shock ,different types , mechanism and their management

1. VCP 411
submitted by : Safeer ahmad
submitted to : Dr. R B Khushwaha

2. :
Shock is a life threatening clinical
syndrome of cardiovascular
collapse characterised by:
• Inadequate perfusion of
cells & tissues.hypoperfusion
• An acute reduction of
effective circulating volume.hypotension

6. How body reacts
Poor tissue perfusion / Hypovolaemia
Loss of baroreceptor stretch (aorta & carotid arteries)
Medulla oblongata
Stimulates sympathetic nervous system
Epinephrine & Nor-Epinephrine release
↑ed HR & contractility
↑ed intravascular volume and cardiac output
(Neurohumoral response)

7. Different types
of shock

10. Shock Syndromes
• Hypovolemic Shock
–blood VOLUME problem
• Cardiogenic Shock
–blood PUMP problem
• Distributive Shock
[septic;anaphylactic;neurogenic]
–blood VESSEL problem

11. Hypovolemic Shock
• Loss of circulating volume “Empty tank ”
decrease tissue perfusion general shock response
• ETIOLOGY:
–Internal or External fluid loss
– Intracellular and extracellular compartments
• Most common causes:
Hemmorhage
Dehydration

12. Dec. Venous return to heart
Dec. Effective circulating blood volume
Dec. Supply of oxygen
Dec. Blood volume
Dec. Cardiac output

13. Inflammatory mediators
anoxia
shock

14. Cardiogenic Shock
• The impaired ability of the
heart to pump blood
• Pump failure of the right
or left ventricle
• Most common cause is LV
MI (Anterior)
• Occurs when > 40% of
ventricular mass damage
• Mortality rate of 80 % or >

15. Cardiogenic Shock : Etiologies
• Mechanical: complications
of MI:
– Papillary Muscle
Rupture!!!!
– Ventricular aneurysm
– Ventricular septal
rupture
• Other causes:
– Cardiomyopathies
– tamponade
– tension
pneumothorax
– arrhythmias
– valve disease

16. Cardiogenic Shock:
Pathophysiology
• Impaired pumping ability of LV leads to…
Decreased stroke volume leads to…..
Decreased CO leads to …..
Decreased BP leads to…..
Compensatory mechanism which may lead to …
Decreased tissue perfusion !!!!

17. Cardiogenic Shock: Pathophysiology
• Impaired pumping ability of LV leads to…
Inadequate systolic emptying leads to ...
 Left ventricular filling pressures (preload) leads
to...
 Left atrial pressures leads to ….
 Pulmonary capillary pressure leads to …
Pulmonary interstitial & intraalveolar edema !!!!

18. Anaphylactic Shock
• A type of distributive shock that results from
widespread systemic allergic reaction to an
antigen
• This hypersensitive reaction is LIFE
THREATENING

19. Pathophysiology Anaphylactic Shock
• Antigen exposure
• body stimulated to produce IgE antibodies specific
to antigen
– drugs, bites, blood, foods, vaccines
• Reexposure to antigen
– IgE binds to mast cells and basophils
• Anaphylactic response

20. Anaphylactic Response
• Vasodilatation
• Increased vascular permeability
• Bronchoconstriction
• Increased mucus production
• Increased inflammatory mediators
recruitment to sites of antigen interaction

21. Clinical Presentation
Anaphylactic Shock
• Almost immediate response to inciting
antigen
• Cutaneous manifestations
– urticaria, erythema, pruritis, angioedema
• Respiratory compromise
– wheezing, bronchorrhea, resp. distress
• Circulatory collapse
– tachycardia, vasodilation, hypotension

22. Septic shock
• Acute infection
• Poisonous substance accumulates in
blood streams.
• Decrease blood pressure.
• Impaired blood flow to cell, tissue,
organs.

23. Pathophysiology of Septic Shock
IMMUNE / INFLAMMATORY RESPONSE
Microorganisms enter body

Mediator Release

Activation of Complement, kallikrein / kinin/ coagulation
& fibrinolytic factors platelets, neutrophils & macrophages>>damage to endothelial
cells.
ORGAN DYSFUNCTION

24. NEUROGENIC SHOCK
• A type of distributive shock that results from the loss
or suppression of sympathetic tone
• Causes massive vasodilatation in the venous
vasculature,  venous return to heart,  cardiac
output.
• Most common etiology: Spinal cord injury above T6
• Neurogenic is the rarest form of shock!

