SHOCK

SHOCK
ا. د.كريم الأعرجي
LEARNING OBJECTIVES
At the end of the lecture , the students should be able to:
• Know the definition of shock
• Describe the symptoms &signs of shock
• List the types and the causes of shock
• Discuss the physiopathological consequence and the complications of shock & how they can be prevented .
• Discuss the immediate diagnostic & treatment of shock
• Understand that shock is a life-threatening condition ,requires early diagnosis and immediate correction to prevents permanent organ damage and death



DEFINITION
Shock is defined as an inadequate perfusion and tissue oxygenation of the
vital organs (brain, heart, kidneys ).
CLASSIFICATION OF SHOCK :
1. Hypovolemic shock( Most common ) : Volume loss with high peripheral resistance
A. Haemorrhagic shock : Whole blood loss ; trauma , ectopic , GIT Bleeding
B. Non-haemorrhagic : It is due to poor fluid intake (dehydration) and excessive fluid loss . Plasma : Burn , Body fluids : Diarrhea , vomiting or third space loss
2. Distributive shock : Peripheral vasodilatation with Low peripheral resistance
A. Septic : Sepsis
B. Anaphylactic : Antigen-antibody reactions
C. Neurogenic shock : Loss of sympathetic tone such as spinal cord injury and regional spinal anaesthesia
3. Cardiogenic shock : Poor preload (inflow) such as decrease venous return , pump failure
( Arrhythmia ) or abnormal afterload (outflow ;Obstructive ) such as cardiac temponade , Tension pneumothorax , Pulmonary embolism .
4. Endocrinal shock : Hypo- and hyperthyroidism ,Addison’s disease
5. Traumatic shock : Soft tissue injury in trauma
PATHOPHYSIOLOGY OF SHOCK :
Persistent hypoperfusion will result in hemodynamic derangements, end-organ dysfunction, cell death, and death of the patient if treated late or inadequately . The physiopathological changes may occur at variable levels :
1. Cellular : There is shift from aerobic to anaerobic metabolism with formation of Lactic acid resulting in systemic metabolic acidosis.
As glucose within cells is exhausted, anaerobic respiration ceases and there is failure of the
sodium/potassium pumps . The intracellular lysosomes release autodigestive enzymes and
cell lysis ensues.
2. Microvascular : Hypoxia , Ischaemia , Acidosis will cause injury of the capillary endothelial cells with fluid oozing outside the capillaries .
3. Vascular :Baroreceptors are stimulated resulting in increased sympathetic activity and release of catecholamines into the circulation. This results in tachycardia and systemic vasoconstriction .
4. Respiratory : Metabolic acidosis and increased sympathetic response result in an increased respiratory rate and minute ventilation to increase the excretion of carbon dioxide (and so produce a compensatory respiratory alkalosis).
5. Renal : Decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a decreased urine output. The renin–angiotensin–aldosterone axis is stimulated resulting in further vasoconstriction and increased sodium and water reabsorption by the kidney.
6. Endocrine : There will be activation of the adrenal and renin–angiotensin systems, vasopressin (antidiuretic hormone) is released from the hypothalamus in response to decreased preload and results in vasoconstriction and reabsorption of water in the renal collecting system. Cortisol is also released from the adrenal cortex, contributing to the sodium and water reabsorption and sensitizing the cells to catecholamines.
Ischaemia–reperfusion syndrome
Systemic hypoperfusion, cellular and organ damage progresses because of the direct effects of tissue hypoxia and local activation of inflammation. Further injury occurs once normal circulation is restored to these tissues. The acid and potassium load can lead to direct myocardial depression, vascular dilatation and further hypotension. The cellular and humeral elements activated by the hypoxia (complement, neutrophils, microvascular thrombi) are flushed back into the circulation where they cause further endothelial injury to organs such as the lungs and kidneys. This leads to acute lung injury, acute renal injury, multiple organ failure and death. Reperfusion injury can currently only be attenuated by reducing the extent and duration of tissue hypoperfusion.
Multiple organ failure
MOF is defined as two or more failed organ systems .It results from prolonged systemic ischaemia and reperfusion injury.
