Evaluation of Shock in Adults

1
Evaluation of Shock in Adults

• Charles B. Lehman, MD
• University Medical Center
• Hospitalist Service

2
Hemodynamic profilesof the shock states
3
Introduction

• Definition a physiologic state caused by
  inadequate tissue perfusion leading to decreased
  tissue oxygen delivery.

4
Introduction

• Effects are initally reversible, but lead to
  cellular hypoxia which can cause
• Cell membrane and ion pump dysfuction
• Intracelluar edema
• Leakage of intracellular contents into the
  extracelluar space
• Inadequate regulation of intracelluar pH

5
Introduction

• Effects rapidly become irreversible and lead to
  cell death, end-organ damage, multi-system organ
  failure and finally death.
• Prompt recognition of symptoms is the key to
  treatment.

6
Introduction

• Despite extensive research, mortality rates
  remain high
• Septic 35-40
• Cardiogenic 60-90
• Hypovolemic variable, depends on etiology and
  time to treatment

7
Stages

• Pre-shock
• Shock
• End-organ dysfunction

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Stages Pre-shock

• Warm or compensated shock
• Regulatory mechanisms are able to compensate for
  diminished perfusion.

9
Stages pre-shock

• Low-preload
• Tachycardia
• Peripheral vasoconstriction
• Decrease in blood pressure
• Low-afterload
• Peripheral vasodilation
• Hyperdynamic state

10
Stages shock

• Compensatory mechanisms become overwhelmed,
  resulting in
• Tachycardia
• Tachypnea
• Metabolic acidosis
• Oilguria
• Cool, clammy skin

11
Stages shock

• Usually occur with
• Loss of 20-25 of effective blood volume
• Fall in cardiac index to 2.5 L/min/M2
• Activation of mediators of the sepsis syndrome

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Sepsis end-organ dysfunction

• Decreasing urine output
• Restlessness leading to agitation, obtundation
  and coma
• Mutiple organ system failure which leads to death

13
Physiologic determinants

• Systemic Vascular Resistance (SVR)
• Vessel length
• Blood viscosity
• Vessel diameter

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Physiologic determinants

• Cardiac Output (CO) heart rate x stroke volume
• Stroke volume depends on preload, myocardial
  contractility and afterload

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Physiologic Determinants

• SVR and CO can be used to differentiate between
  forms of shock

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Classification

• Hypovolemic
• Cardiogenic
• Distributive

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Hypovolemic shock

• Result of decreased preload
• CO HR x SV, and SV depends on preload
• Decrease in preload therefore leads to decrease
  in CO

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Hypovolemic shock

• Hemorrhage
• Trauma
• GI bleeding
• Ruptured aneurysm or hematoma
• Hemorrhagic pancreatitis
• Fractures

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Hypovolemic shock

• Fluid loss
• Diarrhea
• Vomiting
• Heat stroke
• Inadequate repletion of insensible losses
• Burns
• Third spacing (intestinal obstruction,
  pancreatitis, cirrhosis)

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Cardiogenic shock

• Results from pump failure and decreased cardiac
  output
• Main categories
• Myopathies
• Arrythimia
• Mechanical
• Extracardiac/obstructive

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Cardiogenic shock

• Cardiomyopathies
• Infarction involving 40 of the LV
• RV infarction
• Dilated cardiomyopathies
• Stunned myocardium following prolonged ischemia
  or cardiopulmonary bypass
• Myocardial depression in advanced septic shock

22
Cardiogenic shock

• Arrythmia
• Loss of syncrhonized filling between the atria
  and ventricles with atrial fibrillation
• Complete loss of CO with ventricular fibrillation
• Decrease in heartrate with bradyarrythmias and
  heart block leads to decrease in CO

23
Cardiogenic shock

• Mechaincal
• Mitral regurgitation from chordae tendineae
• Aortic insufficiency due to dissection of
  ascending aorta into the aortic valve ring
• Critical aortic stenosis
• VSD
• Atrial myxoma

