Cardiovascular - Level 1 Flashcards
First steps in ALS algorithm for cardiac arrests?
- Assess Response
- If no response, assess signs of life - <10 seconds
- If no signs of life, call Resus team
Second steps in ALS algorithm for cardiac arrests?
o CPR 30:2 (if just yourself, chest compressions only until person comes to attach defib)
o Attach defib monitor (one below right clavicle & one at V6 position mid-axillary line)
o Airway – insert iGel airway and ventilate using bag and mask 15L O2
Third steps in ALS algorithm for cardiac arrests?
o Assess rhythm (pause in CPR <5s)
If shockable rhythm (VF and pulseless VT) - what steps to do in cardiac arrest?
• 1 shock (150J)
o Immediately resume CPR for 2 mins and reassess rhythm
• 2nd shock
o Immediately resume CPR for 2 mins and reassess rhythm
• 3rd shock:
o Give IV adrenaline 1mg and IV amiodarone 300mg IV
- Further adrenaline 1mg IV after alternate shocks (3-5 minutes)
- Further IV 150mg amiodarone considered after 5 shocks
• If organised electrical activity compatible with cardiac output seen during rhythm check – check for signs of life, central pulse and end-tidal CO2
o If positive – start post-resuscitation care
o If negative – switch to non-shockable algorithm
• If asystole seen – switch to non-shockable algorithm
If non-shockable rhythm (PEA/asystole) - what steps to do in cardiac arrest?
- Give IV adrenaline 1mg as soon as IV access achieved
- Immediately resume CPR for 2 mins and reassess rhythm
• If electrical activity compatible with pulse seen, check for pulse or signs of life:
o If present – start post-resuscitation care
o If not present – continue CPR, recheck rhythm after 2 mins, further 1mg IV adrenaline every 3-5 minutes
• If VF/VT – change to shockable algorithm
Management in cardiac arrest when return to spontaneous circualtion?
- ABCDE approach
- Controlled oxygenation and ventilation
- 12-lead ECG
- Treat cause
- Temperature control (therapeutic hypothermia)
Management during CPR in cardiac arrest?
Oxygen, advanced airway
Vascular access (IV or IO)
1mg Adrenaline every 3-5 minutes
Correct reversible causes
What are the reversible causes in cardiac arrest? 4 H’s and 4 T’s
Hypoxia Hypovolaemia Hypo/ Hyperkalaemia/ hypoglycaemia/ hypocalcaemia/ acidaemia Hypothermia Thrombosis (coronary or pulmonary) Tamponade Toxins Tension pneumothorax
Management of reversible causes in cardiac arrest?
Hypoxia - Lungs ventilated with maximal possible inspired oxygen during CPR, check tracheal tube not misplaced
Hypovolaemia - Stop haemorrhage, restore intravascular volume with fluid and blood
Hypo/ Hyperkalaemia/ hypoglycaemia/ hypocalcaemia/ acidaemia - IV calcium chloride if hypocalcaemia, hyperkalaemia, CCB overdose
Hypothermia
Thrombosis (coronary or pulmonary)
• If cardiac thought – consider coronary angiography or PCI
• If pulmonary – give fibrinolytic drug immediately, CPR for 60-90 minutes before termination
Tamponade - Resuscitative thoracotomy after USS
Toxins
Tension pneumothorax - USS diagnosis, decompress by thoracostomy or needle thoracentesis then chest drain
Drug management in cardiac arrests?
In shockable rhythm (VF/pulseless VT)
IV adrenaline 1mg after 3rd shock and then alternate shocks (3-5 minutes)
IV amiodarone 300mg refractory to 3 shocks, further 150mg given after 5th shock
Lidocaine an alternative
In Non-shockable (asystole and pulseless electrical activity (PEA))
Give adrenaline IV 1mg when IV access achieved and then alternate shocks (3-5 minutes)
Post-cardiac arrest initial management?
- SpO2 94-98%
- Advanced airway?
- Waveform capnography
- Ventilate lungs to normocapnia
- 12-lead ECG
- Obtain reliable IV access
- Aim for SPB >100
- IV fluids (crystalloid)
- Intra-arterial blood pressure monitoring
- Consider vasopressors/inotropes to maintain SBP
• Control temperature - Constant 32-36oC
Post-cardiac arrests - subsequent management?
Likely cardiac cause?
Yes - ST elevation on 12-lead ECG
o Yes – Coronary angiogram +/- PCI
o No – consider coronary angiogram +/- PCI
Cause identified?
o Yes – admit to ICU
o No – Consider CT brain and/or CTPA
o Treat non-cardiac cause of cardiac arrest
No
• Consider CT Brain and/or CTPA
• Treat non-cardiac cause of cardiac arrest
ICU management in post cardiac arrest?
Temperature 32-35oC for 24h, prevent fever for 72 hours
Maintain normoxia and normocapnia, protective ventilation
Optimise haemodynamics (MAP, lactate, CO, urine output)
Echocardiogram
Maintain normoglycaemia
Diagnose/Treat seizures
Prevention in post-cardiac arrest management?
ICD Insertion – if ischaemic patient with significant LV dysfunction if event occurred later than 24-48h after primary coronary event
Definition of ACS?
- ACS includes unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI)
Pathology of ACS?
- Plaque rupture or erosion of cap in coronary artery with formation of platelet rich clot with vasoconstriction
- Rarely can be due to emboli or coronary artery spasm
Types of ACS?
o UA does not cause serum markers to change
o NSTEMI causes myocardial injury and elevation of troponin and CK
o STEMI is complete occlusion of coronary artery by thrombus and differentiated from NSTEMI by ECG
Epidemiology of ACS?
- 1 in 200 incidence in UK for STEMI
- 1-month mortality of ACS is 50% in community
Risk factors of ACS?
o Age, male sex, FHx
o Smoking, hyperlipidaemia, DM, hypertension, obesity, cocaine use
o Stress, increased fibrinogen
Symptoms and signs of unstable angina?
o Worsening angina or single episode of crescendo angina
o Angina at rest, increased frequency, duration or severity of pain
Symptoms and signs of ACS?
Classical Features
o Acute central chest pain
>20 mins, worsening pain at rest, unrelieved by nitrated, crushing
o Nausea, sweating, dyspnoea, palpitations
o In elderly & diabetics may be no chest pain due to neuropathy
o May present with syncope, epigastric pain, vomiting
Signs o Pallor, sweaty, clammy o Tachycardia o Changed BP o Signs of HF o Later, pericardial friction rub
DDx of ACS?
