Small Animal Cardiology and Respiratory Medicine: Examination, Pathophysiology and Management Flashcards
What signs might a dog with respiratory or cardiac disease present with?
Cough
Respiratory noise
Increased respiratory rate or effort- dyspnoea
Lethargy/exercise intolerance
Collapse
What conditions are of the Resp/CV system are certain breeds predisposed to?
CKC spaniels and other small breeds- Mitral valve disease/MMVD
Dilated cardiomyopathy in Dobermans and large giant breeds of dog
Yorkshire terriers predisposed to tracheal collapse
Cats- hypertrophic cardiomyopathy
What history finddings may suggest cardiac/respiratory disease?
- Coughing- when, productive?, length
- Breathing rapidly, laboured, difficulty- constant/intermittent
- Change in voice- laryngeal problem
- Breathing noise
- Nasal discharge- uni/bilateral
- Excercise intolerance
- Collapse/wobbly episodes- get a full description
How can CV/Resp diseases be physically examined for?
Observation- RR, (20-30 in dogs/cats)
Dyspnoeic patient- look for obstructive- inspiration/expiration/restrictive
MM- cyanosis, anaemic
CRT- <2 seconds
Cardiac output- femoral pulse quality
Warmth of extremities
What are signs of foward heart failure?
- Lethargy, excercise intolerance
- Weak femoral pulses
- Pale mucous membranes
- Quiet heart sounds- precordial impulse difficult
- Cold extremities
- Sometimes core temperature reduced
What are signs of left sided CHF?
Increased respiratory rate often with increased effort
Restrictive breathing pattern
Sometimes- soft inspiratory crackles
Radiographs- gold standard
What are the signs of right sided CHF?
Abdominal distension (ascites) most common in dogs, fluid wave on ballotment
Hepatomegaly- if liver is palpable, due to hepatic venous congestion
May have visibly congested, distended jugular veins
Heptaojugular reflex- gentle cranial abdominal pressure will increase caudal vena cava flow- increased distension of the jugular veins
Pleural effusion can sometimes be due to R-CHF or biventricular failure
What is the normal BPM of dogs and cats?
Dogs- 80-140
Cats- 120-200
What should be listened out for with respiratory auscultation?
Check larynx and trachea
Bronchovesicular sounds are normal
Adventitious lung sounds- crackles- smaller openings, wheezes- narrowing
What are the 5 ways a heart murur is categorised?
Location- point of maximal intensity (3rd, 4th, 5th intercostal space)
Timing- Systolic, diastolic, continuous
Grade
Character
Radiation
How are heart murmurs graded?
I/VI- very quiet- only detected in optimal conditions
II/VI- less loud then heart sounds
III/VI- as loud as heart sounds
IV/VI- louder then heart sounds
V/VI- loud heart murmur with precodial thrill
VI/VI- very loud with a precordial thrill
What are the four characters of murmurs?
Early systolic murmurs
Mid-systolic murmurs
Holosystolic murmus- between S1 and S2
Pansystolic murmurs- At point of maximal intensity only hear the murmur
What is radiation of a heart murmur?
Next loudest position of the murmur from PMI
What do the following point of maximal intensities tell you about the location of heart murmurs?:
Left apex
Left base
Left cranio dorsal
Right side
Left apex- mitral valve
Left base- pulmonic/aortic valve
Left cranio-dorsal- patent ductus arteriosis
Right side- tricupsid valve, ventricular septal defects
What is the reynolds number and how is it calculated?
The change from laminar to turbulent flow
Re ~ velocity of blood x diameter of blood vesels x density of blood / viscocity of blood
What is an innocent murmus in puppies and kittens?
Present initially- get less loud over time
Usually
Diminish with growth
Disappear by 16-20 weeks old due to change of foetal to adult haemoglobin
What creates S1, S2, S3 and S4?
S1- closure of atrioventricular valves
S2- closure of the semilunar valves
S3- sound associated with early diastolic filling
S4- late diastolic filling with atrial contraction
What causes an increased chance of S3 and S4 being heard?
S4 is heard when animals which depend on atrial contraction to achieve ventricular filling- hypertrophic cardiomyopathy
S3- when early diastolic filling is abruptly decelerated in a stiff, poorly compliant LV and filling pressures are high- dilated cardiomyopathy
How is the thorax percussed?
Percussing a cupped hand or directly on the chest wall checking for resonance- reduced with pleural effusion
How can thoracic compressability be assesed in cats?
