gas/rheumatic fever
Echocardiogram
Drug abuse
Blood cultures
Signs and Symptoms
Antibiotics
General Surgical debridement/excision/replacement
Regurgitant murmurs
S/S embolization
Fever with shaking chills
Surgical Wound with Surgical Wound with

Dehiscence Dehiscence
Causes Treatment
•Dehiscence If minor, call MD immediately
If major, call for help immediately
•Evisceration
Signs and Symptoms
Pain “boggy” Sterile NS soaked 4X4’s
Fever stretching of suture line Comfort
Increased WBC Surgical debridement w/wo secondary closure
Antibiotics
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

MRSA
• Penicillin is now completely useless against staph
aureus
• Oxacillin on lab results
• Vancomycin treatment of choice
• Nosocomial strains resistant up to 50% time
Hospital Onset MRSA Infection
(all sites) TARGET: 9 CMS Hospital Compare: MDRO
MRSA Bacteremia CDI
https://www.medicare.gov/hospitalcompare/compare.html#vwgrph=1&cmprTab=3&cmprID=240004%2C240080%2C240001&cmprDist=0.5%2C1.4%2C
5.2&dist=25&loc=55415&lat=44.9758391&lng=-93.2571034
September 2019 Infection September 2019 Infection

Prevention Update Prevention Update

VRE Next up:
• Generally effects only debilitated or • Pseudomonas
immunocompromised pts
• Large cause vanco use for MRSA
• Synercid • Klebsiella
• Linezolid
Other Bug Fighters Infection case study

• 38yo female from Ontario
• Amphotericin B
• Hx HA for 4 days, felt “crappy”
Antifungal • ER 6/10 w/ HA, weak/numb LE’s
Fever, chills, rigors, and n/v • Admitted 8pm
May do test dose first
• CSF cx, yellow glucose 77, hi protiens
Premedicate
Monitor VS q 15” X 1 hr, then q2h
• r/o cord compression, r/o GB, ?viral
May give fluid flush before and/or • Head CT negative
after
• 0800 BP 220/110, 120, 20’s, sats 80’s • Back to CT no change
• SICU ? Guillian‐Barre • Norepi, phenyl, dopamine….swan
• Numb and paralized to above nipple line • Hemodynamics normal
• Drowsy, but oriented • Flash pulm edema…… no cough
• Runs V‐tach, change in voice quality • No brainstem reflexes , fixed pupils
• Intubated and sedated • Ventric ICP 15
• BP 41/28 140

• Work up: • Results
• Infection… culture everything • No growth to date
• Exposed to chicken pox 2 wks ago • No herpes simplex seen in CSF
• Canada • Viral encephalomyelitis of unknown origin
• HIV • + HIV
• Infectious disease consult
• West nile vs rabies
• No change in status, drips, neuro • Repeat CT
• Intraparenchymal hemorrhage in pons and 4th
• 6/11 2000 CT
ventricle
• Significant brain stem swelling, hydrocephalaus
MRI • Removed from support
‐inflamm consistent w/ encephalitis
SIRS
• Systemic Inflammatory Response
Sepsis Syndrome
and • signs and symptoms of infection
without identifiable source
Septic Shock
2 or more:
T>100.4/38C or <96.8/36C
HR>90
RR>20
WBC>12,000 or <4000

Sepsis Severe Sepsis
• HR > 90
• Temp > 38º C (100.4º F) or
< 36º C (96.8º F)
• RR > 20 or PaCO2 < 32 mm
sepsis + signs of organ
Hg system failure,
• WBC > 12K < 4K, or > 10%
bands hypoperfusion, or
• Infection causes
inflammatory response
hypotension
Severe Sepsis
• Definition
Arterial hypoxemia
• Sepsis+ acute oliguria
• Organ dysfunction creatinine increase
• Hypoperfusion coagulation abnormalities
• Hypotension or thrombocytopenia
hyperlactemia
or
arterial hypotension
Sepsis mimics
Septic Shock
• Pancreatitis
• Trauma
• Burns
• Cardiac surgery
sepsis + hypotension +
• ARDS perfusion defects
• Diabetic ketoacidosis
• Neuroleptic malignant syndrome
• Drug reaction
• Aspiration pneumonitis
11/5/2019

