SHOCK

Dr Terence See
Consultant
Emergency Department, TTSH
 Scope
• Definition
• Basic Physiology
• Clinical Features
• Classification

• Case Studies

• Inotropes and Vasopressors

What is Shock?
 Definition
• Not just low BP!

• Clinical syndrome where tissue perfusion

and oxygenation is inadequate to maintain
normal metabolic function of the cells and
organs

• Manifests as haemodynamic disturbances

and organ dysfunction
Consequences
 What determines BP?
• SV x HR = CO
SV = Stroke Volume, HR = Heart Rate,
CO = Cardiac Output

• MAP = CO x TPR
MAP = Mean Arterial Pressure
TPR = Total Peripheral Resistance
PRELOAD AFTERLOAD CONTRACTILITY

STROKE VOLUME X HEART RATE

TOTAL
CARDIAC OUTPUT X PERIPHERAL
RESISTANCE

BLOOD PRESSURE
(MAP)
 Clinical features of Shock
• Look for signs of inadequate organ
perfusion!
- Brain: giddiness, syncope, altered mental
state
- Kidneys: reduced urine output
- Peripheries: venoconstriction, cool clammy
skin, pallor, mottling, prolonged capillary
refill
- Tachypnoea
Early recognition of shock is
critical!
 How vital are the vital signs?
• Initial BP may be normal!

• Often associated with tachycardia, but

bradycardia can also occur

• Many patients in shock have normal HR

 The Blood Pressure
• Hypotension is a late sign!
- Systolic BP < 90 mmHg, or
- Reduction of > 30 mmHg in previously
hypertensive patient
 Normal BP ≠ No Shock

Normal HR may not be

normal!

SBP of 90 is a late finding

CASE SCENARIOS
 Case 1
• 65 year old Chinese Female
• Pedestrian who was knocked down by a
car, found lying by the roadside
• Initial examination: Alert, GCS 15,
peripheries clammy, no obvious external
haemorrhage
• VS: HR 120, BP 102/50, SpO2 95%, RR 26

Is she in shock?
 Case 1 (continued)
• On arrival at ED: examination of the head,
chest and abdomen normal
• Fluid resuscitated with 1.5L of saline
• Cervical and chest x-rays normal
• HR now 130, BP 85/45
• Pt appears to be more drowsy…

What would you do now?

• Open book pelvic fracture – hypovolaemic shock
 #1 Hypovolaemic Shock
• Any cause of volume loss
- Blood loss (eg trauma, BGIT)
- Plasma loss (eg burns, ascites)
- GI loss (eg diarrhoea/vomiting, IO)
- Renal loss (eg polyuria in DM, diuretics)

• Early signs: tachycardia, narrowed pulse

pressure
 Haemorrhagic Shock
• Most common cause of shock in trauma

• External Vs Internal haemorrhage

• Classification

• Management
 Classification of Haemorrhagic
Shock
I II III IV
Blood loss (ml) <750 750–1500 1500–2000 >2000
Blood loss (%) <15% 15–30% 30–40% >40%
Pulse rate
(beats/min) <100 >100 >120 >140
Blood pressure Normal Decreased Decreased Decreased
Respiratory rate
(bpm) 14–20 20–30 30–40 >35
Urine output
(ml/hour) >30 20–30 5–15 Negligible
CNS symptoms Normal Anxious Confused Lethargic
1-1.5L

2-4L
 Treatment
• Fluid resuscitation – crystalloids or blood
• Find the source and control ongoing loss
• Use of inotropes?
 Haemorrhage Control
• External Haemorrhage:
- Direct pressure
- Splinting
- ?Tourniquet

• Internal Haemorrhage:
- Operative control
- Angioembolisation
Back to our patient…
 Haemorrhagic Shock in Pelvic
Fractures
• 90 percent of haemorrhage sources are
venous in origin – arrest by immobilisation
and alignment of the fracture sites
• Aggressive and early fluid resuscitation,
including blood
• Angioembolisation
• External fixation
• Laparotomy
 BP 70/40
• 70 year old Male with
low back pain

