SHOCK-SHOCK

SYNDROME, CARDIOGENIC
SHOCK,HYPOVOLEMIC,ANA
PHYLACTIC,NEUROGENIC,SEPTI
C SHOCK.
1

SHOCK:
Shock occurs when the blood pressure is too
low to sustain a supply of oxygen and
nutrients; and to remove waste products from
body cells, tissues and organs. It may be
hypovolaemic, cardiogenic, distributive or
obstructive.
shock is defined as a condition where the
tissues in the body don't receive enough
oxygen and nutrients to allow the cells to
function. This ultimately leads to cellular
death, progressing to organ failure and
finally, to whole body failure and death.
2

STAGES OF SHOCK:
There are four stages of shock.
Initialstage:
Compensatory
(Compensating)stage:
Progressive (Decompensating)
Refractory (Irreversible)

SHOCK SYNDROME:
Toxic shock syndrome (TSS) is a life-threatening
condition caused by toxins produced by certain
types of infecting bacteria. The condition has
been most often associated with the use of
tampons in menstruating women.
Although this outbreak was linked to toxins
produced by the Staphylococcus aureus bacteria,
TSS can also be caused by toxins from the group
A Streptococcus bacteria. The condition is
sometimes subdivided and referred to as
staphylococcal TSS and streptococcal TSS.
TSS can occur as a complication of surgery or
skin infections.
4

Risk factors :
use of tampons
barrier contraceptive devices in women,
surgery (especially nasal surgery), the use of wound
packings (such as nasal packings), and postoperative
wound infection.
Signs and symptoms :
few days of mild flu-like symptoms before the TSS develops,
but TSS itself is characterized by the rapid onset of specific
symptoms, including high fever, nausea, vomiting, diarrhea,
low blood pressure, and widespread skin rash. This will
usually progress to a worsening of low blood pressure,
dizziness, confusion, peeling of the skin of the palms and
soles of the feet (which develops after one to two weeks of
rash), headaches, and occasionally seizures. Ultimately,
multiorgan failure may develop, and this leads to death in
approximately 5 % of all those affected.
5

 Diagnosis:
thorough physical examination (which
includes a pelvic examination in
women), blood tests -white blood cell
count (to look for signs of infection),
blood cultures (evaluating for possible
bacteria in the bloodstream) and
evaluation of kidney and liver
function. Blood tests to exclude other
diseases may also be ordered.
Chest X-rays or CT scans of the abdomen
or pelvis
6

 MANAGEMENT:
Foreign material such as tampons, contraceptive devices, or
wound packings must be immediately removed. Treatment
may involve a combination of the following:
intravenous (IV) fluids to stabilize the blood pressure,
possibly in combination with medications to raise blood
pressure;
IV antibiotics to fight the source of the infection;
oxygen administration;
removal of tampons, nasal packings, or other
suspected sources of the infection;
surgical interventions to drain the source of the infection
dialysis if kidney failure develops.
Other therapies
IV immunoglobulin has been reported to be beneficial in
severe cases of TSS.
7

CARDIOGENIC SHOCK:
Cardiogenic shock is a physiologic state in which
inadequate tissue perfusion results from cardiac
dysfunction.
Hemodynamic criteria for cardiogenic shock are
sustained hypotension (systolic blood pressure <90
mm Hg for at least 30 min) and a reduced cardiac
index (<2.2 L/min/m2).
Causes
Based on the etiology and pathophysiology,
cardiogenic shock can be divided into systolic
dysfunction, diastolic dysfunction, valvular
dysfunction, cardiac arrhythmias, coronary
artery disease, and mechanical complications.
8

