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CARDIOLOGY > HEART FAILURE > Flashcards

HEART FAILURE Flashcards

1
Q

What is heart failure?

A

a clinical syndrome with typical symptoms (breathlessness, peripheral oedema, and fatigue) and signs (elevated JVP, basal crepitations, and peripheral oedema)
The traditional concept is a low output state as thw heart cannot maintain an adequate cardiac output to meet the demands of the body, resulting in an in creased systemic vascular resistance in an attempt to maintain MAP

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2
Q

What is the difference between acute and chronic heart failure?

A

Acute heart failure is characterised by a rapid onset of symptoms and/or signs of heart failure that is usually life-threatening. This can be a new presentation or decompensaton of a person with existing chronic HF

Chronic heart failure is due to progressive cardiac dysfunction from structural and/or functional cardiac abnormalities. There is a reduction in cardiac output and/or elevated intracardiac pressure at rest or on stress.

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3
Q

How can heart failure be classified?

A

By ejection fraction
By time
By left and right-sided (no longer used!)
Systolic vs diastolic
High output vs low output
By symptomatic severity

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4
Q

What is ejection fraction?

A

a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction.

(Stroke volume / end diastolic volume) x100

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5
Q

How do we measure ejection fraction?

A

Using an echocardiogram

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6
Q

What is a reduced left ventricular ejection fraction?

A

<50%
(Normal is 55-65%)

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7
Q

At what ejection fraction is heart failure with reduced ejection fraction defined?

A

left ventricular ejection fraction of <40%

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8
Q

What is heart failure with mildly reduced ejection fraction?

A

People with a LVEF between 41–49% have a mildly reduced ejection fraction

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9
Q

What is heart failure with preserved ejection fraction?

A

People who have symptoms of heart failure, cardiac structure or function abnormalities, and/or raised levels of natriuretic peptides with a preserved LVEF > 50%

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10
Q

What proportion of pt with heart failure have preserved left ventricular ejection fraction?

A

Nearly 50%

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11
Q

What has replaced the systolic vs diastolic heart failure classification?

A

Heart failure with reduced ejection fraction - typically have systolic dysfunction
Heart failure with preserved ejection fraction - typically have diastolic dysfunction

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12
Q

What is systolic heart failure?

A

refers to a reduction in the left ventricular ejection fraction (LVEF)

Impaired myocardial contraction during systole . The increase in blood at the end of systole leads to ventricular stretch, dilatation, and eccentric hypertrophy (mostly).

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13
Q

What is diastolic heart failure?

A

Impaired ventricular relaxation or filling. Ventricular hypertrophy tends to occur. Characterised by concentric remodelling
Heart failure with preserved ejection fraction as contraction during systole is unaffected

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14
Q

What is the difference between concentric and eccentric hypertrophy?

A

Eccentric - volume overload-induced cardiac hypertrophy = ventricular dilation = new sarcomeres added in-series to existing sarcomeres (often called atheleets heart as its a normal response to healthy exercise) - also occurs in HFrEF and mitral regurgitation (creates a dilated ventricular chamber with relative wall thinning)

Concentric - increase in pressure in ventricles - addition of sarcomeres in parallel which results in an increase in thickness of the myocardium without a corresponding increase in ventricular size (seen in hypertension or aortic stenosis) - thicker walls and smaller chamber sizes

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15
Q

What can cause systolic dysfunction of the heart?

A

Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Infiltration e.g. haemachromatosis or sarcoidosis

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16
Q

What causes diastolic dysfunction of the heart?

A

Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis

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17
Q

What is cardiac remodelling?

A

changes in cardiac size, shape and function in response to cardiac injury or increased load (e.g. exercise)

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18
Q

Is left or right sided heart failure more common?

A

Left

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19
Q

What causes left sided heart failure?

A

Increased ventricular after load e.g. arterial hypertension or aortic stenosis
Increased left ventricular preload e.g. aortic regurgitation resulting in backflow to the left ventricle

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20
Q

What causes right sided heart failure?

A

Increased right ventricular after load e.g. pulmonary hypertension
Increased right ventricular preload e.g. tricuspid regurgitation

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21
Q

What does left ventricular failure typically result in?

A

Pulmonary congestion sympotms and systemic hypoperfusion

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22
Q

What does right ventricular failure typically result in?

A

Venous congestion (peripheral oedema, weight gain, abdominal distention and discomfort, anorexia/nausea, raised JVP, ascites, hepatomegaly) and pulmonary hypoperfusion

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23
Q

What is the combination of left and right failure is known as?

A

Congestive cardiac failure

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24
Q

What is high-output heart failure?

A

In high output failure there is a high cardiac output (i.e. > 8L/min). The heart is unable to meet the increased demand for perfusion despite normal cardiac function.
I.e. when cardiac output exceeds metabolic demand

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25
Q

What causes high output heart failure?

