Cardiovascular Monitoring & Complications

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The goal of cardiovascular monitoring of critically ill patients is to assess and optimize end organ perfusion and ultimately tissue oxygen delivery. Monitoring is essential to the care of the patient in the Neurocritical Care Unit. Clinicians should understand the physiological principles of end organ perfusion and oxygen delivery, the technology underlying various cardiovascular monitoring techniques, and the associated risks and benefits.

Cardiovascular Physiology

Systemic oxygen delivery is the product of cardiac output (CO) and arterial oxygen content (CaO2). Cerebral oxygen delivery is the product of cerebral blood flow (CBF) and CaO2. Both CO and CBF are governed by the Hagen–Poiseuille equation, correlating directly with the pressure gradient across the vascular bed divided by the vascular resistance (8ηL / πr4 where r = radius, η = viscosity, and L = length). In systemic perfusion, the pressure gradient is the mean arterial pressure (MAP) – mean venous pressure (estimated by the central venous pressure or CVP). Systemic vascular resistance (SVR) is the resistance to blood flow by the systemic vasculature (excluding the pulmonary vasculature). Thus, CO = MAP - CVP / SVR. In cerebral perfusion, the pressure gradient is also MAP – intracranial mean venous pressure. However, because intracranial pressure (ICP) is greater than intracranial mean venous pressure, this pressure gradient (referred to as the cerebral perfusion pressure or CPP) is CPP = MAP- ICP. Cerebral vascular resistance (CVR) is the resistance to blood flow by the intracranial vasculature and indirectly proportional to the CBF. Thus CBF = MAP - ICP / CVR.

Arterial oxygen content depends on both oxygen bound to hemoglobin and oxygen dissolved in plasma. Each gram of hemoglobin carries 1.34 mL of oxygen. Dissolved oxygen follows Henry’s law: the amount of oxygen dissolved is proportional to the partial pressure. For each mmHg of PaO2, there is 0.0031 mL of O2/dL dissolved. Thus, arterial oxygen content, the total amount of oxygen in arterial blood, can be estimated by the following formula: CaO2 = (1.34 x hemoglobin x arterial oxygen saturation) + (0.0031 x PaO2). Oxygen dissolved in plasma diffuses into the tissue according to the oxygen pressure differential between the capillaries and the tissue. The following is a comprehensive review of cardiovascular monitoring keeping the framework of blood flow and arterial oxygen content in mind.

Blood Flow

Arterial Blood Pressure


Blood pressure is the overall driving force of blood flow through the tissue bed, and thus it is the key hemodynamic parameter that is monitored in critically ill patients. Blood pressure is the pressure generated in the aorta from contraction of the left ventricle. The systolic blood pressure (SBP) is the maximal aortic pressure following ejection of blood from the ventricle and is determined by the ventricular stroke volume (SV) and the compliance of the aorta. The arterial waveform (Figure 1) is represented as change in pressure over time (∆P/∆t). The systolic component of the arterial waveform is seen as the very steep rise, (A), or upstroke which peaks with the opening of the aortic valve, (B). The steepness of the upstroke generally correlates with the strength of ventricular contractility; however, this relationship is complex. As the left ventricle relaxes and refills, the pressure in the aorta falls, (C). The slope of the arterial downstroke correlates with the degree of resistance in the vascular tree. The dicrotic notch (incisura) interrupts the downstroke and represents the closure of the aortic valve, (D). The diastolic blood pressure (DBP) represents the lowest pressure in the aorta just before the ventricle ejects blood again, (E).

Figure 1 - Arterial Waveform

CVM Chapter_Figure 1_Arterial Waveform

Blood pressure is pulsatile and this pulsatility is represented by the pulse pressure (PP), calculated as SBP – DBP. As the aortic PP travels down the aorta and into smaller distributing arteries, the systolic pressure rises and the diastolic pressure falls; thus, the PP increases. This occurs because of decreased arterial compliance (increased stiffness) in the smaller branching arteries and reflected pressure waves. Pulse pressure is directly proportional to SV and inversely proportional to arterial compliance.

Pulse pressure also correlates with respiration. With spontaneous respiration, because of negative intrathoracic pressure during inspiration, venous return increases, blood pools in the pulmonary circulation and left ventricular filling decreases. Thus, systolic pressure normally decreases slightly during inspiration. When the drop exceeds 5 mmHg, it is referred to as pulsus paradoxicus (initially described in the setting of constrictive pericarditis). The opposite occurs with positive pressure ventilation. Systolic pressure typically increases during inspiration (so called “reversed pulsus paradoxicus”). Such changes in PP across the ventilatory cycle are referred to as Pulse Pressure Variation (PPV), calculated as PPmax – PPmin / PPmean over a respiratory cycle or other period of time. A PPV >10% suggests fluid responsiveness (that is, the SV is sensitive to fluctuations in preload). 1 (see Stroke Volume Variation under Cardiac Output section).

The steady mean is referred to as the mean arterial pressure (MAP), the average pressure generated during one ventricular contraction. Using an invasive intraarterial catheter, the true MAP is calculated by integrating the area under the curve of the pressure-time waveform. When blood pressure is measured by automated noninvasive systems using oscillometric techniques, with such systems as an automated blood pressure cuff, the MAP is calculated by the following equation: MAP = DP + 0.333(PP).2 This equation, initially proposed by Gauer in 1960, assumes that diastole persists for 2/3 of the cardiac cycle and systole for the remaining 1/3 of the cycle, an assumption that is less valid at faster heart rates. There have been many attempts to find a more accurate formula, 3,4 including simply the square root of the SP and DP, 5 an approximation of the geometric mean.


