Diagnosis and treatment of patients with recurrent gastroduodenal bleeding - Shaprynskyi V.O. 2009

Pathogenesis of acute blood loss. Classification of hemorrhagic shock, diagnosis of hypovolemia and assessment of blood loss volume

Pathogenesis of Blood loss

Blood loss of 500 - 750 ml, up to 10% of CBV, does not cause significant hemodynamic disturbances. A CBV deficit of over 2025% leads to a decrease in venous return and, consequently, a fall in Cardiac Output and arterial pressure. In response to arterial hypotension, aortic arch baroreceptors trigger the activation of the sympathoadrenal system, releasing catecholamines (epinephrine, norepinephrine) into the bloodstream. Epinephrine, acting on ß-adrenoceptors, causes tachycardia and spasm of Arteries and Veins containing 70% of CBV. Vasospasm in the Skin, subcutaneous tissue, and gastrointestinal tract can shunt up to 500 — 600 ml of blood into the vascular bed. Norepinephrine, acting on a-adrenoceptors, causes constriction of small vessels — arterioles and venules — which determine total peripheral resistance (TPR). Due to cardiac hyperdynamia, generalized vasospasm, and increased TPR, blood is redistributed, maintaining the cardiac output necessary to ensure adequate perfusion of the Brain and Heart.

A decrease in capillary blood pressure and hydrostatic pressure leads to the influx of interstitial fluid into the bloodstream (autohemodilution) at an initial rate of 100 ml/h. Subsequently, The rate of fluid influx slows down, with CBV returning to normal within 18-48 hours. This process is biphasic. During the first phase (limited to the duration of active bleeding), protein-free fluid enters the blood and is rapidly excreted by the Kidneys. In the second phase (after 2-24 hours), plasma volume is restored by protein-containing interstitial fluid. Through autohemodilution, the body can independently replenish up to 30% of CBV. Clinically, autohemodilution manifests as extracellular dehydration (decreased skin turgor, sunken eyeballs).

Vasoconstriction is a physiologically justified compensatory response that ensures blood flow to The Heart and brain (centralization of Circulation). If CBV is not rapidly normalized, the pathological features of hemorrhagic Shock begin to take center stage.

Vasoconstriction caused by hypercatecholaminemia leads to numerous adverse effects: renal vasospasm against the Background of hypovolemia and arterial hypotension, reduced renal perfusion, clinically presenting as oliguria; cutaneous vasoconstriction and microcirculatory disorders, skin pallor, and mottling. Vasospasm in the TTTКТ bed causes Necrosis of the gastric and duodenal mucosa, forming so-called "stress ulcers"; constriction of the Vessels of the skin, subcutaneous tissue, and Muscles leads to tissue Hypoxia, resulting in the accumulation of underoxidized metabolites (primarily lactate), acidosis (lactic acidosis), and damage to endothelial Cell membranes. Impaired endothelial permeability and increased hydrostatic pressure promote the shift of the liquid part of the blood into the interstitium, forming sludge syndrome: first, platelet aggregation (white sludge), then erythrocyte aggregation (red sludge), which subsequently leads to The Development of DIC syndrome in the pulmonary vasculature and impaired ventilation-perfusion ratios, predisposing to respiratory distress syndrome. In addition to altering blood rheology, microcirculatory disorders lead to blood pooling in capillaries and the exclusion of a significant volume of fluid from the circulation, resulting in pathological pooling ("sequestration"). "Sequestered blood" consists of cell aggregates, fat droplets, active Polypeptides, acidic metabolites, fibrin, and cytokines. "Sequestration" increases the effective volume of blood loss, as a volume of blood exceeding the actual loss by more than 100% is excluded from circulation. Without timely correction during the vasoconstriction stage, consumption coagulopathy and hemorrhagic diathesis mutually reinforce each other; thus, it is well-founded that bleeding is both a cause and a consequence of consumption coagulopathy. All the aforementioned structural elements lead to a decrease in the cellular supply of oxygen and energy substrates, meaning that at this stage, the core pathological mechanism of any shock — impaired tissue oxygenation — is realized.