A

Significant shunting e,g, Arteriovenous malformation or liver cirrhosis

States of increased metabolic demand e.g. Thyrotoxicosis, myeloproliferative disorders

States of reduced vascular resistance e.g. thiamine deficiency causing beriberi, sepsis, chronic lung disease, pregnancy, Paget’s disease, obesity or anaemia

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26
Q

Outline the pathophysiology of high output heart failure?

A

There is reduced systemic vascular resistance either due to arterio-venous shunting or peripheral vasodilatation. This leads to the cardiac output being higher than normal due to increased peripheral demand = circulatory overload = overtime this causes systolic failure and ultimately CO can be reduced to very low levels

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27
Q

What is acute heart failure?

A

a term used to describe the sudden onset or worsening of the symptoms of heart failure. Thus it may present with or without a background history of pre-existing heart failure

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28
Q

What is de-novo acute heart failure?

A

Acute heart failure without a past history of HF

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29
Q

What proportion of cases of acute hear failure are decompensated AHF?

A

66-75%

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30
Q

What causes de-novo HF?

A

Iatrogenic
Sepsis
MI
Arrhythmias

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31
Q

What are the most common precipitating causes of acute decompensated HF?

A

Inter current illness e.g. pneumonia
MI
Arrhythmia
Hypertension
Persons failure to maintain a fluid restriction/diet/meds
Anaemia and hyperthyroidism can also place additional strain on myocardium
Excessive fluid or salt intake and medication that causes retention may also precipitate decompensation

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32
Q

How do we classify heart failure?

A

Into 1 of 4 groups based on whether they are:
With or without hypoperfusion
With or without fluid congestion

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33
Q

How does acute heart failure present?

A

Breathlessness
Reduced exercise tolerance
Oedema
Fatigue
Cyanosis
Tachycardia
Elevated JVP
Displaced apex beat
Bibasal crackles
S3 heart sound

Sometimes it presents of underlyign cause e.g. viral infection or chest pain

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34
Q

What can cause heart failure?

A

Myocardial disease
Valvular heart disease
Pericardial disease
Congenital heart disease
Arrhythmias
High output states
Volume overload
Obesity
Drugs

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35
Q

What myocardial diseases can cause heart failure?

A

CAD
Hypertension
Cardiomyopathies

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36
Q

Whats the most common cause of HF?

A

CAD (35-40% of cases)

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37
Q

What pericardial diseases can cause heart failure?

A

Constructive pericarditis
Pericardial effusion

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38
Q

What arrhythmias can cause heart failure?

A

AF
Other tachyarrhythmias

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39
Q

What causes of volume overload can cause heart failure?

A

End-stage CKD
Nephrotic syndrome

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40
Q

What drugs can cause heart failure?

A

Alcohol
Cocaine

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41
Q

What drugs can worsen pre-existing HF?

A

NSAIDs
Beta blockers
CCB

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42
Q

Outline the epidemiology of heart failure?

A

Prevalence increases slowly with age until 65 and then increases rapidly. 1 in 7 of those over 85!
Average age at first diagnosis is 76
Accounts for 2% of all NHS hospitalised beds
GPS will suspect a new diagnosis in about 10 people annually

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43
Q

Whats the prognosis for HF?

A

Survival for people with end-stage heart failure is poor - only 65% of patients in NYHA class IV are alive at an average follow up of 17 months
50% of those with HF die within 5 years of diagnosis

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44
Q

What are poor prognostic factors for heart failure?

A

Increased age
Reduced election fraction and transitioning from mildly reduced to reduce election
Comorbidities
Worsening severity of symptoms
Raised JVP, third heart sound, low systolic BP, tachycardia
Obesity or cachexia
Smoking
HF caused by MI
Presence of complex ventricular arrhythmias

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45
Q

What are the complications of HF?

A

AF
Ventricualr arrhythmias
Stroke and thromboembolism
Resp - e.g. pulmonary congestion
GI - hepatic congestion
Organ failure
Depression
Cachexia
Anaemia
CKD
AKI
Sexual dysfunction
Sudden cardiac dearh

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46
Q

Whats the most common arrhythmia in people with HF?

A

AF
(50% of those with severe HF)

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47
Q

How common is depression in HF?

A

Up to 20% of pt

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48
Q

What is cachexia defined as?

A

the loss of 6% or more of total body weight within the previous 6–12 months. Wasting occurs in lean tissue (muscle mass) and fat.

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49
Q

How common is cachexia in HF?

A

May occur in 10-15% of people with HF, especially those with a reduced ejection fraction

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50
Q

Why are pt at an increased risk for AKI if they have HF?

A

Low perfusion state or as a result of the medication used to treat HF

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51
Q

What proportion of deaths in patients with HF are related to sudden cardiac death?

A

30-40%

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52
Q

What are the features of chronic heart failure?