25. HYPOVOLEMIC
EXTRACARDIAC
Obstruction CARDIOGENIC DISTRIBUTIVE
Fluid loss,
hemorrhage
e.g., Pericardial
tamponade
Myocardial
injury or
necrosis
Decreased
systemic
vascular
resistance
Myocardiac
dysfunction
Reduced
systolic performance
Reduced
filling
Low cardiac
output
Reduced
preload
Decreased arterial
pressure
Shock
Multiple organ
system failure
High or normal
cardiac output
Maldistribution
of blood flow in
microcirculation

29. shock
hypotensio
n
Dec.
venous
return &
dec.
.cardiac
output
Capillary
stasis
vasoconstri
ction
Tissue
ischemia
Tissue
hypoxia

30. Stages of Shock
Initial stage - tissues are under perfused, decreased CO,
increased anaerobic metabolism, lactic acid is building
Compensatory stage - Reversible. SNS activated by low
CO, attempting to compensate for the decrease tissue
perfusion.
Progressive stage - Failing compensatory mechanisms:
profound vasoconstriction from the SNS ISCHEMIA
Lactic acid production is high metabolic
acidosis
Irreversible or refractory stage - Cellular necrosis and
Multiple Organ Dysfunction Syndrome may occur
DEATH IS IMMINENT!!!!

31. Compensatory stage
Sympathetic activation of water and sodium
Stimulation RAAS system retention
↑sed CO vasoconstriction ↑sed blood
& Na retention volume
↑sed BP

32. Renin - Angiotensin Hypothalamus
Pituitary gland ACTH release
ADH release Adrenal glands
Aldosterone Cortisol EpiN / Nor-EpiN
Liver Vasoctn
& ↑HR
Kidneys (Gluconeogenesis )
(↑Na+ & H2O retenn)
↑ed intravascular volume and CO

33. As shock progresses
O2
supply ↓es & anaerobic metabolism ensues
Constn Precapillary vessels & Diln postcapillary vessels
↓ed venous return
↓ed cardiac output
pooling of blood in veins
thrombus,ischaemia,necrosis
DIC , multi organ failure

34. CLINICAL SIGNS
 Tachycardia
 Tachypnoea
 Cool clammy extremities
 Rapid capillary refilling time (< 1sec)
 Normal to increased blood pressure

35. Early Decompensatory stage
Redistribution of blood flow to heart & brain
↓se in blood flow to other organs
Anaerobic metabolism, lactic acidosis & tissue hypoxia Devp’s
Loss of cellular integrity
Accumiln of Arachidonic acid & its metabolites (LT s, PGs)
Incite the systemic inflammatory response syndrome
Organ responses

36. Intestines: Loss of integrity  Intestinal micro ulceration
 intestinal microflora enters blood stream
Pancreas: Myocardial depressant factor  depresses myocardium
 ↓CO
Pulmonary vasculature: Vasoconstriction  impairment of oxygen
transport
Kidney: Constriction of afferent glomerular arterioles  ↓s blood
flow to kidney  oliguria & tubular necrosis
Reticuloendothelial system: release of inflammatory mediators

37. RRelease of inflammatory mediators
↑TNF-ἀ ↑IL-1 Others
Syn. Of
NO
Vasodilatat-
ion
IL-6,12,8,
PAF
Generation of
Free radicals Hypotention
Free radicals,
↑C3a,C5a

38. CLINICAL SIGNS
 ↓ cardiac output
 ↓ urinary output
 Tachypnoea
 Tachycardia
 Pale mucous membrane
 Prolonged CRT
 Depressed mentation
 Normal to decreased pulse pressure
 Hypothermia

39. Congested mucous membrane Pale mucous membrane

40. Decompensatory (terminal) stage
Is the final event in all types of shock
Prolonged tissue anoxia
1) Auto regulatory escape
(Local responses will override sympathetic mediated vasoconstn)
2) Sympathetic center lost
3) Chronotropic & Ionotropic response lost
Massive vasodilatation occurs in all organs
Complete circulatory collapse

