Acute circulatory failure with inadequate or
inappropriately distributed tissue perfusion
resulting in generalized cellular hypoxia and/or
an inability of the cells to utilize the oxygen.
DUE TO DIMISHED
DIMISHED THE ABILITY
WHICH DECREASE THE
IN THE OUTFLOW
The end result of any type of shock would be-
• INADEQUATE O2
• INADEQUATE NUTRIENTS
• INADEQUATE REMOVAL OF WASTE PRODUCTS
STAGES OF SHOCK
I. NON PROGRESSIVE
Reversible stage where the compensatory mechanism get activated.
Person will fully recover without any external help.
II. PROGRESSIVE STAGE
Failing of compensatory mechanisms. Intervention is necessary to prevent
shock from further progression or progressing to irreversible stage.
III. IRREVERSIBLE OR REFRACTORY STAGE
DEATH IS IMMINENT!!!!
Osmoreceptors in hypothalamus stimulated
ADH (vasopressin) released by posterior pituitary
Constrict peripheral vessels and increase water
Anterior pituitary release ACTH
Stimulate the adrenal cortex to release
Blood sugar levels increases to meet increase
• Other mechanism that return the blood
volume back towards normal
Absorption of large quantities of fluid
from the intestinal tract
Absorption of fluid into blood capillaries
from interstitial space of the body
Increase thirst and appetite for salt.
PATHOPHYSIOLOGY OF SHOCK-PROGRESSIVE STAGE
Decrease cardiac output
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
• If low perfusion persists then shock will progress to
irreversible state where death is imminent.
• Even in irreversible shock, therapy can, on rare
occasions bring the arterial pressure and cardiac
output to near normal but circulatory system
nevertheless continues to deteriorate followed by
death within mins or hours
PATHOPHYSIOLOGY OF SHOCK-IRREVESIBLE STAGE
Clinical features of shock
• mental status-
• Decreased urine output
Feature specific for each type of shock?
• Loss of circulating volume “EMPTY TANK”
‒ Loss of blood- trauma (blunt and penetrating)
BLOOD YOU SEE
BLOOD YOU DON’T SEE
‒ Loss of plasma- severe burns
‒ Loss of body sodium and consequent intravascular water
from diarrhea and vomiting
1. Hx of trauma, bleeding, burns, diarrhea and vomiting?
2. inadequate tissue perfusion
a) Skin- cold, pale, slate-grey, slow capillary filling time,
b) Kidney- oliguria, anuria
c) Brain-drowiness, confusion, irritability
2. Increased sympathetic tone-
a) Tachycardia, narrowed pulse pressure, weak or thready
c) Blood pressure initially may be maintained later causes
3. Metabolic acidosis- compensatory tachypnoea
S/S vary depending on severity of fluid loss:
• 15%[750ml]- compensatory mechanism maintains CO
• 15-30% [750-1500ml- Hypoxemia, hypotension, generalized
vasoconstriction and reduction in urine output to 20-30
• 30-40% [1500-2000ml] -Impaired compensation & profound
shock along with severe acidosis
hypotension, tachycardia over 120, tachypnoea, urine output
under 20 ml/hour and the patient is confused.
• 40-50% - refractory stage:
marked hypotension, tachycardia and tachypnoea. No urine
output and the patient is comatose
loss of volume= death
• Put the patient on the bed.
• Have the person lie flat with the feet lifted about 12
inches to increase circulation. However, if the
person has a head, neck, back, or leg injury
• Nil by mouth
• Aim of Mx
Restoring circulatory volume
Correct the cause
• Early recognition- don’t rely on BP (decreases only
when 30% of fluid is lost )
• Connect to a pulse oximeter – PR, RR, BP
• Give high flow oxygen
• Put two wide bore cannulas.
Blood for grouping, Rh and cross match blood
depending on loss.
