Heart Failure Flashcards
definition of heart failure
A clinical syndrome comprising of dyspnoea, fatigue or fluid retention due to cardiac dysfunction, either at rest or on exertion, with accompanying neurohormonal activation.” Not a final diagnosis
Prevalence of HF
Affects 1-2% of UK population
Increasing in prevalence
prognosis of heart failure
Poor prognosis: 30-40% mortality at 1 year
10% HF patients readmitted within one month, most in one week
-50% HF patients readmitted over 3 months
More mortality than colon, breast, prostate cancer
longest hospital admission after stroke
symptoms of HF
breathlessness • Fatigue • Odema • Reduced exercise capacity
signs of HF
Odema • Tachycardia • raised JVP • chest crepitations or effusions • 3rdheart sound • Displaced or abnormal apex beat
diagnosis of HF
1.
Symptoms or signs of HF (rest or exercise)
and
2. Objective evidence of cardiac dysfunction
and (in doubtful cases)
3.Response to therapy (diuretics
investigations for cardiac dysfunction
ECHO
Radionucleotide Scan
Left Ventriculogram
Cardiac MRI
12 Lead ECG- LVSD very unlikely if ECG normal (90-95% sensitive). Problems with confidence of interpretation in primary care, must be entirely normalor else loses reliability
BNP (brain (B-type) natriuretic peptide)
Amino acid peptide, can be measured easily in blood, Elevated in heart failure, therefore low BNP effectively excludes heart failure
BNP
Highly sensitive test for HF, stable for up to 72hours, ‘bedside’ testing available if desired, relatively inexpensive • Low BNP effectively rules out heart failure or LVSD, elevated BNP indicates need for an echo/cardiac assessment • Caution… Can be elevated due to AF Elderly Valve Disease
structural heart diseases that may cause HF
LV systolic dysfunction –many causes
Valvular heart disease
Pericardial constriction or effusion
LV diastolic dysfunction/heart failure with preserved systolic function/heart failure with normal ejection fraction
Cardiac arrhythmias: tachy or brady
Myocardial ischaemia/infarction (usually via LVSD)
Restrictive cardiomyopathy egamyloid, HCM
Right ventricular failure: primary or secondary to pulhypertension
common causes of LV systolic dysfunction
• Ischaemic heart disease (usually MI) • Severe AV disesase or MR • Dilated cardiomyopathy(DCM): Means LVSD not due to IHD or secondary to other lesion ie valves/VSD
detailed evaluation of patients with LVSD
•
Take a detailed history:
•
it may provide the answer –ie MI, DM, HBP, post partum, alcohol etc
•
Hillwalkers…?lyme’s disease, IVDA…?HIV etc
•
Consider familial DCM: family history
•
Exclude renal failure, anaemia, TFTs
•
Possibly do autoantibodies / viral serology, ferritin
•
Consider need to exclude phaechromocytoma
•
Consider other causes……sarcoid, muscular dystrophy etc etc
•
ECG, CXR, always do an echo
•
Consider coronary angiography –essential if chest pain, patients <70(?)
•
CT coronary angiogram instead of cor angio
•
Consider evaluating for ischaemia/hibernation ie is revascularisation appropriate even if no angina
•
Cardiac MRI: infarction/inflammation/fibrosis
•
Most patients should be assessed by a cardiologist
why is echocardiography essential
• Identify and quantify • LV systolic dysfunction • Valvular dysfunction • Pericardial effusion / tamponade • Diastolic dysfunction • LVH • Atrial/ventricular shunts / complex congenital heart defects • Pulmonary hypertension / Right heart dysfunction • May not identify constriction / may miss shunts (but you will see atrial dilatation)
views on echo
parasternal long axis
parasternal short axis (papillary muscle level)
parasternal short axis (base)
LV ejection fraction
LV ejection fraction is a continuous biological variable
•
Disease / physiological changes can both decrease and increase the LVEF
•
The LVEF may be lower than previous but not pathologically low
hard to see on echo but good with MRI, time consuming
Normal 50-80% • Mild 40-50% • Moderate 30-40% • Severe <30%
biplane modified simpsons rule
Divides LV cavity into multiple slices of known
•
thickness
•
diameter
•
-> volume of each slice
•
= area x thickness(πr2 x thickness)
•
thinner slices -> more accurate volestimate
•
endocardial border traced accurately
•
often major technical difficulty with this method
•
but still one of most accurate method available
•
relatively easy to perform (but not routinely done)
LVEF -MUGA
ionising contrast used in scan of blood pumping in heart Much easier to obtain an accurate figure for the LVEF • Greater reproducibility • centre specific normal range But • Ionising radiation • No additional structural information
LVEF -MRI
Gold Standard for assessment of LVEF • Greater reproducibility • normal range • Added information about Aetiology • Fibrosis • Infiltration • Oedema • Valves • Time consuming –Approx 1 hour • Patient compliance • Long breath holds • Claustrophobic • Ability to lie flat • Specialist centres • Long waiting lists
Grading of heart failure
1-none
2- mild limitation and comfortable at rest or mild exertion
3-moderate limitation and comfortable only at rest
4-severe limitation and any physical activity brings on discomfort and symptoms occur at rest
Heart failure does not equal reduced cardiac output explanation
Normal heart (an orange) end diastolic volume 100mls with 60% EF = 60mls blood ejected per beat x 60 bpm = 3.6litres CO per min
•
Dilated heart (football): with reduced EF: EDV 200mls with 30% EF = 60mls blood ejected per beat x 60bpm = 3.6l CO per min….at 100bpm = 6 litres CO per min!
