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Cardiovascular support 

Cardiovascular support
Chapter:
Cardiovascular support
Author(s):

Heather Baid

, Fiona Creed

, and Jessica Hargreaves

DOI:
10.1093/med/9780198701071.003.0007
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date: 09 May 2021

Cardiac monitoring

The critically ill patient may require complex monitoring during their episode of critical illness.

Monitoring tools that may be used include:

  • continuous ECG monitoring

  • 12-lead ECG recordings

  • blood pressure monitoring

  • central venous pressure monitoring

  • cardiac output monitoring.

A combination of certain or all of these tools may be required, depending on the severity of critical illness. It is vital that the nurse understands:

  • why the patient requires that form of monitoring

  • how to utilize the monitoring tools

  • the advantages of the tools

  • the limitations of the tools.

Continuous ECG monitoring

It is usual for most patients who are admitted to critical care units to have continuous ECG recording. This enables continuous observation of heart rate and rhythm, and also facilitates the setting of alarm parameters to warn of any disturbances to heart rate. ECG monitoring does not replace the need to take the pulse manually, as manual recordings will provide information about the strength and amplitude of the pulse.

The ECG provides a graphical representation of the electrical activity of the heart. Monitoring electrodes are placed on the patient’s chest, and these detect the electrical activity of the heart. Activity moving towards the electrode will produce an upward or positive deflection, whereas activity moving away from the electrode will produce a downward or negative deflection.

The basic ECG waveform is labelled PQRST (and U) (see Figure 7.1).

Monitoring systems may be either 3-lead systems or 5-lead systems.

The 3-lead ECG system

  • The 3-lead systems allow monitoring of leads I, II, and III.

  • Electrodes are placed on the patient’s chest towards the right arm (RA), left arm (LA), and left leg (LL) (see Figure 7.2).

  • It is most usual for patients to be monitored using lead II.


Figure 7.2 Three-lead ECG electrode positioning. RA, right arm; LA, left arm.

Figure 7.2 Three-lead ECG electrode positioning. RA, right arm; LA, left arm.

(Reproduced from Adam SK and Osborne S, Critical Care Nursing: science and practice, Second Edition, 2005, with permission from Oxford University Press.)

The 5-lead ECG system

  • The 5-lead ECG system allows monitoring of any of the 12 leads, and usually two more leads may be displayed on the monitor at any one time (multi-channel ECG).

  • Electrodes are placed towards the right arm (RA), right leg (RL), left arm (LA), left leg (LL), and a central chest lead (C).

  • The clinical situation will normally determine which leads are viewed on the monitor, and discussion with the medical team may be required.

Troubleshooting ECG recordings

Occasional problems may occur with the recording, and you may be required to ‘troubleshoot’ the ECG if continual alarming or problems with the trace occur. Common problems and their solutions are listed in Table 7.1.

Table 7.1 Troubleshooting guide

Problem

Solution

Excessive triggering of alarms

  • Review alarm parameters

  • Check sensitivity

  • Check monitoring lead

  • Are the R waves and T waves of similar heights?

Wandering or irregular baseline

  • Clip the cable to the patient’s clothing to reduce this

  • Check for excessive patient movement or tremor

  • Reapply electrodes and clean the skin appropriately before application

Intermittent trace

  • Check electrode connection to skin

  • Check electrode connection to cable

  • Check cable connection to monitor

  • Check whether cable is damaged

No ECG trace

  • Adjust gain to see if it is set appropriately

  • Check that cables are connected properly to the patient and the monitoring system

  • Has the appropriate lead selector been utilized?

12-lead ECG monitoring

Recording a 12-lead ECG

Recording of a 12-lead ECG may be required in order to provide a more comprehensive view of the heart.

  • Ten electrodes are placed on the patient to enable the monitoring system to view the heart from 12 views (hence ‘12-lead’ ECG).

  • One electrode is placed on each of the limbs, and six electrodes are placed on the patient’s chest.

  • The electrodes should ideally be placed over areas of least muscle mass to minimize electrical interference.

The 12-lead ECG is therefore composed of:

  • three limb leads—I, II, and III. These form a hypothetical triangle with the heart at the centre

  • three augmented (or modified) limb leads—augmented view left (aVL), augmented view right (aVR), and augmented view foot (aVF).

  • six precordial or chest leads (V1–V6).

Twelve-lead ECGs may be recorded using a continuous system or may be serially recorded using a separate 12-lead ECG system. When serial ECGs are being recorded it is vital that the patient’s electrodes are placed in the same position to allow comparison. There is often difficulty in placing the chest electrodes correctly (correct placement is shown in Figure 7.3). The anatomical positions for chest electrode placement are described in Table 7.2.


Figure 7.3 Diagram of chest electrode placement.

Figure 7.3 Diagram of chest electrode placement.

(Reproduced from Chikwe J, Cooke D, Weiss A, Oxford Specialist Handbook of Cardiothoracic Surgery, Second Edition, 2013, with permission from Oxford University Press.)

