Indequate tissue perfusion and oxygenation, leading to multiple
organ failure and death if not treated.
Classes of shock
Haemorrhagic Shock Treatment.
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Septic shock is the biggest cause of death in intensive care
Haemorrhage is the biggest cause of post-injury preventable death.
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The critical determinants of cellular perfusion:
--> note: demand may be increased as well as perfusion reduced.
CO = SV x HR (per minute)
Stroke volume = EDV-ESV.
- determined by preload, myocardial contractility and afterload:
Venous flow depends on a pressure gradient between mean
veinous and right atrium.
Veins can be considered a reserviour with two components
- first the 'zero-pressure' volume which does not contribute to
- second the 'pressure' volume; 70% of the blood volume is in the
--> in blood loss this second compartment is depleted, reducing
Preload also affects contractility.
- venous filling lengthens myocardial fibers, increasing
contractility (Starling's Law).
Resistance to the forward flow.
Resistance is proportional
to vessel length & blood viscosity, and inversely proportional
to fourth power of the vessel radius.
- thus arteriolar smooth muscle tone is the major determinant of
- arteriolar tone, in turn, is reliant on extrinsic and local
Extrinsic factors include
neural (autonomic) and hormonal (eg adrenaline) regulation.
Local factors include the
myogenic response (response to wall tension), metabolic
autoregulation (response to metabolic waste products), &
endothelial-mediated regulation (eg NO from endothelial cells
monitoring the local environment).
Capillary exchange is determined by Starling's Forces (refer oedema
Shock is best classified by the underlying cause of abnormal tissue
Fluid depletion eg burns, renal losses, adrenal insufficiency
- often exacerbated by peri-operative fasting / poor fluids /
Blunt cardiac injury
- (seen in rapid deceleration)
- associated with penetrating thoracic injury in trauma, sometimes
Extracardiac Obstructive Shock
(External obstruction to cardiac output)
Severe pulmonary hypertension
Endocrine, eg Addisons
A pt may have several forms of shock, eg septic shock, with cardiac
impairment-related cardiogenic and distributive shock.
Haemorrhage is the most
common cause of shock.
Cardiogenic, neurogenic, septic or extracardiogenic obstruction
(tension pneumothorax) are other possibilities.
- or combinations of the above.
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Blood loss pathophysiology
Haemorrhage is an acute loss of circulating blood volume.
- 5L in a 70kg man (7% body weight).
- 80-90ml/kg in a child (8-9% bw).
Compensation begins when
>10% blood loss
- clinical signs of shock are thus unreliably late.
- by the time 40% is lost, the pt is dead.
--> diagnose and act on subtle findings.
For classes of shock see below
Baroreceptors activate the adrenal medulla
--> adrenalin, noradrenalin released
--> tachycardia, sweating, raised glucose
Reduced renal perfuson activates the RAAS cascade
--> angiotensin induced vasoconstrition
--> aldosterone induced salt retention
Vasopressin and glucocorticoids are also often
Other hormones with vasoactive properties are released
- histamine, bradykinin,
beta-endorphines, prostanoids and other cytokines
--> profound effects on microcirculation / vascular permeability.
Diastolic BP rises early and pulse pressure reduces (due to peripheral
- sensed by baroreceptors, respond with sympathetic vasoconstriction & tachcardia
--> tachycardia is most
often the earliest measurable circulatory sign of schock
--> the heart brain and kidneys are relatively spared by local
autoreguation (mediators eg PGs).
--> the skin becomes cool,
sweaty and pale, muscle beds lose
--> the viscera become
--> the volume of venous blood falls and the peripheral veins collapse
--> reduced renal blood flow allows fluid conservation (by Na+ retention in
3. Peripheral compensation
Hypotension with precapillary arteriolar constriction and
of fluid from extra to intravascular space (Starling)
Reduced peripheral perfusion causes lactic acidosis
Cellular hypoxia first manifests as endoplasmic reticulum swelling.
Cell swelling follows loss
of membrane integrity
Intracellular Ca++ deposition occurs.
