Shock, circulatory

1
The origin of the term shock is generally
credited to the French surgeon Henri Francois Le
Dran, who in 1737 defined the same as A treatise
of reflections drawn from experience with gunshot
wounds and coined the term choc to indicate a
severe impact or jolt. An inappropriate
translation by the English physician Clare, in
1743, led to the introduction of the word shock
to the English language to indicate the sudden
deterioration of a patients condition when major
trauma has occurred. It was Edwin A. Moses, who
began to popularize the term, using it in his
article A practical treatise on shock after
operations and injuries
2
Shock, circulatory

• DESCRIPTION Inadequate perfusion (oxygen supply)
  of tissues which results in organ dysfunction,
  cellular and organ damage and, if not corrected
  quickly, death of the patient.

3
The problem shock

• Altered circulatory parameters
• Compromised microcirculation
• Persistent severe hypoxia
• Multiple organ failure

4
Main types

• Vasoconstrictive
• Trauma, bleeding, burning, ileus (volumen loss)
• Pulmonary embolism (impaired cardiac filling)
• Myocardial infarction (impaired cardiac
  contraction)
• Vasodilatative
• Anaphylaxis, sepsis (maldistribution of blood
  flow)
• Spinal medullary injury (venous pooling)
• Hypothermia

5
Comparison of types of shock(Early stage)
Malperfusion and organ dysfunction are the
ultimate end point of any shock stage
6
Decreased cardiac output
Decreased venous return
Decreased myocardial function
Decreased coronary perfusion
Decreased myocardial contraction
Decreased blood pressure
Inracellular fluid loss
BP CO x SVR
Metabolic acidosis
Cell hypoxia
Decreased tissue perfusion
Microcirculatory obstruction
Microcirculatory demage
Cellular aggregation
7
Classification (based on cardiovascular
characteristics, which was initially proposed in
1972 by Hinshaw and Cox)

• Hypovolaemic
• Hemorrhagic, Fluid depletion, Increased vascular
  capacitance
• Cardiogenic
• Myopathic, Mechanical, Arrhythmic
• Distributiv
• Septic, etc.
• Obstructiv
• PE, pericarditis, pnumothorax etc.

8
Hypovolemic Shock

• loss in circulatory volume
• Decreased venous return
• Decreased filling of the cardiac chambers
• Decreased cardiac output
• increase in the systemic vascular resistance
  (SVR).

low central venous pressure (CVP), a low
pulmonary capillary wedge pressure (PCWP), low
cardiac output (CO) and cardiac index (CI), and
high SVR. The arterial blood pressure may be
normal or low.
9
HYPOVOLEMIC (oligemic) SHOCK

• Hemorrhagic
• - Trauma
• - Gastrointestinal
• - Retroperitoneal
• Fluid depletion (nonhemorrhagic)
• External fluid loss
• Dehydration
• Vomiting
• Diarrhea
• Polyuria

• Interstitial fluid redistribution
• Thermal injury
• Trauma
• Anaphylaxis
• Increased vascular capacitance (venodilatation)
• - Sepsis
• - Anaphylaxis
• - Toxins/Drugs

10
Cardiogenic Shock

• dependent on poor pump function
• acute catastrophic failure of left ventricular
  pump function

high PCWP, low CO and CI, and generally a high
SVR
11
CARDIOGENIC

• Myopathic
• -Myocardial infarction (Left ventricle, Right
  ventricle)
• -Myocardial contusion (trauma)
• -Myocarditis
• -Cardiomyopathy
• -Post ischemic myocardial stunning
• -Septic myocardial depression
• -Pharmacologic Anthracycline cardiotoxicity
  Calcium channel blockers

• Mechanical
• -Valvular failure Regurgitant Obstructive
• -Hypertropic cardiomyopathy
• -Ventricular septal defect
• Arrhythmic
• -Bradycardia Sinus (e.g.,vagal syncope)Atrioventri
  cular blocks
• -Tachycardia SupraventricularVentricular

12
Distributive or Vasogenic shock

• Poor vascular tone in the peripheral circulation
• maldistribution of blood flow to organs within
  the body also

CO varies, but is usually raised. A common
haemodynamic profile is a low or normal PCWP, a
high CO, a low arterial blood pressure, and low
SVR
13
DISTRIBUTIVE

• Septic (bacterial, fungal, viral, rickettsial)
• Toxic shock syndrome
• Anaphylactic, anaphylactoid
• Neurogenic (spinal shock)
• Endocrinologic
• Adrenal crisis
• Toxic (e.g., nitroprusside, bretyllium)

