The Evaluation and Management of Shock

Alberto Nunez, MD

Hahnemann University Hospital

Department of Trauma

Shock

Shock

• Definition:

Shock is a state of inadequate organ perfusion, which results in an imbalance of tissue oxygen delivery to meet the metabolic demands of tissue

Shock

• Can there be shock without hypotension?

- SBP does not decrease to less than 90mmHg until base deficit is worse than

-20.

- At this point mortality approaches 65%

(Parks JK et al, Am J Surg 2006)

Shock

Shock

• Diagnosis: CLINICAL

Look for signs of hypoperfusion:

1. Altered level of consciousness

2. Decreased urine output

3. Mottled skin

4. Hemodynamic instability

Shock

• Management:

Pathophysiology:

1. Hemodynamic component: initial resuscitation

2. Inflammatory component: leads to multiple system organ failure (MSOF)

ShockManagement

Hemorrhagic Shock Phases of Hypovolemic shock: Phase I: hypovolemia vasoconstriction Impaired organ perfusion Increasing acidemiaPhase II: intracellular and interstitial fluid Respiratory failure Abdominal compartment syndromePhase III: diuresis

Shock

• Management:

GOAL

To restore tissue perfusion in a timely fashion in order to prevent the systemic inflammatory response that would eventually lead to MSOF

Shock

• Classification:

1. Hypovolemic

2. Vasodilatory

3. Cardiogenic

Shock

• Pathophysiology:

1. Hypovolemic/Vasodilatory:

Inadequate venous return to the heart:

1. Hemorrhage

2. Dehydration

3. Widespread vasoplegia: neurogenic

4. Loss of vascular tone: sepsis, anaphylaxis, ischemia-reperfusion syndrome

Shock

• Pathophysiology:

2. Cardiogenic:

Pump failure:

1. Loss of contractility: MI and its complications

2. Impaired diastolic filling: cardiac tamponade

3. Abnormal rate or rhythm

4. Obstruction to flow: valvular conditions, pulmonary embolus

Shock

• Hypovolemic:

1. JVP is low

2. Poor capillary refill

3. Narrow pulse pressure

4. Evidence of bleeding or dehydration

Shock

• Cardiogenic:

1. Narrow pulse pressure

2. Evidence of pulmonary edema

3. Gallop

4. Chest pain, EKG changes, abnormal cardiac enzymes, abnormal echocardiogram

Shock

• Vasodilatory:1. Hyperemic extremities2. Bounding pulses, wide pulse pressure3. Brisk capillary refill4. Hyperdynamic heart sounds5. Occurs in the setting of sepsis,

anaphylaxis, burns, cyanide and CO poisoning, pancreatitis, ischemia-reperfusion injury

ShockAssessment

Primary Survey Airway and Breathing

• Decision to intubate and initiate ventilatory support should be made on clinical basis

• Recognize signs of early respiratory failure: Inability to speak Diaphoresis Labored breathing Cyanosis Tachypnea Mental obtundation Paradoxical breathing Accessory muscle use

ShockAssessment

Primary Survey Airway and Breathing

• Intubate EARLY• Intubate before procedures or transporting patient• Remember: multiple organ hypoperfusion (the definition

of shock) is an indication for intubation and mechanical ventilation

ShockAssessment

Primary Survey Circulation

• Elaborate working diagnosis: hypovolemia vs. vasodilatation vs. pump failure

• Early empiric volume loading:

Children: 20ml/kg

Adults: 2000ml crystalloids• Establish endpoints of resuscitation

ShockManagement

Endpoints of Resuscitation

“To provide the metabolic substrates, i.e., oxygen, to meet the consumptive demands of the tissues”

The point at which these consumptive demands are met is called the Critical Oxygen Delivery (Critical DO2)

ShockManagement

Endpoints of Resuscitation

ShockManagement

Endpoints of ResuscitationSystemic Oxygen delivery (DO2):

DO2 = CO x CaO2

CaO2 = Hb x O2 Sat x 1.39 + (0.003 PaO2)

1. Oxygen Saturation: FiO2, PEEP

2. Hemoglobin concentration: PRBC

3. Cardiac output: Starling curve

ShockManagement

ShockManagement

Endpoints of Resuscitation

Cardiac output:

Blood pressure: ≥ 90mmHg?

