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PA20321 Retake > (chan) 4. Clinical Therapeutic > Flashcards

(chan) 4. Clinical Therapeutic Flashcards

1
Q

What is NHS Health Check Programme?

A
  • Government initiative to reduce cardiovascular disease through early identification of those at risk
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2
Q

Who is the target for NHS Health Check Programme?

A
  • Target 40 - 74 years olds in England every 5 years- Excludes those already with CVD
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3
Q

What are the beneficial outcome estimations of NHS Health Check Programme?

A

PHE estimates it can- Prevent 1600 MIs annually saving 650 lives- Prevent 4000 cases of diabetes annually- Detect 20,000 cases of diabetes and CKD earlier and therefore reduce later complications

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4
Q

What risk factors are measured in NHS Health Check programme?

A
  • Height- Weight- Blood pressure- Total Cholesterol and High density Cholesterol- Blood Sugar- Lifestyle factors: alcohol, physical activity, smoking- Dementia awareness (65-74 Y/O)
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5
Q

NHS Health Check Programme: What are the GP referral results?

A
  • High Blood Sugar- High Blood Pressure- High TC:HDL (>6mmol/L)- High CV risk (>20%)
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6
Q

What are the different types of hypertension?

A
  1. Primary/Essential- 95% of all cases- Quantitative deviation from the norm2. Secondary - 5% of all cases- Secondary to another cause
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7
Q

Is hypertension usually symptomatic or asymptomatic?

A
  • Asymptomatic except in malignant hypertension
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8
Q

What are the classifications of hypertension?

A

Stage 1- Clinic BP greater than or equal to 140/90mmHg (ABPM or HBPM >135/85mmHg)Stage 2- Clinic BP greater than or equal to 160/100mmHg (ABPM or HBPM >150/95mmHg)Severe- Clinic systolic BP greater than or equal to 180mmHg or clinic diastolic greater than or equal to 110mmHg

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9
Q

When do you add pharmacological intervention to different classifications of hypertension?

A

Stage 1 hypertension- Under 80 plus target organ damage +/or established CV disease +/or renal disease +/or CV risk >20%Stage 2 - Of any ageSevere hypertension- Treat immediately

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10
Q

What is blood pressure and what are the targets of BP treatment?

A
  • Blood pressure (BP) = CO x PVRCO = Cardiac OutputPVR = Pulmonary Vascular Resistance- Aim of the treatment is to reduce BP by reducing PVR without reducing CO
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11
Q

Why do we treat patients with diabetes more aggressively when managing BP?

A

Because people with type 2 diabetes are at high risk of- CVD, Diabetes eye damage, Renal diseaseImproving BP control reduces these adverse outcomes and also lower the risk of- Stroke, MI, Blindness, Renal failure

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12
Q

What are the BP targets in patients with hypertension alone?

A

Aim for target BP- 140/90mmHg in people aged under 80- 150/90mmHg in people aged 80 or overFor those with ‘white coat effect (anxiety experienced during a clinic visit), aim for HBPM- 135/85mmHg in people aged under 80- 145/85mmHg in people aged 80 or over

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13
Q

What are the modifiable/non-modifiable cardiovascular risk factors?

A

Modifiable- Hypertension- Hyperlipidaemia- Diabetes- Smoking- ObesityNon-modifiable- Age- Gender- Genetics

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14
Q

What are lifestyle changes known to reduce BP?

A
  • Lower risk alcohol intake (<14 units per week)- Reduce weight if obese (target BMI of 20-25)- Reduce salt intake- Regular physical exercise (> 30mins 3 times weekly)- Be realistic about what patient can achieve (SMART goals)
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15
Q

Which lifestyles are there that do not reduce BP but reduce CV risk?

A
  • Stopping smoking- Reducing total intake of saturated fats- Increasing intake of oily fish
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16
Q

What are 1st line anti-hypertensive drug treatment for the following groups?1. General population2. People of African/Caribbean family origin3. Women who may become pregnant

A
  1. General population- generic ACE inhibitor once daily2. People of African/Caribbean family origin- generic ACE inhibitor plus either a diuretic or a generic calcium-channel blocker3. Women who may become pregnant- generic calcium-channel blocker
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17
Q

What do you substitute for patients with ACE inhibitor intolerance?

A
  • Angiotensin II-receptor antagonist
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18
Q

Briefly explain actions induced from ACEi and ARB

A
  • Either prevents formation of or action of Antiotensin II which is a potent vasoconstrictor- Arterial and venous dilation- Increase K+ by reducing aldosterone
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19
Q

What are the side effects of ACEi and ARB?

