SHOCK

SYAHBUDDIN HARAHAP
SHOCK

 INADEQUATE ORGAN PERFUSION

AND TISSUE OXYGENATION

 INDENTIFY THE PROBABLE CAUSE

OF SHOCK STATE
Effects of inadequate perfusion on cell function.
•Bowel rest/NPO •Cardiac failure •Achlorhydria Intestinal obstruction,
•Malnutrition •Shock •Antacids Ileus, Blind loop,
Opiates, Ca channel
•Stress •Vasopressors •H2 Antagonists blockers

 Mucosal cell  Mesenteric  Gastric pH  Motility

turnover blood flow

Mucosal atrophy Intestinal bacterial

Mucosal sloughing overgrowth

Breakdown
mucosal barrier

Translocation of
bacteria and toxins

Schematic Representation of the Effect of Critical Illness on

Gastrointestinal Function
The Lethal Triad

 SHOCK  Prolonged hypotension

Metabolic Acidosis

DEATH

Coagulopathy Hypothermia
Rotondo MF, Zonies DH. Surg Clin North Am 1997; 77(4): 761-777
Alfred Blalock proposed in 1934 four categories of
shock:

Hypovolemic
Cardiogenic
Vasogenic (septic)
Neurogenic shock

In 1972 Hinshaw and Cox suggested the following

classification which is still used today.
It uses four types of shock:

Hypovolaemic
Cardiogenic
Distributive
Obstructive shock
 Types of shock

HYPOVOLEMIC SHOCK

 BLEEDING
 THIRD SPACE SEQUESTRATION OF FLUID
IN THE GUT LUMEN (BOWEL
OBSTRUCTION)
 LOSS OF PLASMA INTO INJURED TISSUES
( BURNS )
 VOMITING OR DIARRHEA
CARDIOGENIC SHOCK
This type of shock is caused by the failure of the
heart to pump effectively.
This can be due to damage to the heart muscle,
most often from a large myocardial infarction.
Other causes of cardiogenic shock include
arrhythmias
cardiomyopathy
congestive heart failure (CHF)
contusio cordis
cardiac valve problems.
DISTRIBUTIVE SHOCK
 This form of "relative" hypovolaemia is the result of dilation of blood
vessels which diminishes systemic vascular resistance.

 Examples of this form of shock are:

 Septic shock
This is caused by an overwhelming infection leading to vasodilation, such as
by :Gram negative, Gram-positive, fungi ,which release an endotoxin
which produces adverse biochemical, immunological and occasionally
neurological effects which are harmful to the body.
 Anaphylactic shock
Caused by a severe anaphylactic reaction to an allergen, antigen, drug or
foreign protein causing the release of histamine which causes widespread
vasodilation, leading to hypotension and increased capillary
permeability.
 Neurogenic shock
Neurogenic shock is the rarest form of shock. It is caused by trauma to the
spinal cord resulting in the sudden loss of autonomic and motor reflexes
below the injury level. Without stimulation by sympathetic nervous system
the vessel walls relax uncontrolled, resulting in a sudden decrease in
peripheral vascular resistance, leading to vasodilation and
hypotension.
OBSTRUCTIVE SHOCK
In this situation the flow of blood is obstructed which
impedes circulation and can result in circulatory arrest.
Several conditions result in this form of shock.
 Cardiac tamponade in which blood in the pericardium
prevents inflow of blood into the heart (venous return).
Constrictive pericarditis, in which the pericardium
shrinks and hardens, is similar in presentation.
 Tension pneumothorax. Through increased
intrathoracic pressure, bloodflow to the heart is
prevented (venous return).
 Massive pulmonary embolism is the result of a
thromboembolic incident in the bloodvessels of the
lungs and hinders the return of blood to the heart.
 Aortic stenosis hinders circulation by obstructing the
ventricular outflow tract
Recently a fifth form of shock has been introduced
ENDOCRIN SHOCK
Based on endocrine disturbances.
 Hypothyroidism, in critically ill patients, reduces cardiac
output and can lead to hypotension and respiratory
insufficiency.
 Thyrotoxycosis may induce a reversible
cardiomyopathy.
 Acute adrenal insufficiency is frequently the result of
discontinuing corticosteroid treatment without tapering
the dosage. However, surgery and intercurrent disease
in patients on corticosteroid therapy without adjusting
the dosage to accommodate for increased
requirements may also result in this condition.
 Relative adrenal insufficiency in critically ill patients
where present hormone levels are insufficient to meet
the higher demands
There are four stages of shock

