Cardiology Flashcards
List the types of pneumothoraces
Primary (spontaneous) – no known underlying lung disease, more likely in young, tall, thin men (often have emphysematous bullae or blebs which rupture)
Secondary – underlying lung disease e.g. asthma, COPD, lung cancer, cystic fibrosis, Marfan’s
Tension – one-way valve, progressive accumulation of air leads to rapidly increasing thoracic pressure, causes mediastinal shift, impairment of cardiac output and death if not managed rapidly
Traumatic (often tension) – stab injury, fractured rib, iatrogenic e.g. central line insertion, mechanical ventilation
Describe the presentation of pneumothoraces
Sudden onset shortness of breath – can be minor or severe depending on size and patient factors (underlying lung disease, physiological reserve)
Pleuritic chest pain
Rapid haemodynamic instability if tension
Can be asymptomatic if small
Signs:
Hyperresonance to percussion
Reduced air entry
Reduced chest expansion
Tracheal deviation away from side of pneumothorax
Tachycardia, tachypnoea, hypoxia, hypotension
May be penetrating injury through chest wall (tension), check back
How are pneumothoraces assessed and managed?
A-E assessment
If tension suspected do not delay treatment – insert wide bore cannula into 2nd intercostal space, mid-clavicular line (just above 3rd rib to avoid neurovascular bundle), then insert chest drain when stable
If bilateral/haemodynamically unstable insert chest drain
If stable –
CXR – size of pneumothorax and symptoms determine treatment, size measured as interpleural distance at level of hilum
Primary –
Size over 2cm or breathless – aspirate less than 2.5L with 16-18G cannula
If improved (less than 2cm and breathing better) – consider discharge and review in 2-4 weeks as outpatient
If not improved insert chest drain and admit
If initially less than 2cm and not breathless can consider discharge and review as outpatient in 2-4 weeks
Secondary –
More than 2cm or breathless – insert chest drain
1-2cm – aspirate less than 2.5L with 16-18G cannula
If improved with aspiration (size less than 1cm) admit, give oxygen, observe for 24 hours
If not improved insert chest drain
If initial size less than 1cm admit, give oxygen, observe for 24 hours
Where are chest drains inserted?
Triangle of safety – latissimus dorsi lateral edge (or mid-axillary line) laterally, anterior axillary line (or lateral edge of pectoris major) anteriorly, 5th intercostal line (nipple level) inferiorly
What discharge advice should be given to patients who have had a pneumothorax?
Smoking cessation to reduce risk of recurrence
Avoid diving permanently (unless have undergone bilateral pleurectomy with normal lung function and CT chest post-op)
Avoid air travel until fully resolved – 1 week post X-ray if resolved
Return if increasing breathlessness
Follow-up for X-ray to check for resolution
How are recurrent pneumothoraces managed?
High rate of recurrence
Indications for surgical intervention (first line)
2nd ipsilateral pneumothorax
1st contralateral
Synchronous bilateral spontaneous pneumothorax
Persistent air leak despite chest drain insertion (5-7 days)
Spontaneous haemothorax
Profession at risk – divers, pilots
Pregnant
Surgical options – open thoracotomy or video-assisted thoracotomy with pleurectomy, pleural abrasion
2nd line or patient unfit/unwilling to undergo surgery – chemical pleurodesis
Describe the clinical presentation of lung cancer
Cough
Pleuritic chest pain
Dyspnoea
Haemoptysis
Finger clubbing
Recurrent LRTIs
Weight loss
Night sweats
Fever
Fatigue
Lymphadenopathy
Bone pain
Extra-pulmonary manifestations –
SCC – PTHrp secretion, causes hypercalcaemia
NSCLC – ADH and ACTH secretion, limbic encephalitis, Lambert-Eaton myasthenic syndrome
Mass effects – Horner’s syndrome, superior vena cava obstruction, recurrent laryngeal nerve palsy, phrenic nerve palsy
What are the criteria for 2ww referral for suspected lung cancer?
2ww referral:
CXR findings suggestive of lung cancer
>40 with unexplained haemoptysis
Urgent X-ray (2ww):
>40 with two of (or one of if smoker) – cough, weight loss, appetite loss, dyspnoea, chest pain, fatigue
How is lung cancer diagnosed and staged?
