CV PBL ILO’s Flashcards
Outline potential pathways from psychological arousal to physical symptoms
The body releases a surge of hormones when under stress.
These hormones cause the heart to beat faster and the blood vessels to narrow.
These actions increase blood pressure for a time.
Demonstrate knowledge of adherence, including strategies used to enhance adherence to treatment and health advice.
Adherence Definition : the extent to which a patients behaviour (i.e. taking medication, lifestyle changes, or following a diet) corresponds with the advice given by a healthcare provider.
Strategies to improve adherence:
Simplifying regimen characteristics
Imparting knowledge
Modifying patients beliefs
Patient communication
Leaving the bias behind
Evaluate adherence
Demonstrate knowledge of the pro-inflammatory effects of smoking on the cardiovascular system
• Thrombosis
○ Smoking causes walls of blood vessels to become inflamed -> atherosclerosis
○ Atherosclerotic plaque formed: activated monocytes adhere to site of damaged endothelium -> migrate into sub-endothelium -> differentiate into macrophages -> differentiate into foam cells
Rupturing of plaque -> local vasoconstriction and thrombosis
Demonstrate knowledge of the circulatory system, including the anatomy and histology of arteries and veins
The circulatory system has two components: the cardiovascular system and the lymphatic vascular system.
The cardiovascular system is composed of the heart and two separate circuits: the pulmonary circuit that carries deoxygenated blood from the heart to the lungs and oxygenated blood from the lungs to the heart, and the systemic circuit that distributes oxygenated blood from the heart to the rest of the body and returns deoxygenated blood from the tissues of the body to the heart. Blood leaves the heart via vessels that belong to the arterial system , whose members decrease in size the farther away they are from the heart, and return to the heart via vessels that belong to the venous system, whose members increase in size as they approach the heart. The smallest branches of the arterial and venous systems are connected to each other by way of capillaries that form extensive capillary beds .
Anatomy of the heart
Heart is found in the thorax between two lungs, to the left of the midline. It is between ribs 2 and 5, the apex of heart is on the midclavicular line in the 5th intercostal space.
Heart layers: Endocardium, myocardium, epicardium
The pericardium covers the heart – it is made of two layers an inelastic fibrous parietal layer and a smooth visceral layer.
The fibrous skeleton of the heart is between the atria and ventricles and stops electrical impulses passing from the atria to the ventricles in an uncontrolled manner. The heart valves are suspended from the fibrous skeleton.
There are two types of heart valve:
1. Atrioventricular valves (AV)
a. Bicuspid (Right AV valve)
b. Tricuspid/mitral (Left AV valve)
2. Semilunar Valves
a. Aortic
b. Pulmonary
Atrioventricular Valves:
• Between atria and ventricles
• Flow of blood opens valve
• Anchored by chordae tendinae to papillary muscles
• Contraction of papillary muscles prevents eversion of valves and prevents back flow of blood into atria
Semilunar Valves:
• Between ventricles and aorta/pulmonary trunk
• Opened by flow of blood due to ventricle contraction
Closed by back flow of blood pooling in valve cusps
What does the left and right coronary artery bifurcate into?
Left coronary artery bifurcates into:
• Circumflex
• Anterior interventricular
Right coronary artery bifurcates into:
• Posterior interventricular
Marginal
Name the names of the blood vessels layers:
Walls of blood vessels are composed of three separate concentric layers: the tunica intima, tunica media, and tunica adventitia.
Name the three types of arteries:
Arteries are of three types: elastic arteries (conducting arteries),
The aorta and the branches originating from the aortic arch (the common carotid artery and the subclavian artery), the common iliac arteries, and the pulmonary trunk are elastic (conducting) arteries
muscular arteries (distributing arteries),
Muscular arteries are characterized by a thick tunica media that is composed mostly of smooth muscle cells. Muscular (distributing) arteries include most vessels arising from the aorta, except for the major trunks originating from the arch of the aorta and the terminal bifurcation of the abdominal aorta, which are identified as elastic arteries.
and arterioles
Arteries with a diameter of less than 0.1 mm are considered to be arterioles.
Veins:
Veins are classified into three groups on the basis of their diameter and wall thickness: small, medium, and large.
