Heart Failure Flashcards
HF DEFINITION - ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2021
Heart failure is not a single pathological diagnosis, but a clinical syndrome consisting of cardinal symptoms (e.g. breathlessness, ankle swelling, and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles, and peripheral oedema). It is due to a structural and/or functional abnormality of the heart that results in elevated intracardiac pressures and/or inadequate cardiac output at rest and/or during exercise.
What is Heart Failure?
Collection of signs and symptoms
Inability of the heart to pump blood to meet metabolic demand (rather than the heart no longer working).
Body depends on the heart’s pumping action to deliver oxygen- and nutrient-rich blood to the body’s cells.
Normal body function: when the cells are nourished properly.
With heart failure, compromised cardiac function can’t supply the metabolising tissues with enough blood.
This results in signs and symptoms of HF.
Heart failure is a chronic, progressive condition, and usually there’s no cure.
But with changes, people with heart failure can lead normal lives.
Changes:
– Heart failure medications
– Lifestyle changes
– Implantable cardiac devices
Causes of HF
Ischaemic heart disease and MI - COMMON
Hypertension - COMMON
Valvular heart disease
Familial cardiomyopathy or genetic heart disease (Dilated/hypertrophic/obstructive/restrictive/obliterative)
Endocrine or metabolic (thyroid, diabetes, obesity)
Chemotherapy and other cardiotoxic drugs
Rheumatic/autoimmune
Heart rhythm related (tachy-mediated, PVCs, RV pacing)
Myocarditis (infectious, toxin/medication, immunological)
Peripartum cardiomyopathy
Substance abuse
Alcohol
Left-sided heart failure
Categorised into the following:
Systolic Failure - Heart failure with reduced ejection fraction (HFrEF) – 50% of patients
– LV unable to contract normally.
– The heart can’t pump with enough force to push enough blood into circulation.
Diastolic Failure - Heart failure with preserved ejection fraction (HFpEF)
– LV loses its ability to relax normally (because the muscle has become stiff).
– The heart can’t properly fill with blood during diastole.
Right-sided heart failure
Usually occurs as a result of left-sided failure.
When the left ventricle fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the heart’s right side.
When the right side loses pumping power, blood backs up in the body’s veins, causing swelling/congestion in the legs, ankles and abdomen such as the GI tract and liver.
The heart tries to compensate by:
Enlarging. The heart stretches to contract more strongly and keep up with the demand to pump more blood. Over time this causes the heart to become enlarged.
Developing more muscle mass – due to contracting myocardial cells increasing in size. This enables the heart to pump more strongly, at least initially.
Pumping faster. This helps to increase cardiac output.
The body also tries to compensate in other ways:
Blood vessels narrow to keep BP up, trying to make up for the heart’s loss of power.
The body diverts blood away from less important tissues and organs (e.g. kidneys), and towards the heart and brain.
Mortality is significantly better for those who have access to specialist care i.e. those seen by cardiologists or specialist heart failure services (23 per cent).
Incidence and cost
Global pandemic - 26 million worldwide.
Around 920,600 people in the UK today have been diagnosed with heart failure (1.6% population; Bellanca et al., 2023).
Symptomatic and non-symptomatic HF evident in 4% of population.
The incidence of heart failure increases steeply with age, and the average age at diagnosis is 77.
Prevalence in 70-80 yr olds between 10 and 20%.
Overall prevalence increasing due to ageing population.
Average length of hospital stay for HF: 13 days
1 in 7 heart failure patients die in hospital or in the month following discharge.
Within a year of admission, 32% of patients die.
Cost per hospital admission: £3,796.
Heart Failure accounts for:
2% of the total NHS budget (70% of these costs due to hospitalisation, 10% due to medications)
1 million patient bed days per annum.
5% of all emergency admissions (commonest cause of admission in people > 65yrs).
