As proposed by the historians, the first written
definition of shock is made by Celsus (AD 20) after
a penetrating heart injury as “The pulse fades
away, the color is extremely pallid, cold and
malodorous sweats break out the body as if the
body has been wetted by dew, the extremities
become cold and death quickly follows” .
LeDran, a military surgeon, derived a word shock
as “The bullet thrown from the gunpowder
acquires such rapid force that the whole animal
participates in the jarring (shock and agitation)” in
his article in 1743.
The term “golden hour” is widely attributed to R. Adams
Cowley, who in a 1975 article stated, “the first hour after
injury will largely determine a critically injured person’s
chances for survival”—this was in an era characterized by
a lack of an organized trauma system and inadequate
An analogous concept, the “platinum 10 minutes” places a
time constraint on the prehospital care of seriously injured
patients: no patient should have more than 10 min of
scene-time stabilization by the prehospital team prior to
transport to definitive care at a trauma center.
SHOCK- “A PHYSIOLOGICAL STATE OF WAR”
DEFINITION OF SHOCK
“It is defined as a life-threatening, generalized form of acute
circulatory failure associated with inadequate oxygen utilization
by the cells”
Relative incidence of various types of
According to a European multicenter trial,
septic shock Is the most common (62%)
Distributive other than septic (4%), and
obstructive shock (2%)
Pathophysiology of Shock
In general, all forms of shock involve following 3
Reduced effective circulating blood volume.
Reduced supply of oxygen to the cells and tissues with
Inflammatory mediators and toxins released from shock
induced cellular injury
Hemorrhagic shock develops as a result of
intravascular volume loss due to bleeding out of the
body or into the anatomical spaces inside, causing
insufficient oxygen delivery to the cells.
Hemorrhagic shock is a type of hypovolemic shock.
If the bleeding does not stop, inadequate oxygen
supply may lead to death. Hemorrhagic shock in
trauma patients is a predictor of worse outcomes and
contributes to early mortality
Shock may develop due to several reasons
including trauma, maternal hemorrhage,
gastrointestinal hemorrhage, perioperative
hemorrhage, or ruptured aneurysms .
Mortality due to bleeding is substantial on a
global scale. Annually, 1.9 million people in the
world lose their lives due to hemorrhage and
Out of them, 1.5 million people die of physical
trauma around the world each year.
Unexpectedly, it is more common in young
Classification of haemorrhage
I. Based on the source of bleeding:
Arterial: is bright red in colour, spurting like jet along
with pulse of the patient.
Venous: is dark red, steady and continuous flow.
Blood loss may be severe and rapid when bleeding is
from femoral vein, jugular vein, other major veins,
varicose veins, portal vein, esophageal varices.
Pulmonary arterial blood is dark red in colour and
pulmonary venous blood is bright red in colour.
Capillary: Here bleeding is rapid and bright red. It is
often torrential due to continuous ooze.
II. Based on the time of onset of bleeding in
relation to any operative procedure:
1.Primary: Occurs at the time of injury or operation.
2. Reactionary: It occurs within 24 hours after surgery or
after injury (commonly in 4–6 hours).
3. Secondary: It usually occurs in 14 days after surgery
IV. Based on the duration of haemorrhage:
1. Acute haemorrhage: It is sudden, severe haemorrhage after
2. Chronic haemorrhage: It is chronic repeated bleeding for a
long period like in haemorrhoids, bleeding peptic ulcer,
carcinoma caecum, etc. They present with chronic anaemia
with hyperdynamic cardiac failure. in a state of chronic
hypoxia. It is corrected by packed cell transfusion not by
whole blood itself. Cause has to be treated accordingly.
3. Acute on chronic haemorrage: It is more dangerous as the
bleeding occurs in individuals who are already hypoxic, which
may get worsened faster.
V. Based on the possible intervention:
1. Surgical haemorrhage—can be
corrected by surgical intervention.
2. Nonsurgical haemorrhage—is
diffuse ooze due to coagulation
abnormalities and DIC.
Lethal triad of hemorrhagic shock
The lethal triad of
and coagulopathy is
commonly seen in
patients with severe
Each factor in triad
influences the other
factors, and the patients
with this lethal triad
show high mortality in
spite of aggressive
The source of bleeding
In traumatic shock, penetrating trauma such as
stab wounds or gunshot wounds usually has more
obvious source of bleeding than blunt trauma and
requires surgical bleeding control.