Heart rate: 60 to 100bpm

Urine output: ≥ 0.5ml/kg/hr

CVP: 8-15mmHg

ShockManagement

Endpoints of ResuscitationOther:• Lactate level, base deficit• Pulmonary artery capillary wedge pressure

(PCWP)• SvO2

• Right ventricular end diastolic volume index (RVEDVI)

• Left ventricular end diastolic area (LVEDA)

ShockManagement

GOALS 1. DO2 of 500 to 600ml/min/m² 2. Re-establish perfusion early (within 6 h of

injury) 3. Avoid the “bloody vicious cycle/lethal triad” 4. Avoid abdominal compartment syndrome 5. Avoid secondary brain insult in patients with

TBI 6. Minimize the dysfunctional inflammatory

response leading to MSOF

ShockManagement

Goal-directed therapy. Why?• Kern and Shoemaker: Goals: Increased CI and DO2

PACWP ≤ 18mmHG

Results: 23% absolute risk reduction in mortality• Rivers et al:

Goals: CVP 8-12mmHg

MAP ≥ 65mmHg

SvO2 ≥ 70%

Results: Hospital mortality: 30.5% vs. 46.5% (p=0.009)

28 day mortality: 33.3% vs. 49.2% (p=0.01)

ShockManagement

Goal-directed therapy…but

Goals must be achieved EARLY!

How early? Within the initial 6 hours

Why? After onset of organ failure no amount of extra oxygen will restore irreversible oxygen debt or reverse cellular death

ShockManagement

Hemorrhagic Shock Stop the Bleeding!Uncontrolled hemorrhage is responsible for

over 40% of trauma deaths

Injury to the central nervous system: 33%

MSOF: 21%

ShockManagement

Hemorrhagic Shock

Stop the Bleeding!

• M Massive hemorrhage

• A Airway

• R Respiration

• C Circulation

• H Head injury/hypothermia

ShockManagement

• Classification of Hypovolemic Shock - Initial presentation: Class I, II, III and IV

- Response to initial fluid resuscitation: Rapid response Transient response No response

ShockManagement

Hemorrhagic Shock Delayed resuscitation/hypotensive resuscitation:• Delay resuscitation until bleeding is controlled• Resuscitate to the minimal BP required to

achieve adequate organ perfusion Improved survival in patients with penetrating

torso injury:• Increased BP can cause disruption of early

soft thrombus (“pop the clot”)• Hemodilution of clotting factors can initiate

coagulopathy

ShockManagement

Delayed/hypotensive resuscitation:• Bickel et al, 1994:

survival advantage: 70% vs. 62%, p = 0.04• Animal study meta-analysis:

reduced risk of death (RR=0.37)• Committee on Tactical Combat Casualty Care:

no fluids if palpable radial pulse and adequate mentation – First time since Crimean war that KIA rate has ↓ below 20% to around 10% to 14%

ShockManagement

Hemorrhagic Shock

Fluid resuscitation:

• 3:1 rule (8:1 in severe trauma)??

• Colloid vs. crystalloid

• NS vs. LR vs. Hypertonic saline

• Blood and coagulation factors

ShockManagement

Hemorrhagic ShockThe bloody vicious cycle/lethal triad: Dilutional coagulopathy: - 33% to 55% of major trauma patients with pre-hospital

resuscitation have an APTT > 55 secs and a PT > 18 secs

Hypothermia: - Impaired platelet aggregation - At 35˚C all factors have decreased function - In severe trauma patients (ISS>25) mortality is 100% when temp.

is < 32˚C vs. 7% when temp. is > 34˚C

Acidosis: - Coagulation factor activity is significantly reduced at pH < 7.4

ShockManagement

Hemorrhagic ShockPrevent the bloody vicious cycle:• Aim for normothermia• Damage control surgery• Consider use of blood products early: Consider PRBC when patient remains unstable after

initial resuscitation (2000ml) Consider FFP early: If > 4U PRBC given within the first hour FFP:PRBC of 1:1.8 in severe trauma patients

