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Hemodynamic Monitoring

16

 

Sheila Nainan Myatra, Jigeeshu V. Divatia,

and Ramesh Venkatraman

A 55-year-old male patient presented with respiratory distress, heart rate of 140/ min, BP of 70/40 mmHg, and respiratory rate of 34 breaths/min. Core temperature was 34.4°C. He was oliguric and the abdomen was tender, firm, and distended. He remained tachycardic and hypotensive.

Hemodynamic monitoring is an integral part of intensive care unit (ICU) management. These monitoring devices, if applied injudiciously, may also be harmful. Need for invasive monitoring should be assessed carefully, and its indication should be documented clearly. Attention to technical details, correct interpretation of the data, and its application in selecting an intervention should be individualized within the clinical context.

Step 1: Start basic hemodynamic monitoring

Clinical examination—check for central and peripheral pulses, manual blood pressure: follow the trend and compare with patients’ normal values, capillary refill, core temperature, and peripheral temperature at extremities.

Noninvasive—noninvasive blood pressure, pulse oximetry, and plethysmographic signals.

Hourly urine output.

Screening echocardiography (See Chapter 17).

Base deficit (arterial blood gas).

S.N. Myatra, M.D. (*) • J.V. Divatia, M.D., F.I.S.C.C.M.

Department of Anaesthesia, Critical Care and Pain, Tata Memorial Hospital, Mumbai, India e-mail: sheila150@hotmail.com

R. Venkatraman, A.B. (I.M,) A.B.(C.C.M.)

Critical Care Medicine, Apollo Main Hospitals, Chennai, India

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,

125

DOI 10.1007/978-81-322-0535-7_16, © Springer India 2012

 

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Central venous pressure (CVP).

Intra-arterial blood pressure.

Serum lactate level.

Central venous oxygen saturation (ScvO2).

Step 2: Start advanced hemodynamic monitoring in selected cases

These should be initiated in patients with one or more of the following features:

On high vasopressors, high ventilatory support, compromised cardiac and renal function, and where empirical fluid challenge may be harmful

Options of monitoring techniques include one or more of the following:

Cardiac output-minimally invasive (pulse contour analysis, esophageal Doppler monitoring)

Pulmonary arterial catheter monitoring

Pulse pressure/stroke volume variation

Continuous ScvO2 monitoring

Step 3: Set up the pressure transducing system

This consists of a pressure transducing assembly with a flushing system.

The accuracy of invasive pressure measurement will depend on the proper setup and function of the pressure transducing system.

The pressure transducing assembly consists of a coupling system, pressure transducer, amplifier and signal conditioner, analog to digital converter, and microprocessor which converts the signal received from the vein or the artery into a waveform on a bedside monitor.

The flushing system is set up using a 500-mL sterile saline bag encased in a pressurized system to 300 mmHg. At this pressure, the catheter will be flushed with 3 mL saline per hour and help keep the catheter patent. The flushing device helps flush the assembly as required. Before connecting, flush the pressure transducing system with saline using the flushing device, remove all air bubbles, and keep it ready to connect to the catheter. Heparinized saline is no longer routinely used in view of concerns about heparin-induced thrombocytopenia also, continuous heparin flush solution has been shown to affect coagulation studies if the sample is drawn via the indwelling line.

Step 4: Zero the transducer (static calibration) (Fig. 16.1)

To obtain accurate pressure measurements, the air fluid interface must be aligned with the chamber or the vessel being measured.

The reference point is usually at the level of the heart. Use the phlebostatic axis (junction of the fourth intercostal space and the midpoint between the anterior and posterior chest walls).

A spirit level should be used to level this point with the stopcock of the pressure transducing system which is used for zeroing.

The stopcock is opened to air, and the recorded pressure (atmospheric pressure) is used by convention as the reference value of 0 mmHg.

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Fig. 16.1 Phlebostatic axis

Fig. 16.2 Square wave test

Step 5: Check if the system is optimally damped (dynamic calibration) (Fig. 16.2)

Damping indicates the tendency of an oscillating system to return to its resting state.

Underdamped waveform is a narrow and peaked tracing (will record higher systolic and lower diastolic pressure) and seen when long tubing is used or with increased vascular resistance.

Overdamped waveform (will record lower systolic and higher diastolic pressure) is commonly seen when there are air bubbles or blood clots, overly compliant tubing, catheter kinks, stopcocks not properly closed, no fluid in flush bag, or low flush bag pressure.