- MSK
- Pneumothorax
- Oesophagitis
- Pneumonia
- PE
- Aortic Dissection
- Cholecystitis
ECG findings in ACS? Definition of STEMI?
UA
No change/signs of ischaemia
NSTEMI
ST depression, flat or inverted T waves, or normal
STEMI
Definition
• ST elevation >1mm in two or more limb leads
• ST elevation >2mm in two or more chest leads
• New-onset LBBB
Other features
• Hyperacute tall, widened T waves
• Pathological Q waves (>1/3 size of R wave)
• May get T wave inversion later
Bloods performed in ACS?
o FBC, U&E, glucose, cholesterol
o Troponin I&T – stat and 3h post-presentation
Imaging performed in ACS?
CXR (help exclude pulmonary oedema, pneumothorax, pneumonia, PE)
o Cardiomegaly
o Pulmonary oedema
Diagnosis of myocardial infarction?
Rise of cardiac troponin with at least one of following:
History of cardiac-type ischaemic pain
New or presumed new ST changes or new LBBB
Development of pathological Q waves
Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
Intracoronary thrombus on angiogram
Initial management of UA/NSTEMI?
Morphine IV 5-10mg + metoclopramide IV 10mg
Oxygen High Flow 15L/min
Only if SpO2 <94% when aiming for 94-98% or people with COPD to aim 88-92% until ABG available
Nitrates GTN spray (if BP >90)
Sublingual
IV or buccal glycerol trinitrate given if pain unbearable
Aspirin 300mg PO loading-dose (then 75mg OD)
Ticagrelor 180mg
Continued 12 months
NSTEMI & UA if – ECG changes and >60, previous MI/CABG/CVA/TIA/PAD, CAD with 50% stenosis in 2 vessels, DM, CKD
Subsequent management of UA/NSTEMI?
Discuss with cardiologist before further management:
o Fondaparinux SC 2.5mg OD /UFH
Unless coronary angiogram planned within 24 hours of admission - UFH (if likely to undergo coronary angiography within 24 hours/renal impairment)
o Beta-blocker
Metoprolol PO if hypertensive/tachycardia/LV function <40%
After initial management, further management in UA/NSTEMI according to what score?
- GRACE Scoring Assessment (6-month mortality) o Based on HR, BP, renal function, Killip class of HF – Use calculator
Management of low risk (<3%) on Grace-score following UA/NSTEMI?
No chest pain, HF, ischaemia, ECG changes
May be discharged if second troponin negative
Treat medically and arrange further stress test & angiogram
• Can have coronary angiography if ischaemia subsequently
Management of high risk (>3%) on Grace-score following UA/NSTEMI?
Rise in troponin, Dynamic ST, T wave changes
Discuss with cardiology
• IVI of Glycoprotein 2b/3a inhibitors (eptifibatide/tirofiban)
• Coronary angiogram as inpatient (refer within < 72 hours)
o Urgent (<120 mins after presentation) if ongoing angina and evolving ST changes, signs of shock/arrhythmias
o Early (<24h) if high-risk
o Within 72h if lower risk
Definitive management options in UA/NSTEMI?
Revascularisation
o CABG
o PCI
Offer UFH in cardiac catheter lab to patients receiving fondaparinux and undergoing PCI
Other management
o Bed rest 48 hours with cardiac monitoring
o Admit for 4-7 days
General discharge advice to people after NSTEMI?
o Cardiac Rehabilitation Exercise rehab if patient wishes o Resume sexual activity when comfortable to do so, usually after 4 weeks o Physical exercise – gradual increase o Mediterranean diet best o Reduce alcohol to recommended limits o Stop smoking o Offer follow-up with cardiologist
Secondary prevention following NSTEMI? (5)
Atorvastatin 80mg (lifelong)
ACE-I (lifelong) & Beta blocker (12 months)
Offer when haemodynamically stable and titrate up to maximum tolerated dose
Aspirin 75mg OD (lifelong)
Ticagrelor 90mg BD (12 months)
Initial management of STEMI?
o IV Morphine 5-10mg + IV metoclopramide 10mg
o Oxygen High Flow 15L/min
Only if SpO2 <94% when aiming for 94-98% or people with COPD to aim 88-92% until ABG available
o Nitrates GTN spray (if BP >90)
Sublingual
IV or buccal glycerol trinitrate given if pain unbearable
o Aspirin 300mg PO loading-dose (then 75mg OD)
Subsequent management of STEMI?
- Discuss with cardiology before next drugs:
o Ticagrelor 180mg/Clopidogrel 300mg
12 months
o Beta-blocker
Metoprolol PO if hypertensive/tachycardia/LV function <40%
- Eligibility for Coronary reperfusion therapy (primary PCI or fibrinolysis)
Indications, anticoagulation and procedure of coronary angiogram and primary PCI in STEMI?
Indications
• STEMI
• Presentation <12 hours of symptoms onset
• Delivered <120 minutes of time fibrinolysis could be given
PCI + Anticoagulant
• UFH or LMWH (enoxaparin) if primary PCI (prior treatment of ticagrelor)
• Bivalirudin if primary PCI (prior treatment aspirin and clopidogrel)
Procedure
• Thrombus aspiration
• Stent used where clinically appropriate
Indications, procedure and CI of fibrinolysis in STEMI?
Indications
• Present <12 hours of onset of symptoms
• Primary PCI cannot be delivered within 120 minutes of when fibrinolysis can be given
Alteplase/Reteplase + Fondaparinux/LMWH
• ECG within 60-90 minutes
o If residual ST elevation – offer immediate coronary angiography with PCI
• Consider coronary angiography if stable after fibrinolysis
CI
• Previous intracranial haemorrhage, ischaemic stroke <6m ago, GI bleeding <1 month, Bleeding disorder, Aortic dissection, recent surgery/trauma <3weeks
Advice on discharge following STEMI?
o Cardiac Rehabilitation Exercise rehab if patient wishes o Resume sexual activity when comfortable to do so, usually after 4 weeks o Physical exercise – gradual increase o Mediterranean diet best o Reduce alcohol to recommended limits o Stop smoking o Offer follow-up with cardiologist
Secondary prevention following STEMI?
o Atorvastatin 80mg (lifelong)
o ACE-I (lifelong)
Offer when haemodynamically stable and continue indefinitely
Titrate dose upwards every 24 hours until maximum tolerated
o Aspirin 75mg OD (lifelong)
o Beta-blocker (12 months)
Offer when haemodynamically stable and titrate up to maximum tolerated dose
o Ticagrelor 90mg BD (12 months)
Prognosis following myocardial infarction?
o 50% of deaths within 2h of chest pain onset
o Up to 7% die before discharge
o Worse prognosis if elderly, LV failure and ST changes
Complications of myocardial infarction?
o Cardiac arrest o Cardiogenic shock o LVF o AF o UA o Papillary muscle rupture – causes mitral regurgitation within 1st week (inferior infarct) o Bradycardia o Tachyarrhythmias o Pericarditis o Dressler’s Syndrome 1-3 weeks post-MI Late pericarditis Fever Pericardial effusion
Causes of pulmonary oedema?