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Cardiogenic shock

• Obstructive
• Pulmonary embolism
• Tension pneumothorax
• Constrictive pericarditis
• Pericardial tamponade
• Severe pulmonary hypertension
• These can also present as hypovolemic shock if
  the primary disturbance creates decreased preload

25
Distributive shock

• Causes
• Sepsis
• Activation of systemic inflammatory response
  system (pancreatitis, burns, multiple trauma
• Anaphylaxis
• Drug or toxin reactions (insect bites,
  transfusion reactions, heavy metal poisoning)

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Heavy metal poisoning
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Distributive shock

• Causes
• Addisonian crisis
• Myxedema coma
• Neurogenic shock due to CNS or cord trauma
• MI with systemic inflammatory state
• Cardiopulmonary bypass

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Common features

• Hypotension
• SBP
• Occurs in most shock patients
• Initially will be relative to patients baseline
  blood pressure
• Drop in SBP 40 can be an early indicator
• Progresses to profound hypotension, often
  requiring vasopressors

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Common features

• Cool, clammy skin
• Regulatory processes compensating for decreased
  effective tissue perfusion
• Bloodflow redirected to vital organs to maintain
  coronary, cerebral and splanchnic perfusion
• Lack of peripheral flow leads to classic cool,
  clammy picture of shock

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Common features

• Oliguria
• Result of shunting of renal bloodflow to other
  vital organs
• Objective measure of intravascular volume
  depletion
• Related signs tachycardia, orthostatic
  hypotension, poor skin turgor, absent axillary
  sweat, dry mucous membranes

31
Common features

• Mental status changes
• Begins with agitation
• Progresses to confusion/delirium
• Ends in obtundation/coma

32
Common features

• Metabolic acidosis
• May initally have a respiratory alkalosis
• Acidosis will eventually prevail
• Related to accumulation of lactate due to lack of
  clearance by liver, kidneys and skeletal muscle
• Increased anaerobic metabolism due to tissue
  hypoxia contributes in later stages

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Initial approach

• History
• Food/medicine allergies
• Recent medication changes
• Potential acute/chronic drug intoxication
• Preexisting diseases
• Immunosupression
• Hypercoagulable states

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Initial approach

• Physical exam HEENT
• Scleral icterus
• Dry conjunctivae
• Dry mucous membranes
• Pinpoint pupils
• Fixed/dilated pupils
• Nystagmus

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Initial approach

• Physical exam Neck
• JVD
• Delayed carotid upstroke
• Carotid bruits
• Meningeal signs

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Initial approach

• Physical exam lungs
• Tachypnea
• Shallow respirations
• Crackles/rales
• Consolidation
• Egophony
• Absent breath sounds

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Initial approach

• Physical exam cardiovascular
• Arrythmia
• Murmurs or S3 gallop
• Diffuse PMI
• Right or left ventricular heave
• Distant heart sounds
• Rub
• Pulsus paradoxus

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Initial approach

• Physical exam Abdomen
• Tenseness
• Distension
• Tenderness
• Rebound/guarding
• Absent bowel sounds
• Pulsitile masses
• Ascites

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Initial approach

• Physical exam rectal
• Decreased tone
• Blood (hematochezia or melena)

40
Initial approach

• Physical exam extremities
• Calf swelling/palpable cords
• Unequal pulses
• Disparity of blood pressure between upper
  extremities

41
Initial approach

• Physical exam neurologic
• Agitation
• Confusion
• Delirium
• Obtundation
• Coma

42
Initial approach

• Physical exam skin
• Cold, clammy
• Warm, hyperemic
• Rashes
• Petechiae
• Urticara
• Cellulitis

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Initial approach

• Lab evaluation
• CBC with differential
• Basic chemistries
• Liver function tests
• Amylase/lipase
• Fibrinogen and fibrin split products
• Lactate
• Cardiac enzymes

44
Initial approach

• Lab evaluation
• ABGs
• Toxicology screen
• Chest x-ray
• Abdominal x-ray
• Echocardiogram
• Urinalysis