Table 7.2 Anatomical positions for chest electrode placement

Chest lead

Anatomical position

V1

Fourth intercostal space to the right of the sternum

V2

Fourth intercostal space to the left of the sternum

V3

Midway between V2 and V4

V4

Fifth intercostal space, mid-clavicular line

V5

Anterior axillary line at the level of V4

V6

Mid-axillary line at the level of V4

Interpretation of the 12-lead ECG

This is complex and requires appropriate training. Therefore 12-lead ECGs should always be reviewed by a suitably qualified nurse or doctor. A systematic tool is required for the interpretation of the 12-lead ECG, as the latter needs to be reviewed in a logical manner.

Blood pressure monitoring

The accurate monitoring of blood pressure is an essential element of monitoring the critically ill patient. Occasionally this may be performed using non-invasive blood pressure systems, but more frequently a tranduced arterial monitoring system is used.

Non-invasive blood pressure recordings

A non-invasive system may be used for monitoring blood pressure in the early stages of critical illness if an arterial line is not deemed appropriate, or it may be used temporarily until an arterial line has been inserted.

Non-invasive systems are usually a reliable method of recording the patient’s blood pressure, but if used frequently may cause excessive disturbance and discomfort to the patient.

  • Attention should be paid to the size of the cuff, as an incorrectly sized cuff can cause false readings.

  • The cuff bladder width should be 40–50% of the upper arm circumference. The bladder should encircle 80% of the upper arm.

  • The cuff should be at the level of the heart to maintain a true zero level.

  • Repeat interval times should be determined by the severity of the patient’s condition.

Transduced arterial line recordings

Arterial lines allow the continuous monitoring of the systemic arterial pressure, and also provide vascular access for arterial blood sampling. They are generally used for the majority of critically ill patients. The use of transduced arterial monitoring is essential for:

  • unstable patients

  • patients on vasoactive infusions

  • patients who require frequent arterial blood sampling

  • patients for whom therapeutic decisions require an accurate blood pressure measurement.

The arterial line is normally situated in the radial artery, but may be located in other arteries (e.g. the brachial or femoral artery). The patient should ideally undergo an Allen’s test to check for adequate collateral circulation prior to insertion.

There are a number of safety issues to be noted, as there are several risks associated with arterial lines and arterial monitoring. These include:

  • bleeding

  • infection

  • thrombosis

  • accidental disconnection

  • occlusion of distal blood flow.

In order to maintain the safety of the line it is vital to be able to:

  • regularly assess skin colour, temperature, and pulses distal to the cannula

  • observe the site easily

  • set alarm limits appropriately to facilitate early detection of disconnection

  • clearly label and date the line to prevent accidental injection

  • check connections to prevent accidental disconnection.

The transducer system

The transducer system works by transmitting pressures from the intravascular space through a fluid-filled non-compliant tube to a transducer. The transducer then converts this into an electrical signal which is in turn converted by the monitor into a trace and a digital reading.

It is essential that the transducer system is consistently situated as levelled to an external reference point to ensure accurate readings. The reference point will depend upon local policy, but it is usual to use either the phlebostatic axis or the sternal notch.

Once the reference point has been determined, the transducer should be zeroed prior to use and intermittently during use (frequency should be guided by local policy). Zeroing or recalibration is performed by:

  • turning off the three-way tap to the patient

  • opening the transducer to the atmosphere

  • selecting the appropriate zeroing area on the monitor

  • zeroing the transducer according to the manufacturer’s guidelines

  • closing the three-way tap to the atmosphere

  • opening the three-way tap to the patient.

Arterial waveforms

The arterial waveform should be clearly displayed on the cardic monitor at all times. The normal waveform is represented in Figure 7.4 and consists of:

  • a rapid upstroke—produced by the ejection of blood from the left ventricle into the aorta

  • a dicrotic notch—produced by the closure of the aortic valve that marks the end of systole

  • a definitive end point.


Figure 7.4 Normal arterial waveform.

Figure 7.4 Normal arterial waveform.

(Reproduced from Chikwe J, Beddow E, Glenville B, Oxford Specialist Handbook of Cardiothoracic Surgery, 2006, with permission from Oxford University Press.)

The pressures generated by the arterial monitoring include:

  • systolic blood pressure

  • diastolic blood pressure

  • mean arterial pressure (MAP) = diastolic + (systolic-diastolic)/3.

Abnormal arterial waveforms

Variation in systolic blood pressure

Normally, there is only a minimal variation in systolic blood pressure during inspiration and expiration despite changes that occur in intra-thoracic pressure during the breathing cycle. Pulsus paradoxus is when a non-ventilated patient has more than 10 mmHg drop in systolic blood pressure during inspiration as compared to expiration. Reverse pulsus paradoxus, often referred to as a ‘swing’ in the arterial waveform, occurs when the systolic blood pressure of a mechanically ventilated patient increases during inspiration and decreases with expiration. The most common cause of a variation in systolic blood pressure is hypovolaemia. Other possible causes include tamponade, pericarditis, large pulmonary embolus, and tension pneumothorax.

