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Reza

Octavianus, MD. FIHA


Acute Pulmonary Oedema
Acute pulmonary edema is uid accumula?on in
the ?ssue and air spaces of the lungs.
It leads to impaired gas exchange and may cause
respiratory failure.
Acute pulmonary oedema is a life threatening
emergency that requires immediate interven?on
with a management plan
Acute Pulmonary Oedema
Causes :
Cardiogenic

Noncardiogenic
Acute Heart Failure
AHF refers to rapid onset or worsening of
symptoms and/or signs of HF
Most cases, pa?ents with AHF present with
either preserved (90140 mmHg) or elevated
(>140 mmHg; hypertensive AHF) systolic blood
pressure (SBP).
Only 58% of all pa?ents present with low SBP
(i.e. ,90 mmHg; hypotensive AHF), which is
associated with poor prognosis



Acute Pulmonary Oedema
Diagnos?c :
1. Respiratory distress
Respiratory rate > 25x/min or < 8x/min
Use of accessory muscles for breathing
2. Orthopnoea
3. Low O2 satura?on <90% in oxymetry
4. Pulmonary rales bilateral > lungs area
Acute Pulmonary Oedema
Diagnos?c
5. Frothy sputum, diaphoresis, tachycardia
Diagnos?c Test
Upon presenta?on a measurement of plasma
natriure?c pep?de level (BNP, NT-proBNP or MR-
proANP) is recommended in all pa?ents with acute
dyspnoea and suspected AHF to help in the
dieren?a?on of AHF from non-cardiac causes of
acute dyspnoea
(Class of Recommenda?on I, Level of Evidence A)

Diagnos?c Test

a. 12-lead ECG

b. chest X-ray to assess signs of pulmonary conges?on and
detect other cardiac or non-cardiac diseases that may
cause or contribute to the pa?ents symptoms;

c. the following laboratory assessments in the blood:
cardiac troponins, BUN (or urea), crea?nine, electrolytes
(sodium, potassium), glucose, complete blood count, liver
func?on tests and TSH.

A. Cranializa?on of Pulmonary
Vasculature

B. Kerley Lines
Diagnos?c Test
Echocardiography is recommended
immediately in haemodynamically unstable
AHF pa?ents

Posi?on
Posi?on
Oxygen Therapy and Ven?latory
Support
Monitoring of transcutaneous arterial oxygen
satura?on (SpO2) is recommended
Oxygen therapy is recommended in pa?ents with
AHF and SpO2 <90% or PaO2 <60 mmHg (8.0 kPa)
to correct hypoxaemia
Measurement of blood pH and carbon dioxide
tension (possibly including lactate) should be
considered



Oxygen Therapy and Ven?latory
Support
Non-invasive posi?ve pressure ven?la?on (CPAP,
BiPAP) should be considered in pa?ents with
respiratory distress
(respiratory rate >25 breaths/min, SpO2 <90%)
Intuba?on is recommended, if respiratory failure,
leading to hypoxaemia (PaO2 <60 mmHg (8.0
kPa)), hypercapnia (PaCO2 >50 mmHg (6.65 kPa))
and acidosis (pH <7.35), cannot be managed non-
invasively


CPAP BPAP
Diure?cs
Diure?cs are a cornerstone in the treatment
of pa?ents with AHF
and signs of uid overload and conges?on.
Diure?cs increase renal salt and water
excre?on and have some vasodilatory eect.
In pa?ents with AHF and signs of
hypoperfusion, diure?cs should be
avoided before adequate perfusion is akained

Diure?cs
The ini?al approach to conges?on management
involves i.v. diure?cs with the addi?on of
vasodilators for dyspnoea relief if blood pressure
allows.


Diure?cs
Intravenous loop Diure?cs are recommended for
all pa?ents with AHF admiked with sign/
symptoms of uid overload to improve
symptoms. (Class I, LOE C)
In pa?ents with new-onset AHF or those with
chronic, decompensated HF not receiving oral
diure?cs the ini?al recommended dose should be
20-40 mg i.v. Furosemide (or equivalent); those
on chronic diure?c therapy, ini?al i.v. Doses
should be at least equivalent to oral dose. (Class
I, LOE B)
Diure?cs
It is recommended to give diure?cs either as
intermikent boluses or as a con?nous
infusion, and the dose and dura?on should be
adjusted according to pa?ents symptoms and
clinical status. (Class I, LOE B)
Combina?on of loop diure?c with either
thiazide-type or spironolactone may be
considered in pa?ents with resistant oedema
or insucient symptoma?c response
Vasodilators
Intravenous vasodilators are the second most
onen used agents in AHF for symptoma?c relief
They have dual benet by decreasing venous
tone (to op?mize preload) and arterial tone
(decrease anerload).
Consequently, they may also increase stroke
volume.


Vasodilators
Vasodilators are especially useful in pa?ents with
hypertensive AHF, whereas in those with
SBP <90 mmHg (or with symptoma?c hypotension)
they should be avoided.
Dosing should be carefully controlled to avoid
excessive decreases in blood pressure, which is related
to poor outcome.

Vasodilators should be used with cau?on in pa?ents


with signicant
mitral or aor?c stenosis.

