Heart failure Flashcards
Heart failure can also be known as congestive heart failure.
Pathoma has a section on this.
Define heart failure.
Definition:
“Failure of heart to pump blood (=oxygen) at a rate sufficient to meet metabolic requirements of the tissues - caused by abnormal cardiac function.”
Characteristics of heart failure:
- typical haemodynamic changes e.g. _____ _________
- neurohumoral activation (explain what this is)
Characteristics of heart failure:
- typical haemodynamic changes e.g. systemic vasoconstriction
- neurohumoral activation = ‘ increased activity of the sympathetic nervous system, RAAS, ADH and atrial natriuretic peptide (ANP) ‘
Clinical presentation:
think of 3 main ones
Clinical presentation:
- breathlessness
- effort intolerance
- fluid retention (ankle swelling)
Causes of heart failure:
5 common listed, think of the usual
6 less common listed too.
Causes of heart failure:
COMMON:
- hypertension
- coronary artery disease / ischaemic heart disease (same thing), (MI is an example of acute CAD/IHD)
- idiopathic
- toxins (alcohol, chemo)
- genetic
LESS COMMON:
- valve disease
- infections (e.g. Chaga’s)
- Congenital heart disease (abnormalities from birth)
- Metabolic (e.g. haemochromatosis, amyloid, thyroid disease)
- pericardial disease/pericardial effusion (fluid in pericardial cavity) (e.g. TB)
- endocardial disease/endocardial fibroelastosis (defect in which there’s too much supporting connective tissue - collagen, elastic fibres)
Main types of heart failure (HF):
— __-___
> younger
> usually male
> coronary artery aetiology
— __-___
> older
> usually female
> hypertension aetiology
— ______ (‘congestive’)
> present for period of time
— _____ (‘decompensated’)
> a worsening of chronic
or
> new onset
Main types of heart failure (HF):
— HF-REF (reduced ejection fraction)
> younger
> usually male
> coronary artery aetiology
— HF-PEF (preserved ejection fraction)
> older
> usually female
> hypertension aetiology
— Chronic (‘congestive’)
> present for period of time
— Acute (‘decompensated’)
> a worsening of chronic
or
> new onset
Simple pathophysiology steps to heart failure:
- _______ ____
\/\/\/
- ___ ______ ____ ______
\/\/\/
- ______ ______ _ ______ _____ / _____
\/\/\/
- _________ _______ (SNS, RAAS, ADH, ANP)
\/\/\/
- ______ _________ ___ ____ __ ___ ____ _______ (caused by neurohumoral activation)
\/\/\/
_. again, cycle repeats
Simple pathophysiology steps to heart failure:
- Myocardial injury
\/\/\/
- Left ventricular systolic dysfunction
\/\/\/
- Percieved reduction in circulating volume / pressure
\/\/\/
- Neurohumoral activation (SNS, RAAS, ADH, ANP)
\/\/\/
- Systemic vasoconstriction and renal Na and water retention (caused by neurohumoral activation)
\/\/\/
- again, cycle repeats
Signs and symptoms of heart failure
SYMPTOMS (what patient notices)
3 listed
SIGNS (what doctor notices on examination)
6 listed
Signs and symptoms of heart failure
SYMPTOMS (what patient notices)
- dyspnoea (difficult breathing) and cough
- ankle swelling (also legs and abdomen)
- fatigue
SIGNS (what doctor notices on examination)
- peripheral oedema (ankles, legs, sacrum)
- elevated JVP
- third heart sound
- displaced apex (due to cardiomegaly)
- pulmonary oedema (lung crackles, remember because left ventricle can’t pump enough so there is back log)
- pleural effusion
New York Heart Association (NYHA) Functional Classification:
Discuss when symptoms arise and limitations for each.
NYHA class 1 ?
NYHA class 2 (mild) ?
NYHA class 3 (moderate) ?
NYHA class 4 (severe) ?
