Management of Heart Failure Flashcards
Outline the compensatory mechanisms in response to heart failure and how they themselves can lead to CHF
RAAS systems leads to salt/water retention
Fluid builds up in the vessels -especially the veins
Venous pressure rises
High venous pressure leads to fluid being pushed out of veins
Leading to congestion/oedema
But output & CO are restored
Eventually the patient will decompensate and undergo congestive heart failure and disease progression
Backward failure - congestion
Forward failure - poor perfusion
List the systems involved in the compensatory response
SNS
RAAS
ADH (antidiuretic hormone - water retention)
Natriuretic peptides
Atrial stretch
Describe left sided heart faulire
Congestion of the pulmonary venous circulation
-Drain the lungs
Most common
Due to high pressure the effect is more obvious
Leads to fluid in lungs which is life threatening
Describe right sided heart failure
Congestion of the systemic venous circulation
-Drain the body
Explain stage A at assessing severity of HF
Patients at high risk of heart disease but have no identifiable structural disorder of the heart
-breed associated disease
Explain stage B at assessing severity of HF
Patients with structural heart disease (e.g. murmur), but no clinical signs
Stage B1
Asymptomatic patients with no radiographic or echocardiographic evidence of cardiac remodelling
Stage B2
Asymptomatic patients with radiographic or echocardiographic evidence of left-sided heart enlargement.
-Cardiac enlargement (especially LA)
Explain stage C at assessing severity of HF
Patients with past or current clinical signs of heart failure associated with structural heart disease.
Mild: Evidence of limited exercise intolerance
Moderate: Signs evident with mild exercise
Explain stage D at assessing severity of HF
Patients with end-stage disease with clinical signs of heart failure that are refractory to ‘‘standard therapy’’
Advanced
Obvious clinical signs with minimal exercise
Progressively worsens
Obvious clinical signs at rest
Sudden collapse/death
Outline the treatment process of heart faulire
Identifying primary cause of the disease
Non specific treatment of the primary disease
Treatment of congestive heart failure
Identify dysrhythmias and treat if indicated
Identify complicating and coexisting factors
Regular reassessment
What does the owner want?
Explain why there is no singular treatment for heart failure
- Cause of heart disease varies.
- Presenting clinical signs varies.
- Disease progression varies.
- Response to treatment varies.
Describe the process in identifying the primary cause of the disease
Valve degeneration
Mitral
Aortic
Cardiomyopathy
Cause unknown
Cannot treat
Describe what is meant by non specific treatment of the primary disease
Requirement of precise diagnosis of the type of primary disease
In cases of primary disease that cannot be identified or if it is untreatable (valve degeneration) it must be considered if treatment would be possible
Ultrasound (echocardiography) usually required
Explain how dilated cardiomyopathy is treated with non specific targets
Dilated = contractility failure
Drugs that improve contractility = positive inotropes
- Digoxin (digitalis glycosides)
- Pimobendane (“Vetmedin”)
- Dobutamine
Explain how hypertrophic/restrictive cardiomyopathy is treated with non specific targets
Heart fills poorly
Drugs that help heart relax = positive lusitropes
- Calcium channel blockers
diltiazem, verapamil
- Beta blocker
propranolol, atenolol
Describe how Stage B1 of congestive heart failure is treated
No treatment but to consider:
Weight control
Regular reassessment
Client education
Describe how Stage B2 of congestive heart failure is treated
No treatment but to consider:
Pimobendane
Weight control
Regular reassessment
Client education
Describe how Stage C of congestive heart failure is treated
Clinical signs of CHF
Due to oedema formation
Cough/breathing problems in L heart failure
Fluid accumulation in body cavities in R heart failure
Treatment:
Remove fluid - diuretic traditionally used
Vasodilatation Act at kidney to increase urine output Loop diuretics – furosemide, torasemide Aldosterone antagonists - spironolactone ACE inhibitor
Explain how vasodilators are used in treatment for stage C congestive heart failure
Dilate arteries, veins or both break the vicious cycle of heart failure
Act by: Reduce arterial blood pressure - afterload Reduce venous pressure - preload Reduction of load and therefore cardiac work Clinical uses: Treatment of cardiac failure Antihypertensive agents
How do Venodilators work?
During HF salt & water retained leading to high venous pressure, increasing preload. Eventually leads to oedema formation
Venodilators reduce preload by increasing venous capacity, dropping the pressure within veins. Reducing oedema formation
How do arterial dilators work?
During HF vasoconstriction arteries reduces cardiac output and increase the afterload, leading to increased AV regurgitation.
Arterial dilators reduce afterload, by increasing cardiac output. Leads to a reduction work for the heart and this valve leakage decreases
Explain how the use of ACE inhibitor cause decongestion
Reduce level of angiotensin II
Venous dilators
Arterial dilators
Reduce levels of aldosterone
Reduce fluid accumulation
List examples of ace inhibitor
- Imadipril
Prilium
- Enalapril
Enacard
- Benazepril
Benfortin
Nelio
Prilben
Fortekor
Kelapril
- Ramipril
Vasotop
Outline other treatments used in congestive heart disease
Low salt diet – efficacy??
Exercise regime
exercise within capacity
Aspirate fluid – pleural/abdominal
Acute onset of left heart failure
Severe respiritory distress
-Cage reset
-Oxygen therapy
Outline the process of identifying dysrhythmias and treatment
Dysrhythmias are common in patients with heart disease
These will require characterisation with an ECG
Specific antidysrhythmic therapy may be required
e.g. beta blocker, calcium channel blocker, digoxin
FEW VETERINARY LICENSED
Discuss what is meant by regular assessment in the therapeutic treatment process
- Assess patient for side effects, toxicity etc
- Drug doses may need to be adjusted
There is rarely a standard dose - Regular blood chemistries are advisable
- Repeat investigations if indicated
- Weigh
Aim is resolution of clinical signs
Rarely a cure
Understand mechanisms by which drugs may fail to be effective
Therapy failure
Dose too low – dose by surface area not weight?
Administration failure?
Absorption if given by mouth?
Tachyphylaxis
Outline how there may be adverse effects to therapy
Dose too high - lean weight/fluid presence
Idiosyncratic reaction Complicating factors - renal dysfunction Co-existing disease - liver dysfunction
Effect of combinations - polypharmacy?