Apoptotic self-destruction and free radical damage are central.
Compensation usually fails at >20-25% blood loss.
Multiple organ failure
Cell death causes local mediator release, particularly from the gut.
--> overstimulation of activated leukocytes.
--> self-amplifying mediator production loop
--> shock becomes irreversible.
Widespread peripheral vasodilation
occurs in response
--> loss of autotransfusion mechanism
--> further loss of intravascular volume
Multiple Organ failure
Clinical presentation is variable & depends on cause, severity,
and state of pt's various organs.
Myocardial dysfunction exacerbates ischaemia (another viscous
- ischaemia aggravated by high O2 need of compensating
tachycardic heart and decreased compliance.
Toxins and mediators also depression myocardium.
Cerebral abnormality is a cardinal feature of shock.
Hypoperfusion, hypoxaemia, pH and electrolyte disturbances all
Cerebral autoregulation compensates down to mean arterial pressures
of <60 mmHg
Dysfunction occurs early.
Hypoperfusion impairs gas exchange, 'shunting' under-oxygenated
--> exacerbates the poor delivery of O2 to tissues.
Severe under-perfusion of cells leads to loss of membrane integrity.
--> pulmonary fluid infiltration of alveolar spaces occurs (ARDS)
--> increases work of breathing, worsening hypoxaemia
--> ventilatory failure ensues.
Initially, glomerular control mechanisms compensate, maintaining
When shock worsens, GFR must drop and ATN follows.
Unlike other organs, eg heart & kidney, the gut (and skin)
cannot autoregulate to preserve blood supply.
--> intestinal hypoperfusion can occur despite normal HR and BP.
Blood is diverted, and gut is a major source of mediators from cell
--> systemic inflammation
Stress ulceration, malabsorption, ileus and perhaps pancreatitis or
cholecystitis may occur.
Haemodilution / haemorrhage leads to pancytopaenia.
DIC can follow activation of the clotting cascade within the
Clotting factor consumption and thrombocytopaenia can cause
Compensation aims to restore CO through above mechanisms.
External Obstructive Shock
May be acute or sub-acute.
Subacute can be
compensated in the short term by increased adrenergic stimulation
and fluid retention.
Organ blood flow may appear adequate, but a mediator-induced
'metabolic block' may exist at the tissue level, preventing
utilisation of oxygen and other nutrients.
Classically septic shock (see card).
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Look for decreased tissue perfusion.
- don't be reassured by normal BP and HR
- however a lucid pt with a good cap refill, dry skin and good urine
output is very likely OK.
750ml may be lost from a tibia / humerus
1500ml from a femur
Liters from a pelvic # (retroperitoneal).
Profound circulatory shock is easy
- clouded sensorium.
- organ shutdown
- cutaneous vasoconstriction
Signs of injury
- although shock in trauma
is usually haemorrhagic it may not be.
- if injuries above the diaphragm are present, consider cardiogenic,
tamponade, tension pneumothorax.
Any injured pt cool and tachycardic is in shock until
- elderly, athletes, children and beta-blocked may not show
--> CO = SV x HR so only HR can improve CO in the
Narrowed pulse pressure
- suggests significant blood loss and compensation
- do not rely on BP or
recognition will be delayed.
- remember: hypotension
is a decline in MAP of 40mmHg, regardless of figure (hypertensive
pts have a higher baseline).
The picture is modified by high cardiac filling pressures
And other features of heart failure.
JVP usually elevated
And other features of underlying cause.
See septic shock card
Classically hypotension without tachycardia or cutaneous
Narrowed pulse pressure is not seen.
Clues to diagnosis
Examine past history and medications carefully
Look at fluid balance chart and urine outputs
Are the signs or risk or sepsis?
Classes of Shock
* Age, severity of injury, time to treatment, pre-hospital fluids,
comorbidities and meds alter the classic haemodynamic response.
* Local-mediator induced peripheral vasodilation from soft-tissue
injuries may have a profound additional effect on intravascular
Do not wait until precise category made before Tx given.