Sepsis is now defined as Early is key
• “a life‐threatening organ dysfunction caused by • Infection no longer defined
dysregulated host response to infection” • SIRS and severe sepsis removed from definitions
• “life threatening condition that arises when the • Septic shock:
bodies response to an infection injures its own • A subset of sepsis
tissues and organs” • Circulatory, cellular, metabolic alterations assoc. with
• Response is excessive, creating an increased risk of higher mortality than sepsis alone
morbidity and mortality
CMS, research, and you qSOFA
• CMS still supports SIRS and old definitions • Bedside screening tool
• Research still uses severe sepsis definitions • One point for each:
• Altered mentation
• YOU need to know when you patient is getting sicker
• SBP 100 mmHg or less
and how to manage them
• RR 22 or greater
• Two or more points is a positive screen
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
11/5/2019

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? Risks
• being in a health care setting • Artificial devices
• having natural defenses broached • Inappropriate antibiotics
• immunocompromise: age, HIV, diabetes • Poor nutrition
• co‐morbid conditions • *** greatest risk may be the pathogens that medical
and nursing professionals carry on unwashed
• surgery, trauma, or necrosis of abdomen
hands!***
Causative Organisms After Exposure...
Gram negative organisms Release of Cytokines
Klebsiella, E.coli, enterobacter Vasodilation  Capillary
permeability
Inadequate tissue
Gram positive organisms Third-spacing
perfusion
GAS, strep
Opportunistic organisms Hyperdynamic state
yeast, aspergillus
Hypodynamic state
C diff

Cytokine Released by Effect Hyperdynamic Stage

TNF‐α Dendritic cells Attracts other inflammatory cells
Macrophage Fever, catabolism
Neutrophil Edema, vasodilation Early ‐ Fix them now!
T‐cell
IL‐1 Dendritic cells Similar to and synergistic with
Macrophage TNF‐α Tachycardia High cardiac output
T‐cell BUT
Hypotension Low SVR
NO Many Vasodilation
TGF‐β T‐cell Suppresses lymphocytes
IL‐10 B‐cell Suppresses pro‐inflammatory
T‐cell cytokines
Enhance B‐cell function
11/5/2019
Symptoms More Symptoms

 Endocrine
– Insulin resistant
 Labs
– Lactate/pH
– WBC’s
– Platlets/albumin
– ABG/SVO2
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

Care of the Septic Patient: Source Hemodynamic Support

Control
Fluid resuscitation
Find source of infection Crystalloids
Can’t ID bug up to 70 % of the time Colloids (not trauma)
6-10 L, retain 25%
Treat source Vasopressor/Inotropic Support
•Surgical
Dopamine
•Medical
Dobutamine
•Antibiotics Norepinephrine
Phenylephrine
Prevent new infections
Supportive Care Hypodynamic Stage

Pulmonary Management Late!
Decrease O2 demands
Tachycardia Low cardiac output
ARDS/PEEP AND
Hypotension High SVR
Prone positioning
Nutrition
Family Support
Symptoms More Symptoms
 Cardiovascular
– Tachy, low BP… low HR • Neurological
– Low CO, hi SVR/PAWP • Coma
– Cool, clammy, mottled
– hypothermic
• Gastrointestinal
 Pulmonary
•No BS
– Crackles, ARDS
•Lg NG output
– Acidotic
•Transmigration of
– PEEP, PCV bacteria

More Symptoms
 Renal
– Anuric
– Hi BUN/Cr
 Hepatic
– LFT’s up
– DIC ?
– bleeding
More Symptoms
•Endocrine
•Insulin resistance…hi
glucose…low….
•MDF lowers HR
Laboratory 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)

