2.  64 YOM with pmhx notable for
CHF/CAD presents with 3 days
worsening dyspnea with exertion.
He can usually easily walk from room
to room in his home however in the
last three days he has been unable to
cross a room without stopping to
catch his breath. The patient denies
outright chest pain/ diaphoresis any
recent cough/congestion, fevers or
chills. This episode is reminiscent of
his “heart failure acting up” He has
been using his medications as
prescribed. At presentation he has
mild increased work of breathing; he
is speaking in 5-7 word sentence
fragments. He is awake/alert.
 T 98.7 P 110 BP 180/80
O2 92% (ra), RR 22
 Gen: WDWN, anxious
 CV: Tachycardic, RR,
cr<3 sec.
 Pulm: Lungs show poor
air movement with rales
from the mid lung
fields to the bases
bilaterally.
 Abd: s/nt/nd
 Ext: no cy/cl/ed

4. Note mild interstitial pulmonary edema in a patient with likely poorly controlled
hypertension and hypertensive cardiomyopathy.
PA/Lateral films show signs of interstitial pulmonary edema (increased interstitial
markings).
Lateral radiograph—Thickened interlobar fissures (subpleural edema) (12B,
black arrowheads),

5.  Pulmonary
 100% O2 by face mask should be administered to achieve O2
saturation of >94% by pulse oximetry.
 If hypoxia persists despite O2 therapy: apply biphasic positive
airway pressure via face mask.
 Unconscious or visibly tiring patients should be intubated.

6.  Cardiac
 Nitroglycerin should be administered 0.4 mg sublingually (may be
repeated q1–5 minutes) or as a topical paste in 1–2 in. If no response
or ECG shows ischemia, NTG 10 mcg/min should be initiated as an
IV drip and titrated to BP and symptomatic improvement
 For hypotensive patients or patients in need of additional inotropic
support start dopamine 5–10 mcg/kg/min and titrate to systolic BP
of 90–100 mm Hg
 When indicated administer a potent IV diuretic, such as furosemide
40–80 mg IV

7.  Medical management
 For patients with resistant hypertension or those who are not
responding well to NTG: nitroprusside may be used, starting at 2.5
mcg/kg/min and titrated.
 In the setting of ESRD the definitive treatment of pulmonary edema
is volume management with dialysis.
 Etiology
 Until excluded, AMI should be considered as the cause of
exacerbation.
 Acute mitral valve or aortic valve regurgitation should be
considered, especially if the heart is of normal size, because the
patient may need emergency surgery.

8. Septal lines
(Kerley B lines)
were present
initially.
Septal lines
(Kerley B lines)
later resolved
after diuresis

9. Blurred vascular margins and
cephalization later resolved
arrowheads.
Peribronchial cuffing also resolved
(white arrow).
-Blurred vascular margins and
distension of upper zone blood
vessels (Cephalization). arrowheads
-Peribronchial cuffing (black arrow)

10. Pulmonary edema resolved after several days treatment with diuretic medications.
Cardiac enlargement and hilar venous distension (upper zone vascular prominence) also
improved.
Lateral radiograph shows improvement of thickened interlobar fissures (subpleural
edema).