Shock what is shock stages of shock types of shock, their presentation and management presentation is made for medical students using kumar and clark and guyton.

1. SHOCK
Dilki Punchihewa

2. 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.

3. CIRCULATORY
SHOCK
CIRCULATORY SHOCK
DUE TO DIMISHED
CARDIAC OUTPUT
CIRCULATORY SHOCK
CAUSED WITHOUT
DIMISHED CARDIAC
OUTPUT
(DISTRIBUTIVE SHOCK)
CARDIAC
ABNORMALITIES THAT
DIMISHED THE ABILITY
TO PUMP
FACTORS THAT
DECREASE THE
VENOUS RETURN
WHICH DECREASE THE
CARDIAC OUTPUT
RESTRICTED
CARDIAC FILLING
AND OBSTRUCTION
IN THE OUTFLOW
TRACT
CARDIOGENIC
SHOCK
HYPOVOLEMIC
SHOCK
OBSTRUCTIVE
SHOCK
SEPTIC SHOCK
ANAPHYLACTIC
SHOCK
NEUROGENIC
SHOCK

4. The end result of any type of shock would be-
• INADEQUATE O2
• INADEQUATE NUTRIENTS
• INADEQUATE REMOVAL OF WASTE PRODUCTS

5. 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!!!!

6. PATHOPHYSIOLOGY OF SHOCK- COMPENSATORY STAGE

7. Osmoreceptors in hypothalamus stimulated
ADH (vasopressin) released by posterior pituitary
gland
Constrict peripheral vessels and increase water
retention

8. Anterior pituitary release ACTH
(adrenocorticotropic hormone)
Stimulate the adrenal cortex to release
glucocorticoids
Blood sugar levels increases to meet increase
metabolic needs

9. • 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.

10. PATHOPHYSIOLOGY OF SHOCK-PROGRESSIVE STAGE
Decrease cardiac output
Tissue hypo-perfusion
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
mitochondria damage
Cell death

12. • 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

13. Clinical features of shock
Generalized shock
• mental status-
LOC
restless
Irritable
unresponsive
• Decreased urine output
Feature specific for each type of shock?

14. • 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
HYPOVOLEMIC SHOCK

15. Decreased intravascular volume
Decreased venous return
Decreased ventricular filling
Decreased stroke volume
Decreased cardiac output
Inadequate tissue perfusion
Compensatory
mechanism
activation

16. 1. Hx of trauma, bleeding, burns, diarrhea and vomiting?
2. inadequate tissue perfusion
a) Skin- cold, pale, slate-grey, slow capillary filling time,
clammy
b) Kidney- oliguria, anuria
c) Brain-drowiness, confusion, irritability
2. Increased sympathetic tone-
a) Tachycardia, narrowed pulse pressure, weak or thready
pulse
b) Sweating
c) Blood pressure initially may be maintained later causes
hypotension
3. Metabolic acidosis- compensatory tachypnoea

17. 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
ml/hour.
• 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

18. • 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
Tissue perfusion
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

19. • Put two wide bore cannulas.
Blood for grouping, Rh and cross match blood
depending on loss.
Take blood for FBC, urea and electrolytes
Blood sugar
• ABG- acidosis
• Catheterize and UOP > 30ml/hr
• Trauma- no signs of external bleeding, look for
internal bleeding.
CT SCAN- Head injuries
USS- abdomen (blunt force trauma to abdomen)
• Transfuse blood if hemorrhage
• Electrolyte imbalance- correct it

20. • 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.

21. • Resuscitate using crystalloids such as Normal saline,
hartmann solution.
• Insert a CVP line.
• If in pain iv anaglegics
• Control bleeding – surgery may be needed

22. • the impaired ability of the heart to pump
blood.
Causes
CARDIOGENIC SHOCK
Systolic
dysfunction
Diastolic
dysfunction
Increase after
load
Valvular
structural
abnormalities
Arrhythmias
MI Ventricular
hypertrophy
Aortic stenosis Papillary muscle
rupture
Ventricular
tachyarrhythmia
Myocardial
depressants-
antiarrythmics,
beta blockers,
calcium channel
blockers.
Restrictive
cardiomyopathy
Cardiac
tamponade
Malignant
hypertension
Aortic and mitral
regurgitation

23. Impaired pumping ability of left ventricle leads to
↓Stroke volume
↓Cardiac output
↓BP
↓Tissue perfusion
Inadequate systolic
emptying
↑Left ventricular filling
pressure (preload)
↑Left atrial pressure
↑Pulmonary artery and
capillary pressure
Pulmonary odeama

24. 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

25. • 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

27. • Insert a urinary catheter to measure the UOP.
• Do a arterial blood gas analysis to identify metabolic
acidosis

28. • Ideally following parameter should be measure
a) Central venous pressure via a CVP Line
b) Mean arterial pressure via an arterial
pressure line
c) Pulmonary capillary wedge pressure
through a pulmonary artery catheter

29. 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
CVP.

