Curves.pdf

8/18/2019 Curves.pdf

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Curves

1. Patient ventilator-dyssynchrony

2. ECGs

3. Capnographs

4. Arterial waveforms

5. Flow-volume loops

6. ICP waveforms


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Patient-ventilator dyssynchrony

1. Trigger

2. Flow

3. Exhalation

Case

An old age lady with the history of COPD is ventilated in the ICU. When he sedation is being

weaned off she becomes agitated, restless and sweaty.

What are the differential diagnoses?

Pain

Anxiety

Hunger

Mechanical complications: Pneumothorax, sputum plug. Haemorrhage, cardiac

ischemia/APO, tube dislodgement

Pulmonary embolism

Dys-synchrony with the ventilator

What is the next step in her managements?

Resuscitation

Finding out the cause of the problem

ASSESSMENT

Examination

work of breathing

respiratory pattern

audible sounds (e.g. cuff leak, stridor, wheeze)

chest findings (e.g. hyperexpansion, dullness, crackles)


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Monitor

vital signs

ETCO2

SpO2

Ventilator

waveforms

alarms

Chest x-ray

MANAGEMENT

Resuscitation

address life threats

disconnect patient from ventilator and replace with BVM if required

Address patient factors

treat patients respiratory pathology affecting resistance and/ or compliance (e.g. sputum,

bronchospasm, chest wall eschar, pneumothorax)

treat other patient factors (e.g. hunger, pain, weakness, sleep ,sedation, nutrition, physiotherapy)

Correct problems with the endotracheal tube

kinking

obstruction (e.g. secretions blocking)

impingement on carina or between cords

Correct problems with the ventilator

choose appropriate ventilator

choose appropriate mode

ensure sensitivity is not too low or high

choose appropriate ventilator rate set appropriate flow rate

check that patient isn’t auto-triggering (cardiogenic oscillations, high sensitivity, circuit

leaks, water condensation in the circuit)

sedate patient to reduce agitation

taking over ventilation if fatigue is apparent


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Address ineffective triggering

address PEEPi: — apply increased externally applied PEEP — decrease tidal volume andrespiratory rate — increase expiratory time — bronchodilators

address weakness: — nutrition — reduce sedation — physiotherapy

adjust trigger sensitivity threshold (may lead to inappropriate triggering)

Exhalation dysynchrony

treat underlying patient factors (e.g. COPD, asthma)

adjust exhalation sensitivity or change to time-control cycling between inspiration andexpiration or change to a volume-cycled mode


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Figure 1 Genuine patient triggering (middle) and auto-triggering (right) and with the ventilator

set to pressure trigger and PEEP>0

Autotriggering

triggering of the ventilator in the absence of inspiratory muscle contractionmay result from:

circuit leakcoughing/hiccupswater in circuitseizurescardiogenic oscillations

trigger sensitivity set too low

most common cause for this is a circuit leak. This results in a fall in circuitpressure (figure 1) or a discrepancy between flow leaving the ventilator andreturning to the ventilator.


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Figure 2. Trigger delay indicated by a negative deflection in pressure waveform prior to delivery

of breath and a change in slope of flow waveform. Shaded area on pressure waveform

represents work of triggering

Figure 3. Trigger failure


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Oesophageal pressure (Peso) and flow tracings in the context of patient inspiratory effort. In the

Peso tracing, note that in addition to the effort which starts an inspiratory cycle, there is a second

effort that proves ineffective (hollow arrow).

Oesophageal pressure monitoring is more sensitive than ventilator flow measurement in the

assessment of ineffective triggering.

Causes

1. Patient factors

high PEEPi (must generate enough effort to overcome PEEPi)

weakness

incorrect ventilator settings

ventilator dysfunction

2. ventilator factors

o high level of pressure support or high tidal volume causing gas trapping and

intrinsic PEEP (see above)


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o expiratory asynchrony with delayed opening of exhalation valve

PEEPi is one of the cause of ineffective triggering

Double triggering

Causes

inspiratory time too short> controlled modes


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inspiratory flow rate too low

set tidal volume low> ARDS

coughing and hiccups

Figure 4. Inadequate inspiratory flow

Another example of flow dyssynchrony> inadequate inspiratory flow

Clinically, this presents as upper airway obstruction with signs such as accessory muscle

use,paradoxical breathing, tracheal tug.