CXR – first line, signs e.g. opacity, hilar enlargement, pleural effusion, lobar collapse
CT chest is gold-standard imaging and CT CAP used for staging
Bronchoscopy and biopsy – required to make diagnosis, confirm subtype, presence of targetable mutations e.g., EGFR
May also use PET-CT for staging
Isotope bone scan for bone mets
U+Es – hypontraemia due to SIADH in SCLC
Calcium – hypernatraemia if bone mets or PTHrp secretion in SCC
How is lung cancer managed?
Metastatic – chemotherapy +/- radiotherapy
Often prophylactic brain radiotherapy given for SCLC, usually have mets at diagnosis
Surgery – perform spirometry before to calculate likely post-op capacity and guide options
Curative, first-line in NSCLC
Lobectomy and mediastinal lymph node dissection is standard
Can also do pneumonectomy, wedge resection or sleeve resection
Targeted therapy – immune checkpoint inhibitors, used in NSCLC in patients with target mutations
EGFR – gefitinib, Osimertinib
ALK – alectinib
ROS1 – crizotinib
List complications of lung cancer
Pancoast tumour (lung apex) – Horner’s syndrome (miosis, ptosis, anhidrosis, enophthalmos), superior vena cava obstruction (facial swelling, flushing, arm swelling, venous distention)
Recurrent laryngeal nerve palsy – hoarse voice
Phrenic nerve palsy – diaphragm paralysis, respiratory compromise
Paraneoplastic syndromes:
SCC – PTHrp secretion leading to hypercalcaemia
SCLC – ADH secretion (SIADH, hyponatraemia), ACTH secretion (Cushing’s), Limbic encephalitis (anti-Hu antibodies), Lambert Eaton myasthenic syndrome
Metastases – most commonly to local lymph nodes, brain, bones, liver
Describe the cause, clinical consequences, and presentation of aortic stenosis
Cause:
Calcification with age – most common in over 65s
Congenital bicuspid aortic valve – most common in under 65s
Rheumatic fever
Consequences:
Reduced blood flow from left ventricle, increased pressure on left ventricle leading to hypertrophy to maintain stroke volume
Eventually decompensates leading to heart failure
Shearing forces degrade VWF, can cause coagulopathy e.g. GI bleeding
If calcified commonly have concurrent aortic regurgitation
Presentation:
Can be asymptomatic
Exertional dyspnoea
Angina – increased oxygen demand of LV
Syncope
Signs of heart failure
On examination –
Ejection systolic murmur, loudest in aortic region, radiates to carotids
Slow-rising pulse with narrow pulse pressure
ECG features – signs of LV hypertrophy (tall S in V1, tall R in V5/6 - over 35mm, ischaemic ST/T changes)
How is aortic stenosis managed?
Asymptomatic, valve gradient less than 40mmHg and no signs of left ventricular dysfunction – observe
Symptomatic or valve gradient more than 40mmHg or signs of left ventricular dysfunction – surgery
Surgery:
Open aortic valve replacement – young or low/medium risk
Transcatheter aortic valve replacement – high operative risk
Balloon valvuloplasty – children with no calcification, adults not fit for replacement
Describe the cause and presentation of aortic regurgitation
Cause:
Calcification
Post-rheumatic fever – most common in developing world
Connective tissue disease e.g. RA, SLE, Marfan’s, Ehler-Danlos
Bicuspid aortic valve
Spondyloarthropathy e.g. AS
Hypertension
Syphilis
Acute – infective endocarditis, aortic dissection
Presentation:
Can be asymptomatic
Exertional dyspnoea
Features of LV hypertrophy then heart failure
Collapsing pulse – Corrigan’s pulse (distension and collapse of carotids)
Early diastolic murmur loudest over aortic area, louder sitting forward in expiration
Quinke’s sign – nailbed pulsation
De Musset’s sign – head bobbing
Mid-diastolic Austin-Flint murmur
Muller’s sign – uvular pulsation
Traube’s sign – pistol shot sound on auscultation of femoral arteries
ECG –
LV hypertrophy
LA enlargement (P wave abnormalities in II and V1)
T inversion
ST depression in chest leads
How is aortic regurgitation managed?
