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MSRA Content > Cardiovascular - Level 1 > Flashcards

Cardiovascular - Level 1 Flashcards

1
Q

First steps in ALS algorithm for cardiac arrests?

A
  • Assess Response
  • If no response, assess signs of life - <10 seconds
  • If no signs of life, call Resus team
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2
Q

Second steps in ALS algorithm for cardiac arrests?

A

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

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3
Q

Third steps in ALS algorithm for cardiac arrests?

A

o Assess rhythm (pause in CPR <5s)

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4
Q

If shockable rhythm (VF and pulseless VT) - what steps to do in cardiac arrest?

A

• 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

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5
Q

If non-shockable rhythm (PEA/asystole) - what steps to do in cardiac arrest?

A
  • 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

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6
Q

Management in cardiac arrest when return to spontaneous circualtion?

A
  • ABCDE approach
  • Controlled oxygenation and ventilation
  • 12-lead ECG
  • Treat cause
  • Temperature control (therapeutic hypothermia)
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7
Q

Management during CPR in cardiac arrest?

A

 Oxygen, advanced airway
 Vascular access (IV or IO)
 1mg Adrenaline every 3-5 minutes
 Correct reversible causes

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8
Q

What are the reversible causes in cardiac arrest? 4 H’s and 4 T’s

A 
	Hypoxia
	Hypovolaemia
	Hypo/ Hyperkalaemia/ hypoglycaemia/ hypocalcaemia/ acidaemia
	Hypothermia
	Thrombosis (coronary or pulmonary)
	Tamponade
	Toxins
	Tension pneumothorax
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9
Q

Management of reversible causes in cardiac arrest?

A

 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

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10
Q

Drug management in cardiac arrests?

A

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)

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11
Q

Post-cardiac arrest initial management?

A
  • 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

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12
Q

Post-cardiac arrests - subsequent management?

A

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

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13
Q

ICU management in post cardiac arrest?

A

 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

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14
Q

Prevention in post-cardiac arrest management?

A

 ICD Insertion – if ischaemic patient with significant LV dysfunction if event occurred later than 24-48h after primary coronary event

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15
Q

Definition of ACS?

A
  • ACS includes unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI)
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16
Q

Pathology of ACS?

A
  • 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
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17
Q

Types of ACS?

A

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

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18
Q

Epidemiology of ACS?

A
  • 1 in 200 incidence in UK for STEMI

- 1-month mortality of ACS is 50% in community

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19
Q

Risk factors of ACS?

A

o Age, male sex, FHx
o Smoking, hyperlipidaemia, DM, hypertension, obesity, cocaine use
o Stress, increased fibrinogen

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20
Q

Symptoms and signs of unstable angina?

A

o Worsening angina or single episode of crescendo angina

o Angina at rest, increased frequency, duration or severity of pain

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21
Q

Symptoms and signs of ACS?

A

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
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22
Q

DDx of ACS?

A
  • MSK
  • Pneumothorax
  • Oesophagitis
  • Pneumonia
  • PE
  • Aortic Dissection
  • Cholecystitis
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23
Q

ECG findings in ACS? Definition of STEMI?

A

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

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24
Q

Bloods performed in ACS?

A

o FBC, U&E, glucose, cholesterol

o Troponin I&T – stat and 3h post-presentation

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25
Q

Imaging performed in ACS?

A

CXR (help exclude pulmonary oedema, pneumothorax, pneumonia, PE)
o Cardiomegaly
o Pulmonary oedema

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26
Q

Diagnosis of myocardial infarction?

A

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

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27
Q

Initial management of UA/NSTEMI?

A

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

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28
Q

Subsequent management of UA/NSTEMI?

A

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%

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29
Q

After initial management, further management in UA/NSTEMI according to what score?

A 
-	GRACE Scoring Assessment (6-month mortality)
o	Based on HR, BP, renal function, Killip class of HF – Use calculator
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30
Q

Management of low risk (<3%) on Grace-score following UA/NSTEMI?

A

 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

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31
Q

Management of high risk (>3%) on Grace-score following UA/NSTEMI?

A

 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

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32
Q

Definitive management options in UA/NSTEMI?

A

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

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33
Q

General discharge advice to people after NSTEMI?

A 
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
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34
Q

Secondary prevention following NSTEMI? (5)

A

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)

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35
Q

Initial management of STEMI?

A

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)

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36
Q

Subsequent management of STEMI?

A
  • 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)
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37
Q

Indications, anticoagulation and procedure of coronary angiogram and primary PCI in STEMI?