- LV failure (post-MI or IHD)
- Valvular Heart Disease
- Arrhythmias
- Malignant hypertension
- ARDS (trauma, malaria, sepsis)
- Fluid overload
- Nephrotic syndrome
Symptoms and signs of pulmonary oedema?
- Symptoms
o SOB, orthopnoea
o Pink frothy sputum
- Signs o Distressed, pale, sweaty, sitting forwards o Tachycardia, tachypnoea o Pink frothy sputum o Raised JVP o Fine lung crackles
Initial investigations of pulmonary oedema?
o ECG o CXR Cardiomegaly, bilateral shadowing, Kerley B lines, blunting of costophrenic angles o Bloods (FBC, U&E, troponin) o Urinalysis o ABG o BNP Rule out heart failure if BNP <100 (or N-terminal pro-BNP <300)
Further investigations of pulmonary oedema?
o Transthoracic Echo if stable with acute LV failure
Management of pulmonary oedema?
Sit patient up Oxygen 15L/min via Non-rebreathe mask ABG CXR IV access Bloods – FBC, U&E, LFT, CRP, troponin, BNP, Echo ECG – treat arrhythmia Furosemide 40-80mg IV bolus/infusion (larger doses needed in renal failure) Specialist advice before giving: • Diamorphine IV slowly • GTN spray • Isosorbide dinitrate IVI to keep BP >90mmHg
Further management of pulmonary oedema?
Continuous positive airway pressure (CPAP) if oxygen and diuretics do not improve condition
Once stable, what management is needed in pulmonary oedema?
Weigh daily decrease weight 0.5kg/day
Repeat CXR
Change to oral furosemide
Pacing?
Treatment after stabilisation of LV failure?
o Beta-blocker
o If reduced ejection fraction:
ACEi
Diuretic (aldosterone antagonist)
Follow up after acute heart failure?
o Specialist HF clinic in 2 weeks
Definition of hypertension? Stages of hypertension? What is white coat hypertension?
- Persistently raised arterial blood pressure
- Based on two separate readings
- Classification
o Stage 1 Hypertension – clinic BP ≥140/90 and subsequent ABPM/HBPM ≥135/85
o Stage 2 Hypertension – clinic BP ≥160/100 and subsequent ABPM/HBPM ≥150/95
o Stage 3 Hypertension – clinic BP ≥180/120 - White coat effect – persistently high BP where ABPM is >20/10 less than clinic readings
Epidemiology of hypertension?
- 30% of adults in UK
- More common in Afro-Caribbean
- Increases with age
Aetiology of hypertension?
- Primary Hypertension has no identifiable cause (90% of hypertension)
- Secondary Hypertension
o Conn’s adenoma, renovascular disease, phaeocytochroma, Steroids, Cushing’s
o Drugs, alcohol
o Thyroid disease - White Coat Hypertension
o Raised BP when measured during consultations with clinicians but normal in ‘non-threatening situations’
Risk factors of hypertension?
- Age
- Sex – males more
- Ethnicity
- Genetics
- Social Deprivation
- Smoking, alcohol, excess salt, obesity, lack of exercise
- Anxiety and emotional stress
Symptoms of hypertension?
o Usually asymptomatic
o Secondary causes may give other symptoms
Phaeocytochroma – sweating, increased HR
Signs of hypertension?
o LVH, retinopathy, proteinuria
o In end organ damage:
CVS
• Loud second heart sound, LV heave, 4th heart sound
Retina
• Grade 1 – Tortuous arteries with silver wiring walls
• Grade 2 – AV nipping
• Grade 3 – Flame haemorrhages, soft cotton wool exudates
• Grade 4 – Papilloedema
Investigations and management of that in primary care of hypertension?
- If blood pressure ≥140/90, take second reading and record lower
- If BP between 140/90-180/120, confirm with ABPM/HBPM:
o 24-ABPM at least 2 measurements per hour taken during waking hours (14 values a day) and take average
o HBPM record BDS, 2 readings seated and 1 minute apart, ideally 7 days – discard first day values
Investigations to perform whilst waiting for confirmation of hypertension diagnosis with ABPM/HBPM?
Assess QRISK2 – 10-year risk of CVD
Fundoscopy
Dipstick Urine - Haematuria
Urine Sample - Albumin/creatinine ratio
Bloods - U&Es, fasting lipids, HbA1c
ECG
Diagnosis of hypertension?
o Clinic BP >140/90 +
o ABPM or HBPM average >135/85
When to refer hypertension for same-day assessment with specialist?
o BP ≥180/120 with signs of papilloedema and/or retinal haemorrhage or new-onset confusion, chest pain, signs of heart failure, AKI
o Suspected phaeocytochroma (labile or postural hypotension, headache, palpitations, abdominal pain, diaphoresis)
Management of postural hypotension?
- If postural hypotension (systolic falls >20mmHg when standing)
o Review meds and follow-up
o If persistent then refer to cardiology
Lifestyle advice given in hypertension?
o Diet and Exercise – discourage excessive coffee/caffeine, encourage keeping sodium low
o Stress management
o Smoking
o Alcohol consumption
Management of people with Stage 1 hypertension and <40 years old?
o Consider, seek evaluation of secondary causes
When to offer antihypertensives in hypertension?
- Offer antihypertensives after ABPM/HBPM for:
o Stage 1 Hypertension (≤80 years) with 1 of following:
Target organ damage, established CVD, renal disease, diabetes, ≥10% QRISK2
Stop taking OCP recommend
Consider in Stage 1 if >80 and >150/90 or <60 with QRISK <10%
o Stage 2 Hypertension - If severe hypertension:
o Start antihypertensive immediately
Drug management in hypertension?