• 30 year old Female

with lower abdominal
pain
 Case 2
• 45 year old Indian Male
• Chest pain, SOB, diaphoresis for the past
2 hours
• History of DM
• VS: HR 45, BP 88/50, SpO2 94%, RR 22

What would be the first test you

would do?
• Cardiogenic shock secondary to inferior AMI with
complete heart block
 #2 Cardiogenic Shock
• Primary cause is pump failure – most common
cause is AMI

• Other causes include malignant arrhythmias,

sudden valvular rupture etc.

• Results in decreased cardiac output

• Cool clammy peripheries, poor capillary refill,

low urine output, tachycardia
• Stroke Volume x Heart Rate = CO
 Cardiogenic Shock
• Main aims of management
- Improving myocardial contractibility and
pump function
 fluids, inotropic support
 pacing in CHB
In AMI: restore perfusion ASAP to salvage as much
myocardium as possible!
 Thrombolysis
 Percutaneous Intervention (PCI)
 Case 3
• 67 year old Malay Male
• Fishmonger
• Right forearm pricked by fish fin few days
ago
• Now came to ED for fever, right forearm
pain and swelling
• VS: T 38, HR 108, BP 86/58, SpO2 97%,
RR 22
• Septic shock, likely
necrotising fasciitis

Subcutaneous
air tracking
down to
periosteum
 #3 Distributive Shock
• Vasomotor dysfunction

• Characterised by decreased vascular

resistance or increased venous capacity

• Clinical features: high cardiac output,

warm peripheries with good capillary refill,
hypotension with wide pulse pressure
 Distributive Shock
• Septic shock
 Septic Shock
• Inflammatory response to infecting
organism
- Reduced vascular resistance
- Relative hypovolaemia
- (Myocardial depression)
 Clinical Features
• Fever/chills, lethargy, anxiety,
delirium/confusion/AMS
• Early stages: cardiac output well
maintained  warm skin and peripheries
• Later stages with progression of sepsis:
poor peripheral perfusion (may be
indistinguishable from other types of
shock)
 Clinical Features
• May have atypical presentation in elderly,
very young and immunocompromised
- May not have fever
- May not have localising signs of infection

• Common sources of infection: lung,

urinary tract, abdomen, skin, lines etc.
 Treatment
• Fluid resuscitation
• Inotropic support
• Antibiotic therapy
• Source control
 Case 4
• 40 year old Chinese Male

• Referred by GP for eye/lip swelling, breathlessness and

hoarseness of voice after taking diclofenac

• VS: HR 93, BP 82/46, Sp02 100% on 2L INO2

DIAGNOSIS?
 Distributive Shock
• Septic shock
• Anaphylactic shock
 Anaphylactic Shock
• Life-threatening emergency!
• Distributive shock due to massive
histamine release
• Severe allergic reaction; rapid in onset
• Common precipitating factors: drugs,
insect stings, food allergies
Features of Anaphylactic Shock
• Urticaria
• Brochospasm
• Decreased vascular
tone and capillary
leakage  hypotension
• Angioedema of tongue,
soft palate and larynx
can quickly progress to
upper airway
obstruction with stridor
 Anaphylactic Shock
• Treatment:
- Stop/remove offending agent
- Airway management
- IM Adrenaline 0.3mls
- IV fluids
- Anti-histamines
- Nebulisers
- Steroids
 Case 5
• 20 year old Malay Male
• Motorcyclist involved in RTA, flung off bike
• Found lying by the roadside, alert but
complains that he cannot move his arms
and legs
• VS: BP 80/50, HR 60, RR 20

