Cardiovascular Lecture ILO’s Flashcards
1
Q
Mean Arterial Blood Pressure =
A
Cardiac Output x Total Peripheral Resistance
2
Q
Describe the pathological process that leads to hypertension:
A
3
Q
Risk Factors for ATHEROMA
A
A - Arterial Hypertension
T- Tobacco
H- Hereditary (Familliar Hypercholesterolaemia)
E- Endocrine (diabetes, hypothyroidism, postmenopausal oestrogen deficiency)
R- Reduced physical activity
O- Obesity
M- Male gender
A- Age
Common sites: Aorta, Coronary, Carotid, Cerebral, Renal, Iliac, femoral, popliteal and intestinal arteries.
4
Q
Complications of atheroma
A
Developed atheroma can lead to thrombosis or aneurysm
Expansion of intima reduces the size of the vessel lumen
Reduced perfusion can lead to transient or permanent ischaemia.
• Coronary arteries -> angina
• Leg arteries -> intermittent claudication
• Mesenteric arteries -> ischaemic colitis
• Cerebral and vertebral arteries -> cerebrovascular events
• Severe ischaemia from partially occluded vessels can cause infarction
5
Q
Describe the key factors that contribute to BP regulation
A
• Circulatory volume (therefore stroke volume)
• Force of ventricular contraction
• Elasticity of arteries
• Peripheral resistance
6
Q
Describe the role played by arterial baroreceptors and atrial stretch receptors
A
Atrial stretch
When venous return is raised (e.g. in the case of increased circulatory volume):
Atrial myocytes release atrial natriuretic peptide (ANP), which is a vasodilator and
1. Promotes Na+ excretion – H20 follows
2. Inhibits secretion of ADH (antidiuretic
hormone or vasopressin)
7
Q
Describe the circumstances in which hypotension or hypertension may arise
A
Stress
Hormonal Factors
Type 2 Diabetes
Shock
Orthostatic (postural) hypotension
Dehydration
Arrhythmias
Shock (from severe infection, stroke, anaphylaxis, major trauma, or heart attack)
8
Q
Describe the role of the renin angio tensin aldosterone and other hormonal systems play in longer term regulation of blood pressure
A
• Renin-Angiotensin- Aldosterone System
Renin is released from cells in the walls of the afferent arterioles of kidney glomeruli.
It is released in response to lowered kidney perfusion pressures caused by, amongst other things, lowered BP.
Renin acts on a protein called angiotensinogen (gen – erates angiotensin) and cleaves this precursor at specific sites to form angiotensin I (which is inactive)
Angiotensin converting Enzyme (ACE) then converts angiotensin 1 to angiotensin 2
Angiotensin 2:
Potent vasoconstrictor
Stimulates ADH production
Activates aldosterone secretion (increases sodium production)
• Adrenaline
(Shifts the blood from one place to another)
Released from the adrenal medulla in response to lowered BP.
Does two things:
1. Speeds heart rate and force of ventricular contraction.
2. Dilates the skeletal muscle and constricts splanchnic vascular beds.
Therefore: increases cardiac output and systolic BP, but often has little effect on mean arterial BP
• Antidiuretic hormone
(ADH, vasopressin)
Released from the posterior part of the pituitary in response to decreased blood pressure and increased plasma osmolality. Release is slowed by ethanol/alcohol
Two mechanisms of action:
Promotes reabsorption of water in the kidney
Constricts blood vessels if present at a high enough concentration.
Thus, ADH increases SV and TPR, keeping BP up
• Atrial natriuretic peptide (ANP) (decreases blood pressure)
Released from the atria in response to stretch by increased blood volume.
Three mechanisms of action:
1. Promotes sodium (and thus water) excretion in the kidney.
2. Inhibits ADH and aldosterone secretion. 1. Acts as a vasodilator.
4. Can slow renin release.
Thus, ANP lowers SV and TPR, keeping BP down
9
Q
Describe the different types of muscle.
A
Smooth, skeletal and cardiac.
Skeletal:
Connected to bone, striated, voluntary, high power, usually relaxed, different fibres for different energy systems, fatigue, multi nucleated, cells fees together
Cardiac:
Striated, Involuntary, High power, Pump (cyclic), uninucleated, non fatiguing
Smooth:
Location hollow organs, Smooth, Involuntary, Low power, Usually contracted
10
Q
Explain the sliding filament theory:
A
• Calcium ions diffuse into myofibrils from sarcoplasmic reticulum
• Ca2+ cause movement of tropomyosin on actin
• This movement causes exposure of the myosin head binding sites on the actin
• Myosin heads attach to binding sites on actin forming actinomyosin bridges
• Hydrolysis f ATP on myosin heads causes them to nod
• Nodding pulls actin molecules over the myosin
• Attachment of a new ATP to each myosin head causes myosin heads to detach from actin sites and separates it from actin, returning to its original shape
11
Q
Describe an action potential within a neurone:
A
• Voltage gated sodium channels open and sodium diffuse into the axon
• This reverse potential difference across axon membrane to +40 mV (depolarisation)
• Voltage gated sodium channels close and voltage gated potassium channels open, potassium diffuses into the axon reversing the potential difference across the membrane as the axon becomes more negative (repolarisation)
• Potassium channels remain open and the membrane become hyperpolarised (-90mv, below resting potential)
• The sodium potassium pump re establish resting potential
12
Q
Describe how a resting potential is established within a neurone:
A
• 3 sodium out
• 2 potassium in
• Via sodium potassium pump
• In axon cell membrane
• Per ATP
• Membrane impermeable to sodium ions (all sodium ion channels closed)
• Some potassium channels open
• Potassium moves back out down electrochemical gradient
• Overall uneven disruption of ions resulting in more negative -70mv resting potential in the neurone
13
Q
Describe how an action potential is carried across a cholinergic synapse
A
• Action potential arrives at the pre synaptic knob and causes voltage gated calcium ions to diffuse in to the neurone
• This causes synaptic vesicles to move to the pre synaptic membrane and release acetylcholine into the synaptic cleft
• Acetly choline diffuses across the synapse and binds to receptors on the post synaptic membrane
• This causes voltage gated sodium channels to open and sodium diffuses into the post synaptic neurone
• If enough sodium enters, an action potential will be generated
• Acetyl choline is broken down by cholinesterase and products are taken up by pre synaptic membrane.
