– 11 year old M Lab with history of cough 2 month duration and exercise intolerance wt. 57.2 kg
– speaking with the owner, the cough sounds like he is clearing his throat and only seems to happen when excited or barking
– he is stiff with djd and moderately overweight
Chest rads were sent to a radiologist with the following conclusions:
– 11 year old M Lab with history of cough 2 month duration and exercise intolerance wt. 57.2 kg
– speaking with the owner, the cough sounds like he is clearing his throat and only seems to happen when excited or barking
– he is stiff with djd and moderately overweight
Chest rads were sent to a radiologist with the following conclusions:
RADIOGRAPHIC CONCLUSIONS
1. Generalized cardiomegaly; Expiratory radiographs make the heart look bigger due to decreased surrounding
thoracic volume. DCM is a consideration and echocardiography may be considered for further assessment.
2. Mild diffuse bronchointerstitial pattern; compatible with age-related fibrosis, possible component of bronchitis
3. Normal abdomen
4. T6-7 and T9-10 chronic intervertebral disc disease
– I did an echo on him today and despite sedation with BAA, he panted profusely and loudly (possible Lar Par?) and we could not get him to stop panting even with holding his mouth and blowing on his face ( I was sweating during the exam!)
– as a result, the m-mode is terrible so I took 2-D LV measurements which showed normal LV in sys and dia but a low FS of around 14%
– subjectively I thought the right and left heart looks normal (chambers/walls)
– there was no LAE, no MR, no TR seen, AO Max Vel and Pul Max Vel were wnl, I could not rule out PAH but could not see any major structural changes that would indicate it (possibly some bowing of the PV?)
– the contractility looks a little depressed though? The owner did indicate that he had not given him any food or water since last night and the scan was done in the afternoon so I am wondering if he was dehydrated as he was worked up and panted the whole time at the clinic?
Anyway, I do think this pet’s cough/clearing of the throat is likely more related to Lar Par or possibly lower airway disease, but the FS% is concerning. Any thoughts? Could decreased preload be influencing it as the LVIDs is normal?
Comments
I agree the L side of the
I agree the L side of the heart looks OK. Large breed dogs often have lower FS- but not this low. Where were your M modes taken. Sometimes I think I have been a bit to close to the apex and get understated FS.
When I was going through EVP course I made a paper for myself and I called it the “Pathophysiology of Cardiac Change”. I share it with you- for what it is worth. Helps me.
Pathophysiology of Cardiac Change:
L Atrium:
Too large:
1. L ventricular systolic dysfunction (e.g. DCM)
2. Left ventricular diastolic dysfunction (e.g. HCM)
3. Mitral valvular disease (e.g. endocardiosis)
4. L to R shunting
5. Iatrogenic (e.g. fluid overload)
To small:
1. Hypovolemia
Not empty:
1. Thrombus (cats>dogs)
2. Spontaneous echo contrast (e.g. “smoke”)
3. Mass (e.g. neoplasia, abscess)
L Ventricle:
Too large:
1. Volume overload (e.g. DCM, endocardiosis, L to R shunt)
2. High output state (e.g. anemia, hyperthyroidisim)
3. Iatrogenic (fluid overload)
Too small:
1. Hypovolemia
2. Severe concentric LV hypertrophy (e.g. HCM)
3. Right ventricular volume or pressure overload
LV Posterior Wall:
Too thick:
1. Outflow obstruction (e.g. systemic hypertension, SAS)
2. Inappropriate hypertrophy (e.g. HCM, RCM)
3. Infiltrative disease
Too thin, poor motion:
1. DCM
2. Prior myocardial infarction
Too Bright:
