SHOCK

RODERICK T. VITO, MD
Department of Emergency Medicine
 Shock
• Inadequate oxygen delivery to vital organs
• Cells most sensitive to lack of oxygen:
– Heart
– Lungs
– Brain
• Adequate airway and proper ventilation is
most critical
 Definitions
• Shock is defined physiologically as inadequate
delivery of substrates and oxygen to meet the
metabolic needs of tissues1
• Undifferentiated shock – shock whose etiology
of has not been determined
• Hypotension2
a) Systolic BP < 90 mmHg
b) 30% reduction from patient’s baseline systolic BP
c) Mean BP of < 60 mmHg

1Schwarz, A: Shock. In eMedicine, Feb 2008

2Worthley, L: Shock: A Review of Pathophysiology and Management, Part I and II.

Crit Care Resusc. 2000; 2:55-84

 Physiology of Shock

• The amount of oxygen delivered to the tissues of

the body per minute is designated as DO2
• Hypoxic shock – absolute deficiency of oxygen
delivery (DO2)
• Hypoxic-ischemic shock –combination of hypoxia
and insufficient delivery of substrates, e.g.
glucose

Schwarz, A: Shock. In eMedicine, Feb 2008

 Determinants of Tissue Oxygen
Delivery
DO2

Oxygen content Cardiac output

Hemoglobin O2 saturation Heart rate Stroke volume

Airway Breathing FiO2 Preload Afterload Contractility

Schwarz, A: Shock. In eMedicine, Feb 2008

 Shock
• Clinical diagnosis
• Signs and Symptoms
– Tachycardia and fever
– Tachypnea
– Altered mental status
– Oliguria
– Cool, clammy, pale skin
– hypotension
 Etiologic Classification of Shock

• Hypovolemic
• Traumatic
• Distributive
 Neurogenic
 Anaphylactic
• Septic
• Cardiogenic
 Intrinsic (pump failure)
 Compressive
 Obstructive
• Hypoadrenal
Modified from Maier, R: Approach to the Patient With Shock, Chap 264
Harrison’s Textbook of Internal Medicine 17th ed, p.1693
 Hypovolemic shock

• Decrease in intravascular volume

• Decrease peripheral tissue perfusion resulting
in decrease oxygen delivery to tissues
 Causes of Hypovolemic Shock
• Causes:
• Whole blood loss
 Trauma
 Surgery
 GI bleeding
 Ectopic pregnancy
• Plasma and / or interstitial fluid loss
 Burns
 Endocrinologic causes: diabetes insipidus, diabetic ketoacidosis,
congential adrenal hyperplasia
 Gastroenteritis
 Pancreatitis
 Peritonitis
 NGT, fistula or enterostomy losses
 Diuretic therapy
 Sodium losing nephropathy

Modified from; Worthley, L: Shock: A Review of Pathophysiology and Management,

Part I and II. Crit Care Resusc. 2000; 2:55-84
 Classification of Hypovolemic Shock

Class Volume loss % of blood Clinical

(ml) volume features
Class I 500-750 10-15% None

Class II 750-1500 15-30% Postural

hypotension

Class III 1500-2000 30-40% Hypotension;

tachycardia

Class IV > 2000 > 40% Severe shock;

death
 Hypovolemic Shock
Mild Moderate (20- Severe
(<20%) 40%) (>40%)
Blood volume Blood volume Blood volume
Cool extremities Same, plus: Same, plus:
Increased Tachycardia Hemodynamic
capillary refill Tachypnea instability
Diaphoresis Oliguria Marked
Collapsed veins Postural changes tachycardia
Anxiety Hypotension
Mental status
deterioration
Maier, R: Approach to the Patient With Shock, Chap 264 Harrison’s Textbook
of Internal Medicine 17th ed, p.1693
 Cardiogenic Shock

• State of end-organ hypoperfusion due cardiac

pump failure
• Occurs in 5 – 8% of STEMI pts
• Hemodynamic parameters:
– Systolic BP < 90 mmHg
– Cardiac index < 1.8 L/min/m2 without support
– LVEDP > 18 mmHg
– RVEDP > 10 mmHg