Cranial to the heart- usually springy
With a mediastinal mass or large pleural effusion is is reduced
How can you distinguish between CV and Resp diseases with the following:
HR, Rythm, Coughing, Murmur, Diastolic gallops
How is heart disease classified with ACVIM?
ABCD
A- no risk/abnormality
B- structural abnormality, no clinical signs
B1- no evidence of remodelling, B2- evidence of significant remodelling
C- Congestive heart failre- acute or chronic
Moderate- home treatment, Severe- Hospitalisation
D- Persistent or end stage
How does ISAHC classify heart disease?
Class 1- no clinical signs
1a- no signs of compensation, 1b- mild chamber enlarmgent
Class 2- mild heart failure- signs only on strenuous excertion
Class 3- moderate- severe failure
3a- home treatment, 3b- hospital treatment
How does the NYHA classify heart disease?
Class 1- heart disease present
Class 2- heart disease- signs only after strenuous excertion
Class 3- comfortable at rest, signs on modest excertion
Class 4- Sever clinical signs even at rest
What is the definition of preload?
The venous return to the heart
This influences the degree of end-diastolic stretch and cardiac output by the frank starling mechanism- stretch increases contraction- too an extent
What is theh definition of afterload?
The resistance or impredance to ventricular ejection during systole
What are the major consequences of congestive heart failure?
Oedema and effusions
Peripheral vasoconstriction
Tachycardia/Arrhythmias
Remodelling and fibrosis of the myocardium
These result from neuro-hormonal activation
How does congestive heart failure increase sympathetic drive?
Fall in blood pressure due to low cardiac output causes baroreceptors mediated increase- stimulation of:
- Cardiac B1 adreno-receptors results in increased HR to try and increase cardiac output
- B1 receptors on the juxtaglomerular apparatus of nephron results in renin release
- alpha 1 Adreno-receptors on vascular smooth muscle causes vasoconstriction
How does congestive heart failure activate the RAAS system?
- Renin is released from the JGA by B1 receptro stimulation, reduced perfusion of the kidney, reduced sodium concentration
- Renin is an enzyme which converts angiotensin I in the liver
- Angiotensin to angiotensin II by ACE
- ACE also results in the breakdown of bradykinin
- Angiotensin II acts on the zona glomerulosa of the adrenal cortex to stimulate aldosterone release
How do the different components of the RAAS affect the CV system?
Angiotensin II-
Potent vasoconstrictor
Potentiates sympathetic activity- central activation enhancing adrenergic tone, facilitating ganglionic transport, enhances the release of noradrenaline
Causes vasopressin release from the posterior pituitary
Effects within cardiomyocytes resulting in hypertrophy and fibrosis
Aldosterone
Causes sodium and water retention
Causes myocardial fibrosis and remodelling
Vasopressin from An II release causes excessive sodium and water retention resulting in oedema and effusions
What causes Atrial natriuretic peptide and Brain natriuretic peptide release and what do they cause?
ANP- is released due to atrial stretch
BNP is released due to increased LV pressures
These are natural opponents of the adverse effects of angiotensin II- causing diuresis, natriuresis and vasodilation
How can heart failure be diagnosed?
ANP and BNP can be assayed to demonstrate the presence of heart failure but have a short half life
The inactive N-terminals are more stable and a longer half life and can be assayed by ELISA
What causes endothelin release and what does it do?
Increases are mediated in part by elevated angiotensin II but also endothelial damage
Endothelin is a potent vasoconstrictor and plays a role in myocardial fibrosis and remodelling
What is the La Place relationship?
Compensatory remodelling to attempt to normalise wall stress
Wall stress = radius x pressure / 2 x wall thickness
What does volume overload lead to and what conditions can lead to this?
One or more chambers see and increased volume of blood leading to chamber dilation and usually compensatory hypertrophy- eccentric hypertrophy (wall thickness to chamber size preserved)
Mitral regurgitation
VSD- volume overload of RV, LA, LV
PDA- volume overload of pulmonary vasculature
Tricupsid regurgitation
What does pressure overload lead to and what conditions can cause it?
Increased resistance results in concentric hypertrophy (thick walls)
Aortic stenosis
Systemic hypertension
Pulmonic stenosis
Pulmonary hypertension
What is adaptive remodelling and maladaptive remodelling?
Adaptive- changes in heart chamber and all dimesions as a results of the underlying lesion which normalise wall stress
Maladaptive- change in thickness or geometry of a heart chamber and wall stress is increased
Why does left sided backwards CHF lead to pulmonary oedema?
Elevate filling pressures in the left side of the heart
Increased pressures gets transmitted to the pulmonary vasculature causing fluid to leave the pulmonary circulation and capillaries to result in pulmonary oedema
Why does right sided backwards CHF lead to ascites?