Symptomatic or asymptomatic with LV systolic dysfunction – valve replacement
Describe the cause, clinical consequences, and presentation of mitral stenosis
Cause:
Rheumatic fever – most common cause by far
Infective endocarditis
Causes increased pressure in LA, LA dilation leading to atrial fibrillation, reduced cardiac output, congestive heart failure
Presentation:
Heart failure
Atrial fibrillation
Haemoptysis – pink frothy sputum or sudden haemorrhage due to increased pulmonary pressure and vascular congestion
Low-pitched rumbling mid-diastolic murmur, loudest in mitral region in left lateral decubitus position
May have loud S1 or opening snap
Malar flush
Low volume pulse
How is mitral stenosis managed?
AF – anticoagulation, warfarin if moderate/severe, DOAC if mild
Asymptomatic – monitor with regular echo
Symptomatic – percutaneous mitral balloon valvotomy, mitral valve surgery (commissurotomy or replacement)
Describe the cause, clinical consequences, and presentation of mitral regurgitation
Cause:
Mitral valve prolapse due to myxomatous degeneration of valve leaflets and chordae tendinae
Rheumatic fever
Infective endocarditis
Papillary muscle rupture – MI
Congenital
Cardiomyopathy
Causes backflow of blood into left atrium which leads to reduced cardiac output, meaning left ventricle increases stroke volume to compensate
Eventually causes ventricular dilatation, reduced left ventricular ejection fraction and heart failure
Presentation:
Asymptomatic
Heart failure
Pansystolic murmur, best heard in mitral region with radiation to left axilla
3rd heart sound
Displaced, hyperdynamic apex beat
ECG – LA enlargement, LV hypertrophy +/- ischaemia
How is mitral regurgitation managed?
Management of heart failure
Acute, severe regurgitation – surgical repair preferred over replacement when possible
Describe the cause and presentation of tricuspid regurgitation
Causes:
RV enlargement secondary to pulmonary hypertension
Rheumatic fever
Infectious endocarditis – especially in IVDUs
Carcinoid syndrome
Congenital
Presentation:
Pansystolic murmur
Raised JVP
V waves in jugular veins
Hepatic pulsation
Ascites
Oedema
Describe the cause and presentation of pulmonary regurgitation
Cause:
Pulmonary hypertension
Infective endocarditis
Congenital
Presentation:
Usually asymptomatic
Early diastolic murmur
Describe the cause and presentation of tricuspid stenosis
Cause:
Rheumatic fever
Congenital
Infective endocarditis
Presentation:
Mid-diastolic murmur, usually inaudible
Raised JVP with big A waves
Peripheral oedema, ascites
Describe the cause and presentation of pulmonary stenosis
Cause:
Tetralogy of Fallot
Turner’s syndrome
Noonan syndrome
William’s syndrome
Rheumatic fever
Carcinoid syndrome
Presentation:
Ejection systolic murmur
Raised JVP with A waves
RV heave
Right heart failure signs
How is valvular disease assessed and managed?
Assessment – SCRIPT
S – site (where is it loudest?)
C – character
R – radiation
I – intensity (grade)
P – pitch
T – timing (systolic or diastolic)
Grading:
1 – difficult to hear
2 – quiet
3 – easy to hear
4 – easy to hear with palpable thrill
5 – can hear with stethoscope off chest
6 – can hear from across room
ECHO – transthoracic or transoesophageal
Management:
Catheter-based interventions
Transcatheter aortic valve implantation (TAVI) most common
Open surgery
Valve repair – mitral regurgitation
Valve replacement – mechanical or tissue valves
Mechanical are lifelong but require lifelong anticoagulation with heparin then warfarin, better for younger patients
Tissue have shorter lifespan but do not require anticoagulation, better for older patients
Describe the mechanism of action of warfarin
Vitamin K antagonist to inhibit synthesis of vitamin K-dependent clotting factors – II, VII, IX, X, as well as proteins C and S
Describe the indications for warfarin therapy
VTE prophylaxis in mechanical heart valves, rheumatic heart disease, valvular atrial fibrillation, symptomatic inherited thrombophilia
2nd line (after DOACs) for VTE, AF
How are patients on warfarin monitored? What factors can impact the therapeutic effect of warfarin?
