SHOCK

Dr. R. Lalchhandama
Asst. Professor Dept. of Surgery
ZMC, Falkawn
Introduction
• Shock is a systemic state of low tissue perfusion that is inadequate for
normal cellular respiration.
• With insufficient delivery of oxygen and glucose, cells switch from aerobic
to anaerobic metabolism.
• If perfusion is not restored in a timely fashion, cell death ensues.
• Death may occur rapidly due to a profound state of shock, or be delayed
due to the consequences of organ ischaemia and reperfusion injury.
• Shock is the most common and the most important cause of death of
surgical patients.
Classification of shock
• Hypovolaemic shock

• Cardiogenic shock

• Obstructive shock

• Distributive shock

• Endocrine shock
 Hypovolaemic shock
• Is due to a reduced circulating volume
• Haemorrhagic or non-haemorrhagic causes
• Non-haemorrhagic causes include
A) poor fluid intake (dehydration)
B) excessive fluid loss due to vomiting, diarrhoea
C) urinary loss (e.g. diabetes),
D) evaporation, or ‘third-spacing’ where fluid is lost into the gastrointestinal tract and interstitial spaces, as for
example in bowel obstruction or pancreatitis.

• Hypovolaemia is probably the most common form of shock, and to some degree
is a component of all other forms of shock.
 Cardiogenic shock
• Due to primary failure of the heart to pump blood to the tissues.
• Causes of cardiogenic shock include myocardial infarction, cardiac dysrhythmias,
valvular heart disease, blunt myocardial injury and cardiomyopathy.

• Cardiac insufficiency may also be due to myocardial depression caused by

endogenous factors (e.g. bacterial and humoral agents released in sepsis) or
exogenous factors, such as pharmaceutical agents or drug abuse.

• Evidence of venous hypertension with pulmonary or systemic oedema may

coexist with the classical signs of shock.
 Obstructive shock

• In obstructive shock there is a reduction in preload due to mechanical obstruction

of cardiac filling.

• Common causes of obstructive shock include cardiac tamponade, tension

pneumothorax, massive pulmonary embolus or air embolus.

• In each case, there is reduced filling of the left and/or right sides of the heart
leading to reduced preload and a fall in cardiac output.
 Distributive shock
• Distributive shock describes the pattern of cardiovascular responses characterising a
variety of conditions, including septic shock, anaphylaxis and spinal cord injury.
• Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low
systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac
output.
• In anaphylaxis, vasodilatation is due to histamine release, while in high spinal cord injury
there is failure of sympathetic outflow and adequate vascular tone (neurogenic shock).
• The cause in sepsis is less clear but is related to the release of bacterial products
(endotoxin) and the activation of cellular and humoral components of the immune system.
• There is maldistribution of blood flow at a microvascular level with arteriovenous
shunting and dysfunction of cellular utilization of oxygen.
 Endocrine shock

• Causes of endocrine shock include hypo- and hyperthyroidism and adrenal insufficiency.
• Hypothyroidism causes a shock state similar to that of neurogenic shock due to disordered
vascular and cardiac responsiveness to circulating catecholamines.
• Cardiac output falls due to low inotropy and bradycardia.
• There may also be an associated cardiomyopathy.
• Thyrotoxicosis may cause a high-output cardiac failure.
• Adrenal insufficiency leads to shock due to hypovolaemia and a poor response to
circulating and exogenous catecholamines.
• Adrenal insufficiency may be due to pre-existing Addison’s disease or be a relative
insufficiency due to a pathological disease state, such as systemic sepsis.
 Severity of shock
Compensated shock
• As shock progresses, the body’s cardiovascular and endocrine compensatory responses reduce
flow to non-essential organs to preserve preload and flow to the lungs and brain.
• In compensated shock, there is adequate compensation to maintain central blood volume and
preserve flow to the kidneys, lungs and brain.
• Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there
may be no other clinical signs of hypovolaemia.
• However, this cardiovascular state is only maintained by reducing perfusion to the skin, muscle
and gastrointestinal tract.
• There is a systemic metabolic acidosis and activation of humoral and cellular elements within the
underperfused organs.
• Although clinically occult, this state will lead to multiple organ failure and death if prolonged, due
to the ischaemia–reperfusion effect.
Decompensation
• Further loss of circulating volume overloads the body’s compensatory
mechanisms and there is progressive renal, respiratory and cardiovascular
decompensation.