 Systolic dysfunction
Acute MI or ischemia ,anterior MI, severe myocarditis, end-stage cardiomyopathy
(including valvular causes), myocardial contusion, and prolonged
cardiopulmonary bypass.
Diastolic dysfunction
late stages of hypovolemic shock and septic shock
Valvular dysfunction
Acute mitral regurgitation secondary to papillary muscle rupture or dysfunction is
caused by ischemic injury.
Rarely, acute obstruction of the mitral valve by left atrial thrombus
Aortic and mitral regurgitation reduce forward flow, raise end-diastolic pressure,
and aggravate shock associated with other etiologies.
Cardiac arrhythmias
Ventricular tachyarrhythmia, bradyarrhythmias, Sinus tachycardia and atrial
tachyarrhythmias contribute to hypoperfusion and aggravate shock.
Coronary artery disease
Cardiogenic shock is generally associated with the loss of more than 40% of the
left ventricular myocardium.
Mechanical complications
Complication of acute MI, such as acute mitral regurgitation, large RV infarction,
and rupture of the interventricular septum or left ventricular free wall, are other
causes of cardiogenic shock.
9

Pathophysiology
Myocardial pathology
Cellular pathology

10

Procedures
Invasive hemodynamic monitoring
Swan-Ganz catheterization.
pulmonary capillary wedge pressure (PCWP) greater than 15 mm Hg
and a cardiac index of less than 2.2 L/min/m 2.

Coronary artery angiography

MANAGEMENT:
fluid resuscitation to correct hypovolemia and hypotension,
unless pulmonary edema is present.
Central venous and arterial lines are often required.
Swan-Ganz catheterization and continuous percutaneous
oximetry are routine.
Oxygenation and airway protection are critical; intubation
and mechanical ventilation are commonly required.
Correction of electrolyte and acid-base abnormalities, such
as hypokalemia, hypomagnesemia, and acidosis, are essential.

11

 aspirin and heparin.

The glycoprotein IIb/IIIa inhibitors improve the
outcome of patients.
Thrombolytic therapy
Intra-aortic balloon pump
Ventricular assist devices
Surgical management:
Percutaneous transluminal coronary
angioplasty
Reestablishing blood flow in the infarct-related
artery may improve left ventricular function and
survival following MI.

Coronary artery bypass grafting

12

NEUROGENIC SHOCK:
Neurogenic shock occurs after an injury to the
spinal cord. Sympathetic outflow is disrupted
resulting in unopposed vagal tone. The major
clinical signs are hypotension and bradycardia.
Neurogenic shock is shock caused by the sudden
loss of the autonomic nervous system signals to
the smooth muscle in vessel walls. This can result
from severe central nervous system (brain and
spinal cord) damage. With the sudden loss of
background sympathetic stimulation, the vessels
suddenly relax resulting in a sudden decrease in
peripheral vascular resistance (vasodilation) and
decreased blood pressure.
13

PATHOPHYSIOLOGY:

Injury to the spinal cord or cervical injury

Loss of balance between sympathetic and parasympathetic stimulus.

Predominant parasympathetic stimulus

Vasodilatation for an extended period of time.

Hypovolemic state

However blood volume is adequate, because of dilatation blood volume id

displaced.

Hypotensive state

Drastic decrease in patients systemic vascular resistance and bradycardia.

Inadequate blood pressure- insufficient perfusion of tissues and cells.

14

EMERGENCY
MANAGEMENT;
rapid identification and stabilization of life-threatening
injuries.
Airway control should be insured with spinal immobilization and
protection.
Crystalloid IV fluids should be infused to maintain a mean
arterial blood pressure
If fluid resuscitation is inadequate to ensure organ perfusion,
inotropic agents such as dopamine 2.5 to 20.0 g/kg per
min and dobutamine 2.0 to 20.0 g/kg per min may be
added to improve cardiac output and perfusion pressure.
If necessary, severe bradycardia may need to be treated with
atropine 0.5 to 1.0 mg IV (every 5 min for a total dose of
3.0 mg) or with a pacemaker.
In the presence of neurologic deficits, high-dose
methylprednisolone therapy should be instituted within 8 h of
injury.
15