A

dyspnoea (particularly on exertion)
Pulmonary oedema - cough: may be worse at night and associated with pink/frothy sputum
orthopnoea
paroxysmal nocturnal dyspnoea
Fatigue
wheeze
weight loss
bibasal crackles on examination
signs of right-sided heart failure: raised JVP, ankle oedema and hepatomegaly

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53
Q

Why might cardiac cachexia be hidden in HF?

A

Due to weight gained secondary to oedema

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54
Q

What are the primary determinantsa of stroke volume?

A

Preload
Myocardial contractility
Afterload

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55
Q

What is mean arterial pressure?

A

the average arterial pressure throughout one cardiac cycle.
It can be calculated as follows:
diastolic blood pressure + 1/3rd of the pulse pressure

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56
Q

What is pulse pressure?

A

Systolic - diastolic bp

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57
Q

What is systemic vascular resistance?

A

the amount of force exerted on circulating blood by the vasculature of the body, excluding the pulmonary vasculature

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58
Q

What determines systemic vascular resistance?

A

Vasodilation and vasoconstriction of blood vessels

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59
Q

What is preload?

A

stretching of cardiomyocytes at the end of diastole.

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60
Q

What is afterload?

A

pressure or load against which the ventricles must contract.

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61
Q

What influences preload?

A

Increased venous return
Increased ventricular filling pressure
Increased compliance of ventricle walls
Increased atrial force of contraction
Reduced HR which increases ventricular filing time
Increased aortic pressure

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62
Q

What influences afterload?

A

Vascular resistance: vasoconstriction increases the pressure the heart has the pump against decreasing SV
Valvular disease: stenotic valves increases the pressure the heart has to pump against decreasing SV

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63
Q

What influences contractility of the heart?

A

Muscular function: increased muscular bulk (e.g. hypertrophy) is a physiological and pathological response to increase SV
Autonomic nervous system: innervation from the parasympathetic and sympathetic nervous systems alter the strength of contraction

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64
Q

Outline the pathophysiology of the failing heart?

A

Systolic dysfunction is decreased contractility -> decreased EF and increased end-diastolic volume + increase systemic vascular resistance + endures state of hypoperfusion which causes compensation. As a heart fails the amount of blood left after each contraction increases i.e. the ejection fraction decreases. This increased end-systolic volume (ESV) means the myocardium experiences greater stretch. In a normal heart, this would lead to an increase in myocardial contractility by the Frank-Starling principle. However, in a failing heart, this causes a reduction in stroke volume (and thus cardiac output). This is because the relationship between cardiomyocyte stretch and contractility cannot continue unfettered. There is a physiological limit.

Diastolic dysfunction is decreased compliance leading to problems with filling of the heart

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65
Q

How does the body compensate for the failing heart/decreased cardiac output?

A

The earliest change is sympathetic nervous system stimulation due to reduced CO - peripheral arteriolar constriction, increase in force of myocardial contraction and increased HR
Activation of RAAS due to relative ischaemia of kidneys - angiotensin 2 causes vasoconstriction to increase peripheral resistance and aldosterone causes sodium and water retention + metabolic alkalosis

Frank-starling mechanism - Increasing preload to increase venous pressures and increase end-diastolic volume = increase in CO

66
Q

Whats the problem with the compensatory mechanisms of the heart?

A

Large increases in end diastolic volume can result in pulmonary oedema, ascites and peripheral oedema
Chronic activation of sympathetic nervous system triggers myocyte death

While activation of compensatory measures may be beneficial in the short-term, it is the long-term sustained stimulation that leads to disease progression through ventricular remodelling due to myocardial hypertrophy and fibrosis and then failing to meet the demands of the body

67
Q

What are the risk factors for heart failure?

A

CAD
Viral infection
Hypertension
Arrhythmias
Metabolic syndrome
Smoking
Drugs and alcohol
FHx HF or sudden cardiac death under the age of 40

68
Q

What should you examine for in HF?

A

Tachycardia and pulse rhythm
Laterally displaced apex beat, heat murmurs, third or fourth heart sounds
Hypertension
Raised JVP
Hepatomegaly
Respiratory signs
Dependant oedema
Ascites
Obesity

69
Q

How do you assess heart failure?

A

Detailed history and clinical examination
Arrange admission if person has severe symptoms
Measure N-terminal pro-B-type natriuretic peptide level
12-lead ECG

Consider CXR, blood tests, urine dipstick, lungs function tests
Assess for and manage any underlying causes

70
Q

What is B-type natriuretic peptide?

A

Aka brain natriuretic peptide (BNP)

a hormone produced mainly by the left ventricular myocardium in response to strain.

71
Q

Whats the difference between BNP and NT-proBNP?

A

BNP is biologically active as a hormone whereas NT-proBNP is cleared passively from the body and is not biologically active. Therefore, BNP has a much shorter half-life, NT-proBNP has a longer half-life.

72
Q

What can cause raised BNP?