• In general, loss of around 15% of the circulating blood volume is within normal
compensatory mechanisms.

• Blood pressure is usually well maintained and only falls after 30–40% of
circulating volume has been lost.
Mild shock
• Initially there is tachycardia, tachypnoea, a mild reduction in urine output and the patient may exhibit mild
anxiety.
• Blood pressure is maintained although there is a decrease in pulse pressure.
• The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock).
Moderate shock
• As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below
0.5 mL/kg per hour.
• There is further tachycardia, and now the blood pressure starts to fall.
• Patients become drowsy and mildly confused.
Severe shock
• In severe shock, there is profound tachycardia and hypotension.
• Urine output falls to zero and patients are unconscious with laboured respiration.
 Consequences
Unresuscitatable shock
• Patients who are in profound shock for a prolonged period of time become ‘unresuscitatable’.
• Cell death follows from cellular ischaemia and the ability of the body to compensate is lost.
• There is myocardial depression and loss of responsiveness to fluid or inotropic therapy.
• Peripherally there is loss of the ability to maintain systemic vascular resistance and further hypotension
ensues.
• The peripheries no longer respond appropriately to vasopressor agents.
• Death is the inevitable result.
• This stage of shock is the combined result of the severity of the insult and delayed, inadequate or
inappropriate resuscitation in the earlier stages of shock.
• Conversely, when patients present in this late stage, and have minimal responses to maximal therapy, it is
important that the futility of treatment is recognised and valuable resources are not wasted.
Multiple organ failure

• As techniques of resuscitation have improved, more and more patients are surviving shock.
• Where intervention is timely and the period of shock is limited, patients may make a rapid, uncomplicated
recovery.
• However the result of prolonged systemic ischaemia and reperfusion injury is end-organ damage and multiple
organ failure.
• Multiple organ failure is defined as two or more failed organ systems.
• There is no specific treatment for multiple organ failure.
• Management is supporting of organ systems, with ventilation, cardiovascular support and
haemofiltration/dialysis until there is recovery of organ function.
• Multiple organ failure currently carries a mortality of 60%; thus, prevention is vital by early aggressive
identification and reversal of shock.
 RESUSCITATION
• Immediate resuscitation manoeuvres for patients presenting in shock are to ensure a patent airway and
adequate oxygenation and ventilation.
• Once ‘airway’ and ‘breathing’ are assessed and controlled, attention is directed to cardiovascular
resuscitation.
Conduct of resuscitation
• Resuscitation should not be delayed in order to definitively diagnose the source of the shocked state.
• However, the timing and nature of resuscitation will depend on the type of shock and the timing and severity
of the insult.
• Rapid clinical examination will provide adequate clues to make an appropriate first determination, even if a
source of bleeding or sepsis is not immediately identifiable.
• If there is initial doubt about the cause of shock, it is safer to assume the cause is hypovolaemia and begin
with fluid resuscitation, and then assess the response.
 Fluid therapy
• In all cases of shock, regardless of classification, hypovolaemia and inadequate preload must be
addressed before other therapy is instituted.
• Administration of inotropic or chronotropic agents to an empty heart will rapidly and permanently
deplete the myocardium of oxygen stores and dramatically reduce diastolic filling and therefore
coronary perfusion.
• Patients will enter the unresuscitatable stage of shock as the myocardium becomes progressively
more ischaemic and unresponsive to resuscitative attempts.

• First-line therapy is intravenous access and administration of intravenous fluids.

