NIV in CPE

2. By
Dr . Samiaa Hamdy Sadek
Assiut University

3. Cardiogenic pulmonary edema (CPE)
is a form of acute hypoxaemic
respiratory failure characterized by
pulmonary edema due to increased
capillary hydrostatic pressure
secondary to elevated pulmonary
venous pressure.

5.  Pulmonary capillary blood
and alveolar gas are
separated by the alveolar-
capillary membrane, which
consists of 3 anatomically
different layers:
(1) the capillary endothelium;
(2) the interstitial space,
which may contain connective
tissue, fibroblasts, and
macrophages; and
(3) the alveolar epithelium

6.  In the normal lung, fluid and protein leakage occur
primarily through small gaps between capillary
endothelial cells.
 Fluid and solutes that are filtered from the
circulation into the alveolar interstitial space
normally do not enter the alveoli because of the very
tight junctions of the alveolar epithelium.
 once the filtered fluid enters the alveolar interstitial
space the lymphatic circulation removes most of this
filtered fluid from the interstitium and return it to
the systemic circulation and movement of larger
plasma proteins is restricted.

7.  The hydrostatic force for fluid filtration across the
lung microcirculation is approximately equal to the
hydrostatic pressure in the pulmonary capillaries
which is partially offset by a protein osmotic
pressure gradient.
Mechanism of CPA:
 Imbalance of Starling forces: increased pulmonary
capillary pressure, decreased plasma oncotic
pressure, increased negative interstitial pressure
 Damage to the alveolar-capillary barrier
 Lymphatic obstruction
 Idiopathic (unknown) mechanism

8.  The Starling relationship determines the fluid balance
between the alveoli and the vascular bed.
 Q = K(Pcap - Pis) - l(Pcap - Pis)
 Q is net fluid filtration; K is a constant called the
filtration coefficient; Pcap is capillary hydrostatic
pressure, which tends to force fluid out of the capillary;
Pis is hydrostatic pressure in the interstitial fluid, which
tends to force fluid into the capillary; l is the reflection
coefficient, which indicates the effectiveness of the
capillary wall in preventing protein filtration; the
second Pcap is the colloid osmotic pressure of plasma,
which tends to pull fluid into the capillary; and the
second Pis is the colloid osmotic pressure in the
interstitial fluid, which pulls fluid out of the capillary.

9. For pulmonary edema to develop secondary to
increased pulmonary capillary pressure, the
pulmonary capillary pressure must rise to a level
higher than the plasma colloid osmotic pressure.
Pulmonary capillary pressure is normally 8-12 mm
Hg, and colloid osmotic pressure is 28 mm Hg.

10. The lymphatics play an important role in maintaining an
adequate fluid balance in the lungs by removing solutes,
colloid, and liquid from the interstitial space at a rate of
approximately 10-20 mL/h.
An acute rise in pulmonary capillary pressure (ie, to >18
mm Hg) may increase filtration of fluid into the lung
interstitium, but the lymphatic removal does not increase
correspondingly. In contrast, in the presence of chronically
elevated LA pressure, the rate of lymphatic removal can be
as high as 200 mL/h, which protects the lungs from
pulmonary edema.

11. 1. As pulmonary congestion increases, oxygen
saturation decreases, resulting in decreased
myocardial oxygen supply. This leads to ischaemia
in regions with already borderline blood supply,
further impairing cardiac performance
2. Hypoxemia and increased fluid content in the lungs
induces pulmonary vasoconstriction increasing the
right ventricular pressure. This compromises left
ventricular function through the ventricular
interdependence mechanism
3. finally, circulatory insufficiency results in metabolic
acidosis

12. The progression of fluid accumulation in CPE can
be identified as 3 distinct physiologic stages:
Stage 1
In stage 1, elevated LA pressure causes distention
and opening of small pulmonary vessels. At this
stage, blood gas exchange does not deteriorate, or it
may even be slightly improved.

