Veterinary Clinical Medicine-I (General and Systemic)

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.