W3 Clinical Management of Heart Failure Flashcards
What is Heart failure?
What is this caused by?
What are the treatment aims?
-Heart cannot function, resulting in raised pressure inside the heart and/or inadequate cardiac output
-Usually caused by left ventricular and myocyte dysfunction from a MI, but can have other causes
-Progressive disease without a cure
* Treatment aims to slow progression
* Prognosis depends on cause, but survival is ~5 years after diagnosis
* Common condition (affects ~2% adult population)
* Prevalence increases with age**
Heart Failure Terminology:
What is Acute (Decompensated) Heart Failure?
Sudden deterioration in HF, which can lead to hospitalisation
Heart Failure Terminology:
Whatis Chronic (Compensated) Heart Failure?
Established diagnosis of HF or gradual onset of symptoms
Heart Failure Terminology:
Ejection Fraction?
HF with reduced EF?
Left / Right ventricular dysfunction?
- % blood pumped out of a filled ventricle when it contracts
- Normal EF = ~50%
- Heart failure with ejection fraction below 40%
- HF caused by issues with left / right ventricle
What are the 3 main features of heart failure?
Fatigue, Oedema, Breathlessness
Diagnosing HF:
What is diagnosis based on?
- Presence of signs and symptoms
- Patient history (e.g. history of MI, hypertension, CAD, diabetes etc)
- Blood levels of NT-proBNP
- ECG (will unlikely be normal in HF)
- Exercise tolerance test
- Transthoracic echocardiography (“echo”) to assess ventricular function
- Patients will likely undergo lots of other tests to confirm HF and to rule out other conditions too
- E.g. full bloods, thyroid function tests, chest X rays, peak flow
What is NT-proBNP?
When is NT-proBNP released?
When may its levels be reduced or elevated?
- N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a peptide released in response to changes in pressure inside the heart
- Blood levels can confirm/rule out diagnosis of HF
- Level under 400ng/L = less likely to be HF
- Very high levels (>2,000ng/L) = poor prognosis
- Can be used to monitor progress
- Goes up = deterioration in HF, improves/steady = HF under control
BUT!
* Levels may be reduced in obesity / African-Caribbean family background / current treatment w ACE inhibitors, ARBs, or mineralocorticoid receptor antagonists
* Levels may be elevated in age over 70 / LV hypertrophy / renal dysfunction / sepsis / COPD/diabetes / ischaemia
* Can’t rely on this alone- must still consider clinical picture
What are the Aims of Heart Failure Treatment? (6)
Incurable condition. Treatment will therefore not get rid of it
Condition will get progressively worse. Treatment may therefore need to change as condition progresses- monitor!
Aims:
* Improve symptoms, functional capacity and quality of life
* Slow condition progression
* Prevent hospitalisation
* Reduce mortality
* Cornerstone of treatment = Pharmacological Interventions
* Role for non-pharmacological intervention alongside it
Managing Heart Failure with Preserved EF:
What is the % of preserved EF?
What should be offered?
Preserved EF = EF over 40%
* Offer loop diuretic
* E.g. furosemide
* Titrate dose as needed (usually up to 80mg/day)
* Purpose is to relieve congestive symptoms and fluid retention (symptomatic relief)
* Only other option is to optimally manage other co-morbidities, e.g. hypertension, AF and diabetes
* To keep EF high and slow deterioration
Managing heart failure with reduced ejection fraction:
What is the symptomatic relief?
What is first-line treatment? (2)
What is added in?
Symptomatic relief: Loop Diuretic
* E.g. furosemide to manage oedema
First line: ACE inhibitor & Beta Blocker
1. ACE Inhibitor: E.g. Ramipril
-Dec morbidity and mortality; improve symptoms
-Start with low dose and gradually INC to max tolerated dose
2. Beta Blocker: E.g. Bisoprolol
* DEC Morbidity and mortality; improve symptoms
* Start with low dose and gradually INC to max tolerated dose
3. Add in: Mineralocorticoid Receptor Antagonists
* E.g. spironolactone or eplerenone
Dec mortality and hospitalisation; improve symptoms
Add in if still having symptoms despite ACEi and BB
ACE Inhibitors: First line in Chronic HF (preserved EF)
What is the MoA?
Mechanism of Action
-Inhibit angiotensin converting enzyme
-Stops conversion of angiotensin I to angiotensin II
-Reduces vasoconstriction and aldosterone synthesis
-Less vasoconstriction = dilation of vessels = improve blood flow = reduces amount of work heart does
to keep organs perfused
-Less aldosterone = increased sodium and water excretion = lower blood pressure
Monitoring
-Sodium, potassium and renal function
before starting, 1-2 weeks after starting and
after dose increments
-Blood pressure before and after each dose
increment
Common Side Effects
Alternative
-If cannot tolerate cough,
stop drug
-May also be less effective in
patients of African / African-
Caribbean origin (lower renin
levels)
-Give Angiotensin Receptor
Blocker instead
-e.g. losartan
1st LineACE
Inhibitor
s
Example Dose
-Ramipril 2.5mg BD
-Lisinopril 2.5mg OD
ACE Inhibitors: First line in Chronic HF (preserved EF)
What are the common SE?
-Dry, persistent cough
-Dizziness or light-headedness (Dec BP)
-Headache
-Diarrhoea
-Mild skin rash
-Inc K+, Inc Na+, Dec BP,
-Dec GFR
ACE Inhibitors: First line in Chronic HF (preserved EF)
What are the red flags?
-Jaundice (liver impairment)
-Severe stomach pain (pancreatitis)
-Pale, fatigue, dizzy, bleeding, sore throat, fever, catching infections easy (blood or bone marrow disorder)
-Blood in pee / not peeing (kidney issues)
ACE Inhibitors: First line in Chronic HF (preserved EF)
What is the example dose?
Monitoring requirements?:
Alternatives?
-Ramipril 2.5mg BD
-Lisinopril 2.5mg OD
Loop diuretics:
What are the examples to treat heart failure?
-Furosemide 20mg mane
-Furosemide 40mg mane and 40mg midday
