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Course of Study:
(CNA772) Interpreting Patient Deterioration

Title of work:
Critical care nursing, Fourth edition. (2019)

Section:
Chapter 21. Pathophysiology and management of shock, pages 722-724 pp. 722--724

Author/editor of work:
Aitken, Leanne; Elliott, Doug; Chaboyer, Wendy; Australian College of Critical
Care Nurses

Author of section:
L Aitken

Name of Publisher:
Elsevier
 ossa

Critical Care Nursing

4e
Leanne Aitken
RN, PhD, BHSc(Nurs)Hons, GCertMgt, GDipScMed(ClinEpi),
FACCCN, FACN, FAAN, Life Member - ACCCN
Professor of Critical Care, School of Health Sciences,
City, University of London, UK
Professor of Critical Care Nursing, School of Nursing and Midwifery,
and Menzies Health Institute Queensland,
Griffith University, Qld, Australia

Andrea Marshall
RN, PhD, MN(Research}, BN, Grad Cert Ed Studies (Higher Ed),
IC Cert, FACCCN, FACN, Life Member - ACCCN
Professor of Acute and Complex Care Nursing,
School of Nursing and Midwifery and
Menzies Health Institute Queensland,
Griffith University, Qld, Australia
Intensive Care Unit, Gold Coast Hospital
and Health Service, Qld, Australia

Wendy Chaboyer
RN, PhD, MN, BSc(Nu)Hons, Crit Care Cert, FACCCN, FAAN,
Life Member - ACCCN
Professor and Deputy Head of School (Research},
School of Nursing and Midwifery and Person-Centred Health
Services Group Leader, Menzies Health Institute Queensland,
Griffith University, Qld, Australia

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722 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

