Shock

Nasman Puar, dr.SpAn

Bagian Anestesiologi
Fakultas Kedokteran Unand/
RSUP Dr. M. Djamil Padang
What is Shock?
= hypotension ?
= low blood pressure ?
= haemorrhage ?
= unconscious ?
 Shock =
• Clinical syndrome
• Associated with signs of hypoperfusion:
mental status change, oliguria, acidosis,
etc
• May be associated with hypotension
• Inadequate organ perfusion and tissue
oxygenation to meet tissue oxygen
demand
 Physiological response to
shock
• Normally the body can compensate for
some decreased tissue perfusion
through a variety of mechanisms
• When compensation fails, shock
develops and if uncorrected becomes
irreversible
 Physiological response to
shock
• Sympathetic Nervous System – Adrenal response
(neuro-humoral)
• Systemic response
– Progressive vasoconstriction
– Increased blood flow to major organs
– Increased cardiac output
– Increased respiratory rate and volume
– Decreased urine output (water retention)
– Decreased gastric activity
 Pathophysiology
• Initially, neurohumoral compensatory
mechanisms maintain perfusion to vital
organs
• If appropriate treatment is not promptly
instituted, these compensatory
mechanisms are overwhelmed,
producing ischemia, cellular damage,
multiple organ failure and death
 Shock at the cellular level
• Decreased blood flow to the tissues causes
cellular hypoxia
• Anaerobic metabolism begins
• Cell swelling, mitochondrial disruption, and
eventual cell death; tissues die; organs fail;
organ systems fail
• If Low Perfusion States persists 
compensatory response fail

Irreversible  Death imminent!!

 Normal Hemodynamic
Venous Return Cardiac Output
A V
VR CO

4800 = 60 x 80 cc
Perfusion

VR equals CO
CO = Heart Rate x Stroke Volume
SV = f . EDV. C. TPR
Reaksi kompensasi
 Pathophysiology
• Imbalance between organ perfusion &
oxygen demand
• DO2 = Oxygen content x Cardiac output
• Oxygen content depends on Hb & SaO2
• SaO2 depends on Airway & Breathing
• Cardiac Output & Hb are parts of
Circulation matters
 Volume
(preload)

SVR (afterload)
Rate
(f)
CO
Pump
(contractility)

CO = HR x SV
Preload Contractility Afterload
 Common features of shock

Mentation change
Heart rate 
Blood pressure 
Pulse pressure 
Arterial pH 
Shock

Respiratory rate  Urine output 

- Neonate < 2 ml/kg/hour Peripheral perfusion
- Infant < 1,5 ml - cold, pale , clammy
- Pre school age < 1 ml
- Adult < 0,5 ml
 Shock Categories
1. Hypovolemic : haemorrarghic,
dehydration
– Blood volume problem

2. Cardiogenic : AMI, severe dysrhytmia,

pericardial tamponade
– Blood pump and/or rate problem
 Shock Categories
3. Distributive: septic shock,
anaphylaxis, neurogenic shock
– Blood vessel problem

4. Obstructive: aortic stenosis, massive

pulmonary embolus
– Blood flow problem
 Rapid formulation of working
Dx
Defining features of shock
• Heart rate 
• Respiratory rate 
• Mentation changes
• Blood pressure 
• Urine output 
• Arterial pH 
 Rapid formulation of working Dx
• Defining features in compensatory shock
• Can be difficult to detect with subtle indicators
– Tachycardia
– Decreased skin perfusion
– Alterations in mental status
• Some condition such as medications, age,
pregnancy can hide signs and symptoms
 Rapid formulation of working Dx
Is cardiac output reduced?
High-output hypotension Low-cardiac-output
(CO ) (CO )
Septic shock Cardiogenic &
Hypovolemic

Is CO reduced? No Yes
Pulse pressure  
Diastolic pressure  
Peripheral perfusion Warm Cool
Capillary refill time Rapid Slow
Heart sounds Crisp Muffled
Temperature  or  
White cell count  or  
Site of infection ++ -
 Rapid formulation of working Dx
Is the heart too full?
Reduced pump function Reduced venous return
Cardiogenic shock Hypovolemic shock

Is the heart too full? Yes No

Symptoms clinical context Angina, ECG Hemorrhage, diarrhea,
burns
Jugular venous pressure  
S3, S4, gallop rhythm +++ -
Respiratory crepitations +++ -
Chest radiograph Large heart Normal (small)
 Upper lobe flow
Pulmonary edema
 Rapid formulation of working Dx
What does not fit?
Overlapping etiologies (septic-cardiogenic, septic-
hypovolemic, cardiogenic-hypovolemic)
Other etiologies
High output High right atrial Nonresponsive
hypotension pressure hypotension hypovolemia

Liver failure Pulmonary Adrenal insufficiency

Severe pancreatitis hypotension Anaphylaxis
Trauma + SIRS Right ventricular Neurogenic shock
Thyroid storm infarction
Arteriovenous fistula Cardiac tamponade

Get more information

Echocardiography, CVP, Swan-ganz catheterization, etc
 Shock management
• Recognize inadequate organ perfusion
• Identify the cause (working diagnosis)
– Hypovolemic
– Cardiogenic
– Distributive
– Obstructive
• Restore the organ perfusion and tissue
oxygenation
– Oxygen and ventilatory support ABC
– Fluid therapy resusitasi
– Inotrope or vasoactive drugs
– Treat the cause
 Goals of Respiratory Management
• To protect the airway
• To correct inadequate oxygenation and
ventilation
• To rest the respiratory muscle

A-B
• Caution in cervical trauma!
 Goals Therapy of Shock
• Reverse the pathophysiologic
abnormalities
• Avoid adverse consequences of excessive
therapy
• Titration: “too little vs too much”
• Test  Response

• Maintain body temperature!

