Cryptic shock

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Pre-shock is also known as compensated shock, or cryptic shock [1] [2] describes the state in which the human body is still capable of offsetting the abnormally reduced tissue perfusion by exerting compensatory mechanism [1] . For instance, in sole hypovolemia without formally entering shock state, the body is able to constrict peripheral vessels, accelerate heart rate, and boost myocardial contractility to compensate for the negative impacts out of a certain percentage reduction in total effective arterial blood volume. Thus, the person, particularly for those non-elderly who have higher physical reserve, might not be symptomatic of such blood loss accounted for certain amount of total blood volume in the body and might even manifest a normal systolic pressure as well as diastolic pressure. Taken together, tachycardia, a modest change in overall blood pressure in either trend--increase or decrease--, or hyperlactatemia that is not deemed to be moderate to severe, are the likely only early signs of clinical shock [2] .

Hypovolemia also known as volume depletion is a state of decreased blood volume or diminished body fluid; more specifically, decrease in volume of blood plasma. It is thus the intravascular component of volume contraction, but, as it also is the most essential one, hypovolemia and volume contraction are sometimes used synonymously.

Heart rate is the speed of the heartbeat measured by the number of contractions (beats) of the heart per minute (bpm). The heart rate can vary according to the body's physical needs, including the need to absorb oxygen and excrete carbon dioxide. It is usually equal or close to the pulse measured at any peripheral point. Activities that can provoke change include physical exercise, sleep, anxiety, stress, illness, and ingestion of drugs.

Myocardial contractility represents the innate ability of the heart muscle (cardiac muscle or myocardium) to contract. The ability to produce changes in force during contraction result from incremental degrees of binding between different types of tissue, that is, between filaments of myosin (thick) and actin (thin) tissue. The degree of binding depends upon the concentration of calcium ions in the cell. Within an in vivo intact heart, the action/response of the sympathetic nervous system is driven by precisely timed releases of a catecholamine, which process determines the concentration of calcium ions in the cytosol of cardiac muscle cells. The factors causing an increase in contractility work by causing an increase in intracellular calcium ions (Ca++) during contraction.

Clinical shock aka uncompensated shock is termed overt shock. [3]

Reference

  1. 1 2 Shoemaker, WC (1996). "Temporal physiologic patterns of shock and circulatory dysfunction based on early descriptions by invasive and noninvasive monitoring". New Horizons (Baltimore, Md.). 4 (2): 300–18. ISSN   1063-7389. PMID   8774804.
  2. 1 2 Chien, S (1967). "Role of the sympathetic nervous system in hemorrhage". Physiological Reviews. American Physiological Society. 47 (2): 214–288. doi:10.1152/physrev.1967.47.2.214. ISSN   0031-9333. PMID   5342872.
  3. Puskarich, Michael A.; Trzeciak, Stephen; Shapiro, Nathan I.; Heffner, Alan C.; Kline, Jeffrey A.; Jones, Alan E. (2011). "Outcomes of patients undergoing early sepsis resuscitation for cryptic shock compared with overt shock". Resuscitation. Elsevier BV. 82 (10): 1289–1293. doi:10.1016/j.resuscitation.2011.06.015. ISSN   0300-9572. PMC   3179778 . PMID   21752522.

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