If <55 or T2DM
ACEi/ARB (ARB for Afro-Caribbean)
If >55, do not have T2DM or Afro-Caribbean or any age without T2DM:
CCB
If still not controlled:
ACEi/ARB + CCB
If still not controlled:
ACEi/ARB + CCB + Thiazide-like diuretic (indapamide)
If still not controlled:
ACEi/ARB + CCB + Thiazide-like diuretic + further diuretic (low-dose spironolactone if K<4.5 or high dose TLD if K>4.5, or alpha or beta blocker)
Aims of BP in hypertension?
o Age <80 (ABPM/HBPM 5 less in each)
Clinic BP ≤140/90
o Age 80 and above (ABPM/HBPM 5 less in each)
Clinic BP ≤150/90
o Type 1 Diabetic
135/85 mmHg
130/80 mmHg - If albuminuria or 2 or more features of metabolic syndrome
o Type 2 Diabetic
Clinic BP ≤140/80
Follow up in hypertension?
o How?
Clinic BP
Measure standing and seated BP in hypertension with – T2DM, symptoms of postural hypotension or age >80
o When?
High normal – 5-yearly
If only lifestyle measures advised – after 3 months
Well-controlled – Annually
Monitor response to treatment – 4 weeks after starting drug
Initiation and monitoring of ACEi/ARBs in hypertension?
o ACEi
Ramipril, lisinopril, perindopril
Oral, start at 2.5mg and titrate up to maximum 10mg dose, change dose after 4 weeks
Take first dose before bed to reduce systematic hypotension
Check U&Es before treatment, repeat 1-2 weeks into treatment and after changing dose
o ARB
Losartan, candesartan
Used when ACEi cough not tolerated
Oral dose, 50mg initially and then titrate up to maximum dose over weeks
First dose before bed
Check U&Es before treatment, repeat 1-2 weeks into treatment and after changing dose
Initiation and monitoring of CCBs in hypertension?
Amlodipine, nifedipine
May get ankle swelling
Oral, daily, 5-10mg – swallowed whole and not crushed
Check pulse and ECG before treatment
Initiation and monitoring of thiazide-like diuretics in hypertension?
Indapamide
Oral, 2.5mg daily
Take tablet in morning to prevent diuresis in sleep
Measure U&Es before starting, at 2-4 weeks and any change in dose
Complications of hypertension?
o Heart Failure
o CVD/CVA
o Chronic Kidney Disease
o Peripheral arterial disease
Definition of chronic heart failure?
- Impaired ability of heart to maintain circulation of blood due to structural/functional impairment of ventricular filling or ejection
Classifications of chronic heart failure?
o Ejection fraction – reduced or preserved
o Time-course – acute or chronic
o Left or Right Sided
o Systolic or Diastolic – ventricles either cannot contract (EF<40%) or relax (EF>50%)
Pathology of chronic heart failure?
When heart fails, compensatory mechanisms attempt to maintain output and perfusion but becomes pathogenic:
Sympathetic activation - Increase HR and contractility, venous vasoconstriction increases preload - Increased arteriole vasoconstriction causes increased afterload and decreases cardiac output
RAAS activation - Decreased CO and increased sympathetic leads to renal hypoperfusion - RAAS causes fluid and salt retention to maintain SV, causes oedema and pulmonary congestion
Natriuretic peptides - Released by endothelium, ANP/BNP/c-type peptide causes hypotension but inadequate
Ventricular Dilatation - Decreased SV and increased blood in ventricles stretches fibres and myocardial contraction initially restored
Ventricular remodelling - Hypertrophy, loss of myocytes and fibrosis
Epidemiology of chronic heart failure?
- Prevalence increases with age, average onset 76 years
- 1-3% of general population
- 10% among elderly patients
Risk factors of chronic heart failure?
- CAD, MI, hypertension, AF, DM
- Drugs, alcohol
- Family history
Aetiology of chronic heart failure?
- CCF
o IHD, cardiomyopathy, hypertension, valvular disease, congenital heart disease, arrhythmias
o Alcohol, cocaine, obesity, chemotherapy
o Pericardial disease
o Chagas disease
o Anaemia, thyrotoxicosis, sepsis, liver failure
Symptoms of chronic heart failure?
o LHF Exertional dyspnea, orthopnoea, paroxysmal nocturnal dyspnea Fatigue Nocturnal cough – pink frothy sputum Wheeze (cardiac asthma) Nocturia Cold peripheries Weight loss
o RHF Peripheral oedema Ascites Nausea Anorexia Facial engorgement Epistaxis
Signs of chronic heart failure?
Cyanosis Wheeze Tachycardia Hypertension Cardiomegaly Displaced apex beat 3rd/4th HS – gallop rhythm Increased JVP Bi-basal crackles Pleural effusion Oedema Ascites Tender hepatomegaly
Investigations in chronic heart failure?
- Bloods o U&Es, FBC, TFTs, LFTs, HbA1c, lipids, BNP - Urinalysis - ECG o Underlying causes and hypertrophy in hypertension - CXR o Alveolar Oedema (Bat wings) o Kerley B lines (interstitial oedema) o Cardiomegaly o Dilated upper lobe vessels o Pleural Effusion
Diagnosing chronic heart failure?
- Diagnosing
o If previous MI – specialist assessment and Doppler echo within 2 weeks
o If no previous MI – measure NT-proBNP
If high >2000ng/l then 2-week referral to specialist and transthoracic-echo
If raised 400-2000ng/l then 6-week referral and echo)
• BNP reduced in obesity, Afro-Caribbean origin, ACEi/ARBs, diuretics
• BNP raised in age >70, LVH, tachycardia, renal dysfunction - Echocardiogram
o Shows ventricular function, wall motion abnormalities and valve disease
What severity score is used in chronic heart failure?
- Symptomatic Severity NYHA score:
o Class I — Ordinary physical activity does not cause symptoms
o Class II —Comfortable at rest but ordinary physical activity results in undue breathlessness, fatigue, or palpitations.
o Class III —Comfortable at rest but less than ordinary physical activity results in undue breathlessness, fatigue, or palpitations.
o Class IV —Symptoms at rest can be present. If any physical activity is undertaken discomfort is increased
General advice in management of chronic heart failure?