* For a 70kg man.
|N or Up
* Fluids on 3:1 rule: 300ml electrolyte soln needed for every 100ml
Minimal symptoms (if otherwise physiologically normal)
Does not require replacement
Compensations restore volume within 24 hours.
Symptoms, narrowing pulse pressure (normal BP).
Become anxious, frightened, hostile.
Devastating blood loss, classic signs of shock.
Blood pressure drops.
Transfusion almost always needed (priority is to stop haemorrhage).
Note it takes only a modest further loss to shift to this.
Immediately life threatening.
Rapid transfusion and surgical intervention required.
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- Hb or haematocrit is unreliable and inappropriate for diagnosing
- massive blood loss may only produce a minimal acute decrease.
- a very low haematocrit after injury suggests massive blood loss or
Coagulopathy may cause haemorrhage
More often coagulopathy results from ongoing low-grade haemorrhage
and replacement by cold transfused blood deficient in clotting
Blood gases (shows metabolic acidosis).
FAST (Focused Assessment Sonography in Trauma) can also identify
pericardial fluid and tamponade.
CVP and pulmonary artery catheters may help.
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Intensive care setting with continuous monitoring.
Resuscitate, diagnose, treat
Treat before irreversibility sets in.
Maintain mean arterial pressure.
Ensure adequate perfusion with O2 and nutrient delivery.
Want serum lactate going down, not up.
Specific therapies aimed at cause.
though applies to most forms of
NOTE: RECENT EVIDENCE SHOWS:
1. Excessive crystalloid prior to
hemorrhage control is harmful
--> dislodges clots, dilutes coagulation factors,
--> activates dysfunctional inflammation, worsens oedema (harm to
all organs), assoc. with abdo compartment syndrome
--> increased MOF, morbidity and mortality
2. Early high-ratio transfusion of plasma and platelets to RBCs
- 1:1:1 emerging
O2 at 12-15 L/min
Sats monitoring (want >95%).
- be aware that poor perfusion leads to poor signal.
The first priority unless it is slow bleeding
- do not be reassured by empty drains post-op.
- operative control may be needed
- prolonged attempts at resuscitating pts with a major haemorrhage
lead only to coagulopathy, hypothermia and death.
2 16g cannulae (short and large calibre).
- antecubitals or forearm
- else Saldinger technique for central access, saphenous cutdown or
- be aware of complications of central access and follow up with a
Draw blood for type, crossmatch, FBC, U+Es, toxicology and pregnancy
Obtain an ABG
Use fluid warmers (39o) and rapid infusion pumps as required.
Most nonhaemorrhagic shock states also respond partially to volume,
so it is a good strategy.
Use warmed crystalloids initially.
- Ringer's lactate is the fluid of choice, N saline second
(potential for hperchloremic acidosis, esp if renal fx impaired).
Give max 1-2L (trauma; ATLS guidelines) then move to blood.
- initially 10 ml/kg if normotensive
- or 20ml/kg boluses if hypotensive
Catheterise and attach a graduated measuring bag.
Detects arrythmias and myocardial ischaemia.
- particularly in cardiogenic shock, myocardial disfunction, direct
thoracic injury and sepsis
Arrythmias are more likely when there are electrolyte or acid-base
Every 30mins or so, at least.
Inadequate volume resuscitation is the most common complication
Look for normalising vital signs and cerebral function.
- however these do not exactly relate to organ perfusion
CVP and skin circulation help, but are difficult to quantitate.
Urine output is reasonably sensitive for
renal perfusion and so a prime monitor for pt response.
- 0.5ml/kg/hr is adequate in an adult
- 1ml/kg/hr in a child
- 2ml/kg/hr in a child under 1
Using your hand, assess skin temperature
- a core/peripheral gradient is a useful indicator
- initial hyperventilation-induced metabolic alkalosis gives way to
worsening acidosis as shock progresses.
- normalising of metabolic acidosis suggests adequate resuscitation
- the base deficit may help estimate the severity of the perfusion
- the pH should normalise with treatment, else search for reason.