•
……and yet that person will possibly have severe heart failure….So it is NOT all about cardiac output
Modern Pharmacological treatment of heart failure (due to LV systolic dysfunction)
• Diuretics • Furosemide/Bumetanide • Symptomatic relief • ACE inhibitors/ARBs • Ramipril, enalapril • Candesartan/valsartan • Betablockers • Carvedilol/Bisoprolol • Aldosterone receptor blockers • Spironolactone/Eplerenone • ARNI’S • Entresto
Congestive Heart Failure
Heart failure is the state in which the heart is unable to pump blood at a rate commensurate with the requirements of the tissues or can do so only from high pressures
Types of Heart Failure
Systolic heart failure (HFrEF)
Decreased pumping function of the heart, which results in fluid back up in the lungs and heart failure
Diastolic (or relaxation) heart failure (HFpEF)
Involves a thickened and stiff heart muscle
As a result, the heart does not fill with blood properly
This results in fluid backup in the lungs and heart failure
Risk Factors for Heart Failure
Coronary artery disease Hypertension (LVH) Valvular heart disease Alcoholism Infection (viral) Diabetes Congenital heart defects Other: Obesity Age Smoking High or low hematocrit level Obstructive Sleep Apnea
Frank-Starling Law
if the muscle of a healthy heart is stretched it will contract with greater force and pump out more blood.
In the failing or damaged heart this relationship is lost
As circulatory volume increases the heart dilates, the force of contraction weakens and cardiac output drops further
Decreased cardiac output then activates the RAAS further
The result is a vicious cycle in which the RAAS is activated, circulatory volume increases and cardiac performance deteriorates further
As the heart starts to dilate the cardiac myocytes undergo hypertrophy and then fibrosis and thus the heart is further weakened
Usual treatment today has two aims
To improve symptoms
Diuretics
Digoxin
To improve symptoms and survival
ACE inhibitors/ARBs
Spironolactone
Valsartan-sacubitril
To improve survival
Beata-blockers
Ivabradine
Symptomatic treatment
Inhibition of detrimental neurohormonal adaptation
Enhancing beneficial hormonal changes drugs
Natriuretic peptide system
ANP/BNP
Atrial natriuretic and Brain peptides are potent natriuretic agents and vasododilators
Metabolised by neutral endopeptidase
Neprolysin prevents metabolism and enhances ANP/BNP actions
RAAS Activation
drugs
Angiotensin II
Two groups of drugs available to block the effects of angiotensin II
ACE Inhibitors (Ramipril )
Angiotensin antagonists (Valsartan, Losartan) but these are not as effective (ELITE II)
Aldosterone
Effects blocked by SPIRONOLACTONE
Produces a significant reduction in morbidity (RALES)
Loop Diuretics
the mainstay of symptomatic treatment
FUROSEMIDE or BUMETANIDE
Removes excess salt and water
The loop diuretics induce profound diuresis
Inhibit the NA-K-Cl transporter in the Loop of Henle
Work at very low glomerular filtration rates
Prevent the reabsorption of 20% of filtered sodium and water
In diuretic resistant patients can use in combination with thiazide diuretics
This combination is powerful and may induce a diuresis of 5-10 litres a day
Blocking detrimental hormonal changes drugs
Sympathetic activation
CARVEDILOL, BISOPROLOL and METOPROLOL are beta blockers which are of proven benefit in the treatment of CHF
Enhancement of cardiac function drugs
Positive Inotropes
These drugs improve the ability of the heart to pump and so improve cardiac status
DIGOXIN is the only drug in common use
Vasodilators
The nitrovasodilators by reducing preload and after load improve cardiac function (ISOSORBIDE MONO or DINITRATE
Hydralazine an arterial dilator has also been shown to improve cardiac function
Mortality in HF with therapies
ACEi Relative risk reduction 35% (mortality and hospitalizations)
Blockers Relative risk reduction 38% (mortality and hospitalizations)
Loop diuretics adverse drug reactions
Dehydration Hypotension Hypokalaemia, Hyponatraemia Gout Impaired glucose tolerance, diabetes
Drug Drug Interactions for Loop Diuretics
Frusemide and aminoglycosides aural and renal toxicity lithium renal toxicity NSAIDs renal toxicity antihypertensives profound hypotension vancomycin renal toxicity