HYPOVOLEMIC SHOCK:
Hypovolemic shock refers to a medical or surgical condition
in which rapid fluid loss results in multiple organ failure due
to inadequate circulating volume and subsequent
inadequate perfusion. Most often, hypovolemic shock is
secondary to rapid blood loss.
ETIOLOGY:
Traumatic causes can result from penetrating and blunt
trauma.
Vascular disorders that can result in significant blood loss
include aneurysms, dissections, and arteriovenous
malformations.
GI disorders -bleeding esophageal varices, bleeding peptic
ulcers, and aortointestinal fistulas.
Pregnancy-related disorders include ruptured ectopic
pregnancy, placenta previa, and abruption of the placenta.
16

Pathophysiology
the hematologic, cardiovascular, renal, and
neuroendocrine systems.
The hematologic system responds to an
acute severe blood loss by activating the
coagulation cascade and contracting
the bleeding vessels (by means of local
thromboxane A2 release).
In addition, platelets are activated (also
by means of local thromboxane A2
release) and form an immature clot on
the bleeding source.
17

 cardiovascular system- initially

increasing the heart rate, increasing
myocardial contractility, and constricting
peripheral blood vessels. This response
occurs secondary to an increased
release of norepinephrine and
decreased baseline vagal tone .
The cardiovascular system also responds
by redistributing blood to the brain,
heart, and kidneys and away from
skin, muscle, and GI tract.
18

 The renal system -stimulating an

increase in renin secretion from the
juxtaglomerular apparatus.
The neuroendocrine system -by
causing an increase in circulating
antidiuretic hormone (ADH). ADH is
released from the posterior pituitary
gland in response to a decrease in BP
(as detected by baroreceptors) and a
decrease in the sodium
concentration (as detected by
osmoreceptors).
19

classification.
Class I hemorrhage (loss of 0-15%)
In the absence of complications, only minimal tachycardia
is seen.
Usually, no changes in BP, pulse pressure, or respiratory
rate occur.
A delay in capillary refill of longer than 3 seconds
corresponds to a volume loss of approximately 10%.

Class II hemorrhage (loss of 15-30%)

Clinical symptoms include tachycardia (rate >100 beats
per minute), tachypnea, decrease in pulse pressure, cool
clammy skin, delayed capillary refill, and slight anxiety.
The decrease in pulse pressure is a result of increased
catecholamine levels, which causes an increase in
peripheral vascular resistance and a subsequent increase
in the diastolic BP.
20

CLASSIFICATION
Class III hemorrhage (loss of 30-40%)
By this point, patients usually have marked tachypnea and
tachycardia, decreased systolic BP, oliguria, and significant changes
in mental status, such as confusion or agitation.
In patients without other injuries or fluid losses, 30-40% is the
smallest amount of blood loss that consistently causes a decrease in
systolic BP.
Most of these patients require blood transfusions, but the decision to
administer blood should be based on the initial response to fluids.

Class IV hemorrhage (loss of >40%)

Symptoms include the following: marked tachycardia, decreased
systolic BP, narrowed pulse pressure (or immeasurable diastolic
pressure), markedly decreased (or no) urinary output, depressed
mental status (or loss of consciousness), and cold and pale skin.
This amount of hemorrhage is immediately life threatening.

21

 Imaging Studies
ultrasonographic examination - if an abdominal
aortic aneurysm is suspected.
If GI bleeding is suspected, a nasogastric tube should
be placed, and gastric lavage should be performed.
An upright chest radiograph should be obtained if a
perforated ulcer is a possibility.
Endoscopy can be performed (usually after the patient
has been admitted) to further delineate the source of
bleeding.
A pregnancy test should be performed in all female
patients of childbearing age.
Computed tomography (CT) scanning typically is
performed in the stable patient.
If long-bone fractures are suspected, radiographs should
be obtained.
22

Prehospital Care
Direct pressure should be applied to
external bleeding vessels to prevent
further blood loss.
The cervical spine must be
immobilized.
Splinting of fractures can minimize
further neurovascular injury and blood
loss.
securing an adequate airway, ensuring
ventilation, and maximizing circulation.
use of military antishock trousers (MAST).
23

Emergency management:
Three goals: (1) maximize oxygen
delivery - completed by ensuring
adequacy of ventilation, increasing
oxygen saturation of the blood, and
restoring blood flow,
(2) control further blood loss, and
(3) fluid resuscitation.