Effects of organ failure :
Lung Acute respiratory distress syndrome
Kidney Acute renal insufficiency
Liver Acute liver insufficiency
Clotting Coagulopathy
Cardiac Cardiovascular failure
There is no specific treatment for multiple organ failure. Management is by supporting organ systems with ventilation, cardiovascular support and haemofiltration/dialysis until there is recovery of organ function. Multiple organ failure currently carries a mortality rate of 60%. Thus, prevention is vital by early aggressive identification and reversal of shock.
PHYSIOLOGICAL COMPENSATIONS IN SHOCK
These mechanisms aim to maintain oxygenation and blood supply of vital organs such as the brain , heart and kidneys and also they explain some of the clinical features of shock .
The quickest response is baroreceptors which lead to sympathetic nervous system response . The second intermediate response is Juxtaglomerular Apparatus of the kidneys with increases renin leading to vasoconstriction (splanchnic) .The last response is Adrenal Cortex with increased aldosterone secretion with Na and fluid reabsorption .
Stages of shock :According to degree of compensation and treatment interventions , shock is categorized into :
1. Compensated shock or occult shock
– Normal physiological compensation will lead to complete recovery
– External interventions not necessary
2. Progressive shock
– Progressively worse in the absence of external interventions
3. Irreversible shock
– Death is inevitable in spite of all forms of therapy
CLINICAL FEATURES
The CF depends on Severity , Cause , Type , Grade : 1 ,11 , 111, V1 ,Age : Old , atherosclerotic ,General condition &Drugs : B-Blockers , Aspirin , Warfarin
? General features ; In case of hypotension and reduced tissue perfusion , patient presents with:
? Confusion , anxiety leading to unconscious state
? Sweating
? Tachycardia
? Hypotension , usually postural
? Feeble pulse with low jugular neck venous pressure (JVP )
? Narrow pulse pressure
? Cold extremities (except septic shock); cold clammy skin
? Breathlessness / Hyperventilation
Clinical features according to specific types of shock :
Hypovolemic : Classical features of shock with presence of a cause of blood , fluid or plasma loss
Septic :Classical features , the patient may be worm or hot with presence of sepsis such as peritonitis, UTI , Pneumonia , Skin infection etc.
Neurogenic : Spinal cord injury and spinal anaesthesia . Hypotension with bradycardia
Cardiogenic :Shock with congested neck veins , Hypotension with increased JVP .

Degrees of hypovolaemic shock : Depending on amount of blood loss , hypovolaemic shock is divided into 4 classes
Type % Blood loss Ml Blood BP PR Puls. P(Post. Hypo.)
? I 0-15% <750 ml N. <100 N.
? II 15-30% 750–1500 May be >100 Dec.
? III 30-40% 1500- 2000 Dec. >120 Dec.
? IV >40% > 2000 < 60Sys. >140 Dec.
Complications of shock
The main complications of severe shock include:
1. Shock lung (ARDS)
2. Acute renal failure
3. Gastrointestinal ulceration
4. Disseminated intravascular clotting
5. Multiorgan failure
6. Death
Therefore, a patient in shock requires immediate emergency treatment. Early diagnosis and immediate correction of shock prevents permanent organ damage and death.
MANAGEMENT OF SHOCK
Management aim at restoring oxygen delivery to the cells of vital organs as rapidly as possible such as brain , heart and kidneys . Treatment is initially empiric ,diagnosis for the cause of shock is not always possible .It includes :
I. General management
II. Specific management according to the cause
III. End points of Resuscitation
IV. Recent advances in shock management
I. General management
1. Resuscitation ( ABC ) , Oxygen by mask : Ensure a patent airway , Adequate oxygenation and ventilation ,Cardiovascular resuscitation.
2. IVFluids and blood if indicated
3. Stop bleeding
4. Head down position
5. Monitoring of resuscitation effectiveness: e.g. determine hourly urine output, blood pressure and pulse rate
6. Inotropic drugs
11. Specific management : Treatment of the underlying cause
Hypovolemic Shock: The goal of treatment is to restore vascular volume. This is effected by:
• General approach as above
• Fluid and blood replacement , 2 large cannula 14G in upper extremity .
• Oxygen support by nasal cannula etc.