INR monitoring – ratio of patients PT to normal PT
INR targets:
2-3 – VTE, AF, mitral valve disease, inherited symptomatic thrombophilia
2.5-3.5 – mechanical heart valves
(targets vary)
Long half-life, can take 5 days to achieve stable INR in therapeutic range
Initially induces hypercoagulable state, if develop an acute VTE need heparin until INR is in therapeutic range
Things which increase action of warfarin:
CYP450 inhibitors – oral contraceptives, St John’s wort, cranberries
Liver disease
Acute illness
Things which decrease action of warfarin:
CYP450 inducers – alcohol, allopurinol, paracetamol, SSRIs, lipid-regulating drugs, influenza vaccine, foods high in vitamin K (e.g. leafy green vegetables)
Many antibiotics/antivirals interact with warfarin – check before prescribing
Describe the potential adverse effects of warfarin and reversal of warfarin
Adverse effects:
Bleeding
Teratogenic – can be used when breastfeeding
Skin necrosis
Procoagulant state when first started – concurrent heparin given
Warfarin reversal – in order of least to most potent options:
Withhold warfarin
Vitamin K – oral or IV
Prothrombin complex concentration – contains factor II, VII, IX, X
If major bleeding – do all three (withhold warfarin, give vitamin K, give PCC) and give FFP
INR >8 with minor bleeding – withhold warfarin and give vitamin K, restart when INR less than 5
INR >8 with no bleeding – withhold warfarin, give vitamin K, restart when INR less than 5
INR 5-8 with minor bleeding – withhold warfarin, give vitamin K, restart when INR less than 5
INR 5-8 with no bleeding – withhold 1 or 2 doses of warfarin, reduce subsequent maintenance dose
Describe the mechanism of action, indications, and reversal of commonly used direct oral anticoagulants
Indications:
Prevention of stroke in non-valvular AF (that meets risk factor requirements)
Prevention of VTE following surgery (hip and knee)
Treatment/prevention of DVT and PE
Dagibatran
Direct thrombin inhibitor
Mostly renal excretion
Reversal – idracizumab
Rivaroxaban
Direct factor Xa inhibitor
Mostly hepatic excretion
Reversal – andexanet alfa
Apixaban
Direct factor Xa inhibitor
Mostly faecal excretion
Reversal – andexanet alfa
Edoxaban
Direct factor Xa inhibitor
Mostly faecal excretion
No authorised reversal agent
Describe the types of heparins, their mechanisms of action, side effects and monitoring requirements
Unfractionated (standard) heparin
IV administration
Short duration of action – useful for those at high risk of bleeding, can be terminated rapidly
Mechanism of action – activates antithrombin III, forms a complex that inhibits thrombin, factors IXa, Xa, XIa and XIIa
Side effects – bleeding, heparin-induced thrombocytopaenia, osteoporosis
Monitoring – APTT
Low molecular weight heparin e.g., dalteparin, enoxaparin
Subcutaneous administration
Longer duration of action
Mechanism of action – activates antithrombin III, forms a complex that inhibits factor Xa
Side effects – bleeding, lower risk of osteoporosis
Monitoring not done routinely – can monitor anti-factor Xa
Used for prophylaxis and treatment of DVT and PE, may be used for treatment of ACS but not first line
Describe the types, mechanism of action, indications and side effects of antiplatelet drugs
Aspirin:
Inhibits COX1 and 2, prevents thromboxane A2 formation in platelets which reduced platelet aggregation
Indications – secondary prevention in cardiovascular disease, dual therapy for ACS if medically treated, PCI, second line for TIA, ischaemic stroke or peripheral arterial disease
Side effects – bleeding, dyspepsia, Reye’s syndrome in children
Thienopyridines – clopidogrel, ticagrelor, ticlopidine
Antagonise P2Y12 adenosine diphosphate (ADP) receptor, inhibiting activation of platelets
Indications – ticagrelor and aspirin for medical management of ACS, ticagrelor and aspirin for PCI, clopidogrel first line for TIA, ischaemic stroke, peripheral arterial disease
Side effects – bleeding, GI upset, PPIs decrease efficacy
Describe the management of anticoagulant drugs pre-operatively
Clopidogrel stopped 7 days prior to surgery
Warfarin stopped 5 days prior to surgery, start on therapeutic dose LMWH if high risk for VTE (usually need INR less than 1.5 for surgery to go ahead)
Aspirin usually continued
Stop taking COCP 4 weeks before surgery
Define acute coronary syndrome and describe how the subtypes are differentiated