In nontraumatic hemorrhagic shock, the
approximate source of bleeding could be
determined by the patient’s symptoms such as
If a source of bleeding is identified, immediate
procedures for bleeding control should be
considered unless initial resuscitation is
Unidentified Source of Bleeding
In contrast, a patient without obvious source of bleeding
should undergo further investigation.
In traumatic shock, early diagnostic imaging techniques such
as ultrasonography or contrast enhanced computed
tomography (CT) are recommended for the detection of free
fluid in patients with torso trauma .
Ultrasonography is a rapid, noninvasive imaging technique for
detection of intra-abdominal fluid and can be performed in
bedside without moving the patients.
Extended focused assessment with sonography for trauma
(eFAST) was introduced for trauma as a screening test for
blood in the pericardium, abdominal cavity, or pleural space,
and also for a pneumothorax. The six areas that are examined
are subcostal (subxiphoid), RUQ (hepatorenal recess), LUQ
(perisplenic space), pelvis, and thorax
The CT scan has been widely used to detect the
source of bleeding in patients with hemorrhagic
shock in both trauma and non-trauma, and the
usefulness of the CT scan has been well known.
Recently, multi-detector CT (MDCT) may require
less than 30 s for scanning the whole body, and
the usefulness of the CT scan has been well
In addition, contrast enhanced CT scan could
detect active bleeding more accurately than non-
enhanced CT scan.
Clot size of a clenched fist
is 500 ml.
Weighing the swab before
and after use is an
important method of on-
table assessment of blood
Laboratory tests are a part of diagnostic workup for patients
with hemorrhagic shock. They can help assess the condition and
severity of the patient and identify the patients who may require
aggressive diagnostic and therapeutic interventions.
1. Hemoglobin and hematocrit,
3. base deficit, and
4. tests for coagulation.
Initial Management of Hemorrhagic Shock
The goal of initial resuscitation for hemorrhagic shock is to
arrest ongoing bleeding, to restore the effective circulating
blood volume, and to restore tissue perfusion.
Management protocol of hemorrhagic shock has
developed based on the treatment of trauma patients.
There was a concept of damage control surgery (DCS) as
a surgical approach to the trauma, and this has been
expanded to the early management of trauma patients as
damage control resuscitation (DCR).
Early recognition of the patients with high risk and
prevention of lethal triad of coagulopathy, hypothermia,
and acidosis are main purposes of the DCR.
Restoration of the intravascular fluid volume
Four issues should be considered when treating hemorrhagic
type of fluid to give, how much, how fast, and what the
therapeutic end-points are.
The ideal fluid for resuscitation has not been established.
The three-to-one rule(that is, 3 ml of crystalloid (Ringers
lactate or normal saline) for every 1 ml of blood loss replaced).
has been applied to the classification of hemorrhage to
establish a baseline for guiding therapy , and use of crystalloid
(Ringers lactate or normal saline) is recommended by the
American College of Surgeons .
Although resuscitative end-points are similar
when using Ringers lactate or normal saline,
metabolic hyperchloremic acidosis has been
reported when infusing large volumes of normal
saline (>10 l)
Colloidal solutions, such as albumin and
hetastarch (6% hydroxyethyl starch in 0.9%
NaCl), can be administered to increase
circulatory volume rapidly.
the use of albumin solutions in the initial
resuscitation stages has not proven to be more
effective than crystalloid.
Tranexamic acid is a synthetic lysine analogue and an
antifibrinolytic agent as a competitive inhibitor of
In a prospective cohort study, tranexamic acid reduced
organ failure and mortality in traumatic shock patients .
A prospective randomized study showed that early
administration of tranexamic acid reduced mortality in
trauma patients with shock and the rate of thrombosis was
not increased with the use of tranexamic acid.
The recommended dose is a loading dose of 1 g over
10 min, followed by infusion of 1 g over 8 h, and tranexamic
acid is not recommended more than 3 h after injury.
Hypocalcemia is a common complication of massive
transfusion. Low ionized calcium concentration was
associated with increased mortality and massive
transfusion. Therefore, ionized calcium concentration
should be monitored and maintained within normal range.
1. Acute blood loss following trauma, >15% of total body
volume in otherwise healthy individuals (liver, spleen,
kidney, GIT injuries, fractures, hemothorax, perineal
2. A hypotensive patient who fails to respond to 2 l crystalloid in
the phase of probable hemorrhage should be treated with
blood and blood products.
3. During major surgeries—
4. Following burns.
5. In septicemia.
6. As a prophylactic measure prior to surgery.
7. Whole blood is given in acute blood loss. Packed cells are
given in chronic anemia.