1. ischemia and/or fibrosis
Interventricular Septum:
Too thick:
1. Outflow obstruction (e.g. systemic hypertension, SAS)
2. Inappropriate hypertrophy (e.g. HCM, RCM)
3. Infiltrative disease
4. Right ventricular outflow obstruction (e.g. PS, PH)
Too thin, poor motion:
1. DCM
2. Prior myocardial infarction
Too bright:
1. ischemia and/or fibrosis
Piece Missing:
1. VSD
Flattening:
Right ventricular pressure or volume overload
Paradoxical Septal Motion:
1. RV overload as for flattening
2. Conduction disturbances
Global LV Function:
Increased:
1. High output states (e.g. anemia, fever, increased T4)
2. Hypertrophic Cardiomyopathy
3. Mitral insufficiency (“hyper-dynamic)
Decreased:
1. DCM
2. Restrictive cardiomyopathy (some)
3. Severe hypothyroidism
4. Sepsis
5. Concurrent tachyarrythmia
LFOT/Aortic Valve:
LV outflow tract too narrow (visible ridge)
1. SAS
Thickened valve +/- abnormal valve movement
1. Valvular aortic stenosis
2. Aortic endocarditis
Aorta:
Too wide:
1. Post stenotic dilation
2. Systemic hypertension
Too narrow:
1. Hypovolemia
2. Poor Cardiac output (e.g. DCM)
Pathophysiology of Cardiac Change
Right Atrium:
Too large:
1. Tricuspid valvular disease (e.g. endocardiosis, TV dysplasia
2. Atrial septal defect
3. Iatrogenic (fluid overload)
Too small:
1. Hypovolemia
2. Collapse due to pericardial effusion/cardiac tamponade
Tricuspid Valve:
Too Thick:
1. Tricuspid valvular dysplasia (+/- long, tethered appearance)
2. Chronic degenerative valvular disease (endocardiosis)
Abnormal motion:
1. Tricuspid stenosis- restricted movement during diastole
Multiple double lines crossing valve:
Heartworm disease
Right Ventricle:
Too large:
1. Volume overload (e.g. DCM, tricuspid insufficiency)
2. Iatrogenic (fluid overload)
Too small:
1. Hypovolemia
2. Cardiac tamponade
Thickened Walls:
1. Pressure overload (e.g. PS, Pulmonary hypertension
2. Infiltrative disease
Pulmonic Valve and PA:
Thickened Valve:
1. Pulmonic stenosis
Dilated Pulmonary artery:
1. Post-stenotic dilation
2. Pulmonary hypertension
Pathophysiology of Cardiac Change
I agree the L side of the
I agree the L side of the heart looks OK. Large breed dogs often have lower FS- but not this low. Where were your M modes taken. Sometimes I think I have been a bit to close to the apex and get understated FS.
When I was going through EVP course I made a paper for myself and I called it the “Pathophysiology of Cardiac Change”. I share it with you- for what it is worth. Helps me.
Pathophysiology of Cardiac Change:
L Atrium:
Too large:
1. L ventricular systolic dysfunction (e.g. DCM)
2. Left ventricular diastolic dysfunction (e.g. HCM)
3. Mitral valvular disease (e.g. endocardiosis)
4. L to R shunting
5. Iatrogenic (e.g. fluid overload)
To small:
1. Hypovolemia
Not empty:
1. Thrombus (cats>dogs)
2. Spontaneous echo contrast (e.g. “smoke”)
3. Mass (e.g. neoplasia, abscess)
L Ventricle:
Too large:
1. Volume overload (e.g. DCM, endocardiosis, L to R shunt)
2. High output state (e.g. anemia, hyperthyroidisim)
3. Iatrogenic (fluid overload)
Too small:
1. Hypovolemia
2. Severe concentric LV hypertrophy (e.g. HCM)
3. Right ventricular volume or pressure overload
LV Posterior Wall:
Too thick:
1. Outflow obstruction (e.g. systemic hypertension, SAS)
2. Inappropriate hypertrophy (e.g. HCM, RCM)
3. Infiltrative disease
Too thin, poor motion:
1. DCM
2. Prior myocardial infarction
Too Bright:
1. ischemia and/or fibrosis
Interventricular Septum:
Too thick:
1. Outflow obstruction (e.g. systemic hypertension, SAS)
2. Inappropriate hypertrophy (e.g. HCM, RCM)
3. Infiltrative disease
4. Right ventricular outflow obstruction (e.g. PS, PH)