Invasive Arterial Blood Pressure Monitoring

In 1828, Poiseuille was the first to measure the arterial blood pressure in a human using a mercury manometer connected directly to an arterial cannula. Invasive arterial measurement represents the gold standard for blood pressure monitoring in critically ill patients as it provides continuous blood pressure measurement. It is accomplished by inserting a cannula into a large artery (usually the radial, femoral, or axillary artery) and connecting it to a transducer. 6 This device is commonly referred to as an arterial line. The pressure wave generated by contraction of the left ventricle travels through fluid-filled incompressible tubing to a transducer and displaceable sensing diaphragm, which converts the pressure wave into a proportional electrical signal (Figure 2). The signal is amplified and digitally displayed. The system requires calibration to a reference point which, for cardiovascular pressures, is the right atrium, located externally at the phlebostatic axis (fourth intercostal space, midaxillary line).

Also, a certain amount of damping of the signal is required. Without damping, pressure waves reverberate in the tubing and lead to the formation of harmonics and an overestimation of the systolic blood pressure. This phenomenon is referred to as “underdamping” of the system, and the waveform is typically narrow and peaked (Figure 2). Causes of underdamping include stiff tubing and increased vascular resistance. Underdamping artifacts may be seen in about a third of critically ill patients. 7 Conversely, with too much damping, the arterial waveform loses energy leading to underestimation of the systolic blood pressure. This is referred to as “overdamping” of the system and the waveform is blunted and rounded (Figure 2). Causes of overdamping include compliant tubing, air-bubbles, clots or fibrin within the tubing, catheter kinks, no fluid or low flush bag pressure. Underdamping and overdamping can be determined by the “fast flush test” or “square wave test.” Squeezing the fast flush valve produces a waveform that rises sharply, plateaus, and then drops off when the valve is released. An accurate waveform will then only have two oscillations. An over-damped waveform will lose its dicrotic notch and will have one oscillation. This often happens when there is clot in the catheter tip or an air bubble in the tubing. An under-damped waveform will overestimate the systolic pressure and there will be several post-flush oscillations (at least 2 or more). Damping errors can often be resolved by flushing the tubing, repositioning the patient and/or catheter, and ensuring sufficient saline and pressure are in the system. Though the MAP is less affected by damping artifacts, recognizing this phenomenon is critical for accurate blood pressure monitoring and decision making. Without such recognition, the intensivist may risk over- or undertreating the blood pressure.8 Despite the potential for artifact, invasive blood pressure monitoring is a very valuable tool and is essential for monitoring when antihypertensive, inotropic or vasopressor drugs are being used in a critically ill patient, as it allows for constant blood pressure readings to direct care. Additionally, an added benefit of an arterial line is that it allows for arterial blood sampling without frequent arterial sticks. 9 Arterial lines are not without risks and require constant monitoring for infection, hematoma formation, bleeding from the site and the incidence of air embolism6. Careful attention should be taken during placement due to the risk of pseudoaneurysm formation. 6

Figure 2 - Examples of Normal, Overdamped, and Underdamped Arterial Pressure Waveforms
CVM Chapter_Figure 2_Examples of Arterial Pressure Waveforms

Noninvasive Arterial Blood Pressure Monitoring (NIBP)

Noninvasive measurement of blood pressure (NIBP), using counter pulsation with sphygmomanometry and auscultation, was introduced by Korotkoff in 190510 followed by the oscillometric method blood pressure measurement introduced in 1976. The oscillometric method is the most common method used for noninvasive measurement of blood pressure. Though arm, leg, or ankle are accurate, the arm is the preferred method for NIBP measurement.11 With an inflated cuff, small oscillations from pulsations of the underlying artery are detected using plethysmography. Systolic and diastolic pressures can be estimated indirectly by detecting oscillations that begin approximately at systolic pressure and continue below diastolic pressure. The most common device is the Dinamap (Direct Indirect Assessment of Mean Arterial Pressure) (GE Healthcare, Waukesha, WI) introduced in 1976. This offers advantages over invasive arterial lines such as avoidance of bleeding, infection risk, and use outside the intensive care unit (ICU) . However, oscillometric blood pressure monitoring is intermittent rather than continuous and there are differences in measurements when compared to invasive arterial blood pressure monitoring. Oscillometric SBP measurements tend to be lower compared with invasive monitoring, especially at extremely high blood pressures. Conversely, at extremely low blood pressures, oscillometric SBP measurements tend to be higher than when obtained by invasive monitoring. 9,12 Finally, the methodology of noninvasive blood pressure devices is not standardized between manufacturers. That is, different devices use different proprietary-limited algorithms to measure the blood pressure. 12 Thus, when accurate blood pressure measurements are required in critically ill patients, intraarterial blood pressure monitoring is preferred.

Finally, while blood pressure monitoring is the foundation of ICU monitoring, exactly which component of blood pressure - SBP, DBP, or MAP - that should be monitored and targeted has been uncertain and has varied depending on the patient’s specific condition. For example, the American Heart Association’s definition of hypertension is based on SBP and DBP only. 13 In the management of acute ischemic stroke, both SBP and DBP have been emphasized14whereas in the management of intracerebral hemorrhage, only SBP is targeted. 15 The Society for Critical Care Medicine has utilized both SBP and MAP for defining sepsis-induced hypotension, whereas MAP is used in setting therapeutic goals, 16 especially when low blood pressures are a main concern such as in shock states. 9This is in part because SBP and DBP can vary depending on where the measure is taken, while MAP remains rather constant within the system. 17 Similarly, MAP has been used as the target blood pressure goal following cardiac arrest. 18 (Note that because the coronary arteries fill during diastole, the coronary perfusion pressure is the DBP – left ventricular end diastolic pressure, estimated by pulmonary capillary occlusion pressure, PAOP). And finally, the Brain Trauma Foundation guidelines emphasize MAP in the calculation of CPP for the management of traumatic brain injury. 19,20 Therefore, it is important to closely follow the recommended, evidence-based practice guidelines for hemodynamic management of patients in the Neurocritical Care Unit in order to optimize patient outcomes.

