Blood pressure is the most important of the six vital sign. Organ blood flow is driven by the difference in the pressure between the arterial and venous sides of the circulation. The mean arterial pressure (MAP)¹ minus the central venous pressure (CVP) is the driving force for organ blood flow while the difference between post-arteriolar and venular pressure determines microcirculatory flow. As discussed in Chap. 12, venous pressure has a much greater effect on microcirculatory flow than the MAP. As long as the MAP is within an organs autoregulatory range (see below), the CVP becomes the major determinant of capillary blood flow. Microcirculatory flow and organ function “is best” with a higher MAP and a lower CVP (not higher CVP).

It should however be realized that CO and TPR and interdependent with changes in CO effecting TPR and changes in TPR effecting CO.

MAP = cardiac output (CO) × total peripheral resistance (TPR).

Shock is traditionally defined as “circulatory failure that results in inadequate cellular oxygen utilization” [25]. This definition is problematic as oxygen delivery has to fall to very low levels before oxygen consumption falls and most patients with “shock” have normal levels of oxygen consumption. Ronco and colleagues determined the critical oxygen delivery threshold for anaerobic metabolism in critically ill humans while life support was being discontinued [26]. The critical oxygen delivery threshold was 3.8 ± 1.5 mL/min/kg (266 mL/min in a 70 kg patient); assuming a hemoglobin concentration of 10 g/L this translates into a cardiac output of approximately 2 L/min; it is likely that only pre-terminal moribund patients with “shock” would have such a low cardiac output. Furthermore, while an elevated lactate concentration is widely believed to be a marker of anaerobic metabolism, an overwhelming body of evidence suggests that in most clinical situations, that lactate is produced aerobically as part of the stress response (see Chap. 13). While it is unclear how best to define shock, we believe “circulatory shock” is best defined as “a potentially life threatening reduction in systemic organ blood flow.” The clinical diagnosis of shock is then based on a constellation of clinical and hemodynamic features which include hypotension, tachycardia, increased respiratory rate and decreased urine output. Typically, the SBP is less than 90 mmHg or the MAP is less than 65 mmHg. While altered mentation, notably obtundation, disorientation and confusion is common, patients may be remarkably lucid despite profound hemodynamic compromise (due to blood flow redistribution to the brain).

Shock results from four potential, and not necessarily exclusive, pathophysiological mechanisms: (i) hypovolemia, (ii) decreased systolic cardiac function, (iii) circulatory obstruction (e.g., pulmonary embolism, cardiac tamponade, or tension pneumothorax) or distributive factors (sepsis or anaphylaxis) [25]. The first three mechanisms are characterized by low cardiac output while distributive shock is characterized by decreased systemic vascular resistance. Characterization of the type(s) and cause of shock is essential in order to provide appropriate therapy.

Sinus tachycardia is always an ominous sign. The HR is increased usually due to a fall in SV and/or a hypermetabolic state with an increased oxygen demand. In most critically ill patients, tachycardia is a compensatory response following a fall in SV. Assuming a normal heart rate of 70/min; a heart rate of 140/min would indicate that the SV has halved… a very bad situation. Always determine the cause of a sinus tachycardia (ECHO, SV determination) … and NEVER EVER treat an unexplained sinus tachycardia with a beta-blocker … this will predictably result in DEATH (a few exceptions do exist, e.g. Thyrotoxicosis). The higher the heart rate the more life threatening the situation… AND a tachycardia >110/min in an elderly patient is a VERY ominous sign. Tachycardia in combination with hypotension (SBP <110 or MAP <75 mmHg) and a high respiratory rate (>20/min) is a deadly TRIO [1]. ICU patients with cardiac risk factors and a persistent tachycardia (HR >95/min) are at an increased risk of having an acute cardiac event [27].

More common causes of sinus tachycardia

A ‘breath’ is an inspiration followed by expiration and can be seen by observing the movement of the chest wall. The normal respiratory rate in adults is between 12 and 20/min. and should be counted for one full minute. Depth of breathing should also be recorded, as either ‘shallow’, ‘normal’ or ‘deep’, along with whether accessory muscles are used. The depth of breathing can easily be followed on the bedside monitor which uses trans-thoracic impedance to determine the respiratory rate and produce a respiratory waveform (see Fig. 14.4). The respiratory rate, depth of breathing, patient position (supine vs upright) and work of breathing should be evaluated. A patient lying flat (on one or two pillows) breathing comfortably with good chest excursions at a rate 16–18 breaths/min is “A” okay. However an increase in the depth and rate of breathing (hyperventilation) indicates impending respiratory failure (type 1), while a low respiratory rate (bradypnea) is a sign of type II respiratory failure. A respiratory rate above 20/min is an early warning sign of patient decompensation; while a rate above 26/min indicates impending “doom”. Kussmaul breathing is usually associated with a metabolic acidosis (e.g. ketoacidosis) while Cheyne-Stokes breathing is seen in moribund patients most notably with severe systolic heart failure. Biot’s respiration is an abnormal pattern of breathing characterized by groups of quick, shallow inspirations followed by regular or irregular periods of apnea. It generally indicates a poor prognosis. Biot’s respiration is caused by damage to the medulla oblongata due to strokes or trauma or by pressure on the medulla due to uncal or tentorial herniation. Ataxic respiration is an abnormal pattern of breathing characterized by complete irregularity of breathing, with irregular pauses and increasing periods of apnea. As the breathing pattern deteriorates, it merges with agonal respirations. Ataxic respiration is related to Biot’s breathing, having similar causes.