- Specialist heart failure MDT care plan
- Report worsening symptoms
- Monitor weight weekly/biweekly
- Lifestyle advice
o Lose weight
o Enquire about salt and fluid intake
o Stop smoking
o Do not exceed NHS recommended alcohol levels
o Regular physical activity
Rehabilitation programmes designed for heart failure - Inform DVLA
- Annual flu vaccine & pneumococcal (once)
- Avoid NSAIDs, NHP CCB, flecainide, TCAs, corticosteroids, antipsychotics, cytotoxics, pioglitazone
Drug treatment in all patients with chronic heart failure?
o Loop diuretic – furosemide/bumetanide Titrate dose up and down Add spironolactone if K <3.2 o Anticoagulant if history of VTE, LV aneurysm o Statin if needed
Drug treatments in heart failure with preserved ejection fraction (>40%)?
o Loop diuretic (furosemide up to 80mg)
o Specialist advice if does not improve
Drug treatments in heart failure with redcued ejection fraction (<40%)?
1st line
ACEi/ARB - Hydralazine & Isosorbide dinitrate if not responding to ACEi
Beta-blocker - Start low dose and titrate up
Loop diuretics (furosemide) - For relief of congestive symptoms and fluid retention, titrated according to need
If still symptomatic:
Spironolactone
• If continuing to have symptoms of HF on DAB
Further management of heart failure with reduced ejection fraction (<40%) if 1st line therapy does not work?
Ivabradine • In class 2-4 with systolic dysfunction, HR >75bpm, EF <35%
Sacubitril Valsartan • In class 2-4 NYHA with LVEF <35% and already on ACEi/ARB
Amiodarone
• Need 6-month TFTs, LFTs
Digoxin
Important drug interaction to avoid in chronic heart failure?
AVOID NDHP-CCB IN HF WITH REDUCED EF, REDUCES CARDIAC CONTRACTILITY
Specialist devices/surgery used in chronic heart failure?
Implantable devices
ICDs, CRT with -Defib or -Pacing recommended when EF<35%
Assessed using QRS interval and NYHA classes
Surgery
- Transplant if severe refractory symptoms or refractory cardiogenic shock
When to refer to cardiologist in chronic heart failure?
- Severe HF – class 4
- Non-responsive to ACEi and BB treatment
- Valvular disease
- EF <35%
Follow up in chronic heart failure?
- 2 weeks if condition or drugs change
- 6 months if stable
- Done with HF nurse
o Assessment of functional capacity, fluid status, cardiac rhythm, nutritional status
o Review meds
o Assess U&Es, eGFR
o BNP in specialist care when <75 with reduced EF HF and eGFR >60
Prognosis in chronic heart failure?
Mortality is 50% in 5 years
Complications in chronic heart failure?
- AF, VF
- Depression
- Cachexia
- CKD
- Sudden Cardiac Death
Definition of DVT?
- Formation of a thrombus (blood clot) in a deep vein, which partially or completely obstructs blood flow
- Thrombus can dislodge and travel in the blood, especially to the pulmonary arteries – PE
Types of DVT?
o Provoked DVT – DVT associated with transient risk factor
o Unprovoked DVT – DVT in absence of risk factor
Epidemiology of DVT?
- DVT occurs in 1 in 1000 people a year
- Untreated DVT associated with 1-2% mortality from PE
- ½ with DVT will develop post-thrombotic syndrome – lifelong pain and swelling of leg
Risk Factor of DVT?
o Bedbound >3 days or recent surgery <12 weeks ago o Malignancy o Paralysis/Paresis/recent plaster immobilisation of lower leg o Sepsis o IVDU o Pregnancy/pelvic masses o OCP o Smoking o Previous DVT/PE, varicose veins o Thrombophilia o FHx of VTE
Symptoms of DVT?
o Unilateral leg pain o Swelling o Warm o Tender o Dilated superficial veins
When to refer in primary care for same-day assessment in DVT? What to test?
People:
• If pregnant woman or given birth in 6 weeks, IVDU
• Well DVT score of 2 or more (DVT likely)
Testing
• Proximal leg USS within 4 hours
o If unable to carry out proximal leg US within 4 hours - blood D-dimer, parenteral anticoagulation and leg vein USS within 24 hours
Management of Well’s score of 1 or less in primary care of DVT?
D-Dimer – if positive, refer for proximal leg US within 4 hours
If unable to carry out proximal leg US within 4 hours - parenteral anticoagulation and leg vein USS within 24 hours
Initial management of patient with DVT?
o Record pulse rate, RR, BP, SpO2 and Temp in all patients
o Full history and examination
Signs of plethora, deep vein tenderness, swelling (measure both legs 10cm below tibial tuberosity), oedema and dilatation
Signs of PE
o Bloods
FBC, U&Es, CRP, glucose
D-Dimer (If Wells’ score 1 or less)
• If D-Dimer normal and DVT unlikely, DVT is ruled out
What is the Well’s DVT score and how to interpret it?
A total score of 1 or less DVT is unlikely, 2 or more signifies likely DVT
- Paralysis, paresis, or recent plaster immobilization of the legs +1
- Entire leg swelling +1
- Active cancer +1
- Recently bedridden ≥3 days, or major surgery <12 weeks +1
- Localized tenderness along the distribution of the deep venous system +1
- Calf swelling by >3 cm compared with asymptomatic leg +1
- Pitting oedema (greater in symptomatic leg) +1
- Dilated superficial veins +1
- Previously documented DVT +1
- Another diagnosis more likely than DVT -2
Management of Well’s DVT score 2 or more?
- Offer - Proximal leg vein US within 4 hours – if negative, D-Dimer
- OR offer - D-Dimer test and interim 24-hour dose of parenteral anticoagulation (if proximal leg US cannot be carried out within 4 hours) then proximal leg US carried out within 24 hours
- Repeat proximal leg US 6-8 days later for all patients with positive D-Dimer and negative proximal leg US
Management of Well’s DVT score 1 or less?
Offer D-Dimer – if positive:
o Proximal leg vein US within 4 hours
o D-Dimer test and interim 24-hour dose of parenteral anticoagulation (if proximal leg US cannot be carried out within 4 hours) then proximal leg US carried out within 24 hours
Pharmacological management of diagnosed DVT within calf/thigh?
