Recognising and managing shock

CHAPTER 18 Recognising and managing shock



Carol Ball





Introduction 535

The pathophysiology of shock 535
The stages of shock 536

Types of shock 538
Hypovolaemic shock 538

Cardiogenic shock 539

Obstructive shock 539

Distributive shock 539

Septic shock 539

Neurogenic shock 541

Spinal shock 541

Anaphylactic shock 541

General principles of the management and treatment of shock 541
Management and treatment of hypovolaemic shock 542

Management and treatment of cardiogenic shock 545

Management and treatment of septic shock 545

Management and treatment of anaphylactic shock 546

Monitoring the patient in shock 546
Monitoring cardiac status 546

Monitoring respiratory status 547

Monitoring oxygen saturation 547

Monitoring haemodynamic status 547

Monitoring level of consciousness 548

Monitoring renal function 548

Monitoring body temperature 548

Observing skin condition 548

Laboratory and diagnostic tests 549

Summary – key nursing issues 549

Reflection and learning – what next? 549

References 549

Further reading 550


Introduction


Despite advances in diagnosis, treatment and management, shock remains one of the leading causes of death in the acutely ill patient (Dellinger et al 2008). It is important that nurses from all areas of clinical practice have the knowledge required to identify patients at risk and ensure timely and appropriate intervention is carried out. Identification of the acutely deteriorating patient is a key function of the nurse. The timely and accurate recording of vital signs is an essential part of this identification. Allied to this is the appropriate escalation of management to the appropriate personnel (NICE 2007). The aim of this chapter is to help you understand the pathophysiology of shock and the associated care as this is the responsibility of all nurses.


In any clinical environment, awareness of the predisposing factors which may lead to shock, early detection and prompt action are vital for a good prognosis. Caring for patients who are suffering from shock requires not only an understanding of the pathophysiology of shock and the principles of its treatment and management, but also an awareness of the devastating psychological and social impact such a sudden change from health to illness can have on patients and their families.



The pathophysiology of shock


Circulatory homeostasis exists when the circulating blood volume and the vascular tone of blood vessels are in dynamic equilibrium (Marieb & Hoehn 2007, pp. 733–742). Shock is a state in which tissue perfusion is inadequate to maintain the supply of oxygen and nutrients necessary for normal cellular function and disequilibrium ensues. If there is an inadequate supply of oxygen and nutrients to two or more organs this is known as multi-organ dysfunction and indicates that the patient is at significant risk of becoming critically ill if appropriate treatment is not given immediately (Richards & Edwards 2003).


Tissue perfusion is reflected by the arterial blood pressure (Marieb & Hoehn 2007, pp. 723–733). Hypotension (systolic blood pressure below 90 mmHg or a mean arterial pressure of below 70 mmHg) is a result of either inadequate cardiac output or low systemic vascular resistance. Glomerular filtration (see Ch. 8) is dependent on an adequate blood pressure and in the presence of hypotension the urine output will drop (Marieb & Hoehn 2007, pp. 1007–1011). Inadequate perfusion to the brain may induce a change in behaviour which could be manifested through decreased arousal or agitation. Decreased arousal can be assessed using a simple mnemonic, AVPU – Alert; responds to Voice; responds to Pain; Unconscious (McNarry & Goldhill 2004). In order to maintain cardiac output, in the presence of hypotension, the heart rate will rise (Marieb & Hoehn 2007, pp. 698–705). To maintain adequate oxygenation it is likely that the respiratory rate will also increase. Thus shock is evident in the presence of:


• a systolic blood pressure below 90 mmHg (or 40 mmHg below the usual systolic pressure)

• a rising heart rate (particularly if this is over 100 beats per minute) and respiratory rate (over 25 breaths per minute)

• a lowered urine output (below 0.5 mL/kg/h or less than 30 mL/h)

• an altered level of consciousness.

Of these the most important observation is a fall in blood pressure, which will require immediate attention.