A
  • Renal Impairment- Hyperkalamia (High Blood Potassium)
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20
Q

What does Calcium Channel Blockers (CCB) do?

A

Interfere with inward displacement of calcium ions through the channels into cell membranes.Relaxation of vascular smooth muscle causes vasodilatation

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21
Q

What are the 3 types of Calcium Channel Blockers and what do they do?

A
  1. Dihydropyridines- cause vasodilatation of coronary and peripheral blood arteries with little effect on heart rate2. Phenylalkalamines- rate limiting drug that reduces heart rate3. Benzothiazipine- rate limiting drug that reduces heart rate
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22
Q

How does Beta-Blockers work on Heart, Kidneys and CNS&PNS?

A
  • Heart: reduces HR- Kidneys: reduces renin- CNS&PNS: reduces release of neurotransmitters & sympathetic nervous activity
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23
Q

Define Cardiovascular risk

A

Chance of someone experiencing a heart attack or a stroke at some point in the next 10 years if nothing about their current lifestyle changes

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24
Q

Which drug is used in primary prevention of cardiovasular risk?

A

Atorvastatin 20mg to people with a 10% or higher QRISK2 level

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25
Q

What are monitoring parameters and targets of cardiovascular risk prevention? So

A
  • Measure liver transaminase enzymes within 3 months of starting treatment and at 12 months - Measure ‘total cholesterol, HDL cholesterol and non-HDL cholsterol’ in all patients who have been started on high intensity statin treatment at 3 months of treatment and aim for >40% reduction in non-HDL cholesterol
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26
Q

Case Example- A 49 year old lady, Mrs A, no existing medical conditions. - All bloods (renal function) and ECG come back normal- CV Risk calculated to be 13%- BP in clinic = 152/94mmHgWhat would you do for Mrs A?

A

Send for HBPM (Home Blood Pressure Monitoring)——————————-Mrs A continuedHBPM mean = 152/94mmHgThis repesents- Stage 1 hypertension but as CV risk <20% and no target organ damage, focus on lifestyle- Weight loss- Reduced Salt- Reduced Stress- Reduced Caffeine- Increased Exercise- Reduced Saturated Fat- Increased Oily fish- Balanced Diet- Reduced alcohol- Smoker?Follow up- Review BP and lifestyle modifications in 3 months and at 12months- Repeat Lipids screening

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27
Q

Define Acute Coronary Syndome (ACS)

A

A range of conditions including unstable angina, non-ST elevation MI and ST elevation MI

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28
Q

What is ischaemic event?

A

Reduced blood flow to the heart, causing pain- reduced blood to muscles when exercising, blood diverted elsewhere, therefore pain experienced

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29
Q

What are the typical symptoms of ACS?

A
  • Chest Pain- Nausea- Sweaty- Clammy- Breathlessness- Palpitation
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30
Q

Which investigations help determine the urgency and type of treatment the patients receive regarding ACS?

A
  • ECG trace- Blood Test (troponin)- Individual assessment of CV risk by using a scoring system
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31
Q

What is ECG and what does it tell us?

A
  • Cardiology test showing the rhythm and electrical activity of the heart including:waves, segments and complexes- Vital in determining the type of ACS event. Also area of the heart affected for appropriate intervention treatment
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32
Q

What is Troponin?

A
  • Cardiac enzymes released as a result of cardiac tissue death due to infarction- STEMI/NSTEMI have detectable troponin 3-12 hrs from onset of chest pain (peak at 24-48 hrs) ;measured at hospital presentation and again >6hrs after onset
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33
Q

what is GRACE score?

A
  • NICE recommendation to score risk at admission - Predict 6 month mortality- Determines treatment options
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34
Q

Characteristics of Unstable Angina, NSTEMI and STEMI regarding Troponin and ECG?

A

Unstable Angina- Troponin Negative- Normal/Unchanged ECGNSTEMI- Troponin positive- ST segment depression and or T wave inversionSTEMI- Troponin positive- ST segment elevation >1mm

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35
Q

What causes ACS?

A
  • Fatty deposits - Damage to artery lining- Plaques developping- Exposure of atheroma
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36
Q

What is pathophysiology of UA/NSTEMI

A

partial blockage of blood flow caused by a thrombus

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37
Q

What is pathophysiology of STEMI?

