Shock Management

Video Transcript

Hypovolemic shock

By the end of this topic, you will be able to:

• Identify the causes of hypovolemic shock and

• Discuss the treatment and management of hypovolemic shock

Shock can be defined as a state of acute circulatory failure resulting in decreased organ
perfusion, with inadequate delivery of oxygenated blood to tissues and end-organ dysfunction.

The mechanisms that can result in shock are divided into 4 main categories. They are:

• Hypovolemic

• Distributive

• Cardiogenic and

• Obstructive

In this topic, we will be focusing on Hypovolemic shock, its causes, treatment and management.

Hypovolemic Shock

It is an acute life-threatening condition characterized by rapid fluid loss resulting in multiple

organ dysfunction due to the insufficient circulatory volume and tissue perfusion. It is a
medical or surgical emergency which must be recognized early and intervention initiated timely
to prevent progression and mortality. Let’s now take a look at the causes of hypovolemic shock.

• Hypovolemic shock is primarily caused by fluid and blood loss which may be internal or
external.

• Causes of external fluid loss include hemorrhage, gastrointestinal losses, renal loss,
endocrine loss, and cutaneous loss.

• Causes of internal fluid loss include occult gastrointestinal bleeding, ruptured ectopic
pregnancy, and bleeding into potential spaces, such as hemoperitoneum, hemarthrosis,
and hemothorax.

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• Hemorrhagic shock is the commonest example of hypovolemic shock.

• It is caused typically due to trauma, surgical complications, vascular disorders such as

ruptured abdominal aortic aneurysm, and GI disorders including bleeding peptic ulcer
disease or esophageal varices.

• The hemorrhagic shock also includes pregnancy-related disorders such as placental

abruption, postpartum hemorrhage, and placenta previa.

Now let’s understand the pathophysiology of the hypovolemic shock.

The primary dysfunction in hypovolemic shock is the insufficient tissue perfusion. As perfusion
declines, oxygen supply to the cells also becomes inadequate, resulting in a shift to anaerobic
cellular metabolism. This, in turn, results in increased carbon dioxide or CO2 production and
elevated blood levels of lactic acid. In hypovolemic shock, the inflammatory and clotting
cascades are activated in areas that are insufficiently perfused. The hypoxic endothelial cells
activate white blood cells which, in turn, bind to the endothelium releasing pro-inflammatory
mediators including leukotrienes and cytokines, and toxic substances such as reactive oxygen
species and proteolytic enzymes.

As substrates are reintroduced in circulation and to tissue capillaries, neutrophil activity

increases and leads to production of toxic superoxide and hydroxyl radicals. In addition, on
reperfusion, pro-inflammatory chemokines are circulated and delivered to the organs and
tissues. This combination of direct and indirect injury resulting from reperfusion causes Multiple
Organ Dysfunction Syndrome or MODS. With persistent hypovolemia, renal hypoperfusion
results in acute tubular necrosis which is manifested as oliguria and rising levels of serum
creatinine. In the heart, persistent hypovolemia results in reduced coronary perfusion and
together with the increased levels of pro-inflammatory chemokines, result in reduced
myocardial contractility and down-regulation of the β-receptors. In addition, in the GI tract,
untreated hypovolemic shock results in hepatic hypoperfusion and diffuse hepatocellular
necrosis and reduced production of clotting factors.

Let’s take a closer look at the clinical presentation of hypovolemic shock.

History is crucial in a patient with possible hypovolemic shock. External hemorrhagic shock is
often obvious on presentation and easily diagnosed, however, internal hemorrhage may not be
easily diagnosed. Symptoms of hypovolemic shock includes weakness, confusion, and

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lightheadedness. In patients who are conscious, history should include the site of pain, nature of
the pain, and mechanism of injury in trauma patients. Systolic BP should not be used as a
determinant or an indicator for the severity of shock, as compensatory mechanisms may mask
BP decline until blood volume is lost by 30%. In hemorrhagic shock and dehydration, clinical
manifestations depend on the percentage of extracellular fluid or blood volume loss.

