Heart Failure

Question 1

definition of heart failure

Answer 1

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

Question 2

Prevalence of HF

Answer 2

Affects 1-2% of UK population

Increasing in prevalence

Question 3

prognosis of heart failure

Answer 3

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

Question 4

symptoms of HF

Answer 4

breathlessness
•
Fatigue
•
Odema
•
Reduced exercise capacity

Question 5

signs of HF

Answer 5

Odema
•
Tachycardia
•
raised JVP
•
chest crepitations or effusions
•
3rdheart sound
•
Displaced or abnormal apex beat

Question 6

diagnosis of HF

Answer 6

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

Question 7

investigations for cardiac dysfunction

Answer 7

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

Question 8

BNP

Answer 8

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

Question 9

structural heart diseases that may cause HF

Answer 9

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

Question 10

common causes of LV systolic dysfunction

Answer 10

•
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

Question 11

detailed evaluation of patients with LVSD

Answer 11

•
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

Question 12

why is echocardiography essential

Answer 12

•
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)

Question 13

views on echo

Answer 13

parasternal long axis
parasternal short axis (papillary muscle level)
parasternal short axis (base)

Question 14

LV ejection fraction

Answer 14

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%

Question 15

biplane modified simpsons rule

Answer 15

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)

Question 16

LVEF -MUGA

Answer 16

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

Question 17

LVEF -MRI

Answer 17

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

Question 18

Grading of heart failure

Answer 18

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

Question 19

Heart failure does not equal reduced cardiac output explanation

Answer 19

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

Question 20

Modern Pharmacological treatment of heart failure (due to LV systolic dysfunction)

Answer 20

•
Diuretics
•
Furosemide/Bumetanide
•
Symptomatic relief
•
ACE inhibitors/ARBs
•
Ramipril, enalapril
•
Candesartan/valsartan
•
Betablockers
•
Carvedilol/Bisoprolol
•
Aldosterone receptor blockers
•
Spironolactone/Eplerenone
•
ARNI’S
•
Entresto

Question 21

Congestive Heart Failure

Answer 21

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

Question 22

Types of Heart Failure

Answer 22

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

Question 23

Risk Factors for Heart Failure

Answer 23

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

Question 24

Frank-Starling Law

Answer 24

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

Question 25

Usual treatment today has two aims

Answer 25

To improve symptoms Diuretics Digoxin To improve symptoms and survival ACE inhibitors/ARBs Spironolactone Valsartan-sacubitril To improve survival Beata-blockers Ivabradine

Question 26

Symptomatic treatment

Answer 26

Inhibition of detrimental neurohormonal adaptation

Question 27

Enhancing beneficial hormonal changes drugs

Answer 27

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

Question 28

RAAS Activation | drugs

Answer 28

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)

Question 29

Loop Diuretics

Answer 29

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

Question 30

Blocking detrimental hormonal changes drugs

Answer 30

Sympathetic activation | CARVEDILOL, BISOPROLOL and METOPROLOL are beta blockers which are of proven benefit in the treatment of CHF

Question 31

Enhancement of cardiac function drugs

Answer 31

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

Question 32

Mortality in HF with therapies

Answer 32

ACEi Relative risk reduction 35% (mortality and hospitalizations)  Blockers Relative risk reduction 38% (mortality and hospitalizations)

Question 33

Loop diuretics adverse drug reactions

Answer 33

``` Dehydration Hypotension Hypokalaemia, Hyponatraemia Gout Impaired glucose tolerance, diabetes ```

Question 34

Drug Drug Interactions for Loop Diuretics

Answer 34

``` Frusemide and aminoglycosides aural and renal toxicity lithium renal toxicity NSAIDs renal toxicity antihypertensives profound hypotension vancomycin renal toxicity ```

Question 35

Reducing Mortality Drugs

Answer 35

Angiotensin Blockade Beta receptor blockade Aldosterone blockade ANP/BNP enhancement

Question 36

What does a renin inhibitor block

Answer 36

angiotensinogen > angiotensin I

Question 37

What does an ACE inhibitor block

Answer 37

Angiotensin I > Angiotensin II | BUT this can be done also by alternative enzymes such as chymase in heart tissue

Question 38

What does Valsartan block

Answer 38

Angiotensin II > AT1/AT2

Question 39

Functions of the AT1 receptor

Answer 39

``` 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

Question 40

Angiotensin Converting Enzyme Inhibitors examples

Answer 40

RAMIPRIL, ENALAPRIL, LISINOPRIL,

Question 41

what do ACE inhibitors do

Answer 41

Competitively block angiotensin converting enzyme Prevent the conversion of angiotensin I to angiotensin II Reduce preload and after load on the heart

Question 42

What morbidity do ACEI decrease

Answer 42

``` 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 ```

Question 43

Adverse drug reactions for ACEI

Answer 43

``` First dose hypotension Cough Angioedema Renal impairment Renal failure Hyperkalaemia ```

Question 44

Drug-drug interactions for ACEI

Answer 44

NSAIDs - acute renal failure Potassium supplements - hyperkalaemia Potassium sparing diuretics - hyperkalaemia

Question 45

Angiotensin Receptor Blockers

Answer 45

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

Question 46

AT2 receptors

Answer 46

Mostly in the foetus, | Vasodilation, antiproliferation and apoptosis

Question 47

Valsartan-Sacubitril (ARNI)

Answer 47

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

Question 48

Aldosterone Antagonists

Answer 48

``` 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 ```

Question 49

Beta Blockers

Answer 49

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

Question 50

Ivabradine

Answer 50

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.

Question 51

Positive Inotropes

Answer 51

``` 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 ```

Question 52

Anticoagulants

Answer 52

WARFARIN Dilated ventricle gives rise to thrombus formation and thrombo-embolic events Warfarin has proven value in preventing these events

Question 53

Therapeutic Regime

Answer 53

``` 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)

Question 54

How to monitor benefit

Answer 54

``` 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 ```