critical that other signs and symptom s are identifie d early organs, hyp erglycaemia , immunomodulation and proco-
by frequent observations to detect a patient's deteriorat- agulation. This universal response to impending shock is
ing state and resp ond before irreversible shock ensues.7 particularly effective in compensating fo r loss of circulat-
No single vital sign is adequate in determining the level ing blood volume, but may be counterp roductive w hen
or extent of sh ock 5 nor is there a sp ecific laboratory test pump failure occurs or is 'uncoupled' in distributive
that diagnoses the cause of the sh ock syndrom e. shock states.
In this chapter an overview of the pathophysiology As adaptive resp onses fail, cardiac output becomes
of sh ock, the com monly described categories and asso- insufficient to provide adequate organ p erfusion despite
ciated pathologies, along w ith appropriate m onitoring increasing tissue oxygen consumption (see C hapters 9
and interventions for m anaging a patient in shock are and 10). When oxygen is 'supply dependent', oxygen
described . delivery is decreased and , to comp ensate, increased
oxygen extraction occurs to enable continued tissue
oxygen consumption . H owever, w hen oxygen delivery
Pathophysiology falls below a critical threshold, and extraction demand
Sh ock is classified by aetiology 2 : hypovolaemic, cardio- rises above the available blood oxygen levels, this com-
genic, distributive 8 and obstructive (Fig. 21. 1). 9 Each typ e p ensation m echanism fails and oxygen debt results.5
has a sp ecific mechanism of action that leads to altered H yp op erfusion m ay also exist despite a relatively
tissue perfusion and oxygen and nutrient uptake at the nom1al cardiac output, and may not be immediately clin-
cellular level (Table 21.1 ). In practice, it is common ically evident.5 This results in maldistribution of blood
fo r diffe rent shock types to be existent in the same flow to som e tissues w hile other areas receive more
presentation ; fo r example, a patient w ith septic shock blood flow than needed 6 •8 ·10 and is often referred to as
might also be hypovolaemic and/ or have myocardial distributive shock. This response is typical of the shock
dysfu nction. types that affect vasom otor tone, fo r example septic,
Shock occurs w hen there is an inability of the body neurogenic and anaphylactic sh ock. M aldistribution m ay
to m eet m etabolic dem ands of the tissues; hypoperfusion leave some organ system s ischaemic fo r long periods
(decreased blood flow to the tissues) results in cellular leading to p ersistent organ dysfunction and failure .5
dysfunction, as there is hom eostatic imbalance between There is also evidence supporting the presen ce of cyto-
nutrient supply and dem and, and adaptive responses can pathi c hyp oxia as a result of excessive p rodu ction of
no longer accom modate circulatory changes .8•10 T hese cellular proinflammatory m ediators such as nitric oxide
adaptive resp onses are m oderated via numerous 'sensors' and tumo ur necrosis fac tor-alpha. Adenosine triphos-
thro ughout the thorax and large vessels in particular, phate stores becom e depleted due to this impaired mito-
w hich detect subtle changes in pressure (barorecep- ch ondrial oxygen utilisation 11 interfering w ith electron
tors) or biochemical changes (ch em oreceptors) . These transport and m etabolism. Nitric oxide is associated with
receptors feedback to the hypothalamus, w hich regu- vascular relaxation and is a m aj or contributor to alter-
lates, through the pituitary gland and adrenal cortex, the ations in microvasculature and capillary leak in sepsis. 12
release of a number of h ormones including antidiuretic Organ systems have varying responses in shock and
hormone and adrenocorticotrophic hormone to target are not m easured directly. Often surrogate markers of
organs such as the kidney. The adrenal cortex m edi- global hypop erfusion are used to indicate the severity
ates the mineral and glucocorticoid response to counter of sh ock. Lactate and acid- base disturbances, such as
the developing effects of shock. T his concurrent direct an increase in stro ng ion gap, have been suggested as
fe edback stimulates the sympathetic nervous system to early m arkers of m itoch ondrial dysfunction and cellular
act on blood vessel ton e, particularly the arterioles, and hypop erfusion (Fig. 21. 2). 7 •9 T hese 'surrogate' biochem-
organs such as the adrenal gland and kidney to respond ical m arkers of hypop erfusion (pH, serum lactate and
via the release of endogenous catecholamines (adrenaline standard base excess) assess acidaemia and provide some
and noradrenaline), mineral and glucocorticoids (aldos- insight into the degree of sh ock. 13 Lactate, a stro ng anion
terone, cortisol) and the renin-angiotensin- aldostero ne with basal produ ction of approximately 1300 mmol/
system . Activation of the renin-angiotensin- aldostero ne day, 14 is a product of m etabolism . Increased levels are
system results in synthesis of angiotensin II , a p owerful present in tissue hyp oxia, hyp ermetabolism , decreased
vasoconstrictor that further potentiates th e reductio n in lactate clearance, inhibition of pyruvate dehydroge nase
p eripheral blood vessel capacity. and activation of inflammatory cells, all characteristics
Collectively, these responses form a sympatho- of developing sh ock (T able 21.2). Increased lactate pro-
endocrine-adrenal axis that m oderates the systemi c duction is a warning sign of impending organ failure , as
response to shock. The axis m aintains circulation to the it is indicative of anaerobic m etabolism. Blood lactate
vital organ system and combines w ith the inflamma- levels have been directly linked to deteriorating patient
tory response to limit local and systemic tissue dam age outcom es in shock. 13 · 15
and ultimately confer a survival advantage. Combined Serum concentrations greater than 5 mmol/L in
responses include profo und vasoconstriction, oligoanu- the setting of m etabolic acidosis are indicative of high
ria (fluid retention), redirection of blood flow to vital m ortality. 14
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 723

FIGURE 21.1 Types of shock. (A) Signs of tissue perfusion; (B) types of shock; (C) cardiac changes . CVP: central
venous pressure; SvO 2 mixed venous oxygen saturation.

m Arterial hypotenslon
l]J Types of shock
62%
Distributive (septic)