ShockManagement

Hemorrhagic ShockMassive transfusion: > 10 units PRBC in 24 hrs. 1 blood volume Blood loss ≥ 5000 ml > 10 units: thrombocytopenia, ↓ fibrinogen, ↑ PT > 25 units/24hrs: mortality approx. 50% Cause: massive systemic inflammatory response TNFα, IL 1, IL 6, IL 8, other pro-inflammatory lipids

ShockManagement

Cardiogenic Shock• Mortality: 50% to 80%• Initial approach should include fluid resuscitation

unless patient is in pulmonary edema• Vasoactive therapy is usually indicated• Echocardiogram early to r/o tamponade or acute

valvular dysfunction, evaluation of LVEDA• IABP should be considered• Thrombolytic therapy?• Early revascularization is beneficial in patients <

75 years (survival 51.6% vs. 33.3%)

ShockManagement

Septic Shock• Initial management requires fluid resuscitation• Vasoactive therapy is usually necessary• Definitive management requires surgical

debridement of necrotic tissue, drainage of purulent collections and antibiotic therapy

• Mortality rate has changed little over time• Duration of antimicrobial therapy: 7-10 days• Tight glucose control (80-110mg/dl) improves

survival?

ShockManagement

A word on vasoactive therapy• Adequate Cardiac Output is more important than

Blood Pressure• β agonists are used for cardiac contractility• α agonists are used for maintenance of

perfusion pressure• No randomized controlled trials • Titrate to SBP or MAP that achieves the goal of

restoring autoregulation• Confirm adequacy of CO/CI, SvO2, lactate

ShockManagement

ShockManagement

Steroids• Consider IV hydrocortisone for adult septic shock when hypotension

responds poorly to adequate fluid resuscitation and vasopressors

• Hydrocortisone is preferred to dexamethasone

• ACTH stimulation test is no longer recommended to identify the subset of adults with septic shock who should receive steroids

• Hydrocortisone dose should be ≤ 300 mg/day

• Steroid therapy may be weaned once vasopressors are no longer required

Surviving Sepsis Campaign Guidelines, Crit Care Med 2008

ShockManagement

Recombinant human activated protein C (Xigris®)• Anti-thrombotic serine protease with anti-inflammatory

properties• Associated with a reduction in the relative (19.4%) and

absolute (6.1%) risk of death in patients with organ failure due to acute infection

• Indicated in shock patients with end-organ dysfunction, acidosis, oliguria or hypoxemia

• Should be started within 24hrs. of initial organ failure• Increased risk of bleeding

ShockManagement

Use of Vasopressin (AVP) in hemorrhagic Shock• AVP decreases crystalloid requirements to

maintain target MAP (avoidance of secondary injury in TBI patients and ALI/ARDS in patients requiring massive resuscitation?)

• AVP is an alternative when response to α agonists ↓ due to down-regulation

• AVP is associated with worsening hemodynamic (↓ CI) and metabolic parameters (↑ lactate)

ShockManagement

Sodium Bicarbonate for Lactic Acidosis• Myocardial contractility ↓ with lactic acidosis?• Coagulation factor activity decreases at pH < 7.4• Correction of acidosis with sodium bicarbonate does not

improve hemodynamics or catecholamine responsiveness, even in the face of severe acidosis (pH < 7.2)

• Bicarbonate has been shown to raise PCO2 and lactic acid production. ↑ in CO2 can cause pH in intracellular spaces and CSF to drop

• Bicarbonate administration is not recommended for pH > 7.15

ShockManagement

Summary• Shock is an Emergency.• Early resuscitation is key (first 6 hours)• Continuous bedside evaluation, resuscitation

and re-evaluation are required• Initial management: intubation, ventilation and

volume support• Vasoactive therapy is started after the patient is

well volume-resuscitated

ShockManagement

Summary

• Vasoactive therapy consists of inotropic (β) support for cardiogenic shock and pressor (α) therapy for vasodilatory shock