13. Stage 2
 Fluid and colloid shift into the lung interstitium
from the pulmonary capillaries
 Initial increase in lymphatic outflow efficiently
removes the fluid. The continuing filtration of liquid
and solutes may overpower the drainage capacity of
the lymphatics.
 The accumulation of liquid in the interstitium may
compromise the small airways, leading to mild
hypoxemia.
 Tachypnea at this stage is mainly the result of the
stimulation of juxtapulmonary capillary (J-type)
receptors (nonmyelinated nerve endings located
near the alveoli) J-type receptors are involved in
reflexes modulating respiration and heart rates.

14. Stage 3
With further accumulations, the fluid crosses
the alveolar epithelium in to the alveoli,
leading to alveolar flooding.
increase in airway resistances, a decrease in
lung diffusion capacity,
 a drop in functional residual capacity, and an
increased intrapulmonary shunt effect.
 Decrease in respiratory system compliance,
increased airway resistance, air trapping,
arterial hypoxaemia, and hypercapnia is
attributable to respiratory muscle fatigue as a
result of increased work of breathing

15. The respiratory muscles have to generate large
negative swings in pleural pressure to start
inspiratory flow and maintain adequate tidal
volumes. This increase in negative intrathoracic
pressure aggravates pulmonary edema by
increasing both preload and afterload

17. Medical treatment of ACPE has 3 main
objectives:
(1) reduced venous return (preload reduction);
(2)reduced resistance of systemic vascular (afterload
reduction); and
(3) inotropic support in some cases.
 Treatment that can be administered includes: vasodilator
when there is normal or high BP,
 Diuretics when there is volume overload or fluid retention, and
 Inotropic drugs when there is hypotension or signs of organ
hypoperfusion.

18. It is recommended to administer oxygen as
early as possible in hypoxaemic patients to
achieve 95% arterial oxygen saturation
(90% in COPD patients).
Caution should be taken in patients with
severe airway obstruction to avoid
hypercapnia

19. International guidelines recommend the use of
noninvasive ventilation (NIV) (continuous positive
airway pressure -CPAP or noninvasive positive
pressure ventilation -NPPV) in dyspnoeic patients
with ACPE to improve breathlessness and reduce
hypercapnia and acidosis

20. Noninvasive ventilation is well suited for patients
with cardiogenic pulmonary edema.
CPAP and BiPAP modalities both are effective, with
CPAP may be considered the first option in selection of
NPPV due to more evidence for its effectiveness and
safety and lower cost compared with bilevel NPPV.
The greatest benefits are realized in relief of
symptoms and dyspnea.

21.  In a Cochrane review(1), including 21 studies and
1071 subjects, NIV compared to standard care,
significantly reduced the need for endotracheal
intubation, There was also a significantly reduction
for hospital mortality.
 Similar results were reported by Winck et al(2) in
their meta-analysis, who showed that, in ACPE
patients, CPAP and NPPV both significantly
decrease the need for endotracheal intubation, and
CPAP significantly reduces mortality when
compared to standard medical therapy.
1.Masip J. (2008) Noninvasive ventilation in acute cardiogenic pulmonary edema.Curr Opin Crit Care. 14(5):531-5
2. Winck JC, Azevedo LF, Costa-Pereira A, et al. (2006) Efficacy and safety of non-invasive ventilation in the treatment of acute
cardiogenic pulmonary edema--a systematic review and metaanalysis.Crit Care. 10:R69

22. Patients with hypercapnic respiratory acidosis may
derive the greatest benefit from noninvasive
ventilation.
Importantly, adjust to standard therapy, including
diuresis.
Benefit may be seen with as few as 2 hours of support.

24. The effective filling and emptying of the heart is
determined by the pressure difference between the
inside of the heart and the intrathoracic pressure,
known as the cardiac transmural pressure (PTM).
The more positive the PTM is during diastole, the
greater the filling of the heart (preload). The more
positive the PTM is during systole, the higher the
workload is for the heart (afterload).

25. Increase in intrathoracic pressure reduces the
venous return, decreasing the right and left
ventricular preload
Increases pericardial pressure, reduces
transmural pressure, and thus decreases
afterload
Increase cardiac output and myocardial
contractility.