14
Q
P Wave
A
Depolarisation of atria
Right atrial activation begins first
Relatively little muscle
Small amplitude
Normal P waves may have a slight notch
15
Q
P-R Interval
A
•Time for conduction through AV node, Bundle of His, Purkinje fibres
•Time from onset of atrial depolarisation to onset of ventricular depolarisation
•Measured from start of P wave to 1st deflection of QRS complex (irrespective of whether the QRS complex begins with a Q wave or an R wave)
•Duration 0.12 – 0.20 s (3small squares to 5small squares)
If prolonged- AV node problem eg heart block
16
Q
QRS Complex
A
0.08-0.12s (3ss)
Problem with impulses in ventricles if abnormal
● Ventricular Depolarisation
● Large muscle mass of LV results in
QRS predominantly representing LV
Definitions
Q Wave: Any initial negative deflection
R Wave: Any positive deflection
S Wave: Any negative deflection after R
Normal Values
QRS Duration: < 120 ms
R wave height variable
S wave depth < 30 mm
17
Q
Q waves:
A
•Normal Q waves can be found in leads facing the left ventricle (I, II, aVL, V5, V6 )
•Occasionally occur in lead III
•< 2 mm in depth ( two small squares)
•< 40 ms in duration (one small square)
18
Q
ST Segment:
A
• QRS complex ends at J Point
• ST Segment: J Point to start of T Wave
• End of ventricular depolarisation to beginning of
repolarisation. Muscle is depolarised and is contracting -
isoelectric ≠ inactive!
• Usually level ± 1 mm from baseline - may slope slightly upwards
19
Q
QT Interval
A
0.36 - 0.45/0.47s men/female
If prolonged could be ventricular tachycardia
Total time for depolarisation & repolarisation of the ventricles
20
Q
T and U Wave
A
T Wave
• Ventricular repolarisation
• Asymmetrical
• Rarely exceeds 10 mm
U Wave
• Small deflection after T Wave
• Many ECGs have no discernable U Wave
21
Q
How to work out heart rate on an ECG?
A
300/ RR interval (in big squares)
22
Q
Which part of the heart does V1 - V6 measure on an ECG?
A
V1 - V2 Septum
V3 - V4 Anterior
V5 - V6 Lateral
23
Q
What is the difference between stable and unstable angina?
A
Stable- predicted by exercise/ change in temp
Relived by GTN spray
Unstable- sudden deterioration in angina symptoms
No ST elevation or raised troponin levels
24
Q
What is the difference between a STEMI and NSTEMI
A
STEMI- Complete blockage by thrombus
ST Elevation
Plaque ruptures leading to thrombosis
Myocardial ischemia with irreversible necrosis
NSTEMI- narrowing of the arteries
Myocardial necrosis present
Risk of progressing to STEMI
25
Describe the two methods of reperfusion therapy:
Primary PCI- putting in a wire through the femoral artery high blasts away thrombus
Thrombolysis
26
Secondary prevention of CAD
Low dose aspirin - decrease risk of death by 25%
Statins
Smoking
Diet and weight modifications
Limit alcohol
Increased exercise
Control diabetes/ alcohol
27
Describe the secondary prevention medical management after an MI (6A’s)
Aspirin - 75 mg once daily
Another antiplatelets eg clopidogrel or ticagrelor (low risk of bleeding) for up to 12 months
Atorvastatin - 80mg once daily
ACE Inhibitors (eg ramipril titrated as tolerated to 10mg once daily)
Atenolol or other beta blocker (bisnoprolol) titrated as high as tolerated
Aldosterone antagonist for those with clinical heart failure (ie eplerenone titrated to 50mg once daily)
28
NICE guidelines for stable angina:
Either a beta blocker or a calcium channel blocker first line
If the symptoms are not adequately controlled (or cannot tolerate) consider switching to an alternative or use a combination of the first two
If the patients symptoms are not adequately controlled by one or a combination then consider a third line – long acting nitrate, ivabradine or ranolazine
If in combination with a beta blocker – not verapamil or diltiazem
Only if patient cannot tolerate calcium channel blockers or beta blockers should monotherapy with nitrate, ivabradine or ranolazine be offered.
Triple therapy should be considered whilst awaiting revascularisation
29
Management of NSTEMI/ Unstable angina:
Sub lingual GTN or IV nitrates § Morphine
Oral Beta Blockers
Aspirin
Ticagrelor / Clopidogrel § ACE inhibitor
Statin
Fondaparinux
30
Acute NSTEMI treatment:
B- Beta blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)
M – Morphine titrated to control pain
A – Anticoagulant: Low Molecular Weight Heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm
O - oxygen only if their oxygen saturations are dropping (i.e. <95%).
31
Initial treatment for MI:
§ Pain relief & antiplatelets
§ Diamorphine / Morphine
§ Oxygen
§ Sublingual GTNitrate or IV
§ Aspirin
§ Cyclizine or metoclopramide
§ Thrombolysis with or without heparin
§ IV beta blockers, IV nitrates (if suitable)
§ Aspirin , ACE inhibitors , oral beta blockers . Lipid lowering agents, dual antiplatelets
§ Angiography as needed , revascularisation as needed
32
Chest Pain consultation
SOCRATES
• Site: Where exactly is the pain?
• Onset: When did it start, was it constant/intermittent, gradual/ sudden?
• Character: What is the pain like e.g. sharp, burning, tight?
• Radiation: Does it radiate/move anywhere?
• Associations: Is there anything else associated with the pain, e.g. sweating, vomiting.
• Time course: Does it follow any time pattern, how long did it last? • Exacerbating / relieving factors: Does anything make it better or
worse?
• Severity: How severe is the pain, consider using the 1-10 scale?
33
What is an aortic dissection and how is it diagnosed?
Aortic dissection/ intra-mural haematoma
Tear between intima and media in the aorta due to high pressure environment.
Often described as a tearing pain and often the worst pain they have experienced in their life time.
The pain may radiate from the chest to the back and sometimes to the abdomen.
Often has a sudden onset and can be associated with syncope and sudden collapse.
Chest X ray often shows widened aortic arch.
Can be diagnosed by contrast CT, aortic MRI or transoesophageal echocardiography
• CT scan is the most commonly used due to its high diagnostic accuracy and widespread availability.
