Concept of extreme conditions The most important extreme

states:
• Intensive-care medicine or critical-care medicine is a
branch of medicine concerned with the diagnosis SHOCK
and management of life threatening conditions
requiring sophisticated organ support and invasive • SHOCK Shock is a state of organ
monitoring. • COLLAPSE hypoperfusion with
• COMA resultant cellular dysfunction
• A critically ill patient is one at imminent risk of death; and death.
the severity of illness must be recognized early and Inadequate peripheral perfusion leading to
appropriate measures taken promptly to assess,
failure of tissue oxygenation
diagnose and manage the illness.
Þ may lead to anaerobic metabolism

Ultimate Effects of Anaerobic Metabolism Shock is a condition in which the cardiovascular

system fails to perfuse tissues adequately
Inadequate
Cellular
Oxygen
Delivery
• An impaired cardiac pump, circulatory system, and/or
volume can lead to compromised blood flow to
tissues-hipoperfusion
Lactic
Inadequate
Energy Anaerobic Acid
Production Metabolism Production
l These three parts
can be called the
“perfusion triangle.”
Metabolic Metabolic – When a patient is in
Failure CELL Acidosis
DEATH shock, one or more of
the three parts is not
working properly.
 Pathogenic classification Hypovolemic shock
1. Hypovolemic shock
(hemorrhagic,anhydremic) 1. Blood loss - hemorrhagic shock

2. Cardiogenic shock 2. Loss of blood plasma at massive

exudative inflammation - burn shock
connected with disturbances of pump function of
heart
3. Dehydration - anhydremic shock
3. Vascular forms of shock
(anaphylactic, painful shock at which the central
regulation of blood circulation is damaged)

Hypovolemic shock Cardiogenic shock

• Hypovolemic Shock = Low Volume • Cardiogenic Shock = Pump Failure

–Trauma –Acute MI –Mechanical

–Vomiting
–Non-traumatic –CHF obstruction
–Diuresis
blood loss –Bradyarrhythmias ( distributive shock )
–Sweating ¨Cardiac tamponade
¨Vaginal –Third space losses –Tachyarrhythmias ¨Tension pneumothorax
¨GI ¨Pancreatitis ¨Pulmonary embolism
¨GU ¨Peritonitis
–Burns ¨Bowel obstruction
–Diarrhea
 Reduction of the general peripheral
resistance: Vasogenic shock
1. Fall of neurogenic tone of arterioles • Vasogenic Shock = Low Resistance

2. Reduction of basal tone of vessels –Spinal cord trauma

under action of biologicaly active • neurogenic shock
substances (anaphylactic, pancreatic –Depressant drug toxicity
shock) or toxic products (traumatic, –Simple fainting
infection-toxic shock).

Shock Shock
• Mixed Shock
–Septic Shock • Mixed Shock
• Overwhelming infection –Anaphylactic Shock
• Inflammatory response occurs • Severe allergic reaction
• Blood vessels • Histamine is released
–Dilate (loss of resistance) • Blood vessels
–Leak (loss of volume)
–Dilate (loss of resistance)
• Mixed Shock –Leak (loss of volume)
–Septic Shock • Mixed Shock
• Fever –Anaphylactic Shock
– Increased O2 demand • Histamine release
– Increased anaerobic metabolism • Extravascular smooth muscle spasm
• Bacterial toxins –Laryngospasm
– Impaired tissue metabolism –Bronchospasm
 Etiological classification of shock What is shock?
1. Traumatic
2. Hemorrhagic Generalized State of Hypoperfusion
3. Burn
Inadequate oxygen delivery
4. Anhydremic (dehydrative)
6. Cardiogenic Catecholamines and other responses
8. Septic
9. Anaphylactic Anaerobic metabolism