8. Blood fractions are given in ITP, haemophilias.
Note: Blood transfusion is required if
Hb% is < 8 g%
Collection of Blood
Blood is collected in a sac containing 75 ml of
CPD (Citrate phosphate dextrose) solution and
stored in special refrigerators at 4 degree celcius.
CPD blood lasts for 3 weeks.
Adenosine can be added to increase the storage
life of the blood up to 5 weeks; it is called as CPDA
In storage period, RBCs lose their ability to
release oxygen in 7 days even though RBCs last
for 3 weeks; so blood should be transfused within
7 days ideally. WBCs are destroyed in 2 days.
Platelets and clotting factors are destroyed very
early in 1–2 days
Infusing Packed Red Blood Cells
Whole blood is not available for replacement of blood loss,
and erythrocyte losses are replaced with stored units of
concentrated erythrocytes called packed red blood cells.
Each unit of packed RBCs has a hematocrit of 55% to 60%,
which imparts a high viscosity
As a result, packed RBCs can flow sluggishly unless diluted
with saline. When infused alone, the flow rate of packed RBCs
through average sized (18-gauge or 20-gauge) peripheral
catheters is 3–5 mL/min, which means that one unit of
undiluted packed RBCs (which has a volume of about 350 mL)
can be infused over 70–117 minutes (about 1–2 hours).
This is sufficient for replacing erythrocyte losses in
hemodynamically stable patients, but more rapid flow rates
may be needed for patients with active bleeding.
Dilution of packed rbcs with 100 ml of isotonic
saline results in 7-fold to 8-fold increases in
infusion rates, while dilution with 250 ml saline
increases flow rates over 10-fold.
At the highest infusion rate of 96 ml/min in the
16- gauge catheter, one unit of packed rbcs (350
ml plus 250 ml saline) can be infused in 6–7
More rapid rates require pressurized infusions,
which can increase infusion rates to 120 ml/min
using a 16-gauge catheter
Conclusion Of hemorrhagic shock
Hemorrhagic shock can be rapidly fatal. The primary
goal is to stop the bleeding. Resuscitation may well
depend on estimated severity of hemorrhage.
patients who have moderate hypotension from
moderate bleeding may well benefit from a delay in
massive resuscitation in order to reach a definitive
On the other hand, when patients are obviously in
severe hemorrhagic shock, the use of intravenous
crystalloids or colloids and blood products when
available can be life saving. Uncertainties remain
regarding the best method for resuscitation, what
type of fluid, how much, when, and how fast
A hemoglobin level of 7–8 g/dl is an appropriate
threshold for transfusion in critically ill patients
with no risk factors for tissue hypoxia.
Maintaining a hemoglobin level of 10 g/dl is a
reasonable goal for patients who are actively
bleeding, the elderly, or individuals at risk for a
Moreover, hemoglobin concentration should not
be the only therapeutic guide in actively
bleeding patients. Instead, therapy should be
aimed at restoring intravascular volume and
adequate hemodynamic parameters.
Cardiogenic shock is a serious complication of acute
myocardial infarction and is an important cause of hospital
death. Cardiogenic shock is a condition in which, myocardium
unable to pump enough blood to meet your body’s needs. The
condition is most often caused by a severe heart attack.
Cardiogenic shock is rare, but it’s often fatal if not treated
immediately. If treated immediately, about half the people who
develop the condition survive.
Definition of Cardiogenic Shock
Cardiogenic shock is a life-threatening medical condition
resulting from an inadequate circulation of blood due to
primary failure of the ventricles of the heart to function
The incidence of cardiogenic shock is about 5% in patients
with acute myocardial infarction (AMI) and three times more
in ST-segment elevation myocardial infarction (STEMI) than
Treatment and Management
A patient in cardiogenic shock should undergo
immediate comprehensive assessment.
electrocardiogram (ECG), and
echocardiography are required immediately in
all patients with suspected cardiogenic shock.
Chest X-ray can be a useful test for the diagnosis
of cardiogenic shock. Pulmonary venous
congestion, pleural effusion, interstitial or
alveolar edema, and cardiomegaly are the most
specific findings for cardiogenic shock
ECG is rarely normal in cardiogenic shock. It is
also helpful in identifying underlying cardiac
disease and potential precipitant
The first definition of sepsis, published in 1992, was
based on the presence of a suspected or proven infection
with two or more criteria of the systemic inflammatory
response syndrome (SIRS) .
