Chapter 2 Shock is the commonest indication for ICU admission of the surgical patient. It is therefore essential that the intensivist has a clear understanding of the definition, pathophysiology, classification, and principles of management of shock in order to guide therapy. In this chapter, these topics will be presented with a major surgical focus. Although shock has been defined differently by many clinicians and physiologists, the underlying abnormality and its sequelae arise from decreased tissue perfusion. Shock may be defined, therefore as a generalized state of cellular hypoperfusion. Tissue perfusion is responsible for the delivery of oxygen and other substrates to the cells. Decrease in this perfusion therefore leads to cellular hypoxia, anaerobic metabolism, activation of a myriad of systemic responses including initiation of an inflammatory process, endocrine, microvascular, hemodynamic, and organ dysfunction resulting in eventual death if left unabated. Although shock may be categorized in many ways the most commonly used classification is based on the mechanism responsible for the hypoperfused state as this mechanism affects the pumping function of the heart, circulating volume and the state of the conduits transporting the blood volume i.e., the blood vessels. Shock may thus be classified as: (a)Hypovolemic: Related to inadequate circulating volume as seen in blood loss. (b)Obstructive: Due to extracardiac obstruction to blood flow e.g., cardiac tamponade. (c)Cardiogenic: Due to pump failure secondary to decreased myocardial contractility, dysrhythmia, etc. (d)Distributive: Due to maldistribution of blood flow and volume e.g., septic or neurogenic. Conceptually, decreased tissue perfusion may be considered to arise from abnormality in one or all of the determinants of cardiac output or blood flow viz blood volume (preload), cardiac contractility or systemic vascular resistance (afterload). Cardiac output or blood flow is the product of stroke volume and heart rate. As preload decreases such as in hypovolemia the stroke volume decreases because of the decreased ventricular volume and stretch of the myocardial muscle (Starling’s Law). Cardiac output is then maintained by an increase in heart rate. This compensatory response is limited by the maximum heart rate attainable and the limitation of stroke volume as heart rate increases limiting time for cardiac filling. Systemic blood pressure which is the product of cardiac output and systemic vascular resistance (determined by the tone of the peripheral vasculature) is maintained and may even be elevated in early hypovolemic states due to the increase in peripheral vascular resistance secondary to the vasoconstrictive effect of catecholamine release. This blood pressure is however maintained at the expense of a decrease in systemic blood flow to the tissues. Decreased circulating blood volume is the sine qua non of hypovolemic shock and although it may arise from loss of fluids from third spacing, as in ileus, peritonitis, bowel obstruction, burns, other gastrointestinal disorders and pancreatitis, the commonest cause in the surgical patient is hemorrhage. The prime goal then is to identify the source of hemorrhage, stop it, and replace the volume loss. The source is identified by external examination (extrinsic source) when control is affected by direct pressure or in some instances the application of tourniquets. Internal sources are identified by a systematic assessment of the chest (by physical examination and chest X-ray, occasionally a chest tube insertion); abdominal examination including ultrasound; Pelvic X-ray with examination and assessment of the retroperitoneum (the extremities are included in the search for an external or extrinsic source). When the source of the bleeding is in the abdomen, chest, pelvis or retroperitoneum surgical intervention is frequently required (see chapters on chest trauma, abdominal trauma and pelvic and extremity injuries). Initially, volume replacement is by crystalloid but when major blood loss is obvious or anticipated massive transfusion protocol is initiated which includes early red blood cell, plasma, platelets, cryoprecipitate, and fibrinogen infusion (see chapter on massive transfusion). The underlying mechanism is mechanical obstruction to cardiac output resulting in decreased tissue perfusion. Cardiac tamponade, tension pneumothorax massive pulmonary thromboembolus, air embolism are causes of this type of shock and are described elsewhere in the text. This results from primary pump failure which may be secondary to myocardial infarction, dysrhythmias, cardiomyopathy, ventricular outflow obstruction (aortic dissection or valvular stenosis), ventricular septal defect, etc. In the