• MRI can be used and is considered to be the gold standard but due to poor availability often not used.
34
How is aortic dissection treated?
TYPE A dissection (ascending aorta) MORE COMMON
Surgery as medication to lower blood pressure has poor response rate.
Surgery involves root repair / grafting.
TYPE B dissection (descending aorta)
Type B dissection/haematomas (descending aorta) are usually managed medically (surgery doesn’t affect overall outcomes)
• Emergency treatment is with rapid titratable beta-blockade with labetalol most commonly used.
• Aggressive blood lowering medication is then used using standard combinations of antihypertensive mediation and following the ACD antihypertensive management Rule.
• Some patients appear to benefit from subsequent aortic endovascular repair (stenting )
35
What is pericarditis?
• Pericarditis is an inflammation of the membrane surrounding the heart called the pericardium.
• Characteristic changes are visible in the ECG. Similar ST elevation but different to STEMI changes.
• Viral and bacterial infections may sometimes be the cause of the inflammation.
The chest pain of pericarditis however is aggravated by deep breathing and influenced by changes in body position.
• The pain eases for example when the breath is held or if the patient leans forward.
• Frequently pericarditis mistaken for MI as has similar Signs & Symptoms and similar but different ST elevation on the ECG.
36
What is the treatment for pericarditis and how does it sound?
NSAIDS - ibroprofen
PPI omeprazole
Pericardiocentris (needle in heart t drain fluid if patient is unstable)
Friction rub is how it sounds
37
What is myocarditis?
Involves infection of the heart causing inflammation to the myocardium.
Often due to infection by common virus (parvovirus B19) and other less common infections such as Lyme disease.
Often recent history of viral infection including fever, rash diarrhoea, sore throat and joint pain.
Myocarditis can occur alone or often seen along with pericarditis.
Typically patient presents with raised CRP and ESR and has ECG changes similar to pericarditis (saddled (bend in ST elevation). Elevated troponin levels.
38
Describe Costrocondritits (Tietze’s Syndrome).
Inflammation and swelling of the cartilage between the rib & breastbone(costochondra l or chondrosternal joint) is known as Tietze’s syndrome.
Such chest pain tends to be superficial rather than deep, is aggravated by breathing, and is very tender if the area is pressed.
• In female patients it can be missed diagnosed as mastitis pain.
• In Tietze’s syndrome pain is localised but can radiate to arms and shoulder.
• Often results from repeated coughing, sneezing or vomiting or sometimes from impacts to the chest.
39
What is the name of fluid in the capillaries and the interstitial space?
Capillary - plasma
Interstitial space- interstitial fluid
Fluid moves from the arterial end of the capillary into the interstitial space
Fluid moves from the interstitial space back into the capillary at the venous end
40
Describe capillary exchange.
Capillary blood pressure (CPB) pushes fluid out of the capillary into the interstitial fluid (taking nutrients, gases etc) - filtration
Blood colloid osmotic pressure (BCOP) pulls fluid back into capillary (bringing wastes, gases etc) – reabsorption - BCOP is mainly due to plasma proteins - re absorption
CBP decreases with progression along capillary where as BCOP remains relatively constant
CBP is greater than BCOP at the arterial end → filtration BCOP is greater than CBP at the venous end → reabsorption
Approximately 85% of fluid is reabsorbed
The remainder must be removed from the interstitial space otherwise oedema will result
The remaining 15% is picked up by the lymphatic capillaries
41
Describe the removal of excess interstitial fluid:
Lymph capillaries are blind ended tubes that are located adjacent to capillary beds
The excess interstitial fluid enters the lymphatic capillary and is called lymph Lymph passes through the lymphatic circulation and returns to the blood system
42
Describe the order of lymphatic drainage.
lymph capillaries
lymph vessels
lymph nodes
lymph trunks
thoracic duct (near bottom rib) drains lymph from remainder of the body - left subclavian vein
or
right lymphatic duct (near first rib) drains lymph from the right side of the head and thorax and right upper limb - right subclavian vein
Therefore lymph re enters the blood vascular circulation
43
How would a patient describe their palpitations?
Fluttering
Flip Flop
Pounding
Actual definition - unpleasant awareness of forceful, rapid or irregular beating of the heart
Benign vs life threatening?
Remember its a symptom and not a diagnosis
44
Name some general causes of palpitations.
Cardiac 43%
Psychiatric 31%
Miscellaneous (drugs, caffeine, thyroid etc) 10%
Unknown 16%
45
Name some cardiac causes of palpitations.
Cardiac arrhythmias due to:
• Underlying structural heart disease (e.g, cardiomyopathy, prev. MI)
• Identifiable conduction abnormality (e.g, long QT syndrome, WPW, complete heart block) • Idiopathic
• Tachyarrhythmias, bradyarrhythmias, ectopic beats
• Valvular heart disease (e.g mitral valve prolapse)
• Pacemaker syndrome (AV dysynchrony due to single chamber pacing)
• Atrial myxoma (tumour)
• High output cardiac states
46
Cardiac etiology of palpitations:
More common if:
Male
Described as irregular
Personal history of heart disease
Lasting longer than 5 mins
47
Non cardiac causes of palpitations
Psychiatric disorders
• Panic attacks
• Anxiety and Stress
• Generalised anxiety disorder
• Somatization
Other causes
• Medications
• Substance abuse
• Endocrine disorders
• Metabolic abnormalities
• Caffeine, nicotine
• Exercise
• Phaeochromocytoma
• Pregnancy
• Fever
48
Which narrow complex tachycardia has an abnormal p wave before the regular QRS complex?
Atrial tachycardia
49
Which narrow complex tachycardia has regular QRS complexes however has flutter waves
Atrial flutter
50
Which narrow complex tachycardia has no PO waves or atrial activity just after regular QRS complexes?
AVNRT or AVRT
51
Which narrow complex tachycardia has multiple p waves morphologies before irregular QRS complexes?
Multi focal atrial tachycardia
52
Which narrow complex tachycardia has flutter waves and irregular QRS complexes?
Atrial flutter with variable conduction
53
Which narrow complex tachycardia has no P waves or organised atrial activity?
Atrial fibrillation
54
What is AVNRT and how is it managed?