Management at scene?
Immobilise first, ask
questions later!
Case 5 (continued)
• ABCs
• Cervical
immobilisation
• Spinal board
• Start fluid
resuscitation
 Distributive Shock
• Septic shock
• Anaphylactic shock
• Neurogenic shock
Suspect spinal injury when…
• Any major trauma
• Unconscious
• Mechanism of injury
• Significant head injury
• Any neck pain or neurological symptoms
• Pre-existing spinal disease
 Clinical Features of Spinal
Injury
• Neurogenic shock: hypotension,
bradycardia and peripheral vasodilation

• Spinal shock: flaccid & hyporeflexia

• Can feel above but not below clavicle
• Paradoxical breathing
• Priapism
• Lax anal tone
 Neurogenic Shock
• Distributive shock
• Usually in injuries above T6
• Interruption of sympathetic nervous
system in the spinal cord  loss of
sympathetic vascular tone
• Vasodilation, increased venous pooling
• Hypotension and Bradycardia
Management of Neurogenic
Shock
• Exclude other causes of hypotension
first! (blood loss, tension PTX)
• Maintainance fluids (CVP monitoring
useful)
• Atropine
• KIV inotropic support
 Case 6

• Young man with SLE

• Complains of giddiness, vomiting and feeling unwell
• Hasn’t been taking his usual SLE medication recently
• VS: T 37, BP 76/50, HR 98, RR 20
 “Endocrine” Shock
• Distributive shock
• Addisonian crisis / acute adrenal cortical
insufficiency
• Most common cause: sudden withdrawal
of chronic steroid therapy
• Other precipitating factors: trauma,
infection, stress
 HPA Axis

Function of adrenal gland: excretes corticosteroids in response to stress!

 Management
• Fluid resuscitation
• Correct hypoglycaemia
• Steroids: IV hydrocortisone 100mg 6H
• Treat precipitating factors
 #3 Distributive Shock
• Septic shock
• Anaphylactic shock
• Neurogenic shock
• Addisonian crisis
 Case 7
• 22 year old Indian
Male
• Stabbed in the chest
• Screaming in pain
• VS: HR 130, BP
71/52, RR 24

Should the knife be removed?

Why is the patient in shock?

Fluid in pericardial sac

 #4 Obstructive Shock
• Any physical obstruction to great vessels
or heart
• Causes:
- Cardiac tamponade (blunt/penetrating
cardiac trauma, aortic dissection)
- Tension pneumothorax
- Pulmonary embolism
Management?
Diagnosis?
 SHOCK - Classification
• Hypovolaemic

• Cardiogenic

• Distributive (neurogenic, septic,

anaphylactic, endocrine causes)

• Obstructive
 SHOCK – General Approach
1. Treat the underlying cause

2. Manage the deranged haemodynamics

3. Supportive care
 SHOCK – General Approach
• Airway and Breathing
• Maximise O2 delivery
• Secure large bore IV access
• Fluid resuscitation: crystalloids, colloids,
blood
• Determine and treat the underlying cause
• ECG, CXR
• IDC
 Vasoactive Agents
• Inotropes (eg dopamine) or vasopressors
(eg noradrenaline) may be useful in
managing shock
• Only after adequate volume resuscitation!
• Not for haemorrhagic shock
• Targets certain receptors (alpha and beta)
 Vasoactive Agents
Drug Usual Dose Pharmacological
Range Effects
Adrenaline 0.01- Lower doses: mainly beta
Noradrenaline 0.2mcg/kg/min Higher doses: mainly alpha

Dopamine 2-10mcg/kg/min Mainly beta

10-20mcg/kg/min Beta + alpha
Dobutamine 1-20mcg/kg/min Beta1 and beta2

Alpha: peripheral vasoconstriction, increase in SVR

Beta1: inotropy and chronotropy, increase in cardiac contractility and
heart rate
Beta2: smooth muscle relaxation, peripheral vasodilation,
bronchodilation
 SUMMARY
• Shock is a clinical syndrome – not just low
BP alone
• Normal VS ≠ No shock
• Early recognition of shock is crucial
• Multiple causes – but aetiology can often
be determined by history and physical
examination
• Can often be multi-factorial
• Exclude hypovolaemia in all cases
Thank you