Damping

Accurate arterial blood pressure monitoring requires a monitoring system which is optimally damped and is confirmed by:

  • normal arterial waveform with a dicrotic notch

  • comparable invasive blood pressure readings as the non-invasive blood pressure measurement

  • after square wave form from flushing, only 1-2 oscillations occur before quickly returning to normal waveform.

Overdamping and underdamping may affect the reliability of the continuous blood pressure results (see Table 7.3). Troubleshooting actions for a problem with damping abnormalities include:

  • checking cannula is not constricted and is in correct place

  • checking all connections

  • aspirating blood back and flushing

  • ensuring flush bag is not empty with pressure set to 300 mmHg.

Table 7.3 Abnormal damping of arterial waveforms

Problem

Signs

Causes

  • Overdamping

  • (Underestimation of systolic and overestimation of diastolic)

  • Flattened waveform

  • No dicrotic notch

  • After square wave form from flushing, slowly returns to baseline waveform without oscillations

  • Kink in cannula

  • Air bubbles

  • Blood clot

  • Arterial spasm

  • Loose connection

  • Underdamping

  • (Falsely high systolic and falsely low diastolic)

  • Overshooting of systolic waveform (whip)

  • After square wave form from flushing, multiple oscillations (ringing) occur before returning to baseline

  • Catheter artefact

  • Stiff tubing

  • High cardiac output

  • Tachycardia

  • Arryhthmias

Removal of an arterial line

The cannula may be removed if there are problems associated with its use (e.g. poor distal perfusion) or if it is no longer required. It is vital that care is taken to minimize complications associated with removal. Care should be taken to apply adequate pressure for sufficient time to ensure haemostasis.

Further reading

Nirmalan M and Dark PM. Broader applications of arterial pressure wave form analysis. Continuing Education in Anaesthesia, Critical Care and Pain 2014; 14: 285-90.Find this resource:

Romagnoli S et al. Accuracy of invasive arterial pressure monitoring in cardiovascular patients: an observational study. Critical Care 2014; 18: 644.Find this resource:

Central venous pressure monitoring

The central venous pressure (CVP) is recorded by using a central line that is normally inserted into either the internal jugular vein or the subclavian vein.

The tip of the line is situated in the superior vena cava and reflects the pressure in the right atrium. It is theoretically suggested that in a healthy patient this provides information about intravascular blood volume and right ventricular end diastolic pressure, although a recent meta-analysis questions the reliability of this.1 See Cardiovascular support p. [link].

Nevertheless, the CVP may be used as a guide to treatment, but it is important to remember that no single measurement should be used to guide patient treatment. An overview of the trend in the patient’s assessment results is much more likely to be clinically useful in relation to guiding fluid management.

There are a number of safety issues to be noted, as there are several risks associated with CVP monitoring, and complications may occur in up to 15% of patients. These include problems during insertion, such as:

  • pneumothorax

  • trauma to the surrounding tissue

  • arrhythmias

  • incorrect positioning

  • air emboli.

Problems may also be noted after insertion. These include:

  • infection

  • thrombosis

  • air embolism

  • acting upon inaccurate CVP results.

Transducing the CVP

It is essential that the transducer system is adequately zeroed to an external reference point to ensure accurate readings. The reference point will depend upon local policy, but it is usual to use either the phlebostatic axis or the sternal notch.

Once the reference point has been determined the transducer should be zeroed prior to use and intermittently during use (frequency should be guided by local policy). Zeroing or recalibration is performed by:

  • turning off the three-way tap to the patient

  • opening the transducer to the atmosphere

  • selecting the appropriate zeroing area on the monitor

  • zeroing the transducer according to the manufacturer’s guidelines

  • closing the three-way tap to the atmosphere.

CVP values and waveforms

Normal CVP is considered to be in the range 2–10 mmHg (positive pressure ventilation and addition of PEEP will increase CVP values).

The normal waveform consists of an A, C, and V wave (see Figure 7.5). Each of these waves represents a different part of the cardiac cycle.

  • A wave represents atrial contraction, and the downward slope represents arterial relaxation.

  • C wave represents tricuspid valve closure.

  • V wave represents the pressure generated to the right atrium during contraction of the right ventricle.


Figure 7.5 Normal CVP waveform.

Figure 7.5 Normal CVP waveform.

(Reproduced from Adam SK and Osborne S, Critical Care Nursing: science and practice, Second Edition, 2005, with permission from Oxford University Press.)

The CVP may be altered by changes in the patient’s condition, but it is important that these are viewed alongside other clinical data from the CVS assessment.