Central Venous Pressure


Central venous pressure (CVP) is the pressure in the superior vena cava near the right atrium. It is an estimate of right atrial pressure (RAP) and, in theory, right ventricular end-diastolic pressure (RVEDP). The normal CVP waveform is shown in Figure 3. CVP has often been used as an estimate of right ventricular end-diastolic volume, or preload, and therefore is used as an indirect estimate of intravascular volume. It has been widely believed that patients with a low CVP are volume-depleted and those with a high CVP are volume-overloaded; however, this is overly simplistic. Normal CVP is variable and depends not only on intravascular volume, but also on patient position, venous tone, intrathoracic pressure, and cardiac valvular disease. Depending on the circumstances, a value anywhere between 6 and 20 mmHg could be compatible with normovolemia. Also, a patient with a high CVP may still have an under filled left ventricle that is fluid responsive in the setting of acute right ventricular infarction. 21,22 Thus, CVP measurements correlate poorly with intravascular volume because of multiple assumptions and the effect of complex cardiopulmonary interactions. 22,23 As a result, routine CVP monitoring is done less frequently in practice, unless this is the only means of measuring patient volume status until a more accurate means is established.

Figure 3 -
Central Venous Pressure (CVP) Waveform

a) Atrial contraction (end diastole); c) Isovolemic ventricular contraction, tricuspid valve elevation into the right atrium (early systole); v) Back pressure from systolic filling of right atrium (late systole); x-descent = Atrial relaxation, descent of the contracting right ventricle (mid-systole); y-descent = Tricuspid valve opens in early ventricular diastole (early diastole).

CVM Chapter_Figure 3_CVP Waveforms


Central venous catheters used for monitoring CVP are usually inserted into the subclavian or the internal jugular vein, via the Seldinger technique, and extended into the superior vena cava (SVC) above the level of pericardial reflection. Various landmarks, 24,25 simple formulae, 26,27 and sophisticated techniques like right atrial ECG 28,29 and transesophageal echocardiography30 have been developed to ensure correct placement of the central venous catheter tip. The subclavian vein placement is commonly the preferred location for placement in the Neurocritical Care Unit because of the concern that, theoretically, internal jugular vein cannulation may impede cerebral venous blood return31, though several studies have not shown significant reduction in jugular venous flow with internal jugular cannulation. 32,33 Standard central venous catheters have risks that have been well described, including pneumothorax, vessel dissection, hematoma formation, thrombosis, and even hemopericardium that can occur during line placement. 34,35 To minimize complications, several national guidelines now recommend the use of ultrasound to guide insertion.36 A chest x-ray is done to confirm proper placement prior to use for both subclavian and internal jugular vein access.

Cardiac Output


Cardiac output (CO) is the volume of blood being pumped by the heart in one minute. It is the product of SV and heart rate (HR). The gold standard for measuring CO has been the pulmonary artery catheter (PAC). Within the last decade, a number of “minimally invasive CO monitors” have been introduced and measure CO without the need for placing a PAC. Cardiac output is a key component of blood pressure (BP = CO x SVR) and thus perfusion. Additionally, CO is independently associated with perfusion outside the Hagen–Poiseuille equation and thus is valuable to monitor separately from blood pressure.


Pulmonary Artery Catheter

A pulmonary artery catheter (PAC) can be inserted into either the subclavian or internal jugular vein and the distal port is connected to a pressure transducer. With the balloon at the tip inflated, the catheter is advanced from the superior vena cava into the right atrium, right ventricle, and pulmonary artery. As it wedges into a pulmonary artery branch, the systolic component of the pressure disappears (Figure 4). What remains is the pulmonary artery occlusion pressure (PAOP) or “wedge pressure,” an estimate of the left atrial pressure (LAP) and, in theory, left ventricular end-diastolic pressure (LVEDP) and volume (LVEDV) (assuming the measurement occurs post-isometric LV relaxation once the mitral valve is fully opened). Thus, the PAOP has been used as an estimate or surrogate of the LVEDV or cardiac preload. Like the CVP, the reliability of this correlation is dubious. 22 A normal PAOP is between 6 and 12 mm Hg. Cardiac output can be estimated using a thermodilution technique. When a small amount of cold fluid is injected into the proximal port of the catheter (which lies within the right atrium when the tip is in the pulmonary artery), the temperature of the blood downstream in the pulmonary artery will be transiently reduced in proportion to the blood flow. This temperature change can be detected by a thermistor at the end of the catheter. Cardiac output is inversely proportional to the blood-temperature decrease and the duration of the transit of cooled blood (i.e., the area under the curve). The computer integrates this area under the curve. Cardiac index (CI) is CO expressed in relation to body surface area or BSA (CI = CO/BSA) (Table 1). From these calculations, one can derive a set of hemodynamic parameters (Table 2).

Figure 4 - Schematic of the Distal Portion of a PAC and Corresponding Pressure Tracings as the Catheter Travels Through the Heart.
(The PAOP reflects left atrial pressure; RA, right atrium; RV, right ventricle; PA, pulmonary artery)
CVM Chapter_Figure 4_Schematic of PAC and Pressure Tracings as catheter travels through the heart

Table 1 - Key Hemodynamic Calculations Associated with the Pulmonary Artery Catheter
CVM Chapter_Table 1_Key Hemodynamic Calculations

Table 2 - Hemodynamic Parameters Generated from a Pulmonary Artery Catheter
CVM Chapter_Table 2_Hemodynamic Parameters Generated from a Pulmonary Artery Catheter

Because multiple randomized controlled trials have reported no evidence of benefit or even harm37-41 and some literature has indicated an increase in complications, 42,43 use of the PAC has decreased over the last decade in the Neurocritical Care Unit, especially with the introduction of minimally invasive cardiac output monitors.

Minimally Invasive Cardiac Output Monitors

Minimally invasive cardiac output monitors typically relate the contour of the arterial pressure waveform to SV and SVR. 44 An algorithm is then used to determine the CO by integrating the area under the curve. The specific algorithm used varies with each device. 45 In general, there are two types of devices that utilize the arterial waveform analysis to calculate CO: calibrated and non-calibrated. Calibrated devices take into consideration the patient’s specific compliance and impedance profiles and are more accurate. Non-calibrated devices estimate compliance and impedance based on average age, sex, and size specific values.

