Shock

Thanks to Dr. Ian Daniel for this review of shock...

In the setting of trauma, shock is a very important consideration. As many of our patients arrive to the trauma unit in extremis, it is very important to be aware and knowledgeable about the different types of shock and our established treatment algorithms.

Shock can be divided into 5 broad categories

1.   Hypovolemic shock

2.   Septic Shock

3.   Cardiogenic Shock

4.   Neurogenic Shock

5.   Anaphylactic Shock

In the trauma unit, the first four need to be understood in order to efficiently and safely care for patients. This review will discuss these types of shock and algorithms for treatment.

1.   Hypovolemic shock

a.    Hemorrhagic

b.   Non-Hemorrhagic (3^rd spacing)

Hemorrhagic hypovolemic shock has been studied extensively. There are 4 classes of hemorrhagic shock.

Class I: 500-700ml blood loss (10-15% blood volume in a 70kg person). Results in minimal tachycardia, otherwise asymptomatic.

Class II: 750-1500 ml (20-30% loss). Tachycardia, narrow pulse pressure, decreased capillary refill, anxiety

Class III: 1500-2000ml (30-40% loss). Hypotension, tachycardia, oliguria, pallor, diaphoresis, confusion

Class IV: >2000ml (>40% loss). Hemodynamic instability, inadequate end-organ perfusion

The hemodynamic changes that accompany hypovolemic shock are unique. As the body attempts to accommodate the loss of volume, peripheral vessels constrict, preserving blood flow for the heart and brain. This results in increased Systemic Vascular resistance (SVR). In addition Venous Oxygen Saturation (SvO2) decreases as the remaining blood volume is delivered to oxygen starved tissues. It goes without saying that Cardiac Output (CO) and Central Venous Pressure (CVP) are decreased as there is a decreased volume of blood available for return to, or departure from, the heart.

2.   Septic Shock

Defined as a systemic inflammatory response to infection associated with hypotension, these patients are encountered usually after initial presentation. Many patients in the ICU have sustained injuries that make them particularly susceptible to infection and the possibility of septic shock

Hemodynamically, septic shock can be divided into early and late stages.

A.   Early stage -  characterized by peripheral vasodilation (decreased SVR and increased SvO2), warm extremities and increased cardiac output (CO). CVP is variable in these patients

B.   Late stage - characterized by impaired myocardial contractility (decreased CO), poor peripheral perfusion, vasoconstriction (increased SVR), oliguria, and hypotension. Again CVP is an unreliable marker, as is SvO2 in late stage septic shock

3.   Cardiogenic Shock

Decreased cardiac output despite adequate intravascular volume. The primary problem is the heart itself (whether it be muscle, the conduction system or valves). In the trauma setting blunt cardiac injury (BCI) and tension pneumothorax are significant concerns. However, cardiogenic shock can also be seen in pulmonary embolus, myocardial infarction or pulmonary hypertension. Classic physical findings include cardiac tamponade, Beck’s triad (decreased arterial BP, jugular venous distension, muffled heart sounds). CVP is usually normal or increased in these individuals, CO is decreased, SVR is increased in an effort to preserve blood flow for the heart and brain and SvO2 is decreased as the circulating volume is stripped of its oxygen by starved tissues.

4.   Neurogenic Shock

Inability of the CNS to provide adequate PVR resulting in inadequate end-organ perfusion. Classic findings are warm, flushed extremities, paraplegia, confusion, oligueia, hypotension. Typically, SVR is decreased in these patients, SvO2 is decreased as well, as is CVP and CO.

The table below summarizes the above information and serves as a basis for treatment as will be discussed next

TREATMENT

Treatment of shock has changed significantly over the last 15 years as goal-directed studies have shifted existing paradigms in both the surgical and medical worlds. Resuscitation from shock, especially hypovolemic and septic shock (the most commonly seen in the trauma unit) revolve around judicious administration of fluids.

As the above table depicts, shock is initially treated with fluid if the CVP is less than 12. The decision between crystalloid and colloid is outside the scope of this discussion. If the patients vital signs stabilize, then continued monitoring is prudent.

However, if the patients CVP reaches 12 and the patient is still unstable (or starts with a CVP> 12 and is unstable) then other monitoring modalities may be employed.

In the trauma unit in the acute setting, it is not feasible to perform a pulmonary artery catheter to calculate cardiac index or wedge pressure or echo every unstable patient with a CVP > 12 as suggested in the algorithm. As a result, the mean arterial pressure (MAP: calculated as diastolic pressure + 1/3 pulse pressure) is used extensively. For patients with MAP > 60 and CVP > 12 but still hemodynamically unstable, an inotrope (usually dobutamine) should be considered. For patients with CVP>12 with MAP < 60, a vasopressor should be considered.

In essence, the algorithm breaks down into 3 basic tenets:

1.   If the tank is empty (CVP<12), fill it (administer fluids)

2.   Squeeze the peripheral vessels if the MAP <60 (peripheral vasopressors)

3.   Bolster the function of the heart if MAP > 60 with low cardiac index (positive inotropes)

This algorithm should serve simply as a guideline to treat your patient. As always, diligent monitoring and individualized care for the specific needs of each patient are paramount.