Recognition and diagnosis of shock

Recognition and diagnosis of shock

Shock may be profound and easily recognised or it may be - subtle and only diagnosed with directed clinical examination and cardiovascular and metabolic monitoring. Compensated shock As shock progresses, the body’s cardiovascular and endocrine compensatory responses reduce flow to non-essential organs to preserve preload and flow to the lungs and brain. In compen - sated shock, there is adequate cardiovascular compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain. Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there may be no other clinical signs of hypovolaemia. However, this cardiovascular state is only maintained by reducing perfusion to the skin, muscle and gastrointestinal tract. These organs are underperfused: their cells are respiring anaerobically and sustaining ischaemic damage. There is sys - temic metabolic acidosis and both local and systemic activation of humoral and cellular inflammation. - Although clinically occult, this state will lead to multiple organ failure and death if prolonged. Patients with occult hypoperfusion (metabolic acidosis despite normal urine output and cardiorespiratory vital signs) for more than 12 hours have a significantly higher mortality , infection rate and incidence of - multiple organ failure (see Multiple organ failure ). Decompensation Further loss of circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation. In general, loss of around 15% of the circulating blood volume is within normal compensatory mechanisms. Blood pressure is usually well maintained and only falls after 30–40% of circulating volume has been lost. Mild (compensated) shock - Initially there is tachycardia, tachypnoea, a mild reduction in urine output and the patient may exhibit mild anxiety . Blood pressure is maintained, although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock). Moderate shock As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5 /uni00A0 mL/kg/hour. There is further tachycardia, and now the blood pressure starts to fall. Patients become drowsy and mildly confused. Severe shock In severe shock, there is profound tachycardia and hypoten sion. Urine output falls to zero and patients are unconscious with laboured respiration. Clinical features The classic cardiovascular responses described ( Table 2.2 not seen in every patient. It is important to recognise the limita tions of the clinical examination and to recognise patients who are in shock despite the absence of classic signs. Capillary refill Most patients in hypovolaemic shock will have cool, pale peripheries, with prolonged capillary refill times. However, the actual capillary refill time varies so much in adults that it is not a specific marker of whether a patient is shocked, and patients with short capillary refill times may be in the early stages of shock. In distributive (septic) shock, the peripheries will be warm and capillary refill will be brisk, despite profound shock. Tachycardia Tachycardia may not always accompany shock. Patients who are on β -blockers or who have implanted pacemakers are unable to mount a tachycardia. A pulse rate of 80 in a fit young adult who normally has a pulse rate of 50 is very abnormal. Furthermore, in some young patients with penetrating trauma, where there is haemorrhage but little tissue damage, there may be a paradoxical bradycardia rather than tachycardia accom panying the shocked state. Blood pressure It is important to recognise that hypotension is one of the last signs of shock. Children and fit young adults are able to main tain blood pressure until the final stages of shock by dramatic increases in stroke volume and peripheral vasoconstriction. These patients can be in profound shock with a normal blood pressure. Elderly patients who are normally hypertensive may present with a ‘normal’ blood pressure for the general population but be hypovolaemic and hypotensive relative to their usual blood pressur e. β -blockers or other medications may prevent a tachy - cardic response. T he diagnosis of shock may be di ffi cult unless one is alert to these pitfalls.

Compensated Mild Lactic acidosis + Urine output Normal Conscious level Mild anxiety Respiratory rate Increased Pulse rate Increased Blood pressure Normal Uncompensated Moderate Severe ++ +++ Reduced Anuric Drowsy Comatose Increased Laboured Increased Increased Mild hypotension Severe hypotension

Recognition and diagnosis of shock

Shock may be profound and easily recognised or it may be - subtle and only diagnosed with directed clinical examination and cardiovascular and metabolic monitoring. Compensated shock As shock progresses, the body’s cardiovascular and endocrine compensatory responses reduce flow to non-essential organs to preserve preload and flow to the lungs and brain. In compen - sated shock, there is adequate cardiovascular compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain. Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there may be no other clinical signs of hypovolaemia. However, this cardiovascular state is only maintained by reducing perfusion to the skin, muscle and gastrointestinal tract. These organs are underperfused: their cells are respiring anaerobically and sustaining ischaemic damage. There is sys - temic metabolic acidosis and both local and systemic activation of humoral and cellular inflammation. - Although clinically occult, this state will lead to multiple organ failure and death if prolonged. Patients with occult hypoperfusion (metabolic acidosis despite normal urine output and cardiorespiratory vital signs) for more than 12 hours have a significantly higher mortality , infection rate and incidence of - multiple organ failure (see Multiple organ failure ). Decompensation Further loss of circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation. In general, loss of around 15% of the circulating blood volume is within normal compensatory mechanisms. Blood pressure is usually well maintained and only falls after 30–40% of circulating volume has been lost. Mild (compensated) shock - Initially there is tachycardia, tachypnoea, a mild reduction in urine output and the patient may exhibit mild anxiety . Blood pressure is maintained, although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock). Moderate shock As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5 /uni00A0 mL/kg/hour. There is further tachycardia, and now the blood pressure starts to fall. Patients become drowsy and mildly confused. Severe shock In severe shock, there is profound tachycardia and hypoten sion. Urine output falls to zero and patients are unconscious with laboured respiration. Clinical features The classic cardiovascular responses described ( Table 2.2 not seen in every patient. It is important to recognise the limita tions of the clinical examination and to recognise patients who are in shock despite the absence of classic signs. Capillary refill Most patients in hypovolaemic shock will have cool, pale peripheries, with prolonged capillary refill times. However, the actual capillary refill time varies so much in adults that it is not a specific marker of whether a patient is shocked, and patients with short capillary refill times may be in the early stages of shock. In distributive (septic) shock, the peripheries will be warm and capillary refill will be brisk, despite profound shock. Tachycardia Tachycardia may not always accompany shock. Patients who are on β -blockers or who have implanted pacemakers are unable to mount a tachycardia. A pulse rate of 80 in a fit young adult who normally has a pulse rate of 50 is very abnormal. Furthermore, in some young patients with penetrating trauma, where there is haemorrhage but little tissue damage, there may be a paradoxical bradycardia rather than tachycardia accom panying the shocked state. Blood pressure It is important to recognise that hypotension is one of the last signs of shock. Children and fit young adults are able to main tain blood pressure until the final stages of shock by dramatic increases in stroke volume and peripheral vasoconstriction. These patients can be in profound shock with a normal blood pressure. Elderly patients who are normally hypertensive may present with a ‘normal’ blood pressure for the general population but be hypovolaemic and hypotensive relative to their usual blood pressur e. β -blockers or other medications may prevent a tachy - cardic response. T he diagnosis of shock may be di ffi cult unless one is alert to these pitfalls.