A

Age over 70 years
Heart failure
Left ventricular hypertrophy, myocardial ischaemia and tachycardia
Right ventricular overload
Hypoxia
Pulmonary hypertension
PE
CKD (due to reduced excretion)
Sepsis
COPD
Diabetes
Cirrhosis of the liver

73
Q

What can cause falsely low levels of BNP?

A

Obesity (BMI >35), diuretics, ACE inhibitor treatment, beta blockers, angiotensin receptor antagonists and aldosterone antagonists
African-Caribbean family origin

74
Q

What does it mean when you say BNP has an excellent negative predictive value?

A

It’s good at excluding HF

75
Q

What are the effects of BNP?

A

Vasodilation
Diuretic and natriuretic
Suppresses sympathetic tone and RAAS

76
Q

What is natriuresis?

A

the process of sodium excretion in the urine through the action of the kidneys

77
Q

How should you analyse BNP levels?

A

If the NT-pro-BNP level is above 2000 ng/L (236 pmol/L), refer urgently for specialist assessment and echocardiography to be seen within 2 weeks.
If the NT-pro-BNP level is between 400–2000 ng/L (47–236 pmol/L), refer for specialist assessment and echocardiography to be seen within 6 weeks.
If NT-pro-BNP is <400 ng/L (47 pmol/L), be aware that a diagnosis of heart failure is less likely. Consider discussion with a physician with subspeciality training in heart failure if a clinical suspicion of heart failure persists.

Be aware that:
European Society of Cardiology guidelines suggest a lower threshold for normal values of 125 pg/mL

78
Q

What are differential diagnoses for heart failure?

A

Conditions causing breathlessness such as:
COPD
Asthma
Pulmonary embolism
Lung cancer
Anxiety
Acute respiratory distress syndrome (to distinguish - diffuse crackles, no S3 heart sounds and increased work of breathing on exam)

Conditions causing peripheral oedema such as:
Prolonged inactivity or venous insufficiency causing dependent oedema.
Nephrotic syndrome.
Drugs - dihydropyridine CCB, NSAIDs
Hypoalbuminaemia - from renal or hepatic disease
Pelvic tumour

Other conditions such as:
Obesity
Severe anaemia or thyroid disease
Bilateral renal artery stenosis

79
Q

How do you classify symptom severity for heart failure?

A

The New York Heart Association (NYHA)

80
Q

Outline the New York Heart Association classifications?

A

Class I — no limitation of physical activity. Ordinary physical activity does not cause undue fatigue, breathlessness, or palpitations.

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 out any physical activity without discomfort. Symptoms at rest can be present. If any physical activity is undertaken discomfort is increased.

81
Q

How should I manage a person with confirmed heart failure with reduced ejection fraction?

A

Ensure drugs which may cause or worsen heart failure are reviewed and stopped if appropriate.
Where symptoms of fluid overload are present, prescribe a loop diuretic.
ACEi/ARB and beta blocker
(Add on a mineralocorticoid receptor antagonist if symptoms are not controlled with A and B)
If stil symptomatic then refer to cardiology
Consider if antiplatelet drug and statin therapy is indicated
Ensure any causes, comorbidities or precipitating factors are optimally managed
Screen for depression and anxiety
Refer to a supervised exercise-based group rehabilitation programme for people with HF
Ensure the pt gets annual influenza vaccines and once-only pneumococcal vaccine
Give general info about HF
Assess nutritional status and aim for healthy BMI
Offer a discussion regaling advanced care planning and advanced decisions if appropriate
Arrange follow up in primary care

82
Q

Whats first line drug management for chronic heart failure and how should you start the treatment?

A

ACE inhibitor
Beta Blocker
Aldosterone antagonist when symptoms not controlled with A and B
Loop diuretics improves symptoms

generally, one drug should be started at a time. NICE advise that clinical judgement is used when determining which one to start first - an ACEi first if they have diabetes or fluid overload
Once the person is stable on the first drug, add the second drug
ACEi should be started at lowest dose and double dose every 2-4 weeks until target dose is achieved
Beta blockers also double dose every 4 weeks until target dose is achieved

83
Q

How is confirmed heart failure with mildly reduced ejection fraction managed differently to HFrEF?

A

As well as considering prescribing ACEi and beta blocker, consider an aldosterone antagonist or sacubitril valsartan

84
Q

What is a supervised exercise-based group cardiac rehabilitation programme?

A

A programme for when a persons HF is stable
a medically supervised program that includes exercise, support, counseling and education.

85
Q

How is HF with preseved ejection fraction managed differently to HF with reduce EF?

A

No beta blocker or CCB
You can offer a loop diuretic and consider whether a statin/antiplatelet is needed but no direct drug management

Instead we manage comorbidities and offer a personalised-based cardiac rehabilitation programme (unless HF is unstable)

86
Q

When can pt be regarded as being in end-stage HF?

A

if they are at high risk of dying within the next 6–12 months.

87
Q

What are some common symptoms in end-stage heart failure?