absence of a surgically correctable lesion which should be sought, treatment is guided by response to volume infusion, inotropes and vasoactive drugs to modify cardiac contractility, afterload and preload as described below. This type of shock is usually ascribed to a septic etiology but many other entities (spinal cord injury, anaphylaxis, and liver dysfunction) may manifest signs of distributive shock in which there are the following signs: decreased systemic vascular resistance, normal to low cardiac filling pressures and increased cardiac output. In spite of increased cardiac output, signs of diminished oxygen extraction are present and many theories have been put forward to explain this including the notion that in early septic shock there is cellular inability to utilize oxygen in face of supernormal to normal oxygen delivery which may be related to an effect of endotoxin on the cells. Depression of myocardial contractility has also been demonstrated in these patients frequently ascribed to the endotoxin as well. Neurogenic shock, another form of distributive shock is described elsewhere in this text. In this conundrum, it is important to utilize parameters of endpoints of resuscitation to guide therapy as described below. In septic shock, however, the main goals are to identify the septic focus, administer specific antimicrobial therapy, and eradicate the septic focus which frequently requires surgical or image guided drainage while managing the hypoperfused state. Recognizing the responses to the shock state is not only important in diagnosing its presence but also its response to treatment. Reversal of the parameters manifested in the shock state is a sign of effectiveness of treatment measures. Baro and chemo receptors in response to the shock state stimulate activation of the hypothalamic — pituitary — adrenal axis resulting in release of catecholamines. The effects of the released catecholamine are many, including: Tachycardia maintains cardiac output which is the product of stroke volume and heart rate. The increased heart rate compensates temporarily to maintain cardiac output in spite of the decreased preload, but there is a point of diminishing return when the heart rate is so high that the decreased cardiac filling time decreases stroke volume and cardiac output. Volume loading to increase preload should be instituted early in hypovolemic states in order to reverse this process. Vasoconstriction maintains blood pressure by increasing peripheral vascular resistance, blood pressure being the product of stroke volume and peripheral vascular resistance. Note that blood pressure is maintained at the expense of hypoperfusion resulting from the vasoconstriction, so that hypotension is a late sign of hypovolemic shock. Both pre and post capillary sphincters initially constrict decreasing capillary hydrostatic pressure with movement of fluid into the capillaries (plasma refill). Later, under acidotic conditions the pre capillary sphincters relax but the post capillary sphincters remain constricted leading to pooling in the capillaries and “stagnant” circulation. Cold clammy extremities with pallor and decreased capillary refill are due to the vasoconstriction and stimulation of secretory glands at the base of hair follicles. Regional differences in perfusion are because of differences in vasoreactivity in vascular beds — vascular beds such as cardiac and cerebral preferentially perfused versus splanchnic, skin and muscle with relative decreased perfusion. ADH and aldosterone release preserves sodium and water, maintaining vascular volume. Anaerobic metabolism leads to lactic acidosis with compensatory hyperventilation. Optimum pH for cellular enzyme function is disrupted with cellular dysfunction. Lower ATP generation under anaerobic conditions leads to lower energy availability for cellular function. Energy requiring mechanism such as the ‘sodium pump’ for maintaining higher sodium to potassium ratio extracellularly is disrupted leading to movement of sodium (with water) intracellularly with cellular edema, further diminishing extracellular circulating volume exacerbating the hypovolemic state and hyperkalemia. Intracellular lysozymes are released and auto digest cells leading to cell death, tissue death, organ death, and finally organism death unless the cycle is broken by therapeutic intervention.
Shock: Cardiovascular Dynamics, Endpoints of Resuscitation, Monitoring, and Management
Jameel Ali
Chapter Overview
Definition of Shock
Classification of Shock
Hypovolemic shock
Obstructive shock
Cardiogenic shock
Distributive shock
Responses to the Shock State
Endocrine and catecholamine release
Anaerobic metabolism
Reperfusion Injury
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