PRESSURE MONITORING ARTERIAL MONITORING PRESSURE MONITORING

PRESSURE MONITORING
Indirect & intermittent measurements of vascular pressures are considered
inadequate in unstable critical patients
Direct measurement involves the connection of a transducer system via fluid-filled
manometer tubing to a cannula placed in an appropriate vessel
ADVANTAGES;
1. Continuous information on the arterial & venous pressures
2. Information available from the waveform
3. Blood sampling (via arterial)
POTENTIAL SOURCES OF ERRORS:
1. Zero errors:
- inaccurate zeroing of transducer
- imprecise placement of the transducer
2. Kinks, clots, bubbles in the manometer tubing leading to ;
- Damping: Flattening of the pressure trace which underestimated systolic
& overestimates the diastolic pressure. MEAN is accurate
- Resonance: Overshoot of the pressure waveform due to resonant
oscillations within the measuring system. Overestimates systolic &
underestimates the diastolic pressure. MEAN is accurate.
ARTERIAL PRESSURE MONITORING
Arterial cannulation with continuous pressure waveform display remains the
accepted standard for BP monitoring
Indications and Advantages
- Frequent ABG’s and blood sampling
- Continuous real-time monitoring when rapid, moment-to-moment BP
changes are anticipated, i.e. CV instability, major fluid shifts or EBL
- Failure of indirect BP monitoring i.e. morbid obesity, burned extremity
- Deliberate induced induced hypotension
- Cardiac surgery for cardiopulmonary bypass
- Major vascular surgery
- Administration of vasoactive drug infusions

The arterial tree starts with the aorta and the major branches of this vessel. The
aorta and its branches stretch to receive blood from the left ventricle and recoil
to distribute the blood and to maintain arterial pressure. Arteries and arterioles
control blood pressure through vasoconstriction or vasodilation. Arterioles are the
primary sites that contribute to systemic vascular resistance (SVR).


Arterial pressure is measured at its peak, which is the systolic blood pressure
(SBP), and at its trough, which is the diastolic blood pressure (DBP).
Pulse pressure is the difference between systolic and diastolic pressure.
A normal pulse pressure in the brachial artery is approximately 40 mm Hg.
An increased pulse pressure may be the result of increased stroke volume or
ejection velocity and is common during fever, exercise, anemia, and
hyperthyroidism. Other causes of increased pulse pressure include bradycardia
(increased stroke volume), aortic regurgitation, and arterial stiffening, which is
most noticeable after the age of 50 to 60 years.
An acute decrease in pulse pressure may indicate an increase in vascular
resistance, decreased stroke volume, or decreased intravascular volume.
Systemic mean arterial pressure (MAP) is defined as the mean perfusion pressure
throughout the cardiac cycle. MAP is sensed by baroreceptors located in the
carotid sinuses and the arch of the aorta. These receptors control arterial pressure
mainly by adjusting heart rate and arteriolar vessel radius. MAP is also the basis
for autoregulation by some organ systems such as the kidney, heart, and brain.

Over damping causes slurred upstroke, absent dicrotic notch, and loss of fine
detail
Causes include blood clots, air bubbles in the tubing, and kinked catheters


Under damping produces exaggerated peaks and troughs in the waveform

It can cause falsely high systolic pressures and low diastolic pressures
Causes include long connecting lines (>1.4 mm), small tubing (<1.5 mm internal
diameter), or when the catheter occlude the vessel
Transducer Leveling and Zeroing
The pressure transducer is exposed to atmospheric pressure to establish the zero
pressure reference value against which all intravascular pressures are measured
In the supine patient, pressure transducers are leveled most often to the midchest
position in the midaxillary line.
In other than supine positions (head injuries, CHF etc.), the transducer should be
placed at the level of the aortic root (Chest 2001; 120:1322-1326)
The central MAP and particularly the aortic mean is the key component in coronary
and cerebral perfusion as well as the pressure that is sensed by baroreceptor
mechanisms. This is the pressure that is indirectly measured using standard
noninvasive BP techniques.
The Arterial Waveform in relation to the ECG