- sodium bicarbonate should not routinely be used.
- FBC, U+Es, Hcrit, lactate.
Algorithm for response:
* The haemodynamically normal pt has
no signs of inadequate tissue perfusion
|Est. bld loss
|Need 4 Fluid?
|Need 4 Bld?
* The haemodynamically stable
pt may be still in shock.
* Blood pressure is proportional
to CO and afterload - therefore an increase in BP does not
necessarily mean an increase in cardiac output.
Balance and CVP monitoring
Transfer unstable pts early to ICU for invasive monitoring
- but do not waste time inserting a CVL in the overtly hypovolaemic.
--> complication with pneumothorax can be fatal in an
CVP is relatively simple and a standard guide to assess (R) heart
ability to cope with fluid boluses.
- don't over-rely on CVP as it is not especially sensitive; cardiac
funcion relates to SV and EDV
- initial CVP may not relate to actual blood volume
--> may elevate in COPD, vasoconstriction and rapid fluid
Note that static measurements may
be unreliable (though <5 or >20 are obviously telling
- a minimal rise in an
initially low CVP suggests urgent need for volume expansion
- a declining CVP suggests
ongoing fluid loss and need for volume (transient responder)
- an abrupt elevation in
CVP suggests adequate replacement (or poor cardiac fx)
- pronounced elevations may signify overload or heart dysfuncion /
tamponade / tension pneumothorax.
--> if high (>15) and signs of failure & inadequate
perfusion, suspect cardiogenic shock, call for help.
The CVP Fluid Challenge is useful
- measure before and after 100-200ml bolus
- if CVP does not rise, further fluid can be given
- if it does rise, further fluid will overtransfuse.
Adequate CVP (>8) but
- conisder inotropic support, senior help mandatory.
type of blood?
Fully x-match bld is
- takes ~1 hr; so only for the rapid responder.
Type specific bld (ABO and
Rh) is second best"
- takes ~10mins; use for the transient responder.
Type O packed cells for
- Rh -ve for females of childbearing age.
- Type specific bld is preferred, unless >1 unknown casualties
being treated simultaneously.
Colloids may increase circulating volume to a greater degree than
--> but redistribute within hours in same manner anyway.
- carry a slight risk of anaphylaxis and coagulopathy
1. Both types of fluid are good enough in most situations given in
2. Crystallized theoretically given in 3x volume of colloid.
3. Greater weight gain and oedema follows crystalloid use.
4. No fixed relationship between serum [albumin] and colloid osmotic
pressure until albumin <15.
5. In septic shock / SIRS both will pass out the basement membranes.
6. Colloid can interfere with coagulation
7. No evidence for benefit of colloids over crystalloids (Cochrane)
Hartmann's solution fine; leave colloids to anaesthetists and ICU
Used to be thought rare in the first hour.
Now we understand Trauma-Induced-Coagulopathy
Now understood there is an inappropriate
over-activation of protein C in severe trauma / bleeding,
causing an excessive anti-clotting response
- prompted by endothelial damage activating protein C
- causes inactivation of clotting factors (Va and VIIIa) -->
major reduction in thrombin formation.
There is also hyperfibrinolysis
- due to activation
of the fibrinolytic system, hypothermia, acidosis, metabolic
Massive transfusion can dilute clotting factors
- and hypothermia inhibits clotting (so warm fluids)
- some synthetic colloids can worsen coagulopathy (esp dextrans)
Obtain baseline coag studies, esp if pt takes anticoagulants
Transfuse platelets, cryoprecipitate, FFP as required.
- now know 1:1:1 ideal; generally
4u blood then give 4u FFP +/- more blood, then after ~6+ bag of
platelets (really 6u) + cryo.
FFP contains II, VII, IX, X, XI
Cryo contains Factor VIII, fibrinogen and vWF, XIII, Fibronectin
If non-responding, consider:
1) persistent blood loss
2) unrecognised / underestimated fluid loss
3) nonhaemorrhagic shock eg underlying sepsis
4) underlying cardiovascular effects
5) cardiac tamponade, tension pneumothorax, ventilatory problem,
acute gastric distention, MI, diabetic acidosis, hypoadrenalism,
Disability - neurological exam
Determine LOC, pupils, best motor response and sensation.
