2. Aims of the Session
• Definition
• Classification
• Factors leading to the progression of shock
and tissue hypoperfusion
• Description and discussion of the four
stages of shock
• Assessment & systematic review
• Overview and treatment of Shock
3. Definition of Shock
“Shock is a condition in which the
cardiovascular system is no longer able to
meet the body's metabolic and oxygen
needs. Note that this definition does not
include blood pressure limits. Although
many practitioners believe that shock exists
when the systolic blood pressure falls
below 80 mmHg, some patients will still be
able to maintain relatively normal
metabolic function below this level.”
Trauma Secrets 2nd ed 2003.
4. Shock
…Is potentially life threatening it can
affect many organs and must be
reversed. Nurses need to be alerted to
initial signs of shock to allow early
intervention of treatment, prevent
deterioration or death.
5. Events leading to inadequate
tissue perfusion
• Decreased cardiac output
• Decreased blood volume
• Pump failure
• An increase in peripheral vasodilatation
• Increased vascular permeability
6. Shock
Patient assessment
Instigate
Immediate appropriate
action
Accurate interpretation
of situation
7. Factors in the Progression of Shock
Hypovolaemic Shock Cardiogenic Shock
MI
Endotoxaemia Haemorrhage Myocarditis
Burns Diarrhoea Tamponade
Trauma Dehydration
Anaphylaxis
Decreased CO
Decreased Decreased
Increased Blood Venous Decreased
Vascular volume Return Tissue
permeability
Perfusion
Anoxic
Endothelial Cell
damage injury
8. Factors in the Progression of
Shock Metabolic
acidosis
Decreased CO
Heart Failure
Decreased tissue Anaerobic
perfusion Glycolysis in
Muscle
Anoxic cell
injury Renal Failure
9. Four Stages of Shock
• Initial
• Compensatory
• Progressive
• Refractory
10. Initial Phase
• Cardiac output , tissue perfusion ,
oxygen delivery and nutrients to cells
aerobic metabolism is and anaerobic
metabolism begins to take over.
11. Compensatory Stage
The body tries to overcome these
effects with physiological adaptations
Neural Hormonal Chemical
12. Neural
• As C.O. & BP fall, Baroreceptors in the
aorta & carotid arteries send a message to
the medulla, stimulating the sympathetic
nervous system, the adrenal medulla
releases catecholamines – Adrenaline &
noradrenaline.
• Increase in myocardial contractility, rate &
vasoconstriction
13. Hormonal
• The sympathetic stimulation:
• Renal & spanchnic blood flow decreased
• Juxtaglomerular cells in nephron stimulated
to release renin
• Renin-angiotensin-aldosterone system
activated.
14. Chemical
• Increased production of aldosterone by the
adrenal cortex
• Increased production of catecholamines by
the adrenal medulla
• Increased production of ADH by the
pituitary gland
• Effects of acidosis, oxygenation and carbon
dioxide.
15. Progressive Stage
Compensatory mechanisms begin to fail to perfuse
vital organs
• Reduced Cardiac Output
• Reduced coronary perfusion
• Decreased filling pressure
• Increased capillary permeability
• K+ leaks out of the cells
• Metabolic acidosis
20. Hypovolaemic Shock
• Causes
Commonly due to sudden blood loss –
Burns and Dehydration are the most common
forms of shock
• Research of therapies vast
21. Clinical Findings Associated
with Volume Loss
• < 500 mls = none
• 500 – 1000 mls = HR, BP, Urine, Resp,
CO =, SVR
• 1000 – 2000 mls = As above & worsening, O2
consumption , affected conscious level, skin
perfusion, CO , SVR
• 2000 – 3000 mls = as above & worsening anuria,
loss of consciousness, pulses, cold, pallor.
22. Management
• Replace loss
• ?Crystalloid vs Colloid vs Blood
• O2 Therapy
• Observations
• Monitor blood results
23. Cardiogenic shock
Definition
“…is the result of the loss of critical contractile
function of the heart”
(Hudak & Gallo 1997)
Causes
• MI
• Tamponade
• Cardiomyopathy
• Ventricular septal rupture
24. Cardiogenic Shock
A decrease in CO leads to compensatory
measures to restore function. Cardiogenic
shock is a result of the cycle of progressive
deterioration. A reduced cardiac output
leads to tissue hypoperfusion & increased
myocardial workload leads to lactic
acidosis then worsening contractility
25. Management
• Myocardial and tissue oxygenation
• Increase contractility
• Minimise risk of extension to injury
• Reduce afterload
• Possible surgery
26. Septic Shock
• Development of septicaemia usually bacterial,
occasionally viral
• Immune and inflammatory response causing
vasodilatation, reduced venous return, reduced
cardiac output.
• Increased O2 requirements from anaerobic
metabolism
• Cell damage as a result of released endotoxins –
capillary permeability
27. Clinical Presentation
• Initially – may be pyrexial, flushed,
tachycardic, tachypnoeic, ? Normal BP or
slightly reduced, urine output.
• Cold, clammy, pallid, altered level of
consciousness, cyanosed, hypoxic, acidotic,
hypotensive, tachycardic,
tachypnoeic/reparatory failure, oliguric,
anuric
28. Anaphylactic Shock
An allergic reaction to an allergen.
• Hypersensitivity leading to histamine
released causing to increased capillary
permeability.
• Severe onslaught
• Vasodilatation & reduced cardiac output.
32. Further reading
• Daily, E. K, & Schroeder,J.S. Techniques in
Bedside Hemodynamic Monitoring. 5th Edition.
1994. Mosby
• Gideon P. Naude, et al (2003) Trauma Secrets 2nd
Edition. Handley Belfus. Philadelphia.
• Hudak & Gallo. CM (1994) Critical Care Nursing:
A Holistic Approach Lippincott Philadelphia