Disseminated Intravascular
Atelectasis in ARDS Coagulation
 Coagulation &  Fibrinolysis
 Inflammation

Inappropriate
clotting
Microemboli Loss of
clotting factors
Widespread cell Bleeding

death
DIC DIC case study
• Clotting: • 39 yo F, placenta previa, placenta accretia
• Platlets/ fibrinogen sent to stop bleeding and clot • 34 wks bleeding… C‐section
• • Amniotic fluid embolus
Hemorrhage:
• Coded immediately after delivery and went into
• Plasminogen activated…lyses clot
fulminate DIC
• Develop FSP, FDP, D‐dimer (potent anticoagulants)
• Consumption of platlets/fibrinogen
DIC case study DIC case study
• LABS • PT INR PTT fibrin D‐dimer plts
• Hgb ..9.6 (1245) pre op • 13.6 1.3 47.3 94 >1000 140
• 6.3 (1846) code troponin • 20.6 2.0 129.3 66 >1000 90
• 3.7 (1950) in SICU 1.2
• 11.4 (2123) SICU
• 16.1 1.6 68.3 83 63
• 4.9 (2225) 5.5 • Other labs:glucose >200
• 0030 9.5 • Calcium low

DIC blood products DIC case study
• PRBC’s: 50 units • Summary:
• Platlets: 7 6pks • Clotted an 8” section of inf vena cava
• MODS
• FFP: 28 units • Planned transfer to U of M for clot removal, dislodged clot
• Cryo (jumbo): 8 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 balance
Fluids
Diuretics
Dialysis/CVCC
Vasoactive Drugs
Inotropes
Vasodilators
Vasopressors


Other Measures
Other measures
Nitric Oxide
• Pulmonary
management • Vasodilates by inhibiting angiotensin
II and sympathetic vasoconstriction
• Management of DIC
• Inhibits platelet/WBC adhesion
• Family support NO Inhibition -
N-monomethyl-L-arginine = L-NMMA
Vasopressin Insulin
• 0.04 u/min • < 150 recommended by SCCM
• Restores responsiveness to vasopressors • High blood sugar creates sticky leukocytes
• NO mediates inhibition
Adrenal replacement therapy Procalcitonin
• Modulates inflammatory cytokines • 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

Other measures Initial management
• Nutritional assistance • A one‐hour bundle is promoted by SSG:
• Measure lactate level
• Glutamine…. T‐cell improve, bactericidal, essential amino • Obtain blood cultures before administering antibiotics
acid • Administer broad‐spectrum antibiotics
• Selenium …. Less renal problems • Begin rapid administration of 30mL/kg crystalloid for
• Vit C … radical scavenger hypotension or lactate level ≥ 4 mmol/L
• Vit E ….ATP, less peroxidation • Apply vasopressors if hypotensive during or after fluid
resuscitation to maintain MAP ≥ 65 mm Hg
11/5/2019
3 hour bundle 6 hour bundle
• Measure lactate • In addition to 3 hour
• Obtain blood cultures before antibiotics • Vasopressors MAP >65 (after fluids)
• Delay considered > 45” • If lactate >4 or hypotension persists reassess volume
• 2 sets and perfusion
• Administer broad‐spectrum antibiotics • Reassess lactate if initially elevated
• ASAP
Unproven/controversial therapies Sepsis case study
• Methylene blue • 44 yo MVA unrestrained , ejected
• Vitamin C, hydrocortisone, • PMHx: cocaine. ETOH, smoker
thiamine
• Splenic fracture
• Sodium bicarbonate
• Steroids
• Multiple rib fx with flail chest/hemopneumo
• Also dozens of drugs • Intubated
targeting the • Labs unremarkable
inflammatory pathway
• ECMO
11/5/2019

