overview of shock
DESCRIPTION
shock overviewTRANSCRIPT
Overview of Shock
Lecturer: Michelle Hodgkiss2008
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
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 notinclude 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.
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.
Events leading to inadequate tissue perfusion
• Decreased cardiac output• Decreased blood volume• Pump failure• An increase in peripheral vasodilatation• Increased vascular permeability
Shock
Patient assessment
Accurate interpretationof situation
InstigateImmediate appropriate
action
Factors in the Progression of ShockHypovolaemic Shock Cardiogenic Shock
MIMyocarditis Tamponade
Decreased CO
Decreased Tissue
Perfusion
EndotoxaemiaBurns
TraumaAnaphylaxis
HaemorrhageDiarrhoea
Dehydration
Increased Vascular
permeability
DecreasedBlood
volume
Decreased VenousReturn
Endothelialdamage
AnoxicCell injury
Factors in the Progression of Shock
Decreased CO
Decreased tissue perfusion
Anoxic cellinjury
Metabolicacidosis
Renal Failure
AnaerobicGlycolysis in Muscle
Heart Failure
Four Stages of Shock
• Initial• Compensatory• Progressive• Refractory
Initial Phase
• Cardiac output , tissue perfusion , oxygen delivery and nutrients to cells aerobic metabolism is and anaerobic metabolism begins to take over.
Compensatory Stage
The body tries to overcome these effects with physiological adaptations
Neural Hormonal Chemical
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
Hormonal
• The sympathetic stimulation:• Renal & spanchnic blood flow decreased• Juxtaglomerular cells in nephron stimulated
to release renin• Renin-angiotensin-aldosterone system
activated.
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.
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
Refractory Stage
Severe cell destruction Vital organs failedDeath imminent
Assessing the Shocked Patient
• Skin• Colour• Temperature• Conscious level• Respiratory rate & pattern• Heart rate & BP• Perfusion• Decreased urine output
Classification of Shock
• Hypovolaemic• Cardiogenic• Anaphylactic Shock• Septic Shock• Neurogenic Shock
Classifications of Shock
Hypovolaemic
Distributive
Cardiogenic
SepticNeurogenicAnaphylactic
Hypovolaemic Shock
• CausesCommonly due to sudden blood loss –Burns and Dehydration are the most common
forms of shock• Research of therapies vast
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.
Management
• Replace loss• ?Crystalloid vs Colloid vs Blood• O2 Therapy• Observations• Monitor blood results
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
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
Management
• Myocardial and tissue oxygenation• Increase contractility• Minimise risk of extension to injury• Reduce afterload• Possible surgery
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
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
Anaphylactic Shock
An allergic reaction to an allergen.• Hypersensitivity leading to histamine
released causing to increased capillary permeability.
• Severe onslaught• Vasodilatation & reduced cardiac output.
Management
• Hydrocortisone• Adrenaline• Treat cause• Inotropes, fluids, etc
Neurogenic Shock
• Due to lack of neural control• Vasodilatation• As a result of loss of parasympathetic &
sympathetic nervous control
Causes
• Head injury• Spinal injury/shock• Iatrogenic• Pain• Stress/pain
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