Shock may be the result of a reduced amount of blood returning to the heart (inadequate ventricular filling), an inability of the heart to contract with sufficient strength (reduced ventricular contractility) or a decrease in the resistance to blood flow caused by dilation of the blood vessels (decreased systemic vascular resistance). Shock may be classified as follows (Bridges & Dukes 2005):


• hypovolaemic – a reduction in circulating blood volume (e.g. haemorrhage, burns, diarrhoea, inadequate fluid intake, excessive urine output)

• cardiogenic – a decrease in myocardial contractility (e.g. myocardial ischaemia, myocardial infarction)

• obstructive – an obstruction to blood flow in the circulation (e.g. pulmonary embolus, cardiac tamponade)

• distributive – a decrease in systemic vascular resistance (e.g. septic, neurogenic, spinal or anaphylactic shock).


The stages of shock


Shock represents a complex set of physiological reactions which comprise activation of the sympathetic nervous and immune systems, hormonal response and metabolic derangement (Marieb & Hoehn 2007, pp. 740–742). To interpret the signs and symptoms that present and the appropriate management of shock it is necessary to understand these underlying physiological reactions. These can be divided into four stages:


1 initial stage

2 compensatory stage

3 progressive stage

4 refractory stage.

It is important to understand that the stages of shock comprise continuous and complex processes. There is usually no sudden transition from one stage to the next, although some individuals may progress rapidly through the four stages.




The initial stage


At this point there are no signs and symptoms but cellular changes begin to occur in response to a disturbance in cell perfusion and oxygenation.



The compensatory stage


In this stage physiological adaptations occur in an attempt to overcome the original problem, e.g. hypovolaemia. The compensatory stage strives to maintain cardiac output, which comprises stroke volume and heart rate (CO = SV × HR, see Ch. 2). In the absence of direct measurement of cardiac output, blood pressure and central venous pressure are used as surrogates in the assessment of cardiac output. The normal cardiac output is approximately 5 L, as is circulating volume. When circulation becomes inadequate due to a reduction in circulating volume, diminished myocardial contractility or massive vasodilatation, various mechanisms are activated in response to hypotension, hypoxaemia, acidosis or a combination of these.



Sympathetic nervous system

Hypotension leads to decreased stimulation of the aortic and carotid sinus baroreceptors (Marieb & Hoehn 2007, pp. 727–732). This reduces impulses to the vasomotor centre and thus activates vasoconstriction. Stimulation of the sympathetic nervous system occurs, resulting in activation of the stress response. Catecholamines, namely adrenaline and noradrenaline, are released from the adrenal medulla (Marieb & Hoehn 2007, pp. 631). The stimulation of alpha-adrenergic receptors by the catecholamines results in vasoconstriction of the skin, kidneys, gastrointestinal tract and other organs together with a rise in heart rate (Marieb & Hoehn 2007, pp. 543). This demonstrates an attempt to preserve the blood supply to the heart and brain. Conversely, beta-adrenergic receptors stimulate vasodilation in the lungs and skeletal muscle. Vasoconstriction may initially restore the arterial blood pressure to normal, but peripheral resistance will be raised, making the myocardium work harder to maintain cardiac output. Urine output and peristalsis will decrease, and the individual’s skin will become pale and cool. Sympathetic nervous system stimulation will also result in increased respiratory rate and depth, dilated pupils and increased sweat gland activity, causing the ‘clammy’ skin typically found in all forms of shock, other than early septic and anaphylactic shock.