A

 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

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38
Q

Indications, procedure and CI of fibrinolysis in STEMI?

A

 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

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39
Q

Advice on discharge following STEMI?

A 
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
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40
Q

Secondary prevention following STEMI?

A

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)

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41
Q

Prognosis following myocardial infarction?

A

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

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42
Q

Complications of myocardial infarction?

A 
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
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43
Q

Causes of pulmonary oedema?

A
  • LV failure (post-MI or IHD)
  • Valvular Heart Disease
  • Arrhythmias
  • Malignant hypertension
  • ARDS (trauma, malaria, sepsis)
  • Fluid overload
  • Nephrotic syndrome
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44
Q

Symptoms and signs of pulmonary oedema?

A
  • 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
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45
Q

Initial investigations of pulmonary oedema?

A 
o	ECG
o	CXR
	Cardiomegaly, bilateral shadowing, Kerley B lines, blunting of costophrenic angles
o	Bloods (FBC, U&amp;E, troponin)
o	Urinalysis
o	ABG
o	BNP
	Rule out heart failure if BNP <100 (or N-terminal pro-BNP <300)
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46
Q

Further investigations of pulmonary oedema?

A

o Transthoracic Echo if stable with acute LV failure

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47
Q

Management of pulmonary oedema?

A 
	Sit patient up
	Oxygen 15L/min via Non-rebreathe mask
	ABG
	CXR
	IV access
	Bloods – FBC, U&amp;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
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48
Q

Further management of pulmonary oedema?

A

 Continuous positive airway pressure (CPAP) if oxygen and diuretics do not improve condition

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49
Q

Once stable, what management is needed in pulmonary oedema?

A

 Weigh daily decrease weight 0.5kg/day
 Repeat CXR
 Change to oral furosemide
 Pacing?

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50
Q

Treatment after stabilisation of LV failure?

A

o Beta-blocker
o If reduced ejection fraction:
 ACEi
 Diuretic (aldosterone antagonist)

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51
Q

Follow up after acute heart failure?

A

o Specialist HF clinic in 2 weeks

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52
Q

Definition of hypertension? Stages of hypertension? What is white coat hypertension?

A
  • 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
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53
Q

Epidemiology of hypertension?

A
  • 30% of adults in UK
  • More common in Afro-Caribbean
  • Increases with age
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54
Q

Aetiology of hypertension?

A
  • 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’
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55
Q

Risk factors of hypertension?

A
  • Age
  • Sex – males more
  • Ethnicity
  • Genetics
  • Social Deprivation
  • Smoking, alcohol, excess salt, obesity, lack of exercise
  • Anxiety and emotional stress
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56
Q

Symptoms of hypertension?

A

o Usually asymptomatic
o Secondary causes may give other symptoms
 Phaeocytochroma – sweating, increased HR

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57
Q

Signs of hypertension?

A

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

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58
Q

Investigations and management of that in primary care of hypertension?

A
  • 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
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59
Q

Investigations to perform whilst waiting for confirmation of hypertension diagnosis with ABPM/HBPM?

A

Assess QRISK2 – 10-year risk of CVD

Fundoscopy

Dipstick Urine - Haematuria

Urine Sample - Albumin/creatinine ratio

Bloods - U&Es, fasting lipids, HbA1c

ECG

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60
Q

Diagnosis of hypertension?

A

o Clinic BP >140/90 +

o ABPM or HBPM average >135/85

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61
Q

When to refer hypertension for same-day assessment with specialist?

A

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)

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62
Q

Management of postural hypotension?

A
  • If postural hypotension (systolic falls >20mmHg when standing)
    o Review meds and follow-up
    o If persistent then refer to cardiology
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63
Q

Lifestyle advice given in hypertension?

A

o Diet and Exercise – discourage excessive coffee/caffeine, encourage keeping sodium low
o Stress management
o Smoking
o Alcohol consumption

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64
Q

Management of people with Stage 1 hypertension and <40 years old?

A

o Consider, seek evaluation of secondary causes

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65
Q

When to offer antihypertensives in hypertension?

A
  • 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
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66
Q

Drug management in hypertension?

A

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)

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67
Q

Aims of BP in hypertension?

A

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

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68
Q

Follow up in hypertension?

A

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

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69
Q

Initiation and monitoring of ACEi/ARBs in hypertension?

A

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

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70
Q

Initiation and monitoring of CCBs in hypertension?