The most common calibrated device is the Pulse index Continuous Cardiac Output (PiCCO) system (Pulsion Medical Systems, Munich, Germany). It uses a thermistor-tipped arterial catheter, placed primarily axillary, femoral, or brachial, attached to a pressurized bag of normal saline to measure the aortic pressure waveform morphology. 46 An algorithm determines the CO by pulse contour analysis (essentially integrating the area under the curve). A central venous catheter, placed in either the subclavian or internal jugular vein, is used to calibrate the system using a transpulmonary thermodilution technique, similar to the PAC, however less invasive and easier to use at the bedside by injecting a known volume of cold isotonic saline 46 (Figure 5). Repeated calibration allows the system to accurately estimate the CO based on the patient's real-time hemodynamic status. Cardiac output monitoring utilizing pulse contour analysis generally shows good agreement with CO measurements made using a PAC. However, monitors based on pulse contour analysis rely on an optimal arterial signal; over- or under-damped waveforms may lead to inaccurate CO measurements. Arrhythmias, aortic regurgitation, and the use of an intra-aortic balloon pump also have been shown to decrease accuracy. It is recommended that PiCCO catheters only remain in place for up to ten days. 46

Figure 5 - Calibration of Pulse Contour Analysis by Means of Thermodilution
CVM Chapter_Figure 5_Calibration of PUlse Contour Analysis

The LiDCO system (LiDCO, Cambridge, UK) is another calibrated device. Its algorithm, however, is based on pulse power analysis or the law of conservation of mass (the input of mass or SV equals the output of mass or flow into peripheral vessels). It uses a standard arterial catheter but because it uses power analysis rather than contour analysis, it is less dependent on the quality of the waveform. Like the PiCCO monitor, it requires calibration using indicator dilution technique with lithium chloride injected into a central or peripheral vein and then the concentration is measured by an ion sensitive electrode attached to the arterial line. The most common non-calibrated CO monitor is the FloTrac/Vigileo system (Edwards Lifesciences, Irvine, CA, USA). This device utilizes a blood flow sensor attached to a standard arterial catheter and calculates the standard deviation of the pulse pressure over 20 seconds. This value correlates with SV, which is then multiplied by HR to derive CO. Studies of accuracy and reliability have been mixed. 47

Additional volume parameters can be calculated by multiplying the CO with characteristic time variables of the thermodilution curve (Table 3):

Table 3 - Hemodynamic Parameters Generated from PiCCO Monitor
CVM Chapter_Table 3_Hemodynamic Parameters generated from PiCCO Monitor

  • Global End-Diastolic Volume (GEDV) is the total amount of blood left in all four heart chambers, i.e. atria and ventricles, at the end of diastole.
  • Global End-Diastolic Index (GEDI) is the GEDV divided by body surface area and can be used to determine the patient’s volume status.
  • Intrathoracic Blood Volume (ITBV) represents the total amount of blood in the thorax.
  • Intrathoracic Blood Index (ITBI) is the ITBV divided by body surface area.
    • GEDV and ITBV reflect the circulatory volume status and are indicators of cardiac preload.
  • Extravascular Lung Water (EVLW) quantifies the extravascular fluid volume in the lungs. It reflects the development of interstitial pulmonary edema and represents the water in the lungs outside the blood vessels.
  • Extravascular Lung Water Index (EVLWI) is the EVLW divided by body surface area. There is a positive relationship between EVLWI and mortality in critically ill patients.
  • Global Ejection Fraction (GEF) depends on right and left ventricular contractility and is derived from the ratio of four stroke volumes divided by GEDV.
  • Stroke Volume Variation (SVV) with respiration, SVV increases when preload is low; patients with SVV ≥ 15% are more likely to respond to fluid resuscitation.
  • Cardiac Index (CI) assess the patients cardiac output based on the patient’s size.

Nursing Assessment Key Points

Key nursing considerations to remember when using a PiCCO monitor include the following:

Supplies needed for PiCCO monitoring include:
  • Central venous line (preferably subclavian or internal jugular)
  • The PiCCO arterial catheter with a thermistor-tipped arterial catheter on a pressurized bag of normal saline. The ideal location for the PiCCO line is preferably the femoral site, however due to the risk of infection, axillary is commonly used.
    • Note: Locations of arterial and venous catheters need to be appropriately entered into the system to ensure adequate measurement.
  • The PiCCO monitoring kit
  • Three boluses of cold normal saline, ideally less than 8°C, administered through the most distal lumen of the central venous catheter, based on the patients’ body weight (0.2mL/kg) with a maximum bolus of 20mL, should be administered in less than seven seconds.
  • PiCCO monitor
  • The patient’s gender along with height and weight need to be entered accurately into the PiCCO system in order to obtain correct values as the system bases its calibration on predicted body weight.
  • A rapid flush test should be performed prior to each measurement to determine if there is damping of the waveform and to verify the pressurized bag is adequately inflated.
  • The pressure transducer should be leveled at the phlebostatic axis and should be zeroed to atmospheric pressure.
  • The PiCCO monitor should be calibrated every 8 hours.
  • An appropriate CVP needs to be entered for each measurement in order to calculate the SVR.


  • If the cold saline injection is administered too slowly or stopped during the administration, an error message will appear and the curve will be deformed.
  • The patient does not need to be in the supine position while obtaining PiCCO measurements if the patient will not tolerate being supine.
  • While the patient is being monitored with the PiCCO system, CO can be measured on a continuous basis46,48.

Heart Rate and ECG


The electrocardiogram (ECG) measures the electrical activity of the heart and displays it on the monitor as a waveform and a number. Though invented by Willem Einthoven in 1901, continuous ECG monitoring did not become available in the ICU until the 1970s and was not standardized until the 1980s. Today, ECG monitoring is the foundation to cardiovascular monitoring. The goals of ECG monitoring include heart rate monitoring, diagnosis of complex arrhythmias, detection of myocardial ischemia, and the identification of a prolonged QT interval.