Venules are similar to but larger than capillaries; larger venules possess smooth muscle cells instead of pericytes. As the blood pools from the capillary bed, it is discharged into small venules ( postcapillary venules )
Medium veins are less than 1 cm in diameter. Medium veins are the ones draining most of the body, including most of the regions of the extremities
Large veins return venous blood directly to the heart from the extremities, head, liver, and body wall. Large veins include the vena cava and the pulmonary, portal, renal, internal jugular, iliac, and azygos veins.
Demonstrate understanding of applications of behavioural theories to weight loss
Making specific and small goals to calorie intake, physical activity, and diet.
Calorie deficit
150 minutes of moderate activity per week
Reduce amount of saturated fat and salt and sugar intake
Demonstrate knowledge of the benefits of physical activity in managing hypertension:
Strengthens heart- improves its ability. To pump blood around the body with less effort. Decreases force on the arteries
Exercise leads to post exercise hypotension therefore frequent exercise can sustain lower blood pressure.
Demonstrate knowledge of the pathophysiology of hypertension, including management options.
Involves the impairment of renal pressure natriuresis, the feedback system in which high blood pressure induces an increase in sodium and water excretion by the kidney that leads to a reduction of the blood pressure.
The principal neuroendocrine mechanisms involved in the regulation of blood pressure. RAAS, natriuretic peptide roles, endothelial dysfunction, sympathetic nervous system (SNS) and the immune system. A disruption in any of these systems can lead to hypertension
Management - https://www.nice.org.uk/guidance/ng136
· Lifestyle interventions:
· Weight management
○ BMI 18.5-24.9 Kg/m2
o Dietary advice, use of slimming clubs
· No more than 14 units alcohol per week
· Reduce salt to 4.4g/day
Exercise – should be enjoyable and part of daily routine
Physiological mechanisms involved in development of essential hypertension
Cardiac output
Peripheral resistance
Renin-angiotensin-aldosterone system
Autonomic nervous system
Demonstrate knowledge of the pathophysiology of hypercholesterolaemia in the cardiovascular system.
Hypercholesterolaemia -> elevated cholesterol levels in the blood stream.
Cholesterol travels through the blood on two lipoprotein subtypes
• Low density lipoproteins (LDL), ‘bad’ cholesterol, which makes up most of your body’s cholesterol
• High density lipoproteins (HDL), ‘good’ cholesterol, absorbs cholesterol in the blood and flushes it back to the liver.
Pathophysiology
• When the blood has elevated LDL levels, it can lead to the disposition of cholesterol in vascular walls. This creates fatty streaks, which over time become fibrous plaques, this is termed atherosclerosis. This causes narrowing of the arteries at the located site, which restricts blood flow. This increases TPR and causes an increase in BP.
• As the body responds to atherosclerosis it causes inflammation, resulting in the plaques to become unstable, resulting in plaque rupture.
• Some of the material is thus made evident in the blood vessel and into the circulatory system, which can lead to thrombosis.
• This can affect the hearts ability to pump blood sufficiently and if blood clots form in one of the arteries leading to the heart, angina or a heart attack can occur.
Aetiology of hypercholesterolaemia
1. Genetic Causes : familial dyslipidaemia
Secondary : obesity, diet, excessive alcohol intake, hyperthyroidism, diabetes, inflammatory disease, liver disease, nephrotic syndrome, chronic renal failure, medications.
Diagnostic Factors of hypertension:
headache
visual changes
dyspnoea
chest pain
sensory or motor deficit
Risk factors of hypertension:
obesity
aerobic exercise <3 times/week
moderate/high alcohol intake
metabolic syndrome
diabetes mellitus
black ancestry
age >60 years
family history of hypertension or coronary artery disease
sleep apnoea
sodium intake >1.5 g/day
low fruit and vegetable intake
dyslipidaemia
Demonstrate knowledge of arterial blood pressure and its relationship to cardiac output and peripheral resistance
Blood pressure or systemic arterial pressure → pressure measured within large arteries in the systemic circulation
Mean arterial blood pressure = cardiac output x total peripheral resistance
Cardiac output = Heart rate x stroke volume
Therefore any changes in the heart rate or stroke volume can impact on the cardiac output and therefore BP
Peripheral vascular resistance factors:
Blood viscosity
Vessel Length
Vessel Diameter
Describe the health risk from tobacco smoking at the individual and population levels
Common health risks include:
· Cancer
· Heart disease
· Stroke
· Lung disease
· Diabetes
COPD which includes emphysema and chronic bronchitis
· CVD – 20% of all deaths from CVS are due to smoking
· Respiratory disease – 40% of all are due to smoking, increases risk of pneumonia and TB
Smoking is the main cause of premature death and preventable illness in the UK
Long term effects of smoking:
Increase risk of cancer
Increase risk of heart attack and heart disease
Increase stroke risk
Increase psoriasis risk
Increase T2 diabetes
Increase osteoporosis risk
Increase mental health problems
Increase risk of vision changes
Increase risk of gum disease
Increase risk of chronic lung disease
Delayed wound healing
Fertility problems
What are the two main types of cells in the heart?