A

thrombus causing complete occlusion/blockage of blood flow

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38
Q

what are the risk factors of atherosclerosis and ischaemia?

A
  • High BP- High cholesterol- Diabetes (high sugars damage blood vessels)- Smoking- Alcohol- Stress- High BMI- Lack of exercise (unhealthy heart)
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39
Q

What are the aims of ACS treatment?

A
  • Alleviate pain and anxiety- Limit further ischaemia caused by thrombosis- Prevent and reduce risk of having another event
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40
Q

What is Acute initial management of ACS from first medical contact i.e paramdemic/A+E setting?

A
  • Oxygen (to avoid hypoxia)- GTN spray sublingually (to reduce ischaemic pain)- Morphine 1-2mg IV STAT/PRN (pain relief)- Metoclopramide 10mg IV STAT up to TDS/PRN (nausea associated with event/morphine)- Aspirin 300mg orally STAT (to stop further platelet aggregation)
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41
Q

What is Percutaneous Coronary Intervention (PCI)?

A
  • Non-surgical widening of the coronary artery using a balloon catheter to dilate the artery from within
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42
Q

What are ACS secondary prevention medications?

A
  • Anti-platelets: aspirin/ticagrelor- Beta-blocker: bisoprolol- ACEi: ramipril- Statin: atorvastatin- GTN spray sublingually PRN- Follow NICE guidlines/Local protocols
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43
Q

What monitorings should be down following ACS treatments?

A
  • Observation: BP and heart rhythm/rate- Renal function- Blood - platelets and Hb- Any side effects e.g dry cough with ACEi
44
Q

What is ECHO report ?

A
  • Aimed at all STEMI patients (NICE)- ACS can cause damage to the heart: Heart failure- ECHO determines extent of weakness caused by the ischaemic event- Medications may be started to prevent/support weakened heart
45
Q

What is Cardiac Rehabilitation?

A
  • Formal cardiac rehabilitation programme with an exercise component- reduces mortality and improves quality of life
46
Q

Pharmacist’s role in lifestyle changes for ACS

A
  • Counselling of medications (compliance)- Smoking cessation- Weight loss support- Promotion of exercise- Promotion of healthy diet- Management of diabetes
47
Q

What is Type 1 Diabetes?

A
  • Autoimmune disease that results in destruction of beta cells of pancreas- Results in complete lack of endogenous insulin
48
Q

What are the 2 phases of insulin release?

A

First Phase- begins within 2 mins of nutrient ingestion and continues for 10-15 mins- promotes peripheral utilization glucose, suppress hepatic glucose production, and limits postprandial glucose elvationSecond Phase- prandial insulin secretion which is sustained until normoglycemia is restored- Aim of insulin therapy is to imitate this pattern

49
Q

What are the complications of diabetes?

A
  • Diabetic ketoacidosis (extreme hyperglycaemia- Cardiovascular disease and stroke- Retinopathy and blindness- Kidney disease- Neuropathy and amputations
50
Q

When does Hypoglycaemia occur and what are the symptoms?

A
  • When blood glucose levels fall below 4mmol/L - Feeling shaky- Sweating- Hunger- Tiredness- Blurred vision- Lack of concentration- Headache- Feeling moody- Going pale
51
Q

When does Hyperglycaemia occur and what are the symptoms?

A
  • When blood glucose level goes above 7mmol/L before a meal or 8.5mmol/L 2 hours after meal- Due to missed dose of medication- Eaten more carbohydrate than the body or medication can cope- Stress- Infection- Thirst
52
Q

What is Diabetic Ketoacidosis?

A
  • due to consistently high blood glucose level- occurs when a severe lack of insulin results breaking down fat as an alternative energy; Ketones are produced as a by-product- Ketones are poisonous chemicals which cause body to become acidic- Life-threatening and requires admission to hospital for IV insulin and fluids
53
Q

What is VTE?

A
  • Venous Thromboembolism - Blood clotting in venous system
54
Q

What is VTE?

A

Venous Thromboembolism- undesirable blood clotting in the venous system

55
Q

Which conditions are there under VTE?