A

 Amlodipine, nifedipine
 May get ankle swelling
 Oral, daily, 5-10mg – swallowed whole and not crushed
 Check pulse and ECG before treatment

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71
Q

Initiation and monitoring of thiazide-like diuretics in hypertension?

A

 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

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72
Q

Complications of hypertension?

A

o Heart Failure
o CVD/CVA
o Chronic Kidney Disease
o Peripheral arterial disease

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73
Q

Definition of chronic heart failure?

A
  • Impaired ability of heart to maintain circulation of blood due to structural/functional impairment of ventricular filling or ejection
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74
Q

Classifications of chronic heart failure?

A

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%)

75
Q

Pathology of chronic heart failure?

A

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

76
Q

Epidemiology of chronic heart failure?

A
  • Prevalence increases with age, average onset 76 years
  • 1-3% of general population
  • 10% among elderly patients
77
Q

Risk factors of chronic heart failure?

A
  • CAD, MI, hypertension, AF, DM
  • Drugs, alcohol
  • Family history
78
Q

Aetiology of chronic heart failure?

A
  • 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
79
Q

Symptoms of chronic heart failure?

A 
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
80
Q

Signs of chronic heart failure?

A 
	Cyanosis
	Wheeze
	Tachycardia
	Hypertension
	Cardiomegaly
	Displaced apex beat
	3rd/4th HS – gallop rhythm
	Increased JVP
	Bi-basal crackles
	Pleural effusion
	Oedema
	Ascites
	Tender hepatomegaly
81
Q

Investigations in chronic heart failure?

A 
-	Bloods
o	U&amp;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
82
Q

Diagnosing chronic heart failure?

A
  • 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
83
Q

What severity score is used in chronic heart failure?

A
  • 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
84
Q

General advice in management of chronic heart failure?

A
  • 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
85
Q

Drug treatment in all patients with chronic heart failure?

A 
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
86
Q

Drug treatments in heart failure with preserved ejection fraction (>40%)?

A

o Loop diuretic (furosemide up to 80mg)

o Specialist advice if does not improve

87
Q

Drug treatments in heart failure with redcued ejection fraction (<40%)?

A

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

88
Q

Further management of heart failure with reduced ejection fraction (<40%) if 1st line therapy does not work?

A 
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

89
Q

Important drug interaction to avoid in chronic heart failure?

A

AVOID NDHP-CCB IN HF WITH REDUCED EF, REDUCES CARDIAC CONTRACTILITY

90
Q

Specialist devices/surgery used in chronic heart failure?

A

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

91
Q

When to refer to cardiologist in chronic heart failure?

A
  • Severe HF – class 4
  • Non-responsive to ACEi and BB treatment
  • Valvular disease
  • EF <35%
92
Q

Follow up in chronic heart failure?

A
  • 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
93
Q

Prognosis in chronic heart failure?

A

Mortality is 50% in 5 years

94
Q

Complications in chronic heart failure?

A
  • AF, VF
  • Depression
  • Cachexia
  • CKD
  • Sudden Cardiac Death
95
Q

Definition of DVT?

A
  • 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
96
Q

Types of DVT?

A

o Provoked DVT – DVT associated with transient risk factor

o Unprovoked DVT – DVT in absence of risk factor

97
Q

Epidemiology of DVT?

A
  • 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
98
Q

Risk Factor of DVT?

A 
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
99
Q

Symptoms of DVT?

A 
o	Unilateral leg pain
o	Swelling
o	Warm
o	Tender
o	Dilated superficial veins
100
Q

When to refer in primary care for same-day assessment in DVT? What to test?

A

 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

101
Q

Management of Well’s score of 1 or less in primary care of DVT?

A

 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

102
Q

Initial management of patient with DVT?

A

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

103
Q

What is the Well’s DVT score and how to interpret it?

A

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
104
Q

Management of Well’s DVT score 2 or more?

A
  • 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
105
Q

Management of Well’s DVT score 1 or less?

A

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

106
Q

Pharmacological management of diagnosed DVT within calf/thigh?

A

• 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
107
Q

Thrombolyic therapy of diagnosed DVT within calf/thigh?

A

• 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

108
Q

What investigations to look for cancer & thrombophilia are performed following DVT?

A

• 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

109
Q

General advice given to patient with DVT?

A
  • 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
110
Q

When is VTE assessed in hospital?

A

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

111
Q

General steps to prevent VTE?

A

 Encourage mobilise ASAP

 Do not allow dehydration

112
Q

When to give VTE prophylaxis in medical patients?