Conditions that may cause CVP to rise include:

  • right ventricular failure

  • pericardial tamponade

  • fluid overload

  • pulmonary hypertension

  • tricuspid regurgitation

  • pulmonary stenosis

  • peripheral vasoconstriction

  • superior vena cava obstruction

  • pulmonary embolism.

Conditions that may cause CVP to fall include:

  • hypovolaemia

  • excessive diuresis

  • vasodilatation.

Removal of a CVP line

It may be necessary to remove the CVP line in order to replace it if there are signs of infection. A new line will need to be inserted prior to the removal of the old line if vasoactive or other infusions are utilizing the CVP line. The patient may also no longer require the line.

It is vital that no complications arise from the removal of the CVP line. Therefore, if the patient’s condition permits, the procedure should be performed as follows:

  • The patient should be positioned lying flat or with their head at a downward angle.

  • Infusions through the CVP line should be discontinued.

  • The catheter should ideally be removed during expiration to prevent air emboli.

  • The catheter should be slowly withdrawn.

  • Once the catheter has been removed a sterile occlusive dressing should be applied.

  • It may be necessary to send the catheter tip to the microbiology lab (local policy should be followed).

Reference

1 Marik PE and Cavallazzi R. Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense. Critical Care Medicine 2013; 41: 1774–81.Find this resource:

Cardiac output monitoring

The last decade has seen a significant increase in the number of cardiac output measurement tools available in critical care units. Some units may utilize a variety of systems, whereas in others there may be only one tool or a limited range available. Different cardiac output systems will provide additional data to estimation of cardiac output. The choice of cardiac output measurement tool is dependent on:

  • the equipment available in the local unit

  • the measurements required for the patient

  • the severity of the patient’s illness.

For decades the pulmonary artery catheter has been regarded as the gold-standard tool for cardiac output monitoring. However, increasingly a variety of other tools are being utilized to measure cardiac output. Many of the newer systems are less invasive than traditional methods. The critical care nurse may use systems such as the following:

  • pulmonary artery catheter

  • pulse contour cardiac output (PiCCO)

  • lithium dilution cardiac output (LiDCO)

  • trans-oesophageal Doppler system.

Pulmonary artery (PA) catheter

This is used to measure cardiac output, and also provides other measurements that may be useful in clinical practice. The pulmonary artery catheter is situated in the right side of the heart and enters the pulmonary artery. It is therefore able to measure:

  • right atrial pressure (RAP)

  • right ventricular pressure (RVP)

  • pulmonary artery pressure (PAP)

  • indirectly, left atrial pressure (pulmonary artery occlusion pressure, PAOP, which is also known as pulmonary artery wedge pressure, PAWP).

Cardiac output is measured using thermodilution. Other variables are also calculated, including:

  • systemic vascular resistance (SVR)

  • pulmonary vascular resistance (PVR)

  • oxygen consumption (VO2)

  • mixed venous oxygen saturations (SVO2).

The pulmonary artery catheter typically consists of four lumens.

  • The distal lumen (located in the pulmonary artery) is attached to the transducer for the measurement of cardiac output, and measures PAP. Mixed venous blood may be withdrawn from this lumen.

  • The proximal lumen (located in the right atrium) may be used for measurement of RAP.

  • The thermistor detects the patient’s blood temperature and receives input from a thermistor at the tip of the catheter.

  • The balloon inflation lumen is used to inflate the balloon for measurements of PAOP.

Insertion of a PA catheter

The nurse’s role is to assist with insertion, and a strict aseptic technique is required. The catheter is inserted through a large vein (subclavian or internal jugular vein). The catheter is advanced through the right side of the heart into the pulmonary artery and eventually into the ‘wedged’ position. The nurse may need to observe the monitor during insertion to advise about waveform alterations and monitor for signs of cardiac arrhythmias. It is important that the balloon is deflated after insertion, and that the line is secured firmly to the patient.

Complications related to PA catheter insertion and use include:

  • CVP line insertion complications (see Cardiovascular support p. [link])

  • ventricular arrhythmias

  • air embolism

  • misplaced catheter or knotting of the catheter

  • pulmonary artery rupture

  • pulmonary artery ischaemia or infarction

  • rupture of the right atrium

  • valve damage

  • infection.

Measuring cardiac output

Thermodilution

Older pulmonary artery catheter systems determine cardiac output by thermo dilution.

  • A measured volume of cold fluid (normally saline) is injected into the PA catheter in the appropriate port.

  • The temperature changed is sensed by a thermistor at the catheter tip and cardiac output is calculated from a temperature change curve that is generated by the computer as the cold fluid is injected.

  • Techniques used should follow manufacturer guidelines to ensure accuracy of cardiac output measurement.

Thermofilament

Newer pulmonary artery catheter systems allow for continual cardiac output monitoring without the need for insertion of cold fluid.

  • Distal section of catheter has a 10 cm thermal filament.

  • Catheter emits pulses of heat from the filament resulting in a change in blood temperature which is measured to generate cardiac output value.