The biological defense of Cells is so well "designed" by nature that even in this situation, Organ and tissue death does not occur immediately. Cell viability is maintained, but under conditions of Anaerobic METABOLISM with signs of lactic acidosis. Acidosis triggers further organ dysfunction, including of the heart, promoting arrhythmias up to circulatory arrest. It must be remembered that under anaerobic metabolism, a pathological triad inevitably develops: ATP deficiency — impaired Protein Synthesis — failure of the potassium-sodium pump. This determines the irreversibility of shock, as potassium efflux from The Cell leads to cellular hypernatremia, causing cell Swelling and increased lysosomal membrane permeability, which results in the release of large amounts of active lysosomal Enzymes and degraded cellular Proteins. Entering the bloodstream, all these elements damage virtually all Organs, primarily the heart, critically reducing cardiac output.

If we add to this nitric oxide (N0), which is produced in large quantities in the endothelium under The Influence of cytokine cascade activation, with its ability to cause pathological vasodilation, it becomes obvious that TPR and ТЗЛК will decrease even further, ultimately driving The Mechanism of thanatogenesis.

Based on the above, the development of hemorrhagic shock can be divided into compensated (low output syndrome, centralization of circulation), decompensated reversible (blood sequestration, transmineralization, microcirculatory disorders, and acidosis), and decompensated irreversible (worsening acidosis, organ dysfunction, paralysis of venules and arterioles due to the pathological action of N0, and a critical reduction in TPR) shock.

Thus, a structural Analysis of the pathogenesis of hemorrhagic shock clarifies the Morphology/3.html">MAIN DIRECTIONS OF intensive care. In the intensive care of hemorrhagic shock, as the name suggests, infusion-Transfusion Therapy (ITT) plays a central role. When developing an ITT program, it is essential to know the volume of blood loss, the severity of shock, and the qualitative COMPOSITION OF THE infusion fluids intended for use.

Diagnosis of hypovolemia and blood loss volume

The diagnosis of hemorrhagic hypovolemia is usually straightforward. The Clinical presentation largely depends on the volume of blood lost, the rate of bleeding, and the body's ability to utilize compensatory mechanisms.

A crucial step in a physician's management of blood loss is determining the CBV deficit. The most accessible Methods for a clinician are the following.

1. Determination of the Algover-Gruber index (shock index). The Algover-Gruber index is The ratio of heart rate to systolic blood pressure. Normally, it is equal to 0.5. An increase in the index by every 0.1 corresponds to a blood loss of 0.2 l. The margin of error of this method is 15% (Table 1).

Class="center">Table 5.1 Estimation of blood loss volume based on the Algover-Gruber index

2. Estimation of blood loss using the formula: Blood loss volume (l) = (predicted CBV) x (predicted Ht - actual Ht / predicted Ht); Blood loss volume (l) = predicted CBV x (predicted Ht - actual Ht / predicted Ht) (Table 2).

CBV_pred - normal circulating blood volume.

Ht_pred - normal hematocrit.

Ht_act - actual hematocrit.

Table 5.2 Determination of predicted CBV based on the patient's body constitution

3. Estimation of blood loss using the method of M.I. Borovsky and V.S. Zhukova — based on hematocrit and blood viscosity using the formulas:

CBV deficit in men: 1000*V0 + 60*Ht - 6700;

CBV deficit in women: 1000*V0 + 60*Ht - 6000.

4. Method of the Institute of General and Urgent Surgery of the Academy of Medical Sciences of Ukraine — determination of circulating blood deficit solely by blood hematocrit.

The calculation is performed using the following formulas:

EBV in men: 6152 - 158*Ht;

EBV in women: 5456 - 156*Ht.

Table 5.3 Severity of acute blood loss (according to N.A. Kuznetsov, 2003)

Laboratory methods involve determining hematocrit, hemoglobin concentration, and relative blood density.

Table 5.4 Estimation of blood loss volume by blood density or hematocrit

5. Classification of hemorrhagic shock by severity.

It should be noted that acute blood loss is defined as a loss of 25 ml/min or more. Depending on the volume of acute blood loss, four types of bodily response are distinguished:

Type 1. A CBV deficit of up to 15% is compensated for by the body's adaptive responses and does not significantly affect the patient's overall functional state. Clinically, thirst, resting tachycardia, and orthostatic tachycardia (an increase in standing HR compared to supine HR of at least 20 bpm) are observed.

