HEART FAILURE Flashcards

Question

What causes high output heart failure?

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

Acute heart failure without a past history of HF

Answer 5

Iatrogenic Sepsis MI Arrhythmias

Answer 6

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

Answer 7

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

Answer 8

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

Answer 9

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

Answer 10

CAD Hypertension Cardiomyopathies

Answer 11

CAD (35-40% of cases)

Answer 12

Constructive pericarditis Pericardial effusion

Answer 13

AF Other tachyarrhythmias

Answer 14

End-stage CKD Nephrotic syndrome

Answer 15

Alcohol Cocaine

Answer 16

NSAIDs Beta blockers CCB

Answer 17

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

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

AF (50% of those with severe HF)

Answer 22

Up to 20% of pt

Answer 23

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.

Answer 24

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

Answer 25

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

Answer 26

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

Answer 27

Due to weight gained secondary to oedema

Answer 28

Preload Myocardial contractility Afterload

Answer 29

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

Answer 30

Systolic - diastolic bp

Answer 31

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

Answer 32

Vasodilation and vasoconstriction of blood vessels

Answer 33

stretching of cardiomyocytes at the end of diastole.

Answer 34

pressure or load against which the ventricles must contract.

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

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

Answer 44

Aka brain natriuretic peptide (BNP) a hormone produced mainly by the left ventricular myocardium in response to strain.

Answer 45

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.

Answer 46

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

Answer 47

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

Answer 48

It’s good at excluding HF

Answer 49

Vasodilation Diuretic and natriuretic Suppresses sympathetic tone and RAAS

Answer 50

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

Answer 51

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

Answer 52

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

Answer 53

The New York Heart Association (NYHA)

Answer 54

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.

Answer 55

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

Answer 56

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

Answer 57

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

Answer 58

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

Answer 59

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)

Answer 60

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

Answer 61

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

Answer 62

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.

Answer 63

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

Answer 64

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

Answer 65

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.

Answer 66

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

Answer 67

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.

Answer 68

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

Answer 69

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

Answer 70

Dry cough Hyperkalaemia Renal impairment Light headedness Fatigue GI disturbance Angioedema

Answer 71

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

Answer 72

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

Answer 73

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.)

Answer 74

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

Answer 75

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

Answer 76

transthoracic echocardiography

Answer 77

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

Answer 78

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)

Answer 79

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

Answer 80

Normal - <100 Raised 100-400 High >400

Answer 81

Normal <400 Raised 400-2000 High >2000

Answer 82

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

Answer 83

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

Answer 84

CAD MI Arrhythmia Chronic hypertension

Answer 85

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)

Answer 86

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

Answer 87

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

Answer 88

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

Answer 89

Cardiomyocyte death and fibrosis = chronic neurohumural activation = Ventricualr remodelling

Answer 90

Secondary to heart failure

Answer 91

1.5-2kg in 2 days

Answer 92

as these drugs reduce cardiac contractility Amlodipine

Answer 93

Loop diuretics such as furosemide, bumetanide, or torasemide

Answer 94

bisoprolol, carvedilol and nebivolol

Answer 95

Spironolactone and eplerenone

Answer 96

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

Answer 97

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

Answer 98

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

Answer 99

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)

Answer 100

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

Answer 101

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

Answer 102

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

Answer 103

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

Answer 104

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

Answer 105

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

Answer 106

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)

Answer 107

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

Answer 108

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

Answer 109

Hypotension Hyponatraemia and hypokalaemia

Answer 110

Headache Palpitations Flushing

Answer 111

Dizziness Blurred vision GI disturbances Arrhythmias

Answer 112

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

Answer 113

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

Answer 114

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

Answer 115

Amlodipine

Answer 116

Amlodipine

Answer 117

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.

Answer 118

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

Answer 119

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

Answer 120

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

Answer 121

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

Answer 122

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

Answer 123

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

Answer 124

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.

Answer 125

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

Answer 126

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

Answer 127

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

Answer 128

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

Answer 129

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.

Answer 130

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

Answer 131

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

Answer 132

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

Answer 133

Addisons disease Hypercalcaemia Hyponatraemia Refractory hypokalaemia Symptomatic hyperuricaemia Caution with diabetes, gout, hypokalaemia, SLE, elderly

Answer 134

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

Answer 135

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.

Answer 136

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