The patient’s temperature is the “least vital” of all the vital signs. However, patients’ temperature should be measured on presentation and at least 6 hourly once in the ICU. Core rather than peripheral temperatures should be recorded. Alterations in temperature are important in the diagnosis of infection. (See Chap. 18, Fever in the ICU).

Pulse oximetry is invaluable in the assessment and management of patients with hypoxemia; cyanosis only becomes obvious clinically at saturation below 80 %… much too late. The value of pulse oximetry in patient care has been so great that pulse oximetry has been referred to as the “fifth vital sign” and arguably the greatest advance in patient monitoring since electrocardiography [28, 29]. Continuous monitoring of arterial saturation (SaO₂) by pulse oximetry is now considered the standard of care in the ICU, OR and PACU. In addition, continuous pulse oximetry is required in all patients undergoing conscious sedation as well as ER patients with respiratory failure, those patients receiving supplemental oxygen and during endotracheal intubation [30]. While pulse oximetry is the standard of care in these settings there is no data that proves that this technology improves outcome [31]. Moller et al. performed a remarkable study (published in 1993) in which 20,802 surgical patients in Denmark were randomly assigned to be monitored or not with pulse oximetry in the OR and PACU [32]. In this study there was a 19-fold increase in the incidence of diagnosed hypoxemia in the oximetry group as compared to the control group, however, the two groups did not differ in cardiovascular, respiratory, neurologic, or infectious complications. Despite the findings of this study “common sense” should dictate that pulse oximetry improves the safety of patients managed in the ICU, OR, PACU and ER, and that the failure to prove a benefit does not mean that the technology is not beneficial. By alerting the clinician to the presence of hypoxemia, pulse oximeters can lead to a more rapid treatment of serious hypoxemia and possibly avoid serious complications. Moreover, pulse oximetry can reduce the requirement/frequency of arterial blood gas analysis. Pulse oximetry is invaluable in the titration of fractional inspired oxygen concentration (FiO₂) and flow rate (nasal canula) in patients’ receiving supplemental oxygen/assisted ventilation. In these settings pulse oximetry should prevent hypoxemia (PaO₂ < 60 mmHg) as well as hyperoxia (PaO₂ >200 mmHg) conditions associated with an increased risk of death (see below).

Pulse oximetry provides an estimation of the arterial oxygen saturation of hemoglobin (SaO₂), which is related to the partial pressure of oxygen in arterial blood (PaO₂). Compared with the measurement standard (multiwavelength CO oximeter), pulse oximeters have a mean difference (bias) of between 0.2 and 1 % and a standard deviation (precision) of less than 2 % when SaO₂ is above 80 % [33]. With modern pulse oximeters the bias is about 1.5 % and the precision less than 2 % with oxygen saturations between 60 and 80 % (data from Nellcor). Patients with hemoglobinopathies (e.g. Sickle hemoglobin) are at risk of having inaccurate pulse oximetry readings. A falsely elevated SaO₂ will be obtained in patients with elevated levels of carbon monoxide and methemoglobin. In addition, patient movement, arrhythmias, nail polish (black, green, blue), hypotension and skin pigmentation can affect pulse oximetry readings [33–37]. Pulse oximetry has been found to be reliable with SBP readings greater than 80 mmHg [37]. Low perfusion states such as hypotension, low cardiac output, vasoconstriction, vasoactive drugs and hypothermia produce a low signal-to-noise ratio resulting in inaccurate readings. Several studies comparing black and white patients reported no significant pigment-related errors in pulse oximeters at normal saturations [38, 39]. “Older” generation pulse oximeters overestimated SaO₂ in dark-skinned individuals at saturations below 80 % (bias of 2–4 %), however this discrepancy appears less with newer generation pulse oximeters (data from Nellcor) [40, 41]. High-intensity lighting, typically fluorescent lights, may also lead to false readings. The SaO₂ level displayed should only be assumed to be accurate when there is a high-quality plethysmographic tracing displayed on the monitor (see Fig. 14.5). Ideally, the display will show a pulse wave with a demonstrable dicrotic notch. Ultimately, the clinician must look at the patient, and if the pulse oximeter (or any other monitor) does not seem to be behaving in a way that is consistent with the clinical picture that is presented, the clinician must determine the cause of the discrepancy.

