Shock
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Shock occurs when the circulatory system is no
longer able to deliver enough 02 and vital nutrients to adequately meet the
metabolic demands of the patient.
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Although initially reversible,
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prolonged hypo perfusion will eventually result
in cellular hypoxia and the derangement of critical biochemical processes
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From a
clinical standpoint, shock can be divided into the following subtypes:
1.
Hypovolemic
2.
Cardiogenic
3.
Obstructive
4.
Distributive
Hypovolemic
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Hypovolemic shock results from an inadequate
circulating blood volume owing to either profound dehydration or significant
hemorrhage.
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Traumatic hypovolemia is the most common type
of shock encountered in patients <40 years of age
Cardiogenic
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Cardiogenic shock occurs when the heart is
unable to provide adequate forward blood flow secondary to impaired pump
function or significant dysrhythmia.
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Myocardial infarction is the leading cause of
cardiogenic shock and typically occurs once -40% of the myocardium is
dysfunctional.
Obstructive
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Obstructive shock results from an extracardiac
blockage of adequate venous return of blood to the heart
Example : -
q Pericardial Tamponade ,
q Tension pneumothorax
q Massive pulmonary
embolism [PE)).
Distributive
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Distributive
shock occurs secondary to an uncontrolled loss of vascular tone
v Example
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sepsis
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anaphylaxis,
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neurogenic shock
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adrenal crisis
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Neurogenic shock most commonly occurs in
trauma patients with high cervical cord injuries and a secondary loss of
sympathetic tone and should always be considered a diagnosis of exclusion.
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Classically these patients will present with
hypotension and a paradoxical bradycardia.
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Suspect septic shock in elderly,
immunocompromised, and debilitated patients who are toxic appearing despite
only vague symptoms.
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The prognosis for patients with cardiogenic
and septic shock remains grave ,with mortality rates between 30% and 90%.
Pathophysiology of shock
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The pathophysiology of shock can be divided
into 3 basic categories.
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a systemic autonomic response
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endorgan cellular hypoxia
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The
secretion of proinflammatory mediators .
a systemic autonomic response
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The autonomic system initially responds to
widespread tissue hypoperfusion by globally increasing the overall cardiac
output.
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As tissue perfusion continues to decline,
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the body shunts circulating blood away from
less vital structures including the skin, muscles, kidneys, and splanchnic
beds.
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Reflexively, the kidneys activate the
renin-angiotensin axis, prompting the release of various vasoactive substances,
with the net effect to preserve perfusion to the most critical organs, namely
the brain and the heart.
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When
the preceding response is inadequate despite maximal tissue 02 extraction,
cellular hypoxia forces a conversion from aerobic to anaerobic metabolism.
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By
nature, anaerobic metabolism cannot produce enough adenosine triphosphate to
maintain regular cellular function.
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Tissue
lactate accumulates, resulting in systemic acidosis, and eventually this
breakdown in cellular metabolism leads to widespread tissue death.
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Injured and dying cells prompt the production
and secretion of harmful inflammatory mediators,
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resulting in the development of the systemic
inflammatory response syndrome,
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defined
by the presence of fever, tachycardia, tachypnea, and leukocytosis