Left ventricular contraction creates a pressure pulse or pulse wave. It is the pressure
pulse that a clinician feels when determining a patient's pulse by palpation. The
pressure pulse is also what is sensed by the intra-arterial catheter. The systolic
pressure is measured at the peak of the waveform. The dicrotic (or downward) limb
is demarcated by the dicrotic notch, representing closure of the aortic valve and
subsequent retrograde flow. The location of the dicrotic notch varies according to the
timing of aortic closure in the cardiac cycle. For example, aortic closure is delayed in
patien ts with hypovolemia. Consequently, the dicrotic notch occurs farther down on
the dicrotic limb in hypovolemic patients. The dicrotic notch also appears lower on
the dicrotic limb when arterial pressure is measured at more distal sites in the
arterial tree (Figure 3). The shape and proportion of the diastolic runoff wave that
follows the dicrotic notch changes with arterial compliance and heart rate. Diastolic
pressure is measured just before the beginning of the next systolic upstroke.

1.
2.
3.
4.
5.
6.

Systolic Upstroke
Systolic Peak Pressure
Systolic Decline
Dicrotic Notch
Diastolic Runoff
End-diastolic Pressure


SITES:
1) Radial
2) Ulnar
3) Femoral
4) Dorsalis pedis
Brachial artery to be avoided as it is an end –artery
COMPLICATIONS:
1) Hemorrhage
2) Thrombosis
3) Accidental drug injection with subsequent ischemia (LABEL ACCURATELY)
4) Infection
5) Nerve injury
6) Pseudoaneurysm. Due to weakening of the wall of the artery.
7) AV fistula formation
CENTRAL VENOUS MONITORING

What is CVP?
It is the pressure in the right atrium
It indicates mean right atrial pressure and is frequently used as an estimate of right
ventricular preload
CVP does not measure blood volume directly & is influenced by;
- The right heart function
- Venous return to the heart
- Right heart compliance
- Intra thoracic pressure
- Patient positioning
When should CVP be measured?
- Patients with hypotension not responding to basic clinical management
- Continuing hypovolemia secondary to major fluid shifts or loss
- Patients requiring infusions of inotropes
INDICATIONS:
- Monitoring CVP
- Infusion of irritant solutions
- Infusion of vasoactive drugs
- Inadequate peripheral venous access
- Long-term venous access – TPN, Chemotherapy
- Access to central circulation – pacing, hemodialysis, PA catherisation
SITES:


-

Subclavian vein :
- High incidence of pneumothorax (upto 20%)
- Bleeding from punctured subclavian artery difficult to control
- Comfortable for patient

- Suitable for tunneling
- Internal jugular
- Damage to neck structures
- Risk of pneumothorax
- Reliable access to the right atrium
- Less comfortable to patient
- Femoral vein
- Useful if clotting is deranged or if patient does not tolerate head down
position/tilt
- Convenient site for large bore catheters (Dialysis)
- Higher risk of infection
- Unreliable for CVP, unless catheter is long enough to reach above the
diaphragm
- Antecubital (Basilic vein)
- Convenient
- Avoids damage to structures in the neck & thoracic inlet
- Risk of damage to brachial artery & median nerve
- Difficult to maneuver past the clavipectoral fascia (90% success rate)
- Risk of thrombophlebitis
- External jugular
- Useful for temporary access
- Difficult to pass guidewire into the SVC
- Potentially less damaging

COMPLICATIONS:
A) Of venous puncture:
- Arterial puncture
- Pneumothorax
- Air embolism (minimized by head down tilt)
- Damage to larynx, thyroid, thoracic duct, esophagus, brachial plexus,

recurrent laryngeal nerve.
B) Of Catheter residence
- Sepsis
- Thrombosis
- Phlebitis
- Venous stenosis
- Endocarditis
- Erosion through the vessel
- Arrhythmias