Commonest cause of palpitations in patients with structurally normal heart
It is like an AV node loop
NO ACCESSORY PATHWAY
Slow-Fast (common)
Fast-Slow (uncommon)
• Commoner in women (3:1)
• HR 140-280bpm
• QRS <120ms
• No P waves before the QRS complex retrograde, inverted P waves are visible immediately after QRS complexes (QRS followed by a P wave)
Management:
Depends how tachycardic
Vagal manouvres - blowing into a tube
• Adenosine
• Alternatives include beta blocker, calcium channel blocker, Amiodarone
• DC cardioversion if haemodynamic compromise
• Catheter ablation if medication doesn’t work
55
What is AVRT and how is it managed?
Atrioventricular Re-entry Tachycardia (AVRT) is a form of paroxysmal supraventricular tachycardia that occurs in patients with accessory pathways, usually due to formation of a re-entry circuit between the AV node and accessory pathway. ECG features depend on the direction of conduction, which can be orthodromic or antidromic.
(Ventricles re triggered by extra pathway)
WPW is an example :
Shortened PR interval < 120ms
Slow rise in QRS (delta wave) so QRS prolongation >110ms
Management:
Avoid drugs which block AV Node
Patients that are unstable due to this rhythm require urgent DC cardioversion
If stable follow step wise approach for AVNRT
Vagal manouvres
• Adenosine
• Alternatives include beta blocker, calcium channel blocker, Amiodarone
• DC cardioversion if haemodynamic compromise
• Catheter ablation if medication doesn’t work
56
Name some life threatening palpitations:
Ventricular tachycardia
Ventricular fibrillation
Heart block (third degree)
Fast AF
Atrial Flutter
57
Describe ventricular tachycardia:
Irregular electrical impulse in the ventricles causing the heart to beat much faster
Focal - ventricular cells irritated (hormones, thyroid, hypoxia, stretch in heart tissue, high potassium low calcium, etc) over- fire
• Reentrant- scar on heart tissue (e.g, heart attack, hypertrophic cardiomyopathy/ dilated cardiomyopathy)- electrical conduction loop abnormality- make ventricles beat rapidly
58
Describe ventricular fibrillation:
Cardiac Arrest:
caused by prolonged Vtach- walls spasming + no blood circulating-> death
SVT - VT - VF
59
How do you assess a patient with palpitations?
History
• Physical Exam
• 12 lead ECG
• Lab tests
• Further monitoring
60
What should you ask when taking a history for someone with palpitations?
• Age of onset (since childhood - SVT/ AVRT AVNRT vs older- pSVT,
atrial tachycardia or AF) Older age = red flag
• Duration of palpitations. Instant vs minutes + (over 5 mins usually cardio)
• HR and rhythm regularity – describe the rate + regularity to me- tap it out. (Provide examples if needed)
• Occasional thumps- ectopic
• Pounding in neck could be PVCs, complete heart block, VT
• Fluttering- AF, supraventricular arrhythmia
• Presyncope/ syncope- should prompt concern. Rule out VT, also can be SVT, AF, flutter
• Association with exercise/ stress
• Speed of onset/ resolution-
• random/ episodic/ an instant- premature beats.
• Gradual- sinus tachycardia
• Abrupt onset/ termination- SVT / VT
• Positional change- precipitate arrhythmia/ make person more aware of palpitations.
• AVNRT- standing up straight after bending over
• Prem. Supraventricular beats- left lateral decubitus
• Personal heart disease
• Family history- any sudden deaths in family, pacemaker, WPW syndrome, MI, Cardiomyopathy, mitral valve prolapse, prolonged QT syndrome.
• Psychiatric disorders- anxiety (what came first palps/ anxiety?)
61
Describe heart failure:
Exists when the cardiac output is insufficient to adequately perfuse the tissues despite normal filling of the heart. (Pump mechanism not efficient)
Can be chronic or acute
Can have preserved or reduced ejection fraction
62
What happens in heart failure?
Low cardiac output results in
• increased sympathetic nervous activity
• Stimulating the heart to beat & maintain the blood pressure by increasing the vascular resistance.
• Increase in the resistance against which the heart has to pump (afterload)
• Reduced renal blood flow results in renin secretion and increased plasma angiotensin & aldosterone levels.
• Na & H20 retention to increase the blood volume increasing the central venous pressure (pre-load) – oedema
63
Describe heart failure with preserved ejection fraction:
• the left ventricular wall is stiff and does not relax adequately during diastole,
• often occurring after decades of hypertension.
• left ventricle appears to eject blood effectively, reduced compliance within the ventricular
walls means that it does not fill effectively.
• Pressure then builds up behind the left ventricle (in the left atrium and lungs) giving rise to a similar clinical picture as heart failure with reduced ejection fraction.
64
Describe heart failure with reduced ejection fraction
Common LVF
• Chronic heart failure can be
– “compensated” or “decompensated.”
• In compensated heart failure, symptoms are stable
• In decompensated heart failure refers to a deterioration,
– which may present either as an acute episode of pulmonary oedema or as lethargy and malaise, – a reduction in exercise tolerance,
– and increasing breathlessness on exertion.
65
Name the causes of heart failure:
Coronary heart disease (the biggest cause!)
• Hypertension (left ventricular hypertrophy)
• Myocardial diseases – cardiomyopathies, myocarditis, and valvular diseases
• Volume overload (e.g. valvular heart disease)
• Congenital – atrial septal defect, ventricular septal defects, aortic Coarctation
• Arrhythmias, especially incessant tachyarrhythmias
• Infiltrative disease amyloidosis, sarcoidosis disease
• Iatrogenic (drug/medical cause) includes Beta blockers, antiarrhythmic drugs, calcium channel blockers (rate limiting) pioglitazone.
• Systemic stressors (e.g., anaemia, fever, infection, thyrotoxicosis)
66
What is the New York Heart Association (NYHA) HF Classification?
Class 1: asymptomatic left ventricular dysfunction is included:
No Limitations: Ordinary Physical Activity does not cause fatigue, breathlessness or palpitation
Class 2: symptomatically ‘mild’:
Slight limitation of PA. Comfortable at rest. Ordinary PA results in fatigue, palpitations breathlessness or angina.
Class 3: symptomatically ‘moderate’:
Marked limitation of PA. Although people are comfortable at rest, less than ordinary physical activity will lead to symptoms.