Take blood for FBC, urea and electrolytes
• ABG- acidosis
• Catheterize and UOP > 30ml/hr
• Trauma- no signs of external bleeding, look for
CT SCAN- Head injuries
USS- abdomen (blunt force trauma to abdomen)
• Transfuse blood if hemorrhage
• Electrolyte imbalance- correct it
• Burns- parkland formula
V (volume in ml) = 4 x body mass in kg (%surface area x 100)
Surface area by wallace rule of nine
• fluid replacement within 24 hours. The first half of this
amount is delivered within 8 hours from the burn incident,
and the remaining fluid is delivered in the next 16 hours.
• Resuscitate using crystalloids such as Normal saline,
• Insert a CVP line.
• If in pain iv anaglegics
• Control bleeding – surgery may be needed
• the impaired ability of the heart to pump
Aortic stenosis Papillary muscle
Aortic and mitral
Impaired pumping ability of left ventricle leads to
↑Left ventricular filling
↑Left atrial pressure
↑Pulmonary artery and
Symptoms may vary according to the cause.
• Signs of myocardial failure
a) Elevated JVP
b) gallop rhythm
c) basal coarse crackles
d) reduced pulse volume with tachycardia
e) low BP
• Obstructive – cardiac tamponade
a) Pulsus paradoxus
b) Muffled heart sound
• Symptoms and Signs of pulmonary emboli
a) Sudden onset dyspnoea
b) Tachypnoeic, tachycardia with hypotension
c) Localized Plural rub
d) Massive emboli- severe central chest pain
• Other signs
cold clammy peripheries with pallor and peripheral and central cyanosis
• Put the patient on to the bed.
• Best if the patient was in a coronary care unit.
• Give high flow oxygen via a face mask or if patient is
unconscious endotracheal tube.
• Connect the patient to a pulse oximeter and look for o2
saturation, BP, PR, RR
• Put two wide bore cannulas take blood for cardiac troponin,
FBC, blood gluocose, CRP, ESR, Urea and electrolytes, LFT.
• Meanwhile do a ECG and look for evidence of MI, arrythmias.
• Chest xray- cardiomegally and pulmonary odeama
• Insert a urinary catheter to measure the UOP.
• Do a arterial blood gas analysis to identify metabolic
• Ideally following parameter should be measure
a) Central venous pressure via a CVP Line
b) Mean arterial pressure via an arterial
c) Pulmonary capillary wedge pressure
through a pulmonary artery catheter
a) central venous pressure via a CVP line
adequacy of patients circulating volume and
contractile state of the myocardium.
in cardiac failure venous pressure is usually high;
patient will not improve in response to volume
replacement which will cause further dramatic rise in
b) mean arterial pressure through an arterial
permits the rapid recognition of BP changes
Arterial cannulation also allows repeated arterial blood
gas samples to be drawn without injury to the patient.
Arterial lines can be placed in multiple arteries, including
the radial, ulnar, brachial, axillary, posterior tibial,
femoral, and dorsalis pedis arteries.
But the commonest site is radial artery and second
commonest is femoral artery
c)pulmonary capillary wedge pressure through a
pulmonary artery catheter
pressure measured by wedging a pulmonary catheter with an inflated
balloon into a small pulmonary arterial branch
Indirect measure of left atrial pressure
Gold standard in determining cause of acute pulmonary odeama.
diagnose severity of left ventricular failure and mitral stenosis
pulmonary edema with normal PWP suggested a diagnosis of acute
respiratory distress syndrome (ARDS) or non cardiogenic pulmonary
• Start an infusion of inotropic agents
Dobutamine infusion- if the patient is peripherally
vasoconstricted this is the drug of choice.
Start with 2.5 microgramas/kg/min
Maintain at 2.5-10 micrograms/kg/min
enable the SBP to be kept at 90mmhg.