CVP is measured relative to a reference point – Intersection of the mid-axillary line &
the 2nd/ 3rd intercostals space with the patient in the supine position
Equipment consists of an externally placed measuring device (transducer), the
pressure being transmitted to it by a column of fluid within a centrally placed
catheter.
- Fluid filled manometer (cmH2O)
- No expensive equipment
- No waveform
- No continuous monitoring
- Accidental air embolism
- Zero errors
- Transducer (mmHg)
- Continuous
- Waveform
- Expensive consumables & hardware
- Zero errors
A normal value in spontaneously breathing patient is 5-10 cmH2O , rising 3-5 cmH2O
during mechanical ventilation (10 cmH2O = 7.5 mmHg = 1 kPa)
An absolute value is not as important as serial measurements & the change in

response to therapy.
Should be interpreted alongside other measures of cardiac function such as;
- Pulse
- Blood Pressure
- Urine output
(CVP measurement may be in the normal range in the presence of hypovolemia due
to venoconstriction)
In a normal patient the mean right atrial pressure measured by the CVP closely
resembles the mean left atrial pressure (LAP). At end diastole left atrial pressure is
assumed to equal left ventricular end diastolic pressure (LVEDP), which in turn is
assumed to reflect left ventricular end diastolic volume (LVEDV). Thus, in normal
patients, CVP is assumed to be a reflection of left ventricular preload.
However in patients with a cardiac disease, the right & left ventricles may function
differently. In this scenario, the PCWP is a better indicator of left atrial pressure.
Underfilling or overdistention of the venous collecting system can be recognized by
CVP measurements before clinical signs have become apparent. Under normal
circumstances an increased venous return results in an augmented cardiac output,
without significant changes in CVP. However with poor right ventricular function, or
an obstructed pulmonary circulation, the right atrial pressure rises, therefore
causing a resultant rise in measured CVP. Similarly, although it is possible for a
patient with hypovolaemia to exhibit a CVP reading in the normal range due to


venoconstriction, loss of blood volume or widespread vasodilation will result in
reduced venous return and a fall in right atrial pressure and CVP.
TECHNIQUE: GENERAL PREPARATION
- Sterile
- Head down tilt
- Consent
- All equipment ready

- Know your anatomy well
- Aspirate gently while advancing the needle
- Hold wire while advancing the catheter (Take care not to allow the wire
to be pushed further into the vein)
- Check all lines for patency & flush them with saline.
- X-ray chest post procedure
PROBLEMS:
1) ARTERIAL PUNCTURE:
Possible in a hypotensive or hypoxic patient. Usually obvious. Connect to
saline –
If pulsatile or blood flows to higher than 30 cm vertically, remove &
apply
pressure for at least 10 minutes or longer if necessary
2) PNEUMOTHORAX:
Air may be aspirated into the syringe or patient may become breathless. X-ray
chest followed by ICD insertion.
If CVP monitoring is absolutely necessary, try same side other route or
Femoral
vein for access. DO NOT TRY OPPOSITE SIDE (risk of bilateral
pneumothorax)
3) ARRHYTHMIA –
Withdraw catheter or guidewire
4) AIR EMBOLUS:
In hypotensive, spontaneously breathing patients. Care should be taken to
block open ports. Also prevented by head down tilt.
5) WIRE WILL NO THREAD DOWN THE NEEDLE:
- Check if needle is in vein
- Flush with saline
- Try angling the needle so that the end lies more along the plane of the vessel
- Carefully rotate the needle just in case the end lies against the vessel wall

- reattach syringe & aspirate to confirm the needle is in the vein
- Withdraw wire gently
- If resistance- Withdraw with needle (reduces the risk of the end of wire being
cut off by the needle)
6) PERSISTENT BLEEDING:
Pressure/ Surgical exploration for arterial or venous tear
CARE OF THE CATHETER:
- Sterile technique
- Sterile Dressing


