Shock Obstructivo
Shock
El shock se define desde un punto de vista fisiológico como un estado de disfunción
circulatoria en que la demanda de oxígeno por parte de los tejidos supera la capacidad de
transporte del mismo, lo que lleva a la incapacidad de suplir las demandas metabólicas de los
órganos. Si esta situación se prolonga en el tiempo, se agotan los depósitos energéticos
celulares y se altera la función celular, con pérdida de la integridad y lisis, lo que en última
instancia lleva a un deterioro multiorgánico que compromete la vida del enfermo.
Del punto de vista clínico su definición ha sido más difícil de precisar y descansamos en la
información que nos aporta la evaluación clínica de la perfusión (llene capilar, livideces,
diferencia de temperatura central versus periférica, estado de conciencia, diuresis),
parámetros macrohemodinámicos (ej. presión arterial media) y microperfusión (ej. Lactato
Shock es definido como un estado que amenaza la vida.
Teniendo en cuenta su etiología se pueden clasificar en: hipovolémico, distributivo,
cardiogénico y obstructivo.
Es un síndrome caracterizado fundamentalmente por la inadecuada perfusión sanguínea a
nivel tisular, con reducción de flujo, que si es marcado y sostenido lleva a daño progresivo de
la célula al afectar sus necesidades metabólicas debido a la hipoxia e isquemia.
Shock Obstructivo
El shock obstructivo se debe a una obstrucción del flujo sanguíneo del corazón que produce un
bajo gasto cardiaco, hipoperfusión tisular e hipoxia tisular
Shock obstructivo se debe a una obstrucción mecánica del fl ujo de salida ventricular. Entre sus
causas se encuentran las lesiones congénitas, como la coartación de la aorta, el cayado aórtico
interrumpido y la estenosis valvular aórtica grave, además de ciertas afecciones adquiridas (p.
ej., miocardiopatía hipertrófica). Cuando un recién nacido presenta un shock, deben
considerarse las posibles lesiones obstructivas.
El shock obstructivo se caracteriza por un déficit de llenado cardíaco, es decir, aunque el
corazón es normal, no posee sangre suficiente para bombear. Esto es producto de la
compresión cardíaca o de estructuras circundantes, que pierden la distensibilidad
Fisiopatologia
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Disorders involving impaired diastolic filling and reduced cardiac preload include vena cava
compression syndrome, tension pneumothorax, pericardial tamponade, and high-PEEP
ventilation. A pulmonary artery embolism or mediastinal space-occupying mass increases
right-ventricular afterload, while at the same time left ventricular preload is reduced by
obstructions in the pulmonary flow. The same mechanisms occur with an intracardial mass.
Obstruction of the aortic flow can be distinguished from this, as it leads to a rise in left
ventricular afterload (e.g., Leriche syndrome [aortoiliac occlusive disease], aortic dissection,
and high-grade aortic valve stenosis). After trauma, especially, combined shock forms are seen,
e.g., with tension pneumothorax and hemorrhage. No figures exist for the incidence of
obstructive shock, but it is likely to be the rarest form of shock.
Etiologia
Taponamiento Cardiaco
Pericardial tamponade (PT) is a life-threatening condition caused by accumulation of fluid in
the pericardial sac that causes critical cardiac compression. There is an impaired filling of the
cardiac chambers, leading to a drop in the cardiac output. The spectrum of hemodynamic
compromise in PT varies from mild to critical with varying prognosis.
The pericardium is a sac that contains the heart and includes the outer fibrous sac and the
serosal component. The outer fibrous layer continues as the adventitia of the great vessels
superiorly and is attached to the central tendon of the diaphragm inferiorly.1 The pericardial
cavity is enclosed by the serosal component, which forms the outer parietal (along with fibrous
component) and inner visceral pericardium. The visceral pericardium reflects and becomes
continuous with the parietal pericardium ensheathing the arteries and veins at the base of the
heart. The reflections form the transverse sinus behind the great vessels and the oblique sinus
behind the left atrium separated by the pulmonary veins and inferior vena cava. Pericardial
fluid (normally 15–50 mL) is contained between the visceral and parietal pericardium that
helps in lubrication and equalizes pressures between pericardial chamber and heart chambers.
The accumulation of pericardial fluid beyond the pericardial reserve volume (dependent on the
compliance of pericardium) causes elevation of the intrapericardial pressure, leading to PT.
Equalization of the diastolic cardiac chamber pressures is seen. The cardiac chambers collapse,
which restricts diastolic filling and results in low cardiac output.
PT varies in presentation. The presentation is dependent on the rate of accumulation of
pericardial effusion and underlying cause (Box 6.1). Some patients are asymptomatic when
accumulation of pericardial effusion is slow and chronic. With the chronic accumulation of
fluid, pericardium stretches and becomes more compliant. A compliant pericardium can
accommodate as much as 1 L of fluid without hemodynamic compromise. Clinical
manifestations occur when a critical threshold of intrapericardial pressure is reached. Inthe
cases of acute pericardial effusion where normal pericardium with lower distensibility is
present, this threshold is reached at a lower volume (as low as 100 mL) of pericardial effusion
(see Fig. 24.1). PT clinically manifests as dyspnea, tachycardia (acute bradycardia owing to
vagal response), tachypnea, hypotension, elevated systemic venous pressure, pulsus
paradoxus (PP) (exaggerated inspiratory decrease in arterial blood pressure >10 mm Hg).
Clinical PT represents a later stage in the spectrum of hemodynamic compromise. Most
patients show abnormalities on echocardiography and catheter laboratory hemodynamic
easurements before overt clinical PT is seen
Libro pag 106, 477
Neumotorax
Libro pag 975
Embolismo Pulmonar 906
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