APPROACH TO SHOCK

BY AMIRA ABDULLAH
 Definition

 Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen
consumption or inadequate oxygen utilization.

 Result in inadequate organ perfusion due to circulation fail to meet oxygen and metabolic demand of tissue.

 It is global tissue hypoperfusion and causing metabolic acidosis.

 Shock are divided into 4 clases :

1. Distributive VESSELS
2. Cardiogenic PUMP
3. Hypovolemic VOLUME
4. Obstructive
PHYSIOLOGY
 STAGES OF SHOCK

1. Pre-shock – Also known as compensated shock, or cryptic shock. Aim to maintain

NORMAL BLOOD PRESSURE.
2. Shock – During shock, the compensatory mechanism FAILS and HYPOTENSION
occurs.
3. End-organ dysfunction – Consequences of decompensated shock leading to permanent
cellular and organ damage, multiorgan failure (MOF), and death.
4. Clues to identify each stage :

Compensated Decompensated Multiorgan failure

• Tachycardia • Altered mental status • Refractory acidemia

• Orthostatic hypotension • Poor CCTVR • Anuria
• Decrease u/o • Resp distress • Coma
 Compensatory Mechanism

1. Baroreceptor and Chemo receptor : Activate Sympathetic Nervous System

2. Renin Angiotensin System : vasoconstriction and increase intravascular volume
3. Posterior pituitary : ADH
4. Adrenal Cortex : Aldosterone
5. ACTH : Cortisol
 Approach to shock

 History
 Physical Examination
 Resuscitation

In any patient with life threatening condition, history taking, physical examination and
resuscitation need to proceed SIMULTANEOUSLY
 History Taking

 TARGETED HISTORY TAKING

 Past medical history
 Trauma
 Fever
 Chest pain
 GI loses
 Abdominal Pain
 Bleeding
 Allergic history
 Physical Examination
 Vital signs ?? SHOCK
 BP: postural hypotension? narrowed pulse pressure?
 HR: Tachycardia (earliest sign of shock)
 RR: Tachypnea
 Temperature
 General examination:
 Mental state
 Septic looking
 Lethargy
 CCTVR
 Respiratory effort
 Evidence of trauma
 Physical Examination (cont.)
 CNS
 GCS, pupil
 Movement, reflex
 Lungs
 Air entry
 Added sound : crepitation or rhonci
 CVS
 Murmur
 Muffled heart sound
 Abdomen
 signs of peritonitis: boardlike rigidity, guarding, generalized tenderness
 epigastric mass
 Per rectal
 Limbs
 Limb edema or swelling
 Fracture
 Resuscitation

Initiate ABC’s of Emergency Care: Airway, Breathing and Circulation

AIRWAY:
 Clear airway
 Secure airway, elective ET intubation if necessary
 altered respiratory status
 altered mental status
 Prevent risk of aspiration pneumonia

BREATHING:
 give supplemental O2
 keep SPO2 > 95%
 Resuscitation - Circulation
Colour Gauge Ext. dia. Length Flow rate
Code (mm) (mm) (ml/min)
Orange G14 2.1 45 300
Grey G16 1.7 45 196
 Insert 2 large IV lines Green G18 1.3 45 96
 Draw blood for urgent Ix
 Central line (pt with significant comorbid/ need close monitoring)
 Fluid resuscitation 
 Adequate resuscitation and stabilization is essential to determine outcome of
resuscitation
 Fluid of choice: crystalloid/ colloid/ blood component
 Fluid resuscitation with 10-20cc/kg up to 30cc/kg should be started while assessing
for response, and repeated if necessary
 Insert CBD with hourly urine monitoring
 Resuscitation – Circulation

 Reassess patient post bolus

 Mental status
 Vital signs: MAP >65 and/or SBP >100mmhg
 Pulse volume
 Perfusion
 Urine output
 CVP
 IVC
 Blood gases

 In patients with persistent hypotension (MAP < 65 mmHg) for more than 30 minutes in spite of vigorous
fluid loading, temporary normalization of MAP with a vasopressor can minimize or prevent subsequent
organ dysfunction.
 Investigation

 FBC
 Renal profile/ electrolyte
 Blood gases
 Lactate
 Coagulation profile
 GSH/ GXM
 Blood C+S
 ECG
 Cardiac enzyme (if indicated)
 CXR – pneumonia, cardiomegaly
 Types of Fluid used for Resuscitation
Type Products Content Characteristic Disadvantages

Crystalloid 1. Normal saline Electrolytes and other • Distribute evenly • Large volume
2. Hartmann small molecule that in EC space needed 3:1
3. Dextrose saline moves freely in ECS • Risk of overload