Follow cerebral perfusion, neurologic signs.
hypothermia is critical
Distension may cause hypotension, dysrhythmia and aspiration.
Assess urine and evaluate renal perfusion.
Aim to maintain Hb concentration of 100 g/L
Monitor pulmonary hydrostatic pressure
- reflects transudation of fluid into the pulmonary interstitium
- helps monitor physiological end-points.
- want pulmonary capillary wedge pressure at 14-18 mmHg.
Aim for MAP up to 60 mmHg at least.
Morbidity and mortality increase with age and chronic disease
General reduction in physiological reserve:
- deficit in receptor response to catecholamines.
- less ability to increase HR and SV (less compliant ventricles).
- atherosclerosis leaves organs vulnerable.
- many have pre-existing volume depletion and hypotension is poorly
- B-blocker use masks early symptoms.
- resp effort reduced, less pulmonary compliance and diffusion
- kidney senescence prevents strong volume preservation.
* Prompt aggressive treatment and careful monitoring is required.
--> consider early invasive monitoring to avoid excessive volume
Remarkable ability to compensate blood loss:
- blood volume can increase 15-20%
- CO can increase 6x
- SV can increase 50%
- resting pulse is ~50,
* Usual response to hypovolaemia may not manifest.
--> greater blood loss required to exhibit shock.
--> maternal perfusion abN reflected in the fetus.
B-blockers and Ca++ channel blockers alter haemodynamic response
Monitor BSLs in diabetics on insulin
Chronic diuretics may explain hypokalaemia
NSAIDs may inhibit platelets.
Pacemakers - use CVP to guide fluid requirements.
Trauma victims under influence of ETOH vasodilates and easily
Do not respond normally
Often develop coagulopathy
* Rapidly rewarm
Remember that neurogenic shock compounds haemorrhagic shock and vice
- these pts often have concurrent torso trauma.
Treat initially for hypovolaemia.
--> failure to respond indicates continuing haemorrhag or
CVP monitoring is helpful.
As suits cardiac cause
A mortality benefit using thrombolytics for pts with cardiogenic
shock after MI has not been demonstrated.
Inotropes, eg dopamine & dobutamine can get CO up.
Extracardiac Obstructive Tx
Treat cause, eg exclude or treat tamponade, consider PE.
List of inotropic agents
Fill, pump, squeeze
Adrenergic vs non-adrenergic
Commonly used inotropic and vasopressor medications
Norepinephrine 1–20 μg/min
α1, α2, β1, β2
Inotrope and vasoconstrictor
α1, α2, β1, β2, dopamine Inotrope and
Inotrope and chronotrope
0.25–0.75 μg/kg/min Phosphodiesterase 3
inhibitor Inotrope and vasodilator
U/min Vasopressin V1 and V2
receptors Vasoconstrictor in
Effects of adrenergic and vasopressin receptor subtypes on
(Receptor; Location; Effect)
α1 Systemic arterioles (abdominal viscera,
coronary, skin, skeletal muscle), veins, pulmonary
α2 Presynaptic and postsynaptic sympathetic nerve
terminals, central nervous system Vasodilation
β1 Heart Inotropy, chronotropy,
β2 Systemic arterioles (abdominal viscera,
coronary, skeletal muscle), veins, pulmonary
Dopamine Systemic arterioles (abdominal viscera,
renal, coronary) Vasodilation
V1 Vascular smooth muscle
V2 Renal distal convoluted tubule and collecting
In septic shock
Norepinephrine is a common first-line agent; potent alpha-agonist
with minimal Beta effects
Dopamine is an alternative; greater inotropic but fewer
vasoconstrictive effects (greater O2 consumption can be problematic;
When there is myocardial dysfunction, dobutamine can be added
Vasopressin next if refractory to catecholamines and adequately
- at high doses, get potent peripheral and splanchnic
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