Initial Evaluation

A clinician’s initial evaluation should be a global assessment (Figure 6-1). When walking into a patient’s room, you should think, “What do I see?” and quickly determine whether the patient is in distress or has problems related to the airway or breathing. Look for obvious signs of external hemorrhage, look for evidence of hypoperfusion, and assess the adequacy of intravenous (IV) access. Do not rely solely on blood pressure (BP) readings, as there is no “normal” BP for all patients, and a BP value in the “normal” range does not always equate with adequate tissue perfusion. A patient with a history of poorly controlled chronic hypertension may have signs of hypoperfusion even when the BP is within the normal range (for nonhypertensive patients). Conversely, a patient with cirrhosis may have adequate perfusion despite having a lower-than-normal BP. A quick bedside assessment of tissue perfusion should include evaluation of mental status, urine output, and skin findings (e.g., temperature, diaphoresis, mottling, and capillary refill). If any of these parameters are abnormal, a more urgent approach to treatment must be taken.

Figure 6-1 Initial approach to a patient with low systemic arterial blood pressure. *Adrenal insufficiency, liver failure, post–cardiopulmonary bypass vasoplegia, and anaphylaxis are commonly listed as vasodilatory shock; however, data are inconclusive, and components of other types of shock (hypovolemic, cardiogenic) may be also be present. BP, blood pressure; CO, cardiac output; IABP, intraaortic balloon pump; IV, intravenous; LV, left ventricle; MAP, mean arterial pressure; PE, pulmonary embolism; PTCA, percutaneous transluminal coronary angioplasty; RV, right ventricle; SVR, systemic vascular resistance.

A focused cardiac and pulmonary examination is essential. Seek evidence of jugular venous distention, presence of an S₃ or S₄ heart sound, new or worsening murmurs, or muffled heart sounds. Check for the presence of crackles or rales, and note whether there are absent breath sounds, a finding suggestive of a pneumothorax.

During the initial evaluation, pay close attention to systolic (SBP) and diastolic (DBP) pressures in the context of pulse pressure (PP = SBP − DBP). Diastolic pressure is a reasonable surrogate for systemic vascular resistance (SVR). These basic physiology concepts will be useful in determining the cause and devising a treatment plan.

What Is the Cause?

To help focus the differential diagnosis of a hypotensive patient, it is important to review basic cardiovascular physiology. The first concept to remember is that pressure = flow × resistance, where flow is cardiac output, and resistance is SVR. Because cardiac output is determined by stroke volume (SV) × heart rate, the presence of hypotension means that at least one of these parameters (e.g., SV, SVR, or heart rate) is abnormal.¹ Disturbances in heart rate should be obvious by feeling the peripheral pulse, looking at the cardiac monitor, or evaluating a 12-lead electrocardiogram (ECG). The focus of this chapter is evaluating and treating conditions associated with decreased SV or SVR. By properly measuring pulse pressure and diastolic pressure, the clinician can determine whether the primary cause is a change in SVR or SV.

During systole, the SV is ejected into the proximal arterial conduits. Because more blood is being ejected than the peripheral circulation can accommodate in the arterioles, the arterial walls distend, increasing SBP in a way that is directly proportional to the SV and indirectly proportional to the capacitance (C) of the arterial wall. This relationship is represented by the formula¹:

That is, for a fixed SV, if capacitance is higher, the SBP is lower.

During diastole, the portion of the SV that was “stored” by the distention of the arterial walls during systole fills the peripheral arterioles, leading to a progressive decrease in BP until the next systolic phase. This is the diastolic pressure, a parameter that is directly related to the SVR and capacitance (i.e., low diastolic pressure = low SVR and/or capacitance).¹ When using these basic cardiovascular principles to understand the cause of hypotension, it is important to remember the following: (1) capacitance does not change from heartbeat to heartbeat, and (2) SV depends on preload, afterload, and contractility.