-

Secure the line well to minimize movement
Watch for signs of infection at the site- Remove catheter
Remove catheter as soon as it is no longer needed. The longer the
catheter is left in-situ the greater the risk of sepsis & thrombosis

a wave = atrial contraction
c wave = bulging of tricuspid valve into atrium at start of ventricular contraction
x descent = atrium relaxes and tricuspid valve is pulled downwards
v wave = passive filling of right atrium and vena cavae when tricuspid valve closes
y descent = tricuspid valve opens and blood flows into right ventricle
Disease patterns apparent in CVP waveform
Atrial fibrillation - no a wave
Heart block - cannon waves (large a waves due to atrium contracting against a
closed tricuspid valve)
Nodal rhythm - cannon waves
Tricuspid regurgitation- large c and v waves, loss of the x descent
Tricuspid stenosis - prominent a waves, muted y descent

Interpretation of the CVP
Guide to interpretation of the CVP in the hypotensive patient
CVP
readin
g

Other features that
may be present

Diagnosis to
Treatment
consider

Low

Rapid pulse

Hypovolaemia Give fluid challenges* until CVP


rises and does not fall back
again. If CVP rises and stays up
but urine output or blood
pressure does not improve
consider inotropes

Blood pressure normal or
low
Low urine output

Poor capillary refill
Rapid pulse
Low or
Signs of infection
normal
Sepsis
Pyrexia
or high
Vasodilatation/constriction
Rapid pulse
Normal Low urine output
Poor capillary refill

Ensure adequate circulating
volume (as above) and
consider inotropes or
vasoconstrictors

Treat as above.
Venoconstriction may cause
Hypovolaemia CVP to be normal. Give fluid
challenges* and observe effect
as above.

High

Unilateral breath sounds
Asymmetrical chest
movement
Resonant chest with

tracheal deviation
Rapid pulse

Tension
Thoracocentesis then
pneumothorax intercostal drain

High

Breathlessness
Third heart sound
Pink frothy sputum
Edema
Tender liver

Heart failure

Oxygen, diuretics, sit up,
consider inotropes

Very
High

Rapid pulse
Muffled heart sounds

Pericardial
tamponade

Pericardiocentesis and

drainage

How to give a fluid challenge?
How to give a fluid challenge?
To treat hypovolemia / hypotension; give repeated boluses (250-500 mls) of
intravenous fluid (e.g. 0.9% saline / Ringer's lactate / gelofusine). Observe the effect
on CVP, blood pressure, pulse, urine output, capillary refill etc. If the CVP rises
following the fluid bolus wait 5 – 10 mins and then repeat the CVP reading to see if
the rise is sustained. The fluid challenges should be repeated until the CVP shows a
sustained rise and/or there is an improvement in the other cardiovascular
parameters.


In patients at risk of cardiac failure, the above technique should be followed, but it is
sensible to use smaller fluid boluses (50 – 100 mls) and titrate the total amount of
fluid delivered to the patient’s response as above.
In situations when the CVP rises and stays up but the blood pressure and urine output do not improve, then
inotropes may be considered to support the circulation.

When may the CVP reading be unreliable?
The use of CVP readings to estimate cardiac function and blood volume rely on the
fact that there is no right ventricular disease and normal pulmonary vascular
resistance.

Problem

Effect on CVP

Pulmonary embolus
High intrathoracic

pressure

High pulmonary vascular resistance - left sided pressure
and function may be normal. A higher than normal CVP
may be needed to ensure adequate return of blood to the
left side of the heart.

Left heart failure

Resulting rise in pulmonary venous pressure and right
sided heart strain. Initially CVP may be normal but will
increase with significant failure.