Class 4: symptomatically ‘severe’:
Inability to carry on physical activity with out discomfort. Symptoms of cardiac failure are present even at rest.
67
Risk factors for HF:
Myocardial infarction, coronary artery disease, or angina.
o Atrial fibrillation.
o Diabetes mellitus.
o Hypertension.
o Excessive alcohol consumption.
o Previous cardiotoxic chemotherapy (e.g. doxorubicin, daunorubicin).
o Family history of heart failure or sudden cardiac death from cardiomyopathy at a young age.
68
Signs and symptoms of heart failure:
Symptoms include:
o Breathlessness (on exertion, lying flat, or on waking).
o Fatigue.
o Fluid retention (ankle swelling, abdominal swelling).
o Decreased exercise tolerance
Orthopnoea (shortness of breath)
Paroxysmal nocturnal dyspnoea
Coughing up white froffy pinkish sputum
• Signs include:
o Laterally displaced apex beat.
o Raised jugular venous pressure.
o Enlarged liver (due to engorgement).
o Third or fourth heart sound (gallop rhythm).
o Tachycardia.
o Lung crepitations (persisting after coughing).
69
Initial investigations for suspected heart failure:
• ECG - LVH, evidence of previous MI, conduction defects eg AF, infiltrate cardiomyopathy
• chest x-ray- cardiomegaly, pulmonary oedema / enlarged heart
• blood tests -FBC, U&E’s (fluid status), LFT’s including B natriuretic peptide (BNP). ,
• Echocardiogram
• Myocardial infarction (MI) in the past -urgently referred for specialist assessment and echocardiography.
70
What is the role of an ECHO in diagnosing HF?
Excludes valve disease
Assesses systolic and diastolic function.
Detects intracardiac shunts.
Measures ventricular function - (e.g. LVEF).
An LVEF of 45–50% or more is normal.
Most people with HF have a reduced LVEF.
For people with preserved ejection fraction:
Echo shows normal or only mildly abnormal left ventricular systolic function (LVEF >= 45–50%).
May be evidence of diastolic dysfunction
71
What is BNP (B- natriuretic peptide)?
Released in response to enlarged heart.
• Secreted from the heart wall especially when stretched or when the pressure within it increases.
• Increases renal excretion of sodium and water.
• Relaxes vascular smooth muscle, which leads to vasodilation.
o N-terminalpro-BNP(NT-proBNP)
• Inactive prohormone of BNP.
• Natriuretic peptides help to determine:
o The likelihood of the presence of heart failure.
o The need for referral for specialist assessment and confirmation of the diagnosis by echocardiography.
o The urgency of the referral.
o Baseline levels should be measured on admission to hospital, to determine prognosis in acutely decompensated heart failure
72
Name some causes of elevated BNP other than heart failure:
Age over 70 years.
– Female gender.
– Left ventricular hypertrophy, myocardial ischaemia, or tachycardia.
– Hypoxia.
– Pulmonary hypertension. – Pulmonary embolism.
– Chronic kidney disease (estimated glomerular filtration rate less than 60 mL/min/1.73m2).
– Sepsis.
– Chronic obstructive pulmonary disease
(COPD).
– Diabetes mellitus. – Liver cirrhosis.
73
What BNP level demonstrates heart failure?
• A BNP of >400 pg/ml or an NT pro-BNP >2000 pg/ml suggests a strong probability of heart failure
– Refer these patients Echocardiography and a specialist assessment within two weeks
• Patients who have had a previous myocardial infarction should also be referred urgently (within two weeks) for echocardiography and specialist assessment, without carrying out natriuretic peptide testing first
• A BNP of 100-400 pg/ml or an NT pro-BNP of 400-2000 pg/ml suggests a moderate probability of heart failure
– Refer these patients for ECHO and a specialist assessment within six weeks.
74
How is chronic heart failure diagnosed according to NICE guidance?
Take a detailed history and perform a clinical examination
Measure NT- pro BNP
Perform ECG, chest x ray, blood tests,urinalysis, peak flow/spirometry
NT-proBNP results:
>2000 ng/l (236 pmol/l)
Refer urgently to be seen in 2 weeks
400-2000 ng/l
47-236 pmol/l
Refer urgently to be seen within 6 weeks
<400 ng/l (47 pmol/l)- HF not confirmed, consider other causes of symptoms
Referral:
Specialist clinical assessment including transthoracic echocardiography
If HF confirmed assess severity, establish aetiology and identify correctable causes.
75
What are the 2 aims of treatment for HF?
Provide symptom relief (decrease fluid)
Improve the prognosis for the patient
76
Name the three types of diuretics used for heart failure:
Loop (Targt loop of Henley)
Thiazide (Target distal convoluted tubule)
Aldosterone Antagonist (target last bit of the kidney)
77
Name some loop diuretics
Furosemide , Bumetanide , Torasemide
78
Complications of HF
Complications of heart failure
• Cardiac arrhythmias
• Depression
– Major depressive disorder is present in up to 20% of people with heart failure
• Cachexia (wasting)
– This is defined as 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
• Chronic kidney disease (CKD)
– CKD is common in people with heart failure and is strongly associated with increased morbidity and
mortality
• Sexual dysfunction
– Sexual dysfunction is common in people with heart failure. This may be related to cardiovascular
disease, fatigue, weakness, the use of drugs (such as beta-blockers), or depression and anxiety
• Sudden cardiac death
– About half of the deaths in people with heart failure are related to sudden cardiac death
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Acute Heart Failure
• Develops rapidly and can be immediately life-threatening due to a lack of time to undergo any compensatory changes.
• Due to acute infection (sepsis), acute myocardial infarction, heart valve dysfunction, severe arrhythmias or operations (cardiopulmonary bypass).
• managed by pharmacological, mechanical and surgical interventions despite its aetiology
Symptoms:
Coughing up pink foamy mucus
Lack of appetite/ nausea
Sudden swelling of the abdomen, legs, ankles and feet
Severe shortness of breath
Rapid, irregular heart beat
Fatigue and weakness
Sudden weight gain from fluid retention
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Pathophysiology f acute heart failure:
• Sudden inability of the heart to maintain an adequate cardiac output and blood pressure.
– Reflex arterial and venous constriction.