Reynolds, H & Hochman, J: Cardiogenic Shock: Current Concepts and Improving

Outcomes. Circulation, 2008; 117:686-697.
 Causes of Cardiogenic Shock

• Acute myocardial infarction

 Pump failure
• Large MI
• Small MI with pre-existing LV dysfunction
• Severe recurrent ischemia
 Mechanical complications
• Acute mitral regurgitation
• Ventricular septal defect
• Free wall rupture
• Pericardial tamponde
 Right ventricular infarction
Topalian, S et al: Cardiogenic Shock Crit Care Med. 2008; 36 (Suppl):S66-S74.
 Causes of Cardiogenic Shock
• Other conditions
 End-stage cardiomyopathy
 Myocarditis
 Myocardial contusion
 LV outflow tract obstruction
• Severe aortic stenosis
• Hypertrophic obstructive cardiomyopathy
 Obstruction to LV filling
• Severe mitral stenosis
• Left atrial myxoma
 Acute massive pulmonary embolism
 Tension pneumothorax
 Acute stress (Tako-tsubo) cardiomyopathy
Topalian, S et al: Cardiogenic Shock. Crit Care Med. 2008; 36 (Suppl):S66-S74.
 Pathophysiology of Cardiogenic Shock
Reynolds, H & Hochman, J: Cardiogenic Shock: Current Concepts and Improving
Outcomes. Circulation, 2008; 117:686-697.

Myocardial infarction
Myocardial dysfunction

Systolic Diastolic
SIRS
(IL-6, TNF-,  Cardiac output
 LVEDP
NO, ROS)  Stroke volume
Pulmonary congestion
Hypotension
Hypoxemia
 Coronary perfusion
pressure Ischemia

Compensatory Progressive myocardial dysfunction

vasoconstriction

DEATH
 Distributive Shock

• Due to inappropriate relaxation of vascular

tone
• Results in increase venous capacitance and
relative hypovolemia (no net fluid loss)
• Decreased preload -> reduced CO -> reduce
DO2

Schwarz, A: Shock. In eMedicine, Feb 2008

 Common Causes of Distributive Shock

• Sepsis
• Anaphylaxis
 Medications (eg, antibiotics, vaccines, other drugs)
 Blood products
 Envenomation
 Foods
 Latex
• Neurologic causes
 Head injury
 Spinal shock
• Drugs
Schwarz, A: Shock. In eMedicine, Feb 2008
 Sepsis
• SIRS – Systemic inflammatory response syndrome ( 2 or
more of the following):
– T >38C or <36C
– HR > 90 / min
– RR > 20 / min or PaCO2 < 32 mmHg
– WBC > 12,000 / mm3 or < 4,000 / mm3 or > 10% immature
neutrophils
• Sepsis – SIRS caused by infections
• Severe sepsis – Sepsis with evidence of hypoperfusion,
hypotension, or organ dysfunction
• Septic shock – sepsis with associated hypotension despite
adequate fluid resuscitation

Worthley, L: Shock: A Review of Pathophysiology and Management, Part I and II.

Crit Care Resusc. 2000; 2:55-84
 Septic Shock
• Bacterial cell wall endotoxins secondary to
gram negative bacteremia
• Systemic inflammatory response
• Cytokines dilate peripheral capillary beds
• Capillary leak, third spacing of fluid,
myocardial depression
 Neurogenic Shock
• Autonomic nervous control of the blood
vessel fail
• Peripheral pooling of the blood away from the
vital organs
• Spinal cord injury, DM, pulmonary embolism,
cirrhosis, gastric distension
 Anaphylactic shock
• Severe allergic reaction to a foreign protein
• Insect stings, food, medicine, pollen or inhaled,
ingested, injected substances
• Severity of the reaction is inversely related
between exposure and onset of symptoms
 Pathophysiology of Shock

Ferguson, D: In Cecil’s Textbook of Medicine, Chapter 69, 20th ed 1996.