Heart has 2 main types of cells:
Conducting cells generate and propagate electrical impulses
Contractile cells contract following receipt of electrical impulses. These cells can also propagate and on occasion generate electrical impulses
Where and what is the AV node?
• AVN is a group of specialised cells in atrioventricular septum just above the coronary sinus ostium
• AVN receives electrical impulses from atria and then transmits impulse from the atria to ventricles
Slower conduction velocity (0.05m/sec) than the atria, allowing maximal ventricular filling prior to contraction
Pathophysiology of supraventicular tachycardia.
Pathophysiology
· SVT is caused by the electrical signal re-entering the atria from the ventricles.
· Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria.
· Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12).
· It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.
· Paroxysmal SVT describes a situation where SVT reoccurs and remits in the same patient over time.
What are the types of supraventricular tachycardia’s?
Atrial Fibrillation
Atrial flutter
Atrioventricular reciprocating tachycardia (AVRT)
Atrioventricular modal re entrant tachycardia (AVNRT)
Understand the non pharmacological reduction of cardio vascular risk factors:
Smoking cessation
Control hypertension
Control diabetes
Managing cholesterol
Cardioprotective diet
Avoiding alcohol
Exercise
Managing stress
Maintain healthy weight
What is atrial fibrillation?
Atrial fibrillation (AF) is a cardiac arrhythmia characterised by disorganised electrical activity within the atria resulting in ineffective atrial contraction and irregular ventricular contraction.
Causes of atrial fibrillation:
• Idiopathic
• Ischaemic heart disease
• Heart failure
• Valve disease: mitral stenosis, mitral regurgitation
• Hypertension
• Hyperthyroidism
• Alcohol induced
Familial
Signs of atrial fibrillation
Signs:
• AF is the most common cardiac arrhythmia in adults. The prevalence of AF increases with age, particularly over 65 years, such that 10% of over 85-year-olds have atrial fibrillation.
• The resulting chaotic electrical activity is intermittently conducted through the AVN which gives rise to the characteristic irregularly irregular ventricular rate seen in AF.
• In AF, the ventricular rate is very variable and depends on the speed of AVN conduction. Young patients with slick AV nodes are often very symptomatic and tachycardic.
• The presence of chaotic electrical activity within the atria also results in ineffective atrial contraction. The consequence of this is blood stasis within the atria which increases the chance of thrombosis (Virchow’s triad) and subsequently embolic complications including transient ischaemic attacks (TIA), stroke and systemic embolisation.
• It is most commonly associated with hypertension, obesity and alcohol.
• Irregularly irregular pulse when palpating radial/carotid arteries or auscultating at the apex
Radial-apical deficit: this is important to assess because each ventricular contraction may not be sufficiently strong enough to transmit a pulse to the radial artery and palpating only the radial artery can miss tachycardia.
Symptoms of AF
• Can be asymptomatic
• Common presenting symptoms include breathlessness, chest discomfort, palpitations, dizziness, syncope, dyspnoea and reduced exercise tolerance
• Transient ischaemic attack or stroke can be the presenting feature of AF. Essential that patients presenting with symptoms or signs of a TIA or stroke are also asked about the features of AF.
