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Definition :
inadequate perfusion of body tissues that occurs
when an imbalance develops between cellular
oxygen supply and cellular oxygen demand
• Inadequate tissue perfusion can result in :
- Generalized cellular hypoxia (starvation)
- Widespread impairment of cellular
- Tissue damage  organ failure
- death



• Normotension
• hypoperfusion  hypoxia  tissues are under
perfused, decreased Cardiac Output, increased
anaerobic metabolism  lactic acid is building
• katekolamin
• The baroreceptors detect the resulting hypotension
 release catecholamines (epinephrine &
norepinephrine)  vasoconstriction, increase HR &
contractility of the heart  maintaining adequate CO
 blood pressure 
• Hypoperfusion  Acidosis  hyperventilate
• The body shunts blood from organ such as skin,
kidneys, GIT to ensure adequate blood supply to vital
organs (heart & brain)  patient’s skin is cold, bowel
sounds are hypoactive, urine output decreases
• Renal hypoperfusion  Renin-angiotensin axis &
arginine vasopressin  vasoconstriction
Sign&Symptoms :
• Weakness & lightheadedness – caused by
decreased blood volume
• Thirst – caused by hypovolemia  loss of
extracellular fluid
• Pallor – caused by catecholamine-induced
vasoconstriction and/or loss of circulating red
blood cells
• Tachycardia – caused by the effects of
catecholamines on the heart as the brain
increases the activity of the sympathetic nervous
• Diaphoresis – caused by the effects of
catecholamines on sweat glands
• Tachypnea – caused by brain elevating the
respiratory rate under the influence of stress,
catecholamines, acidosis, and hypoxia
• Decreased urinary output – caused by
hypovolemia, hypoxia, and circulating
• Weakened peripheral pulse – the “thready” pulse
(meaning “threadlike”, the arteries actually shrink
in width as intravascular volume is low)
• Compensatory mechanisms begin to fail 
decreased perfusion of the cells  sodium ions build
up within while potassium ions leak out
• anaerobic metabolism continues  metabolic
acidosis  the arteriolar and precapillary sphincters
constrict  blood remains in the capillaries 
hydrostatic pressure increase & histamine, cytokines
release  leakage of fluid and protein into the
surrounding tissues  edema
• Overworked heart becomes dysfunctional 
body inable to meet increased O2 requirements
 tissue ischemia  failure of cardiac pump
Refractory (Irreversible)
• Shock continues  organ damage is so severe
that the patient does not respond to treatment
and cannot survive. Despite treatment, blood
pressure remains low
• Complete renal & liver failure  compounded by
the release of necrotic tissue toxins, creates an
overwhelming metabolic acidosis  lactic
acidosis  ATP depletet  multiple organ
dysfunction  complete organ failure  death
Sign & Symptoms
• Hypotension – caused by hypovolemia, either
relative or absolute, and/or by diminished cardiac
output seen in mechanical shock
• Altered Mental Status (confusion, restlessness,
combativeness, unconsciousness) – caused by
decreased cerebral perfusion, acidosis, hypoxia,
and catecholamine stimulation
• Cardiac Arrest – caused by critical organ failure
secondary to blood / fluid loss, hypoxia, and
occasionally dysrhythmias caused by
catecholamines and/or low perfusion
Clinical Presentation
• Vital signs
Hypotensive (may be normal or  due to
compensatory mechanism)  <90 mmHg
MAP < 60 mmHg
Tachycardia : weak and thready pulse
Tachypneic : blow off CO2  respiratory alkalosis
• Mental status (LOC)
• Oliguria: urine output <0.5ml/kg/h. Requires at