• Early shock has a hemodynamic component (reversible)

• Late shock has an inflammatory component (not easily reversed)

ShockManagement

Summary• Success in treatment of shock: 1. Early recognition 2. Rapid resuscitation• Aim: 1. Resolution of hemodynamic component 2. Avoid “Second hit” (abdominal compartment

syndrome, intracranial hypertension) 3. Prevention/modulation of inflammatory

component

ShockManagement

Room for Improvement

• Pre-ICU resuscitation monitoring:

1. Near-infrared spectroscopy

2. Central venous Hb oxygen saturation

3. CO monitoring: Trans-thoracic electrical bioimpedance

ShockManagement

Room for Improvement

• Trauma as an immune disease:

- Neutrophil-mediated cytotoxicity

- Activation of adhesion molecules

- Fluid resuscitation and apoptosis

- Blood transfusions and immunosuppresion

ShockManagement

Room for Improvement• Fluid resuscitation: LR: pure L-isomer/ketone-pyruvate based 1. D-isomer up-regulates adhesion

molecules (selectins, integrins) 2. Facilitates neutrophil-mediated

cytotoxicity 3. Increases apoptosis (intestinal mucosa,

smooth muscle, liver, lung)

ShockManagement

Room for Improvement• Hemorrhage control: recombinant activated

Factor VII (rFVIIa)

1. Binds only to exposed subendothelial tissue factor

2. 63% reduction in need for massive transfusion

3. No systemic hypercoagulability

4. Effect on MSOF still unknown

5. Use in acidotic patient still controversial

ShockManagement

Room for Improvement

• Tourniquets?

• Freeze-dried blood and FFP

• Non-antigenic blood

ShockManagement

Room for Improvement

ShockManagement

Room for improvement• Trauma Induced Coagulopathy (TIC)

ShockManagement

Room for improvement

ShockManagement

Room for improvement Damage Control Resuscitation or Early

Hemostatic Resuscitation (EHR):• FFP:PRBC ratio of 1:1• Improves overall mortality in pts with TIC

(28.3% vs. 51.2%)• Pts given 1:3 and 1:4 ratio of FFP:PRBC

were 3.76 and 4.17 times more likely to die in the OR

(Duchesne et al, J Trauma, July 2009)

ShockManagement

Room for Improvement

• Hypotensive Resuscitation:

1. Prevents disruption of early soft thrombus

2. Prevents coagulopathy

3. Prevents hemodilution

ShockManagement

Room for Improvement

• In the absence of traumatic brain injury:

“permissive hypotension”

1. SBP > 80mmHg

2. Consciousness

3. Palpable pulse

4. Control hemorrhage first

ShockManagement

Room for Improvement Epigenetic Transcription Modulation Surviving blood loss without fluid resuscitation

- Hemorrhage causes early transcriptional repression

- ↓ transcription of immediate early response proteins

- Acetylation of histones main mechanism

- Hemorrhage associated with imbalance in HAT/HADC ratio

ShockManagement

Room for Improvement Epigenetic Transcription Modulation- HDACI ( VPA or SAHA) in shock:

up-regulates gene transcription

attenuates organ injury

improves survival

- Survival after 60% blood loss in 60 min:

25% in control group

75% in SAHA group

83% in VPA group Shults et al, J Trauma 2008

ShockManagement

Room for Improvement

Fluid resuscitation:

The best fluid for resuscitation?

Fresh Whole Blood

ShockManagement

Room for Improvement

• Fluid resuscitation: hypertonic saline dextran (HSD)

1. Small volume: avoid second hit

2. Increased perfusion of microcirculation

3. Decreases inflammatory response

4. Might increase bleeding

ShockManagement

The FutureWhat fluids? 1. 5% HTS or HSD, two 250mL boluses. 2. If further volume is needed: L-isomer LR 3. In the hypotensive, bleeding patient: Start blood early FFP:PRBC:Plts ratio 1:1:1 If fresh whole blood is available: use it!

Shock