Common ECG finding include irregular RR intervals and absent p-waves
Complications of AF:
• Stroke and thromboembolism = MAIN COMPLICATIONS
–> dependent of the presence of stroke risk factors though
–> stroke severity greater when stroke is associated with AF
–> Peripheral thromboembolism can also occur
• Heart failure
–> due to disorganised electrical conduction in atria which results in ineffective ventricular filling
• Tachycardia-induced cardiomyopathy and critical cardiac ischaemia as a result of persistently elevated ventricular rate seen in uncontrolled AF
Sudden death
Atrial Fibrillation rate control treatment:
○ Rate Control is first line:
▪ Beta blocker – first line (e.g. atenolol 50-100mg once daily)
▪ Rate limiting CCB – diltiazem hydrochloride / verapamil hydrochloride (not preferable in heart failure)
▪ Digoxin – only as primary treatment in predominantly sedentary / if other rate limiting drugs are unsuitable
○ Used as monotherapies first but if it fails to control rate then use as combination
If combination fails use rhythm control
Atrial Fibrillation rhythm control treatment:
○ Rhythm Control Drugs – pharmacalogical cardioversion
▪ Flecainide
▪ Amiodarone (drug of choice if patient has structural heart disease)
○ Long term rhythm control drugs:
▪ Beta blockers – 1st line
▪ Dronedarone – 2nd line, maintain normal rhythm when they’ve had successful cardioversion
▪ Amiodarone – in patients with heart failure or left ventricular dysfunction
What medication is used for paroxysmal supraventricular tachycardia?
Adenosine initial 6mg, then 12mg, then further 12mg if no improvement
What is digoxin used for?
Slows ventricular response in cases of atrial fibrillation and atrial flutter
What medications are used for supraventricular tachycardia?
Verapamil
Hydrochloride
How can you achieve rapid control of ventricular rate?
IV Beta blockers e.g. esmolol hydrochloride / propranolol hydrochloride
Describe sinus rhythm.
A sinus rhythm is any cardiac rhythm in which depolarisation of the cardiac muscle begins at the sinus node. It is characterised by the presence of correctly oriented P waves on the electrocardiogram
Describe sinus arrhythmia.
Sinus arrhythmia is a commonly encountered variation of normal sinus rhythm. Sinus arrhythmia characteristically presents with an irregular rate in which the variation in the R-R interval vary by more than 0.12 seconds
Name types of ventricular tachycardia’s:
Ventricular tachycardia
Ventricular fibrillation
Name types of bradycardia.
AV Heart Block
Asystole
Supraventricular tachycardia’s:
AV Fibrillation vs AV Flutter
Atrial Fibrillation:
Irregularly irregular
Abnormal P Waves
R to R uneven
Atrial Fluter:
P waves = saw tooth
Normal QRS
R to R can be even or uneven
Typically 2 or more P waves for every QRS
Supraventricular tachycardia’s:
Atrioventricular nodal re entrant tachycardia (AVNRT) vs Atrioventricular reciprocating tachycardia (AVNT)
AVNRT
Originates above the level of the bundle of His
Commonest cause of heart palpitations in patients with no structural abnormality
Slow Fast (Common) P waves often hidden being embedded in QRS complex
Fast Slow (Uncommon) P waves are visible between the QRS and T wave
AVRT: Rate usually 200-300bpm
Orthodromic: Retrograde P waves are usually visible with a long RP Interval
Antidromic: (Rare) Wide QRS complexes due to abnormal ventricular depolarisation
Types of ventricular tachycardia:
Ventricular tachycardia
Ventricular fibrillation
Describe ventricular tachycardia:
Originates from the ventricles
Several different forms - most common monomorphic VT
ECG Features:
Regular broad QRS Complexes
Describe ventricular fibrillation:
Most important shockable cardiac arrest rhythmFatal unless life support is rapidly used
ECG:
Chaotic irregular deflections or varying amplitude
No identifiable P waves, QRS complex, or T waves
Rate 150 to 500 bpm
Name types of bradycardia:
AV Heart Block- First Degree Heart Block, Second Degree heart Block type 1 and 2, Third degree heart block
Asystole
Describe heart block
Arrhythmia where signal delayed or blocked in the conduction system due to damage or fibrosis
First degree heartblock:
PR Interval > 200ms five small squares
There is delay without interruption in conduction from atria to ventricles
Second degree heart block:
Type 1 - Mobitz 1 block (Wenckeback Phenomenon)
Progressive prolongation of the PR Interval
Type 2 - Mobitz 2 (Hay Block)
A form of 2nd degree AV Block in which there is intermittent non- conducted p waves without progressive prolongation of the PR Interval
Third degree heart block
Single blocked completely
Not shockable in cardiac arrest
Symptoms : syncope, confusion, dyspnea, severe chest pain
Risk of dying
ECG:
Severe bradycardia due to absence of AV conduction
AV Dissociation with independent atrial and ventricular rates
Describe Asystole
Flatline
Represents the cessation of electrical and mechanical activity of the heart
Not a shockable rhythm
Aetiology of atrial fibrillation
• The cause is unknown BUT:
• Any condition that leads to inflammation, stress, damage, or ischemia affecting the anatomy of the heart can result in the development of atrial fibrillation.
