Prolonged shock may lead to cellular injury, organ dysfunction and potentially death if not corrected in a timely fashion.

 

Causes of shock are multifactorial. Management of shock should be directed towards the underlying pathophysiology. General categories include:

 

o Volemic

o Distributive

o Cardiogenic

o Mixed (a combination of two or all of the above)

 

The goal of resuscitation is to regain adequate perfusion and maintain adequate oxygen delivery.  “Adequate perfusion” cannot be directly measured. We use surrogate markers such as conversion to aerobic metabolism, (e.g. lactate clearance, resolution of acidosis) and measures of end organ function (e.g. urine output, stabilization of blood pressure, improvement in level of consciousness).

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Hypovolemic shock

The goal in management of hypovolemic shock is to restore circulating volume and minimize further

intravascular losses. Patients can have hypovolemia from hemorrhage or from free water losses

(frequently seen with vomiting, diarrhea, severe dehydration and unregulated diuresis).

 

Hemorrhagic shock:

Hemorrhage can be from trauma, gastro-intestinal, gynecologic, vascular sources, or spontaneous

rupture of solid organs / tumors. Replacement of volume should be primarily with blood and blood

products. Timely control of the bleeding source is paramount with either surgery or interventional

radiology. In the instance of traumatic injury, where the source of bleeding is accessible, point pressure

or the application of tourniquets can allow time for the patient’s circulating volume to be re-established

and logistics of an intervention to be arranged.

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Resuscitation of blood products should attempt to match a 1:1:1 ratio. (PRBCs:FFP:Platelets)

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Hypovolemic, non-hemorrhagic shock:

 

Hypovolemia from loss of free water is often a result of infectious disease. Additionally, there are other etiologies such as severe dehydration from inadequate fluid intake, loss of volume from high output fistula / open cavities, or unregulated diuresis from endocrine and renal dysfunction as in advanced diabetes insipidus, severe hypercalcemia or hyperosmolar states (e.g. severe hyperglycemia or overuse of mannitol). Replacement of free water losses should be in the form of balanced crystalloid solutions. Monitoring of electrolytes in these settings is imperative due to shifts that occur between intracellular and intravascular fluid departments.

 

Measurements of resuscitation:

 

Trend lactate clearance with goal to normalize within the first 6 hours. Volume replacement is the first line therapy for hypovolemic shock. The type of fluid given is determined by the type of hypovolemia you are dealing with (see above definitions).

 

Do not use pressor management to maintain persons in hypovolemic shock, consider more fluid. If patients have been placed on pressors to maintain perfusion during the early phases of resuscitation, wean off of the pressors quickly with addition of volume replacement*. This means the patient is not “fully resuscitated” until pressors are off, OR until other endpoints of resuscitation suggesting

adequate volume status have been achieved. If other indices of resuscitation suggest normovolemia** and the patient still exhibits low perfusion, then the patient has a mixed form of shock: hypovolemic combined with distributive, cardiogenic or both. These diagnoses can be evaluated with ECHO & transhepatic IVC ultrasound to determine direction of therapy (i.e. pressors +/- inotropic support).

 

*One exception to this rule of pressor management is neurologic injury, where low dose pressors may be necessary even in a fully volume resuscitated patient to maintain goal mean arterial pressures (MAP).

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**Signs of adequate volume status:

 

o MAP > 65 mmHg off all pressors

o CVP – PEEP > 5 mmHg

o Corrected lactate over 2 successive measurements within first 6 hours of presentation

o Correction of metabolic acidosis (i.e. normalizing base deficit)

o Minimally compressible or non-compressible IVC throughout respiratory cycle on transhepatic

ultrasound

 

If patient does not correct lactate and show signs of normovolemia within the first 6 hours, consider

ongoing blood loss, systemic inflammatory response and / or missed injuries.

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Distributive Shock

Distributive shock is a result of the vasodilation of the vascular smooth muscles. Due to the vast number

of vascular networks involved in maintenance of ‘vasomotor tone’, small amounts of change in overall

diameter of these vascular networks result in a large change in overall volume of the system. Essentially,

‘pooling in periphery’ results, and lack of perfusion to vital organs occurs.

 

Therapy for this form of shock involves a ‘balanced’ resuscitation that includes adequate volume

replacement and judicious use of pressors.

 

First: Use crystalloid / colloid for re-establisment of normovolemia.

 

Second: Use pressors to re-establish vasomotor tone.

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Common Types of Distributive Shock

o Sepsis (mixed, with prominent distributive role)

o Systemic Inflammatory Response Syndrome SIRS (mixed, with prominent distributive role)

o Neurogenic

o Anaphylactic

o Adrenal

o Pharmacologic

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PRESSORS

 

Norepinephrine: peripheral vasoconstriction (alpha adrenergic), cardiac inotrope and coronary

vasodilation (beta adrenergic)

 

Epinephrine: peripheral vasoconstriction (alpha-1 adrenergic), cardiac inotrope (beta-1 adrenergic)

 

Vasopressin: Acts on the V1 receptors of the vascular smooth muscle to cause vasoconstriction (IP3

signal transductions pathway and Rho-kinase pathway).

 

Phenylephrine: peripheral vasoconstriction (alpha-1 adrenergic)

 

Dopamine: Dose dependent mechanism. A precursor to norepinephrine, has positive ionotropic and

chronotropic effects on myocardium (increased heart-rate and contractility).

 

2 – 5 mcg/kg/min = Beta adrenergic effects

> 10 mcg/kg/min = Alpha adrenergic effects

.5 – 2 mcg/kg/min = Dopaminergic effects

 

Once normovolemia is confirmed (see above), use of pressors to maintain MAP at an initial goal of 65 mmHg, once patient’s perfusion status is determined this target MAP may need to be adjusted to optimize perfusion state and minimize overuse of pressor agents.

 

First line agents for types of distributive shock:

o Sepsis & SIRS: Norepinephrine

 

• Surviving Sepsis Guidelines

o Neurogenic: Norepinephrine

o Anaphylaxis: Epinephrine

o Adrenal: Hydrocortisone

o Pharmacologic: Phenylephrine or Norepinephrine

 

Cardiogenic

o Myocardial Infarction

o Valvular dysfunction

o Septal / ventricular injuries

o Arrythmias

 

Obstructive

o Tension pneumothorax

o Pericardial tamponade

o Large (central) pulmonary embolism

 

 

Mixed

Many etiologies of shock have primary and secondary contributing pathophysiologies. Treatment

algorithms to address these ‘mixed’ types of shock are directed at supporting all aspects of the perfusion

dysfunction. An example of this combined strategy is seen in giving volume and using pressors with ionotropic activity in treatment of septic shock.

The lack of perfusion that causes shock can be due to three primary sources or a combination of them.

• Hypovolemic

• Distributive

• Cardiogenic

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There is no form of shock that exists which cannot be traced back to one or more of these categories.

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