1. Initial shock

2. Compensatory SHOCK

3. Progressive SHOCK

4. Refractory SHOCK
Initial shock
During this stage, the hypoperfusional state
causes hypoxia, leading to the mitochondria
being unable to produce adenosine
triphosphate.
Due to this lack of oxygen,the cell membranes
become damaged and the cells perform
anaerobic respiration.
This causes a build-up of lactic and pyruvic acid
which results in systemic metabolic acidosis.
The process of removing these compounds from
the cells by the liver requires oxygen, which is
absent.
Compensatory SHOCK

This stage is characterised by the body employing physiological

mechanisms including :
1. neural )
2. hormonal ) mechanisms in an attempt to reverse the condition.
3. bio-chemical )
 As a result of the metabolic acidosis  hyperventilate
 The baroreceptors in the arteries detect the resulting
hypotension, and cause the release of adrenaline and
noradrenaline.
-vasoconstriction  increase in blood pressure
-increase in heart rate
 Renin-angiotensin axis is activated and arginine vasopressin is
released to conserve fluid via the kidneys,vasoconstriction of the
kidneys, gastrointestinal tract, and other organs to divert blood to
the heart, lungs and brain.
 The lack of blood to the renal system causes the characteristic low
urine production.
Progressive SHOCK
 Due to the decreased perfusion of the cells, sodium
ions build up within while potassium ions leak out.
 As anaerobic metabolism continues, increasing the
body's metabolic acidosis, the arteriolar and
precapillary sphincters constrict such that blood
remains in the capillaries.
 Due to this, the hydrostatic pressure will increase and,
combined with histamine release, this will lead to
leakage of fluid and protein into the surrounding
tissues.
 As this fluid is lost, the blood concentration and
viscosity increase, causing sludging of the micro-
circulation.
 The prolonged vasoconstriction will also cause the vital
organs to be compromised due to reduced perfusion.
Refractory SHOCK

 At this stage, the vital organs have failed

and the shock can no longer be reversed.
Brain damage and cell death have
occurred.
 Death will occur imminently.
 HYPOVOLEMIC SHOCK
 Rapid volume repletion is indicated in patients with severe
hypovolemia or hypovolemic shock.
 Delayed therapy can lead to
-ischemic injury
-possibly to irreversible shock
-multiorgan system failure.
 Three issues generally need to be considered in this setting:
-the rate of fluid replacement;
-the type of fluid infused
-and the role for buffer therapy in patients with concurrent
lactic acidosis

Vasopressors, such as norepinephrine and dopamine,

generally should not be administered since they do not correct the
primary problem and tend to further reduce tissue perfusion
HYPOVOLEMIC SHOCK

 BLEEDING
 THIRD SPACE SEQUESTRATION OF
FLUID IN THE GUT LUMEN (BOWEL
OBSTRUCTION)
 LOSS OF PLASMA INTO INJURED
TISSUES ( BURNS )
 VOMITING OR DIARRHEA
CILINICAL MANIFESTATION

 Altered mental state

 HYPOTENSION
 TACHICARDIA
 CUTANEOUS VC
 SWEAT GLAND STIMULATION
 NECK VEIN COLLAPSE
 OLIGURIA
Signs and symptoms
 Anxiety, restlessness, altered mental state due to
decreased cerebral perfusion and subsequent hypoxia.
 Hypotension due to decrease in circulatory volume.
 A rapid, weak, thready pulse due to decreased blood
flow combined with tachycardia.
 Cool, clammy skin due to vasoconstriction and
stimulation of vasoconstriction.
 Rapid and deep respirations due to sympathetic
nervous system stimulation and acidosis.
 Hypothermia due to decreased perfusion and
evaporation of sweat.
 Thirst and dry mouth, due to fluid depletion.
 Fatigue due to inadequate oxygenation.
 Cold and mottled skin (cutis marmorata), especially
extremities, due to insufficient perfusion of the skin.
PATHOPHYSIOLOGY