A
  1. DVT- Deep Vein Thrombosis- normally occurs in the leg2. PE- Pulmonary Embolism- fragments of thrombus from DVT may break off and enter arterial circulation, forming a secondary embolus in the pulmonary artery in the lung3. Secondary emboli from DVTs may also block cerebral arteries producing:- Transient Ischaemic Attack (TIA)- Ischaemic Stroke
56
Q

Describe DVT presentation(symptoms)

A
  • May be asymptomatic- Usually unilateral (affecting one side only)- Heavy ache/Warm skin in the affected area- Erythema (red skin)- Pitting oedema- Prominent superficial veins
57
Q

‘Just read’DVT diagnosis - Two Level Wells Score

A

*** put imageLec - Clinical consideration in VTE slide 5

58
Q

Describe PE presentation(symptoms)

A
  • Concurrent DVT- Breathlessness- Cough: Dry / Blood stained (haemoptysis)- Chest / Upper back pain: normally sharp/stabbing- Tachycardia (fast heart rate)- Tachypnoea (fast respiratory rate)- Hypotension- Syncope (fainting)- Hypoxia/cyanosis
59
Q

‘Just read’PE diagnosis - Two Level Wells Score

A

*** put imageLec - Clinical consideration in VTE slide 7

60
Q

What are the 4 types of further investigations for DVT & PE?

A
  1. D-Dimer Test- product formed when thrombus is degraded2. Venous Ultrasound- imaging technique to visualise venous blood clots in situ3. CT pulmonary angiography (CTPA)- imaging technique to visualise thrombus in pulmonary arteries4. Vertilation-Perfusion (VQ) scan- Uses radiopharmaceutical material to visualise the lungs
61
Q

What are the risk factors for blood clotting?

A
  1. Stagnation of blood- Inactivity or immobility- Reduced cardiac output2. Medical conditions assosicated with high clotting risk- cancer and some chemotherapy- CVD- Inflammatory disease (Reumatoid Arthritis)3. Vascular Injury- Broken bones/injuries
62
Q

What is LMWHs and how does it work?

A
  • Dalteparin, Enoxaparin, Tinazaparin- VTE prophylaxis and treatment of DVT/PE- Bind to antithrombin III (ATIII) and increase its inhibitory action on Factor Xa- Given subcutaneously, fixed-dose injection on basis of body weight- Predominantly removed by renal excretion
63
Q

What is UFH (Unfractioned Heparin)?

A
  • Same uses, contraindications and monitoring requirements as LMHW but has much larger polysaccharide chains- Predominantly removed by hepatic metabolism- Loading dose/ Ongoing infusion rate guided by APTT (Activated Partial Thromboplastin Time) ratio
64
Q

What is APTT and APTT Ratio?

A
  • APTT = Activated Partial Thromboplastin Time - APTT measures how quickly the intrinsic and common coagulation pathways cause blood to clot- Normal APTT = apprx 30 seconds- APTT ratio = APTT (patient) ÷ Normal APTT- Target APTT ratio during IV UFH infusion is usually between 2 and 3
65
Q

LMWHs generally preferred over UFH due to longer and more predictable half lives and less intensive monitoringWhen would UFG may be preferred over LMWH?

A
  • Patients with severely impaired renal function: due to UFH being primarily removed by hepatic metabolism- Risk of bleeding: shorter half life so anticoagulant effect can be quickly halted by stopping IV infusion
66
Q

What is Warfarin and when is it used?

A
  • Treatment and secondary prevention of DVT and PE (duration usually 3-6 months after first episode)- Inhibits Vitamin K epoxide reductase and Vitamin K quinone reductase to hinder activation of clotting cascade factors and other proteins associated with clotting- Only Orally available- Target INR depends on condition being treated
67
Q

What are key contraindication, monitoring and adverse effects of Warfarin?

A

Contraindication- Hypersensitivity- Haemorrhagic strokeMonitoring- INR- Full blood count- Liver function test- Signs of bleedingAdverse effects- Bleeding- Skin reaction

68
Q

What is International Normalised Ratio (INR)?

A
  • Prothrombin time (PT) measures speed of clotting mediated by the extrinsic clotting pathway- Normal PT = apprx 12 seconds- INR = PT(patient) ÷ PT(normal)- Target INR normally 2.5 but can be upto 3.5 for certain types of artificial heart valves
69
Q

What are different types of loading of Warfarin and when are they used?

A

Slow loading- may be suitable in patients with AFFast loading- patients with DVT/PE - Usually co-administer treatment dose LMWH until INR consistently >2

70
Q

Why does Warfarin have many significant drug interactions?

A

2 Key reasons1. Warfarin is hepatically metabolised by CYP450 enzymes - Interactions with drugs increasing/inhibiting CYP450 activitiy 2. Warfarin is highly bound to plasma proteins like albumin- Other protein bound drugs compete with warfarin resulting in more free(active) warfarin

71
Q

What does DOAC(Direct Oral Anticoagulants) do?

