TRIPASS XR تري باس

 

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S hock

La u ren M. Smith, MD

Nihja 0. Gordon, MD

Key Points

• Do not wait for hypotension to diagnose shock.

• Early ide ntification and i n itiation of aggressive

therapy can significantly improve patient

survival.

INTRODUCTION

More than 1 million patients present to U.S. emergency

departments annually with shock, and despite continued

advances in critical care, mortality rates remain very high.

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. Although initially

reversible, prolonged hypoperfusion will eventually result

in cellular hypoxia and the derangement of critical bio ­

chemical processes. From a clinical standpoint, shock can

be divided into the following subtypes: hypovolemic, cardiogenic, obstructive, and distributive. Hypovolemic

shock results from an inadequate circulating blood volume

owing to either profound dehydration or significant hemorrhage. Traumatic hypovolemia is the most common type

of shock encountered in patients <40 years of age.

Cardiogenic shock occurs when the heart is unable to provide adequate forward blood flow secondary to impaired

pump function or significant dysrhythmia. Myocardial

infarction is the leading cause of cardiogenic shock and

typically occurs once -40% of the myocardium is dysfunctional. Obstructive shock results from an extracardiac

blockage of adequate venous return of blood to the heart

( eg, pericardia! tamponade, tension pneumothorax, and

massive pulmonary embolism [PE) ). Finally, distributive

shock occurs secondary to an uncontrolled loss of vascular

tone (eg, sepsis, anaphylaxis, neurogenic shock, and adrenal

42

• I n itiate early goa l-directed therapy in patients with

septic shock.

• Early revascu larization is key to improving outcome in

patients with cardiogenic shock.

crisis). 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. Classically these

patients will present with hypotension and a paradoxical

bradycardia. Suspect septic shock in elderly, irnmunocompromised, and debilitated patients who are toxic appearing

despite only vague symptoms. The prognosis for patients

with cardiogenic and septic shock remains grave, with

mortality rates between 30% and 90%.

The pathophysiology of shock can be divided into

3 basic categories: a systemic autonomic response, endorgan cellular hypoxia, and the secretion of proinflammatory mediators. The autonomic system initially responds

to widespread tissue hypoperfusion by globally increasing

the overall cardiac output. As tissue perfusion continues

to decline, the body shunts circulating blood away from

less vital structures including the skin, muscles, kidneys,

and splanchnic beds. 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.

When the preceding response is inadequate despite

maximal tissue 02 extraction, cellular hypoxia forces a conversion from aerobic to anaerobic metabolism. By nature,

anaerobic metabolism cannot produce enough adenosine

triphosphate to maintain regular cellular function. Tissue

lactate accumulates, resulting in systemic acidosis, and

eventually this breakdown in cellular metabolism leads to

widespread tissue death. Injured and dying cells prompt

the production and secretion of harmful inflammatory

mediators, resulting in the development of the systemic

inflammatory response syndrome, defined by the presence

of fever, tachycardia, tachypnea, and leukocytosis.

CLINICAL PRESENTATION

� History

Vague complaints such as fatigue and malaise may be the

only presenting symptoms, especially in elderly patients.

Friends, family, and emergency medical service personnel

will be vital in obtaining a history in patients with altered

mental status. The past medical history including a list of

active medications might reveal risk factors such as immunosuppression, underlying cardiac disease, and potential

allergic reactions.

� Physical Examination

Although hypotension and tachycardia are the cardinal

features of shock, many patients will presents with normal

vital signs owing to physiologic compensation. Because of

the unmet metabolic demands of the central nervous sys ­