Download Shock - cardio

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
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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
Heart rate 
Blood pressure 
Pulse pressure 
Arterial pH 
Respiratory rate 
Mentation change
Shock
Urine output 
- Neonate < 2 ml/kg/hour
- Infant < 1,5 ml
- Pre school age < 1 ml
- Adult < 0,5 ml
Peripheral perfusion
- cold, pale , clammy
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?
Is CO reduced?
Pulse pressure
Diastolic pressure
Peripheral perfusion
Capillary refill time
Heart sounds
Temperature
White cell count
Site of infection
High-output hypotension
(CO )
Septic shock
Low-cardiac-output
(CO )
Cardiogenic &
Hypovolemic
No


Warm
Rapid
Crisp
 or 
 or 
++
Yes


Cool
Slow
Muffled


-
Rapid formulation of working Dx
Is the heart too full?
Reduced pump function
Cardiogenic shock
Reduced venous return
Hypovolemic shock
Is the heart too full?
Symptoms clinical context
Yes
Angina, ECG
Jugular venous pressure
S3, S4, gallop rhythm
Respiratory crepitations
Chest radiograph

+++
+++
Large heart
 Upper lobe flow
Pulmonary edema
No
Hemorrhage, diarrhea,
burns

Normal (small)
Rapid formulation of working Dx
What does not fit?
Overlapping etiologies (septic-cardiogenic, septichypovolemic, cardiogenic-hypovolemic)
Other etiologies
High output
hypotension
High right atrial
pressure hypotension
Nonresponsive
hypovolemia
Liver failure
Severe pancreatitis
Trauma + SIRS
Thyroid storm
Arteriovenous fistula
Pulmonary
hypotension
Right ventricular
infarction
Cardiac tamponade
Adrenal insufficiency
Anaphylaxis
Neurogenic shock
Get more information
Echocardiography, CVP, Swan-ganz catheterization, etc
Shock management
• Recognize inadequate organ perfusion
• Identify the cause (working diagnosis)
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Hypovolemic
Cardiogenic
Distributive
Obstructive
• Restore the organ perfusion and tissue
oxygenation
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Oxygen and ventilatory support
Fluid therapy
Inotrope or vasoactive drugs
Treat the cause
ABC
resusitasi
Goals of Respiratory Management
• To protect the airway
• To correct inadequate oxygenation and
ventilation
• To rest the respiratory muscle
• Caution in cervical trauma!
A-B
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
Volume expansion
Heart
full
Inotrope
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
Mild
Blood loss
Moderate loss
On going losses
Severe
Blood loss
Shock
Non-hypovolemic
Maintenance
Fluid/blood
Fluid/blood
Re-evaluate
Surgical
resuscitation
Get more
information
Surgical
consultation
Surgical
consultation
No response
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
Leukocyte/platelet/RBC aggregation
Primary perpetuators
Microcirculatory flow maldistribution
Leukocyte-mediated cell injury
Cytokine and other mediator
effects, locally and systemically
Gut translocation
Sepsis
Secondary perpetuators
Tertiary perpetuators
Haldane
Hypoxia not only stops the machine
It wrecks the machine!
Time saving is life saving!
Summary
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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!