Based on how much blood is lost, hemorrhagic shock can be categorized into four classes.
They are

Class 1 – (0-15% blood volume loss)

Class II – (15-30% blood volume loss)

Class III – (30-40% blood volume loss) and

Class IV - (loss of 40%)

At Class 1 level, only mild tachycardia occurs and blood pressure (BP), pulse rate, and
respiratory rate are often normal. Capillary refill may be delayed by longer than 3 seconds in this
level.

Clinical symptoms, at Class 2, include tachycardia, tachypnea, col clammy extremities, and
delayed capillary refill.

At class 3 stage, patients develop marked tachypnea and tachycardia, oliguria, decreased
systolic BP, and significantly altered sensorium. In the absence of other injuries and fluid losses,
a decline in blood volume loss by 30 to 40% is the minimal loss.

Class IV – Symptoms at this stage include marked tachycardia, reduction in systolic BP, oliguria
or anuria, depressed mental status, and cold pale skin.

Diagnostic Workup

• History and physical examination should be followed by a comprehensive workup

tailored to the probable cause of the hypovolemia if the patient is regaining stability
upon adequate resuscitation.

• Initial laboratory tests should consist of complete blood count, blood glucose levels,
blood electrolytes, clotting profile, and a urine pregnancy test.

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 Shock Management

• Imaging studies may also be necessary in evaluation of hemorrhagic shock: chest

radiographs may be necessary to exclude to exclude pulmonary hemorrhage, GI
endoscopy to evaluate GI bleeding, and abdominal ultrasonography in evaluating
abdominal bleeding.

Now let’s discuss the Treatment and Management of Hypovolemic Shock

Treatment and Management

Treatment of hypovolemic shock usually begins with prehospital care. The goals of
resuscitation are to optimize oxygen delivery to tissues and control further blood or fluid loss.
Management begins with immediate assessment of patient’s airway, a comprehensive
respiratory examination to assess breath sounds. Supplemental oxygen should be administered
to all patients with ventilator support given if required. An arterial line should be placed in all
patients with severe hemorrhage, this line enables arterial blood gas testing and provision of
continuous blood pressure monitoring.

If the patient regains cardiovascular stability, the patient’s blood should by typed and
crossmatched for blood transfusion. If the patient’s vital signs do not improve upon initial fluid
resuscitation, crystalloid infusion should be continued. The patient should be nursed with the
legs raised while fluid is being administered to improve circulation. Further blood loss may be
controlled by applying direct pressure for external bleeding, and emergency surgical intervention
for internal bleeding. In patients who have lost pulse upon arrival at the hospital, an emergency
thoracotomy with cross-clamping of the aorta may be performed to preserve cerebral blood
flow.

Shock remains a leading cause of mortality and morbidity. Early recognition and prompt
management with diagnostic evaluation can save many lives.

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 Shock Management

Video Transcript

Anaphylactic shock

By the end of this topic, you will be able to:

• Identify the different causes of anaphylactic shock

• Describe the pathophysiology of anaphylactic shock

• List signs and symptoms of anaphylactic shock and

• Discuss treatment and management of anaphylactic shock

Anaphylaxis is an acute, life-threatening multiorgan system reaction caused by an

immunoglobulin E or IgE-mediated immediate hypersensitivity reaction. It involves mast cell and
basophil degranulation release of chemical mediators.
Anaphylaxis reaction typically occurs following exposure to certain sensitized triggers. The
major effects of anaphylaxis on the cardiovascular system are reduced vascular tone and
capillary leakage which causes shock. The classic form of anaphylaxis is characterized by prior
sensitization to an allergen, resulting in clinical manifestations of anaphylaxis upon a later re-
exposure. Now let’s understand the various causes of Anaphylactic Shock

Ig-E mediated anaphylaxis occurs when an allergen elicits an IgE or Immunoglobulin E antibody
response in a sensitized individual who has been previously exposed to it.

These allergens include:

• Foods such as nuts, shellfish, cow’s milk, eggs, wheat, and soy
• Antibiotics like penicillin, cephalosporins.
• Vaccines such as to the influenza vaccine in egg-allergic patients.
• Blood and blood products

Other causes include Insulin and other hormones, Anesthetic agents, Latex allergy and
Antitoxins. Now let us look at the causes of anaphylactoid reactions.