 RELEASE VASOPRESSIN & ANGIOTENSIN ----

PROGRESSIVE VASOCONSTRICTION  HEART,
BRAIN
 ANAEROBIC METABOLISM ---- METABOLIC
FAILURE
-METABOLIC ACIDOSIS
-HYPOTHERMIA
-COAGULOPATHY
BASIC CARDIAC PHYSIOLOGY

 CARDIAC OUTPUT  HR & STROKE VOLUME PER

MINUTE
 STROKE VOLUME - CARDIAC CONTRACTION
 CARDIAC CONTRACTION
PRELOAD-- VR TO THE HEART
MYOCARDIAL CONTRACTILITY
AFTERLOAD-PERIPHERAL VASCULAR
RESISTANCE ( SVR)
 70 % TOTAL BLOOD VOLUME IN THE VENOUS CIRCUIT
 VAS0PRESSOR ARE CONTRAINDICATED
 ISOTONIC ELECTROLYTE SOLUTION COMBAT THIS
PROCESS
CLINICAL CLASSIFICATION OF H.S

 CLASS I BVL 15 %
 CLASS II BVL 15 % - 30 %
 CLASS III BVL 30% - 40 %
 CLASS IV BVL > 40 %
THERAPY

 INITIAL FLUID THERAPY

 BLOOD TRANSFUSION
RESPONSE TO INITIAL FLUID RESUSCITATION

 RAPID RESPONSE
 TRANSIENT RESPONSE
 MINIMAL OR NO RESPONSE
EVALUATION OF FLUID RESUSCITATION

 RETURN OF NORMAL VITAL SIGNS

 MENTAL STATUS
 URINARY OUTPUT
 ACID/BASE BALANCE
 CVP

“PERIPHERAL EDEMA”
HYPOVOLEMIC SHOCK <-> ARF

ACUTE RENAL FAILURE

 PRERENAL
 INTRARENAL
 POSTRENAL

ARF : OLIGURIA < 500 ML/d

SERUM CREATININ > 3MG/dL
TREATMENT PRE RENAL ARF

 INITIAL FLUID THERAPY

 CVP ------15 – 20 CM H20
 NO RESPON TO URINARY OUTPUT---
 OLIGURIA
NO RESPON TO URINARY OUTPUT--- OLIGURIA
 VC RENAL VASCULATURE

TREATMENT
 DIURESIS -- FUROSEMIDE 80-200 MG IV/TWD
 INOTROPIC AGENTS
VD RENAL VASCULATURE
INCREASE MYOCARDIAL CONTRACTILITY
LOW DOSE DOPAMIN /DOBUTAMIN 0,5 -3 ug/kg/min
 DOPAMIN
 Vasodilation — When infused in low doses (0.5
to 3 µg/kg per minute), dopamine dilates the
interlobular arteries and both the afferent
(preglomerular) and efferent (postglomerular)
arterioles .
 At higher concentrations (above 5 µg/kg per
minute), however, dopamine induces renal
vasoconstriction, a response that is mediated
by activation of the alpha-adrenergic receptors
 Septic shock

