Management of shock

Dr Chirengendure
Consultant surgeon
• Sepsis- the body’s response to infection injures its own
tissues.
• Septic shock; sepsis causing inadequate oxygen delivery to
tissues.
Treatment of sepsis/ septic shock
• Initial resuscitation aim for:
- CVP 8-12 mmHg
- MAP ≥ 65 mm Hg
- UO ≥ 0.5 ml/kg/hr
- Correction of metabolic acidosis ( by improved perfusion)
• Culture all “precious body fluids” BEFORE antibiotics
- blood
- pus
- sputum
- urine
- CSF (if indicated)
Treatment summary
a) Source control
b) Antibiotics
c) Fluid resuscitation
- 30 cc/kg fluid challenge
d)Vasopressors if no response
e)Consider adrenal insufficiency (rarely) if no response
• Initial fluid challenge in patients with sepsis- induced tissue
hypoperfusion with suspicion of hypovolemia to achieve a
minimum of 30ml/kg of crystalloids.

• This can be repeated 2 to 3X

• In a patient unresponsive to fluid challenges
• Vasopressor therapy initially to target a MAP of 65 mmHg.
- Norepinephrine (1-4ⴞg/min) is the first choice
- Add epinephrine (1-4ⴞg/min) if no response
- Add vasopressin 0.03units/minute
- Dopamine (1-5 ⴞg/min) is a last choice vasopressor.
• Dobutamine should be used in patients with myocardial
dysfunction as evidenced by elevated cardiac filling pressures
and low CO.

• In general, the rate of fluid administration should be

reduced if cardiac filling pressures increase without
concurrent hemodynamic improvement
steroids?
• Generally NO !
• Consider Adrenal insufficiency in septic shock
• Refractory to standard therapy.
• If you decide to use steroids
- Hdrocortisone 200mg/day in divided doses.

Consideration can be made to discontinue corticosteroid therapy

in patients with a random cortisol level of greater than 25 mcg/dL
Hypovolemic shock
• An abnormality of the circulatory system that results in inadequate
organ perfusion and tissue oxygenation.
Identify the cause
• In trauma most patients have hypovolemic shock, but may suffer from
other forms of shock.
• Tension pneumothorax can reduce venous return and produce
obstructive shock.
• Cardiac tamponade can cause obstructive shock as blood in the
pericardial sac inhibits cardiac contractility and reduce CO. Triad of
cardiac tamponade- muffled sounds, hypotension& distended neck
veins.
We consider these DDx in patients with injuries above the diaghram
Basic cardiac physiology
Cardiac output = the volume of blood pumped by the heart
per minute
= heart rate (beats/min) X stroke
volume(ml/beat)
= HR X SV
Stroke volume = the amount of blood pumped with each
contraction.
- it is classically determined by preload,
myocardial contractility and afterload.
Blood loss pathophysiology
• Early response – compensation
a) Vasoconstriction of the skin, muscles and visceral circulation
to preserve blood flow to kidneys , heart and brain.
b) Increase in HR to preserve the cardiac output – tachycardia
is earliest measurable circulatory sign of shock.
c) Release of catecholamines → increase peripheral vascular
resistance. This will in turn increase diastolic blood pressure
and reduces pulse pressure (systolic – diastolic pressure)
Other hormones released in shock
• These hormone have vasoactive properties.
i) Histamine
ii) Bradykinin
iii) B- endorphins
iv) Prostanoids and cytokines
These substances have profound effects on microcirculation
and vascular permeability.
Venous return in early shock
• Is preserved to some degree by compensatory mechanism of
contraction of volume of blood in the venous system.
• This compensatory mechanism is limited.

Cellular level
• Inadequately perfused and oxygenated cells are deprived of essential
substrates for normal aerobic metabolism and energy production.

• Initial compensation →shift to anaerobic metabolic metabolism

→lactatic acid →metabolic acidosis.
If shock is prolonged
• ATP is inadequate

• Cell membrane loses ability to maintain its integrity and

normal electrical - chemical gradient
Proinflammatory mediators
• Inducible nitric oxide synthase (iNOS)
• Tumor necrosis factor (NTF)
• Other cytokines are released.
→ these set a stage of end organ damage and MODS
Pt treatment is directed towards
a) Reversing the shock state
b) Providing adequate o₂
c) Ventilation
d) Appropriate fluid resuscitation
e) Control hemorrhage.
vasopressors
• Are contraindicated for the treatment of hemorrhagic shock because
they worsen tissue perfusion.
CLASSIFICATION OF HYPOVOLEMIC
SHOCK
Estimated blood loss Based on initial
presentation
Class 1 Class 2 Class 3 Class 4