– Rapid rise in filling pressure of the left ventricle as a result of increased venous return
– Increase the blood retained in the left atrium and cause backflow up through the pulmonary veins which supply blood to the heart from the lungs
• If the heart is unable to expel the extra blood the hydrostatic pressure in the pulmonary veins rises until it exceeds the plasma oncotic pressure and produces pulmonary oedema.
• The principle symptom is breathlessness occurring on exertion in the early stages then at rest with orthopnoea and paroxysmal nocturnal dyspnoea (PND) attacks at night.
81
Main aim of treatment of Acute Heart Failure:
• Treat symptoms - keep patient sat up
• Restore oxygenation
• Improve organ perfusion & haemodynamics
• Limit cardiac & renal damage
• Improve post – discharge outcomes
• Minimise ICU stay
82
A patient comes to ER with suspected acute heart failure, what are the next steps?
Tests:
History/examination/ obs
Chest X Ray
Echocardiogram or NP
ECG
Blood chemistry
Oxygen saturation
FBC
Management:
• Oxygen
• High pre-load – reduce fluid volume – Diuretics
• High afterload – vasodilate – Nitrates
– such as for people with concomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease,
• Poor contractility, signs of hypoperfusion – (e.g. dobutamine, milrinone) Inotropes
• Cardiogenic shock despite treatment with an inotrope –increase blood pressure & organ perfusion – need for a vasoconstrictor– (e.g. dopamine, noradrenaline) Vasopressors
• Fluid management
83
Describe end stage heart failure:
• Breathlessness
o Optimize treatment with diuretics.
o Fluid restriction (between 1.5 L and 2 L daily).
• Pain
o Often caused by cardiac ischaemia.
o Can be relieved with morphine and nitrates.
• Anxiety, insomnia, and depression
o Can be managed with sedatives and hypnotics.
• Constipation, nausea and loss of appetite
o Can be managed with dietary changes and laxatives.
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Name tachyarrhythmias with narrow QRS and regular rhythm
Sinus Tachycardia
Focal Atrial tachycardia
AVRT/ AVNRT
Atrial Flutter
85
Name tachyarrhythmias with narrow QRS and regular rhythm
AF
AFLut with variable block
Multi focal atrial tach
86
Name tachyarrhythmias with wide QRS and regular rhythm
V Tach (monomorphic)
SVT BBB
Antidromic ART
87
Name tachyarrhythmias with wide QRS and irregular rhythm
Polymorphic V tach - long QT - tossades de point
AFib + WPW
AFib + BBB
VFib
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ECG shows
Tachycardia
Narrow QRS <0.12s (3ss)
Regular rhythm
What do you check next?
Are there P waves?
Yes - sinus tachycardia
Yes bu in lead 2 inverted P wave but everything else is normal - Focal Atrial Tachychardia
No
Lead 2,3,AVF+V1 = Saw toothed - Atrial Flutter
No
If P waves aren there/ hidden within QRS - AVRT/ AVNRT
89
What is the treatment for sinus tachycardia?
Give fluid so can see P waves
Treat underlying cause: Infection, Hypoxia?
90
How are narrow regular tachyarrhythmias treated ie Atrial Flutter, AVRT, AVNRT, FAT short and long term?
Short term:
1) Vagal Manouver (increases vagal tone, decreases AV node)
2) Adenosine 6mg (blocks AV node)
3) AFlut or FAT - Beta Blocker/ CCB
4) Cardiovert (No1 if haemodynamically unstable)
Long term:
Catheter Ablation of abnormal tissue causing extra/irregular pathway
91
ECG shows
Tachycardia
Narrow QRS <0.12s (3ss)
Irregular rhythm
What do you check next?
Are there P waves?
Yes-
Are they different shaped P waves? (>3 different shaped P waves)
Yes- multi focal atrial tachycardia (underlying disease most often)
No?
Are there AFib waves with irregular RR intervals?
Yes- Atrial Fibrillation
Are there saw toothed waves with irregular RR intervals?
Yes- Atrial Flutter with variable block
92
Treatment for Atrial Fibrillation/ Atrial Flutter w variable block/ multi FAT (narrow irregular tachychardia?
Short term:
1) Vagal Manouver (increases vagal tone, decreases AV node)
2) Adenosine 6mg (blocks AV node)
3) AFlut or FAT - Beta Blocker/ CCB
4) Cardiovert (No1 if haemodynamically unstable)
(AFIB- CHADVAS- ANTICOAGULATE)
Long term:
Catheter Ablation of abnormal tissue causing extra/irregular pathway
93
ECG shows
Tachycardia
Wide QRS >0.12s (3ss)
Regular rhythm
What do you check next?
Monomorphic V Tach
SVT BBB
Antidromic AVRT
V Tach:
Wide regular rhythm
QRS > 0.14 where as SVT BBB <0.14 >012
AV dissociate (P wave hidden by QRS)
Extreme right axis deviation
History of CVD / > 35
Always treat someone for VTach if not sure if VTach or SVT BBB
94
Treatment for wide regular tachycardia?
PUT PADS ON:
May be VTACH
Treatment:
Amiodarone to reset rhythm
Cardioversion
If certain it is SVT BBB and not VTach:
1) adenosine
2) cardioversion
3) check for underlying cause - MI-PCI? Automatic Implantable Cardiac Defib?
95
ECG shows
Tachycardia
Wide QRS >0.12s (3ss)
Irregular rhythm
What do you check next?
Polymorphic VTach- Dothey have a prolonged QT Interval prior to VTach?
Tossades de point
Do they have a normal QT interval?
AFib WPW (Don’t give ABCD (AVnode blocker)
96
Treatment for tossades de point.
Amiodarone
Cardiovert (may need to DFib)
& then give
Mg Sulphate
Replete K+
Discontinue offending meds
Isoprotenolol to increase HR and decrease QT interval
97
Treatment for AFib BBB
Beta Blocker /CCB
Cardioversion
98
Types of bradyarrhythmias:
Sinus Bradychardia
1st degree heart block
2nd degree heart bock Mobitz type 1
2nd degree heart block Mobitz type 2
Third degree heart block
99
How is bradyarrhythmias treated?
Unstable:
Atropine
Epi
PACE
Once patient is stable treat underlying cause:
Inferior Wall MI
Hypercalemia
Overdose from BB/CCB/Digoxen
Limes disease
100
What is the FrankStarling mechanism?
Ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.