Compensated Mild Lactic acidosis + Urine output Normal Conscious level Mild anxiety Respiratory rate Increased Pulse rate Increased Blood pressure Normal Uncompensated Moderate Severe ++ +++ Reduced Anuric Drowsy Comatose Increased Laboured Increased Increased Mild hypotension Severe hypotension

Recognition and diagnosis of shock

Shock may be profound and easily recognised or it may be - subtle and only diagnosed with directed clinical examination and cardiovascular and metabolic monitoring. Compensated shock As shock progresses, the body’s cardiovascular and endocrine compensatory responses reduce flow to non-essential organs to preserve preload and flow to the lungs and brain. In compen - sated shock, there is adequate cardiovascular compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain. Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there may be no other clinical signs of hypovolaemia. However, this cardiovascular state is only maintained by reducing perfusion to the skin, muscle and gastrointestinal tract. These organs are underperfused: their cells are respiring anaerobically and sustaining ischaemic damage. There is sys - temic metabolic acidosis and both local and systemic activation of humoral and cellular inflammation. - Although clinically occult, this state will lead to multiple organ failure and death if prolonged. Patients with occult hypoperfusion (metabolic acidosis despite normal urine output and cardiorespiratory vital signs) for more than 12 hours have a significantly higher mortality , infection rate and incidence of - multiple organ failure (see Multiple organ failure ). Decompensation Further loss of circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation. In general, loss of around 15% of the circulating blood volume is within normal compensatory mechanisms. Blood pressure is usually well maintained and only falls after 30–40% of circulating volume has been lost. Mild (compensated) shock - Initially there is tachycardia, tachypnoea, a mild reduction in urine output and the patient may exhibit mild anxiety . Blood pressure is maintained, although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock). Moderate shock As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5 /uni00A0 mL/kg/hour. There is further tachycardia, and now the blood pressure starts to fall. Patients become drowsy and mildly confused. Severe shock In severe shock, there is profound tachycardia and hypoten sion. Urine output falls to zero and patients are unconscious with laboured respiration. Clinical features The classic cardiovascular responses described ( Table 2.2 not seen in every patient. It is important to recognise the limita tions of the clinical examination and to recognise patients who are in shock despite the absence of classic signs. Capillary refill Most patients in hypovolaemic shock will have cool, pale peripheries, with prolonged capillary refill times. However, the actual capillary refill time varies so much in adults that it is not a specific marker of whether a patient is shocked, and patients with short capillary refill times may be in the early stages of shock. In distributive (septic) shock, the peripheries will be warm and capillary refill will be brisk, despite profound shock. Tachycardia Tachycardia may not always accompany shock. Patients who are on β -blockers or who have implanted pacemakers are unable to mount a tachycardia. A pulse rate of 80 in a fit young adult who normally has a pulse rate of 50 is very abnormal. Furthermore, in some young patients with penetrating trauma, where there is haemorrhage but little tissue damage, there may be a paradoxical bradycardia rather than tachycardia accom panying the shocked state. Blood pressure It is important to recognise that hypotension is one of the last signs of shock. Children and fit young adults are able to main tain blood pressure until the final stages of shock by dramatic increases in stroke volume and peripheral vasoconstriction. These patients can be in profound shock with a normal blood pressure. Elderly patients who are normally hypertensive may present with a ‘normal’ blood pressure for the general population but be hypovolaemic and hypotensive relative to their usual blood pressur e. β -blockers or other medications may prevent a tachy - cardic response. T he diagnosis of shock may be di ffi cult unless one is alert to these pitfalls.

Compensated Mild Lactic acidosis + Urine output Normal Conscious level Mild anxiety Respiratory rate Increased Pulse rate Increased Blood pressure Normal Uncompensated Moderate Severe ++ +++ Reduced Anuric Drowsy Comatose Increased Laboured Increased Increased Mild hypotension Severe hypotension