Too thin, poor motion:
1. DCM
2. Prior myocardial infarction
Too bright:
1. ischemia and/or fibrosis
Piece Missing:
1. VSD
Flattening:
Right ventricular pressure or volume overload
Paradoxical Septal Motion:
1. RV overload as for flattening
2. Conduction disturbances
Global LV Function:
Increased:
1. High output states (e.g. anemia, fever, increased T4)
2. Hypertrophic Cardiomyopathy
3. Mitral insufficiency (“hyper-dynamic)
Decreased:
1. DCM
2. Restrictive cardiomyopathy (some)
3. Severe hypothyroidism
4. Sepsis
5. Concurrent tachyarrythmia
LFOT/Aortic Valve:
LV outflow tract too narrow (visible ridge)
1. SAS
Thickened valve +/- abnormal valve movement
1. Valvular aortic stenosis
2. Aortic endocarditis
Aorta:
Too wide:
1. Post stenotic dilation
2. Systemic hypertension
Too narrow:
1. Hypovolemia
2. Poor Cardiac output (e.g. DCM)
Pathophysiology of Cardiac Change
Right Atrium:
Too large:
1. Tricuspid valvular disease (e.g. endocardiosis, TV dysplasia
2. Atrial septal defect
3. Iatrogenic (fluid overload)
Too small:
1. Hypovolemia
2. Collapse due to pericardial effusion/cardiac tamponade
Tricuspid Valve:
Too Thick:
1. Tricuspid valvular dysplasia (+/- long, tethered appearance)
2. Chronic degenerative valvular disease (endocardiosis)
Abnormal motion:
1. Tricuspid stenosis- restricted movement during diastole
Multiple double lines crossing valve:
Heartworm disease
Right Ventricle:
Too large:
1. Volume overload (e.g. DCM, tricuspid insufficiency)
2. Iatrogenic (fluid overload)
Too small:
1. Hypovolemia
2. Cardiac tamponade
Thickened Walls:
1. Pressure overload (e.g. PS, Pulmonary hypertension
2. Infiltrative disease
Pulmonic Valve and PA:
Thickened Valve:
1. Pulmonic stenosis
Dilated Pulmonary artery:
1. Post-stenotic dilation
2. Pulmonary hypertension
Pathophysiology of Cardiac Change
The LA/AO is normal so the
The LA/AO is normal so the cough cannot be cardiogenic in origin. There looks to be a tachyarrythmia so that will depress the fs%. ECG?
The LA/AO is normal so the
The LA/AO is normal so the cough cannot be cardiogenic in origin. There looks to be a tachyarrythmia so that will depress the fs%. ECG?
Your descrition of the cough
Your descrition of the cough sounds more typical for tracho-bronchial disease than cardiac disease. As Eric states normal La: Ao, so unlikley that there is cardiac disease but can run a pro-BNP to differentiate cardiac vs respiratory disease:
Oyama MA, et al Assessment of serum N-terminal pro-B-type natriuretic peptide concentration for differentiation of congestive heart failure from primary respiratory tract disease as the cause of respiratory signs in dogs. J Am Vet Med Assoc. 2009;235:1319-1325:
To determine whether serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentration is useful in discriminating between cardiac and noncardiac (ie, primary respiratory tract disease) causes of respiratory signs (ie, coughing, stertor, stridor, excessive panting, increased respiratory effort, tachypnea, or overt respiratory distress) in dogs.
115 dogs with respiratory signs.
Dogs with respiratory signs were solicited for study. Physical examination, thoracic radiography, and echocardiography were used to determine whether respiratory signs were the result of cardiac (ie, congestive heart failure) or noncardiac (ie, primary respiratory tract disease) causes. Serum samples for NT-proBNP assay were obtained at time of admission for each dog. Receiver-operating characteristic curves were constructed to determine the ability of serum NT-proBNP concentration to discriminate between cardiac and noncardiac causes of respiratory signs.