101
Presentation of heart failure:
Presentation
There are some key features that patients with chronic heart failure present with:
Breathlessness worsened by exertion
Cough. They may produce frothy white/pink sputum.
Orthopnoea (the sensation of shortness of breathing when lying flat, relieves by sitting or standing). Ask them how many pillows they use at night.
Paroxysmal Nocturnal Dyspnoea (see below)
Peripheral oedema (swollen ankles)
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How is HF diagnosed?
Diagnosis
Clinical presentation
BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP)
Echocardiogram
ECG
103
Causes of HF:
Causes
Ischaemic Heart Disease
Valvular Heart Disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)
104
Management of HF:
Management
Management focuses on 2 main areas:
1. Provide symptom relief
2. Improve prognosis for the patient
To relieve symptoms of fluid overload:
· Prescribe diuretic e.g. furosemide
· Titrate the dose up/down according to symptoms
· Review the dose and adjust as necessary after introducing other drug treatments for heart failure
· Monitor renal function and serum electrolytes (before starting treatment, 1-2 weeks after starting treatment, after each dose increase) **U+Es need to be monitored closely**
To reduce morbidity and mortality prescribe:
· ACE inhibitor AND a beta blocker
· AIIRA considered in patient develops intolerable side effects to ACE inhibitor
*ACE avoided in those with valvular heart disease until indicated by specialist
Additional management:
Yearly flu and pneumococcal vaccine
Stop smoking
Optimise treatment of co-morbidities
Exercise at tolerated
First Line Medical Treatment (ABAL)
ACE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily)
Beta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily)
Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone)
Loop diuretics improves symptoms (e.g. furosemide 40mg once daily)
105
CHA2DS2VAS vs HASBLED
Congestive heart failure / LV dysfunction 1
Hypertension 1
Age >75 2
Diabetes 1
Stroke 2
Vascular disease (previous MI, PVD) 1
Age 65-74 1
Sex - female 1
Hypertension 1
Abnormal RFT’s and/or LFT’s 1 or 2
Stroke 1
Bleeding 1
Labile INR’s 1
Elderly >65 1
Drugs/Alcohol 1 or 2
score of 3 or more indicates increased one year bleed risk on anticoagulation sufficient to justify caution or more regular review
106
Clinical presentation of deep vein thrombosis (DVT)
Clinical Presentation
•Immobility
•Prominent dilated veins
•Warm tender swollen lower limb or thigh •Pain in leg, usual only in one leg
•Swelling
•Erythema
•Oedema
Positive D-dimers (blood tests to check for clot)
Positive Wells score of 2+
Positive Doppler Scan
107
Suspected DVT diagnosis and anticoagulation management (NICE GUIDELINES)
Determine 2 level DVT wells score
If higher than 2- DVT likely:
Proximal leg vein ultrasound scan within 4 hours
Or
Quantitative D-dimer test if not already done, then
Interim therapeutic anticoagulation
Scan within 24 hours
Scan positive
Diagnose DVT- continue treatment for DVT
If lower than 2- DVT unlikely:
Quantitative D-dimer test if not already done, or
Interim therapeutic anticoagulation
D dimer positive- follow procedure above
D dimer negative- stop any anticoagulation and consider other diagnoses
108
Pulmonary embolism:
Definition
• Is a condition in which one or more emboli , usually arising from a thrombus formed in the veins are lodged in & obstruct the pulmonary arterial system. It can be either provoked or unprovoked.
109
Symptoms of a pulmonary embolism:
Breathlessness
Pleuritic chest pain
Haemoptsis (pulmonary infarction)
Dizziness
Syncope- shocked, pale and sweaty
Severe central chest pain
110
What would an ECG show for a pulmonary embolism?
S-waves in lead 1
Q waves in lead 3
Inverted T waves in lead 3
111
Virchow’s Triad (clotting risk)
Hypercoagulable state:
Malignancy
Pregnancy and peri partum period
Oestrogen therapy
Trauma or surgery of lower extremities, hip, abdomen, pelvis
IBD
Vascular wall injury:
Trauma or surgery
Venepuncture
Chemical irritation
Heart valve disease/ replacement
Atherosclerosis
Circulatory status:
Atrial fibrillation
Left ventricular dysfunction
Immobility or paralysis
Venous insufficiency or varicose veins
112
Risk factors for DVT/PE
Deep vein thrombosis (DVT) is more likely to occur in people with continuing or intrinsic risk factors, such as: Previous venous thromboembolism.
Cancer (known or undiagnosed).
Age over 60 years.
Being overweight or obese.
Male sex.
Heart failure.
Severe infection.
Acquired or familial thrombophilia.
Chronic low-grade injury to the vascular wall (for example from vasculitis, hypoxia from venous stasis, or chemotherapy).
Varicose veins
Smoking
Risk factors that temporarily raise the likelihood of DVT include:
Immobility (for example following a stroke, operation, plaster cast, hospitalization, or during long-distance travel).
Significant trauma or direct trauma to a vein (for example intravenous catheter).
Hormone treatment (for example oestrogen-containing contraception or hormone replacement therapy).
Pregnancy and the postpartum period.
Dehydration.
113
Suspected PE diagnosis and initial management (NICE GUIDELINES)
Determine 2 level PE wells score
Wells score > 4 points
PE likely
Immediate CT pulmonary angiogram
Or
Interim therapeutic anticoagulation while awaiting CTPA
CTPA positive
Diagnose PE and offer or continues treatment
CTPA negative
DVT suspected
Consider proximal leg vein ultrasound scan
Wells score <4 points
PE unlikely
Quantitative D-dimer test and results in. Hours
Or
Interim therapeutic anticoagulation
D dimer positive (follow above treatment)
D dimer negative- stop any anticoagulants- think about alternative diagnosis
114
Complications of PE
• Hypoxemia
• Pulmonary Hypertension
• Right Heart failure
• Respiratory failure
• Cardiogenic shock
• Acute respiratory distress
• Sudden death
115
What is thrombolysis and when is it offered for a PE?
For people who are haemodynamically unstable thrombolytic therapy or embolectomy may be offered
Thrombolysis is the first line treatment for massive PE and may be instituted on clinical grounds alone if cardiac arrest is imminent a
50 mg bolus of Alteplase is recommended.
• Invasive approaches (thrombus fragmentation and IVC filter insertion)
should be considered where facilities and expertise are readily available.
