1. Shock
This session will look at shock and its on going management in The Intensive Care Unit
What is shock.

2. Shock is a state of circulatory failure characterised by tissue perfusion that is inadequate to meet the needs of the body.

3. Oxygen Delivery= Cardiac Output x Oxygen Content
Oxygen Delivery- DO2
Oxygen Delivery= Cardiac Output x Oxygen Content
Cardiac Output is a function of:
Preload
Afterload
Contractility

4. Identify and Treat The Cause!!!
Haemostasis for bleeding
Source control and antibiotics for sepsis
Steroids/antihistamines for anaphylaxis
Coronary intervention for shock resultaing from acute MI.
This is a lecture on how to resuscitate a shocked patient, not a lecture on how to identify and treat the myriad causes of shock.
However in practice, the approach described over the coming slides occurs in simultaneously with diagnostic efforts and attempts to institute treatment aimed at the specifc cause of the shock state.
Failure to adequately treat the cause of shock will lead to perpetuation of the process and will inevitably result in death.

5. Types of shock Distributive Hypovolemic Cardiogenic Cool, pale
Sepsis (commonest)
Anaphylaxis
neurogenic shock
liver failure
adrenal insufficiency
drugs and toxic exposures
Hypovolemic
Bleeding
Dehydration
Cardiogenic
Pump failure
Rhythm abnormalities
Valvular defects
Obstruction to flow
When considering supportive treatment it is often more useful to consider shock according to the underlying physiological disturbance.
Cool, pale
Warm, vasodilated

6. Clinical signs of Shock
Inadequate perfusion
General
systolic BP < 90 mm Hg (or a 30-mm Hg fall in baseline BP)
lactate > 3 mmol/L,
base excess < −4 mEq/L,
reduced capillary refill time
Brain – lethargy, somnolence
Kidneys – low urine output (oliguria/anuria)
Attempted compensation
Tachycardia
Tachypnoea
Assess haemodynamic parameters (hr, bp), but also assess for evidence of adequacy of perfusion. Lactate (produced by tissues with inadequate oxygen supply as they switch to anaerobic pathways to generate ATP).
Urine output is important as it is the only directly measurable indicator of organ function. In shock, a falling urine output indicates that oxygen supply to the kidneys is inadequate, and this can be extrapolated as a more general indicator of organ perfusion.
Not all signs have to be present. Shock can occur with a normal blood pressure and hypotension can occur without shock. Shock is a clinical diagnosis.
Not all signs have to be present. Shock can occur with a normal blood pressure and hypotension can occur without shock

7. Optimising Perfusion
Optimise oxygen delivery to the tissues with basic measures such as:
Ensure adequate oxygen saturations
Ensure adequate ventilation/breathing
Fluid resuscitation (up to 30ml/kg in sepsis)
Ensure adequate haemoglobin concentration to carry the oxygen
Basic resuscitation: A,B,C
A- ensure patent airway to allow breathing
B- ensure adequate ventilation, supplemental oxygen delivery to ensure that blood is fully saturated (plus hypoxia will kill you quicker than shock)
C-resuscitate the circulation- volume expansion/fluid resuscitation followed (when adequate circulating volume has been established), by pharmacological augmentation of cardiac output and systemic vascular resistance
In almost all circumstances, the first step in cardiovascular resuscitation is administration of intravenous fluid- at least 250ml in the first instance, given quickly (squeezed in in less than 10minutes).
Even in florid cardiogenic shock with pulmonary oedema, the patient is normally intravascularly depleted (as all of their fluid has leaked into their lungs). They will still normally respond to IV fluid, and it is unlikely that an additional 250ml of fluid will cause significant deterioration in pulmonary function.

8. Monitoring Regular and repeated assessment of perfusion
Heart rate and respiratory rate trends
Urine output
Repeated ABG and lactate
Conscious level monitoring
If shock persists despite these measures then admission to the Intensive Care Unit may be indicated.
Treatment of shock is a continuous process. Any interventions made must be assessed for efficacy
did the fluid bolus restore blood pressure/reduce heart rate?
did the lactate fall?
Even if initial measures were effective, then repeated assessment is needed to ensure that the benefit is maintained. It is rare for a cause of shock to be rapidly reversed, and a good response to initial resuscitation is rarely maintained without some degree of reversal- return to your patient and reassess them regularly!

