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(Shock - ( continued

When intervention is timely and the period of shock is limited , patient may make rapid uncomplicated recovery , however the result of prolonged systemic  ischemia  and reperfusion  injury is end organ damage and  multiple organ failure. Multiple organ failure means is defined as 2 or more  failed organ systems. There is no specific treatment for multiple organ failure . Management is by supporting organ systems with ventilation ,cardiovascular support and hemofiltration /dialysis until there is recovery of organ function. Multiple organ failure currently carries a mortality rate of 60%.

Resuscitation   :  Immediate resuscitation manoeuvres for patients presenting in shock are to ensure a patent airway and adequate oxygenation and ventilation. Once ‘airway’ and ‘breathing’ are assessed and controlled, attention is directed to cardiovascular resuscitation.

Conduct of resuscitation

It should not be delayed in order to definitively diagnose the source of the shocked state; Rapid clinical examination will provide adequate clues to make an appropriate first determination, even if a source of bleeding or sepsis is not immediately identifiable. If there is initial doubt about the cause of shock it is safer to assume the cause is hypovolaemia and begin with fluid resuscitation, followed by an assessment of the response.

Fluid therapy

Fluid therapy without controlling the site of haemorrhage. Increasing blood pressure merely increases bleeding from the site, and fluid therapy cools the patient and dilutes available coagulation factors. Thus, operative should proceed in parallel with surgery. Conversely, a patient with bowel obstruction and hypovolaemic shock must be adequately resuscitated before undergoing surgery otherwise the additional surgical injury and hypovolaemia induced during the procedure will exacerbate the inflammatory activation and increase the incidence and severity of end organ insult.

Type of fluids

There is no ideal resuscitation fluid  for the management of shock and it is more important to understand how and when to administer them. In most studies of shock resuscitation there is no overt difference in response or outcome between crystalloid solutions (normal saline, Hartmann’s solution, .(Ringer’s lactate) and colloids (albumin

On balance there is little evidence to support the administration of colloids, which are more expensive and have worse side-effect profiles.

Most importantly, the oxygen-carrying capacity of crystalloids and colloids is zero. If blood is being lost, the ideal replacement fluid is blood, although crystalloid therapy may be required while awaiting blood products. Hypotonic solutions (e.g. dextrose) are poor volume expanders and should not be used in the  treatment of shock unless the deficit is free water loss (e.g. diabetes insipidus) or patients are sodium overloaded (e.g. cirrhosis

Monitoring : The minimum standard for monitoring of the patient in shock is continuous heart rate and oxygen saturation monitoring, frequent non-invasive blood pressure monitoring and hourly urine  output measurements. Most patients will need more aggressive invasive monitoring including CVP and invasive blood pressure monitoring 

Monitoring for patients in shock

Minimum *electrocardiogram  *pulse oximetry   *blood pressure   *urine output 

Additional modalities  *central venous pressure   *invasive blood pressure *cardiac output        *base deficit and serum  lactate

Cardiovascular: as a minimum ,cardiovascular monitoring should include continuous heart rate [electrocardiogram (ECG)] ,oxygen saturation and pulse waveform and non-invasive blood pressure. Patients whose state of shock is not rapidly corrected with a small amount of fluid should have CVP monitoring and continuous blood pressure monitoring through an arterial line.  

There is no ‘normal’ CVP for a shocked patient, Some patients may require a CVP of 5 cm H2O, whereas others may require a CVP of 15 cm H2O or higher..CVP measurements should be assessed dynamically as the response to a fluid challenge . A fluid bolus (250_500ml) is infused rapidly over 5-10min.The normal CVP response is a rise of 2-5  cm H2O, which gradually drifts back to the original level over 10-20 min. Patients with no change in their CVP are empty and require further fluid resuscitation. Patients with a large, sustained rise in CVP have high  preload and an element of cardiac insufficiency or volume overload.

Cardiac output : it allows an assessment of not only the cardiac output but also the systemic vascular resistance and, depending on the technique used, end-diastolic volume (preload) and blood volume. Measurement of cardiac output, systemic vascular resistance and preload can help distinguish the types of shock that are present(hypovolaemia ,distributive, cardiogenic) ,especially when they coexist.

Systemic and organ perfusion: Ultimately, the goal of treatment is to restore cellular and organ perfusion. Ideally ,therefore, monitoring of organ perfusion should guide the management of shock (table 4).

Table .4 monitoring for organ /systemic  perfusion clinical

Base deficit and lactate : The degree of lactic acidosis , as measured by the serum Lactate level and/or the base deficit, is a sensitive tool for both the diagnosis of shock and the monitoring of the response to therapy. Patients with a base deficit of over 6 mmo1 1-1 have much higher morbidity and mortality rates than those with no metabolic acidosis. These parameters are measured from analysis of arterial blood gas                                                                                                         Mixed venous oxygen saturation

The percentage saturation of oxygen returning to the heart from the body is a measure of the oxygen delivery and extraction by the tissues. Accurate measurement is via analysis of blood drawn from a long central line placed in the right atrium .Normal mixed venous oxygen saturation levels are 50-70%. Levels below 50% indicate inadequate oxygen delivery and increased oxygen extraction by the cells. This is consistent with hypovolaemic or cardiogenic shock.

High mixed venous saturation levels(>70%) are seen in sepsis and some other forms of distributive shock. In sepsis there is disordered utilization of oxygen at the cellular level and arteriovenous  shunting of blood at the micro vascular level .thus, less oxygen is presented to the cells, cells cannot utilize what little oxygen is presented and venous blood has a higher oxygen concentration than normal.

Patients who are septic should, therefore, have mixed venous oxygen saturation levels of >70%.levels lower than this indicate that the patient is not only in septic shock but also in hypovolaemic or cardiogenic shock. Hypovolaemia should be corrected with fluid therapy and low cardiac output caused by myocardial depression or failure should be treated with inotropes (dobutamine )to achieve a mixed venous saturation level of >70%(normal for the septic state).

Endpoints of resuscitation: A patient may be resuscitated to restore central perfusion to the brain ,lungs and kidneys and yet the gut and muscle beds continue to be underperfused. Thus, activation of inflammation and coagulation may be ongoing and, when these organs are finally perused , may lead to reperfusion injury and ultimately multiple organ failure. this state of normal vital signs and continued under perfusion is termed occult hypoperfusion (OH). Patients with OH for more than 12 hours have a two to three times higher mortality rate than that of patients with a limited duration of shock