• Thrombolysis should not be used as first line treatment in non-massive PE.
116
Absolute contra indications for thrombolysis with Alteplase:
patient currently taking warfarin (seek expert advice);
significant bleeding disorder at present or within last 6 months;
manifest or recent severe or dangerous bleeding;
recent major trauma, surgery or head injury within 3 weeks;
recent stroke within 6 months;
history of haemorrhagic stroke;
GI bleed within 1 month;
haemorrhagic diasthesis;
aortic dissection;
severe liver disease (e.g. known cirrhosis, portal hypertension);
any history of CNS damage (e.g. neoplasm);
recent puncture of a non-compressible blood vessel;
bacterial endocarditis;
pericarditis;
acute pancreatitis;
117
Investigation post VTE:
Unprovoked pulmonary embolism (PE)
investigate for the possibility of an undiagnosed cancer if they are not already known to have cancer.
Consider abdominal-pelvic CT scan (and mammogram in women) in all people over 40 years with a first unprovoked PE who do not have features of cancer based on the initial investigations above.
Consider antiphospholipid testing (anti-cardiolipin or anti-beta glycoprotein I antibodies) before stopping anticoagulants.
In people with an unprovoked PE who have a first-degree relative who has had a DVT or PE, consider arranging hereditary thrombophilia testing (antithrombin, protein C, and protein S testing).
118
DOAC’s side effects:
Common to all to varying degrees
GI disturbance- pain, dyspepsia, diarrhoea, nausea,. Altered liver function, rash & pruritis, epistaxis. Bruising and small haemorrhages
Rivaroxaban
Dizziness, may affect ability to drive headache, tachycardia, dry mouth.
119
Warfarin side effects:
Bleeding
Hypersensitivity
Skin rashes
Alopecia
Diarrhoea
Unexplained drop in haemocrit u Jaundice
Hepatic dysfunction
Purple toes
Skin necrosis
120
How to reverse warfarin and how long does IV vs oral take to work?
Phytomenadione – Vitamin K
How long does IV versus oral take to work?
Complete reversal requires ≥ 5mg IV Vitamin K
Given by IV the response is seen within 4 to 6 hours u Given orally the response is seen within 24hrs.
121
What would you recommend for a patient who has an INR >8 with no bleeding?
Stop warfarin and restart when INR <5
If other risk factors give 0.5mg by slow IV or 5mg by
mouth.
122
How would you treat a major bleed?
How would you treat a major bleed?
Stop warfarin
Give phytomenadione (vitamin K) 5-10mg by slow IV
Give prothrombin complex concentrate or fresh frozen plasma
Beriplex – ensure given Vitamin K
123
Warfarin and surgery
Usually be stopped 5 days before elective surgery;
Phytomenadione (vitamin K1) by mouth should be given the day before surgery if the INR is ≥1.5.
Patients stopping warfarin sodium prior to surgery who are considered to be at high risk of thromboembolism e.g.
-those with a venous thromboembolic event within the last 3 months
-atrial fibrillation with previous stroke or transient ischaemic attack
-or mitral mechanical heart valve
-may require interim therapy (‘bridging’) with a low molecular weight heparin (using treatment dose).
The low molecular weight heparin should be stopped at least 24 hours before surgery;
-If the surgery carries a high risk of bleeding, the low molecular weight heparin should not be restarted until at least 48 hours post surgery
-Patients on warfarin sodium who require emergency surgery that can be delayed for 6– 12 hours can be given intravenous phytomenadione (vitamin K1) to reverse the anticoagulant effect. If surgery cannot be delayed, dried prothrombin complex can be given in addition to intravenous phytomenadione (vitamin K1) and the INR checked before surgery.
124
How do you reverse the action of heparin?
Protamine
125
Supplements bought over the counter that can affect a patients INR
ALFAFA
BILBERRY
CHAMOMILE
CHINESE ANGELICA
CHONDROITIN
CO ENZYME Q10
CRANBERRY JUICE
DANSTREN
DEVILS CLAW
DONG QUAI
EVENING PRIMROSE OIL
FENUGREEK
FEVERFEW
FLAXSEED OILS
FISH OILS
GARLIC
GINGER
GINGKO
BILOBA
GINSENG
GLUCOSAMINE
GRAPEFRUIT JUICE
MULTIVITAMIN SUPPLEMENTS
RED CLOVER
ST JOHNS WORT
VITAMIN E
Foods that contain high levels of vitamin K- liver, broccoli, cauliflower, cabbage, spinach.
126
Drug interactions with DOAC’S
As clearance and mode of action differ so do the interactions
Drugs interacting with all include:
Ketaconazole and Itraconazole
Rifampicin
NSAIDs
Rivaroxaban
All –azole antimycotics
HIV protease inhibitors
Itraconazole and Voriconazole
St John’s Wort
Apixaban
Sulfinpyrazone
127
What is contained in he anticoagulant therapy folders?
The anticoagulant alert card
General information about:
Which AC, INR Range
The safe use of anticoagulants
Blood tests and dosage information
128
Main counselling points of Warfarin:
Indication for warfarin
Duration of treatment
Need for blood tests and importance of keeping appointments
If unexpected bruising or bleeding occurs, consult GP
Dose in mg+colours of tablets
Take warfarin at the same time each day
What to do if doses are missed
Further supplies of warfarin to be obtained from the GP
Avoid aspirin &NSAIDs unless prescribed intentionally
If any new medications are started or stopped,inform person monitoring blood
Ideally avoid sudden changes in diet
Alcohol–1to2 units a day may be drunk,not binge drinking
Take precautions to prevent pregnancy (if applicable)
Explain information in yellow anticoagulant booklet & contact numbers
129
Counselling on DOAC’S
Patient must be told:
How and when to take
What to do if a dose is missed
To carry a drug specific anticoagulant card (available in the product box)
Potential side effects and what to do if they feel they can’t continue taking the drug
What to do in case of unusual bleeding
OTC medicines
Rivaroxaban with food
130
Follow up with DOACS
Patients should be reviewed in the first month of taking to:
Check for side effects
Check compliance
Reinforce counselling and see if they have a warning card
They need U&Es within a year or if any concern about a change in renal function
Some NOACs are black triangle and therefore ALL side effects should be reported via yellow card system