C-E
 Shock management

Heart Inotrope
Volume expansion full Vasoactive drugs
 Fluid challenge
• Fluid deficit may exist in all kinds of shock
• Is the heart too full?
– No :
• Crystalloid 1 – 2 L (20 ml/kg) fast
– Not too full (cardiogenic shock without obvious
fluid overload)
• Crystalloid 250 ml in 20 minute
– Yes :
• No fluid challenge
 Fluid challenge
• Assess patient response
• Next therapeutic decision depend on patient
response
– Better : continue with fluid challenge
– Transient :
• Continue with fluid therapy
• On going losses : find and fix
– No response:
• Severe hypovolemia
– Other etiologies
 Fluid management in
traumatic/haemorrargic shock
Shock

Fluid Loading 1000-2000 ml Warm fluid!!

Good response Transient response No response

Mild Moderate loss Severe Shock

Blood loss On going losses Blood loss Non-hypovolemic

Maintenance Fluid/blood Fluid/blood Re-evaluate

Surgical Surgical Surgical Get more
consultation consultation resuscitation information
 Re-assess Organ Perfusion
Monitor
• Vital signs
• CNS state
• Peripheral perfusion
• Pulse oximetry
• Urine output
 Vasoactive & Inotropic agents
• Use after fluid resuscitation failed
(normovolemia)
– More efficacious if normovolemia
– May obscure hypovolemia

systolic 70 100 mmHg

• epinephrine • nitroglycerin (ischemia)

• norepinephrine • nitropruside
• dopamin • dopamin (shock)
• norepinephrine (+dopamin)
• dobutamin (shock -)
Vasoactive & Inotropic agents
• After fluid resuscitation !!
• Elevate MAP to 60-65 mmHg
• Watch out: Excessive vasoconstriction
 monitor lactate!
– Ischemia
– Contractility 
 Anaphylactic shock
• Severe systemic hypersensitivity reaction
• Characterized by: hypotension & airway
compromise
• Potentially life threatening
• Classic tipe I hypersensitivity reaction
(mediated by IgE)
• Watch out: mild allergic reaction may
progress to severe anaphylaxis
 Anaphylactic shock
• Inadequate perfusion of tissues through
maldistribution of blood flow
• Intravascular volume is maldistributed
because of alterations in blood vessels
• Cardiac pump & blood volume are
normal but blood is not reaching the
tissues
 Anaphylactic shock
• History & physical examination
• Clinical signs of systemic allergic: urticaria,
angioedema, abdominal pain, nausea &
vomiting, bronchospasm, rhinorrhea,
cutaneus flushing, etc
• + Hypotension & airway compromise !!
• Begin: within first hour - 8 hours after
exposure
• The faster onset, the more severe
 Anaphylactic shock
Therapy:
• ABC resuscitation first !!!
• Drug: Epinephrine
– adult: 0,3 - 0,5 mg SC or IM (1:1000)
0,1 mg IV (1:100.000)
– children: 0,01mg/kg SC or IM (1:1000)
only given after ABC resusitasion, no cardiac
arrest, in severe hypotension
may be repeated after 10 - 20 mnt.
 Anaphylactic shock
Subsequent management
• Give antihistamines ( chlorpheniramine 10-20 mg
slowly IV )
• Give corticosteroids (200mg hydrocortisone IV )
• Bronchodilators ( salbutamol 250ugIV or 2.5-5mg by
nebulizer, aminophylline 250mg up to 5mg/kg by
slow IV)
• Refer to ICU
 Old and New Paradigm of
Shock
Shock Shock
Hypoxic Cellular Priming

Ischemic Cellular Damage

Reperfusion Injury Inflammation

Organ Failure

Cellular Damage

Death
Multiple Organ Failure

Death
Trauma Hemorrhage Hypoxia

Prime insult
Cellular ischemia
Resuscitation

Reperfusion injury

Vasoconstriction
Microcirculatory thrombosis Primary perpetuators
Leukocyte/platelet/RBC aggregation

Microcirculatory flow maldistribution

Leukocyte-mediated cell injury

Cytokine and other mediator Secondary perpetuators
effects, locally and systemically

Gut translocation Tertiary perpetuators

Sepsis
 Haldane

Hypoxia not only stops the machine

It wrecks the machine!

Time saving is life saving!

 Summary
• Early recognition of shock state
• Oxygenation and ventilation
• Restore organ perfusion
• Monitor patient response
• Titrate therapy
• Prompt and appropriate action
Thank U 4 your attention!