Stages of HF
Stages Definition and Criteria - AHA, 2022 guidelines
Stage A: At Risk for HF At risk for HF but without symptoms, structural heart disease, or cardiac biomarkers of stretch or injury (eg, patients with hypertension, atherosclerotic CVD, diabetes, metabolic syndrome and obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, or positive family history of cardiomyopathy).
Stage B: Pre-HF No symptoms or signs of HF and evidence of 1 of the following:
Structural heart disease*
- Reduced left or right ventricular systolic function
- Reduced ejection fraction, reduced strain
- Ventricular hypertrophy
- Chamber enlargement
- Wall motion abnormalities
- Valvular heart disease
Evidence for increased filling pressures*
- By invasive hemodynamic measurements
- By noninvasive imaging suggesting elevated filling pressures (eg, Doppler echocardiography)
Patients with risk factors and
- Increased levels of BNPs* or
- Persistently elevated cardiac troponin in the absence of competing diagnoses resulting in such biomarker elevations such as acute coronary syndrome, CKD, pulmonary embolus, or myopericarditis
Stage C: Symptomatic HF Structural heart disease with current or previous symptoms of HF.
Stage D: Advanced HF Marked HF symptoms that interfere with daily life and with recurrent hospitalizations despite attempts to optimize GDMT.
Diagnostic tests
Medical history and physical examination.
12-lead ECG – LVH, LBBB, LAE, AF, sinus tachy.
Echocardiogram
Laboratory tests – BNP (protein indicates myocyte stretch)
Chest X-ray – normal size/slightly enlarged, calcified aortic valve, pulmonary congestion.
What is BNP?
The main stimulus for BNP synthesis and secretion is myocyte stretch and levels are elevated in HF and other conditions such as atrial flutter/fibrillation.
These peptides regulate the circulation. They dilate blood vessels. They also work on the kidneys, causing them to excrete more salt and water. In addition, they reduce the production of hormones that narrow blood vessels, boost the heart rate, or affect fluid retention; examples includeadrenaline, angiotensin,andaldosterone.
Diagnosis of HF (ACC)
- Diagnostic algorithm for patients with suspected HF
Assessment: Clinical hx, Physical Examination, ECG, labs
-> Natriuretic Peptide: NT-proBNP >125pg/mL / BNP > 35pg/mL
–> TTE (indicated with assessment/ assessment and)
-> HF diagnosis confirmed: determine cause and classify
-> HFrEF: LVEF less/equal to 40%
HFmrEF: 41%-49%
HFpEF: LVEF greater than or more than 50%
-> Evaluate for precipitating factors and initiate treatment
Diagnosis of HF (NICE)
Chronic HF suspected -> Take a detailed hx and perform a clinical examination -> measure NT-pro BNP and perform ECG, consider chest X-Ray, blood tests, urinalysis, peak flow or spirometry.
-> NT-proBNP >2,000 ng/l (235 pmol/l) -> refer urgently to be be seen within 2 weeks
-> NT-proBNP 400-2,000ng/l (47-236 pmol/l) -> refer urgently to be seen within 6 weeks
-> specialist clinical assessment including transthoracic echocardiography
-> HF confirmed; assess severity, establish aetiology and identify correctable causes
-> NT-proBNP <400ng/l (47pmol/l) -> HF not confirmed; consider other causes of symptoms with specialist input if concern persists
Diagnosis of HF ESC guidelines
Electrocardiogram (ECG). A normal ECG makes the diagnosis of HF unlikely.63 The ECG may reveal abnormalities such as AF, Q waves, LV hypertrophy (LVH), and a widened QRS complex (Table 7) that increase the likelihood of a diagnosis of HF and also may guide therapy.
Measurement of NPs are recommended, if available. A plasma concentration of B-type natriuretic peptide (BNP) <35 pg/mL, N-terminal pro-B-type natriuretic peptide (NT-proBNP) <125 pg/mL, or mid-regional pro-atrial natriuretic peptide (MR-proANP) <40 pmol/L68 make a diagnosis of HF unlikely. These will be discussed in more detail in section 4.2.69,70
Basic investigations such as serum urea and electrolytes, creatinine, full blood count, liver and thyroid function tests are recommended to differentiate HF from other conditions, to provide prognostic information, and to guide potential therapy.