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Pulmonary arterycatheterization

• Can be used to provide hemodynamic measurements
  such as
• Cardiac output
• Pulmonary artery wedge pressure
• SVR
• Helpful in determining a cause when the
  differential is broad

46
Pulmonary arterycatheterization

• Can also help with
• Monitoring fluid resuscitation
• Titration of vasopressors
• Measuring effects of changes in ventilator
  settings (PEEP) on hemodynamics

47
Pulmonary arterycatheterization

• PA catheters are associated with significant
  clinical risks and have never been proven to
  improve clinical outcomes

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Hemodynamic profilesof the shock states
49
Hemodynamic profilesof the shock states
50
Treatment of Shock in Adults

• Charles B. Lehman, MD
• University Medical Center
• Hospitalist Service

51
Ultimate cure for sepsis

• Chuck Norris tears cure sepsis.
• Too bad hes never cried.
• Ever.

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Therapeutic priorities

• Supportive measures to treat hypoxemia,
  hypotension and impaired tissue oxygenation
• Distinguish between sepsis and SIRS (systemic
  inflammatory response syndrome) so
  medical/surgical treatment of the source of
  infection can be started
• Assess for adequate tissue perfusion

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Initial management

• Resuscitation
• Assess airway, respiration and perfusion
• Supplemental O2 should be given to all patients
• Intubation often required to protect airway
• Mechanical ventilation often needed due to
  development of lung injury or ARDS

54
Initial management

• Monitoring of tissue perfusion
• Hypotension is typically present
• Prompt volume resuscitation and restoration of
  perfusion pressure can limit end organ damage
• Consider arterial catheterization if restoration
  of perfusion pressure is expected to be a
  protracted process

55
Initial management

• Signs of inadequate organ perfusion
• Cool, vasoconstricted skin due to redirection of
  bloodflow to vital organs
• Obtundation/restlessness
• Oliguria/anuria
• Lactic acidosis

56
Initial management

• Restoration of tissue perfusion
• CVP 8 - 12
• MAP 65
• Urine output 0.5 ml/kg/hr
• Mixed venous O2 70
• Can use IV fluids, PRBCs and pressors to achieve
  these goals depending on patients intravascular
  volume, cardiac status and severity of shock

57
Initial management

• IV fluids
• Rapid, large volume infusions are usually
  indicated
• CHF is the primary contraindication
• Relative hypovolemia is often severe
• Not unusual for a patient to require 10 liters
  within the first 24 hours

58
Initial management

• IV fluids
• Should be given in well-defined, rapidly infused
  boluses
• Assess volume status, tissue perfusion, blood
  pressure, and for pulmonary edema before/after
  each bolus
• Colloids have not been proven to have any
  advantage over crystalloids

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Initial management

• May repeat IV fluid boluses until
• Blood pressure, tissue perfusion and oxygen
  delivery are acceptable
• PAWP 18
• Development of pulmonary edema
• Note that septic patients can develop pulmonary
  edema with relatively normal wedge pressures

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Initial management

• IV fluids how much?
• Central venous catheters can be used to monitor
  central venous pressures
• Can also be used to estimate mixed venous oxygen
  content

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Initial management

• Vasopressors
• Second-line agents
• Useful in patients who fail to reach adequate
  blood pressures despite adequate volume
  resuscitation
• Also useful in patients who develop cardiogenic
  pulmonary edema

62
Initial management

• Vasopressors
• Dopamine and levophed recommended and
  first-choice drugs
• Phenylephrine (pure a-adrenergic) can be useful
  when tachycardia or arrythmia due to b-adrenergic
  activity becomes problematic
• Vasopressin can be used in patients refractory to
  first-choice agents

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Properties of Vasopressors
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Monitoring response to therapy

• All patients require close monitoring
• Evidence of deterioration merits a prompt,
  thorough reevaluation

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Monitoring response to therapy

