shock states



  • The shock is a diagnostic and therapeutic emergency, very frequented, putting the vital issue prognosis and requiring care in intensive care or ICU.
  • The diagnosis of shock is clinically, and no diagnostic test should not delay treatment.
  • The etiological variability shock states explained their clinical polymorphism, their pathophysiological complexity and variability therapeutic and prognostic.
  • In this course we will review the clinical aspects, pathophysiological, etiologic and therapeutic various states of shock, and focus our approach on the doctor's specific role of primary care and emergency in the initial management of these patients.


L & rsquo; shock : is an acute circulatory insufficiency, due to an imbalance between the contributions and needs O2, not spontaneously reversible, resulting in cell acute respiratory failure by :

  • A lack of tissue perfusion causing a lack of supply of 02 (cellular hypoxia) and or
  • A lack of ATP production (energy deficiency)

Collapse : C & rsquo; is a significant and sudden drop spontaneously reversible PA (the sympathetic system is effective).

NB : isolated hypotension does not mean shock and shock does not mean hypotension !


1- The autonomic nervous system (SNA) : C & rsquo; is a reflex arc which includes the nerve pathways afferent and efferent, connecting the central nervous system organs. Noradrenergic sympathetic pathway is biased first line treatment of shock.

2- The steps of the & rsquo; tissue oxygenation :

  • 1time step Oxygenation = pulmonary venous blood and definition CaÛ2.
  • 2e step = Arterial transport of & rsquo; oxygen (TaÛ2) : It depends on the CaÛ2 & QC.
  • 3e step = Issuance of’02 tissue or tissue extract 1’02 (EXTO2).
  • 4e step = Cellular metabolism and ATP production of T.


The appearance of a shock occurs in steps :

1- The initiators mechanisms : achieving the steps of tissue oxygenation may be due to a reduced volume, to a failure of the heart pump or vascular :

Non hemorrhagic hypovolemic ↓Masse sanguine ↓RV ↓CaO2 +


hypovolemic Hemorrhagic ↓Hb
cardiogenic failure of the heart pump ↓Qc
Anaphylactic and Neurogenic Failure


Septic ↓EXTO2

2- Compensation schemes :

The reduction in blood volume causes a decrease venous return, therefore, cardiac output and blood pressure (PA). It follows a central response sympatho-- exciter with release of noradrenaline causing arteriolar vasoconstriction and venous, and a tachycardia to maintain PA. otherwise, this phase comprises a hormonal response which goes in the same direction with primarily the release of angiotensin-II positive inotropic and vasoconstrictor.

So, in conscious about, regulatory mechanisms of AP, brought into play by multiple receivers arterial and cardiac, allow the maintenance of PA and participate in a complex redistribution of regional rates favoring cerebral circulations, coronary and kidney at the expense of musculo-cutaneous and splanchnic territories. These mechanisms are put in place very quickly in seconds and are proportional to the importance of volume loss.
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The consequence of tissue hypoxia is the appearance of adaptation phenomena ⇒ compensated shock.

3- The shock decompensated :

ATP production is only possible if oxygen is Transported to cells, Extracted from the blood and used for oxidation of carbohydrates and lipids : therefore shock occurs when O2 needs are not (or poorly) insured.

Tissue hypoxia can lead to :
– Metabolic acidosis.
– Mottled with pale by intense vasoconstriction of the skin. The latter then extends to the skeletal muscles and the viscera.
– Thirst by tr ansfer interstitial fluid to vessels.
– cellular edema, membrane by charge alteration of the water passage from the interstitium to the cells -> Cell death -> multi-organ failure -> irreversible shock


• Hemodynamic consequences define two types of shock :

PA Qc IC RVS PVC reached =
PAPO reached =
hypo-kinetic shock
hyper-kinetic shock
  • Alteration of neurological function.
  • Shock lung : SDRA (respiratory distress syndrome)
  • The multiple organ dysfunction syndrome : multiorgan.


According to the new classification of shock states, based on 3 criteria, We have :

  • Hypovolemic shock (decreased blood volume): hemorrhagic hypovolemic shock and not hemorrhagic hypovolemic shock due to loss of plasma leakage.
  • Shock heart failure (decreased cardiac output) : cardiogenic shock.
  • Shock vascular failure (decrease in systemic vascular resistance or vasoplegia) : Septic shock, anaphyalctique and neurogenic.



→ Background : infection, allergy, digestive diseases and cardiovascular,…etc.

→ Clinique :

Signs related to adrenergic (nice) :

  • tachycardia.
  • Marbrures (knees, extremities), Pallor (absent in the hyperkinetic shock).
  • Pulse rapid and thready.
  • 4P AS (<90 mmHg) AP normal or early, pinch or enlarged pressure differential.
  • polypnoea (> 20 C / min).

