shock - 2.pptx
TRANSCRIPT
Shock
Dr. Naser El-HammuriHead of the Department of Surgery
Hashemite University
Shock
• Definition• Pathophysiology• Ischemic reperfusion syndrome• Classification of shock • Severity of shock• Consequences of shock • Resuscitation & Monitoring• End point of resuscitation • Conclusion
Shock
Definition: Shock is a systemic state of low
tissue perfusion, which is inadequate for normal cellular respiration
Shock
Definition Inadequate delivery of oxygen and nutrients
to maintain normal tissue and cellular function
• The resultant cellular injury is initially reversible• If the hypo-perfusion is severe enough and
prolonged, the cellular injury becomes irreversible
Shock
• The clinical manifestations of shock are result of stimulation of the
- Sympathetic & Neuroendocrine stress response - Inadequate oxygen response - End organ dysfunction• Blood pressure alone is an insensitive measure
of shock• Significant hypoperfusion and cellular death
may be ongoing, despite normal blood pressure
Shock / Pathophysiology
• Tissue hypoperfusion that is insufficient to maintain normal aerobic metabolism
• This represents an imbalance between substrate delivery (Supply) and cellular substrate requirements (Demand)
• The initial insult, whether hemorrhage, injury, or infection, initiates both neuroendocrine and inflammatory mediator response
• The magnitude of physiologic response is proportional to both the degree and the duration of shock
Shock / Pathophysiology
• While the quantitative nature of the physiologic response to shock will vary with etiology of shock, the qualitative nature of the response to shock is similar, with common pathways in all types of shock.
• Persistent hypoperfusion will result in hemodynamic derangements, end organ dysfunction, cell death, and death of the patient if treated late or inadequately
Shock / Neuroendocrine Response
• The goal of the neuroendocrine response to hemorrhage is maintain perfusion to the heart and the brain, even at the expense of other organ system
- Peripheral vasoconstriction - Inhibition of fluid excretion
Shock / Neuroendocrine Response
• The mechanism include (1) Autonomic control of peripheral vascular
tone and contractility. (2) Hormonal response to stress and volume
depletion (3) Local microcirculatory mechanisms that
are organ specific and regulate regional blood flow
Shock
• Tissue hypoperfusion results in: Insufficient delivery of O2 and glucose to
tissue Cells switches from aerobic to anaerobic
metabolism If perfusion not restored, cell death
Shock / Pathophysiology
Pathophysiology (1) Cellular• Accumulation of Lactic Acid results in systemic metabolic
acidosis• Glucose get within cells get exhausted, anaerobic
respiration ceases• Failure of Na/K pump in cell membrane and intracellular
organelles• Intracellular lysosomes release autodigestive enzymes and
cell lysis ensues• Intracellular content including K are released in
bloodstream
Shock / Pathophysiology
Pathophysiology (2) Micro-vascular• Tissue ischemia result in activation of immune and
coagulation system• Hypoxia and acidosis activate complement, prime
Neutrophils, resulting in generation of O2 free radicals and release of cytokine
• This result in injury of capillary endothelial cells which will further activate the immune and coagulation systems
• Endothelial cells losses integrity and becomes leaky• Results in tissue edema
Shock / Pathophysiology
Pathophysiology (3) SystemicCardiovascular• Preload and after load decrease • Compensatory Baroreceptor response Increased sympathetic activity & Release of Catecholamine• Tachycardia & Systemic vasoconstriction
(except in sepsis)
Shock / Pathophysiology
Pathophysiology (3) SystemicRespiratory• The metabolic acidosis and increased sympathetic
response result in increased respiratory rate and minute ventilation to increase excretion of CO2
Shock / Pathophysiology
Pathophysiology (3) SystemicRenal• Decreased perfusion pressure • Decrease glomerular filtration & urine
out put• Stimulation of Renin – Angiotensin –
Aldosterone axis • More vasoconstriction and Na & H2O
reabsorption
Shock / Pathophysiology
Pathophysiology (3) SystemicEndocrine• Release of Antidiuretic hormone from hypothalamus• Release of cortisol from adrenal cortex
Vasoconstriction Reabsorption of Na & H2O
Shock / Pathophysiology
Ischemia – Reperfusion Syndrome• Hypoperfusion• Further injury occurs once normal circulation is restored to
these tissue:• The acid and K load that has build can lead to
myocardial depression , vascular dilatation and further hypotension
• The cellular and humoral elements activated by the hypoxia (complement, neutrophils and microvascular thrombi are flushed back in the circulation where they cause further endothelial injury to organs such as lungs and kidneys
Shock
Ischemia – Reperfusion Syndrome (continue)• This leads to acute lung injury, acute
renal injury, MOF and death
• Reperfusion injury can currently only be attenuated by reducing the extent and duration of tissue hypoperfusion
Classification of Shock
Hypovolemic Shock• (1) Hemorrhagic• (2) Non-Hemorrhagic Poor fluid intake Dehydration Excessive fluid loss
Hypovolemia is probably the most common form of shock and to some degree a component of all other forms of shock
Classification of Shock
Cardiogenic Shock Primary failure of the heart to pump blood
forward to tissue and subsequent tissue hypoxia• MI• Cardiac dysrhythmias• Valvular heart disease• Blunt myocardial injury• Cardiomyopathy
Classification of Shock
Obstructive Shock Reduction in preload because of mechanical obstruction