In both the above situations, the mean arterial pressure (MAP) will not change. Hence, always rely on the MAP, especially when you are not sure whether the system is optimally damped.

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Fig. 16.3 CVP or PAOP measurement in the spontaneously breathing and ventilated patient

Damping can be checked by performing a “square wave test”—activate the flush device, quickly release it, and observe the waveform on the monitor. The waveform sharply rises and “squares off” at the top when the flush is activated, and then, the tracing returns to baseline when it is released. Check the number of oscillations.

1.Optimally damped—one or two oscillations before returning to tracing

2.Underdamped—more than two oscillations before returning to tracing

3.Overdamped—less than one oscillation before returning to tracing

Repeat the square wave test every 8–12 h whenever the waveform looks overor underdamped, when the accuracy of the measurement is doubtful and particularly when implementing interventions based on intra-arterial pressure values.

Step 6: Interpret the CVP

The CVP is used as an index of preload of the heart or as an index of intravascular volume status. However, the CVP is influenced not only by the volume status but also by myocardial contractility, afterload, and intrathoracic and intraabdominal pressures. Hence, the CVP can be confusing at times and difficult to interpret.

A single measurement of the CVP helps somewhat in defining the circulatory status but leaves considerable overlap in possible interpretations. Hence, single values of CVP should not be relied on. Instead, response of CVP to fluid challenge and the trend of values should be used in clinical decision making.

In order to minimize the effects of respiration, the CVP measurement should be taken at end exhalation when the muscles of respiration are at rest and intrathoracic pressure is stable at its resting level (Fig. 16.3). For this, the CVP tracing should be studied on the monitor after freezing the screen or printed out and studied. In mechanically ventilated patients, inspiration is positive and expiration negative, and end-expiratory values should be read just before the beginning of the inspiration. In spontaneously breathing patients, it is the reverse.

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In some patients, “a” and “v” waves are identifiable in CVP tracing. To correctly identify these, a two-channel recorder with a CVP tracing and a concurrent electrocardiogram tracing should be taken. “a” wave is located corresponding to the PR interval and “v” wave to the QT interval. CVP should be measured at the end of “a” wave.

When positive end-expiratory pressure (PEEP) is applied, pleural pressure is transmitted to the right atrium and the CVP increases. However, the transmural right atrial pressure [right atrial pressure (RAP)—intrapleural pressure], which is the true filling pressure, actually decreases, resulting in underfilling of the right side of the heart.

It is best not to remove PEEP for measurements of vascular pressures. The beneficial effect of PEEP on gas exchange is lost very quickly when it is removed and may take a prolonged period to recover when PEEP is reapplied.

Avoid subtracting half or any other proportion of PEEP value (external + auto PEEP) to the CVP measurement to get an approximate of “true” CVP.

In a nonmechanically ventilated patient, the CVP of 8–10 mmHg is judged to be adequate.

If the patient is clinically stable without evidence of hypoperfusion, refrain from giving fluids to attain a particular CVP value.

A higher CVP value of 10–12 mmHg is recommended in some situations such as:

Mechanically ventilated patients

Diastolic dysfunction (e.g., previous hypertension)

Pulmonary hypertension (e.g., chronic obstructive pulmonary disease)

Increased intra-abdominal pressure (e.g., pancreatitis)

A controlled fluid challenge and response of CVP may be used to interpret volume status (see Chap. 18):

Select the type of fluid: usually normal saline or a colloid.

Infuse rapidly. The rate of infusion: 500 mL of crystalloid or 200 mL of colloid over 20–30 min.

Target the desired therapeutic response: the parameters are set empirically by the physician. These could be MAP >70 mmHg, HR <100/min, and hourly urine output >0.5 mL/kg/h.

Set the danger/safety limits: again, they are set empirically by the physician, for example, CVP 16 mmHg or 4–5 mmHg more than the baseline value.

Assess the response to the initial bolus of fluid.

Repeat bolus infusion of fluid if:

Therapeutic target is not reached

Danger CVP value is not reached

Discontinue fluid infusion if:

Therapeutic target is achieved

Danger value of CVP is reached

Reassess at frequent intervals.

Interpret appropriately the change in CVP in response to a fluid bolus. As a rule of thumb, if the increase in the CVP measured before and 5 min after a fluid bolus is 0–3 mmHg, more fluid should be given. If it is 3–5 mmHg, the patient is

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Fig. 16.4 Components of the arterial waveform. 1 Peak systolic pressure, 2 dicrotic notch, 3 diastolic pressure, and 4 anacrotic notch

probably adequately filled, and if the CVP increases more than 5 mmHg after the fluid bolus, fluid loading should be stopped.