Signs related to tissue hypoperfusion :

  • cold extremities, and cyanotic (hot and red ends in hyperkinetic shock).
  • Thirst, sweats, agitation, anguish, psychic troubles.
  • Oligoanuria.

→ Biology :

  • Lactates > 2,5 mmol/1 (unless liver failure)
  • Assessment of visceral impact : GDS = acidosis (4whew, 4HC03-), hyperkaliémie, IRA (îurée / blood creatinine), îtransaminases (=cytolyse), Tlipase (= Gastrointestinal pain), îtroponine (SCA), ÎBNP and Pro-BNP (ICG)… etc.

→ hemodynamic Exploration (PVC, CHAT, Qc, RVS): it is justified in such uncertain or complex states of shock, or to monitor the therapeutic.


Clinique Biology organ failure check
  • Pulse >150 P / min or <50 P / mn
  • P AM <50 mmHg
  • Tachypnée >30 c / mn
  • hemorrhagic syndrome
  • icterus
  • Impaired consciousness
  • Metabolic
  • Hyperkaliémie
  • social

IRA Tubular Necrosis Acute Interstitial

  • ISA : Acute adrenal insufficiency
  • Reaching secondary digestive: Ins. Acute liver, acute gastrointestinal expansion, acute ulcer, colonic necrosis, cholecystitis, pancreatitis… etc
Time elapsed before the therapeutic management


  • Assessment of blood volume :
  • Etiology
  • Elevation of the lower limbs : whether increased PA = hypovolemia.
  • PVC (Central venous pressure) and OPAP (occluded pulmonary artery pressure) : reduced if hypovolemia and increased if hypervolemia.
  • AP differential (Pinch = Hypervolemia and enlargement = Hypovolemia)
  • transthoracic Doppler echo (ONE) cardiac : collapses of the VCI = hypovolémie.
  • Flow Assessment (function) cardiac : Etiology, scan, and measuring Qc
  • Assessment of SVR :
  • Etiology.
  • skin condition (marbrures, coldness = Vasoconstriction, heat, = redness Vasodilation).
  • diuresis (oligurie = vasoconstriction).
  • PA expanded differential (vasodilatation), or pinch (vasoconstriction).
  • Calculation or measurement of SVR = (PAM – PVC) x 80 / IC = 2000

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  • Putting the patient supine and legs elevate (45°)
  • Insert IV line of large caliber device (14 or 16) and make an emergency blood test.
  • O2 probe, +/- catheterization (if unconscious subject) to quantify diuresis.
  • clinical monitoring (State of consciousness. Score de Glasgow, Pulse, PA, FR, SpO2, Coloration, Existence of sweats, diuresis, T°) and biological (especially lactate, GDS, the renal and ionic balance)


  • etiologies : dehydration, skin burns, …etc.
  • Treatment :

→ Vascular Filling Crystalloids (no albumin or hypotonic solution) : 10 ml / kg the first hour and then 5 ml / kg / 30 min (max = 30ml / kg). If & rsquo; sudden onset of dyspnea or hypoxemia (OAP), the fluid infusion volume must be reduced.
→ Monitoring of blood lactate (degree of tissue hypoxia)
→ If persistent HypoTA >>> NA 1st intension of KTC (central catheter)

C- Hypovolemic shock HAEMORRHAGIC :

→ Aetiologies :
– external bleeding : injury (arterial, venous, cutaneous, muscle)
– internal bleeding :
+ Externalized in the gut : UGD, breaking esophageal varices…etc
+ not externalized : hémothorax, haemoperitoneum, retroperitoneal hematoma… etc.

→ Treatment :
+ The HypoTA be tolerated until hemostasis : Target = NOT 80-90mmHg or 60-65mmHg WFP target =. If head injury (GCS<8): WFP must be >80mmHg.
+ vascular filling Crystalloids (no albumin or hypotonic solution) : 10 ml / kg the first hour and then 5 ml / kg / 30 min (limited to the mentioned above targets) with a maximum of 30ml / kg. If & rsquo; sudden onset of dyspnea or hypoxemia (OAP), the fluid infusion volume must be reduced.
+ Monitoring of blood lactate (degree of tissue hypoxia)
+ If persistent HypoTA "> NA 1st intension of KTC
+ Antifibrinolytic unless trauma less than 3hours.
+ Transfusion : Hb cible = 7-9 g/dl :
– Association PFC+CGR : Ratio = l / l or 1/2
– Plq cible : >50000 (>100000 if bleeding or intracranial mass).
– fibrinogen (3g pr 70kg) if rates <1,5 g/1.
– Monitoring the ionized calcium if massive transfusion.
+ If AVK : white k + CCP (prothrombin complex concentrates, still called PPSB).