Causes of Anaphylactoid reactions associated with non-immunologic mechanisms and direct

mast cell degranulation include:

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• Nonsteroidal anti-inflammatory drugs such as aspirin. These reactions in response to

aspirin are IgE or Immunoglobulin E independent as they result from altered arachidonic
acid metabolism. These drugs inhibit cyclooxygenase activity, resulting in a shutdown of
the prostanoid pathway and overproduction of leukotrienes via the 5-lipoxygenase
pathway, causing anaphylactoid symptoms in some patients, especially aspirin-sensitive
asthmatics.

• Radiocontrast media, the medical drugs that are used to improve the visibility of internal
organs

• Other causes of anaphylactoid reactions include: Opioids, sulfites, alcohol, gamma

globulin, antisera, neuromuscular blockers.

Now let’s discuss the pathophysiology of the anaphylactic shock.

• In anaphylaxis, the release of chemical mediators such as histamine, prostaglandins,

leukotrienes, and tryptase result in several systemic responses. These include smooth
muscle contraction, increased mucous secretions and airway edema in the respiratory
tract, increased gastrointestinal contractility, and cardiovascular changes notably
widespread vasodilation and increased vascular permeability.

• Interleukin (IL)-4 and IL-13 also contribute to the initial inflammatory cell responses to
anaphylaxis. Other mediators such as prostaglandin D2, platelet-activating factor or PAF,
and the cysteinyl leukotrienes (LTC4, LTD4, and LTE4) also contribute to the
inflammatory response.

• Vasodilation, a vascular response in anaphylaxis which results in hypotension, is

mediated by both histamine H1 and H2 receptors.

Here is the flowchart that provides an overview of the pathophysiology of an anaphylactic

reaction.

• Anaphylaxis is associated with myocardial ischemia, cardiac arrhythmias, cardiac

conduction abnormalities, and T-wave defects which may cause bradycardia, although
tachycardia is the main heart rate abnormality in anaphylactic shock.

• The peripheral vasodilation also contributes to bradycardia.

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• Venodilation may cause excessive venous poling resulting in reduced venous return
which activates the baroreceptors in the left ventricle causing a reflex stimulation of the
vagus nerve and, in turn, bradycardia.

Now let’s take a closer look at the clinical presentation of anaphylactic shock.

Anaphylactic reactions often develop within minutes usually within an hour of exposure to the
inciting allergen. The reactions are typically more rapid if exposure is parenteral. In rare cases,
however, symptoms may be delayed for many hours. Anaphylaxis may only begin with minor
symptoms such as the cutaneous manifestations and progress to the life-threatening
cardiovascular and respiratory symptoms. Initial symptoms of anaphylaxis include flushing,
pruritus caused by the histamine-mediated stimulation of sensory nerve endings, dyspnea, and
a sense of impending doom. Typically, symptoms involve the skin, eyes, gastrointestinal and
respiratory tracts, and cardiovascular and central nervous systems. Common respiratory tract
symptoms include nasal congestion, rhinorrhea, sneezing, cough, as well as dyspnea and
wheezing which result from severe airway obstruction due to airway edema and bronchospasm.
Eye symptoms include conjunctival injection, eye itch, and tearing. Gastrointestinal symptoms
include vomiting, diarrhea, abdominal cramps, and are more common in cases of food allergy.
The most common cause of death in anaphylaxis is complete airway obstruction.

Diagnosis of anaphylaxis is largely clinical and laboratory investigations are usually not
necessary in evaluating except if the diagnosis is unclear. A history of exposure to a potent
allergen shortly before onset of symptoms often substantiates the diagnosis. In anaphylaxis,
plasma histamine and tryptase are usually elevated. Plasma histamine levels begin to rise
within 10 minutes of onset of the reaction, falling after 30 minutes. Serum tryptase levels peak
an hour after the onset of the reaction, lasting for 1 to 6 hours.

A 24-hour urine analysis for N-amethyl histamine level can also be a helpful alternative.