least 1h to be diagnosed
Weil and Subin :
• the vascular reservoir
(hypovolaemic shock)
• the pump (cardiogenic shock)
• the conduits (obstructive
• distribution of blood flow
among and within the organs
(distributive shock)  septic
shock, anaphylactic shock
Hypovolemic Shock
• Loss of circulating volume  decrease tissue
perfusion  general shock response
• Etiology :
- internal (inflamasi) or external fluid loss
(dehydration, hemorrhage, massive diuresis,
extensive burns)
- intracellular and extracellular compartments
Haemodynamic findings
• decreased cardiac output, high SVR and low
filling pressures
• Venous O2 saturation (mixed venous and
central venous) is typically decreased
• Lactic acidosis is frequent
• Haemoglobin levels can initially be maintained
in haemorrhage  decrease only after
initiation of fluid resuscitation or when shock
is prolonged
Clinical Findings
• Low Blood pressure
• Tachycardia
• Cyanosis
• Capillary Refill Time > 2 seconds
• Collapse of Jugular Venous Pressure
What to measured:
• Arterial Blood gases and assessment of base
deficit  hypoxia  metabolic acidosis
• Haemoglobin
• Lactate
• Haematocrit
These tests are only of value when interpreted
in a series, therefore should be repeated
allgower burri Shock Index
• Management priorities in the bleeding patient
: controlling blood loss, replenishing
intravascular volume and sustaining tissue
• Establishing a patent airway, ensuring
adequate ventilatory exchange and
• Securing venous access
• Urinary catheter  assess urine output
• Controlling blood loss : holding and absorbent
dressing firmly over the area with the heel of
the hand & elevating the bleeding part,
dressing & bandage, arterial tourniquets are
reserved for life threatening bleeding
• 0.9% Normal Saline is also an acceptable
alternative. Large volumes, however may
result in metabolic acidosis.
• Blood transfusion
• Vasopressor (adrenergic agent : Dopamine,
noradrenaline & adrenaline )  improving
blood pressure  help to restore organ
perfusion  additional increase in SVR
(Systemic Vascular Resistance)  further
compromise blood flow in some vascular beds
(especially the skin, splanchnic region and
• Inotropic agents : usually not required
(exception of patients with underlying cardiac
disease or heart trauma)
• Caution ! when applying sedation or analgesia
to patients with hypovolaemic shock  blunt
the release of endogenous catecholamines 
induce vasodilation and myocardial
• Ketamine in contrast to other morphinic
agents, is not associated with these unfa-
vourable haemodynamic effects  considered
as the analgesic agent of choice
what to see within the ressusitation? -
Oxygenation, ABG, heart rate, skin perfusion
and urine output
• Maintaining blood pressure : In bleeding
patients, a SBP of 90mmHg is sufficient to
preserve tissue perfusion
• Brain trauma  SBP of 120mmHg (protect
cerebral perfusion)
Patient’s response
• Urinary output : Adequate resuscitation 
approximately 0.5 mL/kg/hr in adults ; 1
mL/kg/hr for pediatric patients ; For children
under 1 year of age, 2 mL/kg/hour should be
• Acid – base balance : inadequate resuscitation
or ongoing blood loss  Persistent acidosis
• State of inadequate tissue perfusion due to
cardiac failure (impaired contractile function
or to valvular dysfunction).
• Most commonly caused : pump failure in
patients with AMI or mechanical
complications of AMI, myocarditis, myocardial
contusion, stress-induced cardiomyopathy,
intoxication with cardiodepressant substances
(β-blockers, calcium channel antagonists, etc.)