24

Maximizing oxygen delivery

Two large-bore IV lines should be started.
Once IV access is obtained, initial fluid resuscitation
is performed with an isotonic crystalloid, such as
lactated Ringer solution or normal saline.
If vital signs return to normal, the patient may be
monitored to ensure stability, and blood should be
sent for typed and cross-matched
The position of the patient can be used to improve
circulation; one example is raising the hypotensive
patient's legs while fluid is being given.
Autotransfusion may be a possibility in some
patients with trauma.

COMPLICATIONS: Neurologic sequelae , Death

25

ANAPHYLATIC REACTION:
Anaphylaxis is a severe allergic reaction that occurs
rapidly and causes a life-threatening response involving
the whole body. This reaction can lead to difficulty
breathing and shock ultimately leading to death.
Greek words ana (against) and phylaxis
(protection).
For an anaphylactic reaction to occur, a patient must
have been exposed in the past to the substance that
causes the reaction, called the antigen. This is call ed
"sensitization."
A bee sting, for example, may not cause an allergic
reaction the first time.
These reactions usually occur within seconds to minutes
of exposure. Occasionally, they are delayed.
26

CLASSIFICATION:
"true anaphylaxis" and "pseudo-anaphylaxis" or
"anaphylactoid reaction.
"true" anaphylaxis is caused by degranulation of mast
cells or basophils mediated by immunoglobulin E
(IgE), and pseudo-anaphylaxis occurs without IgE
mediation
Biphasic anaphylaxis
Biphasic anaphylaxis is the recurrence of symptoms
within 72 hours with no further exposure to the
allergen.
Anaphylactic shock
Anaphylactic shock is anaphylaxis associated with
systemic vasodilation which results in low blood
pressure. It is also associated with severe
bronchoconstriction .
27

 Pseudoanaphylaxis
It however does not involve an allergic
reaction but is due to direct mast cell
degranulation. This can result from
morphine, radiocontrast, aspirin and muscle
relaxants.
Active anaphylaxis
Active anaphylaxis is what is naturally
observed. After Two weeks, is exposed to
certain allergens, active anaphylaxis (which is
simply called "anaphylaxis") would be elicited
upon exposure to the same allergens.
28

ETIOLOGY:

Prescription and over-the-counter medications

Venom of stinging insects
Transfusion of blood or blood products
Numerous other substances such as latex (natural
rubber)
Dyes and contrast materials used during radiologic
procedures or tests
Sometimes the trigger of the reaction is obvious--a
bee sting, or a new prescription drug. Often,
however, the trigger is unknown.
People with asthma, eczema, or hay fever are slightly
more likely to have an anaphylactic reaction than
people who do not have these conditions.
29

 Any two or more of the following symptoms

within minutes to several hours of allergen
exposure:
a. Involvement of the skin or mucosa
b. Respiratory difficulties
c. Low blood pressure
d. Gastrointestinal symptoms
Prevention:
The greatest success with prevention of
anaphylaxis has been the use of allergy
injections to prevent recurrence of sting
allergy.
30

Septic shock
Septic shock is a serious medical condition
caused by decreased tissue perfusion and
oxygen delivery as a result of infection and
sepsis, though the microbe may be systemic or
localized to a particular site. It can cause multiple
organ dysfunction syndrome (formerly known as
multiple organ failure) and death.
To diagnose septic shock, the following two
criteria must be met:
Evidence of infection, which may include a
positive blood culture
Refractory hypotension - hypotension despite
adequate fluid resuscitation and cardiac output.
31

 In addition to the two criteria, two or more

of the following must be present:
Tachypnea (high respiratory rate) > 20
breaths per minute or, on blood gas, a less
than 32 mmHg of PCO2
White blood cell count < 4000 cells/mm or
> 12000 cells/mm
Heart rate > 90 beats per minute
Temperature > 38.0C (100.4F) or <
36.0C (96.8F)
cold peripheries and increased capillary
refilling time
32

ETIOLOGY:
When microorganisms get into the blood stream,
it produces a condition known as bacteremia. If
the organisms are particularly virulent, or the
host is immunocompromised, then the host
organism may develop a condition known as
systemic inflammatory response syndrome (or
SIRS). Sepsis is bacteremia, combined with SIRS.
Origin of infection
Respiratory tract infection and urinary tract infection
are the most frequent causes of sepsis, followed by
abdominal and soft tissue infections.
The use of intravascular devices is a notorious cause
of nosocomially-acquired sepsis.