• Day 3 • Day 4
• Attempts at weaning fail • Lungs deteriorating
• VS stable except T103 • FiO2 up to 90%
• Labs stable pO2 73 • 99/43 120 14 102T
• QBAL culture gram + cocci • +2 pitting edema
• Plan: early tracheostomy, re‐culture • QBAL >100,000 group A strep
• Treat for ARDS
• Day 5 • Day 6
• Continue with poor ventilatory state, flolan • Echo
• Intubated, sedated, paralyzed • PEEP 15
• 100/60 110 14 103.2 T • PCV
• Swan … SVO2 75% (89%) CO 14 SVR 463 • Troponins continue to rise
• CT negative for PE • Check cortisol levels
• Cultures GAS, staph • proned
• Troponins rising, afib
• Day 7 • Slowly improved to SIMV with periodic trach dome
• FiO2 70% AC 550 R23 PEEP 12 trials
• Sats low 90’s, SVO2 60’s • Transferred to a rehab vent facility after 21 days
• T 102.7
• diuretics

Toxic Shock Syndrome Toxic Shock Syndrome

What bugs?
Treatment
Signs/Symptoms • Early diagnosis
• Mild prodromal symptoms
• Early antibiotics - broad spectrum
• Precipitous acute illness: high fever, n/v,
abdominal pain, severe muscle pain, • Supportive care
headache
• profuse diarrhea, macular erythroderma
Toxic shock case study TS case study
• 28 yo F • Dx: “distributive shock with multi‐organ dysfunction,
• 2 previous cases of toxic shock (14, 18) possibly toxic shock”
• c/o fever, myalgia, ® groin pain • Summary
• Day 3, neuro change… intub…CT neg w/ free fluid in • Day 9
abd… ex lap… compartment syndrome • Fixed, dilated pupils cerebral edema
• No source of infection ID’d
• Day 6, abd open, hypotensive on dopamine and
levophed, low SVR and hi CO…sepsis
Multiple Organ Dysfunction Syndrome MSOF
• Cardiovascular • Causes
• Primary
• Pulmonary • Aspiration leading to ARDS
• Renal • PE
• Trauma to ABD
• CNS • Secondary
• Hepatic • Hypoperfusion
• Microemboli
• Splanchic

APACHE II criteria APACHE II criteria
• Cardiovascular failure • HR </= 54/min • Respiratory failure • RR <5/min or > 49/min

• MAP </= 49mmHg • PaCO2 > 50 mmHg
• V‐tach, V‐fib or both • P(A‐a)O2 .350mmHg
• Serum pH </= 7.24 with • Vent/CPAP dependent
• PaCO2 </= 40mmHg day 4
• Renal failure • UO <479mL/24h or • Hepatic failure • Serum Bilirubin >6

<159mL/8h mg/dL
• Serum BUN > 100mg/dL • PT >4 seconds over
• Serum Creatinine >3.5 control (without
mg/dL systemic
anticoagulation)
• Hematologic Failure • WBC <1000/uL • CNS failure • GCS</= 6 (without

• Platelets < 20,000/uL sedation)
• Hematocrit < 20%

Multiple Organ
Dysfunction 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.



Neurogenic & Anaphylactic
Shock
What is Neurogenic Shock?
Loss of autonomic
nervous system
regulation below level
Sam Johnson was involved in a car accident in which he was driving of injury causes
and hit from behind. When EMS arrived, he was confused but able to massive vasodilation
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
and bradycardia
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.
Causes of Neurogenic Shock Signs of Neurogenic Shock
• Spinal Cord Injury
• T6 or higher bradycardia
profound hypotension
 Anesthesia warm and dry skin below LOI
 Drug overdose May have...

mentation changes paralysis
 Pain
 All interrupt SNS and nausea/vomiting apnea/tachypnea
vasomotor center

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
Anaphylactic
Shock
Four Types of Blood Reactions
• Acute Hemolytic
Transfusion Reaction
• Rx to ABO/Rh
1. Blood Transfusion Reaction • Febrile Non‐Hemolytic
Sarah Reed, 68/yo, is admitted to the MICU with Transfusion Reaction
• Rx to Antibodies or
a GI bleed. She has received 3 units of blood elements
on your shift and you just started her fourth
• Mild Allergic Reaction
unit of blood 20 minutes ago. She complains
• Hives/itch
to you that she “feels funny” and her face is
flushed and her temperature has gone from • Anaphylactic Reaction
36.5 to 38.9C. • Severe RX to protiens