9. Treatment of Shock on ICU
Continuous invasive monitoring:
More accurate fluid resuscitation
Quicker response to changes in patient condition
Use of vasoactive medications to help restore perfusion to vital organs
Specific organ support when organs fail due to hypoperfusion e.g. renal dialysis
Care on a ward may become ineffective- either through ongoing deterioration, limited response to therapy, or instability that requires a greater degree of monitoring than can be provided in a ward environment.
The stage at which this transition becomes necessary is not fixed, and remains a clinical decision often based on an understanding of the underlying condition (eg a patient with intrabdominal bleeding needs transfer to theatre or radiology, not ICU!). Similarly a condition that is known to rapidly reversible may not require ICU however unstable the patient is in the short term.
Once on ICU the patient can be subjected to continuous ecg and beat by beat blood pressure monitoring. Adequacy of perfusion can be assessed by repeated lactate measurements and central venous oxygenation (which gives an estimate of oxygen extraction which is in turn an indicator of the adequacy of oxygen delivery). It also becomes possible to administer vasoactive medications to pharmacologically augment cardiac output or systemic vascular resistance.

10. Invasive monitoring Central Venous Catheter
Central venous pressure (similar to assessing the JVP clinically) is often used as an indicator of fluid staus (ie- is the circulating volume adequate?)
One-off reading of limited use. Trend (particularly after fluid challenge) may be more useful.
Central line is primarily of value to permit the use of drugs that can only be given into central vein e.g. Noradrenaline
However: the common perception on the ward (and even in some critical care units) is that CVP is incredibly useful as a marker of fluid status (it isn’t).
Areterial Line
Permits beat by beat measurement of blood pressure
Permits regular and repeated blood sampling
Analysis of the waveform can give an indication of the adequacy of filling

11. Vasoactive drugs
Inotropes increase the contractility of the heart (and often its rate as well) usually by acting on Beta receptors
Vasopressors cause vasoconstriction of the peripheral vasculature by acting on alpha receptors
Some drugs act on just alpha or beta receptors, some work on both.
If fluid resuscitation has failed to restore tissue perfusion, then it may be necessary to use vasoactive drugs.
Choice of drug depends on the nature of the shock state

12. Types of shock Distributive Hypovolemic Cardiogenic Give Inotrope
When considering supportive treatment it is often more useful to consider shock according to the underlying physiological disturbance.
Give Inotrope
(Dobutamine)
Give vasopressor
(noradrenaline)
Give (more )Fluid

13. Goal Directed Therapy Normalise lactate Urine output ≥ 0.5 mL/kg/hr
Mean arterial pressure (MAP) ≥ 65 mm Hg (or higher if usually hypertensive)
Central venous oxygen saturation >70% (indicating the tissues are receiving adequate oxygen)
Central venous pressure (CVP) 8–12 mm Hg
What are we aiming for?
Normalisation of tissue perfusion- but this is difficult to measure directly
Traditional approach has been to aim for ‘normal’ –at least for that population, and possibly even for that patient (eg a chronically hypertensive patient may need a very high blood pressure to be ‘normal’ in the context of their pre-existing condition.
However- aggressive fluid resuscitation increases tissue leak (Starling forces?), which increases intracapillary distance and worsens tissue oxygenation. Similarly vasopressors may induce tissue ischaemia and inotropes stress the heart and increase myocardial oxygen consumption.
More recently, the trend has been to recognise the above complications and adopt a more permissive approach- resuscitating to the most minimal level that is compatible with physiological stability and attempting to avoid the complications of aggressive resuscitation.

14. However…
The effects of these agents in critically ill patients are complex.
Inotropes can cause arrhythmia as well as increasing the oxygen requirement of the heart leaving it at risk of ischaemia
Vasopressors can increase coronary blood flow and reduce ischemia, but can also cause vasospasm and coronary ischaemia!

15. Shock- What To Do In PracticeB
Circulation- Assess patient
Severity- HR/BP/Lactate/Urine Output
What is the cause of the shock state?
GIVE FLUID- fast, through a big drip
Reassess- has treatment been effective?
Does it need repeating? (if so- get on with it!!)
Does the patient need ‘escalating’
Seek help early

16. Summary Identify shock early
Optimise organ perfusion while TREATING THE CAUSE
Use Intensive Care when basic measures do not reverse shock
The correct use of invasive monitoring and vasoactive drugs can help reverse shock and prevent progression to multi-organ dysfunction and failure.