Overview of Shock, Diagnosis and Management of Hypovolemic Shock

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Shock state

Shock is defined as a pathological state of tissue hypoperfusion and cellular hypoxia characterized by insufficient supply of oxygen and other metabolic substrates essential for cellular integrity and the proper functioning of vital organs.

Types of shock

The pathophysiological shock is classified as:

  1. Hypovolemic: It is triggered by the decrease in vascular content, either by losses or by accumulation of fluid in the third space.
  2. Cardiogenic: It is characterized by primary or intrinsic myocardial dysfunction with the consequence that the heart can not maintain an adequate cardiac output..
  3. Obstructive: It is a consequence of secondary or extrinsic heart failure.
  4. Vasogenic or distributive: It is caused by excessive vasodilation and impaired distribution of blood flow (for example, a direct arteriovenous shunt), and is characterized by a decrease in resistance or increased venous capacity of vasomotor dysfunction.

Evolution stages:

The initial step of managing the shock is to recognize its presence, therefore, identifying it in the early phases is essential for the treatment avoiding complications, the stages to be identified are:

  1. Stage I or compensated shock: In this phase the patient has lost less than 25% of the circulating volume and compensation mechanisms are activated trying to maintain an adequate systemic perfusion resulting in an adequate delivery of oxygen and nutrients while maintaining adequate blood pressure. therefore the clinical manifestations are scarce, being the treatment in this stage effective.
  2. Stage II or decompensated shock: The patient has lost more than 25-30% of the circulating volume that due to lack and energetic wear of the same compensatory mechanisms begin to fail these. It is characterized by the development of neurological and cardiac manifestations, due to the fact that the systemic resistance falls and the hypotension stage begins.
  3. Stage III or irreversible shock: In this phase the mechanisms have mostly failed mainly due to hypoxia and the metabolic imbalance presents multi-organ failure and cell death caused by prolonged hypoxia.

Hypovolemic shock

As already mentioned, hypovolemic shock is defined as the acute decrease in intravascular volume caused by two main etiologies:

1. Oligaemia: (insufficient blood): Bleeding is the main cause of shock in a trauma patient.

  • Traumatic
  • Hemothorax
  • Visceral injury
  • Long bones or pelvis fractures
  • Injury in large vessels

2. No Oligohemetics:

  • Burns
  • Vomiting
  • Diarrhea
  • Diuretics

Pathophysiology

For the pathophysiology, evolution stages must be taken into account.

It begins with the release of endogenous catecholamines increasing the peripheral resistance that maintains the venous return to a certain point.

Stage I: In this stage, the heart to maintain an adequate perfusion with respect to the beat volume increases its frequency per minute. As well as the systemic resistances are maintained. The organism in its eagerness to maintain an adequate perfusion to essential organs (brain, heart and kidney), removes the volume of the splanchnic, dermal and mesenteric beds to support the other essential tissues. There are reports that at this stage hypertension can be found as a compensatory mechanism.

Stage II: The heart continues with increased work to try to maintain the delivery of oxygen and missing nutrients. The respiratory apparatus also increases its respiratory work to increase the supply of oxygen denied to tissues. Hypoxia is increased in organs such as the intestine and kidney.

Stage III: At the cellular level, inadequately perfused and oxygenated cells change anaerobic metabolism for the production of energy, but that leads to the formation of lactic acid and development of metabolic acidosis that triggers cell death. Hypoxia and metabolic imbalance have caused multiple damages to different organs, triggering a cascade of complications derived from a single initial thing: the lack of delivery of oxygen and nutrients causing among the most important complications such as:

  1. Failure of compensation mechanisms.
  2. Bradycardia, secondary to myocardial hypoxia that generates myocardial depressant factor.
  3. Acute renal failure.
  4. Severe metabolic acidosis.
  5. Brain damage due to hypoxia.

That will generally cause the death of the patient in the short term.

Clinical Manifestations and Diagnostic Criteria

The clinical manifestations are presented according to the state of shock in which it is found, among them we find:

Hyperperfusion Indicators:

  • Hypotension occurs when more than 30% of the blood volume has been lost
  • Tachycardia
  • Oliguria
  • Slowed capillary filling
  • Sensory alteration
  • Elevated blood lactate
  • O2 saturation in mixed mixed venous blood

The patient in advanced stages presents paleness, hypothermia, profuse sweating, tachypnea, presenting a rapid and filiform pulse.

The empirically accepted diagnostic criteria for shock are the following:

  • Heart rate> 100 beats / min
  • Respiratory frequency> 22 breaths / min
  • Diuresis
  • Hypotension of more than 20 minutes of duration of 90/65
  • Hyperlacatemia> 1.5

In addition, there are increased baseline deficits, coagulopathy due to consumption, decreased hemoglobin and increased azoate levels

Staging according to the clinic

The classification of the hemorrhagic shock according to the Advanced Trauma Life Support (ATLS) classifies it according to the blood loss and thus be able to handle the appropriate treatment.

Class I

Mild

Class II

Moderate

Class III

Severe

Class IV

Massive

Blood loss(mL)

<750

750-1,500

1,500-2,000

>2,000

Loss of circulating volume (%)

15

15-30

30-40

>40

HR (lpm)

<100

>100

>120

>40

SBP (mmHg)

Normal

Normal

Decreased

Decreased

capillary refill

Normal

Slow

Slow

Slow

BR

14-20

20-30

30-40

>40

Urinary output

>30

20-30

5-15

Despreciable

Estado de conciencia

Mild

anxiety

Median

anxiety

Confusion

Lethargy

Note: If a patient with risk factors of shock and has a BP of 120/80 should investigate the other clinical data as this begins to decline in stage III when you lose 30% volume.