33

 Soft tissue infections are the cause of septic shock in 15%

of patients, and the following are the common pathogens:

S aureus
Staphylococcus epidermidis
Streptococci
Clostridia
Gram-negative bacteria
Anaerobes

GI tract infections are the cause of septic shock in 15% all

patients, and the following are the common pathogens:

E coli
Streptococcus faecalis
Bacteroides fragilis
Acinetobacter species
Pseudomonas species
Enterobacter species
Salmonella species

34

 Microorganisms:
Lower respiratory tract infections are the cause of septic shock in
25% of patients. The following are common pathogens:

Streptococcus pneumoniae
Klebsiella pneumoniae
Staphylococcus aureus
Escherichia coli
Legionella species
Haemophilus species
Anaerobes
Gram-negative bacteria
Fungi

Urinary tract infections are the cause of septic shock in 25% of

patients, and the following are the common pathogens:

E coli
Proteus species
Klebsiella species
Pseudomonas species
Enterobacter species
Serratia species
35

 Foreign bodies leading to infections are the

cause of septic shock in 5% of patients, and S
aureus, S epidermidis, and fungi/yeasts
(Candida species) are the common pathogens.
Miscellaneous infections are the cause of septic
shock in 5% of patients, and Neisseria
meningitidis is the common pathogen.

Anaerobic pathogens are becoming less

important as a cause of sepsis.
Fungal infections are the cause of sepsis in
0.8-10.2% of patients with sepsis, and their
incidence appears to be increasing.
36

Risk factors for severe sepsis and septic shock

Extremes of age ( <10 y and >70 y)
Primary diseases

Liver cirrhosis
Alcoholism
Diabetes mellitus
Cardiopulmonary diseases
Solid malignancy
Hematologic malignancy

Immunosuppression

Neutropenia
Immunosuppressive therapy
Corticosteroid therapy
Intravenous drug abuse
Compliment deficiencies
Asplenia
37

Risk factors

Major surgery, trauma, burns

Invasive procedures

Catheters
Intravascular devices
Prosthetic devices
Hemodialysis and peritoneal dialysis catheters
Endotracheal tubes

Prior antibiotic treatment

Prolonged hospitalization
Other factors - Childbirth, abortion, and
malnutrition
38

Pathophysiology:

39

American College of Chest Physicians

(ACCP)/Society of Critical Care Medicine (SCCM)
Sepsis: This is a systemic inflammatory response to a
documented infection. The clinical features include 2 or more of
the following conditions as a result of a documented infection:
Rectal temperature greater than 38C or less than 36C
Tachycardia (>90 bpm)
Tachypnea (>20 breaths per min)
With sepsis, at least 1 of the following manifestations of
inadequate organ function/perfusion also must be included:
Alteration in mental state
Hypoxemia (PaO2 <72 mm Hg at FiO2 [fraction of inspired oxygen]
0.21; overt pulmonary disease not the direct cause of hypoxemia)
Elevated plasma lactate level
Oliguria (urine output <30 mL or 0.5 mL/kg for at least 1 h)

40

 Severe sepsis: This is sepsis and SIRS 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. The systemic response to infection is
manifested by 2 or more of the following conditions:
Temperature greater than 38C or less than 36C
Heart rate greater than 90 bpm
Respiratory rate greater than 20 breaths per minute
or PaCO2 less than 32 mm Hg
White blood cell count greater than 12,000/L, less
than 4000/L, or 10% immature (band) forms

