Shock

Friday 1st March 2019

  Normal Functioning Heart
 Blood allowed to flow
 Cyclic System
 Anything that impedes
Normal blood flow can result in Veins Artery
Profusion decreased tissue
perfusion
 Negative effect of
tissues and end organs Capillaries
 Severe hypoperfusion =
Shock
 Blood
Heart
Vessels
Perfusion Triad

Blood
 Heart – Pump Function
• Damage to the heart by disease of injury
• Heart is unable to move blood adequately to
support perfusion

Blood Vessels – Container functioning

• If all vessels dilate at once – normal blood
Perfusion Triad volume is insufficient to fill the system
• Inadequate supply to facilitate perfusion

Blood – Content functioning

• If blood or plasm is lost – the volume in the
container is decreased
• Insufficient blood available to allow for perfusion
 •Final Common pathway or many clinical events
•Shock is a result of inadequate energy production to
sustain life.
Shock
•Shock is any condition that causes generalized cellular
hypoperfusion.
•This leads to inadequate cellular oxygenation that
does not meet metabolic needs.
  Any conditions which compromise the flow of blood will
Shock have a direct effect on tissues throughout the body.
 Blood flow may be compromised by
 loss of blood volume
 occlusion of specific vessels
 Inability to pump blood through the system
 Causes hypoperfusion of vital organs.
 Clinically termed shock.
 The body responds by reacting to maintain the blood pressure
 BP = (Stroke Volume x Heart Rate) x Peripheral Resistance
  Hypoperfusion results from:
 Loss of blood (either externally or internally)
 Impaired pumping of blood
 Dilatation of the blood vessels (increased vascular space)

• The end result is a decrease in circulating volume and

Hypoperfusion RBCs moving through the capillary beds to deliver
oxygen to the cells.

• Lack of oxygen impairs metabolism.

Every RBC counts!

  Shock is the final common pathway for a number
of potentially lethal clinical events,
Shock  severe haemorrhage
 extensive trauma
 burns
 large myocardial infarction
 massive pulmonary embolism
 microbial sepsis
 Regardless of the underlying pathology, shock gives rise
to systemic hypoperfusion
 End result is hypotension & cellular hypoxia
 Initially reversible cellular injury
 Persistent shock – irreversible cellular injury
 May result in death
  3 General categories:
 Cardiogenic
Shock  Failure of cardiac pump
 Hypovolemic
 Loss of fluid volume
 Septic
 Cause by microbial infection
 Endotoxic shock
 Three Major Types of Shock
Type of Shock Clinical Examples Principal Mechanisms
Cardiogenic Myocardial infarction
Shock Ventricular rupture Failure of myocardial pump resulting from
Arrhythmia intrinsic myocardial damage, extrinsic pressure,
Cardiac tamponade or obstruction to outflow
Pulmonary embolism
Hypovolemic Haemorrhage
Fluid loss (e.g., vomiting, diarrhoea, Inadequate blood or plasma volume
burns, or trauma)
Septic
Overwhelming microbial infections
Endotoxic shock Peripheral vasodilation and pooling of blood;
Gram-positive septicaemia endothelial activation/injury; leukocyte-induced
Fungal sepsis damage; disseminated intravascular coagulation;
Super antigens (e.g. toxic shock activation of cytokine cascades
syndrome)
Other types of  Anaesthetics accident
Shock  Spinal cord injury (neurogenic shock),
 Loss of vascular tone
Less Common  Peripheral pooling of blood
 Anaphylactic shock
 vasodilation and increased vascular permeability
 caused by an immunoglobulin E hypersensitivity reaction.
 In these situations, acute severe widespread vasodilation
results in tissue hypoperfusion and cellular anoxia.
  Shock is a progressive disorder that if uncorrected leads to
death.
 tends to evolve through three general stages.
 stages have been documented most clearly in hypovolemic
shock but are common to other forms :
1. An initial non-progressive stage
Stages of  reflex compensatory mechanisms are activated
 perfusion of vital organs is maintained
Shock 2. A progressive stage
 tissue hypoperfusion
 onset of worsening circulatory and metabolic imbalances

3. An irreversible stage
 the body has incurred severe cellular and tissue injury
 survival is not possible
The Stages of Shock

Initial Stage Compensatory stage Progressive Stage Refractory Stage

• Body switches from aerobic • Systemic nervous system •  tissue hypoxia • Irreversible cellular damage
to aerobic metabolism stimulated: • Electrolyte imbalance • Irreversible organ damage
• Elevated lactic acid levels   catecholamine release • Metabolic Acidosis • Impending death
• Subtle changes in clinical   renin-angiotensin axis •  lactic acid production
signs   antidiuretic hormone •  tissue pH • Lysosomal leakage
  cardiac contractibility • Respiratory Acidosis • Myocardial contraction
•  vasomotor response weakens
• Neurohormonal response: • Peripheral dilation = • Ischemic to bowel –
 Vasoconstriction (pale/cool oedema intestinal bacteria leakage
skin) • Irregular tachyarrhythmia into circulation
 Blood shunted to vital • Hypotension • Endotoxin shock
organs • Pallor • Renal failure
 tachycardia • Cool
• Clammy Skin
• Aldosterone released • Altered Level of
  urine output Consciousness
  HR
  Glucose levels
 Stage 1:
• Skin warm and flushed
• Peripheral vasodilation
Signs and • Cardiac, cerebral and
Symptoms of pulmonary changes
Septic Shock
Stage 2:
• Renal insufficiency
• Acidosis
• Electrolyte imbalance
  Prognosis depends on:
 Origin of shock
 Duration of shock
 80% - 90% of young healthy patient will recover from
Shock - hypovolemic shock with no complications
 75% mortality rate for cardiogenic and septic shock
Prognosis

Shock Ischemia Infarction Necrosis

  Hemorrhage
 Level of consciousness
 Skin
Patient
Assessment  Pulse
for Shock  Respirations
 Blood pressure
 Confounding factors
 Assume:
 The patient is bleeding somewhere,
Shock without even if you can’t see it.
Obvious Cause  Internal hemorrhage
 Chest, abdomen
 Fracture
 Femurs, pelvis
 • Abdominal organ injury
Injuries • Hemothorax
Commonly • Aortic disruption
Associated • Fractures
with • Rib
• Radius / Ulna
Hemorrhagic • Humerus
Shock • Femur
• Pelvis
 Treatment of Shock
Generalities Hypovolemic Shock
Positioning Maintain / Increase intravascular volume
Avoid hypothermia Decrease any further fluid loss
Maintain adequate oxygenation Give supplementary O2 therapy
Fluid resuscitation
Pain relief Cardiogenic Shock
O2 therapy
Shock - Supportive Therapy Administer cardiac drugs

Treatment Maintain airway and respiratory effort Increase heart action through medication
Maintain cardiac pump
Reverse metabolic acidosis Septic Shock
Restore metabolic equilibrium Restore intravascular volume
Give supplementary O2 therapy
Identify and control source of infection
Administer antibiotics
Remove risk for further infection
 • General treatment:
• Patient kept in cool environment – reduced exposure
to warmth
• Raised lower limb – promotes venous return
• Replacement therapy:
• Hemorrhagic shock – whole blood or blood plasma
Shock - • Hypovolemic shock – electrolyte solutions
Treatment
• Sympathomimetic drugs
• Helpful in neurogenic and anaphylactic shock
• Dopamine, noradrenaline, adrenaline
• Oxygen therapy
• Reduces hypoxia