Unstable angina – partial occlusion of coronary artery, cardiac chest pain not relieved by rest or GTN, no ST elevation/new LBBB, troponin normal
NSTEMI – complete occlusion of coronary artery without infarction of myocardium, cardiac chest pain not relieved by rest or GTN, raised troponin, no ST elevation but may have other ECG changes present (ST depression, T wave inversion)
STEMI – complete occlusion of coronary artery with full-thickness infarction of myocardium, cardiac chest pain not relieved by rest or GTN, lasting >20 minutes, raised troponin, ST elevation or new LBBB on ECG
List the types of myocardial infarction
Type 1 – ischaemia due to coronary event, usually plaque rupture
Type 2 – increased oxygen demand or reduced oxygen supply e.g. hypotension, hypovolaemia, anaemia
Type 3 – sudden cardiac death
Type 4 – associated with intervention e.g. PCI, stenting CABG
Describe the presentation of acute coronary syndrome
Chest pain – central, crushing, radiating to left arm/jaw
Associated symptoms – nausea, vomiting, sweating, SOB, palpitations
Can have ‘silent’ MI – more common in diabetes, women, elderly, features such as dizziness, SOB more prominent
Describe the initial assessment/management of acute coronary syndrome
A-E assessment, haemodynamic status
ECG
Troponin (+ routine bloods)
History of pain
CVD and risk factors
Rule out other causes e.g. CXR
Then can differentiate between unstable angina, NSTEMI, STEMI
Describe the initial management of STEMIs
Determine when pain started – if within 12 hours onset and can get to PCI centre within 2 hours of presentation can get PCI
If not get thrombolysis
O2 if sats less than 94%
If getting PCI:
IV morphine + metoclopramide
Oral aspirin 300mg + ticagrelor
IV heparin (unless already had fondaparinux or enoxaparin)
If getting thrombolysis:
IV morphine + metoclopramide
Oral aspirin 300mg
IV heparin
Oral clopidogrel (instead of ticagrelor)
Tenecteplase (thrombolysis)
Describe the initial management of NSTEMIs/unstable angina
IV morphine and metoclopramide
Oral aspirin 300mg + ticagrelor
IV heparin
NSTEMI – use GRACE score to determine need for PCI (within 4 days of admission)
Unstable angina – use GRACE score to determine whether to discharge or admit
List important causes of raised troponin
ACS – NSTEMI or STEMI
Sepsis
Heart failure
Aortic dissection
Myocarditis
PE
CKD/AKI
List contraindications to thrombolysis
Active bleeding
Previous haemorrhagic stroke/intra-cerebral haemorrhage
Cerebral neoplasm
Major trauma/surgery within 3 weeks
GI bleeding within month
Known bleeding disorder
Aortic dissection
Ischaemic stroke within 6 months
Describe the ongoing management of acute coronary syndrome following initial management
NSTEMI/STEMI – monitor in CCU for complications (arrhythmias, heart failure, myocardial rupture leading to cardiac tamponade, pericarditis, cardiogenic shock)
Secondary prevention:
Lifestyle
ACEi (or ARB if not tolerated)
Dual antiplatelet therapy – aspirin 75mg for life and ticagrelor for 3-6 months
B-blocker – atenolol
Atorvastatin
Management of anginal symptoms:
Calcium channel blockers – amlodipine or diltiazem (if not on B-blocker, don’t use with B-blocker)
Nitrates – isosorbide mononitrate
GTN spray for symptomatic relief
B-blocker
Procedural – PCI with coronary angioplasty or CABG if high-risk angina
Describe the arteries which supply specific areas of the heart and the ECG changes they correspond with
Lateral - circumflex artery
Anterior/septal - LCA
Inferior - RCA
Describe the cause, presentation, and management of Dressler’s syndrome
Cause – occurs post-MI (2-6 weeks), localised autoimmune response which causes pericarditis
Presentation
Fever
Pleuritic chest pain
Pericardial rub
Increased ESR
Cardiomegaly on CXR
ECG – global ST elevation, T wave inversion
Management
Usually self-limiting
1st line – NSAIDs
More severe – steroids
?Pericardiocentesis
How is stable angina managed?
Immediate symptomatic relief – GTN spray
Long-term symptomatic relief – calcium channel blockers, B-blocker, long acting nitrate (isosorbide nitrate)
Secondary prevention – ACEi (or ARB), aspirin, atorvastatin, B-blocker
Procedural – PCI with angioplasty or CABG if high risk/extensive ischaemic heart disease
What is the gold-standard investigation for suspected coronary artery disease?
Coronary angiography
Which vessels are most commonly used for coronary artery bypass grafting?