Septic Shock
• Initial management as above
• Appropriate antibiotics especially for gram-negative microorganisms
• Inotropic support such as adrenaline and dopamine
• Surgical eradication of the infection focus
Cardiogenic shock
• Initial management as above
• Inotropic drugs
• Treat the causes such as cardiac temponade
Neurogenic shock
• Initial management as above
• Pain relief
• Treat the causes, give supportive measures like ephedrine & inotropic support
Types of fluids :
1. Blood
2. Ringer Lactate (Hartmann’s soln. )
3. Normal Saline
4. Hypertonic Saline
5. Colloids
6. Blood Substitutes
Monitoring for patient in shock
Minimum :For all patient
• Electrocardiogram , HR
• Pulse oximetry ,Oxygen saturation
• Blood pressure
• Urine output
Additional modalities
• Patients whose state of shock is not rapidly corrected with a small amount of fluid should have Central venous pressure & continuous Invasive blood pressure through an arterial line
• Cardiac output &peripheral arterial resistance by Doppler ultrasound, pulse waveform analysis and indicator dilution methods , rarely by pulmonary artery catheter .
• Base deficit and serum lactate i.e. :Acid base balance from arterial blood -6mmol/-1
• CVP should be assessed dynamically as the response to a fluid challenge No ‘normal’ CVP (5 -15 cmH2O ). A fluid bolus (250–500 ml) is infused rapidly over 5–10 min. The normal CV response is a rise of 2–5 cmH2O, which gradually drifts back to the original level over 10–20 min. Patients with no change in their CVP are empty and require further fluid resuscitation. Patients with a large, sustained rise in CVP have high preload and an element of cardiac insufficiency or volume overload.
• Cardiac output : Pulmonary artery catheter ( Swan Ganz Catheter )
• Mixed venous oxygen saturation : N: 50–70%. Levels below 50% indicate inadequate oxygen delivery and increased oxygen extraction by the cells.
111. End Points of Resuscitation:
1. Restoration of normal vital signs : Consciousness,PR,BP>90mmHg,RR
2. Adequate Urine output ; 0.5 - 1.0 cc/Kg/hr.
3. Tissue Oxygenation measurement ;Oxygen saturation’SpO2’, Direct and absolute measurement of Hb oxygen saturation in tissues
4. Adequate Cardiac Index
5. Normal Serum Lactate levels
6. Normalization of Oxygen delivery DO2I
V1.Advances in shock management
• Autotransfusion
• Hypertonic Saline ;Hypertonic saline with dextran ,7.5%saline with 6% dextran-70
• Less fluid especially in head injury .
• Hyperdynamic resuscitation, push fluid until no longer needed
• Trauma Vaccine? Ischaemia reperfusion syndrome , ARDS
• Alternatives to Transfusion: Polymerized, Hemoglobin 50 gm. in 500 ml
IVF in shock
Controversies exist whether to give crystalloid solutions(normal saline, Hartmann’s solution, Ringer’s lactate) or colloids (albumin or commercially available products). But preferably crystalloid . Hypotonic solutions (e.g. dextrose) are poor volume expanders and should not be used in the treatment of shock unless the deficit is free water loss (e.g. diabetes insipidus) or patients are sodium overloaded (e.g. cirrhosis).
Dynamic fluid response
• Rapid administration of a fluid bolus. In total, 250–500 ml of fluid is rapidly given (over 5–10 min) and heart rate, blood pressure and central venous pressure (CVP) are observed. Patients can be divided into
• Responders : Sustained improvement ,not actively losing fluid but require filling to a normal volume status.
• Transient responders :improvement but then revert to their previous state over the next 10–20 min. These patients moderate on-going fluid losses .
• Non-responders are severely volume depleted and are likely to have major on-going loss of intravascular volume, usually through persistent uncontrolled haemorrhage.
Role of Inotropic & Vasopressor drugs Support
Vasopressor agents (phenylephrine, noradrenaline) are indicated In :
• Distributive shock states (sepsis, neurogenic shock) when there is peripheral vasodilatation and a low systemic vascular resistance with hypotension
• Cardiogenic shock or when myocardial depression complicates a shock state (e.g. severe septic shock with low cardiac output), inotropic therapy may be required to increase cardiac output and, therefore, oxygen delivery. Dopamine &dobutamine are used but vasodilator dobutamine is the agent of choice .
Role of Steroids in shock
Because severe sepsis is often associated with adrenal insufficiency or glucocorticoid receptor resistance so low doses of hydrocortisone and fludrocortisone for seven-day significantly and safely lowers the risk of death in patients with septic shock .