Management of acute pulmonary edema

Clinical Presentation on Management of Acute Pulmonary Edema for the Department of Internal Medicine, Obafemi Awolowo University Teaching Hospital, Ile Ife.

1. MANAGEMENT OF ACUTE
PULMONARY EDEMA
BY DR. CALISTUS K. OKECHUKWU
A PRESENTATION FOR THE DEPARTMENT OF INTERNAL MEDICINE.
OAUTHC, ILE-IFE.

2. OUTLINE
INTRODUCTION
ETIOLOGY
PATHOPHYSIOLOGY
CLINICAL FEATURES
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
TREATMENT
PROGNOSIS
COMPLICATIONS

3. INTRODUCTION
A life-threatening condition, of sudden onset characterized by fluid
accumulation in the lungs caused by extravasation of fluid from the
pulmonary vasculature into the interstitiumand alveoli of the lungs.
Medical emergency
One of the clinical syndromes seen in acute heart failure (AHF)

4. ETIOLOGY
Broadly classified into;
CARDIOGENIC PULMONARY EDEMA
NON-CARDIOGENIC PULMONARY EDEMA
CARDIOGENIC PULMONARY EDEMA
Impaired cardiovascular function lead to pulmonary capillary pressure and
consequently pulmonary edema.
a.Left ventricular failure (Acute myocardial Infarction/Ischaemia)
b.Severe arrhythmias
c.Aortic dissection with aortic insufficiency
d.Valvularheart disease
e.Hypertrophic cardiomyopathy with severe outflow obstruction
f.Fluid overload (Kidney failure or Intravenous therapy)

5. NON-CARDIOGENIC PULMONARY EDEMA
Damage of pulmonary capillary lining leads to leakage of proteins and
fluid into the surrounding tissue as oncotic forces are shifted from the
vessel to the surrounding lung tissue.
a.Chest trauma
b.Smoke inhalation
c.Sepsis
d.Pneumonia
e.Pulmonary embolism
f.High altitude pulmonary edema
g.Neurogenic e.g. Head trauma, epileptic seizures, subarachnoid
hemorrhage

6. PATHOPHYSIOLOGY
Movement of fluids between the vasculature and interstitial spaces is
maintained in equilibrium by the starling forces;
Hydrostatic pressure: favors movement of fluid out of the vasculature
Oncotic pressure: favors movement of fluid into the vessels
Imbalance between these two forces Accumulation of fluid in the
interstitiumand parenchyma.
Pathophysiology vary for both etiologic types;
CARDIOGENIC PULMONARY EDEMA: Hydrostatic pressure
NON-CARDIOGENIC PULMONARY EDEMA: Oncotic pressure

8. CLINICAL FEATURES
SYMPTOMS
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea(PND)
Cough (±pink frothy sputum)
SYMPTOMS SUGGESTIVE OF UNDERLYING CAUSE
Left ventricular failure: Poor exercise tolerance, fatigue, nocturnal cough
Arrhythmia: Chest pain, dizziness, palpitations
Pneumonia: Fever, chest pain, cough, fast shallow breathing
Aspiration: Fast breathing, impaired voice, regurgitation

9. SIGNS
Respiratory distress
Oxygen saturation < 90% on air
Pale
Peripheral edema
Tachycardia
Tachypnoea
Fine crackles
Rales, rhonchi and wheezes
S3 gallop

10. DIAGNOSIS
CHEST RADIOGRAPH:
i.Peribronchialthickening
ii.Prominent vascular markings in the upper lung zones
iii.Small effusions at costophrenicangles
iv.KerleyB lines
v.Patchy alveolar filling, typically in a perihilardistribution and diffuse alveolar
infilterates(Alveolar edema)
vi.Cardiomegaly
ELECTROCARDIOGRAPHY
ECHOCARDIOGRAPHY
U&E
TROPONIN
ABG
PLASMA BNP: levels suggest heart failure as underlying etiology

12. DIFFERENTIAL DIAGNOSIS
PULMONARY CARDIAC Normalor ↑
Respiratoryeffort
↓ Respiratory
effort
Others
Asthma Cardiac tamponadeAnemia Gullain-Barre
syndrome
Interstitial lung
disease
Corpulmonale Myocardial
infarction
SalicylatetoxicityMyastheniaGravisPleural effusion
Tension
pneumothorax
Pericarditis Flail chest Multiple sclerosisCOPD exacerbation
Anaphylaxis Myocarditis Pneumonia Stroke Congenitalheart
disease
Pulmonary
embolism
Pneumothorax/hem
othorax
Lambert-Eaton
Syndrome
Rib fracture

13. TREATMENT
Treatment of acute pulmonary edema is based on the underlying
etiology.
Life-threatening condition that requires immediate intervention;
Support the circulation
Improve gaseous exchange
Correct accompanying complications; Infection, acidemia, anemia

14. GENERAL PRINCIPLES
SUPPORT OF OXYGENATION AND VENTILATION
REDUCTION OF PRELOAD
TREATMENT OF UNDERLYING CAUSE
MONITORING PROGRESS

15. SUPPORT OF OXYGENATION AND VENTILATION
To ensure adequate oxygen delivery to peripheral tissues and the heart.
OXYGEN THERAPY: Supplemental oxygen
POSITIVE-PRESSURE VENTILATION: Face/nasal masks, endotracheal
intubation

16. REDUCTION OF PRELOAD
To reduce the volume of extravascular fluid in the lungs.
DIURETICS: loop diuretics are effective in most forms of pulmonary
edema. Diuretic of choice is furosemide (0.5-1 mg/kg).
NITRATES: Venodilatorssuch as Nitroglycerin (Sublingual or IV) and
Isosorbidedinitrate. Also IV Nitroprusside which useful in pulmonary
edema and hypertension (requires close monitoring).
MORPHINE: IV given in 2-4mg bolus. Reduces preload while relieving
dyspnea and anxiety.
ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS: Reduce both
preload and afterload and recommended for hypertensive patients.

17. INOTROPIC AND INODILATOR DRUGS: Dopamine and dobutamine
(Inotropic agents), Milrinone(Inodilator) are indicated in cardiogenic
pulmonary edema and severe LV dysfunction.
DIGITALIS GLYCOSIDES: Positive inotropic action. Rarely used at
present.
INTRAAORTIC BALLOON COUNTERPULSATION: IABP or other LV-assist
devices help relieve pulmonary edema
PHYSICAL METHODS: Sitting position with legs dangling along the side
of the bed.

18. TREATMENT OF UNDERLYING CAUSE
Identify underlying cause after thorough investigations and treat
accordingly
MONITORING PROGRESS: Once stable and improving
PULSE OXIMETRY: Target oxygen saturation ˃ 94%
URINE OUTPUT
DAILY WEIGHTS: Aim reduction of 0.5 kg/day
REPEAT CHEST X-RAY

19. PROGNOSIS
Mortality from acute pulmonary edema has fallen over the last
decade, from around 60% to 20%-40%.
Prognosis is dependent on underlying etiology.
When acute pulmonary edema occurs in association with sepsis,
mortality rates remain very high, whereas much lower mortality rates
are to be expected in those with pneumonia, aspiration or chest
trauma.
Mortality rises with increasing age and failure of other organs.
Most of those dying with acute pulmonary edema do so as a result of
MODS and hemodynamic instability rather than impaired gas
exchange.

20. COMPLICATIONS
RESPIRATORY FAILURE
PLEURAL EFFUSION
ANAEMIA
SEPSIS

21. THANK
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