• LMWH as soon as possible for at least 5 days or until INR >2 for at least 24 hours, whichever is longer
o For severe renal impairment (eGFR <30) – Unfractionated heparin (UFH)
• Warfarin offered within 24 hours of diagnosis and continue for 3 months
o Alternatives: NOACs (Apixaban, dabigatran, rivaroxaban)
• If cannot have anticoagulation therapy:
o Temporary inferior vena cava filter
• If recurrent DVT:
o Inferior vena cava filter after alternatives (raise INR 3-4, switching to LMWH)
- Follow-up appointment to anticoagulation services and medical outpatient
- Advise to return immediately if become breathless or chest pain
Thrombolyic therapy of diagnosed DVT within calf/thigh?
• Consider catheter-directed thrombolytic therapy for patient with symptomatic iliofemoral DVT who have:
o Symptoms of <14 days, good functional status, life expectancy >1 year and low risk of bleeding
What investigations to look for cancer & thrombophilia are performed following DVT?
• Cancer investigations for unprovoked DVT:
o Examination
o CXR
o Bloods (FBC, serum Ca, LFTs)
o Urinalysis
o Consider abdomino-pelvic CT scan if >40 with 1st unprovoked DVT
• Thrombophilia testing
o Antiphospholipid antibodies in patients with unprovoked DVT if it is planned to stop anticoagulation therapy
o Hereditary thrombophilia testing – unprovoked DVT with 1st degree relative with DVT/PE if planned to stop anticoagulation
General advice given to patient with DVT?
- Engage in regular walking exercise after discharge
- Elevate affected leg when sitting
- Extended travel (by plane too) delayed until 2 weeks after starting anticoagulation treatment
When is VTE assessed in hospital?
o Assessment on admission
Any tick for thrombosis risk – VTE prophylaxis
Any tick for bleeding risk – consider if bleeding risk is sufficient to preclude pharmacological intervention
General steps to prevent VTE?
Encourage mobilise ASAP
Do not allow dehydration
When to give VTE prophylaxis in medical patients?
Start with 14 hours of admission
LMWH (Minimum 7 days)
• Fondaparinux if LMWH contraindicated
• Renal impairment – LMWH or UFH
When to give VTE prophylaxis in non-orthopaedic surgery patients?
LMWH (Minimum of 7 days)
• Fondaparinux if LMWH contraindicated
• Renal impairment – LMWH or UFH
When to give VTE prophylaxis in orthopaedic surgery patients?
Hip replacement - LMWH for 10 days followed by aspirin 75mg for 28 days (alternatives: LMWH for 28 days and anti-embolism stockings until discharge)
Knee replacement – Aspirin 75mg for 14 days (alternatives: LMWH for 14 days and anti-embolism stockings until discharge)
Fragility fractures – LMWH, starting 6-12 hours after surgery
When to give mechanical VTE prophylaxis?
Anti-embolism stockings
• Surgery patients
• Until mobile/discharged/30 days, whichever is sooner
• CI – acute stroke, PAD
Intermittent Pneumatic Compression
• Acute stroke, start within 3 days of stroke and until mobile/discharged/30 days, whichever is sooner
• Surgery patients
Complications of DVT?
o More serious complication of DVT is PE
o Post-thrombotic syndrome
Chronic venous hypertension causing limb pain, swelling, hyperpigmentation, dermatitis, ulcers and lipodermatosclerosis
Definition of symptoms in acute limb ischaemia?
6 P’s - Pain, paraesthesia, pallor, pulselessness, paralysis and perishingly cold
Epidemiology of acute limb ischaemia?
- Peripheral vascular disease present in 7% of men and 4.5% of females
- Mostly middle aged and elderly
Risk factors of acute limb ischaemia?
o Diabetes o Smoking o Hypertension o Hypercholesteremia o History of TIA/Stroke/MI
Aetiology of acute limb ischaemia?
Commonest causes are embolic or thrombotic
Embolic
• >80% - AF, post MI, prosthetic valves, vegetations, RHD
Thrombotic
• Develop acutely at atheromatous disease, history of IC likely
Compartment syndrome
Trauma
Symptoms of acute limb ischaemia?
o 6 P’s
Pain, paraesthesia, pallor, pulselessness, paralysis and perishingly cold
Signs of acute limb ischaemia?
o Check all pulses
o Mottled skin
o Signs of embolic disease (irregular pulse, abnormal heart sounds, valve clicks)
o If chronic progression – dry skin, hairless, ulceration, increased cap refill
Investigations in acute limb ischaemia?
- Bedside
o ABPI (Normal 1-1.2, PAD 0.9-0.5, limb ischaemia <0.5) and Dopler
o ECG
o Urinalysis (check for myoglobin) - Bloods
o FBC, U&E, lipids, glucose, CK, clotting, cross-match
o ABG - Imaging
o CT angiography to see extent and location
Initial management of acute limb ischaemia?
o IV analgesia (Morphine)
o Correct hypovolaemia
o Unfractionated Heparin 5000U immediately
Definitive vascular management of acute limb ischaemia?
Re-vascularisation within 4-6h
If Compartment syndrome – emergency fasciotomy
If embolic:
Surgical embolectomy (Fogarty balloon embolectomy catheter) or catheter-directed thrombolysis (tPA, streptokinase)
If fails – angiogram and bypass graft considered
If thrombotic:
Intra-arterial thrombolysis (Streptokinase, alteplase, tPA)/Angioplasty/Bypass surgery
If irreversible ischaemia – amputation required
Long-term management of acute limb ischaemia?
o Promote regular exercise, smoking cessation and weight loss
o Clopidogrel 75mg OD lifelong (alternative: aspirin)
o OT and physio assessment and rehabilitation plan
o Thrombophilia screen
Complications of acute limb ischaemia?
- Amputation16%
- Mortality 22%
Definition of superficial thrombophlebitis?
- When superficial vein, usually long saphenous vein, becomes inflamed and blood clots within it
- Usually benign and self-limiting but takes time to resolve
Different types of superficial thrombophlebitis?
- Septic thrombophlebitis – infected superficial thrombophlebitis
- Migratory thrombophlebitis – recurs in same/different/multiple veins and associated with cancer (Trousseau’s syndrome)
Risk factors of superficial thrombophlebitis?
o Varicose Veins o IV cannulation o PHx of superficial thrombophlebitis/DVT o Age >60 o Obesity o Smoking o IVDU o Hypercoagulability:
Symptoms/Signs of superficial thrombophlebitis?
- Superficial vein that is: o Hard and painful to palpate Following injury o Inflamed – hot, red, swollen - Infected superficial thrombophlebitis if features of cellulitis or a fever
Diagnosis of superficial thrombophlebitis?