Low SVR is characteristic of a number of pathologic conditions, including sepsis, adrenal insufficiency, vasodilating medications, neurogenic shock, post–cardiopulmonary bypass (CPB) vasoplegia, and severe liver dysfunction. Decreased SVR should be suspected in the presence of a widened pulse pressure and low diastolic pressure.^2,3

Reduced SV can be due to decreased preload, decreased contractility, or increased afterload. The most common cause of inadequate preload is hypovolemia. Other causes of inadequate preload include increased intrathoracic pressure due to dynamic hyperinflation in mechanically ventilated patients^4,5 or tension pneumothorax, pulmonary embolism,⁶ mitral valve stenosis,⁷ cardiac tamponade,⁸ and right ventricular failure.⁹ Decreased contractility can be caused by myocardial ischemia or infarction, cardiomyopathy, myocarditis, negative inotropic drugs, myocardial stunning after CPB, and direct myocyte toxins, such as chemotherapeutic agents and inflammatory mediators (e.g., tumor necrosis factor [TNF] and interleukin 1-beta [IL-1β).¹⁰ A reduction in SV can be identified by decreased systolic BP and normal or narrow pulse pressure.

Treatment

Hypotension has been associated with higher morbidity and mortality in a variety of disease states, so until proved otherwise, hypotension should be considered synonymous with hypoperfusion and thus treated aggressively. This initial treatment includes monitoring and therapeutic measures. All patients should have adequate IV access, preferably two patent 18-gauge or larger catheters. The patient should be monitored using a standard ECG monitor and pulse oximetry. A 12-lead ECG should be performed to look for evidence of myocardial ischemia. Supplemental oxygen should be given as needed to keep oxygen saturation greater than 92%. A 1-L fluid bolus of an isotonic crystalloid solution should be infused as rapidly as possible while data are being gathered. The history, focused examination, and assessment of pulse pressure, systolic pressure, and diastolic pressure will aid in the formulation of a more specific treatment strategy.

There are several tools that aid in the workup of the hypotensive patient. One option is the use of ultrasound to evaluate inferior vena cava diameter variation during the inspiratory and expiratory phases of the respiratory cycle. Patients with a large variation (>50%) will most likely respond to additional volume.¹¹ Ultrasound, when used in a focused cardiac examination, can also identify the global quality of contractility, ventricular size and volume, obvious wall motion abnormalities, significant valvular abnormalities, and the presence of a pericardial effusion.¹²

An IV fluid bolus should be a first-line option in treating hypotension, but not every patient will have the desired response to fluid administration. The clinician can evaluate “volume responsiveness” by noninvasive or minimally invasive measures. In the nonintubated, supine patient, elevating the patient’s legs in a 45-degree angle above the plane of the bed will cause a rapid temporary increase in venous return to the heart. If the patient’s condition is dependent on additional volume, one will see an increase in SBP that also correlates to an increase in stroke volume. This maneuver increases pulse pressure in “responders.” An increase in pulse pressure of more than 9% noted before and after the passive leg lifts will identify patients who are likely to respond to additional IV fluid administration.^13,14 A more invasive option is to measure pulse pressure or stroke volume variation in the intubated and mechanically ventilated patient. In these patients, a decrease in stroke volume of 13% or more during the inspiratory cycle correlates with preload responsiveness of stroke volume (i.e., stroke volume and therefore cardiac output are likely to increase if intravascular volume is increased by infusing IV colloid or crystalloid solutions). This variation represents a decrease in venous return in conjunction with the increased intrathoracic pressure during the inspiratory phase of the ventilator. This measurement is only accurate when the heart rhythm is regular, so it is an unreliable index of preload responsiveness in patients with many kinds of arrhythmias, in the presence of an intraaortic balloon pump, or when there is loss of integrity in the arterial waveform. It is also only accurate in mechanically ventilated patients who are not experiencing large variations in intrathoracic pressures.^15,16

In those patients where a low SVR is suspected as the primary cause of hypotension, the treatment is different. Large amounts of additional IV fluid will not adequately increase the BP to maintain tissue perfusion alone. Vasoconstrictor agents (e.g., norepinephrine, dopamine, phenylephrine, vasopressin) will be required in these patients. In certain specific cases, other pharmacologic adjuncts may be helpful. Low-dose hydrocortisone in vasoconstrictor-resistant septic shock¹⁷ and methylene blue in post CPB vasoplegia are two examples.¹⁸

Many occurrences of hypotension may have some qualities of both decreased SV and decreased SVR. However, by using a systematic approach, the clinician can rapidly start diagnostic and therapeutic measures needed to treat tissue hypoperfusion.