  • Computes cardiac output over successive 3 minute intervals and then averaged out for continuous monitoring.

Measurement of pulmonary artery occlusion pressure

It may be necessary for PAOP (wedge pressure) to be measured from time to time, as this provides an indication of left atrial pressure and indirectly reflects left ventricular end diastolic pressure. This measurement is obtained by inflation of the balloon, and is best recorded at the end of expiration. It is essential that the correct technique is used.

  • Only use specific syringe which has a maximum of 1.5 ml capacity.

  • Inflate the balloon slowly until the trace flattens.

  • Once the trace has flattened, stop inflating the balloon, to prevent over-inflation.

  • Freeze the monitor and deflate the balloon (do not inflate the balloon for more than 15 s).

  • Move the cursor on the monitor to allow calculation of PAOP at the end of expiration.

  • When PAOP has been calculated, unfreeze the trace.

Normal values for PA catheter measurements

  • Stroke volume: 60–100 mL.

  • Cardiac output: 4–6 L.

  • Cardiac index: 2.5–4 L.

  • PAOP: 6–12 mmHg.

  • Mixed venous O2: 70–75%.

  • SVR: 800–1200 dyne/s/cm.5

Pulse contour analysis

The pulse contour system allows cardiac output studies to be recorded without the need for additional line insertion. The system is able to record continuous cardiac output by using data from the pulse contour of the arterial trace. Therefore cardiac output studies can be recorded without using additional monitoring lines such as a PA catheter.

However, some pulse contour systems do require the use of thermodilution techniques to recalibrate the system to ensure that the data provided are accurate. Some systems use pulmonary thermodilution to recalibrate the calculation system, and will therefore provide some continuous data and some ‘one-off’ measurements that are utilized to calculate other variables.

Because there is no necessity for a PA catheter, some of the measurements traditionally associated with PA studies cannot be recorded (e.g. PAOP). However, other variables that can have an impact on treatment plans can be recorded. Therefore data from pulse contour analysis differ from those produced by other cardiac output measurement systems.

Pulse contour variables that can be measured or calculated include:

  • continuous pulse contour cardiac analysis

  • cardiac index

  • stroke volume

  • stroke volume variation

  • systemic vascular resistance

  • index of left ventricular contraction.

In addition, some pulse contour systems utilize transpulmonary thermodilution to provide the following variables:

  • transpulmonary cardiac output

  • intrathoracic blood volume

  • extravascular lung water

  • cardiac function index.

The equipment required for studies using pulse contour systems varies depending upon the manufacturer. The two main systems are:

  • PiCCO© system (PULSION Medical Systems)

  • FloTrac/Vigileo© system (Edwards Lifesciences).

PiCCO© system

  • This utilizes a specialized thermistor striped arterial line, placed in a distal artery to measure the arterial waveform morphology.

  • An algorithm is used to calculate the cardiac output from the area under the curve of the arterial trace.

  • Transpulmonary thermodilution ensures the accuracy of calculations and is required to recalibrate the system.

FloTrac©system

  • This utilizes a blood flow sensor that is attached to a normal arterial line.

  • Cardiac output is calculated using an algorithm every 20 s.

  • This system does not require external calibration once it has been commenced.

  • No additional lines are required.

Normal values can be found in the user manual for each system.

These systems provide additional data, and the normal values for the additional measurements are listed in Table 7.4.

Table 7.4 PiCCO© and FloTrac© data variables

Measurement

PiCCO©

FloTrac©

Stroke volume variation

< 10%

< 13%

Intravascular blood volume

800–1000 mL/m2

Extravascular lung water

3–7 mL/kg

Cardiac function index

4.5–6.5 L/min

Global end diastolic volume

680–800 mL/m2

Stroke volume index

33–47 mL/beat/m2

Cardiac index

3–5 L/min/m2

2.5–4 L/min/m2

Lithium dilution cardiac output

This method utilizes the injection of lithium chloride to calculate the cardiac output.

  • Lithium is injected via a central or peripheral line.

  • A sensor in the arterial line detects the presence of lithium and calculates a plasma concentration–time curve.

  • This is used to calculate the blood flow.

The system is also able to generate continuous cardiac output by utilizing pulse power derivation, and is not dependent upon waveform morphology to calculate continuous cardiac output measurements.

Cardiac output is measured using the following equation:

Cardiac ouput =lithium dose (mmol) × 60area (1−PCV) (mmol/s)

It is therefore essential to measure the patient’s packed cell volume (PCV) to enable accurate measurements to be obtained.

Because the system utilizes the injection of lithium chloride to calculate the cardiac output, some precautions are necessary. These include:

  • limiting the number of measurements to 12 per day

  • not using the system on patients who:

    • are receiving lithium therapy

    • are receiving non-depolarizing NMBAs

    • weigh less than 40 kg

    • are in the first trimester of pregnancy.