41

 Sepsis-induced hypotension (ie,

systolic blood pressure <90 mm Hg
or a reduction of >40 mm Hg from
baseline
Multiple organ dysfunction syndrome
(MODS): This is the presence of
altered organ function in a patient
who is acutely ill and in whom
homeostasis cannot be maintained
without intervention.
42

Imaging Studies

Chest radiograph
Acquire supine and upright or lateral decubitus abdominal films
Ultrasound
CT scan -intra-abdominal abscess or the retroperitoneal source
of infection.
The presence of soft tissue gas often dictates surgical
exploration.
Obtain a head CT scan in patients with evidence of increased
intracranial pressure (papilledema) and in patients thought to
have focal mass lesions (eg, focal defects, previous sinusitis or
otitis, recent intracranial surgery).
If bacterial meningitis is strongly suspected, then a lumbar
puncture (LP) should be performed.
Additionally, echocardiography has a number of uses in
assessing patients with septic shock.
43

Procedures
Lumbar puncture
Cardiac monitoring, noninvasive blood pressure
monitoring, and pulse oximetry
Supplemental oxygen
A central venous line also can be used to monitor central
venous pressure to assess intravascular volume status.
Use an indwelling urinary catheter to monitor urinary
output, which is a marker for adequate renal perfusion
and cardiac output.
Patients who develop septic shock require a right heart
catheterization with a pulmonary artery (Swan Ganz)
catheter.
These patients need intubation and mechanical
ventilation for optimum respiratory support.
44

Staging
Two well-defined forms

the lungs are the predominant, and often the only, organ
system affected until very late in the disease.
These patients most often present with primary pulmonary
disorder (eg, pneumonia, aspiration, lung contusion, near
drowning, chronic obstructive pulmonary disease [COPD]
exacerbation, hemorrhage, pulmonary embolism).
Progression of lung disease occurs to meet the ARDS
criteria. Pulmonary dysfunction may be accompanied
by encephalopathy or mild coagulopathy and
persists for 2-3 weeks. At this time, the patient either
begins to recover or progresses to develop fulminant
dysfunction in other organ systems. Once another major
organ dysfunction occurs, these patients often do not
survive.
45

 The second form of MODS presents quite differently.

These patients often have an inciting source of sepsis
in organs other than the lung (the common source
being intra-abdominal sepsis), extensive blood
loss, pancreatitis, and vascular catastrophes.
Acute lung injury or ARDS develops early, but
dysfunction in other organ systems also develops
much sooner. The organ systems affected are
hepatic, hematologic, cardiovascular, CNS, and
renal. Patients remain in a pattern of compensated
dysfunction for several weeks and then either recover
or deteriorate further and die.
46

MANAGEMENT:
Treatment primarily consists of the
following. The mnemonic OVERS may be
helpful.
Oxygen administration and airway
support.
Volume resuscitation.
Early antibiotic administration.
Rapid source identification and control.
Support of major organ dysfunction.
47

 The principles in the management of septic shock,

based on current literature, include the following
components:
Early recognition
Early and adequate antibiotic therapy
Source control
Early hemodynamic resuscitation and continued
support
Corticosteroids (refractory vasopressor-dependent
shock)
Drotrecogin alpha (Severely ill if APACHE II > 25)
Tight glycemic control
Proper ventilator management with low tidal
volume in patients with ARDS
48

 Antibiotics
Use of broad-spectrum and/or multiple antibiotics provides the
necessary coverage.
Cefotaxime (Claforan)
Used for treatment of septicemia. Third-generation
cephalosporin with enhanced gram-negative coverage,
especially to E coli, Proteus, and Klebsiella species. Has
variable activity against Pseudomonas species.
1-2 g IV q4h; not to exceed 12 g/m
Ceftriaxone (Rocephin)
Third-generation cephalosporin with broad-spectrum,
gram-negative activity. Lower efficacy against gram-positive
organisms. Used for increasing prevalence of penicillinaseproducing microorganisms. Inhibits bacterial cell wall
synthesis by binding to 1 or more penicillin-binding proteins.
1 g IV q8-12h; not to exceed 4 g/m
49

 Ticarcillin and clavulanate (Timentin)