14
Extracardiac obstructive shock Impaired
diastolic filling (decreased ventricular preload)

• a physical impairment to adequate forward
  circulatory flow involving mechanisms (different
  than primary myocardial or valvular dysfunction)
• Frank decrease in filling pressures (as in
  mediastinal compressions of great veins) or
• trends towards equalization of pressures in the
  case of cardiac tamponade or
• markedly increased right ventricular filling
  pressures

High CVP, low PCWP Cardiac output is usually
decreased with increased SVR.
15
EXTRACARDIAC OBSTRUCTIVE Impaired diastolic
filling (decreased ventricular preload)

• Direct venous obstruction (vena cava)
• Intrathoracic obstructive tumors
• Increased intrathoracic pressure
• Tension pneumothorax
• Mechanical ventilation (with positive
  end-expiratory pressurePEEP, autoPEEP or volume
  depletion)
• Asthma (with auto PEEP

• Decreased cardiac compliance
• Constrictive pericarditis
• Cardiac tamponade
• Acute Post-MI free wall rupture
• Traumatic
• Hemorrhagic
• Chronic Malignant
• Uremic
• Idiopathic

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Symptoms

• Narrowing of pulse pressure
• Tachycardia, hypotension
• Restlessnes
• Disphoria
• Decreased urine output
• Anxiety
• Cool, clammy skin
• Obtundation
• Dyspnoe
• Unconsciousness

17
The compensatory phase of the shock

• Maintenance of mean circulatory pressure
• Maximizing cardiac function
• Redistributing perfusion to vital organs
• Optimizing unloading of oxygen at tissues

18
Maintan Volume

• -Fluid redistribution to vascular space
• From interstitium (Starling effect)
• From intracellular space (Osmotic effect)
• -Decreased renal fluid losses
• Decreased glomerular filtration rate (GFR)
  Increased aldosterone
• Increased vasopressin

19
Mintain Pressure

• Decreased venous capacitance
• Increased sympathetic activity
• Increased circulating (adrenal) epinephrine
• Increased angiotensin
• Increased vasopressin

20
Maximize Cardiac Performance

• Increased contractility
• Sympathetic stimulation
• Adrenal stimulation

21
Redistribution of Perfusion

• Extrinsic regulation of systemic arterial tone
• Dominant autoregulation of vital organs (heart,
  brain)

22
Optimize Oxygen Unloading

• Increased RBC 2, 3 DPG-
• Tissue acidosis
• Pyrexia
• Decreased tissue PO2

23

• (precapillary vasoconstriction)
• (postcapillary vasoconstrction)
• (vasoparalysis)

Treatable
24
Treatment of shock

• Positioning, avoiding hypothermia
• Maintaining adequate oxygenisation
• Fluid resuscitation
• Pain relief ?
• Causal therapy?
• (inotropic treatment?)

25
Early mechanical ventillation

• allows blood flow to be redistributed
• tends to reverse lactic acidosis
• supports the patient until other therapeutic
  measurescan be effective

Tidal volumes in the order of 7-10 mlkg-1 of lean
body mass, an O2 concentration that results in
arterial saturation not less than 92, adequate
ventilator rate and sedation to minimize the work
of breathing.
26
Fluid resuscitation

• Iv line
• Large bore cannula
• More iv line
• Choice of infusion
• Lactated Ringer's solution (initial bolus 10-25
  ml/kg / 10 min.)
• Colloids
• Dextrane
• Hydroethylstrach
• Gelatine
• Small volume resuscitation
• Rate, amount
• General conditions
• parameters ( BP, Pulse, CVP, SatO2 etc)

27
Dextrane

• Molecular weight 40K - 60/70K Dalton
• Concentration 10 (40K) 6 (60/70K)
• Water binding 25 ml/g -- 4 - 6 h
• Plasma expanding effect 180-200 150
• Elimination
• metabolic
• kidney

28
Hydroxyethylstrach

• Molecular weight 450K - 200K - 40K Dalton
• Substitution 0,5 - 0,62 - 0,7
• Water binding 15 - 20 ml/g -- 3 - 6 h
• 6 HES (200K/0,5) -- plasma substitution (100)
• 10HES (200K/0,5) -- plasma expanding (140)
• Elimination
• kidney
• 12 - 24 h (65 - 70 ) --- 168 h

29
Small volume resuscitation
10 HES 200K/0.5 or 10 Dextran 60 and 7.2
NaCl COP70-75 mmHg
Max. vol. eff given vol. x 6 // max. time 30
min
30
Inotropic drugs