Great saphenous vein
Radial artery
Left internal mammary artery if LAD affected
Define aortic dissection and describe the aetiology
Tear in the tunica intima of wall of aorta
Strong association with hypertension
Predisposition in – bicuspid aortic valve, coarctation of the aorta, aortic valve replacement, CABG, Ehlers-Danlos, Marfan’s
Define aortic dissection and describe the aetiology
Tear in the tunica intima of wall of aorta
Strong association with hypertension
Predisposition in – bicuspid aortic valve, coarctation of the aorta, aortic valve replacement, CABG, Ehlers-Danlos, Marfan’s
Describe the types of aortic dissections and the presentation of aortic dissections
Stanford classification
Type A – ascending (2/3)
Type B – descending, distal to origin of left subclavian
DeBakey classification
Type 1 – ascending aorta, extending to arch and possibly beyond
Type 2 – ascending aorta only
Type 3 – originates in descending aorta, rarely extends proximally, extends distally
Presentation:
Classically tearing pain in chest/back (chest more common in type A and back in type B)
Weak or absent carotid, brachial or femoral pulse
Difference in SBP (>20mmHg) between arms
Aortic regurgitation
Hypertension
Focal neurological deficit
Syncope
Haemodynamic instability
Describe the assessment and management of aortic dissections
Investigation of choice is CT angiography CAP (whole aorta) – findings include double lumen, entry tear, aortic dilatation, end-organ malperfusion
Can use transoesophageal echo if too unstable for CT scan
Management:
A-E assessment
Analgesia – IV morphine
BP and HR control – minimise stress on aorta and limit spread of dissection, target HR 60-80, target SBP 100-120 (IV labetalol 1st line)
Surgical management dependent on type:
Type A usually need open resection of aorta and replacement with synthetic graft +/- aortic valve replacement (poor prognosis)
Type B can be managed medically initially if uncomplicated, may need endovascular stent graft placement (thoracic endovascular aortic repair, TEVAR) acutely or in long-term to prevent worsening
What are the potential complications of aortic dissection?
Acute aortic regurgitation
MI
Cardiac tamponade
Aneurysmal dilatation
Ischaemic stroke or paraplegia due to spinal artery dysfunction
Acute limb ischaemia
Renal failure
Bowel ischaemia
Describe the ECG criteria for right bundle branch block and list causes of RBBB
QRS >120
RSR pattern in V1-3
Wide slurred S wave in lateral leads – I, aVL, V5-6
MaRRoW
M in V1
W in V6
Causes:
Normal variant – more common with increasing age
RV hypertrophy
Increased RV pressure e.g. cor pulmonale
PE
MI
Atrial septal defect
Cardiomyopathy or myocarditis
How is hypertension diagnosed? Describe the staging.
Clinic reading >=140/90
Offer ambulatory BP monitoring or home BP monitoring
If 180/120 or more and retinal haemorrhage, papilloedema, life-threatening symptoms, symptoms of phaeochromocytoma refer for specialist assessment
If 150/95 or more treat regardless of age
If 135/85 or more assess cardiovascular risk and end-organ damage
If less than 135/85 not hypertensive, monitor
Assess cardiovascular risk using QRISK (if more than 10% should treat)
Assess for end-organ damage – urine dip for protein/blood, albumin:creatinine, U&Es, fundoscopy, ECG
Other CV risk factors – HbA1c, lipids
Describe management of hypertension
Lifestyle intervention
Low salt – less than 6g/day, ideally less than 3g/day
Reduce caffeine
Smoking cessation, reduce alcohol, balanced diet, exercise, weight loss
Step 1:
Under 55 or T2DM – ACEi or ARB
Over 55 or African-Caribbean – calcium channel blocker
Step 2:
If already taking ACEi/ARB add calcium channel blocker or thiazide-like diuretic
If already taking calcium channel blocker add ACEi or ARB (ARB better if Afro-Caribbean) or thiazide-like diuretic
Step 3:
Triple therapy with ACEi/ARB, calcium channel blocker and thiazide diuretic
Step 4:
If potassium less than 4.5 add spironolactone
If potassium more than 4.5 add alpha/beta-blocker
Refer to specialist
Targets:
Under 80 – aim for less than 140/90 clinic or 135/85 home
Over 80 aim for less than 150/90 clinic or 145/85 home
Describe the Well’s score
Describe the Well’s score
