SHOCK

: Done by
Bayan ayyad
 tissue
perfusion

Tissue
ischemia

Multi-
organ
failure
out of each 5 shocked patients 1
will die
 Tissue perfusion = arterial pressure – venous
pressure

Shock = blood pressure

 blood
pressure

tissue
perfusion

Tissue
ischemia

Multi-
organ
failure
Stages of shock
-blood pressure > decrease tissue perfusion :
e preservation of cellular and organ functionality
-1- anaerobic metabolism > lactic acid start accumulate
stag
2- metabolic waste products accumulation
al
Initi

Activation of compensatory mechanisms:

e -for acidosis >> hyperventilation
stag Tachycardia
-for hypotension : catecholamines > vasoconstriction +
CO. normal BP
y
RAA system > vasoconstriction
ator -For hypovolemia : ADH and RAA system > water retention
pens
Com
Stages of shock
compensation fail to control situation , signs and symptoms
start appearing:
-vasoconstriction >> vascular collapse (Tachycardia ,hypotension)
stage
-lactic acid >> metabolic alkalosis (dyspnea)
- tissue ischemia (confusion ,oliguria..etc
y
sator
mpen
Deco

Tissue necrosis and multi-organ failure

e CNS : altered mental status , coma , death
renal : anuria
respiratory failure
stag
ble heart failure
death
ersi
Irrev
 Clinical presentation of
shock( very early sign ) -1
tachycardia
2- hypotension ( late sign ) and weak pulse
cold extremities, pale skin , blue lips-3
weakness and fatigability headache and thrist -4
lactic acidosis >> rapid shallow breathing -5
: 6 -organ damage
CNS : drowsness, confusion , coma , death -
- renal : olgiuria , anuria
…… etc
specific signs and symptoms due to shock etiology -7
 Diagnosis
Shock is clinically diagnosed based on pt’s signs and
symptoms and vital signs (BP ,T , HR,RR)
:.… other
brief focused History and physical examination (to -1
know etiology)
2-ECG monitoring ( pulse , Pressure )
3-pulse oximetry (O2 sat.)
4- labs: CBC, electrolyte, LFT , KFT,PT,PTT
5- if still not diagnosed do :
- echocardiogram
-pulmonary artery catheter
 Treatment
firstly establish 2 large bore IV line

Control ABC
A: airways : cervical spine protection , keep airway patent
B:breathing : mechanical ventilation
C:circulation :IV fluid ± blood transfusion
specific treatment for each shock type

main indicator for successful*

treatment is urine output
 Shock types
hypovolemic -1 Cold shock
shock - hypovolemic
2- cardiogenic shock
- cardiogenic
3- distributive shock - obstructive
septic - hot shock
anaphylactic-
- distributive
neurogenic -
4- obstructive shock
 A- hypovolemic shock (most common

Acute
types )blood /volume loss

Vomiting
diarrhea External :, penetrating injury, surgical
sweating Internal : rapture AAA , solid organ injury
burns
Signs and symptoms of internal bleeding

hematamesis -1
2- hematochezia , melena
3-haemoptysis
4- hematuria
5-chest or abdominal pain
6- abdominal swelling
7- bruises or skin discoloration
Observation

Crystall
oid

Crystalloid
colloid

Crystalloid Postural
colloid
 Treatment
Initial control over :
1- airway
2- breathing
: 3- circulation
:IV fluid-
colloid (hypertonic ) : plasma substitutes (risk of
pul.edema ,  risk of hepatitis )
crystalloid (isotonic ) : ringer lactate or normal saline ( 
risk of pul.edema )

blood transfusion -
hemorrhage resuscitation :-4
external bleeding : compression initially
internal bleeding : need surgical intervention
B-Cardiogenic shock Cardiomyopat
hy
Arrhythmia
valvular dis
blunt trauma
Most common
diagnosis
A- clinical presentation
hypotension , tachycardia , pulmonary congestion ,
engorged neck veins
B- Diagnosis of primary cause :
ECG
echocardioghram

Treatment
1- ABC (IV fluid are likely to be harmful , instead
we give them diuretics)
2- treat primary cause
3- vasopresser: dopamine
inotrope : dobutamine
4-intra-aortic balloon pump ( after load ,CO. ,  cardiac
 C-Obstructive shock

Restrict cardiac
filling
(preload)

Causes:
Cardiac tampnade (post
traumatic)
tension pneomothorax
Pulmonary embolus
IVC obstruction
Increased intrathoracic
Treatment
Maintain ABC-1
:Treat the cause-2
cardiac Tamponade : pericardiocentesis-
- tension pneuomothorax : chest tube
- surgical management of other causes
D-Distributive shock
An insult cause:

*With normal or even CO.

abnormal distribution of blood into organs
-away from vital organ > tissue ischemia > organ
- toward skin >> hot shock
Types of distributive shock

 
 septic shock ( the most common cause of death-1
*Sepsis :life-threatening organ dysfunction due to dysregulated host
in ICU)
response to infection.
*Septic shock :persisting hypotension requiring vasopressors to maintain a
mean arterial pressure of ≥65 mm Hg and a serum lactate level >2
mmol/L despite adequate volume resuscitation.