Now let’s discuss the treatment and management of Anaphylactic shock

Immediate therapy is required in all patients with positive signs and symptoms as the reaction
may rapidly progress to respiratory failure, shock, and death. In case of suspected imminent
respiratory collapse immediately intubate. Place the patient in a recumbent position. Obtain
large bore IV lines, and ensure continuous monitoring of blood pressure, heart rate, and oxygen

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 Shock Management

saturation. IM epinephrine 0.3 to 0.5 milligram, 1 is to 1000 to anterior or lateral thigh and repeat
in 5 minutes if needed. Do not delay epinephrine administration, and there is NO absolute
contraindication to it. In severe cases, if patient is unresponsive to IM epinephrine, give IV
epinephrine 0.1-0.2 milligram (1 milliliter 1 is to 1000) in 10 milliliter 0.9% Sodium chloride
(0.1milligram per milliliter) 1 to 2 minutes until target response is achieved. If hypotensive,
administer 1 to 2 liters IV 0.9% Sodium chloride fast infusion.

If clinical response is achieved

Treat with histamine (H1 and H2) blockers such as diphenhydramine(H1) 25 to 50 milligram IV
and Ranitidine (H2) 50 milligram IV OR Famotidine (H2) 20 milligram IV.

If no clinical response

Glucagon 1 to 2 milligram IV/IM every 5 minutes till response, if patient is taking outpatient beta
blockers. Continuous IV epinephrine at 0.1 to 1 microgram per kilogram per minute till
response. Continuous and rapid fluid resuscitation. If patient is not intubated, inhaled beta-
agonists such as albuterol 0.5 milliliter 0.5% solution in 2.5 milliliter 0.9% Sodium chloride
nebulized every 15 minutes till effect. If clinical response is achieved, treat with histamine (H1
and H2) blockers such as diphenhydramine (H1) 25 to 50 milligram IV and Ranitidine (H2) 50
milligram IV OR Famotidine (H2) 20 milligram IV.

The management of shock is essential as it helps in the early identification and determination
of etiology to provide appropriate care. There is a need for careful assessment and
individualized approach for management of shock.

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Video Transcript

Septic Shock

By the end of this topic, you will be able to:

• Explain about the causes of septic shock and

• Outline the treatment and management of septic shock

Shock is life-threatening circulatory failure with inadequate tissue perfusion. The human body
usually mounts local and systemic responses to pathogens which invade tissues. Fever or
hypothermia, tachypnea, tachycardia, and leukocytosis are the main signs the systemic
response, and this if called systemic inflammatory response syndrome or SIRS. SIRS may be
caused by an infectious or non-infectious etiology, if the etiology is infectious, it is referred to as
sepsis.

Sepsis may progress to causing dysfunction of organs remote from the site of infection. This
condition is referred to as severe sepsis. In the event sepsis becomes associated with
hypotension and hypoperfusion which cannot be corrected by appropriate fluid resuscitation,
the patient is said to have septic shock, the most severe form of sepsis. The American College
of Chest Physicians/Society of Critical Care Medicine Conference or ACCP/SCCM defines
septic shock as sepsis with hypotension systolic blood pressure less than 90 millimeters of
mercury or 40 millimeters of mercury less than the patient’s normal blood pressure for at least
an hour despite adequate fluid resuscitation.

Now let us understand the causes of Septic Shock:

• Sepsis could be triggered by any class of microorganisms; however bacterial causes

predominate.

• Fungal infections are the second commonest infectious causes of sepsis.

• Sepsis may also be caused by parasites, acute viral infections, and Pneumocystis
infections.

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• Microbial invasion of the bloodstream is not a prerequisite for the development of

sepsis as local inflammation can also trigger a remote organ dysfunction as well as
widespread vasodilatation and hypotension.

• Sepsis and septic shock are largely caused by respiratory infections, accounting for 40
to 50% of all cases.

• Genitourinary and gastrointestinal infections are also common sources of both sepsis
and septic shock, with skin and soft tissue infections, central nervous system infections,
and bone and joint infections occurring relatively less commonly.

Pathophysiology of the hypovolemic Shock:

The first line of host defense in the body is the endothelium, which is often broken through by
microbes to enter the body. The first step in mounting an immune response is identifying the
microbes using certain pattern recognition receptors, the toll-like receptors or TLR. A host
protein called liposaccharide or LPS-binding protein binds to lipid A and transfers the endotoxin
to cluster of differentiation 14 or CD14 on the surfaces of white blood cells including
monocytes, neutrophils, and macrophages. LPS is passed subsequently to myeloid
differentiation factor 2 or MD-2 which is bound to Toll-like receptor or TLR to form a complex
that transduces the LPS recognition signal to the insides of the cell.