A

 Start with 14 hours of admission
 LMWH (Minimum 7 days)
• Fondaparinux if LMWH contraindicated
• Renal impairment – LMWH or UFH

113
Q

When to give VTE prophylaxis in non-orthopaedic surgery patients?

A

 LMWH (Minimum of 7 days)
• Fondaparinux if LMWH contraindicated
• Renal impairment – LMWH or UFH

114
Q

When to give VTE prophylaxis in orthopaedic surgery patients?

A

 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

115
Q

When to give mechanical VTE prophylaxis?

A

 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

116
Q

Complications of DVT?

A

o More serious complication of DVT is PE
o Post-thrombotic syndrome
 Chronic venous hypertension causing limb pain, swelling, hyperpigmentation, dermatitis, ulcers and lipodermatosclerosis

117
Q

Definition of symptoms in acute limb ischaemia?

A

 6 P’s - Pain, paraesthesia, pallor, pulselessness, paralysis and perishingly cold

118
Q

Epidemiology of acute limb ischaemia?

A
  • Peripheral vascular disease present in 7% of men and 4.5% of females
  • Mostly middle aged and elderly
119
Q

Risk factors of acute limb ischaemia?

A 
o	Diabetes
o	Smoking
o	Hypertension
o	Hypercholesteremia
o	History of TIA/Stroke/MI
120
Q

Aetiology of acute limb ischaemia?

A

 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

121
Q

Symptoms of acute limb ischaemia?

A

o 6 P’s

 Pain, paraesthesia, pallor, pulselessness, paralysis and perishingly cold

122
Q

Signs of acute limb ischaemia?

A

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

123
Q

Investigations in acute limb ischaemia?

A
  • 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
124
Q

Initial management of acute limb ischaemia?

A

o IV analgesia (Morphine)
o Correct hypovolaemia
o Unfractionated Heparin 5000U immediately

125
Q

Definitive vascular management of acute limb ischaemia?

A

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

126
Q

Long-term management of acute limb ischaemia?

A

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

127
Q

Complications of acute limb ischaemia?

A
  • Amputation16%

- Mortality 22%

128
Q

Definition of superficial thrombophlebitis?

A
  • When superficial vein, usually long saphenous vein, becomes inflamed and blood clots within it
  • Usually benign and self-limiting but takes time to resolve
129
Q

Different types of superficial thrombophlebitis?

A
  • Septic thrombophlebitis – infected superficial thrombophlebitis
  • Migratory thrombophlebitis – recurs in same/different/multiple veins and associated with cancer (Trousseau’s syndrome)
130
Q

Risk factors of superficial thrombophlebitis?

A 
o	Varicose Veins
o	IV cannulation
o	PHx of superficial thrombophlebitis/DVT
o	Age >60
o	Obesity
o	Smoking 
o	IVDU
o	Hypercoagulability:
131
Q

Symptoms/Signs of superficial thrombophlebitis?

A 
-	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
132
Q

Diagnosis of superficial thrombophlebitis?

A
  • Clinical diagnosis
133
Q

Managing symptoms in superficial thrombophlebitis?

A

o Oral ibuprofen and paracetamol PRN
o Compression stockings (Class 1)
o Warm, moist towel may sooth
o Keep leg elevated

134
Q

Managing risk of VTE in superficial thrombophlebitis?

A

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

135
Q

Managing infected superficial thrombophlebitis?

A

o Flucloxacillin 500mg QDS for 7 days
 Erythromycin or clarithromycin alternative
o If systemic illness – admit

136
Q

Complications in superficial thrombophlebitis?

A

o Septic Thrombophlebitis
o DVT
o Skin hyperpigmentation
o Varicose veins

137
Q

Prognosis in superficial thrombophlebitis?

A

o Usually settles within 3-4 weeks, although may be palpable for months
o Associated with varicose veins and recurrence likely

138
Q

Definition of cannula-related phlebitis?

A

 Inflammation of tunica intima of superficial vein
 Due to irritation by cannula insertion
 20-80% of patients with PVC develop phlebitis

139
Q

Symptoms of cannula-related phlebitis?

A
  • Erythema and swelling along venous track

* Hardened, thickened cord-like track

140
Q

Assessment of cannula-related phlebitis?

A

• Anyone with PVC has cannula checked using Phlebitis scale every day

141
Q

Prophylactic measures in cannula-related phlebitis?

A
  • Good, aseptic practice of insertion

* Appropriate-sized cannula for vein

142
Q

Treatment of cannula-related phlebitis?

A
  • If cannula phlebitis score if high – remove cannula and resite
  • Elevate affected limb
  • Anti-inflammatory gel and analgesic can be given
143
Q

Complications of cannula-related phlebitis?

