Shock

SHOCK
  • Shock is inadequate cellular respiration due to inadequate tissue perfusion, due to any number of causes It is defined as oxygen delivery to the tissue that is insufficient to meet tissue requirements. This may be due to altered hemodynamics, such that the circulatory system is unable to provide adequate pressure to drive perfusion. Or, shock can occur when tissues are receiving adequate flow, but there is either not enough oxygen in the blood or the tissues are unable to extract and utilize the oxygen.

 

  • Shock is a syndrome of clinical signs that has multiple underlying causes.
  • Classically, the signs that indicate the shock state are:
    • Tachycardia (although bradycardia often occurs in cats)
    • Tachypnea
    • Pale mucous membranes
    • Cold extremities
    • Poor peripheral pulses
    • Altered mentation

Brief Pathophysiology

  • Shock is genearlly associated with a decrease in cardiac output, venous return, and arterial blood pressure (sepsis is an important exception to this rule).
  • The decrease in CO and MABP may lead to a self-perpetuating cycle and downward spiral. The ¯ CO and ¯ MABP stimulate the sympathetics, baroreceptors, and the renin-angiotensin system in an attempt to restore MABP.
  • Stimulation of these systems results in an ­ heart rate and intense vasoconstriction. The result of the vasoconstriction and ¯ MABP is ¯ capillary perfusion resulting in deterioration of the microcirculation, stasis of blood, endothelial damage, capillary permeability, development of microthrombi, and disseminated intravascular coagulation. The resultant tissue ischemia results in cellular hypoxia and anaerobic metabolism.
  • Anaerobic metabolism is energy inefficient (94% energy loss) and associated with a lactic acidosis, metabolic acidosis, ¯ cell function, and tissue autolysis. All of these results tend to further depress cardiac output and blood pressure, thus worsening the shock cycle.
  • The clinically observed effects of vasoconstriction are:
  • Decreased blood flow to skin causes cold skin temperature
  • Decreased blood flow to splanchnic vasculature leads to GI hypermotility, followed by stasis and mucosal necrosis ® bacterial proliferation, absorption of bacteria, toxins, etc., and septic shock
  • Decreased renal blood flow results in decreased urine output, renal ischemia, tubular necrosis
  • Decreased blood flow to liver (hepatic artery, portal vein) leads to anaerobic metabolism and the resultant clostridia, toxins
  • Decreased blood flow to pancreas results in MDF
  • Initially, peripheral vascular beds will vasoconstrict to shunt flow to the "essential organs" (brain and heart). This results in reduced perfusion and oxygen delivery to the affected vascular beds.
  • In the dog, the GI tract is considered the shock organ since it takes the brunt of vasoconstriction. Unless shock is rapidly reversed, tissue beds enter an anaerobic state.
  • The products of cellular metabolism build up in tissues, including lactate, acids, nitric oxide, CO2 and adenosine. As ATP stores decrease, membrane pumps are unable to maintain electrochemical gradients, leading to cellular edema.
  • Over time, cellular death will occur, resulting in cell lysis, inflammation, free radical formation and local activation of coagulation. As the by-products of cellular metabolism continue to accumulate, these local factors can eventually overwhelm the vasoconstriction induced by the sympathetic nervous system. This results in vasodilation, systemic hypotension, decompensate, and entry of metabolic byproducts, cytokines, free radical and activated white blood cells into systemic circulation.
  • Many compensatory mechanisms are induced in the shock state. The goals of the compensatory mechanisms are to maintain perfusion to the core organs and restore vascular volume. These include:
    • Mobilization of fluid from the interstitial to intravascular space. This occurs primarily in shock states with low blood volume, especially hypovolemic shock, but can potentially occur in all shock states.
    • Activation of the sympathetic nervous system (SNS). This results in release of norepinephrine and epinephrine. There are many effects of the SNS, including tachycardia, vasoconstriction which may preferentially affect certain tissue beds, and positive inotropy. Activation of the SNS also results in retention of sodium (and therefore water) by the kidneys.
    • Activation of the renin-angiotensin-aldosterone system (RAAS). This results in multiple effects, the most important (and immediate) of which are retention of sodium and water by the kidneys, and peripheral vasoconstriction.
    • Release of Antidiuretic hormone (ADH). This results in retention of water and urine concentration. ADH is also a powerful vasoconstrictor.

Stages of shock

  • The earliest stage of shock is the compensated phase. During this period of time, compensatory mechanisms are able to maintain blood flow to the important organs through peripheral vasoconstriction. Clinical signs are the "classic" signs of shock, and include pale mucous membranes, poor pulse quality and cold extremities secondary to vasoconstriction. Tachycardia is a result of SNS activation, as the body tries to maintain cardiac output. Blood pressure is usually normal to high as a result of vasoconstriction. Remember that the overall goal of compensation is to maintain blood pressure, and a normal blood pressure does NOT mean that perfusion is normal.
  • Over time, the body is either able to "fix" the blood volume and return to normal homeostasis, or it goes into decompensated shock. This phase occurs when local tissue beds that were vasoconstricted begin to vasodilate. Vasodilation leads to pooling of blood and maldistribution of flow to "non-essential" organs. Clinical signs include grey mucous membranes, bradycardia, loss of vasomotor tone leading to hypotension, and severely altered mentation. The patient is often stuporous to comatose. Ventricular arrhythmias can be seen on an ECG. It is important to realize that the progression from compensated to decompensated shock can occur over minutes to hours depending on the cause and severity of injury, and that patients can present anywhere along this spectrum.
  • Cats present a special challenge since they do not always display the classic signs of shock like dogs do. The shocky cat often presents with bradycardia, hypothermia and hypotension, even in the early stages of shock. The causes for this are unknown, although it is documented that cats have species specific alterations in vascular tone and in vascular response to injury.
  • Treatment of the decompensated shock patient may result in resolution of clinical signs of shock, but the patient may decompensate again soon after resuscitation. This is the result of inflammatory mediators and free radicals being flushed back into systemic circulation, setting up DIC and the systemic inflammatory response syndrome, and eventually multi-organ dysfunction. In short, there was simply too much tissue damage to fix despite appropriate shock therapy.

Last modified: Monday, 28 May 2012, 6:44 AM