Medicinski vjesnik, Vol. 26 No. (1-4), 1994.
Pregledni rad
The pathophysiological foundations of the circulatory shock syndromes
Zdenko Kovač
Dražen Belina
Sažetak
Hemodynamic shock syndrome represents an acute circulatory failure leading to a multiple organ failure. Such circulatory failure develops due to a decrease of arteriovenous blood pressure gradient as a consequence of three independent groups of pathogenetic mechanisms (cardiogenic, vasohypotonic and hypovolemic), all of which lead to the common pathogenetic pathways. A decrease of arteriovenous pressure gradient induces vasomotoric responses, reactive body fluids redistribution, endocrine, metabolic as well as tissue energy adjustments. In this review a comprehensive synopsis of pathogenetic processes is shortly outlined. The cardiogenic mechanisms include the acute systolic and/or diastolic heart failure, which produce an increase of venous pressure and decrease of arterial pressure and heart output. Vasohypotonic mechanisms (neurogenic, septic and anaphylactic) are due to vascular tonus missadjustment. Hypovolemia caused by blood, plasma, water and electrolytes losses and/or sequestration, leads to a decrease of pressure gradient as soon as the extent of hypovolemia overcomes the compensatory vascular capacity. The shock syndromes very often consist of parallel pathogenic processes which therefore can be classified as a complex pathogenic forms of the shock. A list of clinical disorders which develop due to a complex shock pathogenesis, are outlined in the paper. Tissue hypoperfusion is direct consequence of the arteriovenous pressure gradient loss. It causes a progressive depletion of cellular ATP concentration (cellular hypoenergosis), which very often falls lower than 0,1 mmol/L. Cellular hypoenergosis plays the critical role in conversion of negative homeostatic regulation into a positive feedback mode. Positive homeostatic regulation (circuli vitiosi) amplifies deterioration of arteriovenous blood pressure gradient, which reversely intensifies the degree of energy depletion in the tissues. Such homeostatic conversion plays a critical role in the development of progressive phase (systemic failure, decompensation) of the shock. Functional restitution, decrease of functional organ capacity, permanent absence of certain organs’ function and death, represent a possible clinical status caused by and developed during the shock syndrome. Progessive pathologic alteration of tissue function and structure correlates well with the degree of tissue hypoenergosis. A short detailed description of the tissue alterations is outlined in the paper. Clinical symptoms and signs, as well as laboratory parameters give a valuable information which points to the level of shock development and reversibility. Correlation of clinical parameters and pathophysiologic processes are summerized. Simple predictive rules are re-discussed in the scope of underlying pathophysiology. In addition, a related hemodynamic disorders are shortly discussed in the paper.
Ključne riječi
Hrčak ID:
192972
URI
Datum izdavanja:
1.12.1994.
Posjeta: 5.434 *