• Electrically active foci within the pulmonary veins.
• Electrical remodeling in the cardiac myocytes causing dilated cardiomyopathy
• Failure of initiation of pharmacological intervention or failure of cardioversion.
• Unresponsive rhythm
What are palpitations or only caused by?
Palpitations are most commonly caused by:
Atrial or ventricular extrasystoles (PACs or PVCs) - additional heartbeats that occur outside the physiological heart rhythm).
Narrow QRS complex tachycardia (heart rate more than 100 beats per minute, QRS duration of less than 120 milliseconds).
Atrioventricular nodal reentry tachycardia (AVNRT) is the most common type of supraventricular tachycardia (SVT).
Wolff-Parkinson-White (WPW) syndrome is a condition that makes the heart suddenly beat abnormally fast, in an abnormal heart rhythm called SVTs - short PR intervals.
Atrial fibrillation or flutter.
Also caused by non cardiac related problems: psychiatric disorders and miscellaneous (i.e. Hyperthyroidism, alcohol)
How do you assess a patient experiencing palpitations?
Assessment of a person who currently has palpitations involves:
Checking for symptoms suggestive of a serious cause or complication, such as breathlessness, chest pain, syncope or near syncope (fainting).
Checking for a history of ischaemic heart disease, heart failure, cardiomyopathy, or valve disease, which could predispose to a serious arrhythmia.
Asking about sudden cardiac death of a relative younger than 40 years of age.
Examining the person’s heart rate and rhythm, blood pressure, and identifying any heart murmurs or lung crepitations - ensure haemodynamic stability.
○ Duration of palpitations -instant vs minutes ○ HR and rhythm regularity – describe the rate + regularity to me - tap it out.
Taking an ECG immediately.
Lab tests - thyroid function test
Cardiac causes of palpitations:
Cardiac causes:
• Underlying structural heart disease (cardiomyopathy - disease of the heart muscle) • Identifiable conduction abnormality (long QT syndrome - heart signalling disorder) • Tachyarrhythmias, bradyarrhythmias, ectopic beats • Valvular heart disease (mitral valve prolapse - valve flaps of the mitral valve don't close smoothly or evenly) • Pacemaker syndrome (AV dyssynchrony due to single chamber pacing) • Atrial myxoma (nonca)ncerous tumor in the atria)
High output cardiac states (resting cardiac output greater than 8 L/min
How to distinguish between causes of heart palpitations:
Supraventricular tachycardia - SVT
Atrioventricular nodal reentry tachycardia - AVNRT
Atrioventricular reentrant tachycardia - AVRT
SINCE CHILDHOOD
Paroxysmal supraventricular tachycardia - pSVT
Atrial tachycardia
Atrial fibrillation - AF
OLDER PATIENTS
Premature ventricular contractions - PVCs
Complete heart block
Ventricular tachycardia - VT
POUNDING IN NECK
Atrial fibrillation - AF
Supraventricular arrhythmia
FLUTTERING
Supraventricular tachycardia - SVT
Atrial fibrillation - AF
Flutter
PRESYNCOPE/SYNCOPE
Supraventricular tachycardia - SVT
Ventricular tachycardia - VT
ABRUPT ONSET AND TERMINATION
Atrioventricular nodal reentry tachycardia - AVNRT
MORE AWAR OF PALPITATIONS ONCE STANDING AFTER SITTING
What are rate medications used for in AF and give some examples and their side effects:
Rate Control medications:
Reduce heart rate to less than 90bpm when resting
Eg Beta Blockers (atenolol, bisoprolol)
Calcium. Channel Blockers (Verapamil, diltiazem)
Digoxin may be prescribed if other drugs are unsuitable
Side effects:
• beta blockers – tiredness, cold hands and feet, low blood pressure, nightmares and impotence
• verapamil – constipation, low blood pressure, ankle swelling and heart failure
Digoxin – arrythmias, cardiac conduction disorder, cerebral impairment, diarrhoea, dizziness, eosinophillia, nausea, skin reactions, vision disorders, vomiting
What are rhythm medications used for in AF and give some examples of medications and their side effects:
Rhythm control medications:
Restore normal heart rhythm
Flecainide, beta blockers (particularly sotalol)
Side effects:
beta blockers – tiredness, cold hands and feet, low blood pressure, nightmares and impotence
flecainide – feeling sick, being sick and heart rhythm disorders
Why are anticoagulations used in atrial fibrillation
Reduce the chance of blood clots forming and casing a stroke
Rationale for anticoagulation choice in atrial fibrillation:
Rationale for anticoagulation choice in atrial fibrillation:
• Pregnancy – warfarin can affect the unborn baby, apixaban, dabigatran, edoxaban and rivaroxaban are also not recommended during pregnancy. Heparin injections can be given while pregnant
• Breastfedding – warfarin is usually ok while breastfeeding, heparin is safe while breastfeeding. Apixaban, dabigatran, edoxaban and rivaroxaban aren’t recommended if you’re breastfeeding because it’s not clear if they’re safe for the baby.
