2. • Shock is defined as circulatory insufficiency that
creates an imbalance between tissue oxygen
supply and oxygen demand.
• The result of shock is global tissue hypoperfusion
and is associated with a decreased venous oxygen
content and metabolic acidosis (lactic acidosis).
• Clinically, shock may have a predominant cause,
but as the shock state persists or progresses to
irreversible end organ damage, other
pathophysiologic mechanisms become operative
3. • Shock is classified into four categories by etiology
(1) hypovolemic (caused by inadequate circulating
volume)
(2) cardiogenic (caused by inadequate cardiac
pump function)
(3) distributive (caused by peripheral vasodilatation
and maldistribution of blood flow)
(4) obstructive (caused by extra cardiac obstruction
to blood flow).
4. Pathophysiology
• The onset of shock -- autonomic responses, many of which serve to
maintain perfusion pressure to vital organs.
• Stimulation of the carotid baroreceptor stretch reflex activates the
sympathetic nervous system leading to:
• (1) arteriolar vasoconstriction, resulting in redistribution of blood
flow from the skin, skeletal muscle, kidneys, and splanchnic viscera;
• (2) an increase in heart rate and contractility that increases cardiac
output;
• (3) constriction of venous capacitance vessels, which augments
venous return;
• (4) release of the vasoactive hormones epinephrine, norepinephrine,
dopamine, and cortisol to increase arteriolar and venous tone; and
• (5) release of antidiuretic hormone and activation of the reninangiotensin axis to enhance water and sodium conservation to
maintain intravascular volume.
• These compensatory mechanisms attempt to maintain DO2 to the most
critical organs—the coronary and cerebral circulation. During this
process, blood flow to other organs such as the kidneys and
gastrointestinal tract may be compromised.
5. • In the early phases of septic shock, these physiologic changes
produce a clinical syndrome called the systemic inflammatory
response syndrome or SIRS, defined as the presence of two or more
of the following features:
• (1) temperature greater than 38°C (100.4°F) or less than 36°C
(96.8°F);
• (2) heart rate faster than 90 beats/min;
• (3) respiratory rate faster than 20 breaths/min; and
• (4) white blood cell count greater than 12.0 x 109/L, less than 4.0 x
109/L, or with greater than 10 percent immature forms or bands.
• 5) As SIRS progresses, shock ensues, followed by multiorgan
dysfunction syndrome (MODS) manifested by myocardial
depression, adult respiratory distress syndrome, disseminated
intravascular coagulation, hepatic failure, or renal failure.
• The fulminate progression from SIRS to MODS is determined by the
balance of anti-inflammatory and proinflammatory mediators or
cytokines that are released from endothelial cell disruption
6. • The cellular response to decreased DO2 ( oxygen delivery
per minute ) is adenosine triphosphate depletion leading to
ion-pump dysfunction, influx of sodium, efflux of
potassium, and reduction in membrane resting potential.
Cellular edema occurs secondary to increased intracellular
sodium, while cellular membrane receptors become poorly
responsive to the stress hormones insulin, glucagon,
cortisol, and catecholamines. As shock progresses,
lysosomal enzymes are released into the cells with
subsequent hydrolysis of membranes, deoxyribonucleic
acid, ribonucleic acid, and phosphate esters. As the cascade
of shock continues, the loss of cellular integrity and the
breakdown in cellular homeostasis result in cellular death.
These pathologic events give rise to the metabolic features
of hemoconcentration, hyperkalemia, hyponatremia,
prerenal azotemia, hyper- or hypoglycemia, and lactic
acidosis.
7.
8. ABCDE tenets of shock resuscitation
•
•
•
•
•
establishing Airway
controlling the work of Breathing
optimizing the Circulation
assuring adequate oxygen Delivery, and
achieving End points of resuscitation
9. Establishing Airway
• Airway control is best obtained through endotracheal
intubation for airway protection, positive pressure
ventilation (oxygenation), and pulmonary toilet.
Sedatives, which are frequently used to facilitate
intubation, can exacerbate hypotension through
arterial vasodilatation, venodilation, and myocardial
suppression. Furthermore, positive pressure ventilation
reduces preload and cardiac output. The combination
of these interventions can lead to hemodynamic
collapse. Volume resuscitation or application of
vasoactive agents may be required prior to intubation
and positive pressure ventilation.
10. Controlling the Work of Breathing
• Control of breathing is required when tachypnea accompanies
shock. Respiratory muscles are significant consumers of oxygen
during shock and contribute to lactate production. Mechanical
ventilation and sedation decrease the work of breathing and have
been shown to improve survival. SaO2 should be restored to greater
than 93 percent and ventilation controlled to maintain a PaCO2 35
to 40 mm Hg. Attempts to normalize pH above 7.3 by
hyperventilation are not beneficial. Mechanical ventilation not only
provides oxygenation and corrects hypercapnia but assists, controls,
and synchronizes ventilation, which ultimately decreases the work
of breathing. Neuromuscular blocking agents are used as adjuncts
to further decrease respiratory muscle, oxygen consumption and
preserve DO2 to vital organs
11. Optimizing the Circulation
• Circulatory or hemodynamic stabilization begins with intravascular access
through large-bore peripheral venous lines. Trendelenburg positioning,
historically considered necessary for maintaining perfusion in the
hypotensive patient, does not improve cardiopulmonary performance
compared with the supine position. It may worsen pulmonary gas
exchange and predispose to aspiration. If a volume challenge is urgently
required, rather than using the Trendelenburg position, an alternative is to
raise the patient's legs above the level of the heart with the patient
supine.