Blood Pressure Regulation

Neural Hormonal Autoregulation

Cardiac Output
Total Peripheral Resistance
Blood Volume

Blood Pressure
Chemoreceptor Reflexes
Hormonal & Cations (K, Ca2+ and Na)
• Epinephrine & norepinephrine  ↑ heart rate &
• Thyroid hormones  enhance cardiac
contractility & increase heart rate
• Elevated of K or Na  decrease heart rate and
• Excess Na blocks Ca2 inflow  decreasing the
force of contraction
• Excess K blocks generation of action potentials
Cardiac Output (CO)
Volume of blood pumped by each ventricle per
minute (not the total amount of blood pumped
by the heart).
Stroke volume
3 factors regulate stroke volume & ensure that the
left and right ventricles pump equal volumes of
• (1) preload, the degree of stretch on the heart
before it contracts; proportional to the end-
diastolic volume (EDV) (the volume of blood that
fills the ventricles at the end of diastole)
• (2) contractility, the forcefulness of contraction of
individual ventricular muscle fibers; and
• (3) afterload, the pressure that must be exceeded
before ejection of blood from the ventricles can
(1) Preload
• EDV : the volume of blood that fills the ventricles
at the end of diastole.

• Two key factors determine EDV:

– duration of ventricular diastole
– venous return

• Frank–Starling law of the heart:

The more the heart fills with blood during
diastole, the greater the force of contraction
during systole.
(> EDV  > SV)
(2) Contractility
• strength of contraction at any given preload
• (+) inotropic : ↑ contractility
– Stimulation of the sympathetic division of the ANS,
hormones (epinephrine & norepinephrine), increased
Ca2 level in the interstitial fluid, & the digitalis drug
• (-) inotropic : ↓ contractility
– inhibition of the sympathetic division of the ANS,
anoxia, acidosis, Calcium channel blockers, &
increased K level in the interstitial fluid
(3) Afterload
• The pressure that must be overcome before a
aortic valve can open
• ↑ in afterload  ↓ stroke volume  more
blood remains in the ventricles at the end of
• Mean arterial pressure (MAP) = the average
blood pressure in arteries, is roughly one-third
of the way between the diastolic and systolic
• MAP = diastolic BP + 1/3 (systolic BP-diastolic
Systemic & Pulmonary circulation
Clinical presentation
• anterior MI : retrosternal pain, severe
tissue/organ hypoperfusion (cyanosis, cold
and clammy skin, slow capillary refilling,
mental changes, obtundation, oligu- ria) &
pulmonary congestion (dyspnoea,
tachypnoea, orthopnoea)
• Hypotension : SBP <90mm Hg / MAP <65mm
Hg / requirement for vasopressor agents to
maintain blood pressure above these levels.
Haemodynamic findings
• tachycardia, low cardiac output, elevated
cardiac filling pressures, increased SVR
• Hypotension : SBP <90mm Hg / decrease of
MAP of >30mm Hg from the patient’s normal
• Hypoperfusion : decreased blood pressure /
elevated lactate levels
• optimal oxygenation, correction of electrolyte
and acid–base disturbances, tight glucose
control, stress ulcus prophylaxis
• Obtaining the aetiological and haemodynamic
diagnosis  haemodynamically stabilized
(fluid challenge in those without pulmonary
oedema & vasopressors in those with
hypotension unresponsive to fluids)
• The changes of haemodynamic variables
(heart rate, arterial pressure, CVP, PAOP,
cardiac output, ScO2) & oxygenation (SaO2)
 monitored closely to prevent pulmonary
oedema, hypoxaemia, and to evaluate the
response to the treatment
• The absolute prerequisite for vasopressor and
inotropic treatment is adequate cardiac
• inadequate cardiac output : inotropic
• Hypotension : dopamine (limited by increase
of heart rate and elevation of pulmonary
• profound hypotension : norepinephrine
• pulmonary congestion : Dobutamine +
nitroglycerin or sodium nitro-prusside
Distributive/Vasodilatory Shock
• The reduction in systemic vascular resistance
results in inadequate cardiac output and
tissue hypoperfusion despite normal
circulatory volume

– Sepsis
– Anaphylaxis
– Neurogenic
• The most common cause of distributive shock (mortality
rate: 20-50%)
• Typically secondary to gram negative bacteremia (E. coli,
Klebsiella, Proteus, Pseudomonas) & less often due to gram
negative anaerobes (Bacteroides)

• Tissue perfusion abnormalities invasion of the body by

microorganisms & failure of body’s defense mechanism.
Endotoxins  inflammatory mediator (systemic inflammatory
Vasodilation & increase capillary permeability
Shock due to alteration in peripheral circulation & massive dilation
Early state (Hyperdynamic Late state (Hypodinamic
compensation) decompensation)

– Massive vasodilation – Vasoconstriction

– Pink, warm, flushed skin – Skin is pale & cool
– Increased Heart Rate Full – Significant tachycardia
bounding pulse – Decreased BP
– Tachypnea – Increase SVR
– Decreased SVR – Decreased CO
– Increased CO – Metabolic & respiratory
– SVO2 will be abnormally acidosis with hypoxemia
• Anaphylaxis: a serious allergic reaction that is rapid in onset
& may cause death
(results from widespread systemic allergic reaction to an
Neurogenic shock
• Etiology :
– traumatic spinal cord injury
– effects of an epidural/spinal anesthetic
• Patophysiology :
– Loss of sympathetic tone with a reduction in systemic vascular
resistance without a compensatory tachycardia.
– Pain, gastric dilation, fright  reflex vagal parasympathetic
stimulation  may stimulate neurogenic shock
• Clinical Presentation :
- Hypotension
- Bradycardia
- syncope
Obstructive shock
• Etiology :
obstruction of the CVS
(most common : Pulmonary embolism & cardiac tamponade)
• Clinical Presentation :
– hypotension
– skin vasoconstriction
– dilated jugular veins
– pulsus paradoxus (frequent)
• Haemodynamic :
– ↓ CO
– ↑ SVR
– ↑ filling pressures
– pulmonary hypertension in pulmonary embolism
• Echocardiography :
– extremely helpful to diagnose obstructive shock and its cause.