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<< Symptomatic Hypotension: ED Stabilization And The Emerging Role Of Sonography

Pathophysiology

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Pathophysiology

Pathophysiology

Normal BP results from a balance between the peripheral vascular resistance and the cardiac output (CO), with total blood volume affecting both. Cardiac output is a product of the stroke volume (SV) and the heart rate (HR):
 

CO = SV x HR

Hypotension results when either the stroke volume or the heart rate is decreased. In addition, blood volume provides the "substrate" that the resistance vessels "push" against in order to regulate BP. Thus, even maximal vasoconstriction will be ineffective if volume status is inadequate. This key point resurfaces in managing many hypotensive patients.

The peripheral vascular resistance (PVR) is regulated by a variety of mechanisms. Only a small proportion of the blood volume is involved in perfusing tissues at any given time. Most of the total blood volume is contained in the venous system. The veins serve as blood reservoirs that are mobilized by the neuroendocrine system in time of need. Certain organs, such as the heart and brain, are autoregulated. Their perfusion is influenced by metabolic factors and not by the neuroendocrine system. Thus, blood flow is preserved and can actually be enhanced in early volume loss.

Adrenergic receptors are located in organs based on their function in the "fight or flight" response to stress. Non essential organs in acute stress events (such as the gastrointestinal tract) have high concentrations of vasoconstrictive alpha-1 (A1) receptors, while those essential to survival in acute stress (the heart, lung, and skeletal muscles) have high concentrations of vasodilatory beta-2 (B2) receptors. Cardiac beta-1(B1) receptors produce increased chronotropy and inotropy with consequent increased oxygen demand. Dopaminergic receptors are primarily located in the splanchnic and the renal beds.

These receptors are stimulated by mediator release from nerve endings (norepinephrine) and the endocrine system (epinephrine). Mediator release is stimulated by the vasomotor centers located in the medulla and hypothalamus. Inhibitory outputs from cardiac, renal, and blood vessel baroreceptors affect these centers. Pathological drops in blood pressure cause decreased outputs to be sent from the baroreceptors, disinhibiting the vasomotor centers. Sympathetic nervous system output or tone is thus  augmented; "vagal tone" is conversely decreased.

In low pressure states, like hypovolemia, there is less baroreceptor stimulation which leads to ADH release. The release of ADH leads to: 1) An increase in water absorption in the distal renal tubules and then an increase in vascular blood volume; and 2) Peripheral vasoconstriction. Other mediators that increase adrenergic tone include carbon dioxide and hydrogen ions.

The kidney plays a role in the regulation of blood pressure through the following mechanisms:

  • Glomerular filtration rate (GFR) decreases in hypotension which decreases sodium transit time in the tubules and increases its absorption. In turn, this increases the absorption of water.
  • Increased water absorption mediated by ADH in the distal tubule.
  • Renin release from granular cells of the afferent arteriole stimulated by adrenergic output, macula densa output, and direct action of low blood pressure on the granular cells themselves. Renin catalyzes angiotensinogen to angiotensin- 1 in the liver which is converted to angiotensin-2 in the lung by angiotensin converting enzyme (ACE). Angiotensin-2 is a direct vasoconstrictor but also stimulates the renal cortex to release aldosterone, further promoting sodium retention.
  • Hypotension causes a decrease in the release of atrial natriuretic peptides which decreases sodium and water loss in the urine.
Publication Information
Authors

Anthony J. Weekes; Ryan J. Zapata; Antonio Napolitano

Publication Date

November 1, 2007

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