Serum NT-proBNP concentration was significantly higher in dogs with cardiac versus noncardiac causes of respiratory signs. In dogs with primary respiratory tract disease, serum NT-proBNP concentration was significantly higher in those with concurrent pulmonary hypertension than in those without. A serum NT-proBNP cutoff concentration > 1,158 pmol/L discriminated between dogs with congestive heart failure and dogs with primary respiratory tract disease with a sensitivity of 85.5% and a specificity of 81.3%.
Measuring serum NT-proBNP concentration in dogs with respiratory signs helps to differentiate between congestive heart failure and primary respiratory tract disease as an underlying cause.
Your descrition of the cough
Your descrition of the cough sounds more typical for tracho-bronchial disease than cardiac disease. As Eric states normal La: Ao, so unlikley that there is cardiac disease but can run a pro-BNP to differentiate cardiac vs respiratory disease:
Oyama MA, et al Assessment of serum N-terminal pro-B-type natriuretic peptide concentration for differentiation of congestive heart failure from primary respiratory tract disease as the cause of respiratory signs in dogs. J Am Vet Med Assoc. 2009;235:1319-1325:
To determine whether serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentration is useful in discriminating between cardiac and noncardiac (ie, primary respiratory tract disease) causes of respiratory signs (ie, coughing, stertor, stridor, excessive panting, increased respiratory effort, tachypnea, or overt respiratory distress) in dogs.
115 dogs with respiratory signs.
Dogs with respiratory signs were solicited for study. Physical examination, thoracic radiography, and echocardiography were used to determine whether respiratory signs were the result of cardiac (ie, congestive heart failure) or noncardiac (ie, primary respiratory tract disease) causes. Serum samples for NT-proBNP assay were obtained at time of admission for each dog. Receiver-operating characteristic curves were constructed to determine the ability of serum NT-proBNP concentration to discriminate between cardiac and noncardiac causes of respiratory signs.
Serum NT-proBNP concentration was significantly higher in dogs with cardiac versus noncardiac causes of respiratory signs. In dogs with primary respiratory tract disease, serum NT-proBNP concentration was significantly higher in those with concurrent pulmonary hypertension than in those without. A serum NT-proBNP cutoff concentration > 1,158 pmol/L discriminated between dogs with congestive heart failure and dogs with primary respiratory tract disease with a sensitivity of 85.5% and a specificity of 81.3%.
Measuring serum NT-proBNP concentration in dogs with respiratory signs helps to differentiate between congestive heart failure and primary respiratory tract disease as an underlying cause.
Thanks Randy – nice summary,
Thanks Randy – nice summary, I am going to print that out for future reference. I almost forgot about the NT-proBNP test. Use to run them all the time before I could do an echo.
As for the tachyarrhythmia, this dog was given a good dose of BAA (butorphanol, acepromazine, atropine)
I wonder if the atropine, along with the profuse panting contributed to the elevated heart rate and thus low FS%? I am going to recommend an ECG to be on the safe side. Have also instrcted the owner to do a few SRR’s at home as this pet was so worked up in the clinic.
Thanks all!
Thanks Randy – nice summary,
Thanks Randy – nice summary, I am going to print that out for future reference. I almost forgot about the NT-proBNP test. Use to run them all the time before I could do an echo.
As for the tachyarrhythmia, this dog was given a good dose of BAA (butorphanol, acepromazine, atropine)
I wonder if the atropine, along with the profuse panting contributed to the elevated heart rate and thus low FS%? I am going to recommend an ECG to be on the safe side. Have also instrcted the owner to do a few SRR’s at home as this pet was so worked up in the clinic.
Thanks all!
If you look on my list under
If you look on my list under Global LV Function you will see
tachyarrythmia as one of the causes of decreased function.
If you look on my list under
If you look on my list under Global LV Function you will see
tachyarrythmia as one of the causes of decreased function.
Yep – that’s great! I suspect
Yep – that’s great! I suspect that this is the reason in this patient as everything else check’s out. Thanks again
Yep – that’s great! I suspect
Yep – that’s great! I suspect that this is the reason in this patient as everything else check’s out. Thanks again