A few weeks ago, I heard an interview on National Public Radio with the editor of a book of synonyms. To hear him talk, the book has wondrous utility. Imagine spending an evening sitting by the fire, with your dog at your feet, reading a copy of the Dictionary of Synonyms to your adoring family ("Gee, Daddy, how many other words are there for "gross"?). I started to think about looking up "shock" in that dictionary because surely we have enough words for shock states to fill a chapter.
The number of terms I use to describe shock in prehospital care has diminished considerably since I attended a lecture some years ago by Dr. Max Harry Weil, a world-renowned specialist in critical care. There, I learned a new classification of shock states that's so simple, it s stunning.
From the standpoint of pathophysiology, shock is a state of inadequate tissue perfusion. Oxygen, glucose and other nutrients don't reach the cells, and metabolic wastes are not removed from body tissues. Fluids in the vascular space transport these substances to and from the cells; when the bloodstream can t reach the target cells, this perfusion fails.
Weil s new system for classifying shock states is rooted in the reasons that intravascular fluids don't reach the tissues. Briefly stated, those reasons are:
- A failure to move fluids (pump failure);
- A blockage in their path;
- A loss of fluid quantity or volume; and
- A movement of fluids to another body space.
All the "named" shock states (cardiogenic, anaphylactic, spinal, septic, etc.) fit into one of these categories.
We re most familiar with shock caused by a loss of fluids. Hypovolemic shock includes blood loss from trauma or gastrointestinal bleeding and fluid deficits from vomiting, diarrhea or hyperthermia. The prehospital treatment is fluid replacement. (Controversy exists regarding the amount of fluids required by the patient with an active bleed, but this is a matter of degree rather than a fluids/no fluids proposition.) Normal saline is my fluid of choice for all shock states. An isotonic fluid, saline stays within the intravascular space and doesn t promote extravascular fluid shifts. These patients have little need for glucose replacement, and (in theory) giving Ringer s lactate solution to a patient with decreased liver blood flow may result in a buildup of lactic acid and critical metabolic acidosis.
Obstructive shock is caused by fluid blockage. Blood clots within vessels (such as pulmonary emboli) or compression of vascular structures from tumors, circumferential burns or external forces may obstruct flow. The situation is similar to putting your thumb over the nozzle of a hose; if the water s destination was your backyard garden, your thumb effectively blocks delivery of liquid to the ground. Vascular obstructions block fluid, oxygen and nutrient delivery to body tissues in a similar way. In the garden, you can overcome the obstruction (your thumb) by turning up the water pressure, overcoming the pressure exerted by your thumb and "blasting" the obstruction clear. In the body, this means pushing more fluids into the system, raising systemic intravascular pressures in an effort to either dislodge the clot or to maximize use of alternate vessels supplying the same body region to bypass this obstruction.
Body fluids are traditionally distributed within the intravascular, extracellular and intracellular space. Distributive shock results from decreased tissue perfusion because of an alteration in the usual balance of fluids within these spaces without external fluid loss. In patients with sepsis, fluids leak out of the vasculature through capillary walls into surrounding tissues; with spinal cord injury, reflex vasodilation means fluids gather in pools within the veins and blood pressure falls. In both cases, effective intravascular circulation is diminished, and shock is the clinical result. Optimal therapy is once again the aggressive use of IV fluids to "fill up the tank" and compensate for loss of volume to other sites.
I ve saved the most interesting concept for last. Fluids don't move within the body, unless the heart is working to push them along. Patients with cardiogenic shock (we ll still use this term) may have pump failure from myocardial infarction (MI), valvular disease or congestive heart failure (CHF). Regardless of cause, intravascular fluids back up into the lungs and pulmonary edema ensues. Standard prehospital care for these patients includes diuretics (furosemide) to dispel excess fluid, vasodilators (nitroglycerin) to decrease the workload of the heart and vasopressors (dopamine) to support the blood pressure, if truly low.
If you give some thought to the use of dopamine, questions arise. If the heart is working hard to get rid of fluids, and you induce a generalized peripheral vasoconstriction with dopamine, doesn t the heart have to work harder (increased afterload), increasing myocardial oxygen demand? And won t venous return to the heart (preload) increase, so the heart is presented with more fluid, magnifying the chance of further fluid buildup in the lungs? Because of these concerns, in this situation some now use dobutamine, which selectively enhances cardiac contractility.
Paradoxically, some feel this increased fluid presentation to the heart may actually be one way in which dopamine improves cardiac output. The reason goes all the way back to the Frank-Starling Law of the Heart (yeah, sure you remember). The law states that as the size of the heart increases, cardiac output will also increase as a result of increased opportunities for interaction between actin and myosin molecules within the myocardial cells. You ll recall that these molecules lay side by side within the cardiac cell, and the cell contracts because of a "ratchet" effect between these filaments. When the heart is small, the overlap is great, and there is not a lot of room available for the ratchet mechanism to work. As the heart expands in size, the cells and filaments stretch, and there is more space to allow the ratchet to do its work, and increased connections between actin and myosin increase myocardial contractility, and the force of contraction grows. This effect persists until the heart grows so large that the stretching myocardial cells separate the molecules, decreasing opportunities for filament interaction and contractility. But given a "small" heart, increased venous return resulting in increased intracardiac fluid volumes may stretch the myocardial cell, enhancing cardiac function.
In the prehospital setting, we can never be sure if a patient has an enlarged heart (certainly we can look for other signs of CHF, but diagnosis requires an X-ray). But even patients with CHF may be relatively dehydrated within the intravascular space. As intravascular pressure rises with fluid buildup (and it s this pressure that causes fluid to leak into extravascular tissues, such as the feet and legs), the kidneys react with a diuresis in an attempt to normalize pressure. As a result, intravascular fluid losses are worsened.
The logical conclusion of this theory is to treat cardiogenic shock with fluids, 250 500 cc of normal saline, and watch for an effect. In a sense, this is not really new advice. ACLS has advised administering fluids as a first-line measure for post-arrest hypotension for many years, but it seldom teaches the physiological reason for it. If the fluid bolus works, and the patient improves, give more fluids.
I ve found that classifying shock as hypovolemic, obstructive, distributive or cardiogenic makes it much easier to conceptualize these patients. More importantly, this system truly simplifies their management: fluids, fluids and more fluids. I hope you find it useful as well.