A

Pain.
Breathlessness.
Persistent cough.
Fatigue.
Limitation of physical activity.
Depression and anxiety.
Constipation.
Loss of appetite and nausea.
Oedema.
Insomnia.
Cognitive impairment.

88
Q

What are some indicators of people likely to have end-stage heart failure?

A

Frequent hospital admissions.
Poor response to treatment and severe breathlessness at rest (New York Heart Association class IV).
Presence of cardiac cachexia.
Low serum albumin.
Progressive deterioration in estimated glomerular filtration rate (eGFR) and hypotension limiting the use of drug treatments.
Acute deterioration and increasingly frequent hospital admissions from comorbid conditions (such as a chest infection).
Poor quality of life and dependence on others for most activities of daily living.
People who are clinically judged to be close to the end of life.

89
Q

How should I manage a person with end-stage heart failure?

A

Liaise with a cardiologist if there is uncertainty about the use of further treatments, and to make sure all treatment options have been considered
Explore the person’s understanding and provide an appropriate explanation of the situation including realistic goals of care with the person and their family/carers
Involve and coordinate care with the MDT
Review the need for medication and provide symptoms relief
Ensure the person has an advance care plan and discuss advance decisions

90
Q

What information and advice should I give to a person with confirmed heart failure?

A

Advise the person about reporting symptoms of worsening heart failure
Consider advising the person to monitor their weight at home to detect fluid retention of worsening heart failure, if practical.
Give advice on avoiding excessive salt intake, maintaining fluid balance, what to do if acutely unwell, smoking cessation, alcohol consumption, physical activity, BMI, sexual activity
Provide sources of information and support e,g. British heart foundation

91
Q

What advice should I give about driving and chronic heart failure?

A

Advise the person that: It is the person’s responsibility to inform the DVLA of any condition that may affect their ability to drive, and people should check with their insurer that they are still covered to drive.

For group 1 entitlement (cars, motorcycles): driving may continue, provided there are no symptoms that may distract the driver’s attention. The DVLA need not be notified.
For group 2 entitlement (lorries and buses): the person is disqualified from driving if symptomatic. Re-licensing may be permitted, provided that the left ventricular ejection fraction is at least 40% and there is no disqualifying condition. Exercise or other functional testing may be required, depending on the likely cause of heart failure.

92
Q

Why can’t you drive with heart failure?

A

When the heart fails to generate adequate cardiac output, the brain is inadequately perfused and temporarily malfunctions, leading to the syncopal event

93
Q

When should I refer a person with HF?

A

if a person has:
Severe heart failure
Heart failure that does not respond to treatment in primary care or can no longer be managed in the home setting
Heart failure resulting from valvular heart disease
Left ventricular ejection fraction of 35% or less
A NT‑pro-BNP level above 2000 ng/L (236 pmol/L). These people should be referred urgently for specialist assessment and transthoracic echocardiography within 2 weeks.
A NT‑pro-BNP level between 400 and 2000 ng/L (47–236 pmol/L). These people should be referred to have specialist assessment and transthoracic echocardiography within 6 weeks.

94
Q

What surgical intervention can be done for HF?

A

Cardiac resynchronization therapy.
Insertion of an implantable cardioverter defibrillator (ICD).
Coronary revascularization.
Cardiac transplantation.

95
Q

How should you follow up a person with HF?

A

Consider monitoring the NT-pro-BNP levels in people less than 75 years of age to guide optimum drug treatment
Assess and monitor symptoms - palpitations, SOB, oedema, syncope and presyncope, HR, heart, fluid status
Assess cognitive status and any psychosocial needs
Provide a self management plan
Assess nutritional status
Review medications
Ensure immunisations are up to date
Ensure the person has been offered a supervised group exercise-based heart failure rehabilitation programme
Monitor renal function every 6 months
Consider if referral is indicated

96
Q

What are the adverse effects of ACEi?

A

Dry cough
Hyperkalaemia
Renal impairment
Light headedness
Fatigue
GI disturbance
Angioedema

97
Q

What are contraindications of ACEi?

A

pregnancy and breastfeeding
aortic stenosis
hereditary or idiopathic angioedema
History of angioedema
Bilateral renal artery stenosis
specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L

98
Q

What are important drug interactions with ACEi?

A

high-dose diuretic therapy (more than 80 mg of furosemide a day) - significantly increases the risk of hypotension

99
Q

What monitoring should be done for ACEi?

A

Renal function and electrolytes should be checked before starting ACE inhibitors (or increasing the dose) and monitored during treatment monthly for 3 months and then at least every 6 months, and if the patient becomes acutely unwell
(a rise in the creatinine and potassium may be expected after starting ACE inhibitors. acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.)

100
Q

What are adverse effects of beta blockers?

A

Bronchospasm
Bradycardia
Cold peripheries
Fatigue
Sleep disturbance - nightmares (blocks release of melatonin)
Erectile dysfunction (can also bind to alpha receptors)
Dizziness

101
Q

What are contraindications of beta blockers?