As the oxygen–hemoglobin dissociation curve is sigmoidal in shape, at high PaO₂, or when the patient is on the “flat part of the curve,” large changes in PaO₂ level will lead to only minor changes in SaO₂ level (see Fig. 14.6). At lower levels of PaO₂, relatively small decreases in oxygen tension can lead to rapid decreases in oxygen saturation. A PaO₂ of 60 mmHg usually is associated with a SpO₂ level of about 90 %. The “knee” of the oxygen–hemoglobin dissociation curve is at about 90 %. Below this value oxyhemoglobin saturation decreases more rapidly as oxygen tension declines (see Fig. 14.6 and Table 14.1). On most pulse oximeters the default setting for the low oxyhemoglobin saturation alarm is therefore 90 %, and this should be regarded as the target for oxygenation in most patients.

Equation for calculation of arterial oxygen content:
As is evident from the arterial oxygen content equation oxygen delivery is dependent almost entirely on the saturation of arterial blood and cardiac output and not on the PaO₂ (which contributes to the small amount of oxygen dissolved in serum). While respiratory failure is usually defined as a PaO₂ <60 mmHg it is in reality the SaO₂ which should be used to make clinical decisions and the titration of oxygen therapy. However, determining the “safe degree of hypoxemia” for an individual subject is exceedingly difficult. The brain is the most sensitive organ to hypoxemia, and visual, cognitive, and electro-encephalographic changes develop when the oxyhemoglobin saturation is less than 80–85 % in normal subjects [42]. Therefore, in most patients, a SaO₂ of 90–92 % results in an adequate level of oxygenation. It is important to note that non-hypoxemic patients do not benefit from oxygen therapy [29]. The recommended target saturation range for critically ill patients not at risk of hypercapnic respiratory failure is 92–96 %; however emerging data suggests that targeting a saturation of 90–92 % may be preferable [43]. In patients with severe acute respiratory distress syndrome (ARDS), a SaO₂ target of 86–90 % is acceptable in order to minimize pulmonary oxygen toxicity. Patients chronically exposed to lower oxygen saturation levels adapt to these conditions; this is clearly evident in patients with cyanotic heart disease and mountain climbers. Patients with Fallot’s tetralogy are able to mentate with arterial saturations in the 60’s [44]. Hillary and Tenzing used supplemental oxygen to achieve the first ascent of Mt. Everest in 1953. Twenty-five years later Messner and Habeler ascended Mt.Everest without supplemental oxygen [45]. The Caudwell Xtreme Everest Research Group performed blood gas analysis (from femoral arterial blood) at the balcony of Mt Everest (27,559 ft) in climbers not receiving supplemental oxygen (see Fig. 14.7) [45]. These data clearly indicate that the “acclimatized” human brain can function at quite low levels of SaO_2. In patients with COPD or other known risk factors for hypercapnic respiratory failure (e.g. morbid obesity, chest wall deformities or neuromuscular disorders), a target saturation range of 86–90 % is generally recommended (see Chap. 24) [29]. However, these patients may tolerate a SaO₂ as low as 80–88 % without cognitive dysfunction. The decision to accept lower values should be based on each individual patient’s circumstances [42].

The SUPPORT study group randomized 1,316 premature infants to a target oxygen saturation of 85–89 % or 91–95 % [46]. Death before discharge occurred more frequently in the lower-oxygen-saturation group (in 19.9 % of infants vs. 16.2 %; relative risk, 1.27; 95 % CI, 1.01–1.60; p = 0.04), whereas severe retinopathy among survivors occurred less often in this group (8.6 % vs. 17.9 %; relative risk, 0.52; 95 % CI, 0.37–0.73; p < 0.001). This study highlights the risks of both hypoxemia and hyperoxia, particularly in the developing brain.

Alveolar hypoventilation is the main form of respiratory failure postoperatively and results from combinations of central respiratory depression, muscular weakness, and upper airways obstruction. Alveolar hypoventilation is also common in patients receiving opiates. As arterial carbon dioxide (PaCO₂) tension rises so does alveolar carbon dioxide tension (PCO₂); alveolar PO₂ falls, leading to arterial hypoxemia. If the patient is breathing room air then the saturation will fall early and is a reasonably sensitive indicator of hypoventilation. The situation is different if the patient is receiving supplemental oxygen. The alveolar PO₂ will now be much higher and alveolar PCO₂ will have to rise much further before hypoxemia sufficient to produce measurable desaturation occurs [37, 47]. It is therefore critical to realize that when patients are receiving supplemental oxygen, they may have normal SpO₂ levels but be in respiratory failure with hypercapnia and respiratory acidosis. These patients may suffer a cardiac arrest despite normal oximetry. End-tidal CO₂ (ETCO₂) monitoring is “mandatory” in these patients.

Oxygen is a treatment for hypoxemia, not breathlessness, nor pain, nor anxiety, nor hemorrhage, nor wound infection, nor cardiac ischemia, nor….. Although supplemental oxygen is often given “automatically” to patients admitted to hospital, oxygen therapy has no proven benefit in non-hypoxemic patients and is likely to be harmful. In addition, a high oxygen fraction has been suggested to prevent adverse outcomes after surgery and anesthesia, including wound infections and postoperative nausea and vomiting (kinda stupid, see below). The deleterious effects of hypoxia are well known and physicians may be overly concerned about avoiding hypoxia and give additional oxygen ‘to be on the safe side’. HOWEVER, hyperoxia is also to be avoided as too much oxygen is toxic.