Heart failure?

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10 year old DSH

-presented for tachypnea, arrhythmia

-no other diagnostics done 

-peripheral pulmonary fluid present on scan of lungs, no pleural effusion present.  No abdominal free fluid.

10 year old DSH

-presented for tachypnea, arrhythmia

-no other diagnostics done 

-peripheral pulmonary fluid present on scan of lungs, no pleural effusion present.  No abdominal free fluid.

Sorry for the image quality – I know it is poor for varying reasons.  I was not able to get many of the measurements that I would normally get.  For now, I had them start lasix while awaiting a more definitive answer from me on whether that is appropriate.  I do not see a lot of structural heart disease but the clinical signs do point strongly to CHF.  I have advised them to get an ECG.

 

Thanks!

Suzanne

 

Comments

EL

No heart failure here… if

No heart failure here… if pulmonary infiltrates or edema are present its not cardiogenic. As a rule la/ao in proper position in the presence of PE or PL effusion needs to be > 1.5… maybe 1.4 with lasix but otherwise no left sided volume overload hence no left chf. Eyeballing here la/ao is about 1.2 so Non cardiogenic effusion and merits an abdominal US to look for a primary cause and a tap to analyze and cytospin to conserve dx cells right away..

smbrowndvm

Wow – fast answer!  There was

Wow – fast answer!  There was no effusion in the abdomen either (I did a quick “drive-by” without shaving and didn’t see anything big and definitely no free fluid).  

I was very unimpressed by this heart but the clinical signs pointed so strongly to a cardiac cause that I really questioned myself.

By PE, are you referring also to pulmonary edema?  By peripheral pulmonary fluid, I was referring to likely pulmonary edema, not fluid in the pleural space.

I would guess bloodwork, BP, ECG are next?

Thanks!!

randyhermandvm

BP and ECG are good ideas-

BP and ECG are good ideas- but I would get chest rads first.

EL

PE= pulmonary edema yes. …

PE= pulmonary edema yes. … there are many non cardiogenic causes of PE:

Frpm my abvp notes and please excise the lumpy verbage and much of this is canine but you may find something that fits for non cardiogenic PE:

 

NCPE Causes:

Increase capillary permeability or hydrostatic pressure

Caudal lung interstitial pattern

PCWP< 18 mmHg

Causes:

Post obstructive: POPE: negative pressure edema: laryngeal dysfunction, aspiration pneumonia, brachycephalic: stenotic nares, elongated sp, reverted laryngeal saccules, Everted tonsils, hypo plastic trachea> acute stress heat exercise intubation POPE aspiration pneumonia>> negative pressure hypoxia sympathetic overstimulation> increase pulmonary vascular volume and pressure > NCPE > surfactant depletion + hypoxia & sympathetic stim > blood pooling > Hypoxia

hypoxia during a POPE event may damage the alveolar epithelium and cause pulmonary vasoconstriction through endothelin

 

POPE Parameters

paO2<80mmHg

Sao2 <95%/93%

Compensatory hyperventilation can increased PaO2 to normal levels

PCWP: Swan Ganz catheter via jugular vein to deep pulm artery= LV end diastolic pressure and la pressure > 18 mm Hg = Cardiogenic volume overload

Sedation removes compensatory hyperactivity of upper airway dilating muscles in brachycephalic breeds

Neurogenic NCPE: seizures, electrocution (NCPE manifests after 1 hour) head trauma CNS hemorrhage creates hydrostatic and permeability changes with a catecholamine storm initiated by the medulla. Volume shift from systemic circulation to pulmonary circulation occurs. Neuro peptide y and endothelin one cause Edema through permeability and vasoconstriction respectively

-An acute increase in hydrostatic pulmonary capillary pressure and secondary damage to tight junctions of the alveoli

ALI/ARDS induced NCPE: sirs, pancreatitis, neoplasia, pneumonia, sepsis, uremia, parvo

Diffuse inflammatory reaction causes pulmonary endothelial and epithelial disruption, edema progresses to fibrosis

Criteria: arterial hypoxia, acute onset, pulmonary Edema, pulmonary inflammation, known risk factor.

Cough with pink foamy sputum in severe cases

All lung fields affected not just caudal dorsal lung***

Drowning NCPE: transfusion related acute lung injury 2-6 hours post-transfusio

Smoke inhalation NCPE:

tissue hypoxia, thermal damage, irritation> secondary pneumonia

OTHER NCPE:
Drug reaction

Anaphylaxis

O2 toxicity

PTE

Starling laws: innate defense against PE

Higher net permeability of capillary endothelium compared with tissues.

Type 1 pneumocytes in alveoli connected by tight junctions that are selective na/k pump. Non selective solute movement if damaged. Loose junctions in capillary endothelium allows passive filtration.

pulmonary capillary endothelium is more permeable to albumin creating a strong oncotic gradient crashing met leakiness avoiding hypoproteinemia induced edema .

Net starling favors intravascular absorption keeping lungs dry

Ventilation also pumps lymphatic and interstitium with one-way valves and fluid can accumulate partially without affecting O2 exchange.

EF:PL ratio > 0.65= NCPE

<0.65=CPE. Edema fluid must be collected from lower airway in early stage of disease

 

NCPE forms when

1) type 1 pneumocyte tight junctions are damaged

2) type 1 pneumocytes are damaged so active na/k transport dies not occur. Aquaporin pump damage

3) local increase in hydrostatic pressure

4) local increase in permeability

 

Tx NCPE

O2 fio2 40-70% nasal Insufflation humidified

Ventilate if Pao2<60 mmHg or Paco2>60 mmHg

Fluid tx colloids lasix for bronchi spasm

EL

any chance he is painful and

any chance he is painful and tachypneic from visceral pain and the PE may be misinterpreted or older lung changes? Can u post the rads?

smbrowndvm

There were no rads done.  It

There were no rads done.  It would make my job easier if there had been a bit more work-up first!

I am just saying it based on the appearance of the U/S.  I will attach a clip of the lung as seen through the liver.  

Thanks so much for your help!

Suzanne

 

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