Sepsis was defined, as the presence of two or more
positive SIRS criteria with a confirmed or suspected
infection as the underlying cause.
If signs of organ dysfunction were seen, the diagnosis
was changed to severe sepsis.
Septic shock was defined by the presence of acute
circulatory failure and arterial hypotension along with
features of sepsis.
SIRS was based on an inflammatory response to an
Many thought the definition was not helpful largely
because the definition place a large emphasis on
inflammation, causing many patients without bacterial
or viral infections to receive empiric antibiotic therapy
and over-resuscitation .
The SIRS criteria were also thought to be remarkably
sensitive, not taking into account any outside factors,
multi-drug resistance and the ability to attain source
control. Based on the old definition of sepsis using the
SIRS criteria, patients have been incorrectly identified
as being septic.
Due to these inaccuracies in the SIRS criteria, the new Sepsis-3
definitions recommend using the SOFA score;
The SOFA score is an aggregate score, from 0 to 4, for each
organ system, including respiratory, coagulation, liver,
cardiovascular, renal and central nervous systems.
An acute increase in the total score of 2 or more reflects an
overall mortality risk in patients suspected of infection.
Calculating the SOFA score at the bedside or in a noncritical
care unit and in patients who do not have full laboratory testing,
is challenging Since the SOFA score is based on biochemical
criteria, clinical qSOFA screening tool which is based on
respiratory rate, systolic blood pressure and altered mental state
was developed .
If 2 of the 3 clinical variables are positive, the predictive validity
is similar to the entire SOFA score when used outside the ICU
In 2016, the Third International
Consensus Definition for
Sepsis and Septic Shock
Defined sepsis as a life-
threatening organ dysfunction
resulting from dysregulated
host responses to infection,
and defined septic shock as a
subset of sepsis in which
cellular, and metabolic
abnormalities are profound
enough to substantially
increase the risk of mortality.
Septic shock may be due to gram-positive organisms,
gram negative organisms, fungi, viruses or protozoal
Septic shock is typically a vasodilatory shock wherein there is
peripheral vasodilatation causing hypotension which is
resistant to vasopressors. This is due to toxin induced release
of isoform of nitric oxide synthetase from the vessel wall
which causes sustained prolonged release of high levels of
Magnitude of infection is quantified as:
1. Sepsis which shows fever, tachycardia, leucocytosis.
2. Severe sepsis which shows low tissue perfusion with
organ dysfunction (lactic acidosis, dysfunction of liver,
1. Septic shock with systemic hypotension (BP < 90 mmHg
in spite adequate fluid therapy), severe organ dysfunction
(acute lung, kidney, liver injury), maldistribution of blood
flow, shunting in microcirculation.
Stages of septic shock
a. 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.
Ventilatory support with ICU monitoring may prevent the patient
going for the next cold stage of sepsis.
b. Hypodynamic hypovolaemic septic shock (cold
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
Anaphylaxis is a life threatening hypersensitivity
reaction that can cause shock. Epidemiology studies
show anaphylaxis and anaphylactic shock is
relatively rare, but its incidence is increasing.
Defined according to the World Allergy Organization
(WAO) definition ‘a severe, life-threatening generalized
or systemic hypersensitivity reaction’
Anaphylactic shock is an end manifestation of
anaphylaxis, occurs when there is inadequate tissue
perfusion causing end organ damage.
Signs and Symptoms
Anaphylaxis causes a generalized systemic reaction affecting
multiple organ systems,
symptoms involving the skin occur in 80–90% of cases,
respiratory tract in 70%, GI in 45%, CV in 45%, and CNS
involvement in 15%.
The cardiovascular and respiratory systems are the principal
shock organs in fatal anaphylaxis. Death occurs in most often
due to shock or acute respiratory distress.
Anaphylaxis develops rapidly with symptoms developing in
minutes. Biphasic reactions, where symptoms resolve and
then reappear later occurs around 20% of the time.
A systematic review of biphasic reactions found the medium
time between resolution of initial symptoms and onset of
delayed symptoms to be 11 h, with a range of 0.2–72 h
Epinephrine is the first line treatment of
anaphylaxis, and delayed administration
increases the likelihood of poor outcomes
In most situations intramuscular
administration is preferred. IM epinephrine
should be given in 0.2–0.5 mg doses (1:1000
dilution), and repeated every 5 min depending
on the resolution of symptoms
Mechanism of action
Epinephrine exerts its effects via alpha and beta adrenergic
receptors in a dose dependent response where beta
receptors effects are dominant at low doses, but alpha
receptors effects are seen at higher doses.