of cardiac filling• Cardiac temponade• Tension pneumothorax• Massive pulmonary embolus• Air embolus Reduced filling of left &/or right sides
of the heart leading to reduced preload and fall in cardiac output
Classification of Shock
Distributive Shock Describes the pattern of cardiovascular
responses characterizing a variety of conditions
• Septic shock• Anaphylaxis• Spinal cord injury
Classification of Shock
Distributive Shock Inadequate organ perfusion is
accompanied by vascular dilatation with hypotension, low systemic vascular resistance, inadequate afterload and resulting in abnormally high cardiac output
• In later phases of septic shock there is hypovolemia from fluid loss into the intestinal spaces and there may be concomitant myocardial depression
Classification of Shock
Endocrine Shock May be present as a combination of
hypovolaemic, Cardiogenic and distributive shock
• Hypo and hyperthyroidism• Adrenal insufficiency
Severity of Shock
Compensated shock• Reduce blood flow to non-essential organs to reserve
preload and flow to lungs and brain• Adequate compensation to maintain central blood volume
and pressure flow to kidneys, lungs and brain• Apart from tachycardia cool peripheries there may be no
other clinical signs of hypovolemia Occult systemic metabolic acidosis, and activation of
humoral and cellular elements within the underperfused organs If prolonged MOF & Death
Severity of ShockDecompensated Compensated
Severe Moderate Mild
+++ ++ ++ + Lactic Acidosis
Anuric Reduced Normal Normal Urine out-put
Comatose Drowsy Mild Anxiety Normal Loss of Consciousness
Laboured Increased Increased Normal Respiratory Rate
Increased Increased Increased Mild increase Pulse Rate
Severe hypotension
Mild hypotension
Normal Normal Blood Pressure
Shock
Remember • Capillary refill
Early shock normalSeptic shock
• Tachycardiaß-blockersPacemakersAdult with normal pulse around 50/min
• Hypotension Late sign of shock in youngHypertensive patients
Consequences of Shock
Patients in profound shock for prolonged period of time become unresuscitable
• Cell death follows from cellular ischemia• Ability of the body to compensate is lost• Myocardial depression and loss of responsiveness to fluid
or inotropic therapy• Peripherally there is loss of the ability to maintain systemic
vascular resistance and further hypotension ensues• The peripheries no longer respond to vasopressor agents
Death is inevitable result
Consequences of Shock
Multiple Organ Failure: Failure of two or more organ systems
• Lung Acute respiratory distress syndrome• Kidney Acute renal insufficiency• Liver Acute liver insufficiency• Clotting Coagulopathy• Cardiac Cardiovascular failure
Consequences of Shock
• Intervention must be timely
and •period of shock must be
limited
Resuscitation
• Should not be delayed• If in doubt about cause of shock, assume
hypovolaemic• Stop bleeding• Resuscitate before surgery (bowel obstruction)• Fluid therapy
Initially no inotropes or chronotropesFluid through short wide-bore access
Resuscitation
Type of fluids• No ideal resuscitation fluid• Crystalloids vs. Colloids• Hypotonic solutions are poor volume
expander• If blood is lost, use blood
Resuscitation
• Dynamic fluid response• Rapid administration of fluid bolus 250 – 500
cc given rapidly over 5 – 10 min, and the cardiovascular responses (HR, BP, CVP) are observed:
ResponderTransient responderNon-Responder
Resuscitation
Vasopressor and Inotropic support• Not used initially• Indicated in Distributive shock Cardiogenic shock
Monitoring
Monitoring of patient in shock• Minimum
ECGPulse oximetryBPUrine output
• Additional modalitiesCVPInvasive BPCardiac out putBase deficit and serum lactate
End Point of Resuscitation
• End point of resuscitation is not by having normal pulse, BP, and Urine output
• The goal in the treatment of shock is restoration of adequate organ perfusion and tissue oxygenation
• Resuscitation is complete when oxygen dept is repaid, tissue acidosis is corrected, and aerobic metabolism restored
• Occult Hypoperfusion
End Point of Resuscitation
Endpoints in resuscitation can be divided into• Systemic or global parameters - Vital signs - Cardiac output - Pulmonary artery wedge pressure - Oxygen delivery and consumption - Lactate
- Base deficit
• Tissue specific parameters• Cellular parameters
End Point of Resuscitation
• Lactate is generated by conversion of pyruvate to lactate by pyruvate dehydrogenase in the setting of insufficient oxygen.
• Lactate is released in the circulation and predominantly taken up and metabolized by the liver and kidneys
• Elevated serum lactate is an indirect measure of the oxygen dept, an therefore an approximation of the magnitude and duration of the severity of shock
• Normalization of serum lactate is considered prognostic factor of outcome
End Point of Resuscitation
• Base deficit is the amount of base in millimoles that is required to titrate 1 L of whole blood to a pH of 7.4 with the sample fully saturated with O2 at 37 C and PaCO2 of 40 mmHg.
• It is usually measured by arterial blood gasses analysis
• The mortality of trauma patients can be stratified according to the magnitude of base deficit measured in the first 24 hours after admission
Conclusion
• State of tissue hypoperfusion• Cellular injury ends up by death• Physiologic response to shock happens at cell, micro-vascular
and systemic levels.• Multiple neuroendocrine and hormonal responses• Common pathways in response to all types of shock• Severity of shock is stratified by level of lactate and base deficit• Outcome depends on degree, duration of shock and the
prompt response. • Endpoint of resuscitation determined by normalization of
serum lactate / base deficit