Signs of a Transfusion Reaction Hemolytic Transfusion Reaction
RX to blood type
Non‐Hemolytic Mild Allergic • Fainting, dizziness,

(antibodies)  Hives
anxiety
• Fever • Chest pain
 Urticaria
• Chills • Hypotension
• >1 degree baseline
• Flushed • Bronchospasm
• Blood urine
• Flank/back pain
• Most common • Nausea/vomiting
Emergency Measures for a Blood COMPLICATIONS
(poor oxygen delivery)
Transfusion Reaction
• Stop the blood!!! • Discomfort
• Anemia
 Assess ABC’s
• Acute kidney failure
• Shock
 Remove blood from the line or • Lung dysfunction
change • Cardiac ischemia
 Medications
• DIC
 Send labs
Massive transfusion
Massive Transfusion
• 1 blood volume replaced in
24 hrs
• Complication is diffuse microvascular
• Mortality 50% (higher in
bleeding or “oozing” coagulopathy
elderly)
• Labs cannot predict
• 45% pts with >10units in • Deplete coag factors to 37% after 10 units
24hrs develop ARDS (many and still have normal coagulation
researchers feel actually • Platelets drop inversely to blood given (50‐
TRALI then ARDS later) 20u)
• Infection rate 50% if >7
units

Massive transfusion complications Antibodies and TRALI
• MSOF, ARDS • Found in donor serum
• Most common cause
• 47% develop coagulopathy
because able to react
• 25u components exposes to 80 different with entire circulating
donors blood pool of WBC’s
• Febrile non‐hemolytic transfusion Rx • Can be in recipient
• Occurs 20%
• Less frequent because
• Risk:
limited # WBC’s in
• 1:5 platelets
donor product
• 1:100 RBC’s
• Delayed hemolytic reaction 1:2500
• 2‐14 days post TX
• Fever, jaundice
• From clearance of antibody coated RBC’s
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
Anaphylaxis: When the Immune
System Goes Nuts
Histamine and other
substances released in
2. Anaphylaxis and Anaphylatic Shock mass
Agnes White is a 56y/o beekeeper who was
tending her bees when she accidentally knocked over Massive vasodilation
one hive. It is estimated that she was stung over 100
times. She is admitted to your unit from the ER, where Increase in capillary permeability
she received 5 liters of fluid. She is edematous, with a
HR of 124, and BP of 70/44.
(IGE stim-mastcell-histamine-platlet activating
factor)

Causes of Anaphylaxis Latex
• Home • Hospital
• Diapers • Ace wraps
• Mouse pads • Electric cords
• Erasers • Shoe covers
• Rug backing • Stethoscope tubing
• Zip lock bags • Injection ports
• lottery tickets • masks
• socks
Symptoms of Anaphylactic Shock
• Hypotension
• Tachycardia
• Decreased SVR
• Edema
• Wheezing/SOB
• Nausea/vomiting

Hemodynamics of anaphylactic shock Treatment for Anaphylaxis
• BP‐ low • ABC’s
• HR‐ high • Epinephrine SQ 1:1000
• CO‐ low Q10‐15” (or IM?)
• RA/CVP‐ low • Steroids
• PAOP(wedge)‐ low (hydrocortisone
5mg/Kg)
• SVR‐ low
• Benadryl
Tx for Anaphylactic Shock
All of anaphylaxis

interventions
 Epinephrine IV 5-10 mcg
 Fluid volume resuscitation (lose
40% into interstitium)
 Epi or dopamine drips
 ?Amrinone or milrinone
(bronchdilates)
Putting It All Together

Case studies
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)