Cellular dysfunction

Cell death

Shock Compensated Shock

•Signs and symptoms due to:
–Hypoperfusion
–Compensatory responses
• Baroreceptors detect fall in BP
–Usually 60-80 mm Hg (adult)
• Sympathetic nervous system activates
–SNS Neurotransmitters & their effects
•Cardiac effects
•Increased force of contractions
•Increased rate
•Increased cardiac output
•Peripheral effects
•Arteriolar constriction
•Pre-/post-capillary sphincter contraction
•Increased peripheral resistance
•Shunting of blood to core organs
Compensated Shock Compensated Shock
• Decreased renal blood flow
–Renin released from kidney arteriole • Insulin
–Renin & Angiotensinogen combine secretion caused by epinephrine
–Converts to Angiotensin I contributes to hyperglycemia
–Angiotensin I converts to Angiotensin II
• Peripheral vasoconstriction • Glucagon
• Increased aldosterone release (adrenal cortex) release caused by epinephrine
– promotes reabsorption of sodium & water promotes liver glycogenolysis & gluconeogenesis
•Decreased blood flow to hypothalamus • ACTH
Release of antidiuretic hormone stimulates adrenal cortex release of cortisol
(ADH or Arginine Vasopressin) from posterior pituitary glucose production
Retention of salt, water
Peripheral vasoconstriction

Decreased
Cardiac
Decompensated Shock
Output
–Cardiac Effects
Aldosterone, Catecholamine
• Decreased RBC oxygenation
ADH Release Release • Decreased coronary blood flow
• Myocardial ischemia
Increased
Increased PVR
• Decreased force of contraction
Blood Volume
–Peripheral effects
Increased •Relaxation of precapillary sphincters
Cardiac •Continued contraction of post-capillary sphincters
Output
•Peripheral pooling of blood
Increased •Plasma leakage into interstitial spaces
Increased
Myocardial Work, Volume Loss •Continued anaerobic metabolism
O2 Demand
•Continued increase in extracellular potassium

Myocardial Compensated Shock Leading to

Ischemia
Decompensation

Decompensated Shock
• Symptoms
–Listlessness, confusion, apathy, slow speech
–Cold, gray, “waxy” skin
–Tachycardia; weak, thready pulse
–Decreased blood pressure
–Moderate to severe orthostatic hypotension
–Decreased body temperature
–Tachypnea
Irreversible Shock
• Presentation
–Confusion, slurred speech, unconscious
–Slow, irregular, thready pulse
–Falling BP; diastolic goes to zero
–Cold, clammy, cyanotic skin
–Slow, shallow, irregular respirations
–Dilated, sluggish pupils
–Severely decreased body temperature
Irreversible Shock
• Post-capillary sphincter relaxation
• Loss of peripheral vascular resistance
•Washout of accumulated products
•Hydrogen ion
•Potassium
•Carbon dioxide
•Microembolise in lungs
•Systemic metabolic acidosis occurs
•Cardiac Output decreases further
Irreversible Shock
• Irreversible shock leads to:
–Renal failure
–Hepatic failure
–Disseminated intravascular coagulation (DIC)
–Multiple organ systems failure
–Adult respiratory distress syndrome (ARDS)
–Death
 Disseminated Intravascular Adult Respiratory Distress
Coagulation (DIC) Syndrome (ARDS)
• Decreased perfusion causes tissue • AKA: Shock Lung , Da Nang Lung
damage/necrosis • Decreased perfusion damages alveolar and
• Tissue necrosis triggers diffuse clotting capillary walls
• Diffuse clotting consumes clotting factors • Surfactant production decreases
• Fibrinolysis begins • Fluid leaks into interstitial spaces and
• Severe, uncontrolled systemic hemorrhage alveoli
occurs • Gas exchange impaired
• Work of breathing increases