Recognition of the invading pathogens leads to the production and release of several host
molecules including cytokines, chemokines, leukotrienes, and prostanoids, which increase
blood flow to the infected tissue, increase local vascular permeability, and recruit neutrophils.
These reactions are features of an acute local inflammation, the body’s primary innate immune
response to eliminate invading pathogens. The cytokines released stimulate leukocytes and
vascular endothelial cells to release cell-surface molecules, improve adhesion of neutrophils to
the endothelium at the site of infection. Chemokines, predominantly interleukin (IL)-8 and IL-17,
act as chemo attractants for migration of neutrophils to the site of infection. During
inflammation, neutrophils and macrophages release large amounts of reactive oxygen species
or ROS which allows these white blood cells to kill the microbes.

Intravascular thrombosis is the hallmark of an acute local inflammatory reaction. This helps to
wall off the microbes and prevent further spread of the infection and inflammation to other

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 Shock Management

tissues. Tissue factor on cell surfaces then binds to factor VII a to form a complex which
activates factors X and IX leading to the activation of the intrinsic and extrinsic coagulation
pathways, culminating in the production of fibrin. As the local and systemic immune response
to the infection increase in intensity, the effects of the circulating cytokines become more
complex and the high concentrations of both pro- and anti-inflammatory cytokines results in a
net anti-inflammatory effect. Despite, the increased blood levels of catecholamines as part of
the systemic immune response, vasodilation persists and is caused by the endothelial
production of nitric oxide, and the release of bradykinin, platelet-activating factor and beta-
endorphins which are potent hypotensive agents.

Clinical Presentation

Symptoms of sepsis are often nonspecific and include fever, chills, disorientation, confusion,
nausea, vomiting, and difficulty breathing. Fever is the commonest symptom, although it may be
absent in the elderly or persons in immunocompromised states. Symptoms should also be
localized to the source of sepsis, such may include:

Headache, neck stiffness, sore throat for head and neck infections, cough, pleuritic chest pain,
difficulty breathing for chest infections, abdominal pain and distention with diarrhea for
gastrointestinal and abdominal infections

Diagnostic Workup

A diagnostic workup should commence once patients are stabilized. Baseline investigative
tests include complete blood count with differentials, coagulation studies, urinalysis, serum
electrolyes, blood glucose levels, liver and renal function tests, and microbiological studies such
as blood cultures, urine cultures, and cultures of tissue samples and secretions. Imaging
studies are also required, as indicated, and include chest and abdominal radiographs, and
computerized tomography or CT and magnetic resonance imaging or MRI of abdomen, brain,
and extremities are essential for determining the primary source of sepsis.

Fluid Management in Septic Shock

On clinical suspicion of sepsis with Systolic Blood Pressure or SBP less than 90 millimeters of
mercury, Mean Arterial Pressure or MAP less than 40 millimeters of mercury. Administer an
initial bolus of 20mls/kg of 0.9% normal saline or lactated Ringers. If SBP less than 90

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millimeters of mercury or MAP less than 40 millimeters of mercury despite initial fluid
administration. Insert a central venous pressure or CVP catheter. If CVP less than 8 millimeters
of mercury, repeat the bolus of at least 20mls/kg of 0.9% normal saline or lactated Ringers
solution. If CVP greater than or equal to 8 millimeters of mercury despite fluid administration,
measure MAP.

If MAP less than 60 millimeters of mercury, administer vasopressors – norepinephrine or

dopamine. If MAP greater than or equal to 60 millimeters of mercury, measure oxygen
saturation of central venous blood or ScvO2. If ScvO2 less than 70%, transfuse if hematocrit less
than 30 with dobutamine if cardiac index less than 3.5L/min.m2. If all goals MAP greater than or
equal to 60millimeters of mercury, SBP greater than or equal to 90 millimeters of mercury, CVP
greater than or equal to 8 millimeters of mercury, and ScvO2 greater than or equal to 70% have
not been achieved despite all above, recommence the therapy from the insertion of CVP
catheter.