New York Heart Association (NYHA) Functional Classification:
NYHA class 1 no symptoms or limitation in ordinary activity (such as walking/stairs)
NYHA class 2 (mild) mild symptoms (mild shortness or breath an/or angina) and slight limitation in ordinary activity
NYHA class 3 (moderate) Symptoms with less than ordinary activity (such as walking short distances), comfortable only at rest
NYHA class 4 (severe) Severe limitations and symptoms at rest, bedbound.
General investigations for heart failure.
Think of the reason for doing each of these:
- ECG
- CXR (chest X-ray)
- Echocardiogram
- Blood chemistry
- Haematology
- Natriuretic peptides
General investigations for heart failure.
Think of the reason for doing each of these:
- ECG = check for MI, LVH, rhythm, rate, QRS duration
- CXR (chest X-ray) = exclude lung pathology, assess pulmonary oedema
- Echocardiogram = chamber size, systolic+diastolic function, check valves (CMR/cardiovascular magnetic resonance is alternative)
- Blood chemistry (to assess U&Es, Creatinine, urea, LFTs, urate)
- Haematology ( Hb, RDW [RBC Distribution Width, checks size of RBCs] )
- Natriuretic peptides (BNP, NT-proBNP)
Heart failure diagnosis:
[ say what each looks for ]
Signs and symptoms -
\/\/\/
Examination -
\/\/\/
Natriuretic peptides and ECG -
\/\/\/
Echocardiography
Heart failure diagnosis:
Signs and symptoms - ones suggestive of HF, such as dyspnoea/fatigue/ankle swelling (symptoms) and raised JVP/third heart sound/displaced apex beat/peripheral oedema/pulmonary oedema (signs)
\/\/\/
Examination - full blood count, blood glucose, U&Es, urinalysis, CXR
\/\/\/
Natriuretic peptides and ECG - BNP, NT-proBNP
(if high BNP or high NT-proBNP or abnormal ECG then continue \/\/\/)
\/\/\/
Echocardiography
Selected patient investigations:
- c_____ a_______ (X-ray with radioactive dye in vessels)
- e_____ t___
- m______ b____
- g_____ t_____
Selected patient investigations:
- coronary angiography (X-ray with radioactive dye in vessels)
- exercise tests
- myocardial biopsy
- genetic testing
SIGN GUIDELINES
- ____ ______ (slows heart) and ___ _______ (reduces BP) [if intolerant to ___ _____ then ARB]
\/\/\/ ongoing symptoms (NYHA II-IV)
- Add _______ _______ _______ (___) (antagonist to aldosterone, so reduces fluid, aka acts a diuretic)
\/\/\/ ongoing symptoms (NYHA II-IV)
- Give ______ (inhibits breakdown of natriuretic peptides [e.g. ANP+BNP] ) and ______ (an ARB).
STOP the ___ ______ and ___.
CONTINUE ___ _____ and ___.
\/\/\/ ongoing symptoms (NYHA II-IV)
- Other shiz:
- ___ (inserted defib, pacemaker action too) or ___-/___- (inserted pacemaker)
- ________ (inhibits sinus node, so slows pace)
then
- digoxin
- hydralazine + isosorbide dinitrate
then
transplant
SIGN GUIDELINES
- Beta blocker (slows heart) and ACE inhibitor (reduces BP) [if intolerant to ACE inhibitor then ARB]
\/\/\/ ongoing symptoms (NYHA II-IV)
- Add Mineralocorticoid Receptor Antagonist (MRA) (antagonist to aldosterone, so reduces fluid, aka acts a diuretic)
\/\/\/ ongoing symptoms (NYHA II-IV)
- Give Sacubitril (inhibits breakdown of natriuretic peptides [e.g. ANP+BNP] ) and Valsartan (an ARB).
STOP the ACE inhibitors and other ARB.
CONTINUE beta blocker and MRA.