The system has shown a good correlation with PA catheter thermodilution as long as there is no indicator loss and there is good blood flow. Repeated blood sampling of 3–4 mL of blood is needed, and concerns have been raised about the need for this in a critically ill patient.2

Variables calculated from the lithium dilution system (LiDCO©) are listed in Table 7.5.

Table 7.5 LiDCO© data variables

Systolic pressure variation

  • < 5 mmHg unlikely to be preload responsive

  • > 5 mmHg may be preload responsive

Pulse pressure variation

  • < 10% unlikely to be preload responsive

  • > 13–15% may be preload responsive

Stroke volume variation

  • < 10% unlikely to be preload responsive

  • > 13% may be preload responsive

Stroke volume index

3.3–4.7 mL/m2/beat

Left ventricular stroke work

58–104 gm/m/beat

Right ventricular stroke work

8–16 gm/m/beat

Coronary artery perfusion pressure

60–80 mmHg

Right ventricular end diastolic volume

100–160 mL

Right ventricular end systolic volume

50–100 mL

Right ventricular ejection faction

40–60%

Doppler cardiac output measurement

Cardiac output can also be estimated by using Doppler ultrasound to measure blood flow through the aorta, and utilizing this to calculate cardiac output. Generally most systems use a probe placed into the patient’s oesophagus to measure blood flow in the descending aorta. Some systems are externally placed (truly non-invasive), and are positioned suprasternally to allow calculation or measurement of flow. However, the oesophageal probe is used most frequently. This system requires no invasive lines and can be utilized in areas outside of critical care by experienced practitioners such as critical care outreach teams.

The systems work by measuring ultrasound waves that are reflected off moving red blood cells.

  • The movement of red blood cells causes a change in frequency proportional to the velocity of the red blood cells within the aorta.

  • When the diameter of the blood vessel is known, it is possible to calculate blood flow using the flow/velocity waveform.

  • A continuous real-time waveform is produced from the Doppler.

  • Continuous wave-contour analysis produces information about the circulation.

  • Continuous cardiac output is calculated using an algorithm based on the Doppler configuration and the patient’s height, weight, and age.

  • Peak velocity is determined by the amplitude of the wave.

  • Flow time is calculated by measuring the width of the base of the waveform.

  • This information can be used to guide and monitor interventions such as fluid therapy and inotropic support.

For the system to work accurately it is essential that the Doppler probe is positioned correctly and that the waveform produced by the Doppler is sharp and well defined. Doppler measurement is useful for most patients. However, caution is needed in the following situations:

  • presence of an intra-aortic balloon pump

  • presence of aortic pathology

  • recent surgery to the mouth, oesophagus, or stomach

  • severe coagulopathy

  • presence of oesophageal varices.

Reference

2 Drummond KE and Murphy E. Minimally invasive cardiac output monitors. Continuing Education in Anaesthesia, Critical Care & Pain 2012; 12: 5–10.Find this resource:

Vasoactive medications

The various monitoring tools discussed in this chapter highlight the need to manipulate blood pressure by using vasoactive medication. Therefore a knowledge of vasoactive drugs and their indications, contraindications, and mechanisms of action is essential for the critical care nurse.

A vasoactive medication is one that is generally used when fluid manipulation in the critically ill patient is unsuccessful. Put simply, a vasoactive medication may be defined as a drug that has the ability to change the diameter of a blood vessel. However, many vasoactive medications also have a direct effect on other elements of the cardiac system, so it is perhaps more appropriate to consider all of the effects of vasoactive medication. These include:

  • vasodilation

  • vasoconstriction

  • inotropic effects

  • chronotropic effects

  • dromotropic effects.

These categories can be summarized as follows:

  • Vasodilators are medications that relax the smooth muscle in the blood vessel wall, thereby facilitating vasodilation. Generally this leads to a decrease in arterial blood pressure, a reduction in cardiac preload, and a decrease in cardiac output.

  • Vasoconstrictors are medications that contract smooth muscle in the blood vessel wall, thereby causing vasoconstriction. This leads to an increase in blood pressure by causing an increase in systemic vascular resistance, cardiac preload, and cardiac output.

  • Inotropes are medications that increase the contractility of the cardiac muscle.

  • Chronotropes are medications that increase the heart rate.

  • Dromotropes are medications that increase conduction through the AV node.

The effects of vasoactive medications are predominantly mediated by the medication binding to a receptor that causes the effect. These include α‎- and β‎-receptors, and it is important to note that medications may bind to more than one type of receptor. The main receptor sites and effects are listed in Table 7.6.

Table 7.6 Receptor sites and effects

Receptor

Location

Action

α‎1

  • Vascular smooth muscle

  • Heart

  • Vasoconstrictor

  • Weak inotrope and chronotrope

α‎2

  • Vascular smooth muscle

  • Heart

  • Peripheral vasodilator

  • Inhibits noradrenaline release

β‎1

Heart

  • Inotropes increase cardiac contractility

  • Chronotropes increase cardiac rate

β‎2

  • Bronchial smooth muscle

  • Vascular smooth muscle

  • AV node

  • Bronchodilator

  • Skeletal muscle vasodilator

  • Dromotrope

Dopaminergic

Vascular smooth muscle

Renal and splanchnic vasodilator

The most common vasoactive medications used in critical illness include:

  • adrenaline

  • noradrenaline

  • dobutamine

  • dopexamine

  • dopamine.