• Access should be through short, wide-bore catheters that allow rapid infusion of fluids as
necessary.
• Long, narrow lines, such as central venous catheters, have too high a resistance to allow rapid
infusion and are more appropriate for monitoring than fluid replacement therapy.
 Monitoring
• The minimum standard for monitoring of the patient in shock is continuous heart rate and oxygen saturation
monitoring, frequent non-invasive blood pressure monitoring and hourly urine output measurements.
• Most patients will need more aggressive invasive monitoring, including central venous pressure and invasive
blood pressure monitoring.
Monitoring for patients in shock
Minimum
• ECG
• Pulse oximetry
• Blood pressure
• Urine output
Additional modalities
• Central venous pressure
• Invasive blood pressure
• Cardiac output
• Base deficit and serum lactate
 EFFECTS OF SHOCK
• Heart: Low perfusion low venous return decreased cardiac output hypotension tachycardia.
• Persistent shock causes hypoxia and release of myocardial depressants leading to further cardiac
damage.
• Lung: Interstitial oedema decreased gaseous exchange pulmonary arteriovenous shunting
tachypnoea Adult/Acute respiratory distress syndrome (ARDS) and pulmonary oedema.
• Metabolic: Shock leads to hypoxia, which activates anaerobic metabolism leading to lactic acidosis.
• Antidiuretic hormone (ADH) is released which increases the reabsorption of water from renal
tubules.
• Other hormones released are ACTH, prostaglandins, histamine, bradykinin, and serotonin to
compensate the effects of shock to increase the perfusion of vital organs like heart, brain and lungs.
• Cellular changes occur in persistent shock due to release of lysosomal enzymes, which alters the
cell membrane permeability causing cell death—sick cell syndrome.
• Sympathetic overactivity alters the microcirculation leading to capillary dysfunction.
• Brain perfusion, when decreases the patient becomes drowsy.
• Brain is the last organ to get underperfused in shock.
• Kidneys: GFR decreases and tubular reabsorption of salt and water increases for compensatory
response. But in severe cases tubular necrosis sets in leading in to irreversible damage.
• Blood: Alteration in cellular components including platelets leads to Disseminated intravascular
coagulation(DIC).
• It causes bleeding from all organs.
• Gastrointestinal tract: Mucosal ischaemia develops causing bleeding from GIT with haematemesis
and malaena.
• It is aggravated by DIC. Hepatic ischaemia leads into increased enzyme levels.
 Stages of Septic Shock
1. Hyperdynamic (warm) shock: This stage is reversible stage.
• Patient is still having inflammatory response and so presents with fever, tachycardia, and
tachypnoea.
• Pyrogenic response is still intact.
• Patient should be treated properly at this stage.
• Based on blood culture, urine culture (depending on the focus of infection), higher antibiotics like
third generation cephalosporins, aminoglycosides, metronidazole are started.
• The underlying cause is treated like draining the pus, laparotomy for peritonitis, etc.
• Ventilatory support with ICU monitoring may prevent the patient going for the next cold stage of
sepsis.
2. Hypodynamic hypovolaemic septic shock (cold septic shock): Here pyrogenic response is lost.
• Patient is in decompensated shock.
• It is an irreversible stage along with MODS (Multi Organ Dysfunction Syndrome) with anuria,
respiratory failure (cyanosis), jaundice (liver failure), cardiac depression, pulmonary oedema,
hypoxia, drowsiness, eventually coma and death occurs - (Irreversible stage).
 Treatment of Septic Shock
• Correction of fluid and electrolyte by crystalloids, blood transfusion.
• Appropriate antibiotics.
• Treat the cause or focus – drainage of an abscess; laparotomy for peritonitis; resection of
gangrenous bowel; wound excision.
• Pus/urine/discharge/bile/blood culture and sensitivity for antibiotics.
• Critical care, oxygen, ventilator support, dobutamine/ dopamine/noradrenaline to
maintain blood pressure and urine output.
• Activated C protein prevents the release of inflammatory mediators and blocks the effects
of these mediators on cellular function.
• Monitoring the patient by pulse oximetry, cardiac status, urine output, arterial blood gas
analysis.