  • pathophysiology : the penetration of an allergen in a previously sensitized subject, causes degranulation of mast cells and basophils PN, with histamine release responsible for intense peripheral vasodilatation with default peripheral tissue perfusion.
  • Clinique : Clinical manifestations are classified 4 increasing severity stages :

– Stade In : mucocutaneous signs widespread (Itching palmar-plantar, urticaria, exanthème, angioedema pharyngeal or laryngeal)
– Stade II : multi-organ damage with moderate mucocutaneous signs, hypotension, tachycardia and airway hyperresponsiveness.
– Stade III : achieving multi-organ threatening life : exp IDM.
– stage IV : circulatory arrest and / or respiratory.

  • Treatment : allergen administration stop, filling vascular and specific treatment depending on the clinical stage :

– Stade In : only general measures suffice.
– Stade II/III : general measures more :
+ Adrenaline : lamp = lmg diluted in 9 ml SSI 0,9%, then injection of lml = 0, l mg IVD to return the AP to normal.
+ corticosteroids : 100 at 200 mg d’HHC (hémisuccinate d&rsquo;hydrocortisone) one IVD.
+ Anti-histaminiques : relay the HHC.
– stage IV : external cardiac massage + 1 mg adrenaline repeated IVD / 3min.


  • etiologies : spinal cord trauma, irreversible coma
  • Treatment :

– vascular filling Crystalloids (no albumin or hypotonic solution) : 10 ml / kg the first hour and then 5 ml / kg / 30 min. If & rsquo; sudden onset of dyspnea or hypoxemia (OAP), the fluid infusion volume must be reduced.
– Monitoring of blood lactate (degree of tissue hypoxia)
– If persistent HypoTA "> NA Here intension on KTC


  • Definitions :

1) Sepsis :
Sepsis is defined by the presence of & rsquo; a documented or suspected infection associated with few signs of the following variables. These may be [6]:

General variables :

  • Fever (> 38,3 °C) or hypothermia (core temperature <36 °C)
  • Heart rate > 90/me.
  • Tachypnée (hyperventilation).
  • altered mental status.
  • significant edema or positive fluid balance (> 20 ml / kg over 24 hours).
  • hyperglycemia (glucose> 1,40 g/1) in the & rsquo; absence of diabetes.

inflammatory variables :

  • Leucocytose (GB> 12 000 pi’1) or Leukopenia (GB <4,000 pi’1) leukocyte count normal or more 10% immature forms.
  • CRP (Plasmatic C-reactive protein) positive.
  • Procalcitonine plasmatique positive.

hemodynamic variables : hypotension (NOT <90 mm Hg, egg P AM <70 mm Hg, or fall > 40 mm Hg in SBP in adults.

Variables dysfunction d & rsquo; organs :

  • arterial hypoxemia (Fo2 / Fio2 <300)
  • acute oliguria (urine output <0,5 ml / kg / h for at least two hours despite adequate fluid resuscitation).
  • Increased creatinine.
  • Coagulation defects (INR> 1,5 or TCA> 60 s)
  • paralytic ileus (lack of bowel sounds)
  • thrombocytopenia (platelet count <100 000 pi’1)
  • Hyperbilirubinémie (Total plasma bilirubin)

Variables tissue perfusion :

  • Hyperlactatémie (> 1 mmol / L).
  • capillary filling decrease or mottling.

2) severe sepsis :
Severe sepsis is defined as a tissue hypoperfusion induced sepsis or
malfunction & rsquo; organs (l & rsquo; one of the following seems to be due to the & rsquo; infection) :
– Hypotension induced by sepsis.
– Lactate above the upper limit of normal
– Urine flow <0,5 ml / kg / hour for more than two hours despite adequate fluid resuscitation
– acute lung injury with Pao2 / Fio2 <250 in the & rsquo; & rsquo absence; pneumonia as a source of & rsquo; infection
– acute lung injury with Pao2 / Fio2 <200 in the presence of pneumonia as a source of & rsquo; infection
– Increased creatinine.
– Hyperbilirubinémie (Total plasma bilirubin)
– The platelet count < 100 000 pi
– Coagulation defects (INR> 1,5 or TCA> 60 s)