Echocardiography is recommended as the key investigation for the assessment of cardiac function. As well as the determination of the LVEF, echocardiography also provides information on other parameters such as chamber size, eccentric or concentric LVH, regional wall motion abnormalities (that may suggest underlying CAD, Takotsubo syndrome, or myocarditis), RV function, pulmonary hypertension, valvular function, and markers of diastolic function.16,71
A chest X-ray is recommended to investigate other potential causes of breathlessness (e.g. pulmonary disease). It may also provide supportive evidence of HF (e.g. pulmonary congestion or cardiomegaly).
Symptoms and signs:
Diagnosis includes assessing patient’s signs and symptoms.
Examination generally difficult in: Obese, Elderly, Lung disease.
Typical symptoms: breathlessness, Orthpnoea (SOB) when lying down and paroxysmal nocturnal dyspnoea (SOB at night which awakens a patient)., dyspnoea, reduced exercise tolerance, fatigue/tiredness/increased time to recover after exercise, ankle swelling, anorexia, confusion/delirium (elderly)
Signs:
Elevated jugular venous pressure
Hepatojugular reflux –distension of jugular vein induced by applying manual pressure over the liver
Third heart sound - gallop rhythm
Laterally displaced apical impulse
Cardiac murmur
Peripheral oedema, ascites (fluid collects in abdomen)
Tachycardia
Irregular pulse
Hepatomegaly (back up of blood into hepatic veins – liver becomes congested and grows)
Cachexia and muscle wasting
Most common ECG changes in HF
Sinus tachycardia; causes decompensated HF, anaemia, fever, hyperthyroidism
Sinus bradycardia; causes beta-blockade, digoxin, ivabradine, verapamil, diltiazem, antiarrhythmics, hypothyroidism, sick sinus syndrome
Atrial tachy/flutter/fib ; hyperthyroidism, infection, mitral valve disease, decompensated HF, infarction
Ventricular arrhythmias; ischaemia, infarction, cardiomyopathy, myocarditis, hypokalaemia, digitalis OD, hypomagnesaemia
M isch/ infarction; coronary artery disease
Q waves; infarction, hypertrophic cardiomyopathy, LBBB, pre-excitation
LV hypertrophy; HTN, AV disease, hypertrophic cardiomyopathy
AV block; infarction, drug toxicity, myocarditis, sarcoidosis, genetic cardiomyopathy, Lyme disease
Low QRS voltage; obesity, emphysema, pericardial effusion, amyloidosis
QRS duration >120ms and LBBB morphology
Most common Echo findings in HF
Parameters related to systolic function;
- LVEF Reduced (<50%)
Parameters related to diastolic function;
- LV diastolic dysfunction parameters
Parameters related to valvular function
- valvular structure and function
Other parameters;
RV function (e.g. TAPSE) (reduced TAPSE<16mm)
TR peak velocity
Common Lab Tests in HF
BNP (biologically active hormone; short half-life).
NT pro-BNP (not biologically active; longer half-life).
Different thresholds for acute/worsening HF and non-acute.
Acute = 300 pg/ml for NT pro-BNP. 100 pg/ml for BNP.
Non-acute = 125 pg/ml for NT pro-BNP. <35 pg/ml for BNP.
Diagnosis HF REF / HF PEF
HF has recently been classified into two main subtypes, namely HF with reduced ejection fraction (HFrEF), HF with preserved ejection fraction (HFpEF) and HF mid-range ejection fraction (HFmrEF).
HF also classified based on severity of patient symptoms with I being the most mild and IV being the most severe.