Flow related. Low flow or too high flow, also called flow dyssynchrony


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(in constant flow modes (eg volume preset assist control) the inspiratory flow rate may be

inadequate to match the patient’ s attempted inspiratory flow rate).

inspiratory asynchrony may be reduced by use of proportional assist ventilation (PAV) or NAVA

Figure 5. Change in flow waveform characteristic of premature inspiratory to

expiratory cycling in pressure support mode > Premature inspiratory-expiratory

cycling

Termination dyssynchrony. Display of flow (top) and pressure (bottom) versus

time reveals an example of “delayed termination dyssynchrony” (solid arrow) as the

patient attempts exhalation before completion of the inspiratory breath, and “prematuretermination dyssynchrony” (dotted arrows) as the patient makes an inspiratory effort

early in the expiratory phase.


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Arterial waveforms

SPV

Arterial pressure rises during inspiration and falls during expiration due to changes in intra-

thoracic pressure secondary to positive pressure ventilation. > 10 is considered significant.

CAUSES OF INCREASED SYSTOLIC PRESSURE VARIATION

•Hypovolaemia

•Tamponade •Constrictive pericarditis

•LV dysfunction

•Massive PE

•Bronchospasm

•Dynamic hyperinflation

•Pneumothorax

•Raised intrathoracic pressure

•Raised intraabdominal pressure

The utility of SVV is limited in the following settings:

•small tidal volumes (tidal volume must be at least 8 mL/kg)

•spontaneous breathing (patient must have 100% controlled mechanical ventilations at a fixed

rate)

•ARDS and low lung compliance (false negatives more likely)


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•PEEP (may increase SVV)

•arrhythmia (R-R interval must be regular on ECG)

•low heart rate/respiratory rate ratio

•open chest

•right ventricular systolic dysfunction •norepinephrine (may decrease SVV)

•vasodilators (may increase SVV)

•b-blocker medication

Over-damped waveform is slurred -looking and under-damped is overshooting.


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Under-damped waveform overestimates the systolic pressure and under-estimate the diastolic

pressure but the MAP is unaffected. Long stiff tubing and increased vascular resistance are the

causes of under-damping.

Over-damped waveform under-estimates the systolic and over-estimate the diastolic pressures

but again MAP is unaffected. Causes include air bubbles, compliant tubing, catheter kink,blood clots/fibrin, stopcocks, no fluid or low flush bag pressure.

Calibrating (‘zeroing’)

ensure the transducer pressure tubing and flush solution are correctly assembled and freeof air bubbles

place transducer at level of the right atrium

‘off to patient, open to air (atmosphere)’

press ‘zero’ -> sets atmospheric pressure as zero reference point

whenever patient position is altered the transducer height should be altered

Square wave test

aka fast flush test

snap flush to generate square wave

check for oscillations as an indicator of the harmonic characteristics of the system

usually only 1 oscillation before returning to baseline

2 or more oscillations before returning to baseline (underdamped)

if no oscillations (overdamped – response speed is too slow)

A good art line trace has a distinct dicrotic notch, and after the fast flush test there are two

oscillations only.

ACCURACY AND MEASUREMENT ERRORS

Conditions that must be met to ensure accuracy

cannula properly placed within the lumen of an unobstructed artery (ie. no spasm,

thrombus, atheroma proximal to cannula)

cannula not kinked or obstructed

cannula connected by short, rigid, wide-bore tubing to the transducer

no air bubbles in tubing or transducer

interface from fluid to transducer accurately transmits deflections

transducer has adequate frequency response (natural frequency > 100Hz)

transducer is leveled and zeroed to desired point (ie. left atrium)

no zero drift

monitor calibrated accurately

Common sources of error


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bubbles in catheter-transducer system -> decreased resonant frequency