• Sports/avoiding injury – anticoagulant medicines can make you more prone to bleeding if you are injured
• Interactions with other medicines and remedies – prescription medicines, over the counter medicines and herbal remedies (St Johns Wort)
Food and drink – important to have a healthy, balanced diet if taking anticoagulants and you should avoid making frequent changes to the amount of green vegetables/foods high in vitamin K you eat if you are taking warfarin. Warfarin is affected by alcohol but the restrictions don’t usually apply if taking apixaban, dabigatran, edoxaban or riaroxaban
What is cardio version?
Cardioversion may be recommended for some people with atrial fibrillation.
It involves giving the heart a controlled electric shock to try to restore a normal rhythm.
Cardioversion is usually carried out in hospital so the heart can be carefully monitored.
If you have had atrial fibrillation for more than 2 days, cardioversion can increase the risk of a clot forming.
In this case, you’ll be given an anticoagulant for 3 to 4 weeks before cardioversion, and for at least 4 weeks afterwards to minimise the chance of having a stroke.
In an emergency, pictures of the heart can be taken to check for blood clots, and cardioversion can be carried out without going on medicine first.
Anticoagulation may be stopped if cardioversion is successful.
But you may need to continue taking anticoagulation after cardioversion if the risk of atrial fibrillation returning is high and you have an increased risk of having a stroke.
What is catheter ablation?
Catheter ablation is a procedure that very carefully destroys the diseased area of your heart and interrupts abnormal electrical circuits.
It’s an option if medicine has not been effective or tolerated.
Catheters (thin, soft wires) are guided through one of your veins into your heart, where they record electrical activity.
When the source of the abnormality is found, an energy source, such as high-frequency radio waves that generate heat, is transmitted through one of the catheters to destroy the tissue.
What is a pacemaker?
A pacemaker is a small battery-operated device that’s usually implanted in your chest, just below your collarbone.
It’s usually used to stop your heart beating too slowly, but in atrial fibrillation it may be used to help your heart beat regularly.
Having a pacemaker fitted is usually a minor surgical procedure carried out under a local anaesthetic (the area being operated on is numbed and you’re conscious during the procedure).
This treatment may be used when medicines are not effective or are unsuitable. This tends to be in people aged 80 or over.
NICE GUIDELINES for AF:
NICE GUIDELINES
Personalised package of care and information
1.4.1 Offer people with atrial fibrillation a personalised package of care. Ensure that the package of care is documented and delivered, and that it covers:
• stroke awareness and measures to prevent stroke
• rate control
• assessment of symptoms for rhythm control
• who to contact for advice if needed
• psychological support if needed
• up-to-date and comprehensive education and information on:
- cause, effects and possible complications of atrial fibrillation
- management of rate and rhythm control
- anticoagulation
- practical advice on anticoagulation in line with the recommendations on information and support for people having anticoagulation treatment in NICE’s guideline on venous thromboembolic diseases
1.4
- support networks (for example, cardiovascular charities). [2014] 1.4.2 Follow the recommendations in NICE’s guideline on shared decision
making. [2014]