Shock Index

Isolated vital signs (eg, heart rate or systolic blood pressure) have been shown to be unreliable in the evaluation of hypovolemic shock. By contrast, the Shock Index (SI), which is defined as the ratio of heart rate to systolic blood pressure, has been proposed to improve the risk of stratifying patients for higher transfusion requirements and early mortality.

Shock index = HR/SBP

Normal

Mild shock

Moderate shock

Severe Shock

<0.6

0.6-1.0

1.0-1.4

>1.4

The shock rate upon arrival at the emergency department can be considered a clinical indicator of hypovolemic shock with respect to transfusion requirements, haemostatic resuscitation and mortality.

Treatment

The diagnosis and treatment of shock must be carried out simultaneously

  1. General measures
  • Placement of patient in supine position in Trendelemburg position
  • Channeling of one and ideally two peripheral venous routes
  • Continuous monitoring of the BP, rhythm and heart rate
  • Continuous monitoring of O2Sa
  • Bladder catheter for diuresis measurement
  • Hourly measurement of Central Venous Pressure

b. Resuscitator treatment:

Simultaneously with the general measures, the resuscitation treatment is initiated, aimed at correcting the hemodynamic deterioration,

  • Respiratory support: Maintain a permeable airway and adequate ventilation SaO must be> 90%
  • Circulation: Control of evident hemorrhages, establishment of venous access and replacement of fluids.

REPLACEMENT OF LIQUIDS:

The reintroduction of oxygen and liquid triggers a complex chain of processes that leads to tissue injury. The tissue injury seems to be secondary to the massive production of free radicals, which exceed the antioxidant capacity of the cell. During reperfusion the cell introduces large amounts of Ca. This loss of balance of calcium metabolism triggers a series of destructive cellular processes, activating phospholipases, proteases and mitochondrial dysfunction.

Therefore, to avoid this imbalance that can be created at the time of initiating hemodynamic management, the American Hearth Association has recommended the administration of rapid charges of crystalloids at 20 cc Kg. Dose in 20 minutes.

Hartman solution:

  1. Corrects acidosis (by the transformation of lactate).
  2. Maintains a balance between the intravascular and interstitial space.
  3. Electrolytes are administered.
  4. Expand the volume.

0.9% physiological solution the only advantage it can offer us over the Hartman is that it expands the volume much better. But it does not improve the acid base and electrolyte imbalance at the same time that hemodynamic resuscitation has started. Another disadvantage is that it can occur in the administration of large amounts of hyperchloremic acidosis

Ringer solution: It is a hydroelectrolytic solution in which part of the sodium of the isotonic saline solution is replaced by Calcium and Potassium, its main indication lies in the replacement of hydroelectrolytic losses with depletion of the extravascular space.

Lactate Ringer Solution: It has a buffer effect since it is first transformed into pyruvate and then into bicarbonate during the metabolism

According to the classification of the ATLS the shock will be handled as follows:

Initially, 1-2 liters of saline should be administered at a rapid drip; The subsequent infusion will depend on the degree of response and the characteristics of the patient.

  • Class I and II hypovolemic shock: Resuscitate with isotonic crystalloid solutions using the 3: 1 rule (300 mL of crystalloids per 100 mL of lost blood) where the volume of replacement crystalloids is equal to three times the calculated blood loss
  • Hypovolemic shock III and IV: Reanimate with crystalloid solutions and initiate blood transfusion, for every 4 units of blood, 1 unit of fresh plasma must be administered, for every 10 units of red blood cells, 5 units of platelets should be administered. Administer 1 gram of calcium for every 5 units of blood. In stage III blood will be administered and in stage IV blood plus blood products should be used

c.Ethological treatment

The same general and resuscitation measures described above are applied, with special emphasis on fluid infusion, and the response is assessed by blood pressure, diuresis and PVC. When hypovolemia is secondary to blood loss and hematocrit is less than 27%, red blood cells or, failing that, whole blood are administered. Bleeding must be stopped or the cause of fluid loss must be treated.

In non-hemorrhagic hypovolemic shock the use of blood is not of great importance, as in burns, so ringer lactate should be used.

Objectives in shock treatment

The goals during the first 6 hours of admission to the emergency room are:

  • Systolic pressure> 90 mmHg
  • Platelets> 5000
  • Temperature> 35 ° C
  • Uresis> 0.5cc / kg / hr
  • Central venous saturation> 70%
  • Lactate
  • Acid-base balance

Bibliography

  • Figueroa A., Diagnóstico y Manejo temprano del choque, boletin AMUP
  • Parra V., Shock Hemorrágico,Revista médica clínica Conder, 2011 May;22(3) 255-264
  • Jiménez L., Montero J., Medicina de urgencias y emergencias guía diagnóstica y protocolo de actuación, 2010, 4ta Edición, Elsevier, 66-87
  • Ramos A., Choque, Manual de terapéutica médica y procedimientos quirúrgicos, 5ta edición, McGraw Hill,, 26-32

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