A

Asthma
Cardiogenic shock
hypotension
marked bradycardia
metabolic acidosis
phaeochromocytoma (apart from specific use with alpha-blockers)
Prinzmetal’s angina
second-degree AV block and third-degree AV block
severe peripheral arterial disease
sick sinus syndrome
uncontrolled heart failure
Concurrent Verapamil use - may precipitate severe bradycardia

102
Q

Whats the main investigation for the confirmation of heart failure?

A

transthoracic echocardiography

103
Q

What does a transthoracic echocardiography look at?

A

The ejection fraction of the heart which helps differentiate suspected HF into HFrEF, HFmrEF, HFpEF

104
Q

When might a cardiac MRI be needed?

A

May be used when transthoracic echo is non-diagnostic
May be used to determine the aetiology of heart failure (e.g. ischaemic versus non-ischaemic in dilated cardiomyopathy)

105
Q

What would you see on CXR in heart failure?

A

Alveolar oedema (batwing perihilar shadowing)
B - Kerley B lines (fluid in septae of secondary lobules)
Cardiomegaly (Cardiothoracic ratio > 50% on PA film)
Dilated upper lobe vessels (aka upper lobe diversion)
Effusion (pleural)
Fluid in horizontal fissure

106
Q

What are normal, raised and high levels of BNP?

A

Normal - <100
Raised 100-400
High >400

107
Q

What are normal, raised and high levels of NTproBNP?

A

Normal <400
Raised 400-2000
High >2000

108
Q

What is acute decompensated HF?

A

A sudden worsening of the signs and symptoms of heart failure, which typically includes dyspnea, leg or feet swelling, and fatigue

109
Q

What causes right heart failure?

A

Most commonly as a result of advanced left sided heart failure
Also caused by right MI and pulmonary hypertension (often occurs secondary to respiratory conditions

110
Q

What causes left-sided HF?

A

CAD
MI
Arrhythmia
Chronic hypertension

111
Q

How do left and right sided heart failure present differently?

A

Left sided tends to cause lung congestion and lung symptoms (left side receives blood from pulmonary veins)
Right sided causes fluid retention in your legs or other parts of the body (right side receives from blood from SVC)

112
Q

What are rales?

A

Small clicking, bubbling, or rattling sounds heard on inspiration in the lungs
Caused by liquid accumulating in alveoli due to left heart pressure overload - alveoli pop open during inhalation

113
Q

What is Cheyne-Stokes respiration?

A

Rare, abnormal breathing pattern - a period of fast, shallow breathing followed by slow, heavier breathing and moments without any breath at all, called apneas. (Cyclical episodes of apnoea and hyperventilation)
Mostly caused by HF

114
Q

What are HF features on ECG?

A

May be normal or reveal clues as to the underlying cause of HF e.g. ischaemic changes or arrhythmias

115
Q

How does an MI cause acute left ventricular failure?

A

Cardiomyocyte death and fibrosis = chronic neurohumural activation = Ventricualr remodelling

116
Q

Whats the most common cause of heart failure in those of African or Afro-Caribbean origin?

A

Secondary to heart failure

117
Q

At what weight gain should they report to their GP or heart failure specialist?

A

1.5-2kg in 2 days

118
Q

Why should rate limiting CCB and short-acting dihydropyridine CCBs be avoided in HF with reduced ejection fraction?
What CCB can be used?

A

as these drugs reduce cardiac contractility
Amlodipine

119
Q

What are the diuretics of choice for managing breathlessness and oedema in heart failure?

A

Loop diuretics such as furosemide, bumetanide, or torasemide

120
Q

Which beta blockers are licensed for HF?

A

bisoprolol, carvedilol and nebivolol

121
Q

What mineralocorticoid receptor antagonists are licensed for heart failure?

A

Spironolactone and eplerenone

122
Q

How can arrhythmias lead to HF?

A

When the heart beats too rapidly for a prolonged period, the muscle can weaken, leading to cardiomyopathy and congestive heart failure

123
Q

Why does Congestive heart failure predisposes to stroke and thromboembolism?

A

low cardiac output = relative stasis of blood in dilated cardiac chambers
regional wall motion abnormalities e.g. left ventricular aneurysm
associated AF

124
Q

Whats the most sensitive clinical sign for acute decompensation of HF?

A

Raised JVP

Others - dyspnoea, orthopnoea, PND, peripheral oedema, pulmonary oedema

125
Q

How do we manage acute decompensated heart failure?

A

The immediate goal is to re-establish adequate perfusion and oxygen delivery to end organs.
Sit the pt up
All pt should get IV loop diuretics
Consider oxygen if sats 94% or less, vasodilators if concomitant MI, severe hypertension or regurgitation aortic/mitral valve disease
Morphine if needed but may increase mortality

CPAP if resp failure
Manage hypotension
Continue regular meds (only stop beta blockers if HR <50, heart block or shock)

126
Q

What is cardiogenic shock?