  • Dgc : It's clinic (signs of shock + severe infection).
  • pathophysiology : Sepsis : microorganisms release products humoral response -► -► production of mediators = immuno-inflammatory response -► defense inéfîcace = loss of self-regulation mechanisms + amplification of inflammation - ► severe sepsis.
  • hemodynamic profile : it is early hyperkinetic, then it becomes hypokinetic by myocardial failure of septic origin.
  • TRT :

peripheral vein + Laboratory tests with GDS (Lactate)
O2 and Sp02 < 94% + bladder survey to estimate diuresis
infectious specimens before antibiotic : Sang (Blood cultures), urine (ECBU), LCR, Coughing, cutaneous,… etc
Administration of broad spectrum antibiotics, adapted to the original site of infection or suspected.
Early vascular filling according to the following strategy vascular filling Crystalloids (no albumin or hypotonic solution) : 10 ml / kg the first hour and then 5 ml / kg / 30 min. If & rsquo; sudden onset of dyspnea or hypoxemia (OAP), the fluid infusion volume must be reduced.
Introduction of noradrenaline (Max = 3 at 5 pg / kg / min) on a central catheter if PAD<40 mmHg : Systematics and whatever the stage of the restoration of blood volume.
adjuvant treatment : According to the recommendations of the SSC :
+ Ventilation : Oxygen if Spo2<94% by nasal tube, mask or intubation depending on the severity of respiratory failure.
+ Transfusion par CGR (Globular Red Socket) if Hemoglobin<7g/dl. The target hemoglobin is 7 at 9 g/dl.
+ glycemic control : early insulin if glycemic >1,8 g/1. The target blood sugar must be <180 mg/dl.
+ Prophylaxis of deep vein thrombosis heparin low weight moluculaire (HBPM) in the absence of thrombocytopenia.
+ Inhibitors of proton pump (IPP) : they have no indication unless risk factors (History of ulcer, …etc.)
+ enteral nutrition (intravenous)with gradual increase in caloric intake suitable for digestive tolerance.
+ HHC (Hémisuccinate d’hydrocortisone) if persistent hypotension after the 6th time.


  • Definition :

The cardiogenic shock, defined as an acute failure of the heart pump, resulting in an inability to generate sufficient blood flow, to the peripheral organs meet their metabolic needs

  • positive diagnosis :

The criteria for the diagnosis of cardiogenic shock are as follows :
– NOT< 90 mmHg 30 mining or PAM< 65 mmHg 30 min or introduction of vasopressors to achieve PAS > 90 mm Hg.
– pulmonary congestion or elevated left ventricular filling pressures.
– organ failure signs of at least one of the following criteria : altered mental state, skin cold and clammy, oligurie, increased blood lactate.

The paraclinical features : ECG, Rx thorax, A cardiaque, GDS, Lactate, troponin the, BNP, Pro-BNP, CRP, transaminases

  • etiologies :

– Abnormalities in FC : arrhythmias or conduction (FATHER, TSV,….).
– Abnormalities preload : ischemic cardiomyopathy or dilated, tamponade, PNO, IM, IAO.
– The anomalies in contractility : IDM, myocardite, toxic attack.
– Abnormalities afterload : pulmonary embolism, cardiomyopathie obstructive, HTA, RAO.

  • symptomatic TRT :

– Improved gas exchange : respiratory support (Non-invasive ventilation or mechanical) depending on the severity of respiratory Tinssufisance.
– Control of blood volume to maintain a preload to its optimum value. The volume expansion and use of diuretics can have a deleterious effect.
– Inotropes et vasopresseurs : use first intension and a central line of the association Dobutamine (inotrope et vasodilatateur) with noradrenaline (vasoconstrictor low inotropic) or Adrenaline (inotrope et vasoconstricteur) in severe forms. levosimendan (calcium stabilizer prolonging the actin-myosin interaction) can be used.
– Correcting fluid and electrolyte disorders, acid-base and thermal (Warming).

  • Trt specific depending on the etiology :

– Acute Coronary Syndrome : coronary revascularization
– acute valvular : valve replacement surgery
– tamponade : pericardial drainage
– Pulmonary embolism : Thrombolyse, embolectomie
– bradycardia : Pacemaker
– Tachyarythmie : Pharmacological cardioversion or electrical
– Sepsis : antibiotics, amines
– Aortic dissection : Getting surgical or medical treatment
– Toxic, drug : Antidotes
– Predominant right ventricular dysfunction : inotropic and vasopressor + volume expansion


  • The diagnosis of shock is based on clinical examination (the occurrence of context) and clinical examination, and not on an isolated figure PA.
  • The severity of the shock depends on the number of organ failure (consequences of cellular hypoxia).
  • The treatment of shock aims to restore good tissue perfusion for adequate tissue oxygenation to the body's needs.
  • The prognosis of shock depends on the diagnosis and early treatment (symptomatic and causal therapy).

Dr I course. Yalaoui – Faculty of Constantine