clotting in arterial catheter

elastic walls causes increased damping

cannula won’t flush – kinked, clotted, tissued

OTHER INFORMATION

Information other than blood pressure can be obtained:

pulse rate and rhythm

effects of dysrhythmia on perfusion

ECG lead disconnection

continuous cardiac output using pulse contour analysis

specific wave form morphologies might be diagnostic

— e.g. slow rising = AS, pulsus alternans = tamponade

pulse pressure variation (suggests fluid responsiveness)

steeper upstroke of pulse pressure = increased contractility area under upstroke = SV

steep downstroke = low SVR

Advantages of using MAP rather than SBP/DBP

least dependent on measurement site or technique (whether invasive or not)

least altered by damping

determines tissue blood flow via autoregulation

COMPLICATIONS

Pain

thrombosis and distal ischaemia

infection

increased diagnostic blood loss and anemia

retrograde air embolism

inadvertent drug/air injection

haematoma (+/- nerve compression)

retroperitoneal haematoma (femoral)

bowel perforation (femoral)

vessel damage may lead to stricture and prevent future AV fistula formation for

haemodialysis

pseudo-aneurysm

arterial dissection

arteriovenous fistula

EVIDENCE


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A 2014 observational study using propensity matching based on the Project IMPACT

database found no mortality benefit for use of arterial catheters in medical ICU patients

requiring mechanical ventilation.


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Capnographs

A, Prolonged phase II, increased α angle, and steeper phase III suggest bronchospasm or airway

obstruction.

B, Expiratory valve malfunction resulting in elevation of the baseline, and the angle between the

alveolar plateau and the downstroke of inspiration is increased from 90°. This is due torebreathing of expiratory gases from the expiratory limb during inspiration.

C, Inspiratory valve malfunction resulting in rebreathing of expired gases from inspiratory limb

during inspiration .

D, Capnogram with normal phase II but with increased slope of phase III. This capnogram is

observed in pregnant subjects under general anesthesia .

E, Curare cleft: Patient is attempting to breathe during partial muscle paralysis. Surgical

movements on the chest and abdomen can also result in the curare cleft. (You have maybe 3minutes to sedate the patient before they begin to waken or start to fight the tube.)

F, Baseline is elevated as a result of carbon dioxide rebreathing.

G, Esophageal intubation resulting in the gastric washout of residual carbon dioxide andsubsequent carbon dioxide will be zero.

H, Spontaneously breathing carbon dioxide waveforms where phase III is not well delineated.

I, Dual capnogram in one lung transplantation patient. The first peak in phase III is from the

transplanted normal lung, whereas the second peak is from the native disease lung. A variation ofdual capnogram (steeple sign capnogram – dotted line) is seen if there is a leak around the


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sidestream sensor port at the monitor. This is because of the dilution of expired PCO2 with

atmospheric air.

J, Malignant hyperpyrexia where carbon dioxide is raising gradually with zero baseline

suggesting increased carbon dioxide production with carbon dioxide absorption by the soda lime.

K, Classic ripple effect during the expiratory pause showing cardiogenic oscillations. Theseoccur as a result of to-and-for movement of expired gases at the sensor due to motion of the

heartbeat during expiratory pause when respiratory frequency of mechanical ventilation is low.

Ripple effect like wave forms also occur when forward flow of fresh gases from a source duringexpiratory pause intermingles with expiratory gases at the sensor.

L, Sudden raise of baseline and the end-tidal PCO2 (PETCO2) due to contamination of the

sensor with secretions or water vapor. Gradual rise of baseline and PETCO2 occurs when sodalime is exhausted.

M, Intermittent mechanical ventilation (IMV) breaths in the midst of spontaneously breathing patient. A comparison of the height of spontaneous breaths compared to the mechanical breaths

is useful to assess spontaneous ventilation during weaning process.

N, Cardiopulmonary resuscitation: capnogram showing positive waveforms during eachcompression suggesting effective cardiac compression generating pulmonary blood.

O, Capnogram showing rebreathing during inspiration. This is normal in rebreathing circuitssuch as Mapleson D or Bain circuit.

Ref. Kodali, Bhavani Shankar Anesthesiology. 118(1):192-201, January 2013.