A
  • Treats or prevents blood clots, often called a’blood thinner’- Directly inhibit Factor Xa by occupying its active site- May increase INR but not significantly
72
Q

Why do DOACs drug interactions occur?

A
  • DOACs are substrates for CYP450 enzymes and P-glycoprotein (P-gp)- Inhibitors of these enzymes induce increase plasma levels and bleeding risk- Inducers of these enzymes decrease plasma level and increase clot risk
73
Q

what Mechanical Thromboprophylaxis are there?

A
  • Anti-embolism stocking (thigh or knee length)- Foot impulse devices- Intermittent pneumatic compression (IPC) devices (thigh or knee length)
74
Q

What is AF?

A
  • A chaotic, often fast, rhythm from multiple foci within atria- Disorganised atrial depolarisation and ineffective atrial contraction- The atriovascular node receives more electrical impulse than it can conduct, resulting in an fast, irregular ventricular rhythm
75
Q

Why is AF a problem?

A
  • Persistence of symptoms- Leads to other problems such as hypotension, cardiac ischaemia, tachycardia, heart faulure- Stroke risk
76
Q

AF presentation(symptoms)

A
  • Palpitation- Irregular pulse- Tachycardia- Breathlessness- Tiredness- Reduced exercise tolerance- Fainting- ECG changes: tiny irregular ‘fibrillation’ waves between heartbeats
77
Q

what are additional investigations for AF?

A
  • Echocardiogram: ultrasound scan of the heart - Chest x-ray- Blood tests
78
Q

What are the common causes of AF?

A
  • Ischaemic heart disease- Hypertension- Valvular heart disease- Hyperthyroidism
79
Q

How are the 3 main elements of AF management?

A
  • Rate control- Rhythm control- Stroke prevention
80
Q

What are the types of drugs used for Heart Rate control?

A
  • Beta-blocker: Atenolol, Acebutolol, Metoprolol, Nadolol- Rate-limiting calcium-channel blocker: Diltiazem (off-label), Verapamil- Digoxin
81
Q

What drugs are used for Heart Rhythm control

A
  • Beta-blocker- Amiodarone- Dronaderone- Pill in the pocket: Infrequent paroxysms +/- known precipitant (caffeine, alcohol)
82
Q

What is Electronic Cardioversion?

A
  • Electronic current being applied to the heart to ‘shock’ back into sinus rhythm
83
Q

What is Cardiac Catheter Ablation?

A
  • Catheter inserted into heart chambers via vene cava which emits radiofrequency energy to damage tiny portions cardiac tissue responsible for generating abnormal electrical activity
84
Q

Why do patients with AF at increased risk of stroke?

A
  • due to risk of clots forming within the fibrillating atria and transferring to the cerebral arteries
85
Q

Which tool is used to assess stroke risk in AF?

A
  • CHA2DS2VASc score toolTakes accounts of (point)- C: Congestive Heart failure/ Left Ventricular dysfunction (1)- H: Hypertension (1)- A: Age >75 years (2)- D: Diabetes (1)- S: Stroke in past (2)- V: Vascular disease (1)- A: Age 65-74yrs (1)- Sc: Sex category = female (1)
86
Q

Which tool is used to assess bleeding risk in AF?

A
  • HAS-BLED scoreTakes accounts of (point)- H: Hypertension (1)- A: Abnormal liver function (1)- A: Abnormal renal function (1)- S: Stroke in past (1)- B: Bleeding history (1)- L: Liable INR (1)- E: Elderly >65 yrs (1)- D: Drugs eg) antiplatelets or NAIDS (1)- H: Harmful alcohol consumption (1)
87
Q

DOAC vs Warfarin in AF

A
  • DOAC requires less monitoring- DOAC better for people with liable INR- DOAC lower risk of bleeding vs warfarin - DOAC very expensive (4x more than warfarin)
88
Q

Define Heart Failure

A
  • complex syndrome that can occur from any structural or functional cardiac disorder that impairs the ability of the heart to fill with and eject blood and therefore to function efficiently as a pump to support physiological circulation
89
Q

What are the common causes of Heart Failure?

A
  • Ischaemic heart disease (35-40%)- Cardiomyopathy (30-34%)- Hypertension (15-20%)
90
Q

What happens in ventricular remodeling post MI?

A
  • After acute MI, normal heart tissue to be replaced by scar tissue, rest of heart starts to remodel itself to replace lost cells- As time goes, heart is left to be less capable
91
Q

What are the clinical syndromes of heart failure?