Antipseudomonal penicillin plus a beta-lactamase inhibitor that
provides coverage against most gram-positive organisms (except
variable coverage against Staphylococcus epidermidis and no coverage
against methicillin-resistant Staphylococcus aureus [MRSA]), gramnegative organisms, and anaerobes.
<60 kilograms: 75 mg/kg IV q6h
>60 kilograms: 3.1 g IV q4-6h
Piperacillin and tazobactam (Zosyn)
Inhibits the biosynthesis of cell wall mucopeptide and is effective during
the stage of active multiplication. Has antipseudomonal activity.
3/0.375 g (piperacillin 3 g and tazobactam 0.375 g) IV q6h
Imipenem and cilastatin (Primaxin)
Carbapenem with activity against most gram-positive organisms
(except MRSA), gram-negative organisms, and anaerobes. Used for
treatment of multiple organism infections in which other agents do not
have wide-spectrum coverage or are contraindicated due to their
potential for toxicity.
500 mg IV q6h; not to exceed 4 g/d

50

 Meropenem (Merrem)
Carbapenem with slightly increased activity against
gram-negative organisms and slightly decreased
activity against staphylococci and streptococci
compared to imipenem. Less likely to cause seizures
and superior penetration of blood-brain barrier
compared to imipenem.
1 g IV q8h
Ciprofloxacin (Cipro)
Fluoroquinolone with variable activity against
Streptococcus species, activity against methicillinsensitive S aureus and S epidermidis, activity against
most gram-negative organisms, and no activity against
anaerobes. Synthetic broad-spectrum antibacterial
compounds.
400 mg IV q12h
51

 Clindamycin (Cleocin)
Primarily used for its activity against anaerobes. Has
some activity against Streptococcus species and MSSA.
600-900 mg IV q8h; not to exceed 4.8 g/d
Metronidazole (Flagyl)
Imidazole ring-based antibiotic active against various
anaerobic bacteria and protozoa. Usually combined
with other antimicrobial agents, except when used for
Clostridium difficile enterocolitis, in which monotherapy
is appropriate.
Loading dose: 15 mg/kg IV over 1 h (1 g IV for 70-kg
adult)
Maintenance dose: 7.5 mg/kg IV over 1 h q6-8h (500
mg for a 70-kg adult), initiated 6 h following loading
dose; not to exceed 4 g/d
52

INVESTIGATIONS:
LAB STUDY FINDINGS

SIGNIFICANCE OF FINDING

Blood
RBC,
haenmatocrit ,
haemoglobin

Normal
Decreased

Remains within normal limits in shock because

of relative hypovolemia and pump failure in
hemorrhagic shock before fluid restoration.

increased
Decreases in hemorrhagic shock after fluid
resuscitation when fluids other than blood are
used.
Increases in non hemorrhagic shock due to
actual hypovolemia because fluid lost does not
contain erythrocytes.
53

DIC
SCREEN:Fibri
n

Increased

split

products
Fibrinogen level Decreased
Platelet count

Decreased

PTT & PT

Prolonged

Thrombin time

Increased

D-dimer

Increased

Creatinine

increased

kinase

Acute DIC can develop within

hours to days after an initial
insult on the body.

Increased in trauma, MI, in response to

cellular damage and /hypoxia.

TROPONIN

Increased

In MI

BUN

Increased

Indicates impaired kidney function due to

hypo perfusion as a result of severe
vasoconstriction or occurs secondary to
catabolism of cells. (ex; trauma)

54

CREATININE

Increased

Indicates impaired kidney function due to hypo

perfusion as a result of severe vasoconstriction
more sensitive indicator than BUN.

GLUCOSE

Increased

Found in early shock because of release of liver

glycogen stores in response to sympathetic nervous
system stimulation and cortisol; insulin insensitivity
develops.

Decreased.

Because

of

hepatocellular

depleted

glycogen

dysfunction

stores

possible

as

with
shock

progresses.
ELECTROLYT
ES
SODIUM

Increased
Decreased

Found in early shock because of increased secretion

of aldosterone causing renal retention of sodium.
May occur iatrogenic ally when excess hypotonic
fluid is administered after fluid loss.

