Shock

Shock = Inadequate perfusion. 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:

Volemic
Distributive
Cardiogenic - nonobstructive and obstructive
Mixed (a combination of two or all of the above)

Ths goal of resuscitation for patients in shock is to regain adequate perfusion and maintain adequate oxygen delivery.

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 patients circulating volume to be re-established and logistics of an intervention to be arranged.

Classifications of Hemorrhagic Shock:

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

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 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.

There is no 'gold standard' measurement of resuscitation!!!!

Some centers check lactate or base deficits... These may reflect a volume deficit, however elevated numbers might also be signalling a loss of tissue 'somewhere' (e.g. in a tight fascial compartment)

Trend urine output with a goal to normalize within the first 6 hours. However, if the patient has started progressing into acute renal failure, decreased urine output may be because the kidneys no longer are functioning as the should and not because the vascular space is volume down!

If patients have been placed on pressors to maintain perfusion during the early phases of resuscitation, weaning off of the pressors should happen in concert with 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. One exception to this rule of pressors is in neurologic injury, where low dose pressors may be necessary to maintain goal mean arterial pressures (MAP).

Signs of adequate volume status:

UOP > .5 cc/kg/hr and normal Cr (& no concern for diabetes insipidus / hyperosmolar diuresis)
Minimally compressible or non-compressible transhepatic IVC throughout respiratory cycle on ultrasound
Adequate filling of right heart on ECHO
MAP > 65 mmHg off all pressors
CVP – PEEP > 5 mmHg
Corrected lactate over 2 successive measurements within first 6 hours of presentation
Correction of metabolic acidosis (i.e. normalizing base deficit)

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.

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.

Common Types of Distributive Shock

Sepsis (mixed, with prominent distributive role)
Systemic Inflammatory Response Syndrome SIRS (mixed, with prominent distributive role)
Neurogenic
Anaphylactic
Adrenal
Pharmacologic

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 of 65 mmHg.

First line agents for types of distributive shock:

Sepsis & SIRS: Norepinephrine
- Surviving Sepsis Guidelines
Neurogenic: Norepinephrine
Anaphylaxis: Epinephrine
Adrenal: Hydrocortisone
Pharmacologic: Phenylephrine or Norepinephrine

Cardiogenic shock is from pathologic states intrisic to the heart anatomy and it's physiology

Myocardial Infarction
Valvular dysfunction
Septal / ventricular injuries
Arrythmias

Whereas Obstructive Cardiogenic Shock relates to factors that are external to the heart yet affect it's performance (e.g. decreases preload, increases afterload)

Tension pneumothorax
Pericardial tamponade
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.