Indequate tissue perfusion and oxygenation, leading to multiple organ failure and death if not treated.
Jump to:
Classes of shock
Haemorrhagic Shock Treatment.

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Septic shock is the biggest cause of death in intensive care settings.
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.

Cardiac Output
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 flow.
- second the 'pressure' volume; 70% of the blood volume is in the veins
--> in blood loss this second compartment is depleted, reducing preload.
Preload also affects contractility.
- venous filling lengthens myocardial fibers, increasing contractility (Starling's Law).
Resistance to the forward flow.

Vascular Factors
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 resistance.
- arteriolar tone, in turn, is reliant on extrinsic and local factors.
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
Capillary exchange is determined by Starling's Forces (refer oedema card).

Shock is best classified by the underlying cause of abnormal tissue perfusion.

Hypovolaemic Shock
Third spacing
Fluid depletion eg burns, renal losses, adrenal insufficiency
- often exacerbated by peri-operative fasting / poor fluids / steroids omitted

Cardiogenic Shock
Cardiac failure
Myocardial ischaemia
Blunt cardiac injury
 - (seen in rapid deceleration)
Air embolus
- associated with penetrating thoracic injury in trauma, sometimes blunt injury

Extracardiac Obstructive Shock
(External obstruction to cardiac output)
Tension pneumothorax
Severe pulmonary hypertension
Mass effect

Distributive Shock
Neurogenic shock.
Endocrine, eg Addisons
Toxic shock

A pt may have several forms of shock, eg septic shock, with cardiac impairment-related cardiogenic and distributive shock.

Aetiology in Trauma
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

1. Endocrine compensation
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 elevated
Other hormones with vasoactive properties are released
- histamine, bradykinin, beta-endorphines, prostanoids and other cytokines
--> profound effects on microcirculation / vascular permeability.

2. Neurogenic compensation
Diastolic BP rises
early and pulse pressure reduces (due to peripheral vasoconstriction)
- 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 blood.
--> the viscera become underperfused
--> the volume of venous blood falls and the peripheral veins collapse
--> reduced renal blood flow allows fluid conservation (by Na+ retention in particular) 

3. Peripheral compensation
Hypotension with precapillary arteriolar constriction and venous collapse
-->  autotransfusion of fluid from extra to intravascular space (Starling)

4.  Cellular Hypoxia
Reduced peripheral perfusion causes lactic acidosis
Cellular hypoxia first manifests as endoplasmic reticulum swelling.
Mitrochondrial damage follows
Lysosomes rupture
Cell swelling follows loss of membrane integrity
Intracellular Ca++ deposition occurs.
Apoptotic self-destruction and free radical damage are central.

5.  Failing homeostasis
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 cycle).
- 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 contribute.
Cerebral autoregulation compensates down to mean arterial pressures of <60 mmHg

Dysfunction occurs early.
Hypoperfusion impairs gas exchange, 'shunting' under-oxygenated blood.
--> 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 GFR.
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 death.
--> 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 microvasculature.
Clotting factor consumption and thrombocytopaenia can cause life-threatening haemorrhage.

Cardiogenic Shock
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.

Distributive Shock
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.


Blood loss
750ml may be lost from a tibia / humerus
1500ml from a femur
Liters from a pelvic # (retroperitoneal).

Profound circulatory shock is easy to recognise:
- clouded sensorium.
- prostration.
- organ shutdown
Early manifestations:
- tachycardia
- 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.


Hypovolaemic shock

Any injured pt cool and tachycardic is in shock until proven otherwise.
- elderly, athletes, children and beta-blocked may not show tachycardia
--> CO = SV x HR so only HR can improve CO in the hypovolaemic pt.

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).
Clouded sensorium

Cardiogenic shock
The picture is modified by high cardiac filling pressures
And other features of heart failure.

Obstructive shock
JVP usually elevated
And other features of underlying cause.

See septic shock card

Neurogenic shock
Classically hypotension without tachycardia or cutaneous vasoconstriction
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 volume.
Do not wait until precise category made before Tx given.

Class I
Class II
Class III
Class IV
Blood loss
(% volume)
Pulse P
N or Up
Resp R
* For a 70kg man.
* Fluids on 3:1 rule: 300ml electrolyte soln needed for every 100ml bld loss.

Class I
Minimal symptoms (if otherwise physiologically normal)
Does not require replacement
Compensations restore volume within 24 hours.

Class II
Symptoms, narrowing pulse pressure (normal BP).
Become anxious, frightened, hostile.

Class III
Devastating blood loss, classic signs of shock.
Blood pressure drops.
Transfusion almost always needed (priority is to stop haemorrhage).

Class IV
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 haemorrhagic shock.
- massive blood loss may only produce a minimal acute decrease.
- a very low haematocrit after injury suggests massive blood loss or pre-existing anaemia.

Coagulopathy may cause haemorrhage
More often coagulopathy results from ongoing low-grade haemorrhage and replacement by cold transfused blood deficient in clotting factors.


Blood gases (shows metabolic acidosis).
Measure electrolytes.


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 underlying cause.

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.

Haemorrhagic Shock
though applies to most forms of shock.


1. Excessive crystalloid prior to hemorrhage control is harmful
--> dislodges clots, dilutes coagulation factors, causes hypothermia
--> 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

Airway, breathing
O2 at 12-15 L/min
Sats monitoring (want >95%).
- be aware that poor perfusion leads to poor signal.

Stop any haemorrhage
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.