A

systemic tissue hypoperfusion secondary to inadequate cardiac output despite adequate intravascular volume and filling pressures
Signs of inadequate perfusion include oliguria, cool peripheries, altered level of conciousness, hypotension and bradycardia

127
Q

How do you manage a pt in cardiogenic shock secondary to heart failure? Why is this so diffiuclt to manage?

A

Inotropic agents e.g. dobutamine
If insufficient response… vasopressors e.g. norepinephrine or mechanical circulatory assistance

Diffiuclt to manage as some of the treatments for acute heart failure e.g. nitrates and loop diuretics, may exacerbate hypotension

128
Q

What are symptoms and signs caused by pulmonary congestion?

A

SOB on exertion
Orthopnoea
PND
Nocturnal cough
Pink, frothy sputum
Tachypnoea
Bibasal fine crackles on auscultation of lungs

129
Q

What blood tests should you do for HF?

A

U&Es to assess renal function for meds and to look for hyponatraemia
LFTs for hepatic congestion
TFTs for hyperthyroidism
Glucose and lipid profile to assess modifiable CV risk factors
BNP

130
Q

What lifestyle modification should be done after diagnosis of HF?

A

Smoking cessation
Salt and fluid restriction to improve mortality
Supervised cardiac rehabilitation

131
Q

What can you give to manage HFrEF if intolerant to ACEi or ARBs?

A

Hydralazine and nitrate (can also give this is first line treatment persists)

132
Q

What can you give to manage HFrEF if first lien treatment isnt sufficient?

A

Replace ACEi or ARB with sacubitril valsartan if EF is <35%
Add ivabradine for sinus rhythm with HR >75 and EF <35%
Add hydralazine and nitrate especially if of African Caribbean descent
Add digoxin in those with AF (worsens mortality but improves morbidity)

133
Q

What are the adverse efefcts of spironolactone?

A

Hyperkalaemia
Renal impairment
Gynaecomastia
Breast tenderness/hair growth in women
Changes in libido

134
Q

Why does spironolactone cause gynaecomastia, breast tenderness, hair growth in women and changes in libido?

A

It decreases testosterone by binding to the androgen receptor and displacing androgens from the receptor, thereby reducing its activation by these hormones

135
Q

What are thr adverse effects of furosemide?

A

Hypotension
Hyponatraemia and hypokalaemia

136
Q

What are adverse effects of nitrates and hydralazine (a vasodilator)?

A

Headache
Palpitations
Flushing

137
Q

What are adverse effects of digoxin?

A

Dizziness
Blurred vision
GI disturbances
Arrhythmias

138
Q

Where are voltage gated calcium channels found?

A

Myocardial cells
Cells of conductin system e.g. glia and neurones
Vascular smooth muscle

139
Q

What are the 3 types of CCB?

A

Verapamil (non-dihydropyridine)
Diltiazem (non-dihydropyridine)
Dihydropyridine (end in dipine)

140
Q

What are dihydropyridine CCB?

A

amlodipine, felodipine, lacidipine, lercanidipine hydrochloride, nicardipine hydrochloride, nifedipine, and nimodipine

141
Q

Which CCB can be used in HF?

A

Amlodipine

142
Q

Which CCB wont increase mortality after an MI?

A

Amlodipine

143
Q

Outline why cardiac muscle and vascular smooth muscle depend on calcium?

A

Voltage-gated calcium channels in the membrane of the muscle cell open when they receive an action potential and this allows calcium ions to flow into the cell from the extracellular space.
The extracellular calcium causes the release of intracellular calcium ions stored in the sarcoplasmic reticulum.
All these calcium ions then bind to troponin regulatory proteins, which change shape and release the thin filaments in the muscle fiber.
This allows the thin filament to bind to the thick filament, eventually leading to muscle contraction.

In the heart, this means greater myocardial contractility. In blood vessels, this means vasoconstriction.

144
Q

How does indication vary between dihydropyridine and non-dihydropyridine CCB?

A

Dihydropyridine CCB mainly act on smooth muscles of blood vessels and cause vasodilation - mainly used to treat hypertension. Can also prevent angina, treat raynauds and prevent cerebral Vaso spasms after subarachnoid haemorrhage

Non-dihydropyridine CCB have a greater efefct on the heart and are less effective for vasodilation. Cause decreased myocardial contractility, have anti-arrhythmic moa and provide moderte dilation of cornary arteries treat tachyarrhythmias and angina

145
Q

What are side effects of dihydropyridine CCB?

A

Flushing
Headache
Dizziness
Peripheral oedema

Others:
Reflex tachycardia - although this is triggered at higher doses than those needed to lower bp. Also more common in shorter acting dihydropyridine e.g. nifedipine
Gingival hyperplasia - cause unclear

146
Q

What are the indications of non-dihydropyridine?

