SHOCK

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

Compensatory

Progressive

Refractory(Irreversible)
 Stages
Initial
Normotension
hypoperfusion hypoxia tissues are under
perfused, decreased Cardiac Output, increased
anaerobic metabolism lactic acid is building
katekolamin
Compensatory
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) patients 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
system
Sign&Symptoms
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
catecholamines
Weakened peripheral pulse the thready pulse
(meaning threadlike, the arteries actually shrink
in width as intravascular volume is low)
Progressive
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
 CLASSIFICATION
Weil and Subin :
the vascular reservoir
(hypovolaemic shock)
the pump (cardiogenic shock)
the conduits (obstructive
shock)
distribution of blood ow
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 ndings
decreased cardiac output, high SVR and low
lling 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 uid 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
 Therapy
Management priorities in the bleeding patient
: controlling blood loss, replenishing
intravascular volume and sustaining tissue
perfusion
Establishing a patent airway, ensuring
adequate ventilatory exchange and
oxygenation
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 ow in some vascular beds
(especially the skin, splanchnic region and
kidneys)
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
depression
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 sufcient to
preserve tissue perfusion
Brain trauma SBP of 120mmHg (protect
cerebral perfusion)
 Patients 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
maintained
Acid base balance : inadequate resuscitation
or ongoing blood loss Persistent acidosis
 CARDIOGENIC SHOCK
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
(-blockers, calcium channel antagonists, etc.)
Physiology

Blood Pressure Regulation

Neural Hormonal Autoregulation

Cardiac Output
Total Peripheral Resistance
Blood Volume

Blood Pressure
Neural
Chemoreceptor Reexes
Hormonal & Cations (K, Ca2+ and Na)
Epinephrine & norepinephrine heart rate &
contractility
Thyroid hormones enhance cardiac
contractility & increase heart rate
RAAS
Elevated of K or Na decrease heart rate and
contractility
Excess Na blocks Ca2 inow 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
blood:
(1) preload, the degree of stretch on the heart
before it contracts; proportional to the end-
diastolic volume (EDV) (the volume of blood that
lls the ventricles at the end of diastole)
(2) contractility, the forcefulness of contraction of
individual ventricular muscle bers; and
(3) afterload, the pressure that must be exceeded
before ejection of blood from the ventricles can
occur.
 (1) Preload
EDV : the volume of blood that lls the ventricles
at the end of diastole.

Two key factors determine EDV:

duration of ventricular diastole
venous return

FrankStarling 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 uid, & the drug digitalis
(-) inotropic : contractility inhibition of the
sympathetic division of the ANS, anoxia, acidosis,
Calcium channel blockers, & increased K level in
the interstitial uid
 (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
systole
 MAP
Mean arterial pressure (MAP) = the average
blood pressure in arteries, is roughly one-third
of the way between the diastolic and systolic
pressures
MAP = diastolic BP + 1/3 (systolic BP-diastolic
BP)
Systemic & Pulmonary circulation
 Clinical presentation
anterior MI : retrosternal pain, severe
tissue/organ hypoperfusion (cyanosis, cold
and clammy skin, slow capillary relling,
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 ndings
tachycardia, low cardiac output, elevated
cardiac lling pressures, increased SVR
Hypotension : SBP <90mm Hg / decrease of
MAP of >30mm Hg from the patients normal
level
Hypoperfusion : decreased blood pressure /
elevated lactate levels
 Therapy
optimal oxygenation, correction of electrolyte
and acidbase disturbances, tight glucose
control, stress ulcus prophylaxis
Obtaining the aetiological and haemodynamic
diagnosis haemodynamically stabilized
(uid 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
preload
inadequate cardiac output : inotropic
 Hypotension : dopamine (limited by increase
of heart rate and elevation of pulmonary
pressure)
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
SIRS
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 bodys defense mechanism.
 Pathophysiology
Endotoxins inflammatory mediator (systemic inflammatory
response)
Vasodilation & increase capillary permeability
Shock due to alteration in peripheral circulation & massive dilation
Early state (Hyperdynamic
compensation) decompensation)
Massive vasodilation
Pink, warm, flushed skin
Increased Heart Rate Full
bounding pulse
Tachypnea
Decreased SVR*
Increased CO & CI
SVO2 will be abnormally
high
Late state (Hypodinamic
Vasoconstriction
Skin is pale & cool
Significant tachycardia
Decreased BP
Increase SVR
Decreased CO
Metabolic & respiratory
acidosis with hypoxemia
 Anaphylaxis: a serious allergic reaction that is rapid in onset
& may cause death
(results from widespread systemic allergic reaction to an
antigen)
 Caused by traumatic spinal cord injury / effects of an
epidural/spinal anesthetic.
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
hypotension, bradycardia, syncope
 Obstructive shock
due to obstruction of the cardiovascular system
(most common : Pulmonary embolism & cardiac
tamponade)
clinical presentation : hypotension, skin
vasoconstriction, dilated jugular veins, Pulsus
paradoxus is frequent
haemodynamic : low CO, high SVR, high lling
pressures, pulmonary hypertension in PE.
Echocardiography : extremely helpful to diagnose
obstructive shock and its cause