If all goals have been achieved and vasopressors are still required, consider adjunctive
therapies. If all goals have been achieved, and vasopressors are no longer required,
resuscitation is complete.

Adjunctive Therapies in Septic Shock

Clinical picture of sepsis and need for vasopressors despite achieving fluid management goals
are the following:

With acute physiology and chronic health evaluation or APACHE II index greater than or equal to
25, in the absence of a “Do not Resuscitate”, bleeding tendency, moribund state, administer
Drotrecogin alfa. If the conditions are present, measure randomly timed cortisol level. If level
less than 15 microgram per milliliters, consider physiologic corticosteroid replacement. If level
15 to 34 microgram per milliliters with an increase in response to corticotropin test, continue
corticosteroid replacement if randomly timed cortisol falls below microgram per milliliters. If
Greater than or equal to 9 microgram per milliliters, corticosteroid therapy won’t be effective. If
level greater than 34 microgram per milliliters, corticosteroid therapy is unlikely to be of benefit.

Antibiotic treatment in Septic Shock

In immunocompromised patients, consult with an infectious disease expert as antibiotics may

include those against the opportunistic pathogens and infecting bacterial pathogens. In non-

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immunocompromised patients, consider treatment for bacterial infection. For community-based

bacterial pathogens that are antibiotic sensitive such as Streptococcus pneumonia, Escherichia
coli, Haemophilus influenza, select monotherapy of ceftriaxone, flouroquinolones,
ampicillin/sulbactam, or macrolides. Modify antibiotic regimen based on results of microbial
investigations. For suspected nosocomial infections Methicillin-Resistant Staphylococcus
Aureus or MRSA, pseudomonas aeruginosa, administer broad-spectrum cephalosporin or
carbapenems or beta-lactam or beta-lactamase inhibitors plus flouroquinolones or
aminoglycoside plus MRSA-sensitive agent such as vancomycin.

The management of shock is important as it helps in the early identification to provide the
necessary care.

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Video Transcript

Cardiogenic shock

By the end of this topic, you will be able to:

• Explain the causes of cardiogenic shock and

• Describe the treatment and management of cardiogenic shock

Cardiogenic shock is a clinical condition characterized by inadequate blood circulation and

organ hypoperfusion caused primarily by cardiac dysfunction. The condition results from failure
of the cardiac pump function resulting in an inability to maintain circulation to vital organs and
tissues which, without treatment, may lead to multisystem dysfunction and Cardiogenic shock
is characterized by prolonged hypotension systolic blood pressure less than 90 millimeters of
mercury associated with severe decrease in cardiac output that is less than 1.8 liters per minute
per square meter without support and less than 2.2 liters per minute per square meter with
cardiac support despite adequate intravascular volume pulmonary capillary wedge pressure or
PCWP greater than 18 millimeters of mercury. Let’s begin with the causes of cardiogenic shock.

Cardiogenic shock has multiple causes which include:

• Acute myocardial infarction

• Post-cardiac arrest

• Acute fulminant myocarditis

• Severe cardiomyopathy with congestive heart failure

• Takosubo’s cardiomyopathy

• Pulmonary embolism

• Myocardial contusion

• Acute or severe valvular heart disease

• Ventricular outflow obstruction – Aortic stenosis or acute mitral regurgitation

• Obstruction to ventricular filling – mitral valve stenosis, pericardial effusion, and

pericardial tamponade

• Medications such as beta-blockers or calcium channel blockers overdose and finally

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• Refractory bradyarrhythmia

Let’s now discuss about the pathophysiology of the Cardiogenic shock.

Cardiogenic shock typically occurs when myocardial dysfunction exceeds a critical pump
threshold from a single large myocardial infarction (typically greater than 40% of the
myocardium), a resultant damage from multiple smaller infarctions, or widespread myocardial
damage secondary to other causes. The reduced coronary perfusion exacerbates ischemia and
causes progression of myocardial dysfunction. Lactic acidosis resulting from tissue
hypoperfusion and hypoxemia from pulmonary edema further worsens the myocardial ischemia
and the resultant hypotension. At pH less than 7.25 (severe acidosis), endogenous and
exogenous catecholamines become ineffective. Decreased systemic perfusion also stimulates
compensatory vasoconstriction which further worsens myocardial dysfunction, leading to
death.