A

Verapamil - angina, hypertension, arrhythmias

Diltiazem - angina and hypertension (not as cardioselective so less potent antiarrhythmic)

147
Q

Which non-dihydropyridine CCB should not be given with beta blockers and why?

A

Verapamil - can cause heart block and bradycardia - CONTRAINDICATED
(Remember its more cardioselective than diltiazem)

Diltiazem - GIVE WITH CAUTION

148
Q

What are side effects of non-dihydropyridines?

A

Worsening CO - heart failure
Bradycardia
Hypotension
Vasodilatory affects - flushing, headaches, ankle swelling (less common than dihydropyridine but still can occur)

Verapamil - constipation
Diltiazem - dizziness, GI disorders, malaise/fatigue

149
Q

Whats the MOA of loop diuretics?

A

inhibiting the Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl and promoting fluid excretion

150
Q

Why may pt with poor renal function need escalating doses of loop diuretics?

A

As loop diuretics work on the apical membrane they must first be filtered into the tubules by the glomerulus before they can have an effect. Therefore patients with poor renal function may require escalating doses to ensure a sufficient concentration is achieved within the tubules.

151
Q

What are indications of loop diuretics?

A

Heart failure (pulmonary oedema i.e. acute HF give IV/chronic HF give oral)
Can be added to Antihypertensive teatment for resistant hypertension, or in those with renal impairment or HF

152
Q

What are adverse efefcts of loop diuretics?

A

hypotension
hyponatraemia
hypokalaemia
hypomagnesaemia
hypocalcaemia
hypochloraemic alkalosis
ototoxicity
renal impairment (from dehydration + direct toxic effect)
Urinary retention if enlarged prostate (unlikely)
hyperglycaemia (less common than with thiazides) - can exacerbate diabetes
Can exacerbate gout

153
Q

What are contra-indications for all loop diuretics?

A

Anuria
Comatose or precomatose states associated with liver cirrhosis
Renal failure
Severe hypokalaemia
Severe hyponatraemia

Caution with diabetes, gout, hypotension, hypovolaemia and urinary retention with prostatic hyperplasia, elderly

154
Q

why do loop diuretics cause hypomagnesemia and hypocalcaemia?

A

Enhances renal excretion of magnesium and calcium
Lumen is electropositive with respective to interstitium due to loss of 2 Cl- for every 1 Na+ (because of Na+/K+/Cl- pump) so calcium and magnesium are lost to balance this

155
Q

Whats the moa of thiazide diuretics?

A

inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter. Potassium is lost as a result of more sodium reaching the collecting ducts.

156
Q

When should thiazide diuretics be given and why?

A

they are usually administered early in the day so that the diuresis does not interfere with sleep as they act within 1-2 hours of oral administration

157
Q

What are indications of thiazide diuretics?

A

Hypertension
Chronic heart failure for oedema (although loop diuretics are better)

158
Q

Which thiazide diuretic is best for managing hypertension

A

Thiazide-like diuretics e.g. indapamide and Chlortalidone
(Used to be bendoflumethiazide but not thiazide-like diuretics are preferred)

159
Q

What are the contraindications for thiazide diuretics?

A

Addisons disease
Hypercalcaemia
Hyponatraemia
Refractory hypokalaemia
Symptomatic hyperuricaemia

Caution with diabetes, gout, hypokalaemia, SLE, elderly

160
Q

What are adverse effects of thiazide diuretics?

A

Dehydration
Postural hypotension
Hyponatraemia
Hypokalaemia
Hypercalcaemia
Hyperuricaemia
Hyperglycaemia
Erectile dysfunction
Alkalosis hypochloraemic
GI disturbance
Dizziness, fatigue, headache

Rare but important - thrombocytopenia, agranulocytosis, photosensitivity rash, pancreatitis

161
Q

What is the referral criteria for heart failure?

A

Refer to a specialist MDT for heart failure or cardiology service for specialist treatment if a person has:
Severe heart failure (NYHA class IV).
Heart failure that does not respond to treatment in primary care or can no longer be managed in the home setting.
Heart failure resulting from valvular heart disease.
Left ventricular EF of 35% or less.
A NT‑pro-BNP level above 2000 ng/L. These people should be referred urgently for specialist assessment and transthoracic echocardiography within 2 weeks.
A NT‑pro-BNP level between 400 and 2000 ng/L. These people should be referred to have specialist assessment and transthoracic echocardiography within 6 weeks.
Consider referral for a person with heart failure and a comorbidity such as chronic kidney disease or chronic obstructive pulmonary disease.
Refer women with HF-REF who are planning a pregnancy for specialist pre-conceptual advice, and refer women who are pregnant for specialist management.
Women who wish to conceive should be advised to continue contraception until they have seen an obstetrician and cardiologist for pre-conceptual advice.

162
Q

Whats the moa of sacubitril?

A

its a prodrug that inhibits the breakdown of natriuretic peptides resulting in varied effects e.g. vasodilation, diuresis and natriuresis

CARDIOLOGY (19 decks)

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