30. b) mean arterial pressure through an arterial
pressure line
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

31. 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
edema

33. • 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.

34. • Dopamine infusion- if the patient is not
peripherally vasoconstricted
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
shock!

35. • 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
Arrythmias- cardioversion
• Correct any metabolic and electrolyte imbalances
• SEEK SPECIALIST ADVICE EARLY.

36. • 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
failure.
SEPTIC SHOCK

37. • 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
permeability
• Alters the peripheral circulation and massive dilation
leads to shock.

39. • Clinical features
a) Fever and rigors
b) Nausea, vomiting
c) Vasodilation so warm peripheries
d) Bounding pulse
e) Rapid capillary refilling
f) Hypotension
g) evidence of infection at local site- lungs, kidneys,
meningies, brain, intra-abdominal.
Other signs
a) Jaundice
b) Come, stupor
c) Bleeding due to coagulopathy
d) rashes- and meningism
e) Hypoglycemia

40. • 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
FBC, CRP
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
open wounds

41. • 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
And or
Epinephrine 1-12 micrograms/mins

42. • 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
DIC
Acute respiratory distress syndrome
• Once culture and ABST reports available treat accordingly

43. ANAPHYLACTIC SHOCK
• Results from widespread systemic allergic
reaction to an antigen
• LIFE THREATENING (Sometimes dead within
minutes)

44. 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
Which causes
1. Increase in vascular capacity because of venous dilation causing
decrease venous return
2. Dilation of the arterioles, resulting in greatly reduced arterial
pressure
3. Greatly increased capillary permeability, with rapid loss of fluid
and protein into tissue space

45. • 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
locally cause
―Vasodilation hence red flares
―Increase local permeability so swelling of skin

46. Present with chocking, coughing, stridor, wheezing,
breathless, LOC, itchy rash.
Hx of previous allergic reaction or anaphylactic
shocks?
1. Signs of profound vasodilation
a) Warm peripheries
b) Low BP
c) Tachycardia
2. Pale cyanosed
3. Erythema, urticaria,pluritus odeama of the face, pharynx and
larynx.
4. Bronchospasms, rhinitis
5. Nausea, vomiting, abdominal pain, diarrhea

47. Management
• Put the patient on the bed
• Establish airway patency and breathing
• If necessary endotracheal intubation, if it fails emergency
cricothyroidotomy
• Consult an anesthetist for advice regarding ventilation
• Give high flow oxygen
•
• Connect to a pulse oximeter and measure the
BP
Oxygen saturation
RR and PR.
• If Hypotensive- head low position

48. • Immediately give 0.5mg im adrenaline 1 : 1000 to vastus
lateralis
Repeat every 5 mins if shock persists
• Meanwhile put 2 large bore (14/16) cannulas
• Give iv chlorphenamine (antihistamine) 10-20mg or 25mg of
promethazine
• 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
urticaria persists

49. Neurogenic shock
• Results from loss or suppression of sympathetic tone
which causes massive vasodilatation in the venous
vasculature therefore venous return decreases and
cardiac output decreases.
• Causes
 Spinal cord injury above the level of T6
 Deep general anesthesia (depress vasomotor centre)
 Spinal anasthesia (block the sympathetic nervous
outflow)
 Brain damage (contusions, concussions, ischemia)

50. 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

51. Present with paralysis below the level of lesion
On patient assessment
• Hypotension
• Bradycardia,
• Hypothermia
• Warm, dry skin
Goal of therapy is to treat or remove the cause and
prevent cardiovascular instability and promote
optimal tissue perfusion

52. • 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,
BP
• Put two wide bore cannulas.
• If hypovolemic- fluid replacement
• Observe closely for fluid overload- pulmonary
odeama
• Hypothermia- warming the patient
• CT/MRI of the spinal cord

53. • 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
neurogenic shock.
• Surgery is needed in case of accident/trauma/
injury/ to the patient.

55. Case scenario
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,
vomiting.
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?

56. It could be hypotension due to streptokinase allergy so
anaphylaxis shock or due to anterior MI causing
cargdiogenic shock or reperfusion arrythmia causing
cardiogenic shock
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
vastus lateralis.
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.

57. 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
cardiac output.
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.