Cardiogenic shock often occurs in a setting of acute myocardial infarction, typically, among
elderly female patients, with previous history of comorbidities such as diabetes,
cerebrovascular disease, renal insufficiency, and prior coronary artery disease. Cardiogenic
shock is most likely to occur in patients with Myocardial Infarction or MI of anterior location.
Clinical features of cardiogenic shock typically occur 6.2 hours after the onset of an MI,
however, most patients develop the features within 24 hours. In a few cases, patients with
cardiogenic shock may develop signs of poor cardiac output and systemic hypoperfusion, but
with normal blood pressure. This condition called normotensive cardiogenic shock.

Diagnostic workup should not delay initial resuscitative therapy and should be initiated
concurrently. A detailed history and physical examination of the patient should be performed.
Routine investigations for evaluation of cardiogenic shock include complete blood count,
electrocardiogram, chest radiographs, and echocardiogram. Pulmonary artery catheterization
and left heart catheterization and coronary angiography may also be used in evaluating patients
with cardiogenic shock in certain cases. Laboratory findings in cardiogenic shock include
elevated white blood cell count with left shift.

Chest radiographs demonstrate features of pulmonary congestion in about two-thirds of

patients. There is often no cardiomegaly in cases resulting from a first MI. Patients with
suspected cardiogenic shock should have a two-dimensional echocardiogram with color-flow

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 Shock Management

Doppler for accurate diagnosis of the cause. This may reveal aortic regurgitation, aortic
dissection, and evidence of pulmonary embolism.

Let’s take a closer look at the treatment and management of cardiogenic shock.

In suspected cardiogenic shock, the Systolic Blood Pressure or SBP less than 90 millimeters of
mercury, signs of cardiac depression.

Initial evaluation and stabilization that should be prompted include:

• Immediate Electrocardiogram or ECG

• Supplemental oxygen/mechanical ventilation
• Blood pressure support. Dopamine at 5 to 15 micrograms per kilogram per minute, if
SBP less than 90 millimeters of mercury on initial evaluation.
• If SBP less than 80 millimeters of mercury despite dopamine infusion, administer
norepinephrine at 1 to 20 micrograms per kilogram per minute. Goal of BP is greater
than 65 millimeters of mercury. Intra-arterial pressure monitoring is indicated in all
patients on vasopressors.

If ECG is positive for Acute Myocardial Infarction:

• Commence immediate reperfusion therapy with thrombolysis or cardiac catheterization.

• Thrombolysis and intra-aortic balloon counter pulsation if cardiac lab is not readily
available
• If Cath lab is available, revascularization is indicated if less than 36 hours from onset of
Acute Myocardial Infarction or AMI, less than 12 to 18 hours from onset of shock, and no
other contraindications to anticoagulation.
• Revascularization should be performed by percutaneous intervention with use of stents
and abciximab.
• If no revascularization method possible, continue supportive therapy.
• If blood pressure stabilizes but cardiac output still low, consider inotropic support with
dobutamine 2.5 to10 Micrograms per min or milrinone 0.375 or 0.75 microgram per
kilogram per min. Avoid milrinone in renal failure and use with great caution in patients
with hypotension.
• Consider for left ventricular assist device or cardiac transplant in refractory shock.

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 Shock Management

If ECG is negative:

• Evaluate Left ventricular or LV and Right Ventricular or RV function and rule out
mechanical complications which may cause cardiogenic shock.
• Pulmonary artery monitoring to confirm cardiac cause.
• Proceed to immediate reperfusion therapy with thrombolysis and cardiac
catheterization. If no revascularization method possible, continue supportive therapy.
• If BP stabilizes but cardiac output still low, consider inotropic support with dobutamine
2.5 to 10 micrograms per minute or milrinone 0.375 to 0.75 micrograms per kilogram
per minute.
• Avoid milrinone in renal failure and use with great caution in patients with hypotension.
• Consider for left ventricular assist device placement or cardiac transplant in refractory
shock.

Shock is defined by critical tissue hypoperfusion. It must be rapidly reversed before organ
damage is sustained and irreversible. Henceforth sound knowledge is required in the
management of shock.

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