Each of these drugs will bind to one or more receptors, and this will result in changes to vasomotor tone, contractility of the heart muscle, and speed of contraction and thus heart rate. Table 7.7 lists the receptors for each of these key medications. Further information about each of these drugs is provided later in this chapter.

Table 7.7 The effect of vasoactive medications on receptors

α‎1-receptor

β‎1-receptor

β‎2-receptor

Dopaminergic receptor

Adrenaline

++

+++

++

0

Noradrenaline

+++

++

0

0

Dobutamine

0

+++

+

0

Dopexamine

0

++

+++

+

Dopamine

Low dose

0

0

+++

Moderate dose

0

++

+

0

High dose

+++

+++

0

0

Vasoactive medications may cause side effects, and it is important that the benefits of the medication are not outweighed by its side effects. Side effects may be dose dependent and include:

  • cardiac arrhythmias

  • myocardial ischaemia

  • decrease in renal perfusion

  • decrease in splanchnic perfusion

  • peripheral ischaemia

  • labile blood pressure

  • lactic acidosis.

Overview of specific vasoactive medications

Noradrenaline

  • Dominant effect on α‎1-receptors.

  • Increases blood pressure by vasoconstriction.

  • Preferred medication for patients presenting with sepsis3 (see Cardiovascular support p. [link]).

  • May cause a reduction in cardiac output as afterload increases.

  • May reduce renal and splanchnic perfusion.

  • May increase coronary blood flow as a result of increase in diastolic pressure.

  • Requires careful titration to ensure that the correct dose is given to maximize effectiveness and minimize side effects.

  • Adverse effects include:

    • arrhythmias

    • poor peripheral perfusion (at high doses)

    • chest pain

    • headache.

Adrenaline

  • Acts on α‎- and β‎-receptors.

  • At low doses predominantly affects β‎-receptors and causes increased cardiac contractility and heart rate.

  • At higher doses predominantly affects α‎-receptors and causes increased blood pressure through vasoconstriction.

  • Net effect is to increase heart rate, blood pressure, and cardiac output.

  • Increases myocardial oxygen requirements as heart rate increases.

  • May decrease renal and splanchnic perfusion at higher doses.

  • May be given as a bolus in emergency situations (see Chapter 15).

  • Increases blood glucose levels.

  • Acts as a bronchodilator (acts on β‎2-receptors).

  • May cause vasodilation at some doses, as it acts on skeletal muscle β‎2-receptors.

  • May worsen acidosis as rate of metabolism increases.

  • Requires careful titration to ensure that the correct dose is given to maximize effectiveness and minimize side effects.

  • Adverse effects include:

    • arrhythmias

    • myocardial ischaemia

    • chest pain

    • headache

    • dizziness

    • increased anxiety and nervousness.

Dobutamine

  • Acts on β‎1-receptors.

  • Effect is mainly inotropic, and causes increased contractility of cardiac muscle.

  • Has some chronotropic properties and increases cardiac rate.

  • Important to ensure adequate preload prior to commencing this medication, as it may cause tachycardia when given to a hypovolaemic patient.

  • Has some effect on β‎2-receptors and may cause vasodilation, and reduce SVR and left ventricular end diastolic pressure.

  • Requires careful titration to ensure that the correct dose is given to maximize effectiveness and minimize side effects.

  • Adverse effects include:

    • arrhythmias

    • tachycardia

    • headache

    • nausea.

Dopexamine

  • A synthetic analogue of dopamine.

  • Acts mainly on β‎-receptors.

  • Has some effect on dopaminergic receptors.

  • Improves blood flow to mesenteric, renal, cerebral, and coronary arteries.

  • Has some effect on decreasing noradrenaline release.

  • Useful inotrope for patients with acute heart failure.

  • May be appropriate for attenuating the inflammatory response in patients with sepsis.

  • Adverse effects include:

    • tachycardia

    • arrhythmias

    • nausea

    • vomiting

    • headaches.

Dopamine

  • Acts on dopaminergic receptors and on α‎- and β‎-receptors.

  • Effect is dose dependent.

  • Low-dose dopamine is not advised because of negative effects on gastric motility, splanchnic oxygen consumption, and the immune system.

  • Higher-dose dopamine is an effective vasopressor and is recommended as a substitute for vasopressor in sepsis in highly selected patients (i.e. those not at risk of tachyarrhythmias).3

  • Moderate doses increase cardiac contractility.

  • Adverse effects include:

    • tachycardia

    • arrhythmias

    • nausea

    • vomiting

    • hypertension.

