Physiology of shock

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Physiology of shock
Late Sciences lecture series Lecture 1

• Mahesh Nirmalan
• Division of Cardiovascular Sciences
• Intensive Care Unit, Manchester Royal Infirmary

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Objectives

• Definition
• Clinical end points
• Classification
• Stages
• Physiological compensation
• Immediate
• Late
• Treatment objectives

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MCQ Shock is defined as

• Sustained reduction in Systolic blood pressure lt
  80 mm Hg
• Sustained reduction in mean arterial pressure lt
  80 mm Hg
• Sustained reduction in diastolic blood pressure lt
  40mm Hg
• Inadequate blood flow to the tissues to meet its
  metabolic requirements
• None of the above

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Compensated shock
MAP is a very poor surrogate of blood flow to the
peripheral tissues Vasoconstriction will maintain
MAP at thee expense of tissue flow Compensated
shock
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Definition of Shock

• Shock is an acute clinical syndrome initiated by
  ineffective perfusion, resulting in severe
  dysfunction of organs vital to survival.
• Shock is not a synonym to hypotension!

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Shock Definition

• Inadequate perfusion to tissues
• Large enough to compromise the supply of
  nutrients and removal of metabolic waste
• Resulting in compromised organ functions
• Usually recognised by clinical features
  suggestive of reduced blood flow
• Reduced capillary fill
• Cold clammy hands or feet
• Widening core-toe temperature gradient
• Reduced urine output
• Raised plasma Lactate-
• Low blood pressure is a late sign- particularly
  in the young previously fit individuals

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Ineffective perfusion

• Organ perfusion may be compromised by an overall
  decrease or maldistribution of cardiac output.

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Classification

• Hypovolaemic Haemorrhage, loss of ECF
• Cardiogenic Tamponade, Infarction, heart failure
  
• Extracardiac obstructive Pulmonary embolism,
  tension pneumothorax
• Distributive sepsis, anaphylaxis

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Physiological factors affecting Arterial
pressure, CO and ventricular performance
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Arterial pressure
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Effect of EDV and contractility on SV
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Stages of shock

• Compensated shock or occult shock
• Normal physiological compensation will lead to
  complete recovery
• External interventions not necessary
• Progressive shock
• Progressively worse in the absence of external
  interventions
• Irreversible shock
• Death is inevitable in spite of all forms of
  therapy

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Stages of shock

• Compensated shock
• Autotransfusion
• De-compensated shock
• Redistribution of blood
• Irreversible shock
• MODS/ delayed death

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CO, MAP and SvO2
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Irreversible shock
Plasma Lactate
A priori groups
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C(n9)
S(n10)
5
G(n10)
4
Plasmalactate (mmol/l)
3
2
1
0
Baseline
Initiation of
End of shock
Post
shock phase
phase
resuscitation
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Effects of prolonged shock on cardiac functions

• Modified Frank- Starling curves
• Dogs bled to a pressure of 30mm Hg
• Maintained hypotensive for variable periods
• Resuscitated in stages to assess ventricular
  functions
• Impaired ventricular functions after 4 hours of
  sustained shock
• Concept of irreversible shock

CO
0
5
10
LAP mm Hg
Adapted from Crowell et al 1962
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Reversible Vs Irreversible shock
Sustained shock can breed more shock
Adopted from Guyton and Hall
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Physiological compensatory mechanisms

• Immediate
• Fluid shifts
• Neural reflexes Autonomic nerves
• Endocrine
• Delayed
• Renal Renin-Aldosterone-Angiotensin
• Hypothalamo-pituitary axis
• ADH
• Thirst

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Starling Forces at the capillary bed
Net Filtering Pressure 5 mmHg
Net Filtering Pressure - 5 mmHg
Hydrostatic Pressure 0 mmHg
Interstitial Fluid
Venous end
Arterial end
Blood
Hydrostatic Pressure 30 mmHg
Colloid Osmotic Pressure 25 mmHg
Hydrostatic Pressure 20 mmHg
In the normal microcirculation
  - At arterial end water moves out of the
capillary Hydrostatic pressure gt COP - At venous
end water moves into the capillary Oncotic
pressure gt Hydrostatic pressure
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Compensation in shock

• In shock, the hydrostatic pressure decreases and
  the oncotic pressure is constant
• The fluid loss from the capillary to the
  extracellular space decreases.
• Re-absorption of fluid return from the
  extracellular space increases
• Partially compensates for the loss in circulatory
  volume
• Never complete
• Fluid shift system
• Re-absorption is aided by the increase in
  osmotically active substances in blood Glucose
• The amount of fluid recruited through the
  metabolic responses may be substantial 20-30m
  Osmol 0.5 liters of fluid
• Hyperglycaemia is an evolutionary survival
  mechanism
• When persistent may have adverse consequences

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Autonomic neural reflexes

• Baro-receptors mediated increase in sympathetic
  outflow
• Chemo-receptor mediated sympathetic outflow
• Ischaemic brain response Late but powerful

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Stages of shock

• Compensated shock
• Autotransfusion
• De-compensated shock
• Redistribution of blood
• Irreversible shock
• MODS/ delayed death

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(No Transcript)
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Autonomic reflex responses to hypovolaemia

• Baroreceptors are stimulated by stretch MAP and
  pulse pressure
• Sympathetic outflow is inhibited by baroreceptor
  affarents
• Direct as well as via the vagal nucleus
• Reduction in baroreceptor affarents therefore
  lead to vasoconstriction and tachycardia
• Compensates for reduction in MAP and pulse
  pressure

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Chemo-receptors

• Central chemo-receptors Medulla
• Peripheral chemo-receptors Carotid body and
  aortic body
• Particularly relevant when MAP lt 60
• H and CO2
• Evoke a powerful sympathetic response

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Sympathetic responses to haemorrhage and shock

• In the absence of sympathetic responses 15-20
  acute haemorrhage is usually fatal.
• In the presence of an intact sympathetic response
  patients may be able to tolerate 30-40 acute
  haemorrhage and recover completely
• Venoconstriction is helpful in maintaining stroke
  volume
• Arterial constriction maintains blood pressure at
  the expense of organ blood flow
• Aimed at preserving coronary and cerebral
  perfusion
• Minimal constriction of the coronary and cerebral
  vessels
• Does not fall until systolic pressure is lt 70 mm
  Hg
• Prolonged arterial-constriction initiates
  secondary changes in organ function

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The early compensatory mechanisms preserve
arterial pressure at the expense of blood flow to
key visceral organs
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Progressive and non-progressive shock
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Generalised cellular degeneration

• Prolonged lack of oxygen and nutrients affect the
  viability of organs
• Tissues with high metabolic activity are more
  prone
• Centri-lobular necrosis of the liver
• Na/K active transport?swelling
• Mitochondrial activity depressed
• Release of lysosomal hydrolases
• Interruption of metabolism
• Lungs
• Heart
• Gut mucosal barrier

Patients resuscitated after prolonged shock
usually die of multiple organ failure Human and
Health care costs
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Delayed compensatory pathways
Restores normalcy
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Treatment priorities in shock

• Use of inotropic agents to restore myocardial
  contractility
• Use of vasoactive drugs to cause
  venoconstriction, vasoconstriction and thereby
  restore venous return and blood pressure
• Restore circulating blood volume to optimise
  cardiac functions
• Increase heart rate to increase cardiac output
• Use of HCO3- to prevent metabolic acidosis

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Tachycardia, though an important compensatory
mechanism always comes at a price
Heart rate Wall tension After load
CPP Diastolic time CO O2 content
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Questions?