Constrictive pericardial
disease

Paradoxical rise in CVP on inspiration and fall on
expiration (opposite of normal in a spontaneously
breathing patient). The absolute level will be higher due
to impeded filling of the heart

Blocked cotton wool at
top of manometer

Fluid will not move in the tube to give a correct reading

Complete heart block

'Cannon waves' on CVP reading the reading will have a
strong pulsatile element when the atrium contracts

against a closed tricuspid valve sending the pressure
wave back into the SVC

Tricuspid
stenosis/regurgitation

Mean CVP will be higher

Catheter removal
Remove any dressing and suture material. Ask the patient to take a breath and fully
exhale. Remove the catheter with a steady pull while the patient is breath holding


and apply firm pressure to the puncture site for at least 5 minutes to stop the
bleeding. Excessive force should not be needed to remove the catheter. If it does not
come out, try rotating it whilst pulling gently. If this still fails, cover it with a sterile
dressing and ask an experienced person for advice.
CLINICAL SCENARIO
A 61 year old man is admitted to the resuscitation room with shortness of breath. He
has a medical history of ischaemic heart disease treated with quadruple coronary
artery bypass grafting five years ago. He has been unwell for the past 48 hours with
a productive cough, lethargy, and fever.
Vital signs on arrival include temperature of 35.2°C, respiratory rate 40/min, pulse
130 beats/min, non-invasive blood pressure 70/40 mm Hg, and oxygen saturation of
90% on 15 l/min face mask oxygen using a non-rebreathing bag. He is poorly
perfused, cold, and shut down. Initial blood gas analysis shows a mixed respiratory
and metabolic acidosis.
CASE PROGRESSION
The patient in the resuscitation room is struggling for breath and is obviously tired.
He is given a 250 ml crystalloid fluid challenge over two minutes with a slight

improvement in blood pressure, to 90/50 mm Hg, but no change in heart rate or
respiratory rate. His peripheral perfusion has improved a little.
A decision is made to proceed with intubation and ventilation, and he undergoes
rapid sequence intubation using etomidate, fentanyl, and suxamethonium. He is
sedated with low dose infusions of morphine and midazolam, paralyzed, and
ventilated with low tidal volumes. Haemodynamically he tolerates this reasonably
well. Further IV fluids are given and a urinary catheter is inserted to assess ongoing
urine output.
Invasive haemodynamic monitoring is started, consisting of a radial arterial line and
a triple lumen right internal jugular central venous catheter. Despite 2.5 liters of IV
crystalloid, his invasive arterial blood pressure remains at 85/45 mm Hg and there is
clinical evidence of peripheral shut down. His urine output is 10 ml in the first hour.
Chest radiography in the resuscitation room shows a right lower lobe pneumonia and
no evidence of pulmonary oedema. A 12 lead ECG shows a sinus tachycardia, Q
waves in leads V2, V3, and V4, but no acute changes.
SUMMARY
Shock is defined by critical tissue hypoperfusion. It must be rapidly reversed before
organ damage is sustained and irreversible. Treatment should therefore begin in the
resuscitation room of the ED and should consist of oxygen therapy with or without
ventilatory support and a rapid appraisal of the likely causes. Patients with
exsanguinating haemorrhage from penetrating torso trauma or ruptured abdominal


aortic aneurysms should be transferred to the operating room for definitive
management using hypotensive resuscitation.
In all other shock states, except cardiogenic shock with left ventricular failure,
intravenous fluids are indicated. Unless this normalises the patient’s condition, more
invasive investigation and treatment should be started promptly. This should consist
of invasive haemodynamic monitoring and repeated IV fluid challenges with CVP
guidance.

In shock states unresponsive to intravascular fluid expansion, or in cardiogenic shock
where fluid challenges may be hazardous, inotrope therapy is required. The choice of
inotrope should be guided by the nature of the problem and the haemodynamic
parameters in individual cases. In all shock states reversible factors should be
rapidly sought and corrected.
Patients admitted to the ED with all but the most simply managed forms of shock
should be transferred to a critical care area once stabilised.