For the heart to pump effectively, the cardiac chambers need to be synchronized. Synchronization occurs by electrical activity spreading through the conduction system. A normal ECG tracing is depicted in Figure 6 below. Initially, the sinoatrial (SA) node (located in the right atrium) generates an electrical impulse that spreads to the left atrium and down to the atrioventricular (AV) node, resulting in atrial depolarization and contraction (P wave). At the AV node, the impulse is delayed as blood is ejected into the ventricles. On the ECG, this delay is represented by the isoelectric activity from the end of the P wave to the beginning of the QRS complex. The impulse is then conducted down to the ventricles through the Bundle of His, right and left bundle branches, and Purkinje fibers causing ventricular depolarization and contraction (QRS complex) followed by repolarization of the ventricles (the T wave). During this period of repolarization, the ventricles are vulnerable to excitation. An ectopic contraction occurring during this period can precipitate ventricular fibrillation (so called R-on-T phenomenon). A small U wave often follows the T wave that is thought to be from repolarization of the Purkinje fibers. Three intervals are typically measured in the ECG. The PR interval (or PQ interval) corresponds with the duration of atrial excitation and atrioventricular conduction (normal 120-200 ms). The QRS interval corresponds with the duration of ventricular depolarization (normal < 110-120 ms) and the QT interval with the duration of ventricular depolarization (normal < 430-450 ms).

Figure 6 - Parts of ECG Waveform
CVM Chapter_Figure 6_Parts of ECG Waveform

Physiologically, the QRS marks the beginning of cardiac systole with initially isovolemic ventricular contraction until the aortic valves open and blood empties out of the left ventricle and into the aorta (SV). This occurs during the ST segment and the T-wave. Cardiac diastole begins with closure of the aortic valve at the end of the T-wave. Thus, in the ECG, cardiac systole is from the Q-wave to the end of the T-wave and diastole is from the end of the T-wave to the next Q-wave (Figure 7).

Figure 7 - ECG and the Cardiac Cycle
CVM Chapter_Figure 7_ECG and the Cardiac Cycle

The ECG measures the electrical activity of the heart by bipolar and unipolar leads. A bipolar ECG lead consists of two surface electrodes of opposite polarity. A unipolar lead consists of one positive surface electrode and a reference point. The original bipolar leads introduced by Einthoven were Leads I, II, and III (I detects the current between right arm and left arm; II detects the current between the left leg and the right arm; III detects the current between the left leg and the left arm). Later, the “augmented vector” unipolar limb leads aVR, aVL, and aVF and then the six-unipolar chest leads (V1-V6) were introduced. A standard “12-lead ECG” requires 10 electrodes placed on the body (1 on each wrist and ankle and 6 across the precordium). In the peri-operative and ICU setting, the four limb electrodes are often repositioned to the torso to reduce muscle artifact during limb movement (Mason-Likar positioning). For basic ECG monitoring in the ICU setting, a 5-lead ECG is typically used, color coded for convenience. The white electrode (RA) is placed below the right clavicle, the black electrode (LA) is placed below the left clavicle, the green electrode (RL) is placed at the right lower thorax/hip region and the red electrode (LL) is placed at the left lower thorax/hip region. Finally, a brown electrode is placed on the chest in the desired V position, usually V1 (fourth intercostal space just right of the sternum). The saying, smoke (black) over fire (red), clouds (white) over grass (green), and brown in the middle can be used to assist with lead placement, knowing that the white lead is always placed on the right side. The 5-electrode ECG allows monitoring of bipolar frontal plane leads I, II, III, aVR, aVL, and aVF, as well as V1 (Figure 8).

Figure 8 - Typical 5-Lead Set Up for ECG Monitoring in the ICU
CVM Chapter_Figure 8_Typical 5-lead set up for ECG Monitoring in the ICU

A 3-lead ECG can also be used but is less common in the ICU; however, a 3-lead ECG is commonly used during a resuscitation requiring advanced cardiac life support (ACLS). This is similar but minus the green electrode (RL) at the right lower thorax/hip region and the brown precordial (V) electrode. This results in the ability to monitor either Leads I, II, or III with a selector switch. In the ICU, ECG monitoring is used to monitor the heart rate, detect cardiac arrhythmias, myocardial ischemia, and prolongation of the QT interval.


Heart Rate Monitoring

Heart rate (HR) monitoring is fundamental to cardiovascular monitoring, as CO is the product of SV and HR. The normal HR ranges between 60 and 120 beats per minute (bpm). Heart rate trend review has been available on most bedside monitors in the ICU since the early 1990s. Heart rate can also be assessed intermittently by cuff sphygmomanometer or continuously by invasive arterial pressure monitoring and pulse oximetry. It should be noted that most monitors use algorithms that combine low and high pass filtering and derivative analysis to detect the beat (R-peak in the QRS complex). The HR number that appears on the monitor is typically a 3-5 second average. More accurate HR monitoring (beat-to-beat interval measurement) requires a higher resolution which is typically not available with commercial monitoring systems. Measuring beat-to-beat intervals has led to the discovery of heart rate variability (HRV), the variation over time of the period between consecutive heartbeats. Because it is a reflection of the interplay between the sympathetic and parasympathetic nervous systems, HRV has been shown in some studies to be a predictor of outcomes and adverse events in critical care. 49,50 For example, in the setting of aneurysmal subarachnoid hemorrhage, HRV may be beneficial in the preclinical detection of delayed cerebral ischemia. 51 In the setting of traumatic brain injury, HRV is significantly associated with increased mortality. 52 Further studies are needed, along with more standardized methodology and reporting, before HRV monitoring can be routinely incorporated into daily care. 50

Detection of Cardiac Arrhythmias

Some monitors have enhanced capabilities for accurate diagnosis of cardiac arrhythmias. During arrhythmia analysis, the monitor continuously filters the ECG signal to remove artifacts and measures signal features such as R-wave height, width, and timing to aid in rhythm analysis. Note that the typical 3-lead set up, while adequate for heart rate monitoring, is generally inadequate for computerized arrhythmia monitoring because a V1 lead, the best lead for bundle-branch blocks and to distinguish ventricular tachycardia from supraventricular tachycardia with aberrant ventricular conduction, is not available.