• Monitoring parameters
• Respiratory PaO2/FiO2 ratio
• Renal urine output, creatinine
• Hematologic platelet counts
• CNS Glascow coma scale
• Hepatobiliary bilirubin, LFTs
• CV blood pressure, arterial lactate
• GI ileus, blood in NG aspirate

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Monitoring response to therapy

• Ebb phase
• Restore arterial perfusion pressures to
  pre-sepsis levels
• Flow phase
• Maintain oxygen delivery to meet ongoing tissue
  needs

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Monitoring response to therapy

• Detection of tissue hypoxia
• Arterial lactate concentration is the most useful
  measure of tissue perfusion
• Limited in that it is a global measure and can
  miss significant injury to a specific organ
  system

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Monitoring response to therapy

• Treatment of tissue hypoxia
• Study compared standard treatment (MAP65, CVP8,
  urine output0.5 ml/kg/hr) to maintaining central
  venous O2 saturation 70

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Monitoring response to therapy

• Results
• Decreased in-hospital mortality (30 vs. 46)
• Lower arterial lactate concentration following 6
  hours of therapy
• Lower APACHE II and SAPS II scores
• Decreased evidence of multiple organ dysfunction

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Monitoring response to therapy

• Red blood cell transfusions were used
  aggressively in this study to maintain DO2 (70
  in study arm vs. 45 in control arm)
• Recommend maintaining Hct 30 to maintain
  adequate tissue oxygen delivery

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Monitoring response to therapy

• If arterial lactate concentrations fail to fall
  with adequate transfusion, cardiac output must be
  increased
• Further IV fluid therapy can be given
• Dobutamine can be given when arterial pressures
  are adequate to tolerate vasodepression
  (phenylephrine/norepineprhine can be added if
  needed)

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Control of septic focus

• Prompt identification and treatment of infectious
  source are critical
• Previously mentioned treatments are supportive
  only

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Control of septic focus

• Identification of septic focus
• Blood cultures (2 sets, aerobic and anaerobic)
• Urine Gram stain and culture
• Sputum in a patient with productive cough
• Intra-abdominal collection in post-operative
  patients

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Control of septic focus

• Investigational methods
• TREM-1 (triggering receptor expressed on myeloid
  cells)
• Elevated serum procalcitonin

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Control of septic focus

• Eradication of infection
• Potentially infected foreign bodies (vascular
  access devices)
• Percutaneous or surgical drainage of abscesses
• Soft-tissue debridement or amputation if necessary

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Control of septic focus

• Antimicrobial regimen
• Should be started promptly after cultures have
  been obtained
• Inappropriate antibiotic selection is
  surprisingly common and has been shown to
  increase mortality
• Time to initiation of treatment has been shown to
  be the strongest predictor of mortality

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Control of septic focus

• If pseudomonas is not likely, vancomycin and
• 3rd/4th generation cephalosporin
• b-lactam/b-lactamase inhibitor
• Carbapenem

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Control of septic focus

• If pseudomonas is likely, vancomycin and 2 of the
  following
• Antipseudomonal cephalosporin
• Antipseudomonal penicillin/b-lactamase inhibitor
• Antipseudomonal carbepenem
• Floroquinolone with good antipseudomonal activity
• Aminolgycoside

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Recombinant HumanActivated Protein C (Xigris)

• Coagulation abnormalities are common in septic
  shock
• Several reports have suggested that protein C
  supplementation may produce clinical benefit,
  epecially in setting of purpura fulminans

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Recombinant HumanActivated Protein C (Xigris)

• PROWESS trial
• Lower 28-day mortality rate (24.7 vs. 30.8)
• Non-significant increase in serious bleeding
• Was of greater benefit in the most acutely ill
  patients (APACHE II 25)

81
Recombinant HumanActivated Protein C (Xigris)

• PROWESS trial limitations
• Excluded patients with chronic renal failure
• Patients with metastatic cancer, pancreatitis and
  organ transplant recipients were excluded after
  720 patients were enrolled
• Cell line used to produce drug was changed during
  the trial