Step 7: Interpret intra-arterial pressure waveform (Fig. 16.4)

The arterial pressure waveform differs at different sites. As the arterial pressure is recorded more distally, the trace gets progressively more peaked and the dicrotic notch migrates away from the peak. The MAP, however, does not vary widely as one measures more distally. Besides more accurate and real-time recording of arterial pressure, other hemodynamic interpretations can be made from the arterial waveform:

Systolic blood pressure variations (swing in the waveform) can be seen during hypovolemia.

Steep slope of upstroke means good contractility and vice versa.

Area under the curve represents the stroke volume.

Position of the dicrotic notch—low (low systemic vascular resistance [SVR]) and high (high afterload).

Slope of the descent—steep (low SVR).

Step 8: Interpreting pulmonary artery occlusion pressure (PAOP)

The four most important measurements obtained from the pulmonary artery catheter (PAC) are the following:

1.PAOP (Pulmonary artery Occlusion pressure)

2.Pulmonary artery systolic (PASP) and diastolic pressure (PADP)

3.Thermodilution cardiac output

4.Mixed venous oxygen saturation

PAOP provides an accurate and indirect measurement of left atrial pressure (LAP) and the left ventricular end-diastolic pressure (LVEDP), which are related to the left ventricular preload: the left ventricular end-diastolic volume (LVEDV).

The PADP displayed on the monitor gives a continuous estimate of the LVEDP, subject to the assumptions in Table 16.1.

Pulmonary artery systolic pressure gives an estimate of pulmonary hypertension and is useful in calculating pulmonary vascular resistance (PVR).

West has described three physiological lung zones that are based on the gravitationally determined relations between pulmonary artery pressure (PAP), pulmonary venous pressure, and alveolar pressure.

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Table 16.1 Assumptions inherent in using PAOP or CVP

Statement

Assumption

Fallacy

LVEDV = LVEDP

Left ventricular compliance

Compliance may change with pathology, for

(preload)

is normal; pressure and

example, left ventricular hypertrophy,

 

volume are linearly related

myocardial ischemia, or infarction; P-V

 

 

relationship is nonlinear

LAP = LVEDP

Mitral and tricuspid valves

It does not hold true if valves are stenotic or

RAP = RVEDP

are normal and fully open in

regurgitant or when A-V valves are closed in

 

diastole

diastole (nodal rhythm, A-V dissociation)

RAP = LAP

Equivalent function of the

Relationship between the right and left sides

 

right and left ventricles

of the heart is affected by several factors

In zones 1 and 2, alveolar pressure exceeds pulmonary vascular pressures. Thus, if the catheter is positioned in any of these zones, it will monitor alveolar or airway pressure instead of the vascular pressures. Fortunately, in most clinical settings where a PAC is inserted, the patient is in the supine position, which facilitates zone 3 formation where alveolar pressure is less than pulmonary venous and arterial pressure thereby reflecting true vascular pressure.

Criteria for confirming the placement of the PAC are:

A tracing consistent with the arterial pressure waveform

A mean wedge pressure lower than mean PA diastolic pressure

Arterialized blood aspirated from the catheter tip with the balloon inflated

Free flow when the catheter is wedged (as determined by the absence of “overwedging” and by ability to aspirate blood through the catheter tip)

The PAC has been regarded as the gold standard for hemodynamic measurements for many years. However, several physiological assumptions are made when stating that the PAOP is a measure of the preload (LVEDV) (Table 16.1).

Lately, the use of PAC has decreased due to availability of other less invasive technique of measuring cardiac output, observational data showing poor outcome with PA catheters and poor training in interpreting PA catheter values, but in selected situation and in proper hands, this catheter is still a useful tool.

Ventilation causes significant swings in pleural pressure. Pulmonary vascular pressure, when measured relative to atmospheric pressure, will reflect these respiratory changes. To minimize this, impact, variables are conventionally measured at the end of expiration. An index of transmission has been described to account for the effects of PEEP (subtract half of PEEP from the pressures). However, the fluid challenge as it is applied to CVP is a method of assessing PAOP during mechanical ventilation with PEEP.

Step 9: Understand the concept of preload responsiveness (Fig. 16.5)

Fluid resuscitation is essential to treat hypovolemia and restore organ perfusion. However, excessive fluid administration will contribute to tissue and pulmonary edema, right ventricular dysfunction, and increased intra-abdominal pressure.