• Dopamine infusion- if the patient is not
Start at 2.5 micrograms/kg/min
Main at 2.5-10 micrograms/kg/min
• If the PCWP is <15mmhg or if not measurable in
the background of hypovolemia and clear lung
field in CXR- give colloids/ plasma expanders
100ml every 15 mins untill PCWP is 15-20mmhg
• Excess fluid can be detrimental in cardiogenic
• Determine the cause of cardiogenic shock
Eg- MI, cardiac arrythmias, acute valvular dysfunction,
aortic aneurysms, cardiac tamponade
• Then treat according
MI- thrombolytics or Percutaneous intervention
Acute valvular dysfunction- surgery
• Correct any metabolic and electrolyte imbalances
• SEEK SPECIALIST ADVICE EARLY.
• Systemic inflammatory response (SIRS) to infection
manifested by two or more of following.
• Temp > 38 or < 36 centigrade
• HR > 90
• RR > 20 or PaCO2 < 32
• WBC > 12,000/cu mm or < 4,000
• Septic shock is SIRS with confirmed infectious
process associated with hypotension and organ
• Initiated by gram negative (most commonly), gram
positive bacteria, fungi or viruses.
• Cell wall of organisms contain endotoxins or exotoxins
(antigenic protien produced by bacteria such as
staphylococcus, streptococcus and pseudomonas )
• Endotoxins causes release of inflammatory mediators
(systemic inflammatory response)
• Which causes vasodilatation and increased capillary
• Alters the peripheral circulation and massive dilation
leads to shock.
• Clinical features
a) Fever and rigors
b) Nausea, vomiting
c) Vasodilation so warm peripheries
d) Bounding pulse
e) Rapid capillary refilling
g) evidence of infection at local site- lungs, kidneys,
meningies, brain, intra-abdominal.
b) Come, stupor
c) Bleeding due to coagulopathy
d) rashes- and meningism
• Put the patient on the bed.
• Hx and examination will be suggestive of septic shock
• Clear the airway and give high flow oxygen
If hypoxia persists intubation and ventilation may be necessary
• Put two wide bore cannulas and take blood for investigations
Blood glucose, urea and electrolytes, CT/BT
• Meanwhile catheterize the patient and send urine for UFR.
Maintain UOP > 30ml/hr
• Culture samples- blood, urine, CSF(meningitis), swabs from
• Chest xray, uss abdomen, KUB
• 2D echo- if suspect endocarditis
• Maintain fluid balance with Normal saline or colloids
• Give fresh whole blood if Hb <10g/dL
• Fever- antipyretics – paracetamol 1 g 6hrly
• Hypotension managed by fluid replacement
If persistant give vasoconstrictor
Norepinephrine 1-12 micrograms/mins
Epinephrine 1-12 micrograms/mins
• Use a combination of broad spectrum antibiotic. Select
appropriately according to the source of infection
• Get advice from a microbiologist
• Identify and drain any collection of pus/ septic foci. Seek
surgical assistance in ressecting dead tissues
• Treat the complications accordingly
Acute renal failure
Acute liver failure
Acute respiratory distress syndrome
• Once culture and ABST reports available treat accordingly
• Results from widespread systemic allergic
reaction to an antigen
• LIFE THREATENING (Sometimes dead within
Expoure to an antigen
Body stimulated produe IgE antibodies specific to the antigen
Rexposure to the antigen
IgE binds to mast cells and basophils
Which release histamine or a histamine like substance
1. Increase in vascular capacity because of venous dilation causing
decrease venous return
2. Dilation of the arterioles, resulting in greatly reduced arterial
3. Greatly increased capillary permeability, with rapid loss of fluid
and protein into tissue space
• Also activated basophils and mast cells release mixture of
leukotrienes called slow reacting substance of anaphylaxis.
These causes spasms of the smooth muscles of bronchioles
• Antigens enter specific skin areas and cause localized
anaphylactoid reactions (urticaria). Histamine release
―Vasodilation hence red flares
―Increase local permeability so swelling of skin
Present with chocking, coughing, stridor, wheezing,
breathless, LOC, itchy rash.