Vasodilators dose
Nitroglycerine ; start with 10-20g/min,
increase up to 200 g/min
Isosorbide dinitrate ; start with 1 mg/h,
increase up to 10 mg/h
Nitroprusside ; start with 0,3 g/kg/min and
increase up to 5 g/kg/min
Neseri?de ; bolus 2/kg + 0.01 g/kg/min
Vasodilators
i.v vasodilators should be considered for
symptoma?c relief in AHF with SBP > 90
mmHg (and without symptoma?c
hypotension). (Class IIa , LOE B)
In pa?ents with hypertensive AHF, i.v
vasodilators should be considered as ini?al
therapy to improve symptoms and reduce
conges?on.
Opiates
Opiates relieve dyspnoea and anxiety.
In AHF, rou?ne use of opiates is not
recommended and they may only be
cau?ously considered in pa?ents with severe
dyspnoea, mostly with pulmonary oedema.
Dose-dependent side eects include nausea,
hypotension, bradycardia and respiratory
depression (poten?ally increasing the need for
invasive ven?la?on).
Rapid arrhythmias or severe
bradycardia/conduc?on disturbance

Severe rhythm disturbances in pa?ents with
AHF and unstable condi?ons should be
corrected urgently with medical therapy,
electrical cardioversion or temporary pacing

For acute control of the ventricular rate in pa?ents
with atrial brilla?on :
Digoxin and/or beta-blockers should be
considered as the rst-line therapy (Class IIa, LOE
C)
Amiodarone may be considered (Class IIb, LOE B)
Opiates may be considered for cau?ous use to
relieve dyspnoea and anxiety in pa?ents with
severe dyspnoea but nausea and hypopnea may
occur (Class IIb, LOE B)

Acute coronary syndrome

Pa?ents presen?ng with ACS should be managed
according to the ESC guidelines on non-ST
eleva?on ACS (NSTE-ACS) and STEMI
Coexistence of these two clinical condi?ons (ACS
and AHF) always iden?es a very-high-risk group
where an immediate (i.e. ,2 h from hospital
admission in pa?ents with NSTEMI, analogous to
STEMI management) invasive strategy

Acute mechanical cause underlying
AHF

may present as a mechanical complica?on of
ACS (free wall rupture, ventricular septal
defect, acute mitral regurgita?on), chest
trauma or cardiac interven?on, or as acute
na?ve or prosthe?c valve incompetence
secondary to endocardi?s

Other Causes
Cardiac Tamponade

Mitral/Aorta valve stenosis


Inotropic Agents
Use of an inotrope should be reserved for
pa?ents with a severe reduc?on in cardiac output
resul?ng in compromised vital organ perfusion,
which occurs most onen in hypotensive AHF.
Inotropic agents are not recommended in cases
of hypotensive AHF where the underlying cause
is hypovolaemia or other poten?ally correctable
factors before elimina?on of these causes.

Inotropic Agents
Inotropes, especially those with adrenergic
mechanisms, can cause sinus tachycardia and may
induce myocardial ischaemia and arrhythmias, thus
ECG monitoring is required.
There is long-standing concern that they may increase
mortality, which derives from studies in which
intermikent or con?nuous infusions of inotropes were
given.
inotropes have to be used with cau?on star?ng from
rather low doses and up-?tra?ng with close monitoring


Inotropic Agents
Short-term i.v infusion of inotropic agents may be
considered in pa?ents with hypotension (SBP <
90) and/or signs/symptoms of hypoperfusion
despite adequate lling status, to increase
cardiac ouput, increase blood pressure, improve
peripheral perfusion and maintain end-organ
func?on (Class IIb, LOE C)
Inotropic agents are not recommended unless
the pa?ent is symptoma?cally hypotensive or
hypoperfused because of safety concern (Class
III, LOE A)
Inotropic Agents
An intravenous infusion of levosimendan or a
PDE III inhibitor may be considered to reverse
the eect of beta-blockade if beta-blockade is
thought to be contribu?ng to hypotension
with subsequent hypoperfusion. (Class Iib,
LOE C)
Vasopressors
Drugs with prominent peripheral arterial
vasoconstrictor ac?on such as norepinephrine or
dopamine in higher doses (>5 g/kg/min) are
given to pa?ents with marked hypotension.
These agents are given to raise blood pressure
and redistribute blood to the vital organs.
However, this is at the expense of an increase in
LV anerload

Vasopressors
Dopamine was compared with norepinephrine in the
treatment of various shock pa?ents.
A subgroup analysis suggested that norepinephrine
would have fewer side eects and lower mortality.
Epinephrine (adrenaline) should be restricted to
pa?ents with persistent hypotension despite adequate
cardiac lling pressures and the use of other vasoac?ve
agents


Vasopressors
A vasopressor (norepinephrine preferably) may be
considered in pa?ents who have cardiogenic shock,
despite treatment with another inotrope, to increase
blood pressure and vital organ perfusion. (Class IIb,
LOE B)
It is recommended to monitor ECG and blood pressure
when using inotropic agents and vasopressors, as they
can cause arrhythmia, myocardial ischaemia, and in
the case of levosimendan and PDE III inhibitors also
hypotension. (Class I, LOE C)


Summary
Acute Pulmonary Oedema can have normo/
hypertension and hypotension clinical
presenta?on
Hypotension comes with worse prognosis
Management of Acute Pulmonary Oedema
diers in these clinical presenta?on

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