Pulse Pressure Variation

Pulse pressure 

is the difference between the systolic and diastolic pressure readings.

It is msured in millimeters of mercury (mmHg). 

It represents the force that the heart generates each time it contracts. 

If resting blood pressure is 120/80 mmHg, pulse pressure is 40

Pulse Pressure Variation

One of the most important concepts in resuscitation is volume responsiveness, or the ability of the cardiac output to increase in response to a fluid challenge. 

As compared to prior static measures of venous filling, such as central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP or wedge pressure), clinicians are increasingly turning to dynamic means of assessing patients’ volume responsiveness.1,2 One such measure is the pulse pressure variation (PPV).1,2



PPV is a reflection of cardiopulmonary interactions. 

As a patient breathes, both spontaneously and with mechanical ventilation, cardiac output varies. 

The more the cardiac output varies with respirations, the more likely that patient is to respond to a fluid bolus with an increase in cardiac output. 

Using this simple principle, clinicians can take advantage the common arterial line tracing to assess a patient’s volume responsiveness.



To measure the PPV in a given patient, that patient must have consistent and demonstrable cardiopulmonary interactions. This means that the patient must:

1. Be in normal sinus rhythm
2. Be intubated and be mechanically ventilated, making no spontaneous respiratory efforts
3. Be ventilated with at least 8mL/kg of tidal volume
4. Have no significant alternations to chest wall compliance, such as an open chest

If all these conditions are met, the arterial waveform can be assessed for variation in a few simple steps.

1. To make measurements easier, condense the waveform to 6.25 mm/sec from the baseline of 25 mm/s. (This is easy to do, and is located under “speed” on most monitor settings.)

2. Identify the maximum (during inspiration) and the minimum (during exhalation) waveforms on the undulating pattern.

3. Using the cursor, find the systolic pressure value for the largest, or maximum, inspiratory waveform, then find the diastolic pressure. Take care to use the systolic and diastolic values on the same form. The difference in these two values is your pulse pressure. The following four figures have been captured from a monitor and enlarged for detail. The first figure below shows the value for the maximum systolic of 109 mmHg.



This figure shows the measurement of the diastolic of the maximum waveform, or 60 mmHg.

4. Repeat step 3 for the minimum form. Here, the systolic is 91 mmHg.

And the diastolic is 54 mmHg.


5. These steps will give you two pulse pressures. The pulse pressure variation is calculated as:

Therefore, in this case, the PPmax is 49, the PPmin is 37, for a mean PP of 43. This leads to a calculated PPV of 27.9%. (12/43 X 100)

Numerous studies have found that a PPV of > 12% is associated with volume responsiveness in the operating room and intensive care unit (ICU) alike. 

A meta-analysis of PPV to predict fluid responsiveness found a sensitivity and specificity of 0.89 and 0.88 respectively.3 

A meta-analysis of 22 studies focused on ICU patients had similar findings, with a pooled sensitivity of 0.88 and pooled specificity was 0.89.2 

To date, no study has specifically looked at PPV in the ED, and this is an area for future study.



The most common pitfalls in using PPV for clinical decision-making involve failing to recognize that the patient does not meet one or more of the required criteria listed above.

 If patients are breathing spontaneously, even while on assist control ventilation, they can vary their intrathoracic pressure and thereby cause exaggerated or blunted responses to the positive pressure breaths.2 

Similarly, clinicians should note that the tidal volumes used in this assessment, of > 8mL/kg,2 are larger than are otherwise used (ideally, around 6mL/kg). 

In our practice, we temporarily increase the tidal volume just for the purposes of this assessment, to ensure that the patient is seeing sufficient positive pressure ventilation to impact hemodynamics. 

However, if these criteria are met, PPV is an easy, rapid means to assess a critically ill patient’s likelihood of volume responsiveness.

A 74-year-old lady with a history of ischaemic heart disease and severe congestive cardiac failure is admitted to the ICU with hypotension and presumed sepsis

A17

A 74-year-old lady with a history of ischaemic heart disease

and severe congestive cardiac failure is admitted to the

ICU with hypotension and presumed sepsis. She is sedated

and ventilated in pressure support mode. On examination

she is confused, BP is 85/35mmHg, HR is 115bpm (sinus

tachycardia), SpO2 is 95% on 60% oxygen. Arterial blood

gas analysis shows a lactate of 4.3mmol/L (39mg/dL).

Which is the BEST guide to the need for further intravenous

fluid replacement?

a. Response of oesophageal Doppler to passive leg raising.
b. Insertion of a pulmonary artery catheter and pulmonary artery
occlusion pressure measurement.
c. Titrate fluid resuscitation against repeated blood lactate
measurements.
d. Assess pulse pressure variation.
e. Urine output measurement.


A

This patient may have hypotension secondary to a variety of causes,

including sepsis and decompensated cardiac failure. 

Pulmonary artery 

occlusion pressure has been shown to be a poor predictor of whether a

fluid bolus will cause an increase in cardiac output (i.e. whether the patient

is volume-responsive). 

Blood lactate is a sensitive marker of shock and

falling levels correlate with improved survival.

 However, this will not

distinguish between cardiogenic shock (where inotropes may be required)

and septic shock (requiring fluids and/or vasopressors). 

Pulse pressure

variation of >13% has been shown to accurately predict response to fluid,

but is only reliable in mechanically ventilated patients without spontaneous

respiratory effort. 

