Shock - 2.pptx

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


• 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


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


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


Pathophysiology (3) SystemicCardiovascular• Preload and after load decrease • Compensatory Baroreceptor response Increased sympathetic activity & Release of Catecholamine• Tachycardia & Systemic vasoconstriction

(except in sepsis)


Pathophysiology (3) SystemicRespiratory• The metabolic acidosis and increased sympathetic

response result in increased respiratory rate and minute ventilation to increase excretion of CO2


Pathophysiology (3) SystemicRenal• Decreased perfusion pressure • Decrease glomerular filtration & urine

out put• Stimulation of Renin – Angiotensin –

Aldosterone axis • More vasoconstriction and Na & H2O

reabsorption


Pathophysiology (3) SystemicEndocrine• Release of Antidiuretic hormone from hypothalamus• Release of cortisol from adrenal cortex

Vasoconstriction Reabsorption of Na & H2O


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


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


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


Distributive Shock Describes the pattern of cardiovascular

responses characterizing a variety of conditions

• Septic shock• Anaphylaxis• Spinal cord injury


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


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


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


• 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


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


• 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


• 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

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Shock - 2.pptx