 Stages of Shock
• Compensatory Shock:
– Usage of normal defense mechanism of the body
– Increase heart rate and blood vessel constricts
– Pale skin, tachycardia and normal BP
– Body corrects within 74 hours
 Stages of shock
• Progressive shock
– Shunting of blood away from the extremities and
abdomen to the lungs and brain
– Medical intervention is needed
– Cyanotic or mottled skin, decreased blood
pressure, altered mental status
 Stages of shock
• Irreversible shock
– No clear immediate sign and symptoms
– Blood is shunted away from the liver and kidney
to the heart and brain
– Blood vessels are unable to compensate to
perfuse the heart and brain
– Death inevitable
 Stages of Shock and Associated
Clinical Signs

Clinical Stage I Stage I I Stage I I I

P aram eter Com pensated Decom pensated I rreversible
Arterial pressure N or   

Heart rate    or 

Pulse pressure   

Respiratory rate N or    or 

Cardiac output *  

Mental status Anxiety Impaired / obtunded Coma

Urine output N or   Anuric

Skin Cool* Mottled Cold, cyanotic

* A high cardiac output and warm skin may be present in early stages of septic shock

Ferguson, D: In Cecil’s Textbook of Medicine, Chapter 69, 20th ed 1996.

 Shock in Children
• Develop early and progresses rapidly
• No symptoms until very late stages
• Pallor and altered mental status
• Changes in the vital signs are late signs of
shock
 Management
• Intubate any patient with persistent hypotension,
altered mental status and hypoxia
• Administer high flow oxygen
• Treat hypovolemic shock with IV fluids or blood
products
• Treat cardiogenic shock with inotropes
• Treat septic shock with IV fluids and antibiotics
 Fluid Resuscitation:
What type of fluid
• No survival benefit using colloids vs
crystalloids
• Volume of crystalloid required 2-3 x that of
colloid
• In pts with low CVP and concurrent
pulmonary edema, a colloid may be used to
avoid large volume of crystalloid

Nguyen, H. B. et al: Severe Sepsis and Septic Shock: Review of the Literature and
Emergency Department Management Guidelines. Ann Emerg Med, July 2006
48;1:28-54.
 Fluid Resuscitation:
How much fluid
• Optimal titration of fluids ideally guided by
invasive monitoring, i.e. central venous or
pulmonary artery catheter
• Various strategies
 Leg raising – one time increases central blood volume
by 100-150 ml
 Fluid challenge: 500 – 1,000 ml boluses q 30 mins
 20-40 ml/kg
• Large volumes (5-10 liters) may sometimes be
needed in cases of septic shock

Nguyen, H. B. et al: Severe Sepsis and Septic Shock: Review of the Literature and
Emergency Department Management Guidelines. Ann Emerg Med, July 2006
48;1:28-54.
 Management
• Do not hesitate to use vasopressor agents
• Early, aggressive treatment of septic shock
improves outcome
• May use CVP line to guide in hydration
 Shock in pregnant woman
• Compromise life of both mother and fetus
• Lack adequate perfusion to the uterus without
signs and symptoms to the mother
• ABCs of life support
• Left lateral decubitus position
 Guidelines for Managing Shock
Abnorm ality I ntervention
Hypotension ICU monitoring, volume
expansion, vasopressor
agents
Tissue ICU monitoring, volume
hypoperfusion expansion, vasopressor
agents, inotropic agents;
 mechanical ventilation
Organ system ICU monitoring, volume
dysfunction expansion, vasopressor
agents; inotropic agents;
 mechanical ventilation
Infection Antibiotics; surgical drainage
Mediators of Mediator inhibition
toxic effects
Therapeutic Goal
MAP  60 mmHg;
PCWP = 14-18 mmHg
Hgb > 10 g/dL
SaO2 > 92%
CI > 2.2 L/min/m2
Normal lactate levels
Normalize values: creat,
BUN, urine output;
PaO2
Eradication of infection
Reversal of toxic effects
Thank you