• Fluid resuscitation begins with isotonic crystalloid; the amount and rate
are determined by an estimate of the hemodynamic abnormality. Most
patients in shock have either an absolute or relative volume deficit, except
the patient in cardiogenic shock with pulmonary edema
• Vasopressor agents are used when there has been an inadequate
response to volume resuscitation or when a patient has contraindications
to volume infusion
12.
13.
14. Assuring Adequate Oxygen Delivery
• Once blood pressure is stabilized through
optimization of preload and afterload, DO2 can be
assessed and further manipulated. Arterial
oxygen saturation should be returned to
physiologic levels (93 to 95 percent) and
hemoglobin maintained above 10 g/dL.13 If
cardiac output can be assessed, it should be
increased by using volume infusion and inotropic
agents in incremental amounts until venous
oxygen saturation (SmvO2 or ScvO2) and lactate
are normalized.
18. Cardiogenic shock
• Cardiogenic shock is defined as a state of
decreased cardiac output (CO) producing
inadequate tissue perfusion despite adequate
or excessive circulating volume.
• Clinical signs of cardiogenic shock include
evidence of poor CO with tissue
hypoperfusion (hypotension, mental status
changes, cool mottled skin) and evidence of
volume overload (dyspnea,
20. Management
• Intra- aortic balloon pump
• Emergency cardiac revascularisation
• Airway ( endotracheal intubation, positive pressure )
• Acute myocardial infarction –aspirin, heparin
• Hypotension managed by small fluid challenge ( NS 100
to 250 ml )
• Vasoconstrictors ( dopamine , dobutamine)
• Phosphodiesterase inhibitor ( amrinone , milrinone )
combined with dopamine or dobutamine
•
21.
22. Septic shock
• Sepsis is a heterogeneous clinical syndrome
that can be caused by any class of
microorganism. Although gram-negative and
gram-positive bacteria account for most sepsis
cases, fungi, mycobacteria, rickettsia, viruses,
or protozoans can cause similar presentations
23. •
Infection = microbial phenomenon characterized by an inflammatory response to the presence of
microorganisms or the invasion of normally sterile host tissue by those organisms.
•
Bacteremia = the presence of viable bacteria in the blood.
•
Systemic inflammatory response syndrome = the systemic inflammatory response to a variety of
severe clinical insults. The response is manifested by two or more of the following conditions: (1)
temperature >38°C or <36°C; (2) heart rate >90 beats/min; (3) respiratory rate >20 breaths/min or
PaCO2 <32 mm Hg; and (4) white blood cell count >12,000/ L, <4000/ L, or >10% immature (band)
forms.
•
Sepsis = the systemic response to infection, manifested by two or more of the following conditions
as a result of infection: (1) temperature >38°C or <36°C; (2) heart rate >90 beats/min; (3)
respiratory rate >20 breaths/min or PaCO2 <32 mm Hg; and (4) white blood cell count >12,000/ L,
<4000/ L, or >10% immature (band) forms.
•
Severe sepsis = sepsis associated with organ dysfunction, hypoperfusion, or hypotension.
Hypoperfusion and perfusion abnormalities may include, but are not limited to lactic acidosis,
oliguria, or an acute alteration in mental status.
•
Septic shock = sepsis-induced hypotension despite adequate fluid resuscitation along with the
presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis,
oliguria, or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor
agents may not be hypotensive at the time that perfusion abnormalities are measured.
•
Sepsis-induced hypotension = a systolic blood pressure <90 mm Hg or a reduction of 40 mm Hg
from baseline in the absence of other causes for hypotension.
•
Multiple organ dysfunction syndrome = presence of altered organ function in an acutely ill patient
such that homeostasis cannot be maintained without intervention.
25. Anaphylactic shock
• Anaphylaxis is a severe systemic
hypersensitivity reaction characterized by
multisystem involvement, which may include
hypotension or airway compromise.
Anaphylaxis is a potentially life-threatening
cascade caused by the release of mediators
from mast cells and basophils in an IgEdependent fashion
27. Treatment
• Emergency treatment: rapid administration of
epinephrine
• First line treatment :
– ABC of resuscitation
– Epinephrine , intravenous fluids and oxygen
• second line treatment :
– Coticosteroids
– Anti histamines
– Agents for allergic bronchospasm ( magnesium
sulphate )
28.
29.
30. Neurogenic shock
• Neurogenic shock, characterized by
hypotension and bradycardia, occurs after an
acute spinal cord injury that disrupts
sympathetic outflow, leaving unopposed vagal
tone