41. Decompensatory Stage
 Bradycardia
 Severe hypotension
 Pale or cyanotic mucous
membrane
 Absent or slow CRT
 Weak or absent pulses
 Decreased heart sounds
 Anuria
 Hypothermia
 Coma

42. Pathophysiology Systemic Level
• Net results of cellular shock:
systemic lactic acidosis
decreased myocardial contractility
decreased vascular tone
decrease blood pressure, preload, and
cardiac output

43. Multi-organ failure in shock
Brain : hypoxic encephalopathy
Heart : focal myocardial necrosis
Lungs : ARDS
Kidney : tubular necrosis
Adrenals : necrosis
GI : haemorrhagic gastroenteropathy
Liver : necrosis
Blood : DIC

45. Guidelines
1. Treat the cause
2. Improve cardiac function
3. Improve tissue perfusion
Guidelines
1. Treat the cause
2. Improve cardiac function
3. Improve tissue perfusion

46. 46
Increase O2
delivery
Decrease O2
demands
Increase O2 contents
Increase cardiac output
Increase blood pressure
Early intubation
Sedation
Analgesia

47. THERAPEUTICS
OBJECTIVE – To improve cardiac output &
O2 delivery to the tissues
 Positive inotropic - poor contractility with
hypotension
 O2 supplementation – either via mask, O2 cage
 Pericardiocentesis for pericardial tamponade

48. Airway and Breathing
 Patent airway is
established and
maintained at all times
 Endotracheal tube is
placed if animal is not
able to breathe on its
own
 Supplemental oxygen is
delivered at high flow
rate @5L/min

49. Water
bottle/ice
pack – in
high temp.
(septic
shock)

50. RESUSCITATION FLUIDS
 Blood
 Lactated Ringers
 Normal saline
 Colloids (whole blood, fresh frozen plasma,
gelatins, dextran, hydroxyethyl starch –
hetastarch & stroma-free Hb)
 Hypertonic saline (10% DNS) Water will enter into
active circulation. This will cause increased urine
output. (Used in cases of oedema)
 Blood substitute (artificial RBC's from bovines)

51.  More volume of colloids are likely to cause
pulmonary edema and increase the venous pressure
 Crystalloid fluid cause significant further
haemodilution – result in serious decreases in colloid
osmotic pressure
 In emergency situation (when much time is not
available for administration of full shock bolus of
crystalloids, hypertonic saline (7.5 %) can be
administered @ 5 ml / kg Animal should be covered
with blanket or sack. SVHSS (small vol of hypertonic
sol) like 7.2%NaCl @ 3-4 ml/kg can be given i/v

52. Crystalloid therapy - balanced isotonic solution @ 90 ml/ kg
in dogs and 60 ml/kg in cats ( sodium chloride, Sod.
Bicarb, Glucose, DNS, NS solns)
Hypoproteinemic - colloids such as hetastarch or dextran @
5 to 10 ml/kg - bolus in dogs and 3 to 5 ml/kg - bolus in
cats - < 20 mg/kg per day to avoid secondary
coagulopathies. They have higher mol. wt. They cannot
pass from active circulation.
(Blood, plasma – natural colloids Hetastarch,
dextran , gelatins – artificial colloids )

53. Monitoring
 Mucous membrane color
 CRT
 Pulse rate
 Pulse quality
 Heart Rate
 Respiration Rate
 Electrocardiography
 Arterial blood pressure
 Packed Cell Volume
 Urine output
 Central Venous Pressure
 Cardiac Output
 Blood gases (arterial and venous)

54. Treatment: Inotropes
54
Agent Site of Action Dose
Mcg/kg/min
Effects
Dopamine Dopaminergic
Beta
Alpha > Beta
1-3
5-10
11-20
Renal vasodilation
Inotrope/vasoconstriction
Increase perip. Vasc. resistance
Dobutamine Beta 1 & 2 1-20 Inotrope
Vasodilation
Epineprhine Beta > alpha 0.05 – 1.0 Inotrope, vasoconstriction
Tachycardia
Norepinephrine Alpha > beta 0.05 – 1.0 Profound vasoconstriction
inotrope
Milranone Phosphodiesterase
inhibitor
0.5 – 0.75 Inotrope
vasodilation