STAGES OF SHOCK NON-PROGRESSIVE STAGE

• Non-progressive Stage Ø NEUROHUMORAL MECHANISMS MAINTAIN

Reflex compensatory mechanisms are activated. CARDIAC OUTPUT AND BLOOD PRESSURE:
Profusion of vital organ is maintained • Baroreceptors reflexes
• Release of catecholamine
• Progressive Stage • Activation of renin-angiotensin axis
• ADH release
Tissue hypoperfusion.
• Generalized sympathetic stimulation
Circulatory & metabolic imbalances leading to
Acidosis. Ø DIFFERENT CLINICAL OUTCOME OF THESE
COMPENSATORY MECHANISMS:
• Irreversible Stage • Tachycardia
• Peripheral vasoconstriction (cool & pale skin)
Cellular & tissue injury.
• Renal conservation of fluid
Even with correction of haemodynamic defects, survival is
not possible.
 IRREVERSIBLE STAGE
PROGRESSIVE STAGE
ØWIDESPREAD CELLULAR INJURY:
ØWIDESPREAD HYPOXIA: • Damage to the organelle of cells
• Leakage of lysosomal enzymes
• Anaerobic glycolysis
• Production of nitric oxide by cells
• Production of lactic acidosis • Worsened myocardial contractility
• pH lead to blunting of vasomotor response leading
to vasodilatation ØDIFFERENT CLINICAL OUTCOME OF
• Peripheral pooling of blood CELLULAR INJURY:
ØDIFFERENT CLINICAL OUTCOME OF THESE • Septic shock (entry of intestinal flora into circulation)
FAILING MECHANISMS: • Complete renal shutdown (acute tubular necrosis)
• Feeble, failing pulse
• Mental confusion

Key Issues In Shock

• Tissue ischemic sensitivity

–Heart, brain, lung: 4 to 6 minutes
–GI tract, liver, kidney: 45 to 60 minutes
–Muscle, skin: 2 to 3 hours

Resuscitate Critical
Tissues First!
 COLLAPSE Orthostatic collapse
Collapse is an acute vascular insufficiency
characterized by fall of a vascular tone:
• Appears at fast transition from horizontal position
• Reduction of venous blood inflow to heart to vertical
• Decrease of heart output
• Fall of arterial and venous pressure • At long time of standing.
• Disorder of tissues perfusion and metabolism
Hypoxia of brain
• At redistribution of blood with increase of total
• Vital functions of an organism are oppressed amount of a venous system
• It is shown in clinic by short-term of
consciousness loss
• At decrease of inflow to heart.

Ortostatic collapse
Cоmа
• In the postoperative period
• At fast removal of ascites liquids Cоmа is a pathological state that is
• As a result of spinal and peridural anesthesias. characterized with deep oppression of functions
of the central nervous system and it is shown by
• Jatrogenic ortostatic collapse sometimes appears loss of consciousness, absence of reflexes on
during wrong use of neuroleptics, ganglioblockers, external irritators and disorders of the vital
adrenoblockers, sympatolytics.
functions.
• Among pilots and cosmonauts ortostatic collapse
may be caused by redistribution of blood.
• It may be observed at practically healthy children
and teenagers.
 Classification. Etiology. Pathogenesis. GLASGOW COMA SCORE

1. Injury and diseases of the central nervous system (insult,

(craniocerebral trauma)
2. Endocrine diseases (diabetic, thyreotoxic, hypoglycemic)
3. Toxic cоmas are observed at endogenic (uraemia, hepatic
insufficiency, infections, pancreatitis) and exogenic
intoxications (alcoholic poisonings, barbiturate poisoning
4. Hypoxia
5. Disturbances of electrolyte, water balance

“Stress”
Most current definitions state that stress
is the mental and physical response and
adaptation by our bodies to the real or
perceived changes and challenges in our
lives.
A stressor is any real or perceived physical, social,
or psychological event or stimulus that causes our
bodies to react or respond.
 This figure shows the individual’s energy and
ability to cope with the stressful situation:
In his early career as an experimental
scientist, Selye noted a triad of adrenal
enlargement, thymic atrophy, and gastric
ulcer appeared in rats he was using for his
studies. These same three changes
developed in response to many different or
nonspecific experimental challenges.

Cortisol in stress response initiation

Sympathetic nervous system activation