- Clinical diagnosis
Managing symptoms in superficial thrombophlebitis?
o Oral ibuprofen and paracetamol PRN
o Compression stockings (Class 1)
o Warm, moist towel may sooth
o Keep leg elevated
Managing risk of VTE in superficial thrombophlebitis?
o If high risk of DVT – consult haematologist to discuss SC LMWH or fondaparinux
o If previous DVT/SP/PE – consider coagulation disorder or malignancy
o All people – continue using affected limb and remain mobile
Managing infected superficial thrombophlebitis?
o Flucloxacillin 500mg QDS for 7 days
Erythromycin or clarithromycin alternative
o If systemic illness – admit
Complications in superficial thrombophlebitis?
o Septic Thrombophlebitis
o DVT
o Skin hyperpigmentation
o Varicose veins
Prognosis in superficial thrombophlebitis?
o Usually settles within 3-4 weeks, although may be palpable for months
o Associated with varicose veins and recurrence likely
Definition of cannula-related phlebitis?
Inflammation of tunica intima of superficial vein
Due to irritation by cannula insertion
20-80% of patients with PVC develop phlebitis
Symptoms of cannula-related phlebitis?
- Erythema and swelling along venous track
* Hardened, thickened cord-like track
Assessment of cannula-related phlebitis?
• Anyone with PVC has cannula checked using Phlebitis scale every day
Prophylactic measures in cannula-related phlebitis?
- Good, aseptic practice of insertion
* Appropriate-sized cannula for vein
Treatment of cannula-related phlebitis?
- If cannula phlebitis score if high – remove cannula and resite
- Elevate affected limb
- Anti-inflammatory gel and analgesic can be given
Complications of cannula-related phlebitis?
- Superficial thrombophlebitis
- Thrombosis
- Infection
- Septic Thrombophlebitis
Definition of bradycardiac?
- Bradycardia is HR <60bpm
What causes sinus bradycardia?
o Athletes, Drugs (BB, CCB, Digoxin, Amiodarone), hypoxia, hypothyroidism, hypothermia
Pathological causes of bradycardia?
o Hypothyroidism, hypothermia, hypoxia, raised ICP, sick sinus syndrome, MI
What is Sick Sinus syndorme?
o Result of ischaemia or degeneration of SA node
o Sinus pauses (>2secs) or sinus arrest
o Escape beats may occur and occasionally tachyarrhythmias may occur (Tachy-brady syndrome)
o Patients present with dizziness, collapse, LOC or palpitations
o Continuous 24hr ECG tape shows arrhythmias
Descriptions of first degree heart block?
o Between SA and AV nodes
o Conduction from atria to ventricles occurs every time but is delayed
o PR >0.2sec (5 small squares on ECG)
Descriptions of second degree heart block?
o Only a proportion of P waves are conducted to the ventricles
o Two types:
Mobitz Type 1 (Wenckebach) – PR interval becomes increasingly lengthened until P wave fails to conduct, in AV node
Mobitz Types 2 – Failure to conduct P waves may occur regularly (e.g. 3:1) or irregularly but PR interval is constant, after AV node
Descriptions of third degree (complete) degree heart block?
o Atrial activity not conducted to ventricles
o Occurs anywhere from AV node down
o Proximal block (at AV node), proximal escape pacemaker in AV node or bundle of His may take over producing narrow QRS complexes at rate of ~50bpm
o Distal AV block, more distal escape pacemaker results in broad bizarre complexes at rate of ~30bpm
o Ventricular asystole can occur if escape pacemaker fails
o P waves and QRS waves are completely unrelated
Initial management of bradycardia according to ALS guideline?
o Assess using ABCDE Assessment Monitor SpO2 – give O2 if hypoxic Monitor ECG and BP Obtain IV access Identify any reversible causes (bloods – electrolytes)
o Any Adverse Features?
Shock, syncope, myocardial ischaemia, heart failure
Management of bradycardias if NO risk of adverse features?
Risk of asystole? – recent asystole, Mobitz Type 2, Complete HB with broad QRS, ventricular pauses >3s
• YES - Give drug measures below
• NO – Observe, stop any drugs (BB, CCB, digoxin, amiodarone), look for cause (Sick Sinus syndrome, hypothyroidism)
Management of bradycardias if YES risk of adverse features?
Atropine (500mcg IV, repeat every 3-5 minutes, up to maximum of 3mg)
• OR, Transcutaneous pacing (if atropine fails)
o Available on most defibs, select external demand pacing at 70bpm and increase pacing current
o Can give IV opioid +antiemetic if uncomfortable
• OR, Isoprenaline 5mcg/min IV
• OR, Adrenaline 2-10mcg/min IV
o Used temporarily prior to transvenous pacing if external pacemaker not available
• Alternatives: Aminophylline, dopamine, glucagon, glycopyrronium bromide
Further management of bradycardias after drug treatments?
o Seek Expert Help
Transvenous cardiac pacing
• Via jugular vein or subclavian vein
• Correctly functioning ventricular pacemaker gives pacing spike followed by widened and bizarre QRS
Permanent pacemakers and ICD
- Indicated in Mobitz Type 2 Heart Block, Complete heart block
Definition of postural hypotension?
- Drop in systolic blood pressure upon standing of >20mmHg (>30 if hypertensive) and/or fall in diastolic blood pressure of >10mmHg within 3 minutes of standing
- On standing, blood pools to lower extremities with failure of counteracting autonomic tachycardia, cardiac contractility and vascular tone
Aetiology of postural hypotension?
o Venous pooling of blood – severe varicose veins, prolonged standing
o Impaired vasomotor tone – diabetic autonomic neuropathy, Shy-Drager syndrome, amyloidosis
o Hypovolaemia – dehydration, bleeding, D&V
o Drugs – hypotensives, levodopa, phenothiazines
o Addisonian – Addison’s, hypopituitarism, abrupt cessation of steroids
Symptoms of postural hypotension?
- Symptoms of cerebral hypoperfusion o Light-headed/dizzy on standing o Blurred vision, scotoma, greying out o Weakness o Confusion o Nausea o Occur in upright posture, improve on sitting or lying down - Blackouts/Syncope
Investigations of postural hypotension?