Detection of Myocardial Ischemia

Unlike computerized arrhythmia monitoring, which is performed automatically, ST-segment analysis generally requires activation of the software for it to work. Like arrhythmia monitoring, the 3-lead set up is also inadequate for ST-segment analysis because it does not provide precordial leads, which are the most sensitive for detecting ischemia. In order to adequately assess for myocardial ischemia, a 12-lead ECG should be completed to assess for myocardial infarction.

Detection of Prolongation of the QT interval

The QT interval, measured from the beginning of the QRS complex to the end of the T wave, reflects ventricular repolarization. When prolonged, there is an increased risk of torsades de pointes ventricular tachycardia. Because ventricular repolarization time increases at a slower HR and decreases at a faster HR, the QT interval is typically corrected for HR (QTc) using Bazett’s formula. A normal QTc is <0.45 second in men and <0.46 second in women. Standard ECG algorithms provide both uncorrected and corrected QT intervals. While any lead can be used to measure the QT interval, Lead II is the one most commonly used.

Cardiac Monitoring

The American Heart Association Practice Standards for ECG Monitoring in Hospitals have published guidelines for which patients would benefit most from ECG monitoring (Table 4). Class I: Cardiac monitoring is indicated in most, if not all, patients in this group. Class II: Cardiac monitoring may be of benefit in some patients but is not considered essential for all patients. Class III: Cardiac monitoring is not indicated because a patient’s risk of a serious event is so low that monitoring has no therapeutic benefit. 53 For patients being cared for in the Neurocritical Care Unit, careful consideration needs to be taken when caring for patients with concomitant cardiac risk factors who may need to remain in the ICU for careful monitoring.

Table 4 - Indications for Cardiac Monitoring
CVM Chapter_Table 4a_Indications for Cardiac MonitoringCVM Chapter_Table 4b

Arterial Oxygen Content


Arterial oxygen content (CaO2) can be estimated by the following formula: CaO2 = (1.34 x hemoglobin x arterial oxygen saturation) + (0.0031 x PaO2). Optimizing CaO2 is a central goal of the management of critically ill patients; therefore, respiratory function is a key parameter that is monitored in the ICU.


Respiratory Rate Monitoring

The normal respiratory rate (RR) ranges between 12 and 20 breaths per minute. Abnormal RR has been shown to be an important predictor of serious events such as cardiac arrest 54,55 and should be closely monitored. The RR can be measured using impedance pneumography, in which a small current is passed between two electrodes on the chest wall (the same electrodes used for ECG monitoring). With chest expansion, the distance between the electrodes increases, impedance increases, and the strength of the current when it reaches the receiving electrode decreases. The reduction in current is processed and converted into a RR. With inductance plethysmography, sensors woven into an elastic band placed around the chest expands with inspiration. This results in changes in magnetic fields around wire coils. Changes in the excitation current are processed and converted into a RR. When both chest and abdominal bands are used, accurate tidal volume measurements can also be generated.

Arterial Oxygen Saturation Monitoring

Arterial hemoglobin oxygen saturation (SaO2) can be continuously measured using pulse oximetry. Most pulse oximeters use spectrophotometry, which sends light through tissue to a photodetector on the other side. Because oxygenated and deoxygenated hemoglobin differ in their capacity to absorb red and infrared light, comparing the degree of absorption allows for the estimation of the relative concentrations of oxygenated and deoxygenated hemoglobin. Pulse oximeters, usually placed on the finger or earlobe, are accurate and precise when SaO2 is greater than 75% and hemoglobin is greater than 5 g/dL. 56 The relationship between SaO2 and PaO2 (arterial partial pressure of oxygen) is described by the hemoglobin dissociation curve; the curve is relatively flat above a SaO2 of 90%. Thus, pulse oximetry is insensitive to changes in PaO2 at higher levels. Pulse oximetry also cannot distinguish between normal hemoglobin, methemoglobin or carboxyhemoglobin. The ECG monitored HR should match that of the pulse oximeter; a difference implies that the pulse oximeter is not detecting arterial pulsation or that an artifact is contaminating the signal. Cardiac arrhythmias usually do not affect the accuracy of pulse oximetry, but the use of vasoactive drugs may lead to under-reading of the SaO2. Pulse oximetry can provide an early warning sign of hypoxia which can lead to respiratory distress.

Mixed Venous Oxygen Saturation Monitoring

Mixed venous blood is blood from the superior and inferior vena cava that has passed through the right heart to the pulmonary artery. The blood can be sampled from the distal port of a PAC, but some catheters have embedded fiberoptic sensors that directly measure O2 saturation. Systemic oxygen extraction can be determined by the arteriovenous oxygen difference (AVDO2), that is the difference between atrial oxygen content (CaO2) and venous oxygen content (CvO2) (AVDO2 = CaO2 - CvO2). This can be estimated by the difference between the arterial hemoglobin saturation and venous hemoglobin saturation (SaO2 − SvO2). This same principle underlies jugular bulb oximetry. The technique involves placing a fiberoptic oximeter (Abbot Opticath, Abbott Laboratories, North Chicago, IL) retrograde into the jugular bulb. The normal range for SjvO2 is 55% to 69% (see Chapter on multi-modal monitoring).

Measurement of pulmonary artery mixed venous oxygen saturation (SvO2) has been advocated as a useful index of tissue oxygenation. Patients with a wide variety of critical conditions such as cardiac failure and sepsis have been shown to have a poorer outcome when the SvO2 is decreased. However, this measurement requires insertion of a PAC. Monitoring central venous oxygen saturation (ScvO2) from a central venous catheter is simpler and can be used to assess systemic oxygen supply and demand. 57

Carbon Dioxide Monitoring

Qualitative End-Tidal PCO2 Measurement

Measurement of end tidal carbon dioxide (ETCO2) with an end tidal CO2 detector is commonly used to confirm placement of the endotracheal tube in the airway. A color change from purple to yellow indicates the presence of CO2 and that the endotracheal tube is correctly placed in the airway. However, if the end tidal CO2 detector remains purple following intubation when exposed to oxygen, this indicates the endotracheal tube is incorrectly positioned within the esophagus and needs to be reinserted. Even with proper endotracheal tube placement, the ETCO2 may remain low with cardiogenic shock or when intubation is attempted during cardiopulmonary resuscitation (CPR).