Immune response

The disorder to blood flow caused by generalised vasoconstriction results in the production of proinflammatory mediators by neutrophils and macrophages (Marieb & Hoehn 2007, pp. 657–660). These include interleukins 1, 6 and 8, TNFα and prostaglandins (Greenwood & Murgo 2007). They are designed to fight foreign antigens and promote wound healing (Marieb & Hoehn 2007, pp. 790–798). At the same time anti-inflammatory mediators are produced to ameliorate the effect of these. If homeostasis is not regained then the proinflammatory mediators proliferate and damage to the endothelium occurs (Marieb & Hoehn 2007, p. 120). Neutrophils adhere to the damaged endothelium and produce more proinflammatory mediators which in turn activate the clotting cascade through the production of platelet activating factor. Small clots form which, in addition to vasoconstriction, disrupt blood flow through the organs resulting in reduced delivery of oxygen and glucose to the cells. The composition of endothelial cells is also disrupted by proinflammatory mediators and the movement of water and plasma proteins from the intravascular to the extravascular space becomes apparent in the formation of oedema.



Hormonal response

Adrenaline (epinephrine) stimulates the anterior pituitary gland to release adrenocorticotrophic hormone (ACTH), which causes the adrenal cortex to release glucocorticoids such as hydrocortisone and mineralocorticoids such as aldosterone (Marieb & Hoehn 2007, pp. 616, 626–629).



Glucocorticoids

raise blood sugar by increasing gluconeogenesis and thereby the availability of glucose for energy. In addition, the glucocorticoids mobilise amino acids from the tissues and decrease protein synthesis. They also reduce glucose uptake by the cells and mobilise fatty acids from the adipose tissue into the plasma. Cortisol shifts cell metabolism from glucose to fatty acids for energy, enhancing fatty acid oxidation, and also reduces tissue destruction by stabilising lysosomal membranes.



Aldosterone

increases reabsorption of sodium and chloride by the kidney. To maintain electrolyte balance at the renal tubular level, the excretion of potassium and hydrogen ions is increased. Thus hypokalaemia can occur. A higher concentration of sodium chloride raises the serum osmolality stimulating the hypothalamic osmoreceptors. In turn this leads to the release of antidiuretic hormone (ADH) from the posterior pituitary gland (Marieb & Hoehn 2007, pp. 627–628).



ADH

stimulates an increase in renal tubular water reabsorption, in an attempt to augment circulating volume and blood pressure whilst restoring normal serum osmolality (Marieb & Hoehn 2007, pp. 617–619). Urine output is diminished.



Renin

is secreted by the kidney in response to secretion of noradrenaline by the adrenal medulla, which results in renal artery vasoconstriction. In the circulation, renin reacts with angiotensinogen, producing angiotensin I. This is converted by an enzyme in the lungs to angiotensin II, which causes venous constriction and increases aldosterone release, thus leading to increased fluid and sodium retention, increased blood volume and therefore increased venous return, blood pressure and renal perfusion (Marieb & Hoehn 2007, p. 628).



Thyroxine

secreted by the thyroid gland sensitises the beta-receptors in the heart to noradrenaline and so increases heart rate, systolic pressure, stroke volume and cardiac output (Marieb & Hoehn 2007, p. 620).


The classic clinical picture at this stage of shock is cool, pale, clammy skin, decreased urinary output and increased heart rate. However, this is not the case in septic, anaphylactic and neurogenic shock, which present with vasodilatation and the skin appears warm and pink. This can be misleading but the disorder to blood flow through the organs, due to a relative reduction in blood volume caused by the vasodilatation, is such that a decreased urine output and tachycardia will still be apparent. The patient may be anxious, restless or confused due to the cerebral effects of hypoxia and sympathetic nervous system stimulation. Anxiety will intensify the physiological responses to stress and thus it is very important for the nurse to provide much needed reassurance to both the patient and any relatives during this major life crisis.



The progressive stage


Now the compensatory mechanisms begin to fail and produce adverse effects. This disturbance progresses to a change from aerobic to anaerobic cellular metabolism, in which production of lactic acid and pyruvic acid leads to metabolic acidosis. Although the compensatory mechanisms may appear at first to reverse the effects of shock, if the cause is not treated appropriately then the next stage of shock soon becomes evident.