Reducing Mortality Drugs
Angiotensin Blockade
Beta receptor blockade
Aldosterone blockade
ANP/BNP enhancement
What does a renin inhibitor block
angiotensinogen > angiotensin I
What does an ACE inhibitor block
Angiotensin I > Angiotensin II
BUT this can be done also by alternative enzymes such as chymase in heart tissue
What does Valsartan block
Angiotensin II > AT1/AT2
Functions of the AT1 receptor
Atherosclerosis* Vasoconstriction Vascular hypertrophy Endothelial dysfunction increased sympathetic tone in brain and vessels
LV hypertrophy Fibrosis Remodelling Cardiomyocyte proliferation Apoptosis in the heart
decreased GFR increased Proteinuria increased Aldosterone release Glomerular sclerosis (hardening) in kidney
which lead to stroke, hypertension, HF, MI, renal failure
Angiotensin Converting Enzyme Inhibitors examples
RAMIPRIL, ENALAPRIL, LISINOPRIL,
what do ACE inhibitors do
Competitively block angiotensin converting enzyme
Prevent the conversion of angiotensin I to angiotensin II
Reduce preload and after load on the heart
What morbidity do ACEI decrease
In CHF patients significantly reduce morbidity mortality Post MI patients to reduce morbidity mortality onset of heart failure Main studies CONCENSUS, SOLVD, SAVE, AIRE, ISSIS-4
Adverse drug reactions for ACEI
First dose hypotension Cough Angioedema Renal impairment Renal failure Hyperkalaemia
Drug-drug interactions for ACEI
NSAIDs - acute renal failure
Potassium supplements - hyperkalaemia
Potassium sparing diuretics - hyperkalaemia
Angiotensin Receptor Blockers
ARBs selectively block the angiotensin II, AT1 receptor.
They are effective NOT AS EFFECTIVE AS ACEIs
At present recommended for use in ACEI intolerant patients.
Major outcome studies Elite II, Charm, ValHeft Valiant
AT2 receptors
Mostly in the foetus,
Vasodilation, antiproliferation and apoptosis
Valsartan-Sacubitril (ARNI)
Combined valsartan and ARB and Neprilysin
ARB blocks AT1 receptor
Neprilysin stops break down of ANP and BNP by neutral endopeptidases
BUT very expensive so not used very much
Aldosterone Antagonists
Spironolactone (RALES Study) Potassium sparing diuretic Inhibits the actions of aldosterone Acts in the distal tubule Used in combination with loop diuretics Particularly useful in resistant oedema Proven to reduce mortality when used in combination with ACEIs
Beta Blockers
CARVEDILOL, BISOPROLOL, METOPROLOL
The use of beta blockers in the treatment of CHF is potentially hazardous and patients must be selected carefully
Block the actions of the sympathetic system
May precipitate severe deterioration in CHF
Have been demonstrated to reduce morbidity and mortality in mild/moderate and severe heart failure by 30%
Should be used only when a patient has been stabilized and not during an acute presentation
Specialist use only
Ivabradine
Ivabradine is a specific inhibitor of the If current in the sinoatrial node.
No action on other channels in the heart or vascular system.
Does not modify myocardial contractility and intracardiac conduction, even in patients with impaired systolic function
Ivabradine can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class II-III) stable chronic HFrEF (LVEF ≤35%) who are receiving stabdard therapy, including a beta blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 bpm or greater at rest.
Positive Inotropes
DIGOXIN (The DIG Study) Increases availability of calcium in the myocyte Shown to reduce number of hospitalisations No effect on mortality Narrow therapeutic index Arrhythmias Nausea Confusion
Anticoagulants
WARFARIN
Dilated ventricle gives rise to thrombus formation and thrombo-embolic events
Warfarin has proven value in preventing these events
Therapeutic Regime
Furosemide ± thiazide Appropriate dose Furosemide + pulsed metolazone ACE Inhibitor Appropriate dose Angiotensin receptor blocker ARNI Beta-blocker ± Ivabradine MRA-spironolactone 25mg Digoxin TDM Warfarin TDM
Therapeutic drug monitoring)
How to monitor benefit
Symptomatic relief SOB, tiredness, lethargy Clinical relief Peripheral oedema, ascites, weight Monitor weight regularly Patient performs daily weight assessment Increase medication according to symptoms or weight Patient education