Elevated right heart filling pressures is transmitted to the great veins
The jugular veins may be distended, elevated central venous pressure affects venous return from the liver- hepatomegaly
Hepatic sinusoids may leak fluid and some protein into the abdominal cavity- Ascites
May result in pleural effusion if any fluid leaks into pleural space
How can oedema and effusions be counteracted with CHF?
Diuretics- high ceiling loop diuretics- always indicated
e.g Furosemide
Why should diuretics not be used as a monotherapy for heart failure long term?
They result in further activation of the RAAS and accelerated deterioration of congestive heart failure
Once diuretics are reuqired they are almost always required life long
If one diuretic alone is not working (furosemide) as the total dose has reached a maximum what can be done?
Switch to a stronger ceiling loop diuretic- torasemide
If further diuresis is required, then additional diuretic drugs can be added, those which act on a different part of the nephron- synergistic effect
e. g spironolactone (competitive antagonist to aldosterone- weak potassium spearing diuretic)
e. g Hydrochlorothiazide and Amiloride
Should pleural and abdmonial effusions be drained?
Pleural effusions should be drained
Abdominal effusions associated with CHF should not be drained, unless the patient is very uncomfortable or breathing is compromised
Re-absorption with assisted drug therapy is preferred
How can neuro-endocrine activation in CHF be counteracted?
ACE inhibitors
Anti-aldosterone drugs
What are the favourable effects of ACE inhibitor drugs for CHF?
Vasodilators- arteries and veins
Reduce release of aldosterone- counteract Na and H20 retention
Prevent Ang II myocardial fibrosis and remodelling
Reduce sympathetic activation
Reduce release of vasopressin
Prevents breakdown of bradykinin (vasodilator)
Ang II- Greater efferent glomerular arteriolar than afferent which results in increased glomerular filtration pressure- ACE inhib couteract this
Why might Ang II receptor blockers be used insted of ACE inhibitors?
ACE inhibiors show side effects- seen in humans
When are anti-aldosterone drugs indicated (spironlactone)?
In patients with adequate ACE inhibition, aldosterone levels can tend to rise despire inhibition of RAAS
What different kinds of vasodilators can be used and what are there effects for CHF?
Arteriodilators- reduce mean arterial pressure, reducing resistance (afterload reducers), reduce wall stresss and myocardial oxygen consumption
Venodilators- increase the capacity of circulation- therefore preload is reduced- left sided filling pressures are reduced- therefore helps alleviate pulmonary oedema
How can pulmonary oedema be controlled in an emergency?
Furosemide IV- potent diuretic and venodilator in IV
Nitroglycerine- topically- venodilation
This combination is used for rapid control of pulmonary oedema
Which two drugs are ‘balanced’ vasodilators?
AVE inhibitors
Pimobendan- also positive inotropic effect
What drugs are indicated with the treatment of mitral regurgiation and why?
For example MDD, ruptured chordae tendinae
Arteriodilators will improve the fraction of forward stroke volume by reducing afterload
What drugs can be used for improving cardiac output and when is it indicated?
Pimobendan- positive inotrope by increasing sensitivty
Indicated in patients with systolic dysfunction- DCM
Haemodynamic improvments and arteriodilation- MMVD
What drug can be used to conuteract the high sympathetic drive in CHF?
What are the indications?
Digoxin
Patients with atrial fibrillation
Antiarrythmic
Sinus tachycardia
Reduced systolic function
How does digoxin reduce high sympathetic drive?
Vagomimetic
Enhances vagal tone and reduces sympathetic tone by:
Direct stimulation of CNS vagal centres
Sensitizes baroreceptors to blood pressure changes
Enhances cardiac pacemaker responses to acetylcholine
Results in- slowing rate of discharge of SAN, slows conduction through AVN
Digoxin is a vagomimetic and enhances vagal tone and reduces sympathetic drive
What are its over all effects?
Negative inotrope- decreases HR
Favourable autonomic effects
Mild positive inotrope
What is the risk of digoxin and what are the signs?
Toxicity- Digitoxity
Signs-
- dull,
- lethargic,
- excessive borborygmi- gurgling from intestines
- Anorexia
- Vomiting/Diarrhoea
- Arrythmias
What is the standard quadruple therapy for CHF?
What additional drugs may be included?
- Furosemide
- ACE inhibitor
- Pimobendan
- Spironolactone
Additional- other diuretics, anti-arrythmics
What is the minimum CHF therapy if there is economic constraints?
Furosemide and Pimobendan
