ED Evaluation of the Critically Ill Patient
Risk assessment and disposition of the critically ill patient is guided by impression of clinical trajectory as well as presumed diagnosis. While diagnosis is often based on historical information and on physician experience and intuition, the clinical trajectory is dictated by the state of tissue perfusion and the patient’s ability to compensate for physiologic perturbations. For example, a patient with a positive troponin, ST changes, and a mean pressure of 65 mm Hg may be having a simple myocardial infarction, while another patient with similar findings may be in cardiogenic shock. Similarly, low blood pressure (BP) in one patient may result from therapeutic lowering of vascular tone (e.g., heart failure), while the same BP in a different individual may signify distributive shock. Differentiating these possibilities enables appropriate disposition and treatment and is essential to the practice of acute care medicine. This chapter focuses on the pathophysiologic roots of organ dysfunction, and demonstrates how an understanding of these principles permits efficient identification of likely diagnoses, institution of timely therapy, and safe patient disposition. Fluency with these principles also enhances communication with other health care providers.
PATHOPHYSIOLOGY OF SHOCK AND ORGAN DYSFUNCTION
Organ dysfunction arising from critical illness can be traced to abnormalities in either one or both of the following physiologic relationships:
1.The autoregulatory curve describing the relationship between organ blood flow and mean arterial pressure (MAP)1
Evaluating these two key homeostatic relationships—MAP/blood flow and oxygen supply/demand (VO2/DO2)—is essential in any patient exhibiting distress, organ dysfunction, or hemodynamic instability. Failure to do so commonly results in misdiagnosis and delayed recognition of clinical deterioration.5–7
Oxygen consumption or demand (VO2) is determined by physical activity, temperature, and body mass, while oxygen delivery (DO2) is the product of cardiac output (CO) and the content of arterial oxygen (CaO2). CO is in turn the product of stroke volume (SV) and heart rate (HR), while arterial oxygen content is primarily determined by hemoglobin concentration and saturation. The graphic representation of these relationships is presented in Figure 61.1. For both curves, the down-sloping limb on the left indicates a region where the patient is at risk for organ failure. Specifically, in curve A, DO2 below the critical threshold signifies a loss of physiologic reserve and a transition to anaerobic metabolism; in curve B, a MAP below the autoregulatory threshold signifies the inability to maintain a constant blood flow to metabolically active regions with an organ. Appreciating the implication of these curves is essential to understanding the impact of different categories of shock.
Figure 61.1 The key determinants of organ perfusion are depicted. A:The relationship between oxygen consumption (VO2) and delivery (DO2) is indicated. Patients usually function on the rightward side of the curve where an excess of oxygen is supplied relative to demand. As delivery decreases relative to consumption, the patient moves in a leftward direction on the curve. A decrease in central venous oxygen saturation (ScvO2) accompanies leftward movement on the curve. In severe cases where delivery is unable to meet metabolic demands, the patient slips beneath the critical DO2 threshold, where VO2 is limited by delivery. Organ dysfunction and lactic acidosis are regarded as evidence of pathologic oxygen supply. B: The autoregulatory curve describing constancy of organ blood flow over a broad range or pressures is shown. Some patients with chronic hypertension have curves shifted to the right relative to the normotensive curve as shown with the dashed line. For both relationships shown, the flat horizontal portions indicate safe ranges, indicative of adequate organ blood flow and intact homeostatic mechanisms. Movement to the down-sloping portions on the left side of the curves indicates decompensation, placing the patient at risk for organ failure. VO2, oxygen uptake/per minute; CaO2, oxygen content of arterial blood (mainly hemoglobin); CO, cardiac output; MAP, mean arterial pressure; SVR, systemic vascular resistance; DO2, oxygen delivery.
For example, the low MAP typically seen in distributive shock becomes life threatening when vascular resistance is unable to maintain MAP above the autoregulatory threshold. Cardiogenic shock may have borderline or low MAP but is differentiated from a simple myocardial infarction by a loss in CO to levels insufficient to meet tissue oxygen demand. Hemorrhagic shock involves both a loss in hemoglobin content and a related loss in ventricular volume—and hence a loss in CO. In severe hemorrhage, these “two hits” on DO2 can result in huge derangements in oxidative metabolism. The hemodynamic indices associated with the prototypic shock states are displayed in Table 61.1. As will be shown throughout the chapter, detection of abnormalities in either maintenance of MAP or DO2 is followed by further differentiation of these parameters as described in Figure 61.2.
TABLE 61.1 Typical Hemodynamic Changes Associated with Three Accepted Categories of Shock
Arrows show degree of change from baseline in mean arterial pressure (MAP), cardiac output (CO), systemic vascular resistance (SVR), and cardiac preload. Additionally, alterations in the relationship between oxygen delivery and demand (DO2/VO2) and mean arterial pressure and organ blood flow (MAP/OBF) are indicated. The asterisk indicates the primary abnormality associated with each shock state.
nl, normal range, arrows showing increases or decreases.
Figure 61.2 A useful scheme organizing the constituents of MAP and DO2 in the context of suspected decompensation. For each key abnormality, physiologic variables are indicated in black, along with the main corresponding medical diagnoses indicated in dark gray. For each, key differentiating findings of laboratory or physiologic monitor data are presented in light gray. (VO2, oxygen uptake; DO2, oxygen delivery; CO, cardiac output; JVP, jugular venous pressure; MAP, mean arterial pressure; SVR, systemic vascular resistance; CVP, central venous pressure; PAP, pulmonary artery pressure; PaOP, pulmonary artery occlusion (wedge) pressure).
EVALUATION OF THE ADEQUACY OF BLOOD PRESSURE
From classic studies, we know that the normotensive brain autoregulates at MAPs between 50 and 150 mm Hg. This corresponds to the flat portion of the curve in Figure 61.1B. A baseline hypertensive patient would operate on a right-shifted antiregulatory curve and may not have normal organ perfusion at mean pressures <65 to 70 mm Hg. Retrospective analyses of trauma registries support the existence of age-related relative hypotension8 and have demonstrated poorer outcomes in these individuals at MAP values previously considered normal.9 Based on an aggregate data on patients with septic shock, studies propose that previously normotensive patients should be considered hypotensive if, after receiving 30 mL/kg crystalloid infusion, they still exhibit a decreased systolic pressure (a drop >40 mm Hg) or a decrease in MAP >30 mm Hg.10