Hx of previous allergic reaction or anaphylactic
1. Signs of profound vasodilation
a) Warm peripheries
b) Low BP
2. Pale cyanosed
3. Erythema, urticaria,pluritus odeama of the face, pharynx and
4. Bronchospasms, rhinitis
5. Nausea, vomiting, abdominal pain, diarrhea
• Put the patient on the bed
• Establish airway patency and breathing
• If necessary endotracheal intubation, if it fails emergency
• Consult an anesthetist for advice regarding ventilation
• Give high flow oxygen
• Connect to a pulse oximeter and measure the
RR and PR.
• If Hypotensive- head low position
• Immediately give 0.5mg im adrenaline 1 : 1000 to vastus
Repeat every 5 mins if shock persists
• Meanwhile put 2 large bore (14/16) cannulas
• Give iv chlorphenamine (antihistamine) 10-20mg or 25mg of
• Give 100mg iv hydrocortisone
• If hypotension persists- 1-2L of normal saline
• Broncospams- nebulize with salbutamol 5mg
• Give oral steroids and antihistamine for 24-48 hrs or longer if
• Results from loss or suppression of sympathetic tone
which causes massive vasodilatation in the venous
vasculature therefore venous return decreases and
cardiac output decreases.
Spinal cord injury above the level of T6
Deep general anesthesia (depress vasomotor centre)
Spinal anasthesia (block the sympathetic nervous
Brain damage (contusions, concussions, ischemia)
Disruption of sympathetic nervous system
Loss of sympathetic tone
Venous and arterial vasodilatation
Decreased venous return
Decreased stroke volume
Decreased cardiac output
Decreased cellular oxygen supply
Impaired tissue perfusion
Impaired cellular metabolism
Present with paralysis below the level of lesion
On patient assessment
• Warm, dry skin
Goal of therapy is to treat or remove the cause and
prevent cardiovascular instability and promote
optimal tissue perfusion
• Put the patient on the bed
• Give high flow oxygen
• Examine the patient and find the level of lesion
• Connect to a pulse oximeter and measure RR, PR,
• Put two wide bore cannulas.
• If hypovolemic- fluid replacement
• Observe closely for fluid overload- pulmonary
• Hypothermia- warming the patient
• CT/MRI of the spinal cord
• Alpha agonist to augment tone if perfusion still inadequate
dopamine (> 10 mcg/kg per min)
ephedrine (12.5-25 mg IV every 3-4 hour)
• Treat bradycardia with atropine 0.5-1 mg doses to
maximum 3 mg
• patient with obvious neurological deficit can be
given I.V. steroids, such as methylprednisolone in
high dose, within 8 hours of commencement of
• Surgery is needed in case of accident/trauma/
injury/ to the patient.
1. A 58 yr patient presented with central chest pain
of tightening nature radiating to the neck and left
arm. It was associated with sweating, nausea,
ECG showed a extensive anterior STEMI.
During the streptokinase infusion patients BP
dropped to 90/60mmhg.
What are the possible causes for hypotension?
How would you treat? And why?
It could be hypotension due to streptokinase allergy so
anaphylaxis shock or due to anterior MI causing
cargdiogenic shock or reperfusion arrythmia causing
Treatment depends on type of shock
If its anaphylaxis due to streptokinase (confirm by looking
for other features like urticaria, swelling, warm
peripheries) streptokinase infusion should be stopped.
Ideally should give IM adrenaline 0.5ml 1:1000 units to
However since this patient is just after a MI, adrenaline
may cause increase contractility of the heart, increase
excitation of the heart making it more prone for
arrythmias, increase the oxygen demand and
vasoconstriction may aggravate the tissue ischemia.
Therefore to correct this patient hypotension in
anaphylaxis shock would be to give a fluid bolus.
If the patient is having a cardiogenic shock due to the MI.
The MI involves the left ventricle hence reducing the
ability to contract. So we can administer dobutamine
which has a positive inotropic effect and which
decreases the afterload therefore improving the
However if the case was an inferior STEMI it will involve
the right ventricle. So rather than giving dobutamine,
giving fluid boluses will increase the venous return to
right heart therefore venous return to left heart will
increase so LV which is functioning normally can pump
the blood to systemic circulation.