\/\/\/ ongoing symptoms (NYHA II-IV)
- Other shiz:
- ICD (inserted defib) or CRT-P/CRT-D (inserted pacemaker)
- ivabradine (slows pacemaker current)
- digoxin
then
- digoxin
- hydralazine + isosorbide dinitrate
then
transplant
Diuretics important in heart failure patients to reduce their fluid retention.
Will help the peripheral oedema and pulmonary oedema.
Name examples of a diuretic (3 listed).
Examples of diuretics include:
- furosemide (loop diuretic, inhibits Na-K-
Cl transporter) - bumetanide (loop diuretic too)
- spironolactone (blocks aldosterone receptors)
What type of medication is Enalapril?
ACE inhibitor
What is the most evidence based medication in heart failure?
Beta blockers
What type of medication is Eplerenone?
It is a selective aldosterone receptor antagonist (SARA), so only blocks aldosterone.
It is a K-sparing diuretic.
Pic of action of sacubitril and valsartan in folder. Here’s it written:
Sacubitril inhibits _______.
_______ breaks down natriuretic peptides (which causes vasodilation, diuresis, inhibits pathological growth/fibrosis).
_______ also breaks down Angiotensin II (which activates ___ receptor to cause vasoconstriction, Na/water retention, fibrosis/hypertrophy).
Valsartan blocks the ___ receptor.
Pic of action of sacubitril and valsartan in folder. Here’s it written:
Sacubitril inhibits Neprilysin.
Neprilysin breaks down natriuretic peptides (natriuretic peptides cause vasodilation, diuresis, inhibits pathological growth/fibrosis).
Neprilysin also breaks down Angiotensin II (which activates AT1 receptor to cause vasoconstriction, Na/water retention, fibrosis/hypertrophy).
Valsartan blocks the AT1 receptor.
______ = sacubitril + valsarta.
______ is a member of a new class of agents called a______ r______-n______ i______ (ARNIs).
ARNIs combine a \_\_\_\_\_\_ \_\_\_\_\_\_ (sacubitril) and \_\_\_\_\_\_\_ \_\_\_\_\_\_ \_\_\_\_\_ /\_\_\_ (valsartan).
LCZ696 = sacubitril + valsarta.
LCZ696 is a member of a new class of agents called angiotensin receptor-neprilysin inhibitors (ARNIs).
ARNIs combine a neprilysin inhibitor (sacubitril) and angiotensin receptor blocker/ARB (valsartan).
Cardiac resynchronisation therapy (CRT)
Pic in folder with table showing when to use. Two types: CRT-P and CRT-D. CRT is simply a multisite pacemaker.
Good info here:
http://www.bostonscientific.com/en-US/patients/about-your-device/crt-devices/how-crts-work.html
ICDs is different. ICD has pacemaker and defibrillation abilities.
Hydralazine plus isosorbide dinitrate.
Discuss.
Used near bottom of SIGN guidelines for heart failure.
Hydralazine is an arterial vasodilator, and isosorbide dinitrate (a nitrate) are predominantly venodilators.
Don’t have good evidence based treatment for HF-PEF (preserved ejection fraction).
I think all the other meds and SIGN guidelines are for HF-REF.
HF-PEF is when the amount of blood pumped from the left ventricle (ejection fraction) is greater than 50%.
Acute heart failure
–> treatments
Lots of pics in folder for acute heart failure. Look at them.
- _________ _______ _______ _______ (reduces preload, increases intrathoracic pressure so venous return is decreased)
- _________, _______ (increases inotropy, which increases strength of contractions)
- ________ (natriuresis, Na put into urine so water follows)
- ______ and _______ causes venodilation
- ______ and ________
causes arterial vasodilation
Acute heart failure
–> treatments
Lots of pics in folder for acute heart failure. Look at them.
- continuous positive airway pressure (reduces preload, increases intrathoracic pressure so venous return is decreased)
- dobutamine, dopamine (increases inotropy, which increases strength of contractions)
- Furosemide (natriuresis, Na put into urine so water follows)
- Nitrates and morphine causes venodilation
- Nitrates and dobutamine
causes arterial vasodilation