Quantitative End-Tidal PCO2 Measurement

More comprehensive information is provided by capnography in which CO2 is measured by infrared absorption and displayed continuously. Capnometers are either placed directly into the airway (mainstream) or adjacent to the airway (side stream). During inhalation, PaCO2 at the airway equals zero. During exhalation, PaCO2 usually rises rapidly until it plateaus. Thus, the peak exhaled ETCO2 in theory represents the alveolar PaCO2. Waveform capnography can be helpful in diagnosing and monitoring respiratory conditions. For example, in patients with expiratory small airway obstruction (e.g., asthma), there is upward sloping of the plateau phase during expiration because of late emptying of poorly ventilated alveoli. In patients with partial obstruction of a main stem bronchus, there may be a ‘‘stepladder’’ appearance at the beginning of expiration. ETCO2 can also be of assistance at the bedside in the Neurocritical Care Unit to closely monitor patients on ventilators to prevent episodes of hypocarbia and hypercarbia, as often patients’ PaCO2 goal in the Neurocritical Care Unit is 35-45 mmHg. Specifically, patients with traumatic brain injury can be highly affected by small changes in their PaCO2 levels. Low PaCO2 (<35 mmHg) can lead to vasoconstriction, decreased cerebral blood flow and ultimately cerebral ischemia. 58 While increased PaCO2 levels (>45 mmHg) can result in vasodilation, increased blood volume, and increased intracranial pressures. 58 In addition, because ETCO2 is partly determined by the amount of blood flow returning to the lungs, it has been used to verify the effectiveness of CPR. Adequate chest compressions are associated with increasing ETCO2 levels greater than 10 mm Hg. Similarly, an abrupt increase in ETCO2 during CPR indicates a return of spontaneous circulation.


The goal of cardiovascular monitoring is to assess and optimize end organ perfusion and tissue oxygen delivery. As oxygen delivery is the product of blood flow and arterial oxygen content, this forms the framework of what parameters are important to monitor in critically ill patients. Understanding these physiological principles are key to monitoring and improving patient outcomes. It is also important to remember that relationships between hemodynamic variables are complex in healthy states but especially in diseased states. In the future, cardiovascular monitoring will be supported by advanced signal processing and analysis that will enable clinicians to synthesize information and form hypotheses that best explain the current situation. Such an integrated system will translate data into actionable information and provide situational awareness.