Colloid 1. Gelafusin Large molecules • Increase • Cost

2. Human albumin intravascular • Allergic reaction
3. Dextran volume

Blood product 1. Whole blood Red Blood Cells • Increase oxygen • Incompatibility
2. Packed cell carrying capacity • Limited resourses
 Hypovolemic Shock

Hemorrhagic Non-Hemorrhagic

Revealed: Poor fluid

-obvious Concealed: intake
external -contained within body dehydration Excessive fluid loss:
hemorrhage cavity vomiting/diarrhea/ urinary
-Trauma: chest, abd, loss(DM) /burn/3rd space
pelvis, retroperitoneum  fluid loss in GI tract
-Non-trauma: GI bleed,
ruptured aneurysm

“Blood on the floor, plus 4 more” – Chest, Retroperitoneum, Abdomen, Pelvis/long bones
Response of initial fluid bolus
 Distributive shock

 Distributive shock is characterized by severe peripheral vasodilation (vasodilatory shock).

 it results from a relative inadequacy of intravascular volume caused by arterial or venous
vasodilation; circulating blood volume is normal.
 Subset of distributive shock :
1. Septic shock
2. Anaphylactic shock
3. Neurogenic shock
 Septic shock

 Septic shock
 Sepsis defined as dysregulated host response to infection resulting in life threatening organ
dysfunction.
 Septic shock is a subset of sepsis that associated with mortality up to 50% and can be identified
by the use of vasopressor and elevated lactate level despite fluid resus.
 Aim of resuscitation :
 MAP > 65mmhg
 U/O .0.5cc/kg/h
 CVP 8-12 mmhg
Anaphylactic shock
Neurogenic shock

 Neurogenic shock is a type of shock caused by the sudden loss of the autonomic nervous
system signals to the smooth muscle in vessel walls
 This results in loss of background sympathetic stimulation, which is responsible for
maintanence of tone of blood vessels. As a result of loss of vascular tone, the vessels
suddenly relax resulting in sudden decrease in peripheral vascular resistance and
decreased blood pressure.
 Usually seen in spinal cord injury involving T6 and above /within 30 mins of injury last
within 6-8 weeks/loss of vasomotor and sympathetic nervous system tone and function
 Cardiogenic Shock

 Cardiogenic shock is a relative or absolute reduction in cardiac output due to a primary

cardiac disorder.
 Mechanism
 Impaired myocardial contractility (Causes; Myocardial ischemia, myocarditis, drugs)
 Abnormalities of cardiac rhythm (Causes; Tachycardia, bradycardia)
 Cardiac structural disorder (Causes; Acute mitral or aortic regurgitation, ruptured interventricular
septum, prosthetic valve malfunction)
Cardiogenic shock
 Obstructive shock

 Obstructive shock occurs when adequate oxygen and nutrient delivered to the organs and tissues of the
body is compromised as a direct result of the an obstruction to flow into or out of the heart
 It is caused by mechanical factors that interfere with filling or emptying of the heart or great vessels.
 Mechanism
 Mechanical interference with ventricular filling (Causes; Tension pneumothorax, cava compression, cardiac
tamponade, atrial tumour or clot)
 Interference with ventricular emptying (Cause; Pulmonary embolism)

 Most common causes are

1. Tension pneumothorax
2. Pulmonary embolism
3. Cardiac tamponade
4. Aortic stenosis
 Vasopressor and Inotropes

 VASOPRESSOR vasoconstriction SVR MAP

 INOTROPES cardiac contractility (most drugs have both effect)

 Know your receptors.

 Alpha1 receptor vasoconstriction blood vessels
 Beta1 receptor cardiostimulant and inotropic heart
 Beta2 receptor vasodilatation blood vessels
 Vasopressor Alpha1 Beta1 Beta2 Dopamine Physiologic effect

Noradrenaline ✔️✔️✔️ ✖️ ✖️ ✖️ ↑ SVR

50-30mcg/min ↑ HR
↑ MAP
↑ COP

Adrenaline ✔️✔️✔️ ✔️✔️ ✔️ ✖️ ↑ HR,

20-200 mcg/min ↓ SVR
↑ SVR (high)

Dopamine ✔️ ✔️ ✔️✔️ ✔️✔️✔️ ↑ HR (low)

1-20 mcg/kg/min ↑ SVR, ↑COP (mod)
↑ SVR, ↑ MAP (high)

Dobutamine ✔️ ✔️✔️✔️ ✔️ ✖️ ↑ HR
2-20 mcg/kg/min ↑ COP
↓ SVR