Fluid resuscitation is commonly guided by static measures of preload (e.g., CVP and PAOP). However, cardiac preload is not preload responsiveness. Preload responsiveness is the increase in cardiac output in response to fluid loading. The

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Pulse Pressure Variation

Stroke Volume Variation

PPmax

 

 

SVmax

 

PPmin

PP% = PPmax – PPmin

SVmin

SVV = SVmax – Svmin

PPmean

 

SVmean

(N < 13%)

(N < 10%)

Fig. 16.5 Pulse pressure variation and stroke volume variation

static measures of preload fail to predict fluid responsiveness in half of fluid challenges, that is, they do not predict whether fluid loading will result in an increase in cardiac output. In addition, fluid has to be given before the response to fluid challenge can be evaluated. This is potentially hazardous in some patients.

Dynamic parameters predict the response to fluid loading without having to give a fluid challenge. Hence, they may avoid the potential hazards of a fluid challenge. The principles of these parameters are outlined below.

During inspiration in a fully controlled mechanically ventilated patient, afterload to the left ventricle decreases due to decrease in transmural pressure (pressure inside the aorta − pressure outside [pleural]) and preload to left ventricle increases due to squeezing of pulmonary capillary blood to the left side of the heart. This causes increase in the left ventricle output during inspiration, leading to increased systolic pressure, increased pulse pressure, and increased stroke volume.

During inspiration, the right ventricle preload decreases due to less venous return (less preload) and afterload increases due to lung inflation resulting in decreased right ventricle output, leading to decrease in systolic pressure, pulse pressure, and stroke volume which is reflected during expiration due to transit time from the rightto the left-sided heart.

During expiration, this phenomenon is reversed.

These changes will result in stroke volume variation (SVV), systolic pressure variation (SPV), and pulse pressure variation (PPV) with the respiratory cycle with increase in these parameters during inspiration and decrease during expiration and are referred to as dynamic indicators of preload responsiveness.

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In hypovolemic patients, these changes are exaggerated. Values more than 13% are indicative of fluid responsiveness.

Volume responsiveness or pressure variation with respiration is a physiological phenomenon related to a normal preload reserve because both ventricles of healthy subject operate on the steep portion of the preload–stroke volume relationship. Therefore, detecting the volume responsiveness must not systematically lead to the decision to infuse fluid. Such a decision must be based on the presence of signs of cardiovascular compromise and must be balanced with the potential risk of pulmonary edema formation and/or worsening gas exchange.

SPV, PPV, SVV cannot be used in patients with spontaneous breathing activity and/or with arrhythmias. They are not reliable in patients ventilated with low tidal volume and in patients with increased intra-abdominal pressure.

In these cases, passive leg raising is an alternative choice.

Passive leg raising maneuver is an endogenous fluid challenge. A continuous monitor of stroke volume, SVV, PPV, or aortic blood flow by esophageal Doppler is required. Increase in stroke volume of more than 10%, aortic blood flow of more than 10%, or decrease in SVV/PPV after PLR predicts a good response to fluid loading.

Step 10: Interpret ScvO2/SvO2

Shock is defined as the disruption of the balance between oxygen demand (VO2) and supply (DO2) to the tissues.

A low DO2 can be because of anemia, hypoxia, low cardiac output, or maldistribution of blood flow in the microcirculation.

VO2 can be increased in sepsis and systemic inflammation.

We thus need to assess the balance between oxygen supply and demand.

SvO2 estimates all components of DO2. It reflects cardiac output (CO) if VO2 and Hb are constant, and most importantly, it reflects the balance between oxygen supply and demand.

An SvO2 below 65% implies low oxygen delivery, while a value below 60% indicates that there is a serious risk of tissue hypoxia if corrective measures are not taken.

A low SvO2 (<40%) implies critical oxygen supply–demand imbalance.

If SvO2 is high (>80%), then either the demand has declined, the O2 supply has increased, or the cells are unable to utilize the oxygen.

Thus, a falling or low SvO2 is an important indicator that the oxygen delivery is compromised and is deficient relative to the needs of the tissues.

The measurement of mixed venous oxygen saturation (SvO2) from the pulmonary artery is an indirect index of tissue oxygenation.

However, sampling of mixed venous blood requires insertion of a PAC, which is an invasive procedure with risks, and is not universally used. An alternative is to

measure ScvO2. Central venous catheterization is a simpler and safer procedure and is commonly used.

In this case, a catheter is positioned in the superior vena cava or the upper right atrium.

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