Reference

3 Dellinger R et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock. Critical Care Medicine 2013; 41: 580–637.Find this resource:

Intra-aortic balloon pump

An intra-aortic balloon pump is a mechanical device that sits in the aorta and is used as a temporary measure to support acute heart failure.

The intra-aortic balloon pump uses counter pulsation to support the failing heart—that is, the balloon inflates during diastole and deflates during early systole. This causes volume displacement of blood within the aorta both proximally and distally. The volume displacement increases coronary blood flow and has the potential to subsequently improve systemic perfusion by increasing cardiac output.

The purposes of the balloon pump are to:

  • increase myocardial oxygenation

  • increase cardiac output

  • increase oxygen delivery

  • increase myocardial oxygen uptake.

It is usually used to support patients:

  • with cardiogenic shock

  • post cardiac surgery

  • post myocardial infarction to support mechanical defects

  • pre-operatively if they are awaiting surgery with unstable angina.

Intra-aortic balloon pumps are contraindicated in:

  • severe aortic valve insufficiency

  • aortic dissection

  • aorta iliac occlusive disease.

The timing of the counter-pulsation therapy is critical, as it is vital that the balloon inflates after the aortic valve has closed and deflates before the opening of the aortic valve. Timings are normally coordinated by using either the ECG complex or the arterial waveform. Suboptimal timing of the counter-pulsation therapy can lead to haemodynamic instability. Therefore it is essential that the console is set up correctly by an expert practitioner.

Nursing care for the patient with an intra-aortic balloon pump involves:

  • monitoring cardiovascular observations

  • monitoring for side effects of the intra-aortic balloon pump

  • psychological care.

Side effects include:

  • distal ischaemia

  • compartment syndrome

  • development of embolisms

  • renal problems

  • aortic damage or dissection

  • haemorrhage.

The device is normally removed once the patient is more stable. This may be indicated by a decreasing need for inotropic support and improved cardiac output. It is important that the intra-aortic balloon pump is gradually weaned, and the device should never be abruptly stopped as this may lead to thrombus formation.

Pacing

Cardiac pacing is normally indicated when there are cardiac conduction problems. These may be related to cardiac ischaemia or damage, or may be linked to other aspects of critical illness.

Pacing is commonly used:

  • to treat heart blocks—usually complete (third-degree) or Mobitz type 2 blocks (see Chapter 6, Cardiovascular support p. [link]).

  • to override arrhythmias and to treat asystole.

  • prophylactically post cardiac surgery (especially valve surgery).

  • non-cardiac diseases such as Guillain–Barré syndrome sometimes require pacing in the event of profound bradycardia that does not respond to medication.

Most pacing in critical care is of a temporary nature, although occasionally permanent systems may be required. Temporary pacing units usually consist of:

  • a pulse generator

  • pacing leads with electrodes.

Pacing systems may be:

  • transvenous

  • epicardial

  • transcutaneous.

Transvenous pacing

  • This type of pacing requires a bipolar venous catheter to be inserted through a large vein.

  • The internal jugular and subclavian sites are preferred.

  • The tip of the catheter is placed in contact with the endocardium of the right ventricular apex.

  • The catheter has a positive proximal electrode and a negative distal electrode.

  • These are connected to the respective generator terminals on the pulse generator.

  • The pulse generator voltage threshold is set to ensure that pacing is adequate.

  • A pacing spike should then be seen before each stimulated complex.

Epicardial pacing

  • Pacing leads are placed during surgery on the epicardium.

  • This approach is commonly used post cardiothoracic surgery as a temporary measure in the event of post-operative inflammation and complications.

  • The wires are connected to an external temporary pulse generator.

  • The threshold is set.

  • A pacing spike should then be seen before each stimulated complex.

  • Wires may be removed externally when they are no longer needed, as directed by the surgeon.

Transcutaneous pacing

  • This type of pacing is generally only used in emergency situations.

  • Large gel pads are placed directly on the chest wall.

  • Normally they are positioned anteriorly to the left of the sternum and posteriorly on the patient’s back.

  • Transcutaneous pacing may be used to treat bradycardia where the patient is haemodynamically compromised, until another system can be inserted.

  • The electrodes need to make good contact with the skin in order for the pacing system to capture effectively (capture refers to successful deporalisation after the pacing impulse has been delivered).

  • An on-demand mode should be used in the patient with bradycardia, to prevent possible arrhythmias.

  • This type of pacing has the potential to cause discomfort to the patient, so is reserved exclusively for emergency situations.

Overriding arrhythmias

Occasionally pacing may be used to ‘override’ fast arrhythmias. This involves the doctor setting the pacemaker to a faster rate than the patient’s tachycardia (normally 10–15 beats/min faster). It may be used to suppress supraventricular tachycardia, atrial flutter, and ventricular tachycardia. However, it is not effective in suppressing atrial fibrillation or sinus tachycardia.