55. Digoxin can given to ↑ heart rate
 It is an inotropic glycoside
 It ↑the intracellular conc. of free Ca2+ ions in the
myocardial fiber, ↑ contractility of myocardium &
thus stimulates the failing heart
 Dose:- 5-8 mcg/kg BW bid for oral maintenance &
2.2-4.4 mcg/ kg BW bid for iv.
• Dopamine is a catecholamine & stimulates the
release of nor epinephrine & also stimulates the
dopaminergic receptors which causes ↑renal
blood flow & diuresis.
 It has +ve inotropic & chronotropic action.
 Dose is 2-10 mcg/ kg BW/ min diluted in saline.
 Dopamine given as constant infusion( ↑ blood
flow & O2 supply to tissues)

56. • Vasoconstrictors like nor-epinephrine are given
in hypotensive shock @ 0.1- 1 mcg/kg BW
• Cox 2 inhibitors like NSAIDS can also be given.
• Anti histaminics are given in anaphylactic shock.
E.g.:- chlorpheniramine maleate( H1 blocker)
@30-50 mg in cattle, 0.4-2 mg/ kg in dogs
• Oxygentherapy:- if no response with fluid therapy,
then the other causes of shock like if there is low
arterial O2 content, that means animal could be
in anemia or if there is abnormal Hb function
leading to poor oxygenation of blood. In this
oxygen therapy is given.

57. Corticosteroid therapy
• Enhance blood pressure → inc. cardiac output.
• Prevent vasoconstrictor effect → Perfusion of
vital organs like lungs and kidneys.
• Inhibit lactic acid formation → ↑es oxygenation
of tissues → prevent acidosis.
• Stabilization of cell membrane .
• Maintain microcirculation → decreasing
viscosity of WBC’s & platelets.
• Neutralizes endotoxins.
• Egs:- dexamethasone(i/v) @ 10-30 mg in cattle,
.5-2 mg in dogs; hydrocortisone(i/m) @ 1-1.5 g
in horse & cattle, 2.2 mg/kg in dog

58. Glucocorticoids?
Beneficial effect:
• Strong anti-inflammatory effect
• Prevention of cytokine
production by macrophages
• Reduce reperfusion injury
• Relax arterioles & venules and
thereby improve
microcirculation
Adverse effects:
• Hypotension in presence of
Hypovolemia
• GI Ulceration
• Contraindicated in SIRS,
Sepsis bcz of –ve effects on
cellular immune response

59. Antibiotics:
Factors …Stage of shock & underlying problem
Compensatory stage× External trauma√
Decompensatory stage√
Bacterial entry will occur from intestinal tract to blood stream during
Decompensatory stage & during reperfusion injury
In initial stages of fluid resuscitation bactericidal antibiotics are
recommended……Continuation is done by monitoring the animal &
cause of shock
Cephalosporins are the first choice…… if animal does not respond……
Aminoglycosides & Fluroquinolones

60. In summary, Treatment of Shock
• Identify the patient at high risk for shock
• Control or eliminate the cause
• Implement measures to enhance tissue
perfusion
• Correct acid base imbalance
• Treat cardiac dysrhythmias

63. CASE SHEET (MEDICINE)
REG NO. 1358 DATE:04-09-2015
SPECIES: Canine BREED: Pomeranian
AGE: 2 months SEX: Male
HISTORY : A/O animal suffered from Vomition and Diarrhoea last week,
anorectic last 2 days, severe worm load and ectoparasite infestation.
PROPHYLACTIC MEASURES :Vaccination and Deworming NOT done.
GENERAL EXAMINATION :
BEHAVIOUR: recumbent EATING/DEFECATION: anorectic
URINATION: anuria MUCOUS MEMBRANE: white

64. • CINICAL EXAMINATION:
Skin tent test : 8 seconds
Temp:96.0 F H.R: 140/min RESPIRATION RATE: 40/min
Dehydration status: >8%