Type 2. A CBV deficit of 15-25%. It is characterized by a systemic cardiovascular response. Clinically, it manifests as pale skin and visible mucous membranes due to vasoconstriction of cutaneous arteries, as well as the collapse and "disappearance" of subcutaneous veins, particularly in the upper extremities. Tachycardia up to 100 bpm is recorded both in the supine position and orthostatically; systolic BP decreases by at least 15 mmHg from baseline. Moderate dyspnea up to 20 breaths per minute is present. Blood viscosity increases.

Type 3. The CBV deficit is 25-40%. The patient's condition in response to blood loss is assessed as moderate to severe. Acute blood loss may cause mild to moderate psychomotor agitation. Marked pallor of the skin and visible mucous membranes is noted. Dyspnea up to 24-28 breaths per minute. Tachycardia of 120 bpm or more. Extrasystoles. Arterial hypotension in the supine position. Oliguria. Restoring the lost volume within the first 15-30 minutes after blood loss helps prevent or rapidly reverse the Development of the hemorrhagic shock symptom complex.

Type 4, so-called massive blood loss, exceeding 40-50% of CBV. The condition is assessed as extremely severe. Acute blood loss of this volume is typically accompanied by stupor, lethargy, and confusion. Breathing is rapid (over 28 breaths per minute) and shallow. Systolic BP drops to 70 mmHg or lower. Tachycardia of 120 bpm or more. Volume replacement in these patients must be performed alongside 100% oxygen inhalation, and one must be prepared to initiate mechanical ventilation.

Some authors distinguish a 5th type - blood loss exceeding 60% of CBV, where the clinical signs of hemorrhagic shock do not have time to develop. Such blood loss presents as primary hemorrhagic collapse with rapid progression to a terminal state and cardiac arrest. This condition is characterized by a rapid (within minutes) drop in BP and respiratory rate accompanied by loss of consciousness, reduced coronary blood flow with myocardial ischemia, and the development of ventricular fibrillation or asystole. A fatal outcome can be prevented by immediate attempts to achieve maximum possible centralization of circulation.

6. Classification of blood loss according to P.L. Marino, 1998)

Table 5.5 Classification of blood loss according to P.L. Marino.

Class I - clinical symptoms are absent or tachycardia is present, primarily when transitioning from a horizontal to a vertical position.

Class II - main clinical signs: orthostatic hypotension or a decrease in BP of more than 15 mmHg when transitioning from a horizontal to a vertical position. In the supine position, BP values are normal or decreased. Urine output is preserved.

Class III - manifests as supine hypotension and oliguria (urine output less than 400 ml/day).

Class IV - characterized by collapse and impaired consciousness progressing to coma.

Table 5.6. Hypovolemic shock: symptoms, signs, therapy.

7. Classification of blood loss severity by A.A. Shalimov, V.F. Saenko (1972, 1987):

Grade I - mild (observed with blood loss not exceeding 20% of the circulating blood volume, which corresponds to up to 1000 ml adjusted for a patient weight of 70 kg). The patient's general condition is satisfactory or of moderate severity; pallor, diaphoresis, clear consciousness, rapid breathing, diminished Reflexes, and oliguria are noted. Blood pressure is 90-100/60 mmHg; pulse is up to 100 beats per minute.

Grade II - moderate (observed with blood loss ranging from 20 to 30% of the circulating blood volume, which corresponds to 1000 to 1500 ml adjusted for a patient weight of 70 kg). The patient's general condition is of moderate severity, the patient is lethargic, and pronounced pallor and profuse diaphoresis are noted. Breathing is shallow, with an increased respiratory rate, and significant oliguria may occur. Blood pressure is 80-90/50 mmHg, pulse is 120 - 130 beats per minute, weak.

Grade III - severe (observed with blood loss exceeding 30% of the circulating blood volume, which corresponds to more than 1500 ml adjusted for a patient weight of 70 kg). The patient's general condition is severe or extremely grave, with pronounced pallor, sometimes with a cyanotic tinge, and profuse diaphoresis. Consciousness may be absent, or a significant decrease in respiratory responses and general lethargy are noted. Breathing becomes rapid and shallow, body Temperature decreases, and oliguria progresses to anuria. Blood pressure is 60-70/50 mmHg or lower, pulse is thready, exceeding 130 beats per minute.