A
  • Left ventricular systolic dysfunction (LVSD): heart failure with reduced ejection fraction: caused by ischaemic heart disease, valvular heart disease : hypertension- Diastolic heart failure: heart failure with preserved ejection fraction: increased stiffness in ventricular wall and increased left ventricular wall thickness: diastolic filling impaired - treat with diuretics- Right ventricular systolic dysfunction (RVSD): secondary to LVSD
92
Q

What are the clinical features of heart failure in terms of symptoms and clinical signs?

A

Symptoms- Fatigue- Exertional dyspnoea- Orthopnoea- Decreased exercise tolerance- Paroxysmal nocturnal dyspnoeaClinical signs- Tachycardia- Cardiomegaly- Fluid retention (oedema)- Elevated venous pressure- Abnormal heart sounds

93
Q

What are the 4 NYHA Classification of heart failure?

A

Class 1- no limitation on physical activityClass 2- slight limitation, comfort at rest but ordinary physical activity cause symptomsClass 3- marked limitation of activity, comfort at rest but less than ordinary activity causes symptomsClass 4- Unable to carry out any physical activity without discomfort, symptoms at rest

94
Q

What is Ejection Fraction(%)?

A
  • An important measurement in determining how well your heart is pumping out blood and in diagnosing and tracking heart failure
95
Q

Describe echocardiogram diagnosis results of heart failure

A

Ejection profile- 60% or above = normal- <30% = severe dysfunction

96
Q

What the the 3 different types of Natriuretic peptides and when are they induced?

A
  1. Atrial Natriuretic Peptide (ANP) - released from atrial myoctes in response to stretch- induces diuresis, natriuresis, vasodilation, supresses renin-angiotensin system- Levels raised in heart failure, correlate with functional class ; prognosis2. Brain natriuretic peptide (BNP)- released by ventricles in response to myocardial wall stress- N-terminal (NT)-proBNP is cleaved from proBNP to release BNP- increased BNP ; NT-proBNP in heart failure3. C-type peptide- has similar effects to ANP & BNP
97
Q

What are the effects of Natriuretic peptides?

A

1.→ Vasodilation → Decreased BP2.→ Decreased Renin & Increased GFR → Decreased Antiotensin II & Aldosterone → Increased NA+, H2O and Increased excretion → Decreased Blood Volume → Decreased BP

98
Q

What Non-pharmacological treatment options are there?

A
  • Exercise- Diet- Weight Reduction- Reduce alcohol consumption- Stop smoking- Infleunza & Pneumococcal vaccinations
99
Q

How is Chronic Heart Failure managed?

A
  • Multi-disciplinary team inc. non-NHS agencies e.g social care- Management of depression- Lifestyle advice: diet, exercise, reduce alcohol- Medication: Keep regimens as simple as possible: consider comorbidities esp hypertension, ischaemic heart disease and diabetes
100
Q

Drug treatment options for all types of chronic heart failure (NICE 2017)?

A
  1. Loop diuretic (furosemide)- Routinely used for relief of congestive symptoms and fluid retention in patients2. Amlodipine- for comorbid hypertension and/or angina3. Anticoagulants- for those with a history of thromboembolism, left ventricular aneurysm, or intracardiac thrombus4. Aspirin- for patients with combination of heart failure and atherosclerotic arterial disease
101
Q

What are first line treatment options for chronic heart failure due to left ventricular systolic dysfunction (LVSD)?

A

ACE-i + b-blocker- Start ACE-i at a low dose and titrate upwards at short intervals until optimal tolerated or target dose achieved- Offer b-blockers licensed for heart failure (Carvedilol, Bisoprolol or Nebivolol) to all patients with LVSD

102
Q

What are second line treatment options for chronic heart failure due to LVSD?

A
  1. Aldosterone antagonists2. Angiotensin II receptor blockers3. Hydralazine in combination with nitrate4. Sacubitril valsartan
103
Q

What are the third line treatment options for chronic heart failure due to LVSD?

A
  1. Digoxin2. Ivabradine
104
Q

Which invasive treatments are there for heart failure?

A
  • Coronary revascularisation- Cardiac Resynchronisation Therapy (CRT)- Intra Cardiac Defibrillators (ICD)- Cardiac transplant
105
Q

Describe Acute Heart failure

A
  • Rapid onset of signs & symptoms of heart failure- Severe dyspnoea- Acute pulmonary oedema

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