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The examiner may ask you : 1). Indications of monitoring the ICP 2) Different methods

available. 3). Management of raised ICP.


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Inflation of the balloon is triggered by the the beginning of diastole, which correlates with the

middle of the T-wave.

The balloon is timed to deflate at the very end of diastole. This correlates with the R-wave on the

ECG, and this is the most commonly used trigger for balloon deflation.


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Unassisted Peak Systolic Pressure? A Diastolic Augmentation / Augmented Peak Diastolic Pressure? D

Balloon Aortic/ Assisted End Diastole Pressure? F

Assisted Peak Systolic Pressure? E

Unassisted End Diastolic Pressure? B

Balloon inflation? C

What features seen on the aortic pressure waveform indicate optimal timing and function of

the IABP?

Optimal timing and function ofIABP has the following features:

inflation of the balloon occurs at the dicrotic notch (forming the sharp ‘V’)

the slope of rise of augmented diastolic waveform is straight and parallel to the

systolic upstroke

the augmented peak DBP at balloon deflation exceeds or is equal to end-systolic BP

the balloon aortic end-diastolic BP (DBP at balloon deflation) is lower than the

preceding unassisted end-DBP by 15-20 mmHg

the assisted SBP (following a cycle of balloon inflation) is lower than the previousunassisted SBP by 5 mmHg

The timing of IABP inflation and deflation should be manually adjusted to achieve these optimalwaveform characteristics if they are absent.


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Deflation of the IAB is too early – it occurred well before the onset left ventricular contraction and the

start of systole.

Waveform features:

There is a sharp drop in pressure immediately following the peak of diastolicaugmentation (peak B).

Diastolic augmentation may be suboptimal but it is difficult to confirm in the absence of

a pressure scale or comparison to an unassisted waveform.

Assisted aortic end-diastolic BP may be sub-optimally increased (trough C), but it is

difficult to say based on the information given. With early deflation a widened U-shaped

trough is typically seen. Early deflation can lead to an assisted aortic end-diastolic BP

that equals or exceeds the unassisted aortic end-diastolic BP (trough F), although this isnot the case in this scenario.

Assisted SBP (peak D) is the same or higher than the unassisted SBP (peak A) – it should be slightly less.


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Inflation of the IAB is occurring too early – it occurred prior to aortic valve closure (indicated by the

absence of a dicrotic notch).

Waveform features:

Diastolic augmentation (peak B) encroaches on the peak corresponding to unassisted

systole (peak A) – the two peaks have merged and are barely distinguishable.

There is no ‘sharp V’ or dicrotic notch between peaks A and B.


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Deflation of the IAB is occurring too late – deflation is occurring as the aortic valve is opening

Waveform features:

The peak corresponding to diastolic augmentation (peak C) is widened.

Assisted aortic end-diastolic BP (trough E) is the same as, not lower than, the unassisted

aortic end-diastolic BP (trough G).

The upstroke of assisted systolic BP (peak F) has a gentle gradient resulting in a

prolonged rise

Triggering of the IABP is usually set according to the patient’s ECG tracing. When an R wave is detected

the balloon is triggered to automatically start inflating in the middle of the T wave.Triggering can be impaired if the patient develops an arrhythmia, is paced or has a poor ECG trace.

If the IABP cannot be successfully triggered using the R waves from the ECG trace, pacingspikes or the arterial blood pressure waveform may used for triggering. Alternatively, the pump

can be set at an intrinsic rate without any physiological triggering. The IABP may automatically

use these other modes as default backups if ECG-triggered timing is not possible.If the patient

remains hemodynamically stable despite the IABP malfunctioning it might be a good time to


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think about removing the IABP… Treating any underlying causes of arrhythmia is also a good

idea!

Inflation of the IAB is occurring too late – it occurred well after the dicrotic notch (B).

Waveform features:

Inflation of the IAB occurs after the dicrotic notch ( B)

Absence of a sharp V at the point of IAB inflation (should occur at B – the dicrotic notch)

The augmented DBP (peak C) is less than the unassisted SBP (peak A) – it should be

higher

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