55

POTASSIUM

Increased
Decreased

Results when cellular death liberates

intracellular potassium.
Found in early shock because of increased
secretion of aldosterone causing renal
excretion of potassium.

ARTERIAL

Respiratory

Secondary to hyperventilation found in early

BLOOD

alkalosis

shock.

Metabolic

Occurs in later shock when organic acids

acidosis

such as lactic acid accumulate in the blood

GASES

from anaerobic metabolism.

BASE
DEFICIT

> -6

Indicates acid production secondary to

hypoxia.\
56

BLOOD

Growth of organisms In case of septic shock.

CULTURES
LACTATE

Increased

Usually increases once significant hypo

perfusion and impaired oxygen utilization
at cellular level have occurred. By product
to of anaerobic metabolism.

LIVER

Increased

ENZYMES
(ALT,

Elevations indicate liver cell destruction in

progressive state of shock.

AST,

GGT)
URINE
SPECIFIC
GRAVITY

Increased

Occurs secondary to the action of ADH.

Fixed at 1.010.

In renal failure.
57

DRUG

MECHANISM OF ACTION

TYPE OF SHOCK

Dobutami

Increase myocardial contractility

Used in Cardiogenic shock with

ne

Decrease ventricular filling pressure

severe systolic dysfunction.

Used in septic shock with normal CO
that

is

not

meeting

increased

metabolic demands.
Dopamine Precursor to epinephrine and nor Cardiogenic shock
epinephrine, Hemodynamic effects
from release of nor epinephrine.
Positive inotropic effects:
Increased myocardial contractility
Increased automaticity
Increased

atrioventricular

conduction
58

Epinephrine LOW DOSES; adrenergic agonist (cardiac Cardiogenic

stimulation, bronchial dilatation, peripheral combined

shock

with

afterload

vasodilation)

reduction.

High doses: adrenergic agonist(peripheral

Anaphylactic shock

vasoconstriction)

Cardiac

arrest,

pulseless

ventricular tachycardia
Ventricular fibrillation
aystole
Nor
epinephrine

1- adrenergic agonist (cardiac stimulation)

adrenergic agonist(peripheral
vasoconstriction)
renal /splanchnic vasoconstriction

Cardiogenic

shock

after

myocardial infarction
Septic shock : works by
increasing vascular tone.
59

Phenyl ephrine

adrenergic agonist

neurogenic shock

Vasoconstriction: renal,
mesenteric, splanchnic,
cutaneous,

and

pulmonary vessels.

Nitroglycerin

Venodilation

Sodium nitroprusside.

Arterial

and

vasodilatation.

Cardiogenic shock
venous Cardiogenic shock with
increased SVR.

60

FLUID THERAPY IN SHOCK:

Crystalloids: Isotonic: 0.9% NACL,
Ringer lactate
Blood and blood products: Whole
blood /packed red blood cells.
Colloids Hetastarch, Human serum
albumin ,Dextran

61

NURSING MANAGEMENT
Decreased cardiac output related to blood loss,
impaired fluid distribution, impaired circulation,
inadequate heart contraction, massive vasodilation.
Impaired gas exchange related to reduced cardiac
output secondary to blood loss, heart failure, altered
body fluid distribution, vasodilation, and bradycardia.
Hypothermia related to haemerrahge
Ineffective tissue perfusion related to hypovolemia or
inadequate cardiac output or inadequate vascular
tone.defecient knowledge related to unfamiliar
condition of shock.

62

COMPLICATINS OF SHOCK
CENTRAL NERVOUS SYSTEM- neurological
defeicits.
CARDIOVASCULAR SYSTEM- cardiac failure
HEMATOLOGICAL SYSTEM- DIC
RESPIRATORY SYSTEM- acute respiratory
distress syndrome.
RENAL SYSTEM- acute renal failure
HEPATIC SYSTEM-coagulopathy
GI- Ischemia and ulceration.
63

THANK YOU

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