Putting It All Together Putting It All Together
Mr. A, a long-time nursing home resident, comes to the Mr. B. is a 57 yo male returning from the PACU after spinal
hospital via ambulance. Physical exam shows: surgery for chronic thoracic back pain. Physical exam
•RR 28, crackles 1/3 up bilaterally shows:
•HR 122, BP 70/46 •RR 10
•Skin warm, sweaty •HR 45, BP 80/44
•UO 150 with cath; foul smelling, cloudy •Skin warm and dry from nipple line down; cool and
clammy from the nipple line up

-the wedge? What will the CVP/RA be?
-the CO? -the wedge?
-SVR? (vasodilated or vasoconstricted) -the CO?
Putting It All Together Putting It All Together

A 46yo female comes to the ER complaining of SOB.
Ms. C. is a 16 yo female who has had uncontrolled diarrhea Physical exam shows:
and vomiting for three days. Physical exam shows: •RR 24, labored
•RR 22 •Inspiratory and expiratory wheezes progressing to audible stridor
•HR 136, BP 84/36 •HR 130, BP 180/94 initially then drops to 80/44, HR 145
•Skin cool and pale •Skin warm and red
•UO 35 through cath; clear

What will the CVP/RA be? -the wedge?
-the wedge? -the CO?
-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
Who Done
•HR 106; BP 120/78
•Skin warm and slightly diaphoretic
•Temp 39.3 C
It????
-the wedge?
-the CO?
The Death of a Cell

The Location Seemore Cell

•Has a lot of things to do
In a quaint little town just
off of a picturesque river, •Has not lived a healthy
there sits a popular lifestyle
vacation spot, known for its
excellent service. •Lots of folks come and
go from his place
everyday
Professor Neuro Genic Miss Anna Fillactic

•Well educated •Has a drug problem
•Likes to control the •Loves to dine on fish in

world around him strawberry sauce
•Kind of “nerdy” •Is the heiress to the

Benadryl family fortune
Princess Scarlet Heart Sir Bach Terria

•Is essential to her peers •Loves adding to his bug
collection
•Likes to be the center of
attention •Makes everyone aware
of his presence
•Likes to “pump”
weights •He’s really “hot”

Mr. Hy Po Volemic Your Mission

•Has a “dry” sense of Seemore Cell was found dead.
humor
Your mission (and you chose to
accept it) is to figure out who
•Enjoys “bloody”
Mary’s while watching
killed Seemore Cell.
“bloodbath” horror
flicks
Scenario Scenario
•All guests were invited to a pool-side party
at the Therapy Pool. The guests were enjoying drinks
and appetizers when Miss Anna
•It would be pot luck as the dietary staff’s Fillactic lets out a very loud
parking location was moved, and they are scream…. Mr. Cell is at the
now on strike.
bottom of the pool!
•The pool was a bit dirty as all chemicals

were used up in preparation for an
important inspection earlier in the week.
Scenario Known Facts

Mr. Cell was removed from the Mr. Cell has a past medical history of:
pool and taken to the nearest •CAD
hospital where he later dies. Upon •Diabetes
autopsy, his death was determined •Alcohol Abuse (many treatments)
to be a homicide. You, Inspector •Hypertension
Assessment, are assigned to the •“Many allergies” but nothing specific
documented
case.

Known Facts Clue #1
• BP RANGE 60‐90/35‐48
Mr. Cell was on the following
medications:
•Zantac • Does this rule any type of shock?
•Lisinopril
•ASA
•Glyburide
•Motrin
Clue #2 Clue #3
• Urine output <30 cc/hr • 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?
• Does this rule out any type of shock?
Clue #4 Clue #5
• Hemodynamics • Skin is warm and flushed.
• CO/CI 3.2/1.6 • Does this rule out any
• RAP 5 type of shock?
• PCWP 5 • Which 3 types of shock can this be?
• SVR 537

Clue #6
• Heart rate has been 40‐
60 (sinus brady)
• “Dead” giveaway?
SO…….
WHO DONE IT?


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