 Septic shock is a serious medical

condition causing such effects as multiple
organ failure and death in response to
infection and sepsis.
 immune systems cannot cope with the
infection
 The mortality rate from septic shock is
approximately 50%.
 Definition of septic shock
 Evidence of infection, through a positive blood culture.
 Hypotension despite adequate fluid resuscitation  ---
------CVP
 In adults it is defined as a :
-systolic blood pressure < 90 mmHg
-or a MAP < 60 mmHg, S + 2D : 3
-or a reduction of 40 mmHg in the systolic blood
pressure from baseline.
 In addition to the two criteria above, two or more of the
following must be present:
 Heart rate > 90 beats per minute.
 Body temperature < 36 or > 38°C.
 Hyperventilation (high respiratory rate) > 20 breaths
per minute or, on blood gas, a PaCO2 less than 32
mmHg.
 White blood cell count < 4000 cells/mm3 or > 12000
cells/mm3
Types Septic Shock
 A subclass of distributive shock, shock refers
specifically to decreased tissue perfusion resulting in
end-organ dysfunction.
 Cytokines TNFα, IL-1β, IL-6 released in a large scale
inflammatory response results in:
- massive vasodilation
- increased capillary permeability
- decreased systemic vascular resistance, and
hypotension.
Hypotension reduces tissue perfusion pressure and thus
tissue hypoxia ensues.
 Finally, in an attempt to offset decreased blood
pressure, ventricular dilatation and myocardial
dysfunction will occur.
Causes Septic Shock

 The process of infection by bacteria or fungi can result in systemic

signs and symptoms that are variously described. In rough order
of severity, these are bacteremia or fungemia; septicemia; sepsis,
severe sepsis or sepsis syndrome; septic shock; refractory septic
shock; multiple organ dysfunction syndrome, and death.
 The condition develops as a response to certain microbial
molecules which trigger the production and release of cellular
mediators, such as tumor necrosis factor (TNF); these act to
stimulate immune response. Besides TNFα, other cytokines
involved in the development of septic shock include interleukin-1β,
and interferon γ.
 The condition can also come about as a result of certain poisons,
such as ricin. For example, Georgi Markov, the Bulgarian dissident
who was assassinated in London, died of septic shock after being
injected with ricin.
 Treatment
 Treatment primarily consists of :
- antimicrobial chemotherapy
- removal of the source of infection
- haemodynamic support
- respiratory support
- metabolic support.
 Antimediator agents may be of some limited use in severe clinical
situations:
- Corticosteroids, especially if combined with a
mineralocorticoid, can reduce mortality among patients who
have relative adrenal insuffuciency
 Activated protein C can reduce mortality in patients with organ
failure
Emergency Department Care:

The treatment for sepsis has evolved considerably over the past 10 years as it
has transitioned from a disease that primarily concerned only critical care
physicians to one that has a major impact in the emergency department. Early
recognition and early aggressive therapy for patients with sepsis have a
significant impact on mortality.

Rivers et al brought this issue to the forefront with their landmark article in the
New England Journal of Medicine in 2001, where they instituted a treatment
protocol for patients with septic shock, termed Early Goal Directed Therapy
(EGDT).
EGDT emphasizes early recognition of patients with potential sepsis in the ED,
early broad-spectrum antibiotics, and a rapid crystalloid fluid bolus, followed by
goal-directed therapy for those patients who remain hypotensive or severely ill
after this initial therapy.
Those patients who did not respond to an initial fluid bolus and antibiotics
received a CV catheter in the internal jugular or subclavian vein to measure
central venous pressure (CVP) and an arterial catheter to directly measure
arterial blood pressure
EGDT is basically a three-step process aimed at optimizing tissue
perfusion.

•The first step involves titrating crystalloid fluid administration to CVP, or

administering 500 mL boluses of fluid until the CVP measures between 8
and 12 mm Hg. CVP is a surrogate for intravascular volume, as excess
circulating blood volume is contained within the venous system. Only after
the CVP is greater than 8 mm Hg should vasopressors be considered.

•The second step, if the patient has not improved with fluid alone, is to
administer vasopressors to attain a mean arterial pressure (MAP) greater
than 65 mm Hg.

•The third step is to evaluate the central venous oxygen saturation (SvO2).
This is obtained from the CV line, which, in turn, is a surrogate for
peripheral tissue oxygenation and cardiac output. An SvO2 of less than
70% is considered abnormal and indicative of suboptimal therapy. In this
case, the hematocrit is checked and blood transfused until a hematocrit
greater than 30% is attained. Once this is attained and the SvO2 is still low,
dobutamine is initiated to increase cardiac output.