26. Although CPAP can decrease cardiac index in
normal subjects, it increases cardiac index in patients
with ACPE
CPAP also causes a significant decrease in the heart
rate, resulting from increased lung inflation
In patients with diastolic dysfunction, who usually
require a comparatively high filling pressure, the
effects of positive pressure therapy compromises
venous return, resulting in deterioration of
haemodynamics

27. It is recommended to use CPAP initially and to
consider switching to NPPV(BIPAP) if the patient is
found to have substantial hypercapnia or
unrelenting dyspnea.
The favourable hemodynamic effect of CPAP is
most likely to occur when filling pressures are high
and ventricular performance is poor.

28. It favors alveolar recruitment and
Increases functional residual capacity, lung
compliance and alveolar ventilation,
Reduction of the intrapulmonary shunt and
respiratory effort, thus improving oxygenation
Reduced transdiaphragmatic pressure swings, and
decreased diaphragmatic activity can lead to a
decrease in the overall work of breathing and
therefore a decreased metabolic demand from the
body.

29. The physiological benefits of BIPAP NIV are the
same as for CPAP but also include:
1-The inspiratory assist which further increase the
mean intrathoracic pressure and therefore potentially
increase the benefits of CPAP, but can further reduce
the work of breathing and therefore the overall
metabolic and oxygen demand of patients with AHF.
2- The expiratory positive airway pressure pressure
(EPAP, or CPAP or PEEP) therefore helps triggering
and, by reducing the inspiratory effort, it improves
comfort

30. Mode: CPAP or BiPAP
A. CPAP: 5cm- up to 15cmH2O
B. BIPAP: (IPAP 10-16 (max 20) cmH2O,
EPAP 4-6 (max 10) cmH2O)
FiO2 titrated to keep SpO2 >92%
Keep HOB >30 degrees

31.  NPPV titration based on patient assessment
1. Assessment will include evaluation of the patients general
appearance, blood pressure, heart rate, breath sounds, SpO2,
ventilating pressures/volumes and when appropriate, ABG
values
2. Allow time for the patient to adjust to the feel of the mask
gas flow
3. Initially start with lower settings and titrate to levels that
reduce work of breathing and allow a reduction in FiO2. This
will improve patient tolerance and cooperation.

32. 4. NPPV titration:
a. To improve ventilation, increase IPAP in increments
of 2-3 cmH2O every 5 minutes until a max of 25 cmH2O
is reached.
b. To improve oxygenation, increase EPAP in
increments of 2 cmH2O until a max of 10 is reached.
Keep pressure support ventilation > 5 cmH2O
c. To improve oxygenation, increase FiO2
d. When increasing EPAP, increase IPAP by same
amount of pressure to maintain the same level of
pressure support.

33. 6. If the patient is not comfortable, assess for the
following:
a. Work of breathing: titrate settings to improve distress
b. Optimize tidal volume >6-7mL/kg
c. Adjust rise time and inspiratory time
d. Leak: re-adjust mask or change mask size
e. Consider lower pressures
 Document final resting settings within 20 minutes of
initial application, a complete assessment performed
every 30minutes x2 then every 4 hours and as needed.
 The efficacy of NPPV is often made in the first hour or
two of therapy. If there is no physiologic improvement,
intubation and mechanical ventilation should be
considered.

34. Reversal or sufficient resolution of underlying cause
of respiratory failure is the most important factor in
complete liberation from noninvasive ventilation.
With a rapidly reversible problem (i.e. cardiogenic
pulmonary edema and atelectasis due to
hypoventilation), simple discontinuation of NPPV is
generally all that is required.
For other causes of respiratory insufficiency,
periodic breaks from noninvasive ventilation should
begin once the FiO2 has been decreased to 35-40%,
IPAP <18 cmH2O, EPAP <12 cmH2O and patient is
able to sustain effective spontaneous ventilation.

36.  Endotracheal intubation and mechanical ventilation
indicated when patients with CPE remain hypoxic
despite maximal noninvasive supplemental oxygenation,
 When patients have evidence of impending respiratory
failure (eg, lethargy, fatigue, diaphoresis, worsening
anxiety), or
 When patients are hemodynamically unstable (eg,
hypotensive, severely tachycardic).
 Mechanical ventilation maximizes myocardial oxygen
delivery and ventilation. Positive end-expiratory
pressure is generally recommended to increase alveolar
patency and to enhance oxygen delivery and carbon
dioxide exchange.