If tissue perfusion is not restored and blood flow through the organs remains erratic then the supply of oxygen and glucose to the cells will be inadequate to produce sufficient adenosine triphosphate (ATP) (Marieb & Hoehn 2007, p. 57). The sodium pump will fail and the amount of intracellular calcium increase. Anaerobic metabolism by the cell, which results from an inadequate oxygen supply, will increase the production of lactic acid resulting in a metabolic acidosis (pH <7.35) (Edwards 2008).


Prolonged disruption to the supply of oxygen and glucose and the consequent impact on cell function will soon compromise the functioning of the vital organs, as follows:


• The lungs will become less compliant as fluid and plasma proteins leak from the pulmonary capillaries into the alveoli, leading to pulmonary oedema and acute lung injury. This in turn affects gaseous exchange reducing the diffusion of oxygen into the blood. Thus, hypoxaemia is evident in a reduced peripheral oxygen saturation (SpO2) and partial pressure of oxygen (PaO2). In the early stages a higher respiratory rate will demonstrate an attempt to increase oxygen supplies, and a corresponding drop in carbon dioxide levels will be apparent. However, in the later stages of shock carbon dioxide levels may increase, even though it is a more soluble gas, if the pulmonary oedema intensifies and the acute lung injury deteriorates to acute respiratory distress syndrome (ARDS, see Ch. 3). Hypercapnia is demonstrated through a rising partial pressure of carbon dioxide (PaCO2).

• Myocardial workload will be increased due to the increased heart rate caused by stimulation of the sympathetic nervous system and the effort made to eject blood from the left ventricle (stroke volume) against the high peripheral resistance caused by vasoconstriction. Even if vasodilatation is evident the heart rate will still be raised due to the relative drop in the amount of blood returning to the heart. The heart will eventually fail as coronary perfusion and oxygen supply become inadequate to meet the demands of the myocardium.

• The kidneys will be unable to filter, reabsorb and excrete fluid normally. Urine will become concentrated in appearance, osmolality will increase and output will be reduced to below 0.5 mL/kg/h. Acute tubular necrosis may occur (see Ch. 8), causing a marked rise in blood creatinine and urea.

• Alteration in cerebral function may have a number of effects, ranging from a dulling of responses to major behavioural changes.

• Ischaemic damage to the intestinal mucosa will potentially result in the release of bacteria and toxins from the gut into the circulation.

• Pancreatic cells will release the enzymes amylase and lipase into the circulation, contributing to the formation of myocardial depressant factor (MDF), which decreases myocardial contractility.


The refractory stage


In this stage pathophysiological processes are set in motion that cannot be arrested or reversed. Death is imminent. Continuing circulatory collapse, an inability to restore circulating blood volume, increasing metabolic acidosis and the formation of micro-emboli will all contribute to decreased tissue perfusion (Marieb & Hoehn 2007). Inadequate ventilation will lead to increasingly inadequate oxygenation. Renal failure will contribute to increasing metabolic abnormalities, and vital centres in the brain will eventually cease to function due to ischaemia and hypoxia. If the refractory stage is reached, shock is irreversible and death will occur.



Types of shock


The following sections describe the distinguishing features of hypovolaemic shock, cardiogenic shock, obstructive shock and the different forms of distributive shock (Skinner & Jonas 2007). It is essential that deterioration in the patient’s condition is communicated effectively and escalated to experienced staff. This is addressed in a later section of this chapter. (See Boxes 18.1, 18.2.)



Box 18.1 Reflection



Prevention is better than cure


Two days ago Mrs R underwent a hysterectomy with bilateral salpingo-oophorectomy to remove a dermoid cyst. She required blood and crystalloid replacement following surgery but is now eating and drinking. The area around her intravenous cannula is now looking red and swollen, her blood pressure is 80/50 mmHg, pulse rate 110 and temperature 39°C.



Activity:



• What might have been done to avoid this problem?

Answer: remove the intravenous cannula when no longer required.