A
  • Superficial thrombophlebitis
  • Thrombosis
  • Infection
  • Septic Thrombophlebitis
144
Q

Definition of bradycardiac?

A
  • Bradycardia is HR <60bpm
145
Q

What causes sinus bradycardia?

A

o Athletes, Drugs (BB, CCB, Digoxin, Amiodarone), hypoxia, hypothyroidism, hypothermia

146
Q

Pathological causes of bradycardia?

A

o Hypothyroidism, hypothermia, hypoxia, raised ICP, sick sinus syndrome, MI

147
Q

What is Sick Sinus syndorme?

A

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

148
Q

Descriptions of first degree heart block?

A

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)

149
Q

Descriptions of second degree heart block?

A

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

150
Q

Descriptions of third degree (complete) degree heart block?

A

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

151
Q

Initial management of bradycardia according to ALS guideline?

A 
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

152
Q

Management of bradycardias if NO risk of adverse features?

A

 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)

153
Q

Management of bradycardias if YES risk of adverse features?

A

 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

154
Q

Further management of bradycardias after drug treatments?

A

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

155
Q

Definition of postural hypotension?

A
  • 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
156
Q

Aetiology of postural hypotension?

A

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

157
Q

Symptoms of postural hypotension?

A 
-	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
158
Q

Investigations of postural hypotension?

A
  • 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
159
Q

Non-pharmacological measures in postural hypotension?

A

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

160
Q

Pharmacological measures in postural hypotension?

A

o Fludrocortisone oral OD
o Midodrine
o Pyridostigmine

161
Q

Definiton of syncope?

A

o Transient loss of consciousness caused by transient global cerebral hypoperfusion characterised by rapid onset, short duration and spontaneous complete recovery

162
Q

Causes of syncope?

A 
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
163
Q

What is the rule of 15% in syncope?

A

These conditions present with syncope in 15%:

PE, aortic dissection, ACS, ectopic pregnancy, ruptured AAA, SAH

164
Q

Causes of collapse?

A 
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

165
Q

Assessment of patient presenting with syncope?

A 
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 &amp; Neck
o	Investigations
	BP – lying and standing
	ECG
	Bloods
•	Glucose, Hb
	CXR?
	CTPA?
	CT brain?
	EEG?
166
Q

What risk assessments used in syncope?

A

o San Francisco Syncope rule
o OESIL Risk Score
o NIH Stroke Scale

167
Q

What is the San Francisco Syncope rule?

A

 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

168
Q

What is OESIL risk score?

A 
	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
169
Q

What is the NIH Stroke Scale?

A

National Institute of Health Stroke Scale

Used to assess stroke risk and severity

170
Q

Managing uncomplicated (vasovagal) or situational syncope?

A

 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

171
Q

Management of suspected epilepsy?

A

 Assessed by epilepsy within 2 weeks

 Do not drive before assessment

172
Q

Management of orthostatic hypotension?

A

 Consider drug therapy

 Discuss treatment options

173
Q

Management of other causes of syncope?

A

 Specialist CV assessment
 Do not drive in this wait
 Investigate for structural, arrhythmias, carotid sinus problems

174
Q

Definition of vasovagal syncope?

A
  • Due to reflex bradycardia +/- peripheral vasodilation provoked by emotion, pain, fear or standing too long
175
Q

Risk Factors of vasovagal syncope?

A 
o	Overwarm
o	Prolonged standing
o	Fright
o	Visual stimuli (blood)
o	Large meals
o	Prolonged starvation
o	Alcohol
o	Pain
o	Fear
176
Q

Precipitating features of vasovagal syncope?

A

o Onset usually preceded by nausea, pallor, sweating and closing in of visual fields (pre-syncope)
o Cannot occur if lying down flat

177
Q

Symptoms/Signs of vasovagal syncope?

A

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

178
Q

Assessment of vasovagal syncope?

A
  • 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
179
Q

When to refer in vasovagal syncope?

A
  • 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
180
Q

When to diagnose vasovagal syncope?

A

o No feature suggesting other pathology

o 3P’s – Posture, provoking factors, prodromal symptoms

181
Q

Management of vasovagal syncope?

A

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

182
Q

When to diagnose situational syncope?

A

o No features suggesting other pathology

o Clearly and consistently provoked by straining during micturition, coughing or swallowing

183
Q

Management of situational syncope?

A

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

184
Q

What is Lemierre’s Syndrome?

A

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

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