Urine output measurement will again not distinguish

between different causes of shock. 

Passive leg raising autotransfuses

about 300ml of blood into the central circulation. 

If stroke volume

increases significantly (>10% as measured by oesophageal Doppler), this

indicates preload-responsiveness. 

An advantage of this technique is that it

is reversible if no improvement is seen, avoiding worsening pulmonary

oedema in the case of cardiogenic shock.

A15 All the following increase the likelihood of a patient
acquiring an antimicrobial-resistant infection EXCEPT:
a. Use of cefotaxime.
b. High nursing workload.
c. Prolonged mechanical ventilation.
d. Brief hospital admission.
e. Understaffing in the ICU.


D
Multi-drug resistant infections are increasing in incidence in the intensivecare unit. Use of broad spectrum antibiotics such as third generationcephalosporins, carbapenems and quinolones is an independent riskfactor for ventilator-acquired pneumonia with a drug-resistant organism, asis prolonged mechanical ventilation.

Methycillin-resistant Staphylococcus aureus rates have been shown to increase with bothovercrowding andunderstaffing of the ICU.


Prolonged hospital admission, the presence ofindwelling devices and poor hand hygiene also contribute to thedevelopment of antibiotic-resistant infections.

A14 A 48-year-old woman is rescued from a house fire during
which she was trapped in a smoke-filled bedroom for 30
minutes. On arrival in the Emergency Room, she has
marked facial burns and a hoarse voice but no stridor. She
is expectorating carbonaceous sputum, appears confused
and has a cherry-red visage. Which statement is FALSE?
a. Early intubation is advisable.
b. A significant thermal injury to the trachea is likely.
c. Lavage with sodium bicarbonate 1.4% has a role in the
management of this patient.
d. Lung function is likely to worsen over the next 12 hours.
e. A cherry red visage has several causes other than carbon monoxide
poisoning.



A14 B
Inhalational injury has three mechanisms: thermal injury to the upper
airway, smoke inhalation causing chemical pneumonitis to the lower
airways, and systemic absorption of toxins (principally carbon monoxide
and cyanide).

Hoarseness and facial burns are signs of upper airway
thermal injury to the pharynx and glottic area.

Pharyngeal oedema is likely
to increase rapidly especially once fluid resuscitation is commenced, and
early intubation is advised.

Most of the heat from hot gas inhalation is
dissipated in the upper airways, so thermal injury below the glottis is
unusual. 

Sodium bicarbonate lavage of the bronchial tree may be
performed following intubation to neutralise acidic deposits and remove
soot contamination, although evidence for the effectiveness of this therapy
is lacking.

Lung function usually worsens over a period of hours following
inhalational injury.

A cherry red visage is a non-specific sign of carbon
monoxide poisoning, and there are many other causes of facial flushing
including alcohol, emotion and heat, all of which are associated with burns
injuries.

A13 Which of the following statements regarding the use of
antifibrinolytic agents is FALSE?
a. Tranexamic acid is a competitive inhibitor of plasminogen and
plasmin.
b. Aprotinin significantly reduces blood loss and transfusion
requirements in cardiac surgery.
c. Use of antifibrinolytics in trauma is supported by several high quality
randomised controlled trials.
d. Arterial and venous thrombosis are uncommon complications of
tranexamic acid use.
e. The risk of anaphylaxis with aprotinin is 0.5%.


A13 C

• Tranexamic acid (TXA) is a competitive inhibitor of plasmin and plasminogen, while aprotinin forms irreversible complexes with a variety of proteases including plasmin. 
• While TXA is synthetic, aprotinin is isolated from bovine lungs and has a high incidence of anaphylaxis (0.5%). 
• A strong evidence base supports the use of antifibrinolytic agents in cardiac surgery, where they have been shown to reduce the requirement for blood transfusion by about 30%. A Cochrane review 1 failed to demonstrate any increased incidence of thrombosis with antifibrinolytics, although a recent study 2 suggested that aprotinin is associated with an increased incidence of myocardial infarction, stroke and renal failure, leading to its withdrawal in the USA. 
• The rationale for use in trauma is extrapolated from evidence in elective cardiac surgery; the ongoing CRASH (Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage) II trial should help determine whether they are effective in this context.

The following are prerequisites for the use of recombinant factor VIIa in bleeding trauma patients EXCEPT:

The following are prerequisites for the use of recombinant factor VIIa in bleeding trauma patients EXCEPT:

a. Platelet count >50x109/L.

b. Temperature >36°C.

c. Fibrinogen >0.5g/L.

d. pH >7.20.

e. Ionised Ca2+ >0.8mmol/L (3.2mg/dL).

B

• ·        Recombinant factor VIIa (rFVIIa) may be helpful to induce coagulation in areas of diffuse small vessel coagulopathic bleeding.

·        It follows that all surgical avenues to control bleeding must first be explored.

·        Adequate platelet numbers are required to generate the ‘thrombin burst’ which the rFVIIa provokes, and adequate fibrinogen must be present to translate this thrombin generation into clot formation.

·        Correction of severe acidosis, hypothermia and hypocalcaemia are also warranted to maximise the chances of success for this expensive and unlicensed therapy.

·        However, a temperature of 36°C is difficult to achieve in such patients; 32°C is considered an appropriate minimum threshold.