The diagnosis of HF-REF requires three conditions to be satisfied:
1. symptoms typical of HF
2. Signs typical of HF
3. Reduced LVEF
The diagnosis of HF-PEF requires 4 conditions to be satisfied:
1. Symptoms typical of HF
2. Signs typical of HF
3. Normal or only mildly reduced LVEF and LV not dilated
4. Relevant structural heart disease (LV hypertrophy/ LA enlargement) and/or diastolic dysfunction
NYHA classification:
Class I - No limitation of physical activity. Ordinary physical activity does not cause undue breathlessness, fatigue, or palps.
Class II - Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in undue breathlessness, fatigue or palpitations
Class III - Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity results in undue breathlessness, fatigue or palpitations
Class IV - Unable to carry on any physical activity without discomfort. Symptoms at rest can be present. If any physical activity is undertaken, discomfort is increased
Pathophysiology of HF-REF
Long-term hypertension can contribute to HF-REF.
Can induce LV remodelling and dilatation and reduced cardiac output.
Stretching and altering of the conduction system.
May lead to electrical and mechanical dyssynchrony.
The change in LV shape and size may lead to tricuspid and mitral annulus dilatation and resultant functional tricuspid and mitral regurgitation.
Myocyte stretching in response to hypertension and valvular disease can lead to atrial dilatation and an increased susceptibility to Aflutter/AF.
Chronic LV dysfunction frequently leads to increased pulmonary vascular resistance and pulmonary hypertension due to endothelial cell dysfunction, vasoconstriction and remodelling, which can ultimately result in concurrent RV dysfunction (Moraes et al., 2000).
Primary myocardial injury e.g. Due to ischaemic heart disease, leads to impaired cardiac structure or function and a reduced ability to efficiently supply blood to the body’s tissues at a rate that meets their oxygen and metabolic demands
Secondary myocardial effects
- LV remodelling
- Contractility
- Hypertrophy
- Apoptosis
- Cytokines
- Fibrosis
- NOS/ROS
- EP
Neurohormones
- Increased SNS activity
Increase RAS
Increased Endothelin
Increased ANP/BNP
Increased cytokines
Endothelium
- vasoconstriction
- NOS/ROS
- structural change
-cytokines
CHF outcomes: Sudden death, progressive pump failure, symptoms
Other useful adjunct testing summary.
DSE/ETT
Angiography
RHC / myocardial biopsy
CMR
Genetic testing
Ambulatory ECG
Treatment
Aim: Keep symptoms under control
The National Institute of Clinical Excellence (NICE) guidelines 2018 in England and Wales, and the Scottish Intercollegiate Guidelines Network (SIGN) guidelines in Scotland, recommend that heart failure patients should be considered for the following medications.
(Start low, aim high).
Stage A and Stage B HF
Stage A - At risk of HF
Patients with HTN - Optimal control of BP
Pts with T2DM and CVD or high risk for CVD - SGLT2i
Patents with CVD - Optimal management of CVD
Patients with exposure to cardiotoxic agents - MDT evaluation for management
First degree relatives of patients with genetic or inherited cardiomyopathies - genetic screening and counseling
Patients at risk for HF - Natriuretic peptide biomarker screening
Patients at risk for HF - validated multivariable risk score
Stage B - Pre-HF
Patients with LVEF <40% - ACEi
Patients with a recent MI and LVEF <40% - ARB if ACEi intolerant
Patients with LVEF <40% - beta blocker
Patients with LVEF <30%; >1y survival; >40d post MI
Patients with non-ischaemic cardiomyopathy - Genetic counselling and testing
ACE Inhibitor
(Angiotensin Converting Enzyme Inhibitor)
Traditionally a 1st line drug. Titration to target dose is essential.
– Long term studies suggest may increase survival by up to 50%.
– All NYHA classes benefit, NYHA IV have shown most benefit.
Relieves symptoms and improves exercise tolerance.
Reduces risk of death and slows disease progression.
Benefits may not be apparent for 1-2 months after initiation.
Help to relax blood vessels, making it easier for heart to pump blood around the body.
Occasional side effects may include a troublesome cough or dizziness.