Box 18.2 Reflection



What type of shock are you observing?


Mr W is obese and has type 2 diabetes. Recently he fell at home, following a non-ST elevation myocardial infarction, and sustained a subdural haematoma. This afternoon he has complained of an ache on the left side of his chest, affecting his arm and jaw. This was thought to be related to his recent fall. You have just taken his observations and note he is very drowsy, temperature 36.5°C, blood pressure 80/60 mmHg, heart rate 80 and the pulse feels ‘thready’, skin is cold to touch and appears cyanosed.



Activity



• What type of shock are you observing?

Answer: cardiogenic shock.



Hypovolaemic shock


This is the most common type of shock. Its primary cause is loss of fluid from the circulation, which may be described as:


• External fluid loss – due to external bleeding, vomiting, diarrhoea, overuse of diuretics or burns.

• Internal fluid loss – due to internal bleeding such as haemothorax or bleeding into tissues at fracture sites after injuries, paralytic ileus, intestinal obstruction or acute dilatation of the stomach. Although hidden, the effects of internal fluid loss can be very serious. For example, 1 litre (approximately 20% of the blood volume of an average person) or more of fluid may be sequestered (i.e. lost from the circulation) in the gastrointestinal tract during paralytic ileus and/or acute dilatation of the stomach, and the same volume or more of blood may escape into the tissues and/or thorax as a result of multiple injuries.

The physiological implications of hypovolaemia are:


image

In early hypovolaemic shock, the compensatory mechanisms described (see above) are activated when the blood pressure starts to fall. These mechanisms will compensate for up to 10% reduction of the circulating volume of a healthy person without the development of marked symptoms. However, if a greater volume of fluid is lost and is not replaced quickly, the compensatory mechanisms may fail quite suddenly, in which case the patient’s condition will deteriorate rapidly. It should be recognised that, in older people, the cardiovascular system is often less able to cope with haemodynamic changes, and the heart may be less able to pump faster and harder in order to maintain cardiac output against high peripheral resistance.




Recognising hypovolaemic shock


The following signs and symptoms of hypovolaemic shock are reliable only if they are considered in relation to one another and the patient’s previous, stable condition. Nevertheless, when several of these indicators occur together the possibility of shock should be considered as a successful outcome depends upon early intervention. It is essential that the measurement of vital signs is done manually as it is impossible to ascertain respiratory rate and the characteristics of a pulse when using electronic machines. The nurse should be alert to the following:


• rapid and deep respirations, in response to sympathetic nervous system stimulation, hypoxia and acidosis

• a rapid, weak, thready pulse, due to low blood flow despite a rapid heart rate

• systolic blood pressure below 90 mmHg

• narrowing of the pulse pressure, i.e. a reduced difference between systolic and diastolic pressures due to decreased stroke volume and increased peripheral resistance indicating vasoconstriction of the skin and viscera, reflecting decreased blood flow

• anxiety, restlessness and confusion, which may indicate decreased cerebral perfusion and oxygenation

• cool, clammy skin and cold peripheries, due to vasoconstriction and sympathetic stimulation of sweat glands

• decreased urinary output, due to renal artery vasoconstriction and endocrine compensatory mechanisms

• lowered body temperature, which may be related to altered metabolism, perfusion and oxygenation and, possibly, heat loss caused by evaporation of sweat from the skin

• thirst and a dry mouth related to fluid depletion and possibly to sympathetic nervous system stimulation

• fatigue, probably related to inadequate perfusion and oxygenation of the tissues and vital organs.

It is relatively easy to diagnose hypovolaemic shock when a patient is bleeding externally. Diagnosis is more difficult when hypovolaemia is developing as a consequence of an internal crisis. Nurses must be alert to recognise the above signs and context of the crisis and to ensure that prompt action is taken and/or help is sought.

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Oct 19, 2016 | Posted by in NURSING | Comments Off on Recognising and managing shock

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