  1. Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med 2009;37:2642-7.
  2. Gauer OH. Kreislauf des blutes. In: Rosemann U, ed. Lehrbuch der Physiologie des Menschen. 28th ed. Munchen: Urban und Schwarzenberg; 1960.
  3. Razminia M, Trivedi A, Molnar J, et al. Validation of a new formula for mean arterial pressure calculation: the new formula is superior to the standard formula. Catheter Cardiovasc Interv 2004;63:419-25.
  4. Chemla D, Hebert JL, Aptecar E, et al. Empirical estimates of mean aortic pressure: advantages, drawbacks and implications for pressure redundancy. Clin Sci (Lond) 2002;103:7-13.
  5. Chemla D, Antony I, Zamani K, Nitenberg A. Mean aortic pressure is the geometric mean of systolic and diastolic aortic pressure in resting humans. J Appl Physiol (1985) 2005;99:2278-84.
  6. Scheer BV, Perel A, Pfeiffer UJ. Clinical review: complications and risk factors of peripheral arterial catheters used for haemodynamic monitoring in anaesthesia and intensive care medicine. Crit Care 2002;6:199.
  7. Romagnoli S, Romano SM, Bevilacqua S, et al. Dynamic response of liquid-filled catheter systems for measurement of blood pressure: precision of measurements and reliability of the Pressure Recording Analytical Method with different disposable systems. J Crit Care 2011;26:415-22.
  8. Romagnoli S, Ricci Z, Quattrone D, et al. Accuracy of invasive arterial pressure monitoring in cardiovascular patients: an observational study. Crit Care 2014;18:644.
  9. Lehman LW, Saeed M, Talmor D, Mark R, Malhotra A. Methods of blood pressure measurement in the ICU. Crit Care Med 2013;41:34-40.
  10. Korotkoff NS. On methods of studying blood pressure [in Russian]. . Bull Imperial Mil Med Acad 1905;11:365-7.
  11. Lakhal K, Macq C, Ehrmann S, Boulain T, Capdevila X. Noninvasive monitoring of blood pressure in the critically ill: reliability according to the cuff site (arm, thigh, or ankle). Crit Care Med 2012;40:1207-13.
  12. Bur A, Herkner H, Vlcek M, et al. Factors influencing the accuracy of oscillometric blood pressure measurement in critically ill patients. Crit Care Med 2003;31:793-9.
  13. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA 2014;311:507-20.
  14. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association Stroke. 2019;50(12):e344‐e418. 
  15. Hemphill JC, 3rd, Greenberg SM, Anderson CS, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2015;46:2032-60.
  16. Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;43(3):304‐377. 
  17. Burdick W, Clarke N, Garlichs R, Priestley J, Richards D. DIFFERENCES IN BLOOD PRESSURE IN THE ARM AND LEG IN NORMAL SUBJECTS. American Journal of Physiology -- Legacy Content 1925;72:169-76.
  18. Neumar RW, Shuster M, Callaway CW, et al. Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2015;132:S315-67.
  19. Carney N, Totten AM, O'Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017;80(1):6‐15. 
  20. Carney N, Totten AM, O'Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017;80(1):6‐15. 
  21. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest 2008;134:172-8.
  22. Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med 2004;32:691-9.
  23. Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med 2004;32:691-9.
  24. Schuster M, Nave H, Piepenbrock S, Pabst R, Panning B. The carina as a landmark in central venous catheter placement. Br J Anaesth 2000;85:192-4.
  25. Stonelake PA, Bodenham AR. The carina as a radiological landmark for central venous catheter tip position. Br J Anaesth 2006;96:335-40.
  26. Czepizak CA, O'Callaghan JM, Venus B. Evaluation of formulas for optimal positioning of central venous catheters. Chest 1995;107:1662-4.
  27. Chalkiadis GA, Goucke CR. Depth of central venous catheter insertion in adults: an audit and assessment of a technique to improve tip position. Anaesth Intensive Care 1998;26:61-6.
  28. Wilson RG, Gaer JA. Right atrial electrocardiography in placement of central venous catheters. Lancet 1988;1:462-3.
  29. Jeon Y, Ryu HG, Yoon SZ, Kim JH, Bahk JH. Transesophageal echocardiographic evaluation of ECG-guided central venous catheter placement. Can J Anaesth 2006;53:978-83.
  30. Andropoulos DB, Stayer SA, Bent ST, et al. A controlled study of transesophageal echocardiography to guide central venous catheter placement in congenital heart surgery patients. Anesth Analg 1999;89:65-70.
  31. Stocchetti N, Longhi L, Valeriani V. Bilateral cannulation of internal jugular veins may worsen intracranial hypertension. Anesthesiology 2003;99:1017-8.
  32. Woda RP, Miner ME, McCandless C, McSweeney TD. The effect of right internal jugular vein cannulation on intracranial pressure. J Neurosurg Anesthesiol 1996;8:286-92.
  33. Vailati D, Lamperti M, Subert M, Sommariva A. An ultrasound study of cerebral venous drainage after internal jugular vein catheterization. Crit Care Res Pract 2012;2012:685481.
  34. Akmal AH, Hasan M, Mariam A. The incidence of complications of central venous catheters at an intensive care unit. Ann Thorac Med 2007;2:61-3.
  35. Kornbau C, Lee KC, Hughes GD, Firstenberg MS. Central line complications. Int J Crit Illn Inj Sci 2015;5:170-8.
  36. Troianos CA, Hartman GS, Glas KE, et al. Guidelines for performing ultrasound guided vascular cannulation: recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr 2011;24:1291-318.
  37. Harvey S, Harrison DA, Singer M, et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial. Lancet 2005;366:472-7.
  38. Sandham JD, Hull RD, Brant RF, et al. A randomized, controlled trial of the use of pulmonary-artery catheters in high-risk surgical patients. N Engl J Med 2003;348:5-14.
  39. Richard C, Warszawski J, Anguel N, et al. Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2003;290:2713-20.
  40. Binanay C, Califf RM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA 2005;294:1625-33.
  41. Shah MR, Hasselblad V, Stevenson LW, et al. Impact of the pulmonary artery catheter in critically ill patients: meta-analysis of randomized clinical trials. JAMA : the journal of the American Medical Association 2005;294:1664-70.
  42. Hartung EJ, Ender J, Sgouropoulou S, Bierl R, Engelhardt W, Engemann R. Severe air embolism caused by a pulmonary artery introducer sheath. Anesthesiology 1994;80:1402-3.
  43. Bristow A, Batjer H, Chow V, Rosenstein J. Air embolism via a pulmonary artery catheter introducer. Anesthesiology 1985;63:340-2.
  44. Erlanger J, Hooker DR. An experimental study of blood pressure and pulse pressure. Johns Hopkins Hopsital Records 1904;12:145-378.
  45. Funk DJ, Moretti EW, Gan TJ. Minimally invasive cardiac output monitoring in the perioperative setting. Anesth Analg 2009;108:887-97.
  46. Hofkens PJ, Verrijcken A, Merveille K, et al. Common pitfalls and tips and tricks to get the most out of your transpulmonary thermodilution device: Results of a survey and state-of-the-art review. Anaesthesiology Intensive Therapy 2014;46:89-116.
  47. Saraceni E, Rossi S, Persona P, et al. Comparison of two methods for cardiac output measurement in critically ill patients. Br J Anaesth 2011;106:690-4.
  48. Cottis R, Magee N, Higgins DJ. Haemodynamic monitoring with pulse-induced contour cardiac output (PiCCO) in critical care. Intensive Crit Care Nurs 2003;19:301-7.
  49. Seely AJ, Macklem PT. Complex systems and the technology of variability analysis. Crit Care 2004;8:R367-84.
  50. Karmali SN, Sciusco A, May SM, Ackland GL. Heart rate variability in critical care medicine: a systematic review. Intensive Care Med Exp 2017;5:33.
  51. Schmidt JM, Sow D, Crimmins M, et al. Heart rate variability for preclinical detection of secondary complications after subarachnoid hemorrhage. Neurocrit Care 2014;20:382-9.
  52. Sykora M, Czosnyka M, Liu X, et al. Autonomic Impairment in Severe Traumatic Brain Injury: A Multimodal Neuromonitoring Study. Crit Care Med 2016;44:1173-81.
  53. Drew BJ, Califf RM, Funk M, et al. Practice standards for electrocardiographic monitoring in hospital settings: an American Heart Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young: endorsed by the International Society of Computerized Electrocardiology and the American Association of Critical-Care Nurses. Circulation 2004;110:2721-46.
  54. Hodgetts TJ, Kenward G, Vlachonikolis IG, Payne S, Castle N. The identification of risk factors for cardiac arrest and formulation of activation criteria to alert a medical emergency team. Resuscitation 2002;54:125-31.
  55. Fieselmann JF, Hendryx MS, Helms CM, Wakefield DS. Respiratory rate predicts cardiopulmonary arrest for internal medicine inpatients. J Gen Intern Med 1993;8:354-60.
  56. Wouters PF, Gehring H, Meyfroidt G, et al. Accuracy of pulse oximeters: the European multi-center trial. Anesth Analg 2002;94:S13-6.
  57. Rivers EP, Ander DS, Powell D. Central venous oxygen saturation monitoring in the critically ill patient. Curr Opin Crit Care 2001;7:204-11.
  58. Carney N, Totten AM, OʼReilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery 2016.

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