BACTEREM
IA
Presence
of
bacteria
or M.O. In
the blood
Pathophysiology of septic shock
Complication :
1- DIC
2- ARDS
3- ATN
4-mutiorgan
failure
5-death
 Clinical presentation
• Hyperdynamic circulation (CO. +
vasodilatation)
• Warm , dry skin
Warm shock • Normal BP
(early phase ,
compensated ) • Tachycardia , tachypnea

• Hypodynamic circulation
( CO. vasoconstriction)
• Cold .clammy skin
Cold shock • Decrease BP
(late phase ,
decompensated) • Tachycardia , tachypnea
 diagnosis
…Clinically diagnosed
: confirmed by
CBC and blood culture-
identifying primary source : pneumonia , pyelonephritis , -
)meningitis , peritonitis ,abscess …etc

Treatment
1. Initially, IV antibiotics (broad spectrum) at maximum dosages.
Antibiotics for more rare organisms or antifungal medications may be
required if there is no clinical response or if suspicion for an atypical
organism (i.e., immunocompromised).
If cultures are positive, antibiotics can be narrowed based on
sensitivity testing.
2. Surgical drainage if necessary.
3. Fluid administration to increase mean BP (may require many liters of fluid).
4. Vasopressors (Norepinephrine, dopamine, phenylephrine) may be used if
hyotension persists despite aggressive IV fluid resuscitation
 Anaphylactic Shock .2
A type of distributive shock
that results from widespread
systemic allergic reaction to
an antigen

 This hypersensitive reaction

is LIFE
THREATENING

Most common causes :

o Antibiotics
o Insects
EX: Exercise , cold , heat , UV light , opiod , ethanol >>
induce allergic reaction without affecting B cell and
produce Ag ,they may :
1- induce non-specific histamine release
2- induce leukocyte synthesis
3-induce complement activation
 Anaphylactic Response

• Vasodilatation
• Increased vascular permeability
• Bronchoconstriction
• Increased mucus production
• Increased inflammatory mediators
recruitment to sites of antigen
• Clinical presentation
Almost immediate response to inciting
antigen:
- Cutaneous manifestations (some of the most
severe cases of anaphylaxis present in the absence of skin
findings).
urticaria, erythema, pruritis,
angioedema
- Respiratory compromise
stridor, wheezing, bronchorrhea, resp.
distress
- Circulatory collapse
tachycardia, vasodilation,
hypotension

*Mild, localized urticaria can progress to full

anaphylaxis
*Symptoms usually begin within 60 minutes of
exposure
*Faster the onset of symptoms = more severe
Diagnosis
• Clinical diagnosis( airway compromise,
hypotension, cutaneous involvement)
• Look for exposure to drug, food, or
insect
Treatment
Nonpharmacotherapy
-Airway management (eg, ventilator support with bag/valve/mask,
endotracheal intubation)
-High-flow oxygen
-Cardiac monitoring and/or pulse oximetry
-Intravenous access (large bore)
-Fluid resuscitation with isotonic crystalloid solution
-Supine position (or position of comfort if dyspneic or vomiting)
with legs elevated
Pharmacotherapy
The primary drug treatments for acute anaphylactic reactions are
epinephrine and H1 antihistamines.
-Adrenergic agonists (eg, epinephrine)
-Antihistamines (eg, diphenhydramine, hydroxyzine)
-H2 receptor antagonists (eg, cimetidine, ranitidine, famotidine)
-Bronchodilators (eg, albuterol)
-Corticosteroids (eg, methylprednisolone, prednisone)
-Positive inotropic agents (eg, glucagon)
-Vasopressors (eg, dopamine)
 3- Neurogenic Shock
rarest form of shock!

failure of the sympathetic nervous system to maintain-

adequate vascular tone (sympathetic denervation) which lead
to massive vassodiletation > tissue ishemia > shock

Causes include spinal cord injury, severe head injury, spinal-

anesthesia, pharmacologic sympathetic blockade
Pathophysiology of Neurogenic
Shock

Disruption of Venous and

Loss of
sympathetic
nervous sympathetic arterial
system vasodilation
tone

Decreased Decreased venous

Decreased
cardiac output return
stroke
volume

Decreased cellular
Impaired tissue Impaired
oxygen supply
perfusion cellular
metabolism
 Clinical presentation
Hypotension
Bradycardia
Warm, dry skin
 CO
Flaccid paralysis below level of the
spinal lesion
 Manegment
Judicious use of IV fluids as the mainstay of .1
treatment
2. Vasoconstrictors to restore venous tone, but
cautiously
3. Supine or Trendelenburg position
4. Maintain body temperature
Pul. Cap. wedge pre.
Indicate volume status