Blood loss(ml) Up to 750 750-1500 1500- 2000 >2000

Blood loss (% volume) Up to 15% 15 – 30 % 30 -40 %  40%

Pulse rate < 100 100- 120 120- 140 > 140

Systolic BP normal normal decreased decreased

Pulse pressure Normal or ↑ ↓ ↓ ↓

Respiratory rate 14- 20 20- 30 30 -40 >40

Urine output (ml/hr)  30 20-30 5 -15 negligible

Mental status Slightly anxious Mildly anxious Confused lethagic

Initial fluid replacement Crystalloid Crystalloid Crystalloid and Crystalloid and

blood blood
HOW DO YOU MANAGE SHOCK
1)
(a) PRIMARY SURVEY
Recognise the presence of shock and stop overt bleeding.

(b)
• AttendCommence
to ABCDEfluid replacement (via 2 by 14G canulae Iv lines).

(c) Assess response to treatment.

(d) Decide upon action.

What do you do!
- Give o2
- Set up two IV lines or check if there is
a good IV access.
-Take blood for labs: FBC, X match,
U/E + creat, ABGs.
-Let the fluid run. Give Normal saline,
Ringers solution, Plasma Supp and
blood if indicated.
Review your ABCDE and recognize what
has caused the shock.
-Insert NG tube and
- urethral catheter.
but remember the
contraindications.
Get the Surgeon early!!!
Neurogenic shock
• a condition characterized by hypotension and bradycardia that results from
interruption of the sympathetic nervous system pathways within the spinal
cord.
• Common causes include :
- sensory stimulation, such as severe pain,
- exposure to unpleasant events or sights,
- high spinal anesthesia,
- and traumatic spinal cord injury.
- Clinical characteristics include a BP that is often low, as in other forms of
shock. However, the pulse rate is usually slower than normal, and the skin is
flushed, warm, and dry
Why low pulse and no cutaneous
vasoconstrition ?
• Ans
• Loss of the sympathetic tone on blood vessels due to sympathetic
denervation.
• CO is reduced secondary to decreased blood return to the heart because of
the increased capacitance of the arterioles and venules.

• Since the heart receives sympathetic input, there is a difference between

injuries above and below T4.

• The former a)depresses the cardiac function and decreases venous return.

b) The bradycardia is caused by sympathectomy of the spinal

injury above the level of T4 with no capacity for compensatory
tachycardia
• Treatment of neurogenic shock secondary to spinal cord injury is
usually more complicated, not only because of more prolonged
hypotension but also because of the presence of coincident
hypovolemic shock resulting from associated injuries.

• Such patients often require ventilatory support as a result of

decreased spontaneous respiration and loss of the accessory muscles
for breathing.

• Aggressive fluid therapy should be instituted early under continuous

cardiovascular monitoring.

• Persistent hypotension necessitates recognition of possible

hemorrhagic shock, and a vasopressor such as ephedrine or
phenylephrine may be needed.
If the injury is below T4
• a pure α-agonist may aggravate the reflex bradycardia.

• Thus, a drug with mixed chronotropic and inotropic effects

(e.g., norepinephrine or dopamine) is preferred.

• A nasogastric tube should be inserted because gastric atony,

dilation, and hypersecretion develop in these patients
Cardiogenic shock
• Most commonly occurs as a result of acute left ventricular infarction.
• However, it may also be due :
a) right ventricular infarction,
b) ruptured papillary muscle,
c) ruptured ventricular wall,
d) acute aortic valvular insufficiency,
e) mitral regurgitation, and a ventricular septal defect.
• However, before assuming that the hypotension is caused by a cardiogenic
mechanism, one must be sure that there is adequate blood volume.
• Therefore, a patient who is hypotensive with low right and left atrial
pressure should undergo fluid administration as the initial management.

• If cardiac performance improves with fluid administration alone,

cardiogenic shock is probably not present.

• If adequate filling pressures are attained and the hypotension persists

in the absence of mechanical defects, arrhythmia, and sepsis, a primary
pump problem probably exists and should be managed with inotropic
agents
One form of cardiogenic shock
• cardiac tamponade,
- which is seen in traumatized patients,
- postoperative cardiac patients,
- and those suffering from uremia and certain malignancies.
- Pericardial tamponade has a trend toward equalization of pressures in
the right and left sides of the heart