The α1 receptors cause vasoconstriction increasing
peripheral vascular resistance and blood pressure and
improving coronary and cerebral perfusion.
The β1 receptors exert positive chronotropic and inotropic
effects which improves cardiac output and increases blood
In the respiratory system, β2 receptors stimulation results in
bronchodilation, and relief and respiratory symptoms. β
receptors also inhibit release of mediators from mast cells
and basophils, via increased cAMP production
Beta blockers may complicate the treatment of anaphylaxis, as
some of the beneficial effects of epinephrine will be diminished . In
patients on betablockers who do not respond to epinephrine , other
vasopressors should be considered.
Glucagon has been reported to be a successful treatment in
several case reports of patients on beta blockers who experienced
Vasopressin or phenylephrine can be used to increase systemic
vascular resistance without further increasing heart rate.
Methylene blue has been reported to be an effective treatment in
cases of severe anaphylaxis not responding to epinephrine, as well
as cases of anaphylaxis without hypotension.
Shock is an imbalance between
tissue oxygen supplement and
utilization, not just a state of low
Fundamental of shock treatment is
restoration of tissue oxygenation
and tissue function.
Close monitoring of perfusion
status and supportive care for
organ dysfunctions is important
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, founder of Baltimore’s renowned Shock Trauma Institute,
Pericardial tamponade compression of heart caused by the fluid in the pericardium
The classification of hemorrhage into four classes based on the initial clinical signs such as vital signs, mental status, and urine output was traditionally introduced and a usefulmethod for estimating the percentage of blood volume loss . The estimated blood volume of normal adults is approximately 7% of body weight, and a 70 kg male has approximately 5 L of circulating blood volume (Table 2.1). There is variability in estimating blood volume, the blood volume of obese adult calculated based on the ideal body weight not on the actual body weight to prevent overestimation.
Normal jvp is 6 to 8 cm of water
Hemorrhage induces tissue hypoperfusion and increased production of lactic acid which results in metabolic acidosis. In addition, aggressive fluid resuscitation with unbalanced crystalloid such as 0.9% sodium chloride solution could also induce hyperchloremic acidosis. Acidosis induces impairment of coagulation cascade characterized by prolongation of clot formation time and reduction of clot strength and decreased myocardial performance, resulting in tissue hypoperfusion and acidosis . Hypothermia is induced by envi
ronmental exposure, massive bleeding, fluid resuscitation, and administration of sedative drugs. Hypothermia could induce platelet dysfunction, destabilization of coagulation factors, and increase in fibrinolytic activity . The importance of the early diagnosis and prevention of coagulopathy has increased significantly in recent years. Endogenous factors related with coagulopathy are endogenous anticoagulation, fibrinogen depletion, hyperfibrinolysis and fibrinolytic shutdown, platelet dysfunction, and endothelial dysfunction . Coagulopathy could be worsened by several factors such as acidosis, hypothermia, anemia, and anticoagulants/ antiplatelets.
Lactate normal level 0.5 to 2.2 mmol
Lactate level is the biomarker for tissure hypoperfusion and anoxia it is associate with the mortality rate in trauma
Base deficit amout of base in mmol required to titrate a liter of whole arterial blood to ph of 7)range 9.3 to -1.5 mmolreflects the tissue hypoperfusion base deficit is superior to ph in determining the outcome of trauma
It is an act of maintaininhg the blood pressure lower than the physiological levels in pt who has suffered from hemorrhagic shock in order to main tain adequate vaso constriction and oran perfusion and to prevent undesirable coagulopathy during initial fluid resuscitation.
. Recent advances in early treatment, technological advancement, and pharmacologic treatment have improved the prognosis of patients and improved long-term survival and quality of life. Therefore, the mortality rate due to cardiogenic shock is also decreasing, and the prognosis of the high-risk patients is better than the previous one
Catecholamine doses = μg/kg/min FiO2 fraction of inspired oxygen, MAP mean arterial pressure, GCS Glasgow coma score
CREAT 0.7 TO 1.35 LIVER BILIRUBIN 0.1 TO 1.2
Glucagon mechanism of action is via direct activation of adenylate cyclase, bypassing the blocked adrenergic receptors.
Methylene blue inhibits NO mediated vasodilation via competitive inhibition of guanylate cyclase decreasing cyclic GMP production and subsequent vasodilation . This mechanism acts independent of adrenergic receptors, and may be effective in patients with refractory anaphylactic shock