82
Recombinant HumanActivated Protein C (Xigris)

• ENHANCE trial
• Similar 28-day all-cause mortality rates
• Increase in incidence of serious bleeding
  (specifically intracranial hemorrhage) was
  significant
• Treatment within 24 hours of first sepsis-related
  organ dysfunction showed significantly lower
  mortality than those treated after 24 hours

83
Recombinant HumanActivated Protein C (Xigris)

• ADDRESS trial
• Patients with APACHE II scores
• Designed to enroll 11,000 patients
• Stopped after 2,600 patients were enrolled
  because it was unlikely to show any benefit

84
Nutrition

• Essential for optimal immune function
• Beneficial in both treatment of and prevention of
  sepsis
• Early enteral nutrition probably offers more
  benefit that parenteral nutrition
• Results in higher neutrophil counts and higher
  albumin levels

85
Glucose control

• Critically ill patients can develop hyperglycemia
  and insulin resistance regardless of a history of
  diabetes
• Several papers have shown improvement in outcome
  with aggressive glucose control

86
Summary

• Initial management secure airway and correct
  hypoxemia. Intubation and mechanical intubation
  are often necessary

87
Summary

• Prompt restoration of tissue perfusion using IV
  fluids, vasopressors, oxygen, PRBCs and
  inotropes
• CVP 8-12
• MAP 65
• Urine output 0.5 ml/kg/hr
• Central venous or mixed venous O2 sat 70

88
Summary

• IV fluids are first-line treatment
• Repeat until BP and perfusion are acceptable,
  patient develops pulmonary edema or PAWP 18
• Assess patient before and after each bolus
• No data to demonstrate using colloids over
  crystalloids

89
Summary

• Vasopressors recommended for patients who remain
  hypotensive after adequate volume replacement
• Dopamine and norepineprhine are preferred agents

90
Summary

• If patient has evidence of ongoing tissue hypoxia
  (increased arterial lactate) despite restoration
  of intravascular volume and perfusion pressure,
  transfusion and inotropes can be used to increase
  oxygen delivery

91
Summary

• Prompt identification of the source of infection
  is essential
• Sputum and urine for Gram stain
• Intra-abdominal fluid should be percutaneously
  sampled
• Blood from 3 distinct sites and from indwelling
  catheters cultured aerobically and anaerobically

92
Summary

• Prompt administration of appropriate antibiotics
  after cultures have been obtained
• Potentially infected vascular devices should be
  removed, abcesses should be drained, and soft
  tissue infections must be debrided or amputated

93
Summary

• Xigris can be administered to patients with
  severe sepsis and a high-risk of death (APACHE II
  25), but has not been shown to be of benefit in
  lower risk patients or in children

94
Summary

• Glucose should be aggressively (goal 80-110)
• Nutritional support can improve outcomes, and an
  enteral route is favored over parenteral

95
GI bleed case study

• 51 year-old white male transferred to University
  Medical Center for severe GI bleeding
• Required total of 18 units of PRBCs in first 3
  days after admission, then continued to require 2
  4 units per day to maintain adequate Hb/Hct

96
GI bleed case study

• EGD extensive ulcerations extending from
  mid-palate to duodenum
• Colonscopy extensive ulcerations from the rectum
  to the terminal ileum with active bleeding noted
  at many sites
• Bleeding scan suggested small bowel involvement
  as well

97
GI bleed case study

• Biopsies obtained from the EGD were consistent
  with Crohns disease
• Attempts to treat with steroid enemas and
  systemic steroids were only partially effective.

98
GI bleed case study

• Case was presented on GI/surgical conference
  rounds.
• They decided that further medical treatment was
  futile, and that a definitive surgical approach
  would be required

99
GI bleed case study

• The patient became the first person in the world
  to undergo an oro-pharyngeo-esophago-gastro-duoden
  o-jejuno-ileo-colectomy with oro-anal anastomosis.

100
GI bleed case study

• Thank God!
• My Crohns disease is
• finally completely
• cured!