- History and examination
o Precipitated by head-up postural change and relieved by lying flat
o Symptoms worsened by speed of positional change, coughing - Lying and standing BP
o Take BP lying down, then measure after 3 minutes standing up - Find cause:
o Blood glucose
o Urinalysis - protein
Non-pharmacological measures in postural hypotension?
o Review medications that cause hypotension
o Patients should sit first when going from supine
o Eat frequent, small meals
o Increase dietary salt and water intake
Pharmacological measures in postural hypotension?
o Fludrocortisone oral OD
o Midodrine
o Pyridostigmine
Definiton of syncope?
o Transient loss of consciousness caused by transient global cerebral hypoperfusion characterised by rapid onset, short duration and spontaneous complete recovery
Causes of syncope?
o Reflex (Neurally mediated) syncope Vasovagal Situational Carotid Sinus Syncope Atypical forms
o Orthostatic Hypotension Primary autonomic failure • MSA, Parkinson’s, Lewy body dementia Secondary Autonomic failure • Diabetes, amyloidosis, uraemia, spinal cord injuries Drug Induced • Diuretics, alcohol, vasodilators, antidepressants Volume Depletion • Haemorrhage, diarrhoea, vomiting
o Cardiac Syncope Arrhythmias • Bradycardia • Tachycardia • Drug-Induced Structural Heart Disease • Cardiac o Valvular disease o MI o Hypertrophic cardiomyopathy o Tamponade • Other o PE, acute aortic dissection, pulmonary hypertension
What is the rule of 15% in syncope?
These conditions present with syncope in 15%:
PE, aortic dissection, ACS, ectopic pregnancy, ruptured AAA, SAH
Causes of collapse?
o HEAD Hypoxia/Hypoglycaemia Epilepsy Affective Dysfucntion of brainstem
o HEART Heart Emboli Aortic obstruction (Stenosis, HOCM) Rhythm disorders Tachyarrhythmias
o VESSELS Vasovagal ENT Situational Sensitive carotid sinus Ectopic pregnancy Low vascular tone Subclavian steal
o Drugs
Antihypertensives
BB
Street drugs
Assessment of patient presenting with syncope?
o History Before, during, after Associated symptoms Recent illness Medications PMH FH
o Examination General appearance CV Resp Neurological • Cranial nerves, PNS • Cerebellar • Gait • AMTS • Fundi • NIHSS • GCS • Pupils • BMG Head & Neck
o Investigations BP – lying and standing ECG Bloods • Glucose, Hb CXR? CTPA? CT brain? EEG?
What risk assessments used in syncope?
o San Francisco Syncope rule
o OESIL Risk Score
o NIH Stroke Scale
What is the San Francisco Syncope rule?
Used to assess risk of adverse outcomes, RED FLAGS (MI, arrhythmias, PE, stroke)
• C – Hx of CHF
• H – Haematocrit <30%
• E – Abnormal ECG
• S – SOB
• S – Triage SBP <90
Refer urgently for CV assessment within 24 hours
What is OESIL risk score?
Each factor scores 1 point: • Age >65y • Hx of CV disease • Syncope without prodromes • Abnormal ECG Score of 2 or more implies risk of cardiac death – gives 12 month mortality
What is the NIH Stroke Scale?
National Institute of Health Stroke Scale
Used to assess stroke risk and severity
Managing uncomplicated (vasovagal) or situational syncope?
Inform GP
Make sure ECG recorded
Reassure person prognosis is good and explain mechanism
Advise – avoid triggers, consult GP if experience different TLoC from this episode
Management of suspected epilepsy?
Assessed by epilepsy within 2 weeks
Do not drive before assessment
Management of orthostatic hypotension?
Consider drug therapy
Discuss treatment options
Management of other causes of syncope?
Specialist CV assessment
Do not drive in this wait
Investigate for structural, arrhythmias, carotid sinus problems
Definition of vasovagal syncope?
- Due to reflex bradycardia +/- peripheral vasodilation provoked by emotion, pain, fear or standing too long
Risk Factors of vasovagal syncope?
o Overwarm o Prolonged standing o Fright o Visual stimuli (blood) o Large meals o Prolonged starvation o Alcohol o Pain o Fear
Precipitating features of vasovagal syncope?
o Onset usually preceded by nausea, pallor, sweating and closing in of visual fields (pre-syncope)
o Cannot occur if lying down flat
Symptoms/Signs of vasovagal syncope?
o Falls to ground, unconscious for ~2 minutes
o Brief clonic jerking of the limbs may occur (reflex anoxic convulsion due to cerebral hypoperfusion) – no stiffening or tonic-clonic acitivity
o May have urinary incontinence but rare
Assessment of vasovagal syncope?
- Determine urgency of treatment:
o If patient sustained injury, not made full return of consciousness, secondary to condition - Assessment
o Record details by witnesses and person
o Before, during, after
o Previous episodes, medical history, family history of cardia disease
o Vital signs, lying and standing BP
o Cardiac and neurological examination - ECG
o Red flags – conduction abnormality, long/short QT, ST segment/T wave changes - Bloods - Blood glucose, FBC
When to refer in vasovagal syncope?
- 24-hour cardiology referral if:
o ECG abnormality, HF, TLoC during exertion, FHx of SCD, SOB or murmur
o Do no drive - Refer patients for specialist epilepsy assessment if one or more of:
o Tongue biting
o Amnesia, unresponsive, unusual posturing, prolonged limb jerking
o History of prodrome
o Post-ictal confusion
When to diagnose vasovagal syncope?
o No feature suggesting other pathology
o 3P’s – Posture, provoking factors, prodromal symptoms
Management of vasovagal syncope?
o Management
Episode usually brief and recovery rapid
No immediate management
Inform GP of diagnosis and take ECG (arrange within 3 days if not done already)
o Advice
Reassure, explain mechanism
How to avoid triggers, keep record of symptoms, consult GP if further TLoC
If symptoms – lie down flat, legs up, squat on heels, aid blood back to brain
When to diagnose situational syncope?
o No features suggesting other pathology
o Clearly and consistently provoked by straining during micturition, coughing or swallowing
Management of situational syncope?
o Management
Episode usually brief and recovery rapid
No immediate management
Inform GP of diagnosis and take ECG (arrange within 3 days if not done already)
o Advice
Reassure, explain mechanism
How to avoid triggers, keep record of symptoms, consult GP if further TLoC
If symptoms – lie down flat, legs up, squat on heels, aid blood back to brain
What is Lemierre’s Syndrome?
Infectious thrombophlebitis of internal jugular vein caused by Fusobacterium necrophorum
Often develops as complication of bacterial tonsillitis in healthy, young people
May lead to sepsis, septic emboli or PE
