Shock is defined as a state of cellular hypoxia due to reduced oxygen delivery or utilization. It can be classified as initial/primary shock which is transient and benign, or true/secondary shock which involves a circulatory imbalance at the cellular level. Hinshaw and Cox classify shock into four categories: hypovolemic, cardiogenic, extracardiac obstructive, and distributive. All forms of shock involve reduced circulating blood volume, reduced oxygen supply to tissues leading to anoxia, and release of inflammatory mediators from cellular injury. Compensatory responses aim to maintain circulation and maximize cardiac function to redistribute perfusion to vital organs. Diagnosis involves monitoring physiology, while management focuses on treating the underlying cause, organ
2. Introduction
Shock is the clinical syndrome that
results from inadequate tissue
perfusion.
Irrespective of cause, the
hypoperfusion-induced imbalance
between the delivery of and
requirements for oxygen and substrate
leads to cellular dysfunction.
3. Definition
Shock is defined as a state of cellular and
tissue hypoxia due to reduced oxygen
delivery and/or increased oxygen consumption
or inadequate oxygen utilization.
Shock is a life-threatening clinical syndrome of
cardiovascular collapse characterised by:
an acute reduction of effective circulating
blood volume (hypotension);
and an inadequate perfusion of cells and
tissues (hypoperfusion).
4. Classification:
“Initial (or primary) shock” is used for
transient and usually a benign vasovagal
attack resulting from sudden reduction of
venous return to the heart caused by
neurogenic vasodilatation and
consequent peripheral pooling of blood.
“True (or secondary) shock” is a
circulatory imbalance between oxygen
supply and oxygen requirements at the
cellular level, and is also called as
circulatory shock.
5. Hinshaw and Cox Classification
•Hypovolemic,
•Cardiogenic,
•Extracardiac obstructive and
•Distributive
It divides the
syndrome
into four
major
categories:
6. HYPOVOLEMIC
SHOCK
• The severity of clinical
features depends upon
degree of blood volume
lost, hemorrhagic shock is
divided into 4 types:
• < 1000 ml: Compensated
• 1000-1500 ml: Mild
• 1500-2000 ml: Moderate
• >2000 ml: Severe
ETI0LOGY
7. CARDIOGENIC SHOCK
• Cardiogenic shock (CS) is
characterized by systemic
hypoperfusion due to severe
depression of the cardiac index
[<2.2 (L/min)/m2] and sustained
systolic arterial hypotension
(<90 mmHg), despite an
elevated filling pressure
[pulmonary capillary wedge
pressure (PCWP) > 18 mmHg
ETI0LOGY
10. PATHOGENISIS
In general, all forms of shock involve
following 3 derangements:
• Reduced effective circulating blood
volume.
• Reduced supply of oxygen to the
cells and tissues with resultant
anoxia.
• Inflammatory mediators and toxins
released from shock induced
cellular injury.
These derangements initially set in
compensatory mechanisms (discussed
below) but eventually a vicious cycle
of cell injury and severe cellular
dysfunction lead to breakdown of
organ function
15. Compensatory responses
• All compensatory responses to shock, whether
hemodynamic, metabolic or biochemical, support oxygen
delivery to vital organs.
• These responses are similar for varying classes of shock
and are divided into four categories):
(a) Maintenance of mean circulatory pressure
(b) Maximizing cardiac function
(c) Redistributing perfusion to vital organs
(d) Optimizing unloading of oxygen at tissues
16.
17. Diagnostic Approach
and Evaluation
• A monitored physiologic
approach to therapy
provides the best
opportunity for successful
outcome and avoidance of
organ dysfunction.
18. Signs and symptoms
• Tachycardia, tachypnea and
oliguria are the hall mark.
• Cool extremities are seen in
hypodynamic shock.
• With progression, blood
pressure falls and frank
hypotension
19. Management:
• Patients in shock should be
managed in ICU with
continuous ECG monitoring
and close nursing support.
20. Specific therapies
Hypovolemic: crystalloid, colloids and blood transfusion
Cardiogenic: inotropes, vasodialators, intra-aortic balloon pump, surgical intervention if necessary
Septic shock: removal of septic focus, antibiotics, intravenous fluids, vasoactive agents, activated
protein C
Anaphylactic shock: oxygenation, adrenaline, intravenous fluids
Neurogenic shock: intravenous fluids, inotropes and vagolytics
Adrenal crisis: ABC, IV fluids, hydrocortisone, treat the precipitating factor
Extra cardiac obstructive shock: pericardial drainage via surgery
Editor's Notes
The cellular injury created by the inadequate delivery of oxygen and substrates also induces the production and release of inflammatory mediators that further compromise perfusion through functional and structural changes within the microvasculature.
This leads to a vicious circle in which impaired perfusion is responsible for cellular injury, which causes maldistribution of blood flow, further compromising cellular perfusion; the latter causes multiple organ failure and, if the process is not interrupted, leads to death
e.g. immediately following trauma, severe pain or emotional overreaction such as due to fear, sorrow or surprise
A classification based on cardiovascular characteristics, which was initially proposed in 1972 by Hinshaw and Cox, is the most accepted one amongst many others that have been given.
Hypovolaemic shock occurs from inadequate circulating blood volume due to various causes. The major effects of hypovolaemic shock are due to decreased cardiac output and low intracardiac pressure.
Shock is an end-stage of a continuum of progressive physiologic derangements. It is imperative, therefore, that clinicians recognize the early stages of shock at a time when it is more responsive to treatment.
Invasive hemodynamic monitoring with arterial and pulmonary artery catheters should be instituted in those indicated i.e., patients in whom etiologic diagnosis is in doubt, whose hemodynamic instability does not quickly resolve with intravenous fluids etc., laboratory tests as mentioned before should be performed the earliest possible. Management of shock can be divided into specific therapy for triggering injury and general therapy of the shock syndrome.
50-100 microgms iv ( 0.5-1mg IM
Hydrocortisone 100-300mg iv