Vascular access
2 16g cannulae (short and large calibre).
- antecubitals or forearm
- else Saldinger technique for central access, saphenous cutdown or interosseous needles.
- be aware of complications of central access and follow up with a CXR.
Draw blood for type, crossmatch, FBC, U+Es, toxicology and pregnancy test
Obtain an ABG
Use fluid warmers (39o) and rapid infusion pumps as required.

Initiate fluid resuscitation
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.

ECG Monitoring
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 disturbance.

Evaluating response
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
Acid/base balance
- 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 deficit.
- 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
Transient response
Remain abN
Est. bld loss
Need 4 Fluid?
Need 4 Bld?
Need Op?
Call Surgeon?
* The haemodynamically normal pt has no signs of inadequate tissue perfusion
* 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.

Fluid 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 unresuscitated pt.
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 replacement.
Note that static measurements may be unreliable (though <5 or >20 are obviously telling you something).
- a minimal rise in an initially low CVP suggests urgent need for volume expansion (non-responder)
- 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 inadequate perfusion
- conisder inotropic support, senior help mandatory.

What type of blood?
Fully x-match bld is preferrable.
- 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 exsanguinating haemorrhage.
- Rh -ve for females of childbearing age.
- Type specific bld is preferred, unless >1 unknown casualties being treated simultaneously.

Crystalloid or Colloid?
Colloids may increase circulating volume to a greater degree than crystalloids.
--> but redistribute within hours in same manner anyway.
- carry a slight risk of anaphylaxis and coagulopathy
Important points:
1. Both types of fluid are good enough in most situations given in enough quantity.
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)
Bottom Line
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 changes.
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, neurogenic.

Disability - neurological exam
Determine LOC, pupils, best motor response and sensation.
Follow cerebral perfusion, neurologic signs.

Preventing hypothermia is critical

Gastric decompression
Distension may cause hypotension, dysrhythmia and aspiration.

Urinary catheterisation
Assess urine and evaluate renal perfusion.
Know contraindications.

Tranfusion target
Aim to maintain Hb concentration of 100 g/L
Monitor pulmonary hydrostatic pressure
- reflects transudation of fluid into the pulmonary interstitium (microvascular pressure)
- helps monitor physiological end-points.
- want pulmonary capillary wedge pressure at 14-18 mmHg.
Aim for MAP up to 60 mmHg at least.

Special Groups


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 tolerated.
- B-blocker use masks early symptoms.
- resp effort reduced, less pulmonary compliance and diffusion capacity.
- kidney senescence prevents strong volume preservation.
* Prompt aggressive treatment and careful monitoring is required.
--> consider early invasive monitoring to avoid excessive volume restoration.


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.

Physiologic hypervolaemia
--> greater blood loss required to exhibit shock.
--> maternal perfusion abN reflected in the fetus.

B-blockers and Ca++ channel blockers alter haemodynamic response significantly
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 becomes hypothermic
Do not respond normally
Often develop coagulopathy
* Rapidly rewarm

Neurogenic Shock
Remember that neurogenic shock compounds haemorrhagic shock and vice versa.
- these pts often have concurrent torso trauma.
Treat initially for hypovolaemia.
--> failure to respond indicates continuing haemorrhag or neurogenic shock.
CVP monitoring is helpful.

Cardiogenic Tx
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.
Maintain perfusion.

Extracardiac Obstructive Tx
Treat cause, eg exclude or treat tamponade, consider PE.
Maintain perfusion.

Septic Shock
See card.

List of inotropic agents
Fill, pump, squeeze
Adrenergic vs non-adrenergic

Commonly used inotropic and vasopressor medications
Medication            Dose Range                Mechanism                            Indications
Norepinephrine     120 μg/min                α1, α2, α1                            Vasoconstrictor
Epinephrine          120 μg/min                α1, α2, β1, β2                        Inotrope and vasoconstrictor
Dopamine             120 μg/kg/min            α1, α2, β1, β2, dopamine    Inotrope and vasoconstrictor
Dobutamine          220 μg/kg/min            β1, β2                                    Inotrope and vasodilator
Phenylephrine       20200 μg/min            α1                                           Vasoconstrictor
Isoproterenol        120 μg/min                β1, β2                                      Inotrope and chronotrope
Milrinone            0.250.75 μg/kg/min    Phosphodiesterase 3 inhibitor    Inotrope and vasodilator
Vasopressin        0.010.04 U/min    Vasopressin V1 and V2 receptors    Vasoconstrictor in catecholamine-resistant shock

Effects of adrenergic and vasopressin receptor subtypes on cardiovascular system
(Receptor;  Location;  Effect)
α1    Systemic arterioles (abdominal viscera, coronary, skin, skeletal muscle), veins, pulmonary arterioles    Vasoconstriction
α2    Presynaptic and postsynaptic sympathetic nerve terminals, central nervous system    Vasodilation
β1    Heart    Inotropy, chronotropy, dromotropy
β2    Systemic arterioles (abdominal viscera, coronary, skeletal muscle), veins, pulmonary arterioles    Vasodilation
Dopamine    Systemic arterioles (abdominal viscera, renal, coronary)    Vasodilation
V1    Vascular smooth muscle    Vasoconstriction
V2    Renal distal convoluted tubule and collecting duct    Antidiuresis

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; worsening outcome)
When there is myocardial dysfunction, dobutamine can be added
Vasopressin next if refractory to catecholamines and adequately fluid loaded.
- at high doses, get potent peripheral and splanchnic vasoconstriction.

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