Absent Signs of tissue hypoperfusion

Brain IK:0!:.
Chronic
hypotension ? state
Syncope
(if transient)

Skin
16% 16%
Cardiogenic Hypovolaemic

~
ECHOCARDIOGRAPHY
In tamponade: pericardia!
effusion, small right and
Normal cardiac Small cardiac left ventricles, dilated
chambers and (usually) chambers and normal Large ventricles and inferior vena cava; in
preserved contractility or high contractility poor contractility pulmonary embolism or
pneumothorax: dilated right
Cardlogenlc shock ventricle, small left ventricle
Distributive shock Hypovolemic shock
Obstructive shock

Distributive shock Hypovolaemic shock Cardlogenic shock Obstructive shock

Source: From Vincent J-L, De Backer D. Circulatory shock. New Engl J Med 2013;369(18):1726-34. Copyright © (2013)
Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.
724 SECTION 2 PRINCIPLES AND PRACTIC E OF CR ITICAL CARE

As the shock state worsens and the body fails to space into the interstitium. 16 This response mechanism
compensate, organ systems begin to fail. This is com- improves the supply of nutrient-rich fluid to the site of
plicated by 'capillary leak' or increased m icrovascular injury; h owever, systemically, fluid shifts lead to hypo-
permeability that leads to interstitial oedema due to volaemia, impaired organ function and development of
alterations to the vascular endothelium. Many immune acute organ injury such as acute kidney injury.16 This
mediators including circulating cytokines, oxygen- free developing organ injury is the precedent to organ failure
radicals and activated neutrophils alter the structure of (see C hapter 22) .
the endothelial cells, creating space to allow larger intra- The next sections of this chapter describe the general
vascular molecules to cross into the extravascular space, assessment and management of shock, different classifi-
with proteins and water moving from the intravascular cations of shock and specific management principles to
avoid or limit tissue injury and the eventual progression
to organ failure.

TABLE 21.1 Patient assessment

Shock types
Critically ill patients often exhibit signs of tissue hypoxia
SHOCK TYPE MAIN CHARACTERISTIC as a result of cardiovascular disturbances. 17 Table 21.3
provides an overview of the physiological changes in
Hypovolaemic A reduction in circulating blood volume
shock. Therapy is targeted to maintain oxygen delivery
through haemorrhage or dehydration or
plasma fluid loss

Cardiogenic Pump failure (impaired cardiac

contractility) usually as a result of TABLE 21.2
myocardial infarction Hyperlactatemia due to tissue hypoxia
Obstructive Characterised by blockage of circulation MECHANISMS SERUM LEVELS CAUSES
to the tissues by impedance of outflow
or filling in the heart (e.g . due to cardiac Increased Lactate >5 mmol/ L Hypoxaemia
tamponade or pulmonary emboli) glycolysis and pH <7.35 Anaemia
Decreased (normal lactate Hypoperfusion
Distributive A maldistribution of circulation from clearance <2 mmol/ L) Shock
sepsis, anaphylaxis or neurogenic injury Sepsis

Adapted from Manji RA, Wood KE, Kumar A. The history Adapted from Phypers B, Pierce JT. Lactate physiology in
and evolution of circulatory shock. Grit Care Clin 2009;25:1- health and disease. Continuing Education in Anaesthesia,
29, with permission. Grit Care Pain 2006;6: 128-32, with permission.

FIGURE 21.2 Blood lactate and shock.

Arterial hypotens1on

Signs of tissue hypoperfusion ?

(oliguria, altered mentation, cutaneous vasoconstriction .)

Present Absent

Blood lactate

r
> 2 mEq/L
l
< 1.5 mEq/L
Chronic hypotension ?
Syncope (if transient)
drug effect
l
Circulatory shock

Arterial catheter
Central venous catheter

Source: Vincent J-L, Ince C, Bakker J